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Li, methanol) Capillaries: v large pores; MW 20,000-30,000 can pass (most brain capillaries aren’t this leaky except at pituitary and pineal gland, median eminence, choroid plexus) 2) Lipid diffusion: through membrane driven by conc grad; must be lipid soluble, though must be dissolved in water in order to reach membrane 3) Facilitated diffusion (via carriers): eg. Needed to cross BBB, for weak acids in PCT of kidney 4) Pinocytosis (receptor mediated endocytosis): for drugs MW>1000 Factors Affecting Drug Permeation Rate of diffusion determined by Fick’s law of diffusion Related to area of diffusion (eg. Lung>stomach) thickness of barrier conc grad – determined by gradient source (ie. Amount of drug administered) gradient sink (ie. Rate of removal of drug near source) - so high blood flow will keep high conc grad, so vasodilating drugs absorbed faster pKa (for lipid diffusion): Weak acids/bases are more water-soluble when ionized (polar) and more lipid soluble when unionized ( pH of environment determines ionization according to Henderson-Hasselbalch equation which measures amount of dissociation: Log (protonated form/unprotonated form) = pKa – pH IN WEAK ACIDS: the PROTONATED is LIPID-SOLUBLE and UNIONISED If result of this calculation is >0 (before doing antilog) then more is PROTONATED (ie. Reabsorbed, not excreted) If result is <0 (before antilog) then more is UNPROTONATED (ionised ( water soluble ( excreted) IN WEAK BASES: the PROTONATED is WATER SOLUBLE and IONISED If result of calculation is >0 then still more protonated, but this time it’s excreted If result is <0 then still more is unprotonated, but this time it’s lipid soluble and reabsorbed Acids: HA (protonated form) ”! H+ + A- (unprotonated form) Alkali: H+ + RNH2 (unprotonated form) ”! RNH3 (protonated form) pKa: the pH at which conc of ionized and unionized forms are equal If pKA is alkaline ( in alkaline urine it will be ionized ( poorly soluble in lipids ( not reabsorbed ( excreted; in acidic urine it will be unionized ( lipid-soluble ( reabsorbed Vice versa if pKa is acidic Degree of ionization v important in body compartments where pH often changes (eg. Gastric, urine) (eg. Phenobarbitol cleared in alkaline urine as pKa is 7.4) Note, some drugs are NOT significantly influenced by pH (eg. Penicillin) Drug Absorption Route of administration: PO: absorption in gut is via lipid diffusion as cells joined by tight junctions; absorption favoured by large SA of GI tract, mixing of contents, pH differences at different levels; can be destroyed by acid (eg. Some penicillins) and enzymes (eg. Insulin is hydrolysed) and microbial activity INH: can be used from agents that vaporize easily (eg. Amyl nitrite) or can be dispersed in aqueous droplets (eg. Ergot derivatives); large SA and high blood flow of lungs aid rapid absorption TOP: transdermal route is using top drugs for systemic effects, slow absorption can cause prolonged drug levels; absorption through skin is through lipid barrier BUCCAL: for drugs that are too rapidly deactivated by liver to be administered PO as portal circ will remove 90% therefore can use lower dose; high blood flow in buccal mucosa, into veins NOT portal circ IV: bypass absorption barriers IM: rapid absorption; depot injections are dissolved in oil to slow absorption SC: slow absorption; if wish to give large amounts must add hyaluronidase to aid spread of injected solution Intra-arterial or intra-thecal: for high local conc of drug; can use higher conc of drug than would be tolerated systemically Drugs Distribution Blood ( compartments Held in blood if strongly binds plasma proteins (eg. Heparin) V. large molecules also stay in blood Water-soluble molecules freely distribute in TBW (eg. Ethanol, mannitol) Lipid-soluble molecules distribute to fat (eg. DDT) Some ions (eg. Heavy metals, lead, fluoride) go to bone Otherwise rate at which leaves blood determined by permeability principles Apparent volume of distribution: total drug present in body / measured plasma conc of drug Since some drugs are 100% bound to tissue structures ( small amount in soln ( v large apparent vol of distribution Determining factors: 1) Protein binding: measured as % drug in blood that is not dialyzable; drugs is bound to inert binding sites on proteins ( can’t diffuse/interact with receptors; in equilibrium with free drug, so alterations in free drug will change amount but not % bound; inert binding sites aren’t specific so diff drugs can compete (inert binding sites must be concentrated for drug to reach therapeutic levels ( if another drug added and displaces drug ( toxic levels); may also bind to proteins outwith vascular compartment 2) Blood flow: determines rapidity of delivery and conc gradient between blood and tissue; liver and kidneys have high blood flow; heart and skin have low blood flow; brain has mod flow, but since small receives high % cardiac output to reaches high conc; muscle has high flow but since large vice versa 3) Membrane permeation 4) Tissue solubility Termination of Drug Effect 1) Excretion a) Kidneys: by glomerular filtration: passive; non-saturatable; removes small molecules; cleared from blood at rate equal to CrCl; can’t occur if bound to plasma protein by tubular secretion: active; in PCT; saturatable (eg. Weak acids such as diuretics, may have to compete with endogenous acid such as uric acid) once in urine, lipid-soluble drug may be reabsorbed, water-soluble readily excreted; metabolism of drugs can produce less lipid-soluble metabolites b) Liver: important in drug metabolism ( drug and metabolites secreted into bile (eg. Cardiac glycosides, ABs) ( duodenum ( some drug may be reabsorbed from intestine into blood (enterohepatic circulation) c) GI tract: drugs may cross lipid membrane from blood to lumen via passive diffusion (eg. Weakly basic morphine (pKa 7.9) diffuses into acidic stomach ( 7.9 – 2.0 = 5.9 therefore more is protonated, therefore it’s 100% ionized and water-soluble ( won’t be reabsorbed and can be lavaged (not excreted, as when passes to alkaline intestine will become un-ionised again) d) Lungs: mostly for gaseous anaesthetics e) Minor routes: sweat and salivary glands, milk Early distribution phass = Extravascular equilibration: steep initial decr in conc of drug as drug passes from vascular into other compartments; this wouldn’t be demonstrated if drug remained in vascular compartment, only in 2-compartment kinetics Slower elimination phase = Exponential decay curve: steep rise in conc when add drug ( slow decr in levels as excreted, rate of decr decreases as the conc gradient driving drug out decreases as it level decreases in blood stream 2) Biotransformation: from active to inactive products DRUG RECEPTORS AND PHARMACODYNAMICS Receptors The component of a cell/MO that interacts with a drug ( biochemical events ( drug effect Receptors determine relation between conc of drug and effect of drug A receptors affinity for a drug determines conc of drug required to form significant no of drug-receptor complexes Total no of receptors limits max effect a drug can produce Receptors determine selectivity of drug action Change in chemical structure of drug change affinities for diff classes of receptors Receptors mediate actions of pharmacological antagonists Pure antagonists bind receptors without altering them ( prevent binding of agonists Receptor may be: Enzyme – can be inhibited/activated by binding of drug (eg. Dihydrofolate reductase) Transport protein – eg. Digitalis on Na-K ATPase Structural protein  eg. Colchicine attaches to tubulin Receptor Desensitisation: Usually reversible, which separates it from down-regulation Eg. ˛-receptor  binding of receptor ( begins to interact with G protein ( phosphorylation of cytoplasmic OH terminal via serine ˛- adrenoceptor kinase ( receptor gets high affinity for ˛-arrestin ( bind, decreasing receptors ability to interact with Gs protein ( reversed when agonist unbinds; Nicotinic Ach receptor NB. There may be multiple receptors for any endogeous ligand, drugs often need to be more selective Signalling Mechanisms and Drug Action Mechanisms of transmembrane signaling: Using a lipid soluble ligand: cross membrane and act on intracellular receptor (can be sited in cytoplasm or nucleus) ( bind to DNA sequences (enhancers) ( stimulate transcription of genes There is a lag-time before effect as it takes time to make proteins; effects can persist long after drug eliminated from system 2Y to slow turnover of enzymes and proteins Eg. Corticosteroids (binding to receptor triggers release of Hsp90 which was covering DNA-binding portion of receptor), mineralocorticoids, sex steroids, vit D, thyroid hormones Using a transmembrane receptor protein: Protein causes intracellular enzymatic actions Consists of extracellular hormone-binding domain and cytoplasmic enzyme domain with protein tyrosine kinase activity Hormone binds ( conformational change in receptor ( receptors bind together ( protein kinases brought together ( become enzymatically active ( tyrosine residues become phosphorylated (cross-phosphorylation which may last longer than receptor activated) ( cellular events (eg. Phosphorylation of substrate protein, transcription factor activation etc…) Regulated by down-regulation (endocytosis and breakdown of receptors) – this process requires tyrosine kinase activity Eg. Insulin, epidermal GF, PDGF Using a ligand-gated channel: Ligand binding opens/closes channel ( change in ion transport ( change in membrane potential V fast response; for transfer across synpases Eg. Ach (opening of nicotinc Ach channel, a pentamer, Ach binds ą subunit ( Na into cells ( depolarisation , gamma-aminobutyric acid, excitatory aa s (all synaptic transmitters) Using a transmembrane receptor protein ( G protein: Ligand binds serpentine receptor (extracellular amino terminal, intracellular carboxyl terminal) ( receptor activates (via interaction at 3rd cytoplasmic loop of receptor) G protein on cytoplasmic side of cell membrane (swapping of GDP for GTP (length of response may be related to length of GTP-bound Gs molecule as opposed to length of binding of ligand-receptor ( amplification of original signal; this creates spare receptors) ( via enzyme / ion channel G protein generates intracellular 2nd messenger ( effect terminated by hydrolysis of GTP Eg. Gs (ą-receptors, glucagons, histamine, serotonin), Go (NT s), Gq (Ach, serotonin), G1+2 (rods and cones), G1+3 (ą1-receptors, Ach, opioids, serotonin) Second messengers Pathways may oppose eachother or work together Reversible phosphorylation is common theme and can result in: Amplification: attachment of phosphoryl group to serine/threonine/tyrosine ( amplification via creation of molecular memory, memory erased by dephosphorylation Flexible regulation: multiple protein kinases regulated by multiple 2nd messengers, many branches, many diff responses possible cAMP made via adenyly cyclase: ( stimulate cAMP-dependent protein kinases via cAMP binding to R dimer of kinase ( C chains released which diffuse through cytoplasm ( transfer phosphate from ATP to (eg.) Lipase in adipocytes, myosin in smooth muscle, glycogen synthase in liver ( agonist binding stops ( cAMP effects terminated by phosphatases, cAMP degraded to 5’-AMP by cyclic nucleotide phosphodiesterases (NB. Caffeine and theophylline prevent this degradation) Effects: mobilization of stored E, conservation of water by kidney, Ca homeostasis, increased contractility of heart, regulates production of adrenal/sex steroids, relaxation of smooth muscle Activated by: ACTH, catecholamines via ˛-receptors, FSH, glucagons, LH, histamine, PTH, vasopressin via V2, serotonin via 5-HT1 Ca/phosphoinositides: May be via G proteins/tyrosine kinase; stimulation of phospholipase C ( hydrolyses PIP2 into diacylglycerol (( activates protein kinase C) and IP3 (triggers release of internal Ca stores) ( Ca binds calmodulin ( activates other enzymes. Reversed by dephosphorylation of IP3, phosphorylation of diacylglycerol, active pumping of Ca from cytoplasm Activated by: lithium, Ach, angiotensin, catecholamines via ą-receptors, PDGF, serotonin via 5-HT2, vasopressin via V1 cGMP: Ligand binds ( guanylyl cyclase produces cGMP ( cGMP-dependent kinase activated; action terminated by dephosphorylation of cGMP and breakdown of substrate Effects: relaxation of vascular smooth muscle (via dephosphorylation of myosin light chains) Activated by: ANF, EDRF, NO (in response to Ach and histamine) Receptor-Effector Coupling Coupling: the transduction process between occupying receptors and drug response; effect of full agonists are more efficiently coupled to receptor occupancy than partial agonists; also determined by biochemical events that transduce receptor occupancy ( cellular response Spare receptors: When max response achieved by agonist when not all available receptors occupied  increase sensitivity to drug eg. Max inotropic response to catecholamine can be achieved even if 90% ˛-receptors blocked by irreversible antagonist Allows agonists with low affinity for receptors and hence rapidly dissociate from receptors, to produce full responses at low concs Occurs because receptor activation may greatly outlast agonist-receptor interaction or if intracellular components rather than receptor limits coupling Explains why sensitivity of tissue to certain conc of agonist doesn’t only depend on affinity of receptor/drug but on concentration of receptors. Eg. There are 100 receptors: If 90% receptors are spare ( 10 receptors need to be occupied for full response ( EC50 occurs at 5 receptors occupied ( EC50 < Kd If receptor conc doubled to 200 and 5 receptors occupied needed for EC50 ( drug will still bind same percentage as above which will be higher no of receptors now and only 2.5% of receptors need be occupied ( “!EC50 as lower conc drug needed  A: max response achieved B: higher conc needed to achieve max response, EC50 increasing C: max response still achieved 2Y to spare receptors used, EC50 still higher D + E: can no longer achieve max response as spare receptors filled with antagonist HAgonists  Partial agonists: Produce lower response at full receptor occupancy Curve similar to that of full agonist in presence of irreversible antagonist May occupy all binding sites but fail to produce maximal effect despite having high affinity for receptors May competitively inhibit responses produce by full agonists Changes receptor confirmation but not to extent for full activation of receptor Efficacy of drug: relation between occupancy of receptors and pharmacologic response Full agonists: Produce higher response at full receptor occupancy Competitive/Irreversible Antagonists Antagonists bind receptors but don’t activate them ( prevent agonists from binding.  Competitive Antagonist: High conc antagonist prevents agonist effect, high agonist can prevent antagonist effect Presence of antagonist increases conc of agonist required for given effect ( agonist conc-effect curve will shift to R Ratio of conc required from certain effect in presence of antagonist v. conc required in absence of antagonist is called dose ratio and is related to Kd (named Kl) of antagonist using Schild equation. - Degree of inhibition depends on conc of antagonist AND agonist, influenced by its metabolism and excretion Irreversible Antagonist May form covalent bonds with receptor If enough antagonist present may not be possible to achieve max agonist response Duration of response not dependent on elimination of antagonist but on rate of turnover of receptors Will prevent response to varying and high level of agonist Eg. Phenobenzamine (ą-antagonist) to control ‘!BP 2Y to pheochromocytoma Chemical Antagonist Antagonist binds DRUG not RECEPTOR Eg. Protamine binds heparin preventing its action Physiologic Antagonism Preventing effect of a drug by preventing effect via a different pathway; effects are less specific and easy to control Eg. Giving insulin to prevent hyperglycaemia caused by steroids Drug Conc and Response  Generally response to drug increases proportional to dose; but as dose increases incremental response decreases until incr in dose has no effect ( hyperbolic curve made using equation: E (effect observed at conc C) = Emax (mac response produced by drug) x C (conc) C (conc) + EC50 (conc of drug producing 50% max effect) Similar to curve made predicting assoc of 2 molecules with given affinity, with equation: B (amount of receptor-bound drug) = Bmax (total conc of receptor sites) x C C + Kd (equilibrium dissociation constant, conc of free drug at which half-maximal binding observed) Kd demonstrates receptor’s affinity for drug – if Kd is low, binding affinity is high. Graph above can be transformed into sigmoid graph with linear midportion by plotting drug effect against log of dose/conc ( makes it easier to compare 2 dose-response curves. Drug Dose and Response  1) Potency: Conc/dose (EC/ED50) of drug required to produce 50% of THAT drugs max effect B is most potent, then A (even though A has higher max efficacy), C, D Note B is partial agonist Depends on Kd (affinity of receptors for drug) and efficiency of drug-effector coupling Determines dose of drug – only comes into play if low potency means drug has to be given in large amounts Relative potency used to compare 2 drugs 2) Maximal efficacy: Reflects limit of dose-response relation on response axis (ie. A,C,D higher than B) This determines clinical effectiveness of drug Affected by drug’s interaction with receptors and efficacy of drug-effector coupling 3) Shape of dose-response curve: Steep curves (eg. D) can result in accidental toxicity esp. if drug has several diff co-operative interactions (eg. Negative inotrope and vasodilator). Can occur if most receptors must be occupied before response seen. Quantal dose-effect curves Made using population data rather than specific drug levels; rather than showing max efficacy of drug, reveals variability of response to drug on Y axis Can calculate median effective dose (ED50) – dose at which 50% population exhibit specified quantal effect Median toxic dose (TD50) – dose for 50% animals to show toxic effect Median lethal dose (LD50) Potency of drugs (ED50 of 5mg more potent than ED50 500mg). Specificity: comparing ED50 of 2 different quantal effects (eg. Cough suppression vs sedation) shows specificity Therapeutic index: relation of dose of drug for required effect to dose that produces toxic effect (ratio of TD50 to ED50) – clinically acceptable risk of toxicity depends on severity of disease being treated Variation in Drug Responsiveness Idiosyncratic response: usually 2Y to genetic diff in metabolism of drug / immune mechanisms Can be hypo/hyperreactive drug (referring to efficacy) Tolerance: becoming hyporeactive to drug Tachyphylaxis: when response diminishes rapidly after administration of drug Mechanisms causing variation: Altered conc of drug reaching receptor: Change in rate of absorption / distribution / rate of clearance Can be estimated by age / weight / sex / renal or liver function Altered conc of endogenous receptor ligand: Eg. Propanolol will “!HR of someone whose endogenous catecholamines are ‘!ed, but won t affect heart of marathon runner Altered no / function of receptors: Incr no receptors / incr efficiency of coupling Agonist may cause down-regulation / desensitization (antagonist may prevent down-regulation, when antagonist withdrawn get large agonist effect – overshoot phenomenon) (may get bad withdrawal when remove agonist 2Y to ongoing down-regulation) – may make it dangerous to discontinue drugs, must wean Sometimes incr in no receptors is caused by other hormones (eg. Thyroid inc ˛ receptors) May explain tolerance, tachyphylaxis Changes in response distal to receptor: Largest cause of variation; physiological mechanisms may compensate to prevent effect of drug Drug Selectivity Drugs bind to many receptors, but will bind to some tighter than others Can be measured in therapeutic vs toxic effects – different effects can occur by 3 mechanisms: Both effects mediated by same receptor-effector mechanism: Toxic effect is direct pharmacological extension of action of drug (eg. Bleeding in anticoagulation, postural hypotension with methyldopa) Manage dose of drug carefully; use other drugs in combination so can decr dose of SE drug Effects mediated by same receptor but different effector pathway: Eg. Digitalis glycosides – incr cardiac contractility; cause GI effects and vision changes; glucocorticoids treat inflammation but cause psychosis Use lowest dose possible, use other drugs as above, use a different route of administration (eg. INH) Effects mediated by different type of receptor: Eg. ą and ˛ receptors, serotonin, histamine, nicotinic/muscarinic; morphine, MAOI, tricyclics, thiazide diuretics PHARMACOKINETICS: ABSORPTION, DISTRIBUTION, ELIMINATION Drug effect controlled by bioavailability, distribution, clearance Relationship exists between therapeutic/toxic effect of drug and con of drug in readily accessible site of body; must weight up toxic effect and efficacy Volume of Distribution Measure of apparent space in body available to contain drug Vd = amount drug in body / conc in blood or plasma Normal plasma vol = 3L Normal blood vol = 5.5L Normal extracellular fluid (minus plasma) = 12L Total body water = 42L Use ideal body weight to determine. Pt’s with oedema/ascites etc… have incr Vd to aminoglycosides Depends on pKa, partition coefficient in fatty tissues, and degree of plasma protein binding Doesn’t represent real vol but size of pool of body fluids required if drug was distributed evenly throughout all body – if you calculate dig level based on plasma conc (low) Vd will be large - but it’s wrong as dig mostly in muscle and adipose tissue. Also if you calculate a drug that strongly binds plasma proteins Vd may be artificially low as drug will be mostly in blood (eg. Frusemide, warfarin). Clearance Rate of elimination of compound relative to plasma drug conc Related to blood flow to extracting organ and extraction ratio CL = rate of elimination / conc in blood or plasma Rate of elimination = (Q(blood flow to organ) x Ci(drug conc entering)) – (Q(blood flow out of organ) x Co(drug conc exiting) Extraction ratio = (Ci – Co) / Ci Dosing rate = CL x Css(steady-state conc)  0 order: rare, only alcohol, aspirin and phenytoin; elimination NOT related to conc, therefore is saturable 1st order: all the others; elimination ą conc, unsaturable; line will be straight on a log scale May need to alter for poor renal function, estimated via CrCl and predicted Cr production rate (lower in women due to decr muscle mass; decr in renal function with age is independent of Cr prod rate Can be blood clearance (CLb), plasma clearance (CLp), clearance based on unbound/free drug conc (CLu) Plasma clearance may also assume proportions that aren’t ‘physiological’ - if drug binds mainly to RBC rather than stays in plasma clearance rates can be incredibly artificially high (eg. Imipramine) Steady-state when dosing rate = clearance rate Max clearance possible determined by blood flow to clearing organ; to determine clearance you must do above equation for conc presented to each organ involved (ie. It’s additive CLrenal + CLliver + CLother = CLsystemic) Major sites: Liver: 1500ml/min; via biotransformation or excretion into bile (eg. Hydralazine, imipramine, lidocaine, morphine, nortriptyline, propanolol, verapamil) If drug absorbed from GI tract, bioavailability determined by extent of hepatic extraction Kidney – renal clearance is level of unchanged drug in urine Poorly extracted by liver – chlordiazepoxide, theophylline, phenytoin, warfarin Half-Life (t1/2) Time required to attain 50% steady state or to decay 50% from steady-state conditions after a change in rte of drug administration T1/2 = 0.693Vd / CL Depends on Vd and clearance – can be affected by disease state If drug distributes into multiple compartments, true ˝ life will be underestimated Difficult to measure in prolonged release formats The longer the half life, the longer to reach steady state NB. 50% of drug remaining after each half life is eliminated in each successive half life; takes 5 half lifes after cessation of therapy for 97% of drug to have gone (opposite relationship occurs with multiple dosing) Bioavailability Fraction of unchanged drug reaching systemic circ following administration – reflected by AUC (area under curve) = availability Can also be used to describe rate (as opposed to extent) at which drug reaches general circulation – reflected by speed at which drug reaches peak conc in plasma  A+C have identical AUC therefore same AVAILABILITY B has lower availability A would reach MEC faster. B would be crap. A+C could be used but A would have higher peaks and lower troughs, but same average concs Important as there is MEC (minimum effective conc) needed to elicit effect, so needed for efficacy – can be dependent on both the rate and fraction as described above, EXTENT more useful than RATE in measuring amount of drug in body; rate important in drugs given as single dose (eg. Sleeping tablets) IV: bioavailability = unity PO: may incompletely absorbed, metabolized in gut/portal blood/liver; may undergo enterohepatic cycling with some excretion in bile Extraction Ratio and First Pass Effect Disposition: what happens to drug after it reaches a site in circ where measurement of drug can be made; can markedly affect extent of availability. Drug given PO must pass through liver before can be measured therefore affect here on availability may be large – first pass effect. May need to give large doses to reach therapeutic levels, but this will result in large no of metabolites. Large amount of first pass in – propanolol, lidocaine Avoid first pass (eg. SL, PR) – PR passes into IVC (except for 50% anastomosis ( some go to portal), UNLESS moves up into rectum ( still hits portal circ Extraction ratio: may be dependent on hepatic function and blood flow if excreted by liver; decr extraction ratio ( incr bioavailability of drug (eg. In disease states, intra/extra-hepatic circ shunting) can have large effect on drug conc Dosage Regimes Main determining factor is CLEARANCE, not vol of distribution of half life Must decide on Amount drug to administer Route of administration Interval between doses: aim to maintain steady-state; rate of drug input = rate drug loss Dosing rate = CL x Css - allows you to calculate it; note that after multiple doses, conc becomes average plasma conc over dosing interval Maintenance dose = dosing rate x dosing interval Remember that in this time there will be peak and trough levels unless being continuously infused. How long to continue drug administration Loading dose: administer dose to promptly raise conc of drug in plasma to steady-state value; amount given is equal to amount that must be IN BODY (as opposed to average conc when in intermittent dosage scheme) when steady state reached – affected by Vd Loading dose = Css x Vd This is assuming there is only 1 compartment ignoring distribution phase; if absorption faster than distribution (always true if IV) the initial conc may be higher than steady-state ( toxicity (eg. IV lidocaine); makes rate of administration important Therapeutic Drug Monitoring Pharmacokinetic Variables Absorption: depends on pt compliance; on extent of transfer from site of administration to blood Clearance: impaired kidney, liver, heart function; hepatic disease does not always affect hepatic clearance; measure CrCl Volume of distribution: binding to tissues makes apparent vol larger, binding to plasma makes apparent vol smaller; old people have less skeletal muscle mass decreasing Vd of digoxin, theophylline distributes in TBW so Vd is proportional to body weight; abnormal accumulation of fluids (eg. Ascites, oedema) can incr Vd of hydrophilic drugs (eg. Gentamicin) Half life: increases with age 2Y to change in Vd, NOT 2Y to change in metabolism Pharmacodynamic Variables Max effect: every drug has conc at which incr in conc will not cause incr effect Sensitivity: reflected by EC50; measure drug conc and compare with conc that are usually assoc with therapeutic effect; sensitivity may decr 2Y to abnormal physiology (eg. Incr K (decr efficacy of dig), drug antagonism (eg. Ca channel blockers decr inotropic response to dig) Interpreting Drug Conc Measurements Avoid drawing blood until 2 hours after PO dose (when absorption is complete); dig and lithium take several hours to distribute to tissues (dig wait at least 6 hrs, lithium as trough); sample near midpoint of dosing interval will be close to Css Clearance: most important factor in determining drug conc; affected by Dose of drug Organ blood flow Function of liver and kidneys Protein binding: may make you think there’s a change in clearance when it’s actually unaltered; factors are Albumin conc: may be low in disease states; albumin binds phenytoin, salicylates Alpha1-acid glycoprotein conc: increased in inflamm processes; binds quinidine, lidocaine, propanolol Capacity-limited protein binding: binding to proteins is conc-related; total drug conc will increase less rapidly than dosing rate would suggest as protein binding approaches saturation DRUG BIOTRANSFORMATION Xenobiotics: foreign substances to which body is exposed Biotransformation may occur in: liver (during first pass, eg. morphine), gut wall (eg. Clonazepam, midazolam, chlorpromazine, cyclosporine, catecholamines), MO’s in lower gut, gastric acid (eg. Penicillin), digestive enzymes (eg. Insulin), lungs, skin, kidney. Pt in liver failure will increasingly rely on gut metabolism Biotransformation in liver may be so great that PO route is useless (eg. Lidocaine) Biotransformation for clearance: pharmacologically active molecules tend to be lipophilic + poorly ionized ( readily reabsorbed from glomerular filtrate; may be bound to p proteins and not filtered into urine ( prolonged duration of action unless metabolized to polar metabolites that can be excreted or inactivated by metabolism Eg. Important for excretion of thiopental, Phenobarbital Biotransformation for activation: metabolism may enhance effect of drug Eg. Steroid hormones, cholesterol, Vit D, bile acids Types of Biotransformation Phase I reactions: convert drug into more polar metabolite by introducing/unmasking functional group (eg. OH, NH2, SH) ( inactive/enhanced product Phase II reaction: product of phase I reaction may be conjugated with glucuronic acid / suphuric acic / acetic acid / amino acid using transferases (catalytic enzymes located in microsomes/cytosol) ( drug conjugates (highly polar product) which are usually readily excreted or inactive. May produce an active product (eg. NSAID, isoniazid) Since substrate combined to drug is endogenous, nutrition plays important role here. Reactions can be glucuronidation (morpine, paracetamol, diazepam, digoxin) Acetylation (eg. Sulfonamides, isoniazid, clonazepam) glutathione conjugation (eg. paracetamol) glycine conjugation (eg. Aspirin) sulfation (eg. Paracetamol, methyldopa) methylation (eg. Dopamine, epinephrine, histamine) water conjugation (eg. Carbamazepine) If drug already has functional group, phase II reaction may occur before phase I Biochemistry of Biotransformation Drug-metabolising enzymes in membranes of smooth endoplasmic reticulum: Mixed function oxidases / monooxygenases – catalyse oxidation-reduction process requiring reducing agent (eg. NADPH) and molecular oxygen ( product becomes oxidized with water as by-product; this is a very non-specific process, all that is needed is for drug to be lipophilic Eg. NADPH-cytochrome P450 reductase Eg. Cytochrome P450 Specific steps in CP450 drug oxidations: Oxidised P450(Fe3+) combines with RH (drug) NADPH donates electron to cytochrome P450 reductase CP450R reduces P450(Fe3+)-RH complex to P450(Fe2+)-RH complex Another electron donated to CP450R from NADPH CP450R reduces molecular O2 ( O2- \O2- binds with P450(Fe2+)-RH complex P450(Fe2+)-RH-O2- complex oxidizes drug ( P450(Fe2+)-ROH ROH is oxidized drug product In human liver, many diff types of CP450 – CYP3A4 metabolised >50% drugs metabolized in liver Enzyme Induction / Inhibition Many lipophilic drugs may remain bound to lipid ER membrane ( induce microsomal enzymes / competitively inhibit metabolism of simultaneously administered drug. INDUCTION: (sedatives, antipsychotics, anticonvulsants, antitubercular) CP450 induced by enhanced rate of synthesis and reduced rate of degradation ( incr metabolism ( decr pharmacological action of drugs / increase action of active metabolites (eg. Need higher doses of warfarin) If you discontinue an inducer, then you may get reduced metabolism of another drug you are taking due to loss of induction. May result in tolerance (progressively reduced therapeutic effectiveness due to increased metabolism) if drug induces its own enzymes Inducers: smoking, insecticides, omeprazole, rifampicin, Phenobarbital, barbiturates, ethanol, St John’s wart, carbamazepine, glucocorticoids, phenytoin. These inducers increase transcription and translation of CP450 genes. Clotrimazole and alcohol increases CP450 by substrate stablisation (ie. Decr degradation) INHIBITION: May result in toxic levels of drugs – be careful with anticoagulants and sedatives Competitive inhibition: drug may bind CP450 heme iron hence preventing CP450 from metabolizing via competitive inhibition (eg. Ketoconazole, cimetidine) Drug may bind CP450 heme iron and render it catalytically inactive (eg. macrolide AB’s) Suicide inhibitors: CP450 may be bound by metabolic substrate of a drug and hence altered (eg. Chloramphenicol, spironolactone, clopidogrel, grapefruit juice) Other inhibitors: clopidogrel, trimethoprim, fluconazole, quinidine, paroxetine, disulfiram, erythromycin, clarithromycin, allopurinol, fluconazole, grapefruit juice, cimetidine Production of Toxic Products May be esp important in OD Eg. Paracetamol (95% glucuronidation and sulfation, 5% with glutathione) ( on OD 95% pathway saturated quickly, glutathione (GSH) mops up as much as poss, but then rest goes down CP450 pathway ( N-acetylbenzoiminoquinone ( hepatotoxicity. Antidote to this metabolite is N-acetylcysteine. Variations in Drug Metabolism Individual differences: metabolism of certain drugs may differ 30x in diff people Genetic factors: usually autosomal recessive Abnormal enzymes (eg. Pseudocholinesterase and succinylcholine; warfarin) Abnormal level of enzymes (eg. acetylation of isoniazid - slow acetylation type) Debrisoquinsparteine oxidation polymorphism – faulty expression of P450 gene ( poor drug Metabolism Aromatic (4)-hydroxylation of CYP2C19 polymorphism – decr metabolism of mephenytoin CYP2C9 – mutuation may lower affinity for substrate or impair interaction with P450 reductase ( decr tolerance for warfarin CYP3A5 – affects metabolism of midazolam Diet: charcoal-broiled foods and cruciferous veggies induce CYP1A; grapefruit juice inhibits CYP3A Environment: smoking and pesticides induce Age: extreme of ages have slower metabolism Sex: males metabolise faster Drug-drug interactions: see inhibitors/inducers Interactions with endogenous compounds: different drugs may compete for same conjugating compounds Diseases: liver disease affects biotransformation (incr halflife of diazepam), heart disease decreases blood flow to liver preventing metabolism of even very easily metabolisable drugs (eg. Amitriptyline, imipramine, isoniazid, lidocaine, morphine, propanolol, verapamil), lung disease (decr metabolism of procainamide), hypothyroidism incr half life of digoxin and beta-blockers GI TRACT DRUGS Anti-Ulcer Medication Caustic effect of acid/pepsin/bile overwhelms GI mucus and bicarb secretion, PG’s, blood flow, regeneration. Decr gastric acidity ( decr bioavailability of drugs needing acid to be absorbed (eg. Ketoconazole, digoxin) Production of Acid: 1) Ach / gastrin binds parietal cell ( incr cytosolic Ca ( stimulates protein kinases ( acid secretion from H/K ATPase on canalicular surface 2) Ach / gastrin binds enterochromaffin-like (ECL) cells ( histamine release ( binds to H2 receptor on parietal cells ( activation of adenylyl cyclase ( incr intracellular cAMP ( activates protein kinases ( acid secretion by H/K ATPase NB. Ach works via M3 receptors in gut Muscosal Protective Mechanisms 1) Gastric mucous – prevent back-diffusion of pepsin and acid 2) Epithelial cell-cell tight junctions – prevent back-diffusion of pepsin and acid 3) Bicarb secretion – pH gradient within mucous layer 4) Blood flow – carries bicarb and nutrients to gastric mucosa 5) Mucosa – quick regeneration of damage, by migration of cells from gland necks 6) Mucosal PG’s – for blood flow and bicarb secretion Antacids: ActionWeak bases that react with HCl ( salt and H2O May promote PG productionIndicationDyspepsiaRoute of administrationPODoseDosing Interval1 hour after a mealAbsorptionBioavailabilityHalf lifeDuration of Action2 hoursDistributionMetabolismExcretionRenalSide effectsBloating, belching (Na bicarb / Ca carb due to production of CO2) Metabolic alkalosis (Na bicarb / Ca carb alkali absorption) (less in MgOH / AlOH due to efficiency of action) Fluid retention 2Y to NaCl absorption (Na bicarb) Hypercalcaemia (Ca carb) Renal insufficiency (Ca carb) Diarrhoea (MgOH; osmotic) Constipation (AlOH)ContraindicationsRenal insufficiency ( metabolic alkalosis Heart failure, HBP ( fluid retentionDrug interactionsCan affect absorption of other meds by binding them or altering gastric pH and hence drugs dissolution/solubility (eg. Tetracyclines, flurorquinolones, itraconazole, iron)PregnancyExamplesNa bicarb (baking soda, alka seltzer): reacts rapidly; forms CO2 and NaCl Ca carb (Tums, Os-Cal): less soluble, slower; forms CO2 and CaCl2 MgOH, AlOH: slow; forms MgCl/AlCl and H20 NB. Acid-neutralisation capacity depends on rate of dissolution, water solubility, rate of reaction with acid, rate of gastric emptying H2-Receptor Antagonists: ActionCompetitive inhibitors (inverse agonist) at H2 parietal cell receptor (not H1/3 receptor) ( effects 2Y decr parietal cell cAMP levels ( decr action of protein kinases ( block histamine (released from ECL cells on gastrin / vagal stimulation) on parietal cells ( decr effect of Ach/gastrin on parietal cell ( decr acid releaseIndicationDyspepsia, NSAID gastritis (if NSAID stopped); IV in stress-related ICU gastritis (ranitidine)Route of administrationPO, IV (not nizatidine)DoseCimetidine: 400-800mg Ranitidine: 150 – 300mg Nizatidine: 150 – 300mg Famoitidine: 20 – 40mgDosing IntervalBD or nocteAbsorptionRapid POBioavailabilityCimetidine: 60-70% (50) Ranitidine – 39-88% (50) Famotidine – 20-66% (50) Nizatidine – >70%Half lifeCimetidine: 2hrs Ranitidine: 2-3hrs Famotidine: 2.5-4hrs Nizatidine: 1-2hrsDuration of ActionDepends on dose given 6 (OTC) – 10 (prescription) hrsDistributionMetabolism1st pass hepatic Famotidine <30% metabolisedExcretionRenal Famotidine is mostly excreted unchanged in urine Dose alteration in renal/hepatic insufficiency/elderlySide effectsV safe; in <3% - diarrhoea, headache, fatigue, myalgia, constipation, dizziness, confusion, rash IV – confusion, hallucinations, agitation; bradycardia and LBP due to blockade of cardiac H2 Cimetidine tolerated less well Cimetidine ( inhibits binding of dihydrotestosterone to androgen receptors, inhibits metabolism of estradiol, increases PL levels ( gynaecomastia, impotence, galatorrhoea, loss of libido Rare: blood dyscrasias, liver chemistry changesContraindicationsDrug interactionsCimetidine interferes with cP450 pathways – inhibits CYP1A2/2C9/2C19/2D6/2E1/3A4 ( prolonging half lives of drugs (eg. Warfarin, theophylline, phenytoin, lidocaine, quinidie, propanolol, labetolol, metoprolol, tricyclic antidepressants, benzos, sulfonylureas, metronidazole, ethanol, OCP); interactis with hydroxychloroquine Competes for renal tubular secretion with eg. ProcainamidePregnancyDO cross placenta, secreted into breast milkExamplesCimetidine, ranitidine (better SE profile, higher efficiency, longer acting), famotidine, nizatidine NB. Decr acid secretion, vol of gastric secretion, conc of pepsin Inhibit 60-70% total 24hr secretion esp nocturnal (90%, less so (60-80%) on meal-stimulated acid Proton Pump Inhibitors: ActionLipophilic weak bases (inactive prodrug) which diffuse readily across lipid membranes into acidified compartments (eg. Parietal cell canaliculus) ( protonated in acid environment to active form ( concentrated in parietal cell canaliculus by Henderson-Hasselbach trapping ( molecular conversion to active form (thiophilic sulfonamide cation) ( reacts with H/K ATPase via covalent disulfide linkage (irreversible) ( inactivates H/K ATPase on parietal cellIndicationErosive and non-erosive GORD (healing in 85-90% pt), PUD – better in duodenal than gastric; may need prophylaxis H. pylori – direct antimicrobial properties, incr pH helping actions of AB’s NSAID gastritis even if still on NSAID Prevent re-bleeding in peptic ulcers (high dose) – pH >6 enhances coag and plt aggregation Prevent stress ulcers in ICU (omeprazole per NG tube) Inoperable gastrinomasRoute of administrationPO / IV (bolus of 80mg then infusion at 8mg/hr needed for optimal trt due to short half life) Immediate release formation of omeprazole availableDoseOmeprazole, esomeprazole: 20 – 40mg Lansoprazole: 30mg Pantoprazole: 40mg Rabeprazole: 20mgDosing IntervalOD 1 hr before meal so peak drug conc = peak acid secretionAbsorptionCapsules/coated tablets ( delay release to protect from gastric acid ( coating dissolves in alkali duodenum ( prodrug absorbedBioavailabilityOmeprazole: 40-65% Esomeprazole: >80% Lansoprazole: >80% Pantoprazole: 77% Rabeprazole: 52%Half lifeOmeprazole: 0.5 – 1.5 hrs Esomeprazole: 1 – 1.5hrs Lansoprazole: 1-1.5 hrs Pantoprazole: 1hr Rabeprazole: 1 – 1.5 hrsDuration of Action24hrs – irreversible inactivation of PP, takes 18hrs to make new H/K ATPase moleculesDistributionMetabolism1st pass hepatic metabolism, cytochrome P450 – metabolites don’t have pharmacological significance; reduce dose in severe liver failure There are poor metabolisers, esp S pacific islandersExcretion80% renal, 20% fecalSide effectsV safe; diarrhoea, headache, abdo pain, N, fatigue, dizziness; rash, itch, flatulence, constipation Reduced cyanocobalamin absorption 2Y to decr acid ( B12 def Incr gastric bacterial conc ( ? incr risk of pneumonia / C diff Raised gastrin due to feedback mechanism ( hyperplasia of ECL cells as gastric is trophic, incr proliferation rate of gastric mucosa ? incr risk of Ca Chornic inflamm in gastric body ( ? atrophic gastritis or intestinal metaplasia Rare: Stevens Johnsons syndrome, acute interstitial nephritisContraindicationsDrug interactionsMetabolised by cP450 enyzmes but due to short half life, rare interactions Omeprazole inhibits metabolisms of diazepam + phenytoin Esomeprazole inhibits metabolism of diazepam Lansoprazole enhances clearance of theophylline Reduce absorption of antifungals Increase digoxin plasma levelsPregnancyUncertainExamplesOmeprazole – racemic mixture of R- and S-isomers; available in powder form containing NaHCO3 to protect prodrug from acid degradation with rapid absorption Esomeprazole – S-isomer of omeprazole (proved to be only effective isomer) Lansoprazole - available in dissolvable version Pantoprazole Rabeprazole – has highest pKa at 5 therefore has faster onset of action NB. Administered as inactive prodrugs Full effect not reached for 3-4 days of dosing as not all PP’s are affected on 1st dosing Block fasting and meal-induced secretion (90-98% 24hr secretion) Triple therapy: 10-14/7 of PPI bd, clarithromycin 500mg bd, amoxicillin 1g bd (or metronidazole 500mgbd), then PPI od for 4-6/52 Muscosal Protective Agents: Sucralfate Action: Sucrose salt complexed to AlOH ( is broken down to sucrose sulphate and Al salt ( forms viscous paste ( (-) sucrose sulphate binds (+) proteins at base of ulcers forming physical barrier and stimulating PG and bicarb secretion Indication: used in ICU Absorption: <3% absorbed Excretion: in faeces SE: may cause constipation, don’t use long term in renal failure Drug interaction: May bind other meds affecting absorption Prostaglandin analogues (eg. Misoprostol (PGE)) Action: Stimulates mucus and bicarb secretion, enhances mucosal blood flow, binds to PG receptor on parietal cell ( decr histamine-stimulated cAMP production ( decr acid production Absorption: rapidly absorbed Half life: 30mins Excretion: renal SE: diarrhoea and abdo pain in large proportion of patients; not in pregnancy Colloidal bismuth (eg. Bismuth subsalicylate/subcitrate/dinitrate) Action: coats erosions, stimulates PG mucus and bicarb, direct antimicrobial effects, binds entertoxins, reduces stool f and liquidity so used in traveller’s diarrhoea Absorption: rapid dissolution in stomach ( absorption of salicylate; <1% bismuth absorbed Distribution: bismuth accumulates in tissue Excretion: salicylate excreted in urine, slow renal excretion of bismuth SE: stools and tongue, avoid in renal insufficiency, prolonged use can cause toxicity Stimulating GI Motility Submucosal and myenteric plexus in gut, contributed to by paraS and sym systems, but also has independent action DOPAMINE is INHIBITORY on gastric motility MOTILIN is EXCITATORY on gastric motility 5-HT3 and 4 most important Release of 5-HT from enterchromaffin cells in mucosa ( stimulate 5-HT receptors on afferent nerves ( via dorsal root ganglia or vagus nerve to CNS ( N+V, abdo pain Release of 5-HT stimulates intrinsic primary afferent nerves (IPAN) ( release of calcitonin gene-related peptide (CGRP) and Ach ( affect myenteric interneurons ( peristalsis (prox bowel contraction via Ach and substance P, distal bowel relaxation via NO and VIP) Dopamine (D2) receptor antagonists: ActionBlock D2 receptors in gut ( cholinergic SM stimulation (as dopamine is inhibitory) Block D2 receptors in chemoreceptor trigger zone in medulla ( antiemetic action Metoclopramide also a mixed 5-HT3 antagonist / 5-HT4 agonistIndicationN+V (effective in post-op, NOT MOTION SICKNESS) Gastroparesis, barium studies, help NG tube placement (incr peristalsis of jejunum and duodenum, incr tone and amplitude of gastric contractions, relaxes pyloric sphincter and duodenal bulb) Promote postpartum lactationRoute of administrationPO / IV, PR domperidone, IM metoclopramideDose10mg metoclopramideDosing IntervalAbsorptionBioavailability>80%Half lifeMetoclopraminde: 5-6hrs Domperidone: 7hrsDuration of ActionDistributionDomperidone doesn’t cross BBB whereas metoclopramide doesMetabolismHepatic Also intestinal in domperidoneExcretion70-85% renal, 2% fecal Breast milk in domperidoneSide effects10-20%: restlessness, drowsiness, insomnia, anxiety, agitation 25% (high dose), 5% (longterm): extrapyramidal SE (oculogyric crisis, dystonia, akathisia, parkinsonism) Tardive dyskinesia in long term Elevated PL levels ( galactorrhoea, gynecomastia, impotence, menstrual disorders Rare: agranulocytosis, SVT, hyperaldosteronism, neuroleptic malignant syndromeContraindicationsPhaeochromocytoma; worsens Parkinsons; may worsen clinical depression; SBODrug interactionsPregnancyExamplesMetoclopramide, domperidone (less SE than maxalon) Cholinomimetic agents: for gastroparesis, acute large bowel distension SE: cholinergic SE – salivation, nausea, vomiting, diarrhoea, bradycardia Eg. Bethanechol - stimulate M3 receptors on muscle cells and at myenteric plexus synapses Eg. Neostigmine – acetylcholinesterase inhibitor Macrolides: stimulate motilin receptors on GI SM, promote onset of migrating complex Eg. Erythromycin Laxatives Bulk-forming laxatives: Action: Indigestible, hydrophilic colloids that absorb water ( bulky emollient gel that distends colon ( peristalsis SE: bloating and flatus 2Y to digestion of plant fibres Eg. Psyllium, methylcellulose, polycarbophil Stool softeners: Action: soften stool ( allows water and lipids to penetrate SE: aspiration of mineral oil ( severe lipid pneumonitis; impair absorption of fat soluble vits Eg. Docusate, glycerin suppository Eg. Mineral oil – lubricates poo preventing water absorption from stool Osmotic laxatives: Action: nonabsorbable osmotically active sugars/salts Eg. Milk of magnesia – hypermagnesemia in renal insufficiency Eg. Sorbitol, lactulose – sugars metabolized by colonic bacteria ( abdo cramps Eg. Magnesium citrate, sodium phosphate – hyperosmolar; ( intravascular vol depletion and electrolyte fluctuations; beware renal insufficiency Eg. Polyethylene glycol (PEG) – isotonic; no significant IV/electrolyte shifts occur; used for bowel cleansing; doesn’t produce cramps/flatus Stimulant laxatives: bed-bound/neurologically impaired patients may need long term Action: stimulation of enteric nervous system; stimulates colonic electrolyte and fluid secretion Eg. Anthraquinone derivatives (aloe, senna, cascara) – poorly absorbed, hydrolysis in colon; long term use causes melanosis coli Eg. Castor oil – hydrolysed in SI to ricinoleic acid; seldom used Serotonin (5-HT4) Agonists: affects IPANS; also causes cAMP-dependent Cl secretion from colon ( stool liquidity Clearance: metabolized by gastric acid-catalysed hydrolysis and hepatic glucuronidation; 66% excreted unchanged in faeces, 33% as metabolite in urine SE: safe; diarrhoea, headaches Eg. Tegaserod – no effect on oesophageal motility, only in SI and LI; bioavailability 10% (take before food); beware in renal/hepatic failure Antidiarrhoeal Agents Do not use in bloody diarrhoea, high fever, systemic toxicity Opioid Agonists: Action: increase colonic phasic segmenting activity through inhibition of presynaptic cholinergic nerves in submucosal and myenteric plexuses ( incr colon transit time and fecal water absorption; decr mass colonic movements and Gastrocolic reflex Eg. Loperamide – doesn’t cross BBB, no analgesic effect, no addiction Eg. Diphenoxylate – higher doses can have CNS effects and cause opioid dependence Colloidal bismuth compounds Kaolin: hydrated MgAl salicate Pectin: indigestive carbohydrate Act as absorbants of bacteria, toxins, fluid; decr stool liquidity and number; no significant adverse Effects Bile-salt binding resins: Action: disease of terminal ileum may cause malabsorption of bile salts ( secretory diarrhoea SE: bloating, flatulence, constipation, fecal impaction, fat malabsorption Drug interaction: may bind other drugs Eg. Cholestyramine, colestipol Octreotide: ActionSimilar to somatostatin which is released from GI tract and pancreas from paracrine cells, D cells, enteric nerves ( inhibit secretion of gastric, CCK, glucagons, GH, insulin, secretin, pancreatic polypeptide, VIP, 5-HT ( reduce intestinal fluid secretion and pancreatic secretion ( slow GI motility, inhibit GB contraction ( cause contraction of vascular SM ( reduced portal and splanchnic blood flow ( inhibit secretion of APG hormonesIndicationNeuroendocrine GI tumours; diarrhoea 2Y to vagotomy, short bowel syndrome, AIDS; GI bleeding Psuedoobstruction, small bowel bacterial overgrowth (low dose)Route of administrationSC, IV, IMDose50 – 250mcg SC; low dose stimulates and high dose inhibits bowel motilityDosing IntervalAbsorptionBioavailabilityHalf life1.5 hrs IVDuration of Action6-12 hrs SCDistributionMetabolismExcretionSide effectsSteatorrhoea, fat-soluble vit def; nausea, abdo pain, flatulence, diarhoea; gallstones; hypo/hyperglycaemia; hypothyroidism; bradycardiaContraindicationsDrug interactionsPregnancyExamplesN/A Irritable Bowel Syndrome Serotonin (5-HT3) Receptor Antagonists: ActionInhibit peripheral visceral afferent 5-HT3 receptors in gut ( decr unpleasant sensations (eg. Nausea, bloating, pain) Inhibition of central 5-HT3 receptors (vomiting centre and chemoreceptor trigger zone) ( reduces central response to visceral afferent stimulation Inhibition of 5-HT3 receptors on terminals of enteric cholinergic neurons ( inhibit colonic motility prolonging transit time No effect on D or M receptorsIndicationSevere IBS where diarrhoea is main symptom (alosetron) N+V (if due to vagal stimulation – postop – or chemo) – not in motion sicknessRoute of administrationIV / PODoseFor chemo: ondansetron 24-32mg, granisetron 1mg, dolasetron 100mg, palonosetron 0.25mg Otherwise: ondansetron 8mgDosing Interval30 mins prior to chemo 8-12hrlyAbsorptionBioavailability50-60% (alosetron)Half lifeAlosetron: 1.5hrs Ondansetron, granisetron, dolasetron: 4-9hrs Palonosetron: 40hrsDuration of ActionDistributionMetabolismHepatic cP450 – may need dose reduction in renal failureExcretionRenal and hepaticSide effectsAlosetron: 30% constipation; ischaemic colitis Headache, dizziness, constipation PROLONGED QT (esp. with dolasetron)ContraindicationsOther meds that prolong QT intervalDrug interactionsPregnancyExamplesOndansetron, granisetron, dolasetron, palonosetron Alosetron – has longer duration of action as binds with high affinity and dissociates more slowly from receptors Anticholinergics: antispasmodic SE: anticholinergic (eg. Dry mouth, visual disturbances, urinary retention, constipation) Eg. Dicyclomine, hyoscyamine Serotonin (5-HT4) Receptor Agonists: see above; for IBS where constipation is main symptom Antiemetics Vomiting centre located in lateral medullary reticular formation; co-ordinates vomiting with CN VIII and X, nucleus tractus solitarius; M1, H1 and 5-HT3 receptors found in vomiting centre. Input from: Chemoreceptor trigger zone in 4th ventricle in area postrema – outside BBB, emetogenic stimuli in blood/CSF triggers; rich in D2, 5-HT3, NK1 and opioid receptors Vestibular system via CN VIII – in motion sickness; rich in M1 and H1 receptors Pharynx via X – gag reflex and retch response GI tract via vagal and spinal afferent nerves – irritation ( release of mucosal serotonin ( 5-HT3 receptors ( vagal afferent input to vomiting centre and chemoreceptor trigger zone CNS – in stress, psych 5-HT3 Antagonists: see above Substituted Benzamides (eg. Metoclopramide, methobenzamide): see above Corticosteroids: enhance effects of 5-HT3 antagonists for chemo patients; unknown mechanism Neurokinin Receptor Antagonists: used with above in chemo Action: block area postrema SE: fatigue, dizziness, diarrhoea Drug interactions: metabolized by CYP3A4, may inhibition metabolism of other drugs (eg. Vincristine); other drugs that inhibit CYP3A4 may increase levels (eg. Ketoconazole, ciprofloxacin, clarithromycin, quinidine); will DECREASE INR if on warfarin Eg. Aprepitant – crosses BBB; bioavailability 65%; halflife 12hrs Phenothiazines: antipsychotics with antiemetic and sedative properties Action: inhibition of D and M receptors (( antiemesis), inhibition of H receptors (( sedative) Eg. Prochlorperazine, promethazine, thiethylperazine Butyrophenones: antipsychotics with antiemetic and sedative properties Action: central D blockade SE: extrapyramidal; hypotension; prolonged QT interval (( VT, torsade de pointes) Eg. Droperidol H1 Antihistamines and Anticholinergics: useful in motion sickness and vertigo SE: dizziness, sedation, confusion, dry mouth, cycloplegia, urinary retention Eg. H1 antihistamine – diphenhydramine, dimenhydrinate, meclizine Eg. Anticholinergic (muscarinic antagonist) – hyoscine Cannabinoids: Clearance: Significant first pass hepatic metabolism; metabolites excreted in faeces and urine SE: euphoria, dysphoria, sedation, hallucinations, dry mouth, increased appetite, tachycardia, conjuctival injection, orthostatic hypotension Eg. Dronabinol, nabilone Inflammatory Bowel Disease Aminosalicylates: ActionWork topically on GI tract via 5-aminosalicylic acid (5-ASA) ( modulate inflammatory mediators from cyclooxygenase and lipoxygenase pathways ( interfere with production of inflammatory cytokines (inhibit activity of nuclear factor şB which is a transcription factor in their production) ( inhibit NKC s, mucosal lymphocytes, macrophagesIndicationInduce and maintain remission in UC; mild/mod distal Crohn sRoute of administrationDoseDosing IntervalAbsorptionRapidly absorbed from SI (80%) so doesn’t reach lower therefore formulated with an inert compound to deliver it to distal segmentsBioavailabilityHalf lifeDuration of ActionDistributionMetabolismIn LI bacteria cleave azo bond via azoreductase enzyme, releasing active 5-ASA ( N-acetylation in gut epithelium and liver to metabolite that has no antiinflamm action ( metabolites either absorbed or excreted in faeces There are slow and fast acetylators – slow have worse SE’sExcretionMetabolite either absorbed from GI tract (20-30% at colon) ( hepatic acetylation and excreted by renal (eg. Sulfapyridine), or excreted in faeces (eg. Balsalazide)Side effectsDue to systemic effects of sulfapyridine molecule - nausea, GI upset, headache, arthralgia, myalgia, BM suppression, malaise, oligospermia, impaired folate absorption Hypersensitivity ( fever, exfoliative dermatitis, pancreatitis, pneumonitis, haemolytic anaemia, pericarditis, hepatitis Other preparations well tolerated – rare hypersensitivity; olsalazine causes diarrhoea, renal tubular damageContraindicationsDrug interactionsPregnancyExamplesAzo compounds - Sulfasalazine (5-ASA bound to sulfapyridine) – 10% active cmpd absorbed, 85% sulfapyridine absorbed (hepatic metabolism and renal excretion) Olsalazine (two 5-ASA bound together) Balsalazide (5-ASA bound to 4-aminobenzoyl-beta-alanine) – 1% active cmpd absorbed, only 30% carrier peptide absorbed Mesalamine compounds - Pentasa (time release granules that release throughout SI) Asacol (coated in pH-senstive resin that dissolves at pH 7 in distal ileum and prox colon) Rowasa and canasa enemas Purine Analogs: ActionInhibition of purine nucleotide metabolism and DNA synthesis and repair ( inhibit cell division and proliferation ( T cell apoptosisIndicationInduction and maintenance of remission of UC and CDRoute of administrationDoseAzathioprine 2-2.5mg/kg/d 6-MP 1-1.5mg/kg/dDosing IntervalAbsorptionBioavailabilityAzathioprine 80% 6-MP 50%Half life<2hrsDuration of ActionThioguanine nucleotides concentrated in cells for days; 17/52 delays before effect seenDistributionMetabolismAzathioprine converted to 6-mercaptopurine ( biotranformation via catabolic enzymes (eg. Xanthine oxidase, thiopurine methyltransferase) ( inactive metabolites ( biotranformation via anabolic pathways ( active thioguanine nucleotides ( effectExcretionSide effectsN+V BM depression (leucopenia, macrocytosis, anaemia, thrombocytopenia), hepatic toxicity; FBC and LFT monitor Hypersensitivity reactions (fever, rash, pancreatitis, diarrhoea, hepatitis) Risk of lymphoma if long termContraindicationsDo not give to pt with absent TPMT activity (catabolises 6-MP)Drug interactionsXanthine oxidase catabolism reduced by allopurinol ( increased active nucleotides ( leucopeniaPregnancyDO cross placentaExamplesAzathioprine, 6-mercaptopurine (6-MP) Methotrexate: ActionInhibition of dihydrofolate reductase (used in production of thymidine and purines) ( inhibit cell proliferation, interfere with inflammatory actions if IL-1, simulate increased release of adenosine (anti-inflammatory autacoid), stimulate apoptosis of T cells Inhibition of aminoimidazolecarbozamide ribonucleotide (AICAR) transformylase and thymidylate synthetase, effects on polymorphonuclear chemotaxisIndicationInduction and maintenance of remission in CD; RARoute of administrationPO / SC / IMDose12-25mg/wk SC until remission; 15mg/wk maintenanceDosing IntervalAbsorption70% POBioavailability50-90% PO, 100% otherwiseHalf life6-9hrsDuration of ActionDistributionMetabolismMetabolised to less active hydroxylated metabolite ( polyglutamated in cellsExcretionUrine; 30% in bileSide effectsBM depression, megaloblastic anaemia, alopecia, mucositis – usually only at higher doses Hepatotoxicity: renal insufficiency increases risk of hepatic accumulation and toxicity Nausea, mucosal ulcers Hypersensitivity lung reaction, pseudolymphomatous reactions Give folate supplementation to decr liver and GI SEContraindicationsDrug interactionsCon increased by hydroxychloroquinePregnancyExamples Glucocorticoids: PO / top (still some absorption); cause disease remission but won’t retain it Action: inhibit production of inflammatory cytokines (eg. TNF-ą, IL-1) and chemokines (eg. IL- 8); decr expression of inflammatory cell adhesion molecules; inhibit gene transcription of NO synthase, phospholpiase A2, cyclooxygenase-2, NF-şB. Eg. Budesonide  synthetic analogue of predisolone, rapid first pass metabolism so low bioavailability; less SE than prednisone Anti-Tumour Necrosis Factor Therapy: 2 weeks to response; may eventually lose response despite higher doses due to development of ab to infliximab Action: dysregulation of TH1 response present, in which TNF-ą involved  it binds to cell surface TNF-ą receptors; infliximab binds free and membrane bound TNF-ą with high affinity preventing it binding receptors / activity; also promotes complement activation and ab-mediated apoptosis and cellular cytotoxicty of T cells and macrophages SE: suppression of TH1 inflammatory response (may allow reactivation of TB, hep B, histoplasmosis etc…); infusion reactions 2Y to development of ab to drug (prevented by preinfusion steroids and paracetamol and concomitant therapy with methotrexate for eg); infusion reactions (eg. Fever, headache, dizziness, urticaria, chest pain, dyspnoea, haemodynamic instability, hypotension, muscle spasms); delayed serum-sickness reaction in 1-2% (eg. Myalgia, fever, rash, urticaria, oedema); acute hepatic failure Eg. Infliximab  chimeric mouse-human ab to human TNF-ą  IV infusion, 1st order elimination, halflife 8-10 days Eg. Adalimumab, certolizumab Pancreatic Enzyme Supplements Decr pancreatic enzymes ( fat and protein maldigestion ( steatorrhoea, azotorrhoea, vit malabsorption, weight loss Pancreatin: low conc of lipase and proteolytic (amylase, protease) enzymes Pancrelipase: high concs; more commonly used; must be either enteric-coated or given with PPI as enzymes inactivated by gastric acid Eg. Creon, Pancrease Bile Acid Therapy for Gallstones Used for dissolution of small cholesterol gallstones in poor surgical candidates; also helpful in early-stage primary biliary cirrhosis Ursodiol: ursodeoxycholic acid; absorbed ( conjugated in liver with glycine and taurine ( excreted in bile ( expands bile acid pool, decreases cholesterol content of bile by reducing hepatic cholesterol secretion, stabilizes hepatocyte canalicular membranes; undergoes enterohepatic circulation; halflife 100hrs; may be dehydroxylated by colonic bacteria ( lithocholic acid ( hepatic toxicity Variceal Haemorrhage Somatostatin and ocretotide: MOA poorly understood Vasopressin (ADH): secreted by hypothalamus, stored in PPG; potent arterial vasoconstrictor ( causes splanchnic arterial vascoconstriction ( decr splanchnic perfusion, decr portal venous pressures; useful in acute GI bleeding by infusion into a mesenteric artery; causes hypertension, MI, mesenteric infarction so give nitroglycerin at same time; also causes hyponatraemia, fluid retention and pul oedema due to ADH effects Beta-blockers: reduce portal venous inflow due to decr CO (beta 1 blockade) and splanchnic vasoconstriction (beta 2 blockade); use non-selective beta-blockers (eg. Propranolol, nadolol) OPIOID ANALGESICS Introduction From Papaver somniferum and P album poppies Opium contains many alkaloids, one of which is morphine Can be full/partial agonists, antagonists; may be agonist at one receptor and antagonist at another Eg. Buprenorphine, pentazocine, nalbuphine have mixed agonist-antagonist properties – high affinity for ź-receptors but low activity, with slow rate of dissociation, therefore acts as antagonist in presence of stronger agonist; alternative to methadone; may diminish analgesia/cause withdrawal if on strong agonist Endogenous Opioid Peptides 3 families of peptides: 1) Endorphins and endomorphins 2) Pentapeptides  met-enkephalin, leu-enkephalin; have higher affinity for ´ receptor 3) Dynorphins 4) Nociceptic / orphanin FQ Derived from precursor proteins: 1) Prepro-opiomelanocortin (POMC)  contains met-enkephalin sequence, ˛-endorphin, several non-opioid peptides (inc. ACTH, ˛-lipotropin, MSH) 2) Preproenkephalin A + B  contains 6 copies of met-enkephalin and 1 copy of leu-enkephlain 3) Preprodynomorphin  several opioid peptides that contain leu-enkephlin sequence (eg. Dynorphin A + B, ą + ˛ neoendorphins) Dynorphin A is found in dorsal horn of SC, role in sensitization of nociceptive neurtotransmission, increased levels after tissue damage and inflammation  increases pain and causes hyperalgesia; this is via binding with NMDA (N-methyl-D-aspartate) receptor, not via opioid receptors Other proteins found with analgesic properties: 1) Endomorphin-1 + -2  high affinity for ź-receptor ActionBind to G-protein linked receptors (@ 3rd intracellular loop) located in brain and SC 3 families of receptors, which have overlapping affinities for these peptides: 1) ź: endorphins > enkephalins > dynorphins; subtypes 1+2; most opioids analgesics work here; responsible for most beneficial and SE of opioids; high densities of receptor presynaptically in periaqueductal gray region, and in dorsal horn of SC; also found in post amygdale, hypothalamus, thalamus, nucleus caudatus, putamen, cortex; found on terminal axons of 1Y afferents in laminae I and II and trigeminal nerve Function: supraspinal and spinal analgesia, sedation, inhibition of respiration, slowed GI transit, modulation of hormone and NT release, euphoria, physical dependence 2) ´: enkephalins > endorphins and dynorphins; subtypes 1+2 Function: supraspinal and spinal analgesia, modulation of hormone and NT release 3) ş: dynorphins >> endorphins and enkephlains; subtypes 1,2+3; has less SE than ź so new drugs developed that selective for this (eg. Butorphanol, nalbuphine) Function: supraspinal and spinal analgesia, psychotomimetic effects, slowed GI transit, miosis a) Present in dorsal horn of SC (on SC pain transmission neurons and on 1Y afferents that relay pain message to them). Via G-protein: Close voltage-gated Ca channels on presynaptic nerve terminals ( reduce NT release (eg. Glutamate, Ach, NE, 5-HT, substance P) from 1Y afferents Open K channels ( hyperpolarize postsynaptic neurons ( inhibition in SC pain transmission neurons b) Inhibit descending (modulatory) pathways ( activation of descending inhibitory neurons (via inhibition of inhibitory neurons) that send processes to SC and inhibit pain transmission neurons ( increase analgesic effect c) Cause release of endogenous opioid peptides (eg. Morphine acts on ź ( release of peptide that works on ´+ş) d) Peripheral ź-receptors in peripheral terminals of sensory neurons ( activation ( decr sensory neuron activity and NT release; these effects are outwith CNS, useful in inflammatory painIndicationAnalgesia: works well on severe constant pain, less well on sharp intermittent pain; fixed interval administration more useful in chronic pain; minimize use in labour as crosses placental barrier (phenylpiperidine drugs eg. Meperidine produce less resp depression); in renal/biliary colic may cause incr SM muscle tone and paradoxically worsen pain Acute pul oedema: reduced anxiety, decr cardiac preload (reduce venous tone), decr afterload (decr peripheral resistance) Anaethesia: used before anaesthetics due to sedative, anxiolytic and analgesic properties; in high doses as 1Y anaesthetic (eg. Fentanyl); used in CV surgery as less CV depression; can be used in epidurals (can still cause resp depression, pruritis, N+V) Antitussive: specific mechanism not known; usually use dextromorphan (produces less constipation than codeine, non-addictive), codeine, levopropoxyphene, noscapineRoute of administrationPO, IV, IM, TD, buccalDoseMorphine: 10mg Methadone: 10mg (will need 80-120mg/day) Fentanyl: 0.1mg Codeine: 30-60mgDosing Interval8hrly methadoneAbsorptionBioavailabilityMorphine: 25% PO, 100% IV Methadone: 40-80% Fentanyl: 92% transdermal, 50% buccal Codeine: 90% POHalf lifeMorphine: 2-3hrs Methadone: 25-52 hrs (varies greatly due to enzyme differences) Fentanyl: 3-12hrs Codeine: 2.5 – 3 hrs Prolonged in renal failureDuration of ActionMorphine: 4-5hrs Methadone: 4-6hrs Fentanyl: 1 – 1.5hrs Codeine: 3-4hrsDistributionBind to plasma proteins with varying affinity, but leave blood rapidly and localize in highly perfused tissues (eg. Brain, lungs, liver, kidneys, spleen); also accumulates in muscle (due to large mass) and fat (esp. if lipophilic, eg. Fentanyl)MetabolismConverted to polar metabolites via 1st pass metabolism (90% hepatic) when PO, variation in 1st pass between people Also occurs in brain and kidneys Glucuronidation – phase II metabolism by enzyme UDP-glucuronosyl transferases 2B7 (UGT2B7) Eg. Morphine ( morphine-3-glucuronide (M3G) ( neuroexcitatory effects via GABA/glycinergic system ( morphine-6-glucuronide (M6G) (10%) ( analgesic properties Eg. Hydromorphine ( hydromorphine-3-glucuronide M6G is potent analgesic but can’t cross BBB so don’t contribute much to effects of morphine Accumulation can cause SE in renal failure / long term administration (eg. Seizures, prolonged opioid action) CNS uptake of M3/6G enhanced by probenecid Hydrolysed Eg. Esters: Heroin (diacetylmorphine) ( hydrolysed to monoacetylmorphine ( morphine ( glucuronidation Hepatic Oxidative Metabolism Eg. Phenylpiperidine opioids (eg. Mepiridine, fentanyl, alfentanil, sufentanil) Eg. Fentanyl ( N-dealkylation by P450 enzyme CYP3A4 in liver and intestine ( inactive metabolites Eg. Codeine, oxycodone, hydrocodone ( metabolism by P450 enzyme CYP2D6 in liver ( active metabolites of greater potency (Eg. Codeine ( morphine); 5-10% codeine converted to morphine, 70% converted to codeine-6 glucuronide, 10% to norcodeine and hydromorphone; ceiling effect at 400mg as codeine must be converted to active form Accumulation of metabolites causes SE’s Eg. Mepiridine ( normepiridine (accumulation in renal failure / longterm ( seizures)ExcretionRenal excretion of polar metabolites (90%) and small amounts of unchanged drug Some conjugates found in bile (10%)Side effectsCNS: mainly due to ź-receptors Analgesia  sensory and emotional compenents Euphoria / dysphoria Sedation  little amnesia; occurs more with compounds related to phenanthrene derivatives (eg. Morphine), less with synthetic agents (eg. Fentanyl, meperidine) Resp depression – inhibit brainstem resp mechanisms; depressed response to CO2 challenge; raised C02 ( cerebral vasoD ( incr cerebral b/ flow ( incr ICp Cough suppression Miosis – little/no tolerance develops to this Truncal rigidity – due to supraspinal actions; reduces thoracic compliance interfering with ventilation; mostly seen when lipid-soluble opioids given rapidly (eg. Fentanyl, sufentanil) N+V – activated brainstem chemoreceptor trigger zone Temp – homeostatic regulation mediated by endogenous opioid peptides in brain Peripheral: CV – bradycardia; hypotension (due to peri vasoD, central depression of vasomotor-stabilising mechanisms, release of H); exception is meperidine which causes tachycardia through antimuscarinic effects GI – constipation (decr motility, incr tone ( delayed passage of fecal mass, incr absorption of H20) Biliary tract – contract biliary SM ( biliary colic; sphincter of Oddi contraction ( reflux of biliary and pancreatic secretions ( raised amylase and lipase Renal – decr renal plasma flow; ź-opioids have antidiuretic effect; enhanced renal tubular Na reabsorption; incr uretal and bladder tone; incr sphincter tone Uterus  may prolong labour due to reduced uterine tone Neuroendocrine  stimulate release of ADH, prolactin, somatotropin; inhibit release of LH Pruritis – flushing, warming, sweating, itching; CNS effects and peripheral H release Immune – effect lymphocyte proliferation, ab production, chemotaxis; inhibit NKC cytolytic activity and lymphocyte proliferative responses to mitogensContraindicationsResp depression; acute pancreatitis (spasm of sphincter of Oddi), renal failure (accum of M6G), raised ICp (raised pCO2 will worsen)Drug interactionsSedatives/hypnotics – incr CNS/resp depression Antispsychotic/tranquilisers – incr sedation, accentuate CV effects MAOI – high risk of hyperpyrexic coma, hypertension SSRI’s – inhibit efficacy of codeine Rifampicin, dexamethasone – increase efficacy of codeinePregnancyFetus may become dependent and demonstrate withdrawal on birth (irritability, shrill crying, diarrhoea, seizures) – control symptoms with diazepam or even opiatesExamplesSTRONG AGONISTS Phenanthrenes (eg. Morphine, hydromorphone, oxymorphone, heroin): useful for severe pain Phenylheptylamines (eg. Methadone) - ź-receptor agonist; also has racemic mixture of D- and L-methadone isomers which block NMDA receptors (therefore antagonist of glutamate which is excitatory NT) and monoaminergic uptake tranporters, and ź receptors  good in difficult pain; slow development of tolerance and physical dependence; slow metabolism and high fat solubility ( long duration of action and high Vd (so less ‘rush’) Phenylpiperidines (eg. Fentanyl, Sufentanil, alfentanil, remifentanil, meperidine): potency sufentanil > fentanyl > alfentanil; good in anaesthesia; rapid effect, short halflife, shorter duration of action; can be buccal / transdermal – distribute in fat as lipid-soluble (careful in cachexic), early CO2 retention, reduced sedation so harder to tell when at toxic doses Meperidine has antimuscarinic effects ( tachycardia, negative inotrope, risk of seizures if renal failure Morphinans (Eg. Levorphanol) MILD/MOD AGONISTS Phenanthrenes (eg. Codeine, oxycodone, DHC, hydrocodone): often combined with aspirin / acetaminophen containing drugs; marketed as salts (codeine sulphate, codeine phosphate); less 1st pass Phenylheptylamines (eg. Propoxyphene): Related to methadone with low analgesic activity Phenylpiperidines (eg. Diphenoxylate, loperamide): Used for treatment of diarrhoea; may be combined with atropine to reduce likelihood of abuse MIXED RECEPTOR ACTIONS Don t give partial agonist / mixed receptor drug with pure agonist due to unpredictable outcome  reduce analgesia, withdrawal Phenanthrenes Eg. Nalbuphine  strong ş-receptor agonist, ź-receptor antagonist; ceiling to resp depressant effect, but resp depression resistant to naloxone Eg. Buprenorphine  parital ź-receptor agonist with long duration of action and slow dissociation from ź-receptors; resistant to naloxone; alternative to methadone Morphinans (eg. Butorphanol) ş-receptor agonist; equivalent to buprenorphine but with more sedation Benzomorphans (eg. Pentazocine): ş-receptor agonist with weak ź-receptor antagonist/partial agonist OPIOID ANTAGONISTS (eg. Naloxone, naltrexone, nalmefene): High affinity for ź opioid binding sites as competitive antagonist, but also reverse agonists at ´+ş sites; work in 1-3mins Naloxone: 1-2hr duration of action, so may relapse into coma after that time; may be also used in low doses to counteract SE of opioids; 2% bioavailability, liver metabolises, urinary and biliary excretion Naltrexone: halflife 10hrs, lasts 48hrs; considered from IV drug addicts due to long duration of action Nalmefene: halflife 8-10hrs Metabolised by glucuronide conjugation Tolerance and Physical Dependence Poorly understood mechanism Possibly due to failure of endocytosis of multiply stimulated ź-receptors ( failure to maintain sensitivity Receptor uncoupling: dysfunction of structural relationship between ź-receptors and G protein, 2nd messenger systems and target ion channels; NMDA-receptor important as NMDA antagonists prevent tolerance Persistent administration can cause hyperalgesia, thought to be due to spinal dynorphin Tolerance: after 2-3/52; rate with which develops and extent varies between pt and drug (eg. Methadone tolerance develops slower than morphine); develops better if large doses at short intervals; tolerance disappears after withdrawal syndrome finishes High: analgesic, sedating (few days to stop), resp depressant (few days to stop), antidiuretic, emetic (several months to stop), euphoric, cough suppressing and hypotensive effects Mod: bradycardia; tolerance occurs to mixed agents but to lesser extent as to pure agonists Low: NOT to miotic, convulsant, constipating; tolerance doesn’t develop to antagonist actions of mixed agonists/antagonists or to pure antagonists NMDA-receptor antagonists (eg. Ketamine) prevent opioid-induced tolerance; can also try using ´-antagonists with ź-agonists Cross tolerance: occurs, esp with ź-agonists; not only to analgesic properties; can be partial/incomplete Physical dependence: characteristic withdrawal syndrome (rhinorrhoea, lacrimation, yawning, chills, piloerection, hyperventilation, hyperthermia, mydriasis, myalgia, vomiting, diarrhoea, anxiety, hostility); time on onset, intensity and duration depends on drug used and halflife Morphine/heroin – in 6-10hrs; peak after 36-48hrs; gone by 5 dys Meperidine – subsides in 24hrs Methadone – several days to reach peak; less intense Antagonist-precipitated withdrawal: by giving antagonist (eg. Naloxone); begin at 3 mins ( peak to 10-20mins ( subside in 1hr Tramadol Centrally acting analgesic; blockade of 5-HT reuptake, inhibits NE transporter function; probable weak ź-receptor agonist Partially antagonized by naloxone SE: seizures, N, dizziness. No clinically significant effects on CV / resp NON-OPIOID ANALGESICS Immune response deleterious when chronic inflammation with no resolution of underlying injurious process (eg. Arthritis) Involves release of mediators which aren’t prominent in acute response ( cell damage ( ( leukocytes release lysosomal enzymes ( arachidonic acid liberated from precursor compounds, eicosanoids synthesised ( arachidonate metabolism via cyclooxygenase (COX) pathway produces PGs and thromboxane A2 ( effects on BV’s, nerve endings, cells COX-1 involved in homeostasis, COX-2 involved in inflammation ( arachidonate metabolism via lipooxygenase pathway produces Leukotrienes (via lipoxygenase pathway) ( chemotactic effect on eosinophils, neutrophils, macropages, bronchoconstriction, altered vascular permeability ( Kinins, neuropeptides, histamine, complement compounds, cytokines ( stimulation of neutrophil membranes ( oxygen free radicals ( reduction of O2 ( superoxide anion ( stimulate production of other reactive molecules (eg. Hydrogen peroxide, hydroxyl radicals) Interaction of these substance with arachidonic acid results in chemotactic substances ( inflamm process Aim to relieve pain and slow tissue-damaging process – via NSAID, steroids, DMARDs NSAID’s ActionInhibition of biosynthesis of PG’s reversibly, or irreversibly (eg. Aspirin irreversibly acetylates and blocks platelet COX 1) at subcortical site Inhibit chemotaxis Down-regulate IL-1 production (from macrophages during inflammation, has antipyretic effect) Decrease production of free radicals and superoxide Interfere with Ca-mediated intracellular events Decrease sensitivity of vessels to bradykinin and H Affect lymphokine production from T cells Reverse vasodilation of inflammation Inhibit urate crystal phagocytosis Aspirin inhibits plt aggregration via inhibition of platelet COX (lasts 8-10 days) and decr production of thromboxane A2 Apirin also buffers and transports protons in mitochondria and induces formation of NO-radicals enabling WBC to fight infections COX selectivity: older NSAIDs aren’t selective for COX-1 or -2, new are more selective COX-2 (celocoxib) – PG synthesis at inflamm; don’t effect platelet function; improved GI safety; may increase incidence of oedema and hypertension; rofecoxib and valdecoxib removed due to CV thrombotic events COX-1 (indomethacin, piroxicam, sulindac): PG synthesis at GI tract, kidneys, plt Both (ibuprofen, meclofenamate, aspirin)IndicationAnalgesic, antipyretic, anti-inflammatory, inhibit plt aggregation (except COX-2) Initial trt of gout instead of colchicines RA; closure of PDA Dysmenorrhoea, metastatic bone pain Indomethacin delays premature labour via blocking uterine contractions caused by PGRoute of administrationDoseAspirin: 1200 – 1500mg tid Diclofenac: 50-75mg qid Ibuprofen: 600mg qid Indomethacin: 50-70mg tid Naproxen: 375mg bdDosing IntervalAbsorptionWell absorbed Aspirin: peak level in 1-2hrsBioavailabilityAspirin: rapid and complete Ibuprofen: 49-73% Diclofenac: 100% Indomethacin: 100% PO, 80-90% PR Food doesn’t alter bioavailabilityHalf lifeAspirin: 0.25hrs as rapidly hydrolysed; increases as dose increases Diclofenac: 1.1 hrs Ibuprofen: 2 hrs Indomethacin: 4-5 hrs Naproxen: 14hrsDuration of ActionDiclofenac: 6-8hrsDistributionFound in synovial fluid after multiple dosing; highly protein bound to albumin so Vd = plasma volMetabolismHighly by liver via oxidation and conjugation ( inactive metabolitels; some by phase I then II, some by direct glucuronidation (phase II alone); via CYP3A and CYP2C families of P450 enzymes Aspirin: hydrolysed to acetic acid and salicylate by esterases in tissue and bloodExcretionRenal; varying degrees of biliary excretion and enterohepatic circulation (which correlates with amount of lower GI irritation) Aspirin: <2% urinary excretion of unchanged drug; increases rate of excretion if alkalinsation of urine Diclofenac: mostly biliary excretion Indomethacin: 60% renal, 33% fecalSide effectsGastric irritants (halfed in COX-2 selective; worst in indomethacin, ketoprofen and piroxicam) Nephrotoxic (due to interference with autoregulation of renal blood flow modulated by PG’s ( salt and fluid retention, hypertension) Hepatotoxic (hepatitis, raised LFT’s) Asthma; CV thrombotic events in COX-2 selective; photosensitivity Aspirin: rashes, salicylism in high doses (vomiting, tinnitus, decr hearing, vertigo, hyperpnoea); toxicity ( resp alkalosis then metabolic acidosis, resp depression, cardiotoxicity, glu intolerance; incr bleeding in menstrual women; Reye’s syndrome in children (fatty degeneration of liver cells; high mortality rate), nephritis Ibuprofen: rash, pruritis, tinnitus, dizziness, headache, aseptic meningitis, fluid retention; rarely agranulocytosis, aplastic anaemia, acute renal failure, interstitial nephritis, nephritic syndrome Indomethacin: diarrhoea, pancreatitis, headache, dizziness, confusion, depression, psychosis, thrombocytopenia, aplastic anaemia, hyperkalaemia, renal papillary necrosis Naproxen: low rate of GI bleeding; allergic pneumonitis, leukocytoclastic vasculitis, psuedoporphyriaContraindicationsAspirin: haemophilia; GI bleeding with alcohol; displaces phenytoin, probenecid, valproic acid, methotrexate from protein binding sites; decr effect of spironolactone Ibuprofen: nasal polyps, angioedema Caution in asthma, renal disease, PUD, diabetes, IBDDrug interactionsPregnancyAvoid – premature closure of FDA, premature birthExamplesAspirin (acetylsalicylic acid, ASA) Non-acetylated Salicylates (eg. Magnesium choline salicylate, sodium salicylate, salicylsalicylate): effective anti-inflamm, poor analgesics; not as effective COX inhibitors (ie. Preferred in asthmatics, bleeding tendancies, renal dysfunction); best for patients with renal impairment COX-2 Selective Inhibitors: Antipyretic, antiinflamm, analgesic; no affect on plt aggregation so no cardioprotective effects Eg. Celecoxib – may cause rashes; interacts with warfarin Eg. Etoricoxib – highest selectivity; monitor hepatic function Eg. Meloxicam – least selectivity; fewer SE’s Eg. Valdecoxib – concerns about CV risk and Stevens-Johnson syndrome Non-selective COX Inhibitors: Eg. Ibuprofen – phenylpropionic acid derivative analgesic but not anti-inflamm effects at lower doses; closes patent ductus arteriosus may inhibit cardioprotective effects of aspirin less effect on urine output and fluid retention than indomethacin; less GI irritation than aspirin Eg. Diclofenac – phenylacetic acid derivative PR good for pre-emptive analgesia Eg. Indomethacin – indole derivative inhibits COX, phospholipase A and C, reduce neutrophil migration, decrease T and B cell proliferation Eg. Naproxen  naphthylpropionic acid derivative Eg. Propionic acid derivatives: Flurbiprofen  S- and R+ enantiomers; S- non-selectively inhibits COX, and affects TNF-ą and NO synthesis; enterohepatic circulation; rarely assoc with cogwheel rigidity, ataxia, tremor, myoclonus Ketoprofen – inhibits COX and lipooxygenase Eg. Acetic acid derivatives: Etodolac – slightly more COX-2 selective; transient impairment of renal function; less GI toxicity Nabumetone – converted to acetic acid derivative in body; half life >24hrs (longer in renal impairment); slightly less GI irritant; SE pseudoporphyria and photosensitivity Eg. Others Diflunisal – salicylic acid derivative; enterohepatic cycle via reabsorption of glucuronide metabolite ( cleavage of glucuronide to reactive; capacity limited metabolism; v good for cancer and dental; clearance via renal also Ketorolac – mainly analgesic; can be used to decr opioid requirements Mefenamic acid – inhibit COX and phospholipase A2’ Piroxicam – oxicam; inhibits polymorphonuclear lymphocyte migration, decreases oxygen radical production, inhibits lymphocyte function; long halflife; SE GI symptoms (high), dizziness, tinnitus, headache, rash Sulindac – sulfoxide prodrug; enterohepatic circulation; inhibits colon, breast and prostate Ca; SE Stevens-Johnson epidermal necrolysis syndrome, thrombocytopenia, agranulocytosis, nephrotic syndrome, elevated serum aminotransferases, cholestatic liver damage Tenoxicam Tiaprofen – half life 1-2hrs; inhibits renal uric acid reabsorption DMARD’s NSAID’s provide symptomatic relief but no effect on disease process May take 6/52 to 6/12 to take effect Combination therapy is good; often use methotrexate as background therapy (except azathioprine, auranofin, sulfasalazine which have no additional benefit) Methotrexate: see above Chlorambucil Action: phenlyacetic acid mustard is metabolite ( cross links DNA ( prevents cell replication Bioavailability: 70% Excretion: complete in 24 hrs SE: dose-related BM suppression; infertility, azoospermia, amenorrhoea; incr risk of neoplasia (eg. Leukaemia) Cyclophosphamide Action: phosphoramide mustard is metabolite ( cross links DNA ( prevents cell replication; suppresses T and B cell function SE: dose-related infertility, bone marrow suppression, alopecia, haemorrhagic cystitis, bladder Ca Cyclosporine Action: inhibits IL-1 and IL-2 receptor production via change in gene transcription; inhibits macrophage-T cell interaction and T cell responsiveness Bioavailability: 20-30% with new microemulsion formula; increased to 62% by grapefruit juice SE: significant nephrotoxicity (monitor Cr); hypertension, hyperkalaemia, hepatotoxicity, gingival hyperplasia, hirsutism Drug interactions: metabolized by CYP3A so large number (eg. Diltiazem, K-sparing diuretics which inhibit) Azathioprine Action: 6-thioguanine is metabolite ( suppresses inosinic acid synthesis, B and T cell function, Ig production, IL-2 secretion Metabolism: may be slow and fast metabolisers; thiopurine methyltransferase (TPMT) metabolises SE: BM suppression, GI disturbance, incr infection risk, lymphomas, acute allergic reaction (fever, rash, hepatotoxicity) Mycophenolate Mofetil Action: mycophenolic acid is metabolite ( inhibits cytosine monophophate dehyrdogenase, inhibits T cell proliferation, interferes with leukocyte adhesion to endothelial cells via inhibition of E-selectin, P-selectin and intercellular adhesion molecule 1 SE: similar to azathioprine Chloroquine and Hydroxychloroquine Used in malaria, not v effective DMARD, but help symptoms; 3-6/12 for response Action: possibly suppression of T cell responses to mitogens, decr leukocyte chemotaxis, stablisation fo lysosomal enzymes, inhibition of DNA and RNA synthesis, trapping of free radicals Absorption: rapid, 50% protein bound in plasma, extensively tissue bound (esp melalin containing tissues, eg. Eyes) Half life: 45 days Elimination: deaminated in liver SE: ocular toxicity; dyspepsia, N+V, abdo pain, rashes, nightmares Gold IM: aurothiomalate, aurothioglucose; PO: auranofin; rarely used; IM more effective Action: altered macrophage function ( inhibit monocyte chemotactic factor-1, IL-8, IL1-˛ production, vascular endothelial GF function; IM alter lysosomal enzyme activity, reduce H release from mast cells, inactive complement, suppress phagocytic activities of polymorphonuclear leukocytes; PO: inhibits release of PGE2 and leukotriene B4 Bioavailability: high; concentrate in synovial membranes, liver, kidney, spleen, LN’s and BM Half life: 1yr Excretion: 66% urine, 33% poo SE: pruritis, eosinophilia, stomatitis; thyombocytopenia, leukpenia, pancytopenia in 1-10%; aplastic anaemia rare; proteinuria ( nephrotic syndrome; rare – enterocolitis, cholestatic jaundice, peri neuropathy, pul infiltrates; nitritoid reactions – sweating, flushing, headaches) Penicillamine Rarely used due to toxicity Sulfasalazine Action: sulfapyridine and 5-aminosalicylic acid are metabolites; sulphasalazine and sulfapyridine cause effects; decr IgA and IgM RF, suppress T cell response, decr B cell proliferation Absorption: 10-20% PO; some enterohepatic circulation ( bacteria break down into metabolites ( some sulfapyrdine absorbed, 5-aminosalicylic acid excreted Half life: 6-17hrs Excretion: some unchanged in urine; sulfapyridine excreted after hepatic acetylation and hydroxylation SE: toxic; N+V, headache, rash; haemolytic anaemia, thrombocytopaenia and methaemoglobinaemia rarely; neutropaenia in 1-4%; pul toxicity; infertility in men TNFą Blocking Agents TNFą important in disease progress  activates membrane bound TNFR1 and 2 receptors ( cytokine effects, T cell and macrophage effects Methotrexate decreases clearance and decreases formation of human antimonoclonal ab in all Common SE: risk of macrophage-dependent infection, screen for TB before starting No evidence of incr risk of solid tumour, but beware of lymphoma May cause formation of dsDNA and ANA, but rarely lupus Infusion site reactions Adalimumab: IgG1 anti-TNF monoclonal ab ( prevents interaction of TNFą with p55 and p75 cell surface receptors by binding TNF ( down-regulation of macrophage and T cell function Infliximab: IgG1 monoclonal ab that binds soluble and membrane bound TNFą; same MOA as above; half life 9-12 days; SE inc URTI, nausea, headache, sinusitis, rash, cough; rarely demyelinating syndromes, leucopenia, hepatitis, activation of hep B, vasculitis Etanercept: 2 soluble TNF p75 receptor moieties linked to Fc portion of human IgG ( binds TNFą, inhibits lymphotoxin-ą; half life 4.5 days Abatacept Action: binds to CD80 and 86 on APC ( inhibits binding of CD28 on T cell to CD80/86 of APC ( prevents activation of T cell Half life: 13-16 days SE: URTI (do not use with TNF agents); hypersensitivity and infusion related reactions; ab formation; possible incr lung ca and lymphoma Rituximab Targets CD20 B cells Leflunomide Action: conversion in intestine and plasma to metabolite A77-1726 ( inhibits dihydroorotate dehydrogenase ( decr ribonucleotide synthesis and arrest of cells in G1 phase of cell growth ( inhibit T cell proliferation and production of autoab by B cells; incr IL-10 receptor mRNA, decr IL-8 receptor mRNA, decr TNFą dependent NF-şB activation Half life: 19 days; good enterohepatic recirculation Excretion: enhanced by cholestyramine by 50% SE: diarrhoea, elevated liver enzymes, alopecia, weight gain, hypertension, leukophenia, thrombocytopenia OTHER ANALGESICS Paracetamol ActionWeak COX inhibitor in peri tissues; modulates endogenous cannabinoid system by inhibiting reuptake of endogenous cannabinoidsIndicationRoute of administrationDoseDosing IntervalAbsorptionRelated to gastric emptying; peak conc in 30-60minsBioavailability100%Half life1-4hrs; affected by liver diseaseDuration of ActionDistributionSlighly bound to plasma proteinsMetabolismBy 90-95% by hepatic microsomal enzymes ( converted to acetaminophen sulfate (inactive) acetaminophen glucuronide (inactive) ( minor pathway is cP450 pathway (CYP2E1, CYP1A2) ( metabolite is N-acetyl-p-benzoquinone (NAPQI) (highly toxic to liver and kidney – at normal doses it is detoxified by combining irreversibly with sulfhydryl groups of glutathione ( non-toxic conjugate excreted by kidneys)ExcretionRenal; <5% unchangedSide effectsMild incr liver enzymes; dizziness, excitement, disorientation 15g ( centrilobular necrosis (N+V, diarrhoea, abdo pain), acute renal tubular necrosis Rare – haemolytic anaemia, methaemoglobinaemiaContraindicationsDrug interactionsPregnancySafeExamplesN/A DRUGS IN GOUT Due to deposition of monosodium urate in joints and cartilage ( phagocytosed by synoviocytes which then release PG, lysosomal enzymes, IL-1 ( chemotaxis and inflamm ( macrophages which ingest crystals ( more inflamm mediators; high serum uric acid (end product of purine metabolism) doesn’t necessarily mean gout Avoid aspirin for analgesia as in low doses it causes net retention of uric acid by inhibiting secretory transporter in PCT Colchicine Relieves pain and inflamm in 12-24hrs without altered metabolism of urates; has largely been replaced by NSAID; used more in prophylaxis but can be used to terminate an attack Action: binds to intracellular protein tubulin ( prevents its polymerization into microtubules ( inhibition of leukocyte migration and phagocytosis; inhibits formation of leukotriene B4; inhibits cell mitosis Absorption: good PO, peaks in 2hrs Half life: 9hrs Excretion: GI tract and urine SE: diarrhoea common; N+V, abdo pain; hair loss, BM depression, peri neuritis, myopathy; OD ( burning throat pain, bloody diarrhoea, shock, haematuria, oliguria Uricosuric Agents Will be long term trt; Decrease body pool of urate in tophaceous gout or increasing f of attacks; not to be used if v high uric acid levels; don’t start until 2-3/52 after an attack Action: uric acid freely filtered at glomerulus ( reabsorbed and secreted in PCT; affect active transport sites to decr net reabsorption ( urinary excretion ( net pool of uric acid decreased ( tophi reabsorbed, arthritis resolves ( uric acid pool accumulates, so must keep good urine output and alkali urine to prevent development of calculi SE: GI irritation, rash, aplastic anaemia; P may cause nephrotic syndrome Drug interaction: inhibits secretion of weak acids (eg. Penicillin) Eg. Probenecid – completed reabsorbed by renal tubules; slow metabolism; half life 5-8hrs Eg. Sulfinpyrazone – rapidly excreted by kidneys; long half life Allopurinol Will be long term trt; use colchicine starting until steady state uric acid level obtained; also used to prevent calculi formation when get uricosuria on trt of blood dycrasias Action: metabolized by xanthine oxidase ( alloxanthine which inhibits xanthine oxidase; purine is formed from aa’s, formate and CO2 in body ( if purine not incorporated into nucleic acids, and purines from nucleic acid degradation converted to xanthine/hypoxanthine then oxidized to uric acid; allopurinol inhibits last step ( decr total uric acid body burden, incr xanthine and hypoxanthine Absorption: 80% Half life: 1-2hrs SE: may cause acute attack of gout; GI (N+V, diarrhoea), peri neuritis, necrotizing vasculitis, BM depression, aplastic anaemia, hepatic toxicity, interstitial nephritis, allergic skin reaction, cataracts Drug interaction: azathioprine dose must be decr by 75%; may incr effect of cyclophosphamide; inhibits metabolism of probenecid and PO anticoagulants; may incr hepatic Fe conc Febuxostat Action: inhibits xanthine oxidase; reduces formation of uric acid AND xanthine Absorption: PO 80% Excretion: metabolized by liver, appears in urine SE: may cause attack of acute gout; liver function, diarrhoea, headache, N STEROIDS STILL TO DO CARDIOVASCULAR DRUGS Cardiac performance determined by: Preload: LV function curve is stroke vol vs LV filling pressure / end-diastolic fibre length; ascending limb represents Frank-Starling relation ( beyond 15mmHg performance plateaus; preload >20-25mmHg causes pul congestion In failure: incr due to incr BV and venous tone; curve lower in failure so >20-25mmHg reached at lower SV; incr fibre length ( incr O2 demand Treatment: decr high filling p via salt restriction and diuretics; venodilators decr preload by redistruting blood from chest to periphery Afterload: resistence against which heart must pump blood (aortic impedence and SVR) In failure: decr CO ( reflex incr SVR via sym mechanism, RAA and ET Treatment: decr arteriolar tone Contractility: decr contractility ( decr velocity of muscle shortening, decr r of IV p development ( decr SV Treatment: use positive inotropes HR: incr HR via sym activation of beta-adrenoceptors is compensatory mechanism Compensating mechanisms for CCF: Baroreceptor reflex reset – decr sensitivity to arterial p ( decr input ( incr sym outflow, dec paraS outflow ( incr HR, contractility, vascular tone ( initial incr CO ( incr afterload, decr EF/CO/renal perfusion ( downregulatory changes in ˛1-adrenoceptor-G-protein-effector system ( decr stimulatory effects; ?cardiac ˛3-receptors mediate negative inotropic effects; XS beta activation ( leakage of Ca from SR ( stiffening of ventricles, arrhythmia Decr renal perfusion ( incr angiotensin II production ( incr aldosterone ( Na and H20 retension, incr afterload, remodeling of heart and vessels Release of ANP, ET Myocardial hypertrophy ( ischaemic changes later, impaired diastolic filling ( remodeling (incr apoptosis of myocytes) and dilatation Drugs can act on various sites in sym reflex arc: Vasomotor centre – central adrenergic neurons modulate baroreceptor reflexes; methyldopa, clonidine, guanabenz, guanfacine Sympathetic ganglia  trimethaphan NOT USED Sympathetic nerve terminals  guanethidine (NOT USED), guanadrel, reserpine ˛-receptors in heart - ˛ blockers Vascular SM  hydralazine, minoxidil, nitroprusside, diazoxide, Ca channel blockers, fenoldopam ą receptors of BV s  ą1-blockers (eg. Prazosin) Angiotensin receptors of BV s  angiotensin receptor blockers (eg. Losartan) ˛ receptors of juxtaglomerular cells that release renin - ˛-blockers Kidney tubules  diuretics Drugs can relax SM in variety of ways: Incr cGMP – cGMP facilitates dephosphorylation of myosin light chains ( prevent interaction of myosin with actin (eg. Na nitroprusside and organic nitrates ( NO causes this) Decr intracellular Ca – Ca is modulator in activation of myosin light chain kinase (eg. Ca channel blockers and beta blockers decr Ca influx into cardiac muscle ( decr rate, contractility, O2 requirements) Stabilise/prevent depolarization of vascular SM membrane – caused by opening K channels (eg. Minoxidil sulphate) Incr cAMP in vascular SM – incr rate of inactivation of myosin light chain kinase (enzyme which triggers interaction of actin with myosin) (eg. Beta2-agonists) Antihypertensives NB: Resistance vessels = arterioles Capacitance vessels = venules ACEi good if chronic renal disease Beta-blockers / Ca channel blockers: good if angina Diuretics / ACEi / angiotensin blockers / beta blockers: good if CCF Alpha blockers: good if BPH Diuretics / Ca channel blockers: good if Afro-Caribbean Diuretic + symathoplegic/ACEi + direct vasodilator = good combination Normal regulation of BP: BP = CO x PVR (precapillary arterioles); regulated at arterioles, postcapillary venules, heart and kidney – all antihypertensives act at 1 of these sites Baroreflexes (rapid changes; central sym neurons in vasomotor area of medulla are tonically active ( incr CO and vasoC; carotid baroreceptors stimulated by stretch ( inhibits central sym discharge, lack of stretch removes inhibition) RAA system (renal for longterm; decr renal b/flow ( release of rennin ( incr production of angiotensin II ( contriction of resistence vessels and stimulation of aldosterone synthesis by adrenal cortex ( incr reabsorption of salt and H20) Vasopressin regulates water reabsorption by kidney Local vasoactive substances (eg. ET-1 constricts, NO dilates) Hypertensive emergency: malignant hypertension due to arteriopathy of arterioles ( vascular lesions in kidneys ( release of renin ( angiotensin and aldosterone ( incr BP ( hypertensive encephalopathy (headache, confusion, apprehension, blurred vision, N+V, FND, convulsions, stupor, coma); rapid normalization may cause cerebral hypoperfusion and brain injury – lower by 25%, DBP no less than 100-110mmHg; use Na nitroprusside, can use fenoldopam, nitroglycerin, labetolol, Ca blocker, diazoxide, hydralazine in conjuction with diuretics DIURETICS: decr BP by 10-15mmHg; see later Sympathoplegic agents: note that the kidney will try to make up for action by incr Na reabsorption, hence combination drug therapy; Decr PVR, inhibit cardiac function, decr venous pooling in capacitance vessels; note that these decr vascular responsiveness CENTRALLY ACTING: ActionDECR AFTERLOAD (PVR) DECR PRELOAD (capacitance vessels) ?EFFECT ON CONTRACTILITY DECR HR Decr CO, renal vascular resistence Decr sym outflow from pressor centres in brainstem, but retain sensitivity to baroreceptor control and reflexes hence less postural drop; possible work by decr NE release due to binding of presynaptic ą2-receptors or inhibit activity of neurons by binding postsynaptic ą2-receptors Methyldopa  decreases PVR, HR, CO; decr renal vascular resistance; enters brain via aa transporter; analogue of L- dopa; converted to ą methyldopamine and ą-methylNE (like synthesis of NE) ( ą-methylNE stored in nerve terminals and released to interact with postsynaptic ą-adrenoreceptors as agonist ( peri vasoC ( ą methyldopamine / ą-methylNE reacts with central ą-adrenoreceptors ( antihypertensive effect Clonidine  decr CO, HR, PVR, renal vascular resistance; relaxation of capitance vessels; lipid soluble so rapidly enters brain; partial ą-agonist so causes transient raised BP; antihypertensive effect due to ą-adrenoreceptors in medulla (decr sym and paraS tone ( decr BP and HR, decr catecholamine levels; also binds imidazoline receptors Guanabenz and guanfacine – work in similar way to clonidineIndicationHypertensionRoute of administrationClonidine: can be transdermalDoseMethyldopa: 1-2g/day Clonidine: 0.2-1.2mg/day; can incr dose for higher effect Guanethidine: 25-50mg/dayDosing IntervalClonidine: bdAbsorptionBioavailabilityMethyldopa: 25% Clonidine: 95% Guanethidine: 3-50%Half lifeMethyldopa: 2hrs Clonidine: 8-12hrs Guanethidine: 5 daysDuration of ActionMethyldopa: max effect in 4-6hrs, can last up to 24hrs, persisting after drug has left system as metabolite does effect Clonidine: shorter as directly related to drug conc Guanethidine: takes 1-2/52 to take effect, lasts same length of timeDistributionMetabolismExcretionSide effectsCentrally acting ( sedation, mental depression, sleep disturbance, vertigo, extrapyramidal SE Methyldopa ( lactation (inhibition of dopamine mechanisms in hypoT), positive Coomb’s test, haemolytic anaemia, hepatitis Clonidine ( dry mouth; life threatening hypertensive crisis after longterm trt then withdrawal (incr sym activity; nervous, incr HR, headache, sweating ( restart trt or give ą/˛ blockersContraindicationsCentrally acting: depression Guanethidine: phaeochromocytoma ( hypertensionDrug interactionsClonidine: blocked by tricylics Guanethidine: blocked by tricyclics; drugs that block catecholamine uptake decr effect (eg. Cocaine, amphetamine, tricyclics, phenothiazines, phenoxybenzamine); long term trt causes supersensitivity of effector SM cells ( sympathomimetic agents cause hypertensionPregnancyExamples GANGLION BLOCKERS: ActionCompetitively block Ach at nicotinic paraS and sym postganglionic autonomic neurons; not used much due to toxicityIndicationHypertensionRoute of administrationDoseDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsGanglion blocking ( profound sym blockade (postural hypoT, sexual dysfunction), paraS blockade (constipation, urinary retention, glaucoma, blurred vision, dry mouth)ContraindicationsDrug interactionsPregnancyExamples ADRENERGIC NEURON BLOCKERS ActionDECR PRELOAD (capacitance vessels) ? EFFECT ON AFTERLOAD/CONTRACTILITY DECR HR Decr CO Prevent release of NE from postganglionic sym neurons ( decr CO, decr HR, relaxed capacitance vessels Guanethidine – transported into nerve by same mechanism as NE (ie. NET) ( concerntrated in transmitter vesicles replacing NE depleting stores in nerve endings; causes local blockade of membrane electrical activity; block sym ( toxic SE’s, rarely used Guanadrel – same as above Riserpine – irreversibly blocks ability of aminergic transmitter vesicles to take up and store amines by interfering with vesicular membrane-associated transporter (VMAT) ( depletion of NE, dopamine and 5-HT in central and peri neurons (inc in adrenal medulla); appears to have central effects at low dosesIndicationHypertensionRoute of administrationDoseRisperine: 0.25mg/dayDosing IntervalAbsorptionBioavailabilityRisperine: 50%Half lifeRiserpine: 24-48hrsDuration of ActionDistributionMetabolismExcretionSide effectsAdrenergic neuron blockers ( sym blockade (inhibited ejaculation, postural hypotension); paraS predominance ( incr gut motility ( diarrhoea; postural hypotension, exercise induced hypotension, may even cause shock; marked compensatory Na and H20 retention Riserpine ( more centrally acting ( little postural hypoT; sedation, mental depression, parkinsonism (dopamine depletion in corpus striatum); diarrhoea, GI cramps, incr gastric acidContraindicationsRiserpine: depression, PUDDrug interactionsPregnancyExamples ADRENOCEPTOR ANTAGONISTS – BETA BLOCKERS – see adrenergic blockers ADRENOCEPTOR ANTAGONISTS: ALPHA BLOCKERS – see adrenergic blockers DIRECT VASODILATORS ActionDECR PRELOAD by redistributing blood peripherally via venodilation DECR AFTERLOAD (dilate resistance vessels) NO EFFECT ON CONTRACTILITY REFLEX INCR HR (except verapamil which is negatively inotropic) No effect/incr CO; may decr longterm remodeling of heart Relax vascular SM ( dilate resistance vessels, incr capacitance; note that these decr vascular responsiveness; activates compensatory responses via baroreceptors and SNS and RAA ( Na and H20 retention (esp. minoxidil); work best in combination with other antihypertensives that oppose compensatory effects and diuretics Can be selective arterial / venous or both Hydralazine: dilates arterioles only; useful in combination therapy Minoxidil: active metabolite is minoxidil sulphate ( opens K channels in SM membranes ( stabilizes membrane at RMP ( contraction less likely; dilates arterioles only; more efficacious than hydralazine Sodium nitroprusside: dilates veins and arterioles ( decr PVR and VR; used in emergencies and severe CCF – rapid effect; activates guanylyl cyclase via release of NO or stimulation of the enzyme ( incr intracellular cGMP ( relax vascular SM ( decr BP, maintains CO Diazoxide: dilates arterioles only; for hypertensive emergencies; decr SCR, incr CO, incr HR; prevents vascular SM contraction by opening K channels and stabilizing RMP Fenoldopam: dilates arterioles; for hypertensive emergencies and postop hyperT; agonist of D1 receptors ( dilates arteries and natiuresis Ca antagonists: see below Synthetic BNP (nesiritide): for acute CCF; incr cGMP in SM ( decr art and ven tone, diuresisIndicationHypertension, CCF (arterial selective one better if fatigue is 1Y symptom as incr forward CO)Route of administrationMinoxidil: PO Na nitroprusside: IV infusion Diazoxide: IV Fenoldopam: IV infusion BNP: IV and infusionDoseHydralazine: 40-200mg/day Minoxidil: 40mg/day Na nitroprusside: 0.5-10mcg/kg/min Diazoxide: 50-100mg q5mins til effect Fenoldopam: 0.1-1.6mcg/kg/minDosing IntervalHydralazine: bd/tidAbsorptionBioavailabilityHydralazine: 25% Minoxidil: 90%Half lifeHydralazine: 1.5-3hrs Minoxidil: 4hrs Diazoxide: 24hrs Fenoldopam: 10mins BNP: 18 minsDuration of ActionHydralazine: longer than half life due to binding to vascular tissue Na nitroprusside: 1-10mins Diazoxide: onset after 5 mins; lasts 4-12hrsDistributionDiazoxide: binds albumin and vascular tissueMetabolismHydralazine: rapidly by liver by acetylation Na nitroprusside: uptake into RBC with liberation of cyanide ( cyanide metabolized to mitochondrial enzyme thiocyanate ( thiocyanate distributed to ECF and elminated renally; thicyanate may accumulate if prolonged course esp in renal failure Diazoxide: partial metabolism Fenoldopam: rapid by conjugationExcretionSide effectsSym reflexes intact so no postural hypoT or sexual dysfunction Hydralazine: headache, nausea, anorexia, palpitations, sweating, flushing; reflex tachycardia ( angina / ischaemic arrhythmias; may cause syndrome with arthralgia, myalgia, skin rashes, fever – fully reversible; peri neuropathy Minoxidil: incr HR, palpitations, angina, oedema, headache, sweating, hirsutism Na nitroprusside: accumulation of cyanide ( metabolic acidosis, arrhythmias, hypotension, death; hydroxycobalamin combines with cyanide to nontoxic cyanocobalamin ; thiocyanate poisoning (>10mg/dl) ( weakness, disorientation, psychosis, muscle spasms, convulsions; thiocyanate may inhibit iodine uptake by thyroid ( hypothyroidism Diazoxide: XS hypotension ( CVA, MI; reflex incr HR ( angina, CCF; inhibits insulin release ( incr BSL; salt and H20 retention Fenoldopam: reflex incr HR, headache, flushing, glaucoma BNP: XS hypotension, renal damageContraindicationsDiazoxide: caution in renal failure and if on beta-blockers (decr HR ( incr hypotension) Fenoldopam: glaucomaDrug interactionsPregnancyExamples BLOCK PRODUCTION/ACTION OF ANGIOTENSIN: decr PVR and blood vol ActionDECR AFTERLOAD (PVR) DECR PRELOAD (decr Na and H20 retention via decr aldosterone secretion) NO EFFECT ON CONTRACTILITY NO EFFECT ON HR (decr sym activity via decr angiotensins presynaptic effects on NE release) CO unchanged; decr longterm remodeling of heart (decr morbidity and mortality, slow progress of dilatation) Decr renal arterial pressure / sym output / incr Na level in renal tubule / decr Na level in blood ( renin release ( splits inactive precursor angiotensin I from angiotensinogen ( angiotensin I converted to angiotensin II by endothelial ACE ( A-II converted to angiotensin III in adrenal gland Angiotensin II = vasoconstrictor, causes Na-retention Angiotensin II + III = stimulate aldosterone release If there is high plasma renin activity (eg. RAS, renal disease, malignant hypertension, essential hypertension, trt with Na restriction, diuretics, vasodilators) angiotensin contributes to maintaining high PVR; angiotensin also produced in other tissues and may cause cardiac hypertrophy ACE inhibitors: inhibitory action on RAA, stimulatory action on kallikrein-kinin system; inhibits peptidyl dipeptidase – plasma kininase (that hydrolyses AI ( AII and inactivates bradykinin – which is a vasoD via release of NO and prostacyclin); useful in CCF Captopril Enalapril – prodrug converted by hydrolysis in liver to enalaprilat Lisinopril – derivative of enalaprilat Benazepril, fosinopril, moexipril, perindopril, quinapril, ramipril, tradolapril – long acting Angiotensin II inhibitors: only if intolerant to ACEi; decr PVR; unchanged CO and HR; no reflex sym activation, safe in IHD; helpful even if not raised renin activity; good in chronic renal disease as decr proteinuria and stabilize renal function (via decr glomerular efferent arteriolar resistance, decr cap pressure) Angiotensin receptor-blockers: losartan and valsartan block angiontensin II type 1 (AT1) receptor; also candesartan, eprosartan, irbesartan, telmisartan; more selective than above as no effect on bradykinin; helpful in heart failure and chronic renal diseaseIndicationHypertension, angina, CCFRoute of administrationEnalaprilat – available for IV use in emergenciesDoseCaptopril: 75-150mg/day Enalapril: 10-20mg od/bd Lisinpril: 10-80mg od Losartan: 25-100mg/dayDosing IntervalAbsorptionBioavailabilityCaptopril: 65% Losartan: 36%Half lifeCaptopril: 2hrs Enalaprilat: 11hrs Lisinopril: 12hrs Losartan: 1-2hrsDuration of ActionEnalapril: peak after 3-4hrsDistributionMetabolismProdrugs converted by hydrolysis in liverExcretionRenal (except fosinpril and moexipril) so decr dose in renal insufficiencySide effectsACEi: Severe 1st dose hypotension if hypovolaemic (diuretics, salt restriction, GI fluid loss); acute renal failure (esp if RAS), hyperkalaemia (esp if renal insufficiency/diabetes), dry cough (due to bradykinin and substance P), wheeze, angioedema; neutropenia and proteinuria if renal insufficiency; altered sense of taste, skin rashes Angiotensin receptor blockers: less cough and angioedemaContraindicationsDrug interactionsACEi: K supplements or K sparing diuretics ( hyperK; NSAID impair effect via blocking bradykinin-mediated vasoD which is PG mediatedPregnancyACEi: not during 2-3rd trimesters – fetal hypotension, anuira, renal failure, malformations Angiotensin receptor blockers: same hazards during pregnancyExamples Drugs in Angina Obviously: antiplt agents and lipid-lowering agents GTN and Ca blockers are vasoD; beta-blockers for prophylaxis ( decr time til onset of angina and ST depression on ETT Use Ca blockers and beta-blockers in hypertensives (in combination is good) (also work in CA spasm); nitrates in normotensives Heart uses 75% O2 even when no stress Determinants of myocardial O2 consumption = wall stress (intraV p, ventricular vol, wall thickness), HR, contractility 1) Decr O2 demand: organic nitrates, Ca channel blockers, beta blockers a) Decr cardiac work: HR, ventricular vol, BP, contractility b) Shift myocardial metabolism to substrates needed less O2 per unit of ATP produced) or incr O2 delivery; heart uses f.a.’s for E production – oxidation of f.a. uses more ATP than oxidation of carbohydrates so drugs that shift this metabolism towards glu (f.a.oxidation inhibitors) may decr O2 demand 2) Incr O2 supply: nitrates, Ca channel blockers Incr coronary blood flow related to Perfusion pressure (aortic diastolic p) Duration of diastole (esp important when tachycardia) Coronary vascular bed resistence (determined by metabolic products and autonomic activity) Arteriolar tone (intraV p > aortic p to eject blood, so arterial BP determines systolic wall stress) Venous tone (determines amount of blood sequestered in venous circ vs amount returned to heart – determines diastolic wall stress) NITRATE AND NITRITES ActionDECR PRELOAD > AFTERLOAD REFLEX INCR CONTRACTILITY AND HR Relaxes all SM but more venous selective (veins>arteries; arterioles and precapillary sphincters20): give diuretics Power failure: give vasodilators / inotropics Severe shock: give vasoactive drugs, inotropics, circulatory assist devices RV infarct: give vol replacement, inotropics; avoid diuretics Mitral regurg / VSD: give vasodilators. Inotropics, circulatory assist devices, surgery DIGITALIS: ActionNO EFFECT ON PRELOAD / AFTERLOAD INCR CONTRACILITY DECR HR Cardiac glycoside (cardenolide) 1) Inhibit Na/K ATPase ( incr intracellular Na level ( decr Ca expulsion via Na-Ca exchanger ( incr free Ca conc during systole ( Ca enters SR via SERCA 2) Prolonged AP initially …. Then …. Shortened AP (mostly plateau phase; due to incr K conductance due to incr intracellular Ca) 3) Causes cardioselective paraS effects via sensitization of baroreceptors, central vagal stimulation, facilitation of muscarinic transmission at cardiac myocyte – affecting atria and AVN > ventricles or Purkinje fibres; useful in arrhythmias Effects: decr r SAN discharge, decr refractory period of atria, decr conduction velocity and incr refractory period of AVN, decr refractory period of Purkinje system and ventricles; incr PR and decr QTIndicationCCF and AF; dilated heart and 3rd HS; will only help in 50% if no AF (try after ACEi/diuretics)Route of administrationDoseSlow loading with 0.125-025mg/dayDosing IntervalAbsorptionDigoxin: 65-80% absorbed PO Other glycosides from 0-100%BioavailabilityHalf lifeDuration of ActionDistributionSolubility not pH dependent; widely distributed to tissues inc CNSMetabolismNot extensiveExcretion2/3 excreted unchanged in urine (proportional to creatinine clearance)Side effectsLevel should be 1ng/mL or less At toxic conc: decr RMP (due to inhibition of Na pump and reduced intracellular K) ( oscillatory depolarizing afterpotentials (delayed afterpolarisations) after normal AP’s due to overloading of intracellular Ca stores and oscillations of free intracellular Ca conc ( if afterpolarisations reach threshold, AP (ectopic beats coupled to normal AP’s, may cause bigeminy) ( when each afterpotential reaches threshold tachycardia and fibrillation At toxic conc: incr sym outflow Effects: decr r SAN discharge, decr refractory period atria, incr refractory period AVN ( arrhythmias, fibrillation, tachycardia, extrasystoles, arrest; giving antiarrhythmics may cause cardiac arrest so best treated with temporary pacing / digoxin immune fab, only cardiovert if VF Also effects GI tract ( anorexia, N+V, diarrhoea Also effects CNS ( vagal and chemoreceptor trigger zone stimulation; disorientation, hallucinations, visual disturbance K and digoxin inhibit eachother’s binding to Na/K ATPase ( hypoK incr action of dig, hyperK decr action Ca facilitates toxic action of dig by accelerating overloading of stores Mg inhibits action of digContraindicationsWPW syndrome – incr probability of conduction of arrhythmic atrial impulses through alternative AV pathwayDrug interactionsPregnancyExamplesDigoxin obtained from Digitalis lanata (white foxglove) Phosphodiesterase inhibitors: phosphodiesterases are enzymes which inactive cGMP and cAMP; positive inotropes and vasodilators eg. Imarinone, milrinone – inhibit phosphodiesterase isoenzyme 3 (PDE-3) ( incr Ca influx during AP, effect SR to alter intracellular movement of Ca, vasodilatory, incr cAMP and contractility; only IV in acute CCF; half life 3-6hrs; 10-40% excreted in urine; SE are N+V, arrhythmias, thrombocytopenia, LFT changes eg. Levosimendan Beta-adrenergics: eg. Dobutamine; incr CO and decr ventricular filling p; tachycardia and incr myocardial O2 consumption; used in acute CCF Non-positive inotropic drugs: diuretics, ACEi, angiotensin receptor antagonists, beta blockers Drugs Used in Cardiac Arryhthmias SAN discharges at 60-100bpm ( atria ( AVN (slow conduction, needs 0.15s) ( His-Purkinje system ( ventricles (endocardial surface at apex of heart 1st, epicardial surface at base of heart last; takes 0.1s); arrhythmia is cardiac depolarization that differs from this in 1 or more ways (site of impulse, rate, regularity, conduction) Water-soluble Na, Cl, K and Ca unable to diffuse across membranes along elec/chem grads, need voltage/ion/metabolic gate-controlled channels to be open ( movement causes AP (see physiology) Use: Na or Ca channel blockade Blockade of sym autonomic effects Aim: Suppress ectopic automaticity and abnormal conduction in depolarized cells ( electrically silent; minimalise effect on normal polarized heart (as dosage increases this is hard ( drug induced arrhytmia) Decr ectopic pacemaker activity (affect ectopic pacemakers > SAN) Drugs reduce phase 4 slope by binding Na/Ca channels ( decr ratio of Na/Ca permeability to K permeability ( MP stabilizes closer to K equilibrium potential; may incr threshold Beta-blockers reduce phase 4 slope by blocking positive chronotropic effect of NE on heart Modify conduction/refractoriness in reentry circuits to disable circus movement Most agents slow conduction ( early extrasystoles not able to propogate ( bidirectional conduction block; via Decr no. available unblocked channels ( decr excitatory currents ( decr propogation Prolong recovery time of channels still working normally ( incr refractory period Affect depolarized (abnormal) > polarized (normal) tissue by selectively blocking Na/Ca channels of depolarized cells Bind activated (phase 0) or inactivated (phase 2) cells but not rested channels; normal channels that are bound by drug will lose it during resting portion of cycle Use dependent: in fast tachycardia (many channel activations/inactivations) State dependent: in loss of RP (many inactivated channels during rest) Classification: CLASS I: Na channel blockade CLASS IA: prolong AP duration, dissociate from channel with intermediate kinetics ActionProcainamide: slows upstroke of AP, slows conduction; Also some K channel blockade Block Na channels: normal cells (+), depolarized cells (+++) Refractory period: normal cells (+), depolarized cells (+++) Ca channel blockade: 0 Effect on pacemaker activity: (-) depressant effect on SAN and AVN Effect on SAN rate: (-) Effect on AVN refractory period: (-) and (+) (anticholingergic and direct depressant effect) Sympatholytic activity: (+) PR interval: (-) and (+) (anticholingergic and direct depressant effect) QRS duration: (++) QT interval: (++) Quinidine: slows upstroke of AP, slows conduction; also some K channel blockade; more pronounce antimuscarinic effect than procainamide Block Na channel: normal cells (+), depolarized cells (++) Refractory period: normal cells (+), depolarized cells (++) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: (+) and (-) (anticholingeric and direct depressant effect, may suppress diseased SAN) Sympatholytic activity: (+) Effect on AVN refractory period: (+) and (-) (anticholingergic and direct depressant effect) PR interval: (+) and (-) (anticholingergic and direct depressant effect) QRS duration: (++) QT interval: (++) Disopyramide: similar to above; even more antimuscarinic effect so will need to be given with a drug that slows AV conduction Block Na channel: normal cells (+), depolarized cells (+++) Refractory period: normal cells (+), depolarized cells (++) Ca channel blockade: (+) Effect on pacemaker activity: (-) Effect on SAN rate: (+) and (-) as above Sympatholytic activity: (0) Effect on AVN refractory period: (+) and (-) as above PR interval: (+) and (-) as above QRS duration: (++) QT interval: (++)IndicationProcainamide: for atrial and ventricular arrhythmias Quinidine: occasionally in AF, rarely in VT Disopyramide: ventricular arrhythmiasRoute of administrationProcainamide: IV, IM, PO Quinidine: PO Disopyramide: PODoseProcainamide: load wih 12mg/kg IV at 0.3mg/kg/min ( maintenance of 2-5mg/min; 2-5g/day needed to control ventricular arrhythmias Disopyramide: 150mg tid, decr in renal impairmentDosing IntervalProcainamide: frequent or SR Quinidine: usually SRAbsorptionBioavailabilityHalf lifeProcainamide: 3-4hrs; note half life of NAPA is longer so it accumulates Quinidine: 6-8hrs Disopyramide: 7-8hrsDuration of ActionDistributionProcainamide: decr vol distribution in CCF so decr dose Quinidine: bound to albumin and alpha1-acid glycoproteinMetabolismProcainamide: liver metabolism to N-acetylprocainamide (NAPA, a metabolite has class 3 activity; accumulation of this may cause torsade de pointes esp if renal failure and rapid acetylators) Quinidine: hepaticExcretionProcainamide: renal elimination of NAPA; decr dose in renal failure and decr renal clearance in CCFSide effectsProcainamide: ganglion-blocking properties ( decr PVR ( hypotension esp with LV dysfunction; toxic at >8mcg/mL procainamide / 20mcg/mL NAPA ( XS prolongation of AP and QT interval, torsade de pointes, syncope, arrhythmias; lupus erythematosus (with arthritis), pleuritis, pericarditis, parenchymal pul disease, incr ANA, nausea, diarrhoea, rash, fever, hepatitis, agranulocytosis Quinidine: when toxic ( XS prolongation of QT, torsade de pointes, slowed conduction throughout heart; diarrhoea, nausea, vomiting, headache, dizziness, tinnitus, thrombocytopaenia, hepatitis, angioneurotic oedema, fever Disopyramide: toxic ( as above; negative inotrope ( CCF; atropine like ( urinary retention, dry mouth, blurred vision, constipation, glaucomaContraindicationsDisopyramide: CCFDrug interactionsPregnancyExamples CLASS Ib: shorten AP duration, dissociate from channel with rapid kinetics ActionLidocaine: Block Na channel: normal (0) (rapidly dissociate at normal RP ( recovery from block between AP with no effect on conduction) depolarized (+++) (more slowly dissociated in depolarized cells so selective depression of conduction in depolarized cells) Blocks activated ( greater effect on cells with long AP’s such as Purkinje and ventricular; blocks inactivated channels) Refractory period: normal (-), depolarized (++) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: 0 Sympatholytic activity: 0 Effect on AVN refractory period: 0 PR interval: 0 QRS duration: 0 QT interval:0 Mexiletine: similar to lidocaine Block Na channel: normal cells (0), depolarized cells (+++) Refractory period: normal cells (0), depolarized cells (++) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: 0 Sympatholytic activity: 0 Effect on AVN refractory period: 0 PR interval: 0 QRS duration: 0 QT interval: 0IndicationLidocaine: arrhythmias assoc with MI; agent of choice for VT and prevention of VF Mexiletine: for trt of ventricular arrhythmiasRoute of administrationLidocaine: IV Mexiletine: PO active version of lidocaineDoseLidocaine: 150-200mg over 15mins, maintenance of 2-4mg/min Mexiletine: 600-1200mg/dayDosing IntervalMexiletine: bd/tidAbsorptionLidocaine: 3% POBioavailabilityHalf lifeLidocaine: 1-2hrs Mexiletine: 12hrsDuration of ActionDistributionLidocaine: plasma alpha1-glycoprotein binds it, decr free drug; vol of distribution and total body clearance decr in CCFMetabolismLidocaine: extensive 1st passExcretionLidocaine: plasma clearance and VOD decr in liver disease ( decr dose and longer til steady state reached; renal disease has no effectSide effectsLidocaine: low incidence of toxicity (>9mcg/mL); proarrythmic effects uncommon; hypotension in large doses; paraesthesia, tremor, nausea, lightheaded, hearing disturbances, slurred speech, convulsions Mexiletine: more common; tremor, blurred vision, lethargy, nauseaContraindicationsDrug interactionsLidocaine: propanolol/cimetidine decr liver blood flow ( decr lidocaine clearancePregnancyExamples CLASS Ic: minimal effect on AP duration, dissociate from channel with slow kinetics ActionFlecainide: potent K channel blocker also; no antimuscarinic effects Block Na channel: normal cells (+), depolarized cells (+++) Refractory period: normal cells (0), depolarized cells (+) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: (-) Sympatholytic activity: 0 Effect on AVN refractory period: (+) PR interval: (+) QRS duration: (+++) QT interval: 0 Propafenone: weak beta-blocker activity Block Na channel: normal cells (+), depolarized cells (++) Refractory period: normal cells (+), depolarized cells (++) Ca channel blockade: (+) Effect on pacemaker activity: (--) Effect on SAN rate: (-) Sympatholytic activity: (+) Effect on AVN refractory period: (+) PR interval: (+) QRS duration: (+++) QT interval: 0 Morcizine: Block Na channel: normal cells (+), depolarized cells (++) Refractory period: normal cells (-), depolarized cells (-) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: 0 Sympatholytic activity: (+) Effect on AVN refractory period: 0 PR interval: (+) QRS duration: (++) QT interval: 0 IndicationFlecainide: supraventricular arrhythmias in normal heart, suppresses premature ventricular contractions Propafenone: supraventricular arrhythmias Morcizine: ventricular arrhythmiasRoute of administrationDoseFlecainide: 100-200mg bd Propafenone: 450-900mg in 3 doses Morcizine: 200-300mg tidDosing IntervalAbsorptionFlecainide: goodBioavailabilityHalf lifeFlecainide: 20hrs Propafenone: 5-7hrs Morcizine: 2-6hrsDuration of ActionDistributionMetabolismFlecainide: hepatic Propafenone: liver Morcizine: multiple metabolitesExcretionFlecainide: renalSide effectsFlecainide: may cause severe worsening of arrhythmia if prev MI, ventricular ectopics, ventricular tachyarrhythmias Propafenone: metallic taste, constipation, exacerbation of arrhythmia Morcizine: dizziness, nausea, arrhythmiasContraindicationsDrug interactionsPregnancyExamples CLASS II: sympatholytic; decr beta-adrenergic activity; only drugs with decr mortality in asymptomatic patient; see adrenergic blockers CLASS III: prolong AP duration and hence effective refractory period; block rapid component of delayer rectifier K current, or enhance inward current (eg. Na channels) ActionAmiodarone: markedly prolongs AP over wide range of HR’s (no reverse-use phenomenon); broad spectrum of action so high efficacy Block Na channel: normal cells (+), depolarized cells (+++) (also blocks inactivated Na channels) Refractory period: normal cells (++), depolarized cells (++) Ca channel blockade: (+) (weak) Effect on pacemaker activity: (--) Effect on SAN rate: (--) Sympatholytic activity: (+) (weak) Effect on AVN refractory period: (+) PR interval: variable QRS duration: (+) QT interval: (++++) (but low incidence of torsade de pointes due to broad spectrum of activity) Bretylium: interferes with neuronal release of NE; lengthen ventricular but not atrial AP, effect most pronounced in ischaemic cells; has +ive inotropic action when first administered due to release of NE Block Na channel: normal cells (0), depolarsied cells (0) Refractory period: normal cells (+++), depolarized cells (+++) Ca channel blockade: 0 Effect on pacemaker activity: (-) (may transiently incr by causing NE release) Effect on SAN rate: (-) (initial stimulation due to NE release) Sympatholytic activity: (++) Effect on AVN refractory period: (+) (initially – due to NE release) PR interval: 0 QRS duration: 0 QT interval: 0 Sotalol: has class III actions Dofetilide: K blockade increases in hypoK with slow rate of recovery Block Na channel: normal cells (0), depolarized cells (0) Refractory period: normal cells (+), depolarized cells ? Ca channel blockade: 0 Effect on pacemaker activity: 0 Effect on SAN rate: (-) Sympatholytic activity: 0 Effect on AVN refractory period: 0 PR interval: 0 QRS duration: 0 QT interval: (++) Ibutilide: Block Na channel: normal cells (0), depolarized cells (0) Refractory period: normal cells (+), depolarized cells ? Ca channel blockade: 0 Effect on pacemaker activity: 0 Effect on SAN rate: (-) Sympatholytic activity: 0 Effect on AVN refractory period: 0 PR interval: 0 QRS duration: 0 QT interval: (++)IndicationAmiodarone: serious ventricular arrhythmias (can be used for prevention); also for supraventricular arrhyhmias; low doses for AF Bretylium: only in emergency setting for VF when lidocaine and cardioversion failed Dofetilide: AF Ibutilide: acute conversion of AFRoute of administrationAmiodarone: PO/IV Bretylium: IVDoseAmiodarone: loading dose 10g with 0.8-1.2g daily doses ( maintenance dose 200-400mg/day Bretylium: 5mg/kg over 10mins ever 4-6hrsDosing IntervalAbsorptionBioavailabilityAmiodarone: 35-65% Dofetilide: 100%Half lifeAmiodarone: slower component over weeks; rapid component 3-10 days (50% of drug) Dofetilide: 7hrs Ibutilide: 6hrsDuration of ActionAmiodarone: effects maintained for 1-3/12DistributionAmiodarone: accumulates in many tissues (heart, lung, liver, skin, tears); pul toxicity (pul fibrosis); abnormal LFT’s and hepatitis; photodermatitis and gray-blue skin discoloration, corneal microdeposits, halos, optic neuritis; blocks peri conversion of T4 to T3 ( hypo or hyperthyroidism; bradycardia and AV blockMetabolismAmiodarone: hepatic; major metabolite, desethylamiodarone, is bioactive; uses CYP3A4 Ibutilide: rapid hepaticExcretionDofetilide: 80% eliminated unchanged by kidneys; change dose in renal failure Ibutlilde: renal excretion of metabolitesSide effectsUnfortunately ‘reverse use dependence’ – AP prolongation least marked at fast rates and most at slow rates (risk of torsade de pointes) Bretylium: initial NE release may cause ventricular arrhythmias; postural hypotension due to sympatholytic effects (prevent with tricyclic antidepressant); N+V Ibutilide: XS QT prolongation, torsade de pointesContraindicationsDofetilide: QTc >450, HR <50, hypoKDrug interactionsAmiodarone: levels increased by drugs that inhibit CYP3A4 – cimetidine; levels decreased by inducers – rifampicin; amiodarone inhibits other liver enzymes ( high levels of digoxin and warfarin Dofetilide: peak conc increased by verapamil due to incr intestinal b/flow; prolonged half life by inhibitors of renal secretion system (cimetidine)PregnancyExamples CLASS IV: Ca channel blockade; slow conduction in areas where AP upstroke is Ca-dependent (ie. SAN< AVN) ActionDECR AFTERLOAD > PRELOAD DECR CONTRACTILITY DECR HR Inhibit Ca influx via blocking L-type Ca channels (selectivity means neurons and secretory glands only minimally affected, Skeletal muscle not affected as uses intracellular pools of Ca and not transmembrane influx) in cardiac and vascular SM; dihydropyridines bind different site to verapamil/diltiazem; drugs act from inner side of membrane and bind more effectively when membrane depolarized ( decr f of opening of Ca channel in response to depolarization ( decr transmembrane Ca current ( relaxation SM (also occurs in bronchi, GI and uterine) arterioles>veins (so less postural hypotension) ( decr BP, decr PVR, decr CA tone, decr IV pressure, decr LV wall stress ( decr O2 requirement ( decr contractility (dose dependent; may decr CO) ( decr HR ( decr O2 requirement ( decr SAN pacemaker rate, decr AVN conduction velocity (Ca dependent AP’s) ( decr HR, incr ejection time ( decr O2 requirement ( verapamil > diltiazem have non-specific antiadrenergic effect ( peri vasoD ( incr end-diastolic vol Dihydropyridines affect vascular more, verapamil and diltiazem affect heart more (less negatively inotropic) Verapamil - negatively inotropic, decr HR and CO; produce less hypotension; antiarrhythmic effect; some Na channel block Block Na channel: normal cells (0), depolarized cells (+) Refractory period: normal cells (0), depolarized cells (+) Ca channel blockade: (+++) – blocks activated and inactivated channels; effect more marked in tissues that fire frequently and those less polarized at rest Effect on pacemaker activity: (--) Effect on SAN rate: (--) – hypotensive action may cause small reflex incr in SAN r Sympatholytic activity: (+) Effect on AVN refractory period: (++) PR interval: (++) QRS duration: 0 QT interval: 0 Diltiazem - intermediately inotropic; produce less hypotension; antiarrhythmic effect; slight Na channel block Block Na channel: normal cells (0), depolarized cells (0) Refractory period: normal cells (0), depolarized cells (0) Ca channel blockade: (+++) Effect on pacemaker activity: (--) Effect on SAN rate: (+) and (-) Sympatholytic activity: 0 Effect on AVN refractory period: (++) PR interval: (+) QRS duration: 0 QT interval: 0 Dihydropyridines (amlodipine, felodipine, isradipine, nimodipine (esp effective in cerebral vascular bed so used in SAH), nicardipine, nifedipine, nisoldipine) – less negatively inotropic (get reflex tachycardia due to lack of negative inotropic effect); safer if AV conduction abnormalities, may worsen hypotension; negligible Na channel blockIndicationAngina, hypertension; felodipine, nifedipine and diltiazem for Raynaud’s phenomenon; nimodipine for SAH; verapamil for migraine and arrhythmias No role in CCF Verapamil: may reverse resistance of cancer cells to drugs; to terminate SVT if no heart failure / nodal disease; also used in AF; occasionally used in ventricular arrhythmias but can cause haemodynamic collapse Diltiazem: similar to verapamil for SVT and AFRoute of administrationNicardipine, verapamil and dilatiazem can be given IVDoseDiltiazem: 30-80mg PO 8hrly; 75-150mcg/kg IV Amlodipine: 5-10mg PO od Felodipine: 5-10mg PO od Nifedipine: 20-40mg PO 8hrly; 3-10mcg/kg IV Nimodipine: 40mg PO 4hrly Verapamil: 80-160mg PO 8hrly; for arrhythmia IV 5mg bolus over 2-5mins then 5-10mg every 4-6hrs or infusion of 0.4mcg/kg/min; 75-150mcg/kg IV for other conditionsDosing IntervalAbsorptionBioavailabilityDiltiazem: 40-65% Verapamil: 20-35% Amlodipine: 65-90% Felodipine: 15-20% Nifedipine: 45-70% Nimodipine: 13%Half lifeDilatiazem: 4-8hrs Verapamil: 6-7hrs Amlodipine: 30-50hrs Felodipine: 11-16hrs Nifedipine: 4hrs Nimodipine: 1-2hrsDuration of ActionDistributionHigh plasma protein bindingMetabolismVerapamil: High 1st pass effect, extensive metabolism; caution in liver failureExcretionSide effectsCardiac depression (incr bradycardia, AVN block, CCF); dihydropyridines may incr risk of adverse cardiac events in patients with hypertension – use SR (though diltiazem decr f of postinfarct angina in non-Q-wave MI); pt on beta-blockers more sensitive to cardiodepressant effects; flushing, nausea, constipation, peri oedema Verapamil: if given IV to a ventricular tachy ( VF; negative inotrope; sinus arrest in SAN disease; constipation, lassitude, nervousnessContraindicationsCareful in CCFDrug interactionsBlock partially reversed by incr Ca levels, and drugs that incr transmembrane flux of Ca (eg. Sympathomimetics) Verapamil (and diltiazem a bit) can incr digoxin blood levelsPregnancyExamples MISCELLANEOUS (do not fit classification) ActionAdenosine: activation of inward rectifier K current and inhibition of Ca current ( marker hyperpolarisation and suppression of Ca-dependent AP’s; more effect on AVN than SAN Block Na channel: normal cells (0), depolarized cells (0) Refractory period: normal cells (0), depolarized cells (0) Ca channel blockade: (+) Effect on pacemaker activity: (0) Effect on SAN rate: (+) and (-) Sympatholytic activity: (+) Effect on AVN refractory period: (+++) PR interval: (+++) QRS duration: 0 QT interval: 0 Magnesium: thought to influence Na/K ATPase, Na channels and some K and Ca channels Potassium: aim to normalize potassiumIndicationAdenosine: SVT Magnesium: digitalis-induced arrhythmias if low Mg; torsade de pointesRoute of administrationAdenosine: IVDoseAdenosine: 6mg followed by 12mg Magnesium: 1g over 20minsDosing IntervalAbsorptionBioavailabilityHalf lifeAdenosine: <10secsDuration of ActionDistributionMetabolismExcretionSide effectsAdenosine: flushing, SOB, chest burning; short-lived highgrade AV block, AF; headache, hypotension, nausea, paraesthesiaContraindicationsDrug interactionsAdenosine: less effective when adenosine receptor blockers present (eg. Caffeine, theophylline); potentiated by adenosine uptake inhibitors (eg. Dipyridamole)PregnancyExamples Diuretics Agents that incr urine vol Physiology PCT: Reabsorbs NaHCO3 (85%, in the early PCT) (dependent on carbonic anhydrase) Na/H exchanger in luminal membrane ( Na enter cell, H enters lumen Na: Na/K ATPase pumps Na into interstitium H: H in lumen binds with HCO3 to form H2CO3 (carbonic acid) H2CO3 ( H20 + CO2 via carbonic anhydrase CO2: CO2 enters cell by simple diffusion ( becomes H2CO3 ( this forms H + HCO3 H used in Na/H exchanger HCO3 actively transported into interstitium NaCl (overall Na 66%; in the late PCT) Na/H exchanger in luminal membrane ( Na enter cell, H enters lumen Na: Na/K ATPase pumps Na into interstitium H: no HCO3 left to bind H ( intraluminal pH falls ( Cl/base exchanger activated ( Cl reabsorbed H20 (60%) passively, maintaining osmolality of PCT constant Note, if large amount of impermeant solute in lumen (eg. Mannitol), the conc of solute will rise ( incr osmolality ( eventually prevent H20 reabsorption Glu (nearly 100%) aa (nearly 100%) Organic solutes In S2 segment; eg. Uric acid, NSAID, diuretics, antibiotics secreted; helps deliver diuretics to lumen where they act In S1 segment: eg. Creatinine, choline K (65%) via paracellular pathway Carbonic anhyrdrase inhibitors act here: block reabsorption of NaHCO3 Desc limb of LOH: H20 (by osmotic forces as hypertonic medullary interstitium; opposed by mannitol) Asc limb of LOH: NaCl (overall Na 25%; active reabsorption) Via Na/K/2Cl cotransporter – accumulates XS K in cell ( K diffuses back into lumen ( lumen +ive electric potential = driving force for cation reabsorption (eg. Mg, Ca) via paracellular pathway Relatively impermeable to H20 so luminal fluid becomes dilute whereas medullary intersitium becomes hypertonic Loop diuretics act here: block Na/K/2Cl cotransporter ( incr urinary excretion of cations and NaCl; decr lumen-positive potential produced by K recycling, so incr Mg and Ca excretion DCT: NaCl (10%) reabsorbed; relatively impermeable to H20 so luminal fluid becomes more dilute Via Na/Cl cotransporter No effect on K ( no effect on electrical potential of lumen Active reabsorption of Ca via Ca channel then Na/Ca exchanger into interstitium (regulated by PTH) Thiazide diuretics act here: block Na/Cl cotransporter; enhance Ca reabsoprtion (in PCT by passive reabsorption due to thiazide inhanced vol depletion, in DCT due to decr intracellular Na ( enhanced Na/Ca exchange in BL membrane) CT: responsible for tight regulation of fluid vol and conc of urine NaCl (2-5%) reabsorbed; note Na delivery to CT regulates amount of K secreted K secreted Principal cells are major site of Na/K/H20 transport Have separate ion channels for Na and K ( more Na reabsorbed than K secreted (aldosterone incr activity) ( Na enters interstitium via Na/K ATPase (aldosterone incr activity) ( negative intraluminal electric potential (this will be even more potent if HCO3 is present, ie. After use of CA inhibitor) ( Cl driven out of lumen into blood via paracellular pathway ( K driven out of cells into lumen H20 reaborption incr by ADH – causes insertion of aquaporin-2 in apical (luminal) membrane via G-protein linked cAMP-mediated process; also causes insertion of urea transporter UT1 into apical membrane – important role in osmolarity of medulla and conc of urine Intercalated cells are major site of H secretion Side effects of diuretics act here: diuretic incr Na delivery to CT ( incr K secreted ( hypoK Note: diuretics incr aldosterone release ( incr Na reabsoption and K secretion also ActionDECR PRELOAD (blood vol ( decr size of heart so can work at better fibre length) DECR AFTERLOAD (after initial incr PVR, PVR decreases) NO EFFECT ON CONTRACTILITY / HR May decr CO due to decr filling p (beware in R heart failure) Na increases BV stiffness and neural reactivity (due to Na/Ca exchange ( incr intracellular Ca stores) Decr Na stores ( initial decr blood vol and CO (PVR may increase) ( after 6/52 CO normalizes and PVR decreases (may have direct vasoD effect) Carbonic anhydrase inhibitors (acetazolamide, dichlorphenamide, methazolamide): act mostly in PCT, inhibits up to 45% NaHCO3 reabsorption; rarely used as diuretics Loop diuretics (frusemide, ethacrynic acid, bumetanide, torsemide): inhibit NaCl reabosrption in aLOH; v efficacious; act on luminal side of tubule; cause incr renal blood flow also Thiazide diuretics (BFZ, indapamide, metolazone, hydrochlorothiazide etc…): act on DCT; may have CA inhibitory action also K-sparing diuretics (spironolactone, eplerenone, amiloride, triamterene): to prevent K depletion esp if on digitalis; antagonize aldosterone at late DCT and CT ( decr Na reabsorption and hence K and H secretion; spironolactone and eplerenone (more selective for aldosterone receptor) are aldosterone antagonists (decr morbidity and mortality in pt with severe CCF on ACEi; aldosterone may cause myocardial and vascular fibrosis and baroreceptor dysfunction); amiloride and triamterene block Na inlux through ion channels in luminal membrane in CCT Osmotic diuretics (mannitol): osmotically active agents that are filtered by glomerulus but not reabsorbed cause H20 to be retained in PCT and dLOH and CT ( incr urine flow rate, decr contact time between fluid and tubular epithelium, decr Na reabsorption also ( H20 and Na diuresis ADH agonists (vasopressin, desmopressin): V2 receptors involved ADH antagonists (conivaptan): inhibit effect of ADH in CT via antagonizing V1a and 2 receptorsIndicationHypertension (thiazides), heart failure (loops) (esp if oedema; thiazide if mild; frusemide if needed; spironolactone/eplerenone if mod/severe CCF as decr morbidity and mortality); loop diuretics useful in mild renal failure with Na retention (eg. Diabetes, SLE); can use K sparing in cirrhotic oedematous states CA inhibitors: decr formation of aqueous humour (glaucoma) and CSF (mountain sickness); urinary alkalinisation (to incr excretion of weak acids – effects last a few days); metabolic alkalosis (if due to XS diuretic use so intraV fluid replacement contraindicated) Loop diuretics: also used in hyperCa (decr Ca reabsorption, given with NaCl), anion overdose (eg. Bromide, iodide, fluoride; give with NaCl), hyperK (excretion of K encouraged by giving concurrent NaCl); ARF(incr urine flow and K excretion) Thiazide diuretics: renal stones due to hyperCa (as enhance Ca reabsorption in DCT), nephrogenic diabetes insipidus (due to decr plasma vol ( decr GFR ( decr NaCl reaborption via decr delivery of fluids down diluting segments) K sparing: mineralocorticoid XS / hyperaldosteronism (eg. Conn’s, ectopic ACTH production / 2Y – CCF, cirrhosis, nephrotic syndrome, overuse of other diuretics) ( K wasting Osmotic diuretics: H20 leaves cells ( decr ICp and intraocular p (within 60-90mins); incr urine vol ( promote prompt removal of renal toxins (eg. Rhabdo) ADH agonists: central diabetes insipidus ADH antagonists: CCF and siADHRoute of administrationCA inhibitors: dorzomalide, brinzolamide are given topically per eye Thiazide diuretics: PO (except chlorthiazide which can be IV) Osmotic: IV ADH antagonists: PODoseAcetazolamide: 250mg 1-4x/day Loop diuretics: bumetanide 0.5-2mg/day Ethacrynic acid 50-200mg/day Frusemide 20-80mg/day Torsemide 5-20mg/day Loop: incr BP response with incr dose Thiazides are more natriuretic at higher doses but when used as single agent incr dose doesn’t incr antihypertensive effect K sparing: spironolactone 25-100mg Triamterene 50-100mg Amiloride 5mg Eplerenone 25-100mg Osmotic: mannitol 12.5-25g every 1-2hrs to keep urine flow rate >100ml/hrDosing IntervalAbsorptionCA inhibitors: good PO Loop diuretics; rapid; torsemide in 1hr, frusemide in 2-3hrs Thiazide diuretics: chorthalidone slowly Osmotic: v poor and will cause osmotic diarrhoeaBioavailabilityHalf lifeLoop diuretics: depends on renal function; short (2-6hrs) K sparing: triamterene has shorter half life than amiloride and is given more often ADH antagonists: conivaptan 5-10hrsDuration of ActionLoop diuretics: frusemide 2-3hrs, torsemide 4-6hrs Thiazide diuretics: chlorthalidone longer K sparing: spironolactone has slow onsetDistributionThiazide diuretics: chlorthiazide is not lipid-soluble and must be given in large doses K sparing: triamterene renal excretion of metabolitesMetabolismLoop diuretics: ethacrynic acid and frusemide have metabolites, ?if active; torsemide has at least 1 active metabolite K sparing: spironolactone inactivated in liver; triamterene in liver Osmotic: noneExcretionCA inhibitors: secretion in PCT S2 segment; decr dose in renal insufficiency Loop diuretics: glomerular filtration and tubular secretion Thiazide diuretics: indapamide has biliary excretion also; most secreted in PCT Osmotic: renal; glomerular filtration within 30-60mins with no reabsorption/secretionSide effectsCA inhibitors: hypercholraemic metabolic acidosis (chronic reduction HCO3 stores and limits use of drug to 2-3 days); effect will decr over several days as HCO3 reaching CT enhances reaborption of NaCl, but metabolic acidosis will continue as long as drug taken; renal stones (phosphaturia and hypercalciuria; Ca insoluble in alkaline urine); K wasting; drowsiness, parasthesia; NS toxicity if accumulates in renal failure; hypersensitivity reactions Loop diuretics: hypoMg; hypokalaemia metabolic alkalosis (incr delivery of NaCl to CT ( incr secretion K and H; correct hypovolaemia and K); ototoxicity (reversible, esp if on other ototoxic drugs eg. Aminoglycosides); hyperuricaemia (can precipitate attacks of gout; hypoV assoc incr reabsorption of uric acid); occasional skin rash, eosinophilia, interstitial nephritis; severe hydration, may cause hypoNa if pt drinks more due to thirst Thiazide diuretics: compete with uric acid for secretion at PCT so incr levels; may unmask hyperCa due to incr Ca reabsorption; hypokalaemic metabolic acidosis as above; hyperlipidaemia; hyperglycaemia (impaired pancreatic release of insulin, decr tissue utilization of glu); hypoNa (hypoV induced incr ADH, incr thirst); photosensitivity, dermatitis, haemolytic anaemia, thrombocytopaenia, weakness, fatigue, paraesthesia K sparing: hyperK (incr risk with renal disease as max K secretion reduced, or drugs that decr renin – beta-blockers, NSAID, or drugs that decr AII – ACEi etc…; avoid by combining with thiazide diuretic); hyperchloraemic metabolic acidosis; gynecomastia, impotence, BPH; renal stones as triamterene is poorly soluble Osmotic: extracellular vol expansion and hypoNa occur prior to diuresis ( pul oedema, headache, N+V; as H20 > Na diuresis, eventually get hyperNa; dehydration; incr intracellular K as H20 leaves ADH antagonists: hyperNa and nephrogenenic diabetes inspidus; ARF K depletion – hazardous if on digitalis, chronic arrhythmia, acute MI, acute LVF; K loss coupled to reabsorption of Na so restriction of dietary Na will decr K loss Decr glu tolerance; risk of RCCContraindicationsCA inhibitors: decr excretion of NH4 so CI in cirrhosis as may cause hyperammonaemia and hepatic encephalopathy Loop diuretics: hepatic cirrhosis, borderline renal failure or heart failure Thiazide diuretics: cirrosis, borderline renal failure or heart failure K sparing: renal failure ( hyperK; careful in hepatic failureDrug interactionsLoop diuretics: effect correlates with secretion, NSAID/probenecid decr secretion by competing for weak acid secretion at PCT; synthesis of renal PG induced and participates in actions of diuretics ( NSAID interfere with this Thiazide diuretics: again NSAID interfere K sparing: again NSAID interfere; triamterene and indomethacin = renal failure; withdraw K supplementationPregnancyExamplesIndapamide – has direct vasodilatory effect, may cause incr CO Amiloride – has direct vasodilatory effect via inhibition of SM responses Some people don’t respond to loop as half life short and between doses incr Na reabsorption ( use loop and thiazide in combination v good as act on 2 diff parts (normally Na reabosption in aLOH or DCT can incr if earlier blocked) In hypoK try NaCl restriction or K supplementation ( if not work, add in K-sparing (avoid in ARF/ACEi etc& ) Adrenoceptors NE (ą1 = ą2; ˛1>> ˛2) E (ą1= ą2; ˛1= ˛2) Direct mode: E and NE directly activated adrenoceptors Indirect mode: cause release of endogenous catecholamines via Displacement of stored catecholamines from adrenergic nerve ending (eg. Amphetamine, tyramine) Inhibition of reuptake of catecholamines (eg. Cocaine, tricyclics) Effects: adrenoceptors are G-protein coupled (Gs – stimulatory of adenylyl cyclase; Gi – inhibitory of adenylyl cyclase; Gq – coupled to phospholipase C) ( dissociation of GDP from ą subunit ( binding of GTP ( ą subunit dissociates ( effector (adenylyl cyclase, phospholipase C, cGMP phosphodiesterase, ion channels) ( hydrolysis of GTP to GDP and phosphate stops Desensitisation: occurs after exposure to sympathomimetic drugs May be 1) Covalent modification of receptor 2) Assoc of receptors with other proteins 3) Change in subcellular location of receptor 4) Phophorylation of receptor by G protein-coupled receptor kinase (GRK) ( incr affinity for ˛-arrestin ( binding this decr ability of receptor to activate G-protein ( possible endocytosis of receptor via binding of ˛-arrestin with clathrin 5) 2nd messenger feedback (eg. Protein kinase A phosphorylates ˛ receptors or G protein) May be homologous – loss of responsiveness of receptors that have be exposed; via process 4 heterologous – loss of responsiveness of some receptors that haven’t been activated by the drug; via process 5 Phenylethylamine is compound all drugs derived from; altered to alter sensitivity Incr size of alkyl substituents on amino group incr ˛ receptor activity Substitution on benzene ring alters potency, bioavailability and distribution of CNS Substitution on alpha carbon blocks oxidation by MAO ( prolongs action Subsitution on beta carbon important for facilitating activation of receptors ReceptorAgonistAntagonistEndogenous agonistsEffectsSite and Actioną receptorsE > NE > isopretenerolą1 type (type 1A, B, D)Phenylephrine, methoxamine (ą2 also but to lesser extent)PrazosinGq protein (phospholipase C) ( polyphosphoinositide hydrolysis ( inositol 1,4,5-triphosphate (IP3) ( release of Ca from intracellular stores and incr influx of Ca from extracellular ( activation of Ca dependent protein kinases; IP3 progressively dephosphorylated to free inositol ( diacylgycerol (DAG) ( activates protein kinase C ( many pathways Also activate signal transduction pathways (eg. Mitogen-activated kinases, polyphosphoinositol-3-kinase ( cell growth and altered gene expressionVascular SM ( contraction Pupillary dilator muscle ( contraction ( dilates pupil Pilomotor SM ( erects hair Prostate ( contraction Heart ( incr contractilityą2 typeClonidine, methylnorepinephrine (ą1 also, but to lesser extent) YohimbineGi protein ( inhibit adenylyl cyclase activity ( decr cAMP Affect other signaling pathways (eg. Ion channels, enzymes) Cause plt aggregationPostsynaptic CNS adrenoceptors ( multiple Plt ( aggregation Adrenergic and cholinergic nerve terminals ( NT release Vascular SM ( contraction (in skin and splanchnic) Fat cells ( inhibition of lipolysisą 2AOxymetazolineą 2BPrazosiną 2CPrazosin ReceptorAgonistAntagonistEndogenous agonistsEffectsSite and Action˛ receptorsIsoproterenol (˛1= ˛2); dobutamine (˛1> ˛2); terbutaline, metaproterenol, albuterol, ritodrine (˛2>> ˛1)PropanololIsopretenerol > E > NEGs protein ( activation of adenylyl cylcaseIncr conversion of ATP to cAMP (which is most important 2nd messenger here) ( in heart causes incr intracellular Ca) Causes relaxation of SM (poss via phosphorylation of myosin light-chain kinase to inactive form B2: May couple to Gq ( activate additional kinases˛ 1DobutamineBetaxololE = NEHeart ( incr HR and contractility˛ 2AlbuterolButoxamineE > NEResp, uterine, vascular SM ( SM relaxation Skeletal muscle ( incr K uptake Liver ( glycogenolysis˛ 3Fat cells ( lipolysis ReceptorAgonistAntagonistEndogenous agonistsEffectsSite and ActionDopamine receptorsDopamine (D1=D2); fenoldopam (D1>>D2)Important in brain, splanchnic and renal vasculatureD1FenoldopamIncr cAMP; stimulation of adenylyl cyclase ( cAMP accumulation ( SM relaxationSM ( dilates renal BV’sD2BromocriptineDecr cAMP; inhibit adenylyl cyclase, open K channels, decr Ca influxNerve endings ( modulates NT releaseD3Decr cAMPD4ClozapineDecr cAMPD5Incr cAMP Organs: BV: ą ( vasoC ˛ ( vasoD D ( vasoD Skin and splanchnic have alpha; muscles have both; renal, splanchnic, coronary, cerebral have D Heart: ˛1 most important ( Ca influx ( +ive chonotropic effect (incr pacemaker activity, incr conduction velocity at AVN, decr refractory period), +ive inotropic effect (incr contractility, faster relaxation) ( decr ejection time, faster change in IVp BP: ą agonist ( incr peri arterial resistence ( incr BP ( baroreceptor mediated decr HR ( decr venous capacitance ( incr venous return ( incr SV ( +ive inotropic effect ˛ agonist ( incr CO ( net effect slight incr SBP, fall DBP ( ˛2 ( decr peri resistance Eye: ą agonist ( mydriasis, incr outflow of aq humour (( decr IOp) ˛ agonist ( little effect ˛ antagonist ( decr production aq humour RS: ˛2 agonist ( bronchodilation ą agonist ( decongestants for URT GI: ą and ˛ agonist ( relaxation of GI SM (ą works via presynaptically decreasing release of Ach) GU: ˛ agonist ( relaxation of uterus ą1 agonist ( contraction of bladder base, urethral sphincter and prostate ( urinary continence ˛2 agonist ( relaxation of bladder ą receptors needed for ejaculation Exocrine: salivary gland have adrenoceptors but sympathomimetics cause dry mouth via central effects Metabolic: ˛3 agonist ( incr lipolysis ( free fa and glycerol ą2 agonist ( decr lipolysis ˛2 agonist ( uptake of K into cells ( prevent hyperK during exercise Sympathomimetics ( enhance glycogenolysis in liver ( incr glu; may cause metabolic acidosis Endocrine: ˛ agonist ( incr insulin secretion ą2 agonist ( decr insulin secretion ˛1 agonist ( incr renin secretion ą2 agonist ( decr renin secretion CNS: catecholamines can t cross BBB unless in high levels ( nervousness etc& ; amphetamine can cross BBB Catecholamines: 1) Epinephrine: ˛1 ( +ive inotrope and chonotrope ( incr SBP ą ( vasoC ( incr SBP ˛2 ( vasoD in muscles ( decr PVR, decr DBP 2) Norepinephrine: ˛1 ( +ive inotrope and chonotrope ( incr SBP; chonotrope effects overcome by vagal stimulation ą ( vasoC ( incr SBP Little effect on ˛2 so incr SBP and DBP 3) Isoproterenol: ˛1 ( +ive inotrope and chonotrope ( incr SBP and CO ˛ ( potent vasoD ( decr DBP and MAP, slight incr/decr SBP Little effect on ą 4) Dopamine: D1 ( vasoD inc renal bed ( decr peri resistance D2 ( suppress NE release ˛1 also activated ( +ive inotrope and chonotrope ( incr SBP ą activated at higher doses ( vasoC inc renal bed ( mimic E 5) Fenoldopam: selective for D1 ( vasoD; for trt of severe hypertension 6) Dobutamine: selective for ˛1( +ive inotrope and chonotrope ( incr SBP and CO Other sympathomimetics: 1) Phenyephrine: almost pure ą agonist ( vasoC ( incr SBP; mydriatic; decongestant; not inactivated by COMT so has longer duration of action 2) Methoaxamine: ą1 agonist ( incr BP, reflex bradycardia 3) Midodrine: ą1 agonist; used for postural hypoT 4) Ephedrine: high bioavailability and long DOA; mild stimulant as crosses BBB 5) Pseudoephedrine: decongestant 6) Xylometazoline, oxymetazoline: ą agonist; used as decongestant 7) Amphetamine: similar to ephedrine but crosses BBB well 8) Methamphetamine: similar to 7 but higher central vs peri effects 9) Phenmetrazine: similar to above but used as anorexiant 10) Methylphenidate and pemoline: similar to above but good in children with ADHD 11) Cocaine: inhibits reuptake at noradrenergic synapses (inc dopamine in brain) ( shorter more intense amphetamine like response 12) Tyramine: given IV causes release of stored catecholamines; intensified effect if on MAO inhibitors ( incr BP Receptor selective drugs: 1) ą2 agonist (clonidine, methyldopa, guanfacine, guanabenz): decr BP via central mechanisms 2) ˛1 agonist (dobutamine, prenalterol): less vasoD so less reflex incr HR; incr CO 3) ˛2 agonist (ritodrine, terbutaline): in asthma and premature labour Applications: 1) Hypotensive emergency: ą agonist for vasoC (NE, phenylephrine, methoxamine); if in shock will already have vasoC so +ive inotrope needed (dopamine, dobutamine) 2) To decr blood flow (eg. in LA, decongestant): ą agonist best (E, cocaine, phenylephrine, ephedrine) 3) 3rd deg HB and cardiac arrest: isoproterenol, E; redistribute blood to CA and brain 4) Asthma: ˛ agonist (isoproterenol), ˛2 agonist (metaproterenol, terbutaline, albuterol) 5) Anaphylaxis: E 0.3-0.5mg IM 6) Eye: phenylephrine for mydriasis; ą2 agonists (apraclonidine, brimonidine) decr IOp in glaucoma 7) GU: ˛2 agonist (ritodrine, terbutaline) relax uterus in premature labour 8) CNS: modanfinil for narcolepsy; methylphenidate/clonidine for ADHD SE: incr BP, cardiac ischaemia, heart failure, incr HR, arrhythmias, occasional CNS SE Adrenoceptor antagonists: Action˛ BLOCKERS: DECR AFTERLOAD (PVR, dilatation of resistence vessels) DECR PRELOAD (dilate capacitance vessels) DECR CONTRACTILITY (negative inotrope ( decr myocardial O2 requirement) DECR HR (negative chonotrope; prevent adverse effects of high NE levels (inc apoptosis and remodeling) and upregulation of beta-receptors; incr coronary perfusion time ( incr coronary perfusion) Decr CO, slight incr EF Undesirable: incr end-diastolic vol and ejection time ( incr myocardial O2 requirement (balance with concomitant use of nitrates); may cause incr PVR due to unopposed ą action as CNS discharges due to decr BP but this effect will decr in time Also decr renin (due to SNS) RS: ˛2 blockade ( incr airway resistence, so ˛1 selective better Eye: decr IOp due to decr aq humour production Metabolism: may decr lipolysis and glycogenolysis; caution in IDDM; decr HDL Some selective for cardiac beta1-receptors, some have intrinsic sympathomimetic activity, some prolong cardiac AP; some direct membrane effects Competitively antagonistic; most are pure antagonists (some are partial/inverse agonists); selectivity is dose-related and decr at higher doses Propanolol: helpful preventing incr HR from trt with direct vasodilators; decr mortality in CCF; non-selective ˛-blockade ( decr CO, inhibits stimulation of renin production by NE+E via ˛1, acts on peri presynaptic ˛-adrenoceptors to decr sym vasoconstrictor nerve activity; doesn t cause prominent postural hypoT; may block 5-HT in brain Block Na channel: normal cells (0), depolarized cells (+) Refractory period: normal cells (-), depolarized cells (++) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: (--) Sympatholytic activity: (+++) Effect on AVN refractory period: (++) PR interval: (++) QRS duration: 0 QT interval: 0 Esmolol: ˛1-antagonist; for trt of op/post-op hypertension esp if assoc with incr HR Block Na channel: normal cells (0), depolarized cells (+) Refractory period: normal cells (0), depolarized cells ? Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: (--) Sympatholytic activity: (+++) Effect on AVN refractory period: (++) PR interval: (++) QRS duration: 0 QT interval: 0 Sotalol: non-selective; has classe 2 and 3 actions; l-isomer has beta-blocking activity, l- and d-isomers prolong AP Block Na channel: normal cells (0), depolarized cells (0) Refractory period: normal cells (++), depolarized cells (+++) Ca channel blockade: 0 Effect on pacemaker activity: (--) Effect on SAN rate: (--) Sympatholytic activity: (++) Effect on AVN refractory period: (++) PR interval: (++) QRS duration: 0 QT interval: (+++) Metoprolol, acebutolol, alprenolol, atenolol, betaxolol, celiprolol, esmolol, bisoprolol – ˛1>˛2; more cardioselective so better if asthma, diabetes or PVD Propanolol, carteolol, penbutolol, pindolol, timolol, nadolol, carvedilol: non-selective Butoxamine: ˛2> ˛1 Pindolol, carteolol, celiprolol acebutolol and penbutolol  partial ˛-agonist; decr PVR; decr CO and HR less than other ˛-blockers as some intrinsic SNS retained via ˛2-receptors, good in bradycardia/asthmatics; may not be as good after MI; less effect on HDLIndicationHypertension, angina  relieve angina and incr exercise tolerance, decr ischaemic time per day; decr mortality with recent MI, improve survival in CVA with hypertension Chronic CCF (decr mortality with bisoprolol, carvedilol, metoprolol – as tachycardia and high NE levels help downward course; initiate cautiously at low doses) Acute MI (relative CI bradycardia, hypotension, LVF, shock, HB, airways disease) Less good at suppressing ventricular arrhythmias, but good in SVT, AF and flutter; decr ventricular ectopic beats; Sotalol for life threatening ventricular arrhythmias; good for arrhythmias in paeds; Esmolol for intraop and acute arrhythmias (esp in thyrotoxicosis and MI) Timolol, levobunolol and betaxolol for glaucoma Also for obstructive cardiomyopathy (decr outflow resistence, incr SV), dissective aortic aneurysm (decr r of development of systolc p), thyroid storm, migraines, anxiety, decr portal vein p in cirrhosisRoute of administrationPropanolol: od/bd Esmolol: given IVDosePropanolol: 80-480mg/day Metoprolol: 200-400mg/day Nadolol: 40mg/day Atenolol: 50mg/day Carteolol: 2.5mg/day Pindolol: 10mg Acetbutolol: 400mg Dosing IntervalAbsorptionUsually well absorbed PO; peak conc 1-3hrs following ingestion; SR propanolol and metoprolol availableBioavailabilityPropanolol: 25% (low but dose dependent) Metoprolol: 40% Sotalol: 100% Atenolol: 40% Carvedilol: 25-35% Esmolol: 0Half lifePropanolol: 3-5hrs Metoprolol: 3-7hrs Bisoprolol: 9-12hrs Esmolol: 9-10mins; steady state achieved quickly Sotalol: 7hrs Nadolol: up to 24hrs as not metabolized and excreted unchanged in urine Atenolol: 6-9hrs Carvedilol: 7-10hrsDuration of ActionNadolol: v longDistributionRapid distribution, large VOD’s Propanolol, carvediolol and penbutolol lipophilic and cross BBBMetabolismPropanolol: extensive 1st pass but becomes saturated so more reached circ at higher doses; variable effect between people as diff amount 1st pass Betaxolol and bisoprolol – in liver Esmolol – rapidly metabolized by hydrolysis by RBC esterases Sotalol – not in liver Celiprolol and pindolol – less completely metabolized Carvedilol – extensive in liverExcretionNadolol, carteolol, atenolol, sotalol – not metabolized, excreted in urine unchanged Propanolol and metoprolol – little unchanged drug appears in urine due to extensive metabolism Elimination prolonged by liver disease, decr hepatic blood flow, hepatic enzyme inhibitionSide effectsNon-selective agents ( worsened asthma and PVD; ˛1 may be better If abnormal myocardial fx, CO may be dependent on sympathetic drive ( CCF, impaired exercise tolerance Central (in lipophilic): fatigue, insomnia, sedation, depression, unpleasant dreams May get withdrawal symptoms poss due to up-regulation/supersensitivity of ˛  adrenoceptors (( nervousness, incr HR, incr angina, incr BP) Also worsened diabetes Decr nadolol, carteolol and atenolol doses in renal failure Sotalol ( dose related torsade de pointes, exacerbation of CCFContraindicationsAsthma, severe bradycardia, AV blockade, bradycardia-tachycardia syndrome, severe unstable LVFDrug interactionsQuinidine and fluoxetine inhibit metabolism of carvedilol Interact with Ca antagonists ( severe hypoT, bradycardia, CCF, conduction abnormalitiesPregnancyExamples Actioną BLOCKERS: Decr arterial p by dilating resistance and capacitance vessels ( postural hypoT after 1st dose; may be reverible/irreversible ( decr PVR and BP NB. ą antagonism can convert pressor effect of E to depressor effect  epinephrine reversal Prazosin, terazosin, tamsulosin, alfuzosin, indoramin and doxazosin  ą1-blockers in arterioles and venules; cause less reflex tachycardia than non-selective ą-antagonists, allowing NE to exert unopposed negative feedback (via presynaptic ą2-receptors); prazosin is reversible; tamsulosin 1A>1B and esp good for prostate Phentolamine  nonselective reversible ą1 and 2-blocker; blocks both pre- and post-synaptic receptors so reflex activation of sym neurons causes greater release of NT onto ˛-receptors so greater cardioacceleration; also minor agonist for muscarinic and histamine receptors, minor antagonist for 5-HT Phenoxybenzamine: irreversible via formation of covalent bonds; slightly ą1-selective; also blocks H1, Ach and 5-HT receptors; also inhibits reuptake of NE; decr BP when sympathetic tone high (eg. upright posture, low BV), reflexes incr CO Rauwolscine, yohimbine, tolazoline: ą2-selective; little clinical use Note: neuroleptic drugs also have alpha-blocking effectsIndicationHypertensive emergencies (esp if due to XS catecholamines eg. sympathomimetic OD); phentolamine and phenoxybenzamine for phaeochromocytoma esp pre- and peri-op (don’t use only beta-blockers as may cause incr BP from incr vasoC); chronic hypertension; male erectile dysfunction; BPH (alpha-1)Route of administrationDose‘-blockers: give nocte Dosing IntervalPrazosin: 10-30mg/day Terazosin: 5-20mg/day Doxazosin: 1-4mg/dayAbsorptionPhentolamine: poor PO Phenoxybenzamine: POBioavailabilityPrazosin: 50-70% Phenoxybenzamine: low Terazosin: high Doxazosin: mod Tamsulosin: high Alfuzosin: 60%Half lifePrazosin: 3-4hrs Terazosin: 9-12hrs Phentolamine: 5-7hrs Doxazosin: 22hrs Tamsulosin: 9-15hrs Alfuzosin: 5hrsDuration of ActionFor reversible – dependent on half life and rate at which dissociates from receptor For irreversible – effects last long after drug has been cleared from plasma, dependent on synthesis of new receptorsDistributionMetabolismTerazosin – little 1st pass; but extensively metabolized in liver Prazosin: extensive degradation in liver Doxazosin, alfuzosin and tamsulosin: extensive metabolism in liverExcretionRenalSide effectsRetention of salt and H20, need to be used with diuretic; can can cause postural hypoT and reflex incr HR (more marked in ą2-blockers of heart, as incr E release further stimulates ˛ receptors); arrhythmia, myocardial ischaemia Dizziness, palpitations, headache, lassitude Miosis and nasal congestion, decr resistance to flow of urine, inhibition of ejaculation Phenoxybenzamine: enters CNS ( fatigue, sedation, nausea prazosin ( ANAContraindicationsDrug interactionsPregnancyExamples Mixed antagonists: labetolol (˛>ą1; reversible; decr SVR without change in HR or CO; helpful for phaeochromocytoma and hypertensive emergencies; 200-2400mg/day), carvedilol (6.25mg bd; 7-10hr halflife, metabolized in liver) DRUGS USED IN CARDIAC ARREST: to do Anticoagulants Physiology: In clotting cascade CF’s undergo proteolysis to become active protease which activates next CF ( ends in formation of thrombin (factor IIa) Vascular endothelial cell layer has anticoagulant phenotype ( vascular injury ( more procoagulant as subendothelial matrix ( release of thromboxane A2 (plt adherence and activation) adenosine diphosphate (plt aggregation, released from plts) 5-HT (vasoconstriction and aggregation) ( Activation of plt ( change in ąIIb˛III integrin receptor ( bind fibrinogen, crosslinks plts ( aggregation ( exposes tissue factor (TF) which binds factor VIIa ( activates factors X and IX (this is regulated by tissue factor pathway inhibitor (TFPI) ( factors Xa and factor Va form prothrombinase complex on activated cell surfaces ( catalyses conversion of prothrombin (factor II) to thrombin (factor IIa) ( proteolytically cleaves peptides from fibrinogen ( fibrinogen polymerises to form fibrin clot ( activates other CF’s (V, VIII, IX, XI) ( propogates more thrombin generation ( activated factor XIII that crosslinks fibrin and stablises clot ( activates protein C pathway that attenuates clotting response Antithrombin inactivates IIa, IXa, Xa, XIa, and XIIa by forming complexes with them (slow process) Protein C and S cause proteolysis of Va and VIIIa ( attenuate clotting cascade Disorders: Mutation in factor V ( factor V Leiden ( resistance to inactivation by protein C/S mechanism ( incr clotting Deficiency of antithrombin, protein C/S ( recurrent thrombosis Plt-rich thrombi (white thrombi) develop in highflow rate arteries; fibrin-rich thrombi (red thrombi) develop in veins FactorSynonymDrugIFibrinogenIIProthrombinHeparin (IIa), warfarin (synthesis)IIITissue thromboplastinIVCalciumVProaccelerinVIIProconvertinWarfarin (synthesis)VIIIAntihemophilic factor (AHF)IXChristmas factor, plasma thromboplastin component (PTC)Warfarin (synthesis)XStuart-Prower factorHeparin (Xa), warfarin (synthesis)XIPlasma thromboplastin antecedent (PTA)XIIHageman factorXIIIFibrin-stabilising factorProtein C and SWarfarin (synthesis_PlasminogenThrombolytic enzymes, aminocaproic acid Fibrinolysis: fibrin digestion by plasmin; vascular injury ( endothelial cells synthesise and release tissue plasminogen activator (tPA) ( converts plasminogen to plasmin ( remodels thrombus and limits extension by protein domains binding exposed lysines on fibrin clot making the process clot specific Endothelial cells make and reslease plasminogen activator inhibitor (PAI) which inhibits tPA ą2 antiplasmin circulates and inactivates plasmin that is not clot-bound Indirect Thrombin Inhibitors: interact with antithrombin and enhance inactivation of factor Xa ActionHeparin: aim for level 0.2-0.4unit/mL (protamine titration) or 0.3-0.7unit/mL (anti-Xa units) (APTT 2-2.5x); measure APTT 6hrs after dose if intermittent SC Binds to antithrombin ( conformational change in antithrombin ( expose antithrombin’s active site ( more rapid interaction with activated CF’s ( heparin then released to interact with another antithrombin; generally given as a Na salt HMWH/UFH: high affinity for antithrombin; inhibit all 3 factors esp thrombin and Xa LMWH (enoxaparin, dalteparin, tinzaparin, danaparoid): less effect on thrombinIndicationRoute of administrationSC/IVDoseIV bolus: 80-100units/kg ( infusion of 15-22units/kg/hr SC: 5000units every 8-12hrs Enoxaparin 40mg od prophylactic, 1mg/kg trt Dalteparin: 5000units od, 200 units/kg for venous disease, 120 units/kg for ACSDosing IntervalHMWH: less frequentAbsorptionBioavailabilityHMWH: higherHalf lifeFondaparinux – 15hrs (od dosing)Duration of ActionDistributionMetabolismExcretionSide effectsBleeding – more prone in renal failure and elderly Thrombocytopenia: in 1-4% on HMWH for 1/52; causes thrombosis – treat with removal of heparin and giving thrombin inhibitor Alopecia, OP, mineralocorticoid deficiencyContraindicationsActive bleeding, hemophilia, thrombocytopenia, purpura, severe hypertension, intracranial haemorrhage, infective endocarditis, active TB, GI ulcers, threatened abortion, visceral Ca, advanced hepatic/renal disease, recent surgery/LP Caution in renal insufficiency or obesityDrug interactionsPregnancyExamplesClose monitoring of APTT needed in HMWH LMWH monitoring not needed as more predictable (except in renal insufficiency, obesity, pregnancy) – measured with anti-Xa units Antidote is protamine sulphate – forms complex with heparin; give 1mg for every 1mg heparin given Direct Thrombin Inhibitors: ActionDirectly bind to active site of thrombin ( inhibit thrombin Hirundin, bivalirudin, lepirudin: bind at active site and substrate recognition site of thrombin; Lepirudin: as independent of thrombin can reach fibrin-bound thrombin in thrombi; little effect on plt or bleeding time Bivalirudin: inhibits plt activation Argatroban, melagatran: bind at thrombin active site Ximelagatran: predictable response so less close monitoringIndicationHIT caused by heparinRoute of administrationIVDoseDosing IntervalAbsorptionBioavailabilityHalf lifeBivalrudin: short Argatroban: shortDuration of ActionBivalirudin and ximelagatran: rapid onset and offset of effectsDistributionMetabolismExcretionBivalrudin: 20% renal, 80% metabolic Argatroban: clearance needs liver functionSide effectsLepirudin: May have severe allergic reaction Ximelagatran: hepatic toxicityContraindicationsLepirudin: Caution in renal insufficiency Argatroban: caution in hepatic insufficiencyDrug interactionsPregnancyExamplesMonitor with APTT Lepirudin: may develop ab to thrombin-lepirudin complex ( enhanced anticoagulant effect Argatroban: increases INR Warfarin and Coumarin Anticoagulants: ActionAdministered as a sodium salt; racemic mixture of S- (most potent) and R-warfarin; block ł-carboxylation of glutamate residues (this reaction is coupled to oxidation of vit K to vit K epioxide) in prothrombin and factors VII, IX and X and anticoagulant proteins C and S ( incomplete CF molecules which are biologically inactive; vit K must be reduced to active hydroquinone form to reactivate it – warfarin prevents thisIndicationRoute of administrationDoseDuring dosing, beyond 0.75mg/kg (up to 10mg) doesn’t inc speed of onset of action; takes a week usually to reach correct dosage (PT incr to 25% less PT activity than norm); INR is PT ratio (patient PT time / mean normal PT time for lab); ISI = 1, International Sensitivity Index, which uses WHO reference standard thromboplastin so diff instruments and stuff will give same INRDosing IntervalAbsorptionBioavailability100%Half life36hrsDuration of Action8-12hr delay in action; inhibition dependent on degradation half life of altered CF’s (6, 24, 40, 60hrs for VII, IX, X, II)DistributionOver 99% bound to albumin, so small VODMetabolismExcretionSide effectsReverse by stopping drug and giving PO/IV Vit K (phytonadione), FFP, PT complex concentrates (Bebilin, Proplex T), recombinant factor VIIa; since warfarin has long halflife may need >1 dose Warfarin resistance – thrombotic event when in therapeutic range, esp occurs with GI CaContraindicationsDrug interactionsCan occur pharmacokinetically – enzyme induction/inhibition, decr plasma binding Pharmacodynamically – synergism (altered clotting), competitive antagonism (vit K) Incr PT time (more anticoagulant effect): PK - amiodarone, cimetidine, disulfiram (inhibit metabolism of S- and R-warfarin) metronidazole, fluconazole, trimethoprim (inhibit metabolic transformation of S-warfarin) phenylbutazone and sulfinpyrazone (inhibit oxidative metabolism of S-warfarin and displacement of albumin- bound warfarin so incr free fraction; most dangerous as also alter plt function and induce PUD) PD – aspirin (inhibit plt’s) hepatic disease, hyperthyroidism (incr turnover rate of CF’s) cephalosporins (3rd gen) (eliminate bacteria in GI tract that produce vit K; inhibit vit K epoxide reductase) heparin Decr PT time (prothrombotic): PK - barbs, rifampicin, (induce hepatic enzymes) Cholestyramine (binds warfarin in intestine, decr absorption and bioavailability) PD – diuretics (incr conc of CF’s) vit K (incr synthesis of CF’s) hypothyroidism (decr turnover rate of CF”s)PregnancyWarfarin crosses placenta readily ( haemorrhagic disorder of fetus and birth defects due to abnormal bone formationExamples Fibrinolytic Drugs ActionCatalyse formation of plasmin from precursor plasminogen Streptokinase: combines with plasminogen, catalyzing its transformation Urokinase: human enzyme made by kidney that directly converts plasminogen to plasmin Anistreplase: purified human plasminogen + bacterial streptokinase; when given acyl group spontaneously hydrolyses ( streptokinase-proactivator complex; has greater clot sensitivity and thrombolytic activity tPA (manufactured as alteplase, reteplase, tenecteplase): preferentially activates plasminogen that is bound to fibrin, so theoretically only lyses thrombus; reteplase is less thrombus-specific, tenecteplase has longer halflife and is more clot-specificIndicationIV – PE with haemodynamic instability, severe DVT, ascending thrombophlebitis of iliofemoral vein Acute MI – streptokinase CVA within 3hrs of symptomsRoute of administrationDoseStreptokniase in MI: 250,000iu loading ( 100,000iu/hr over 24-72hrs Urokinase: 300,000iu over 10minrs ( 300,000iu/hr over 12hrs Alteplase: 60mg over 1st hr ( 20mg/hr for 2hrs Reteplase: 10iu bolus twice Tenecteplase: 0.5mg/kg once In CVA, recombinant tPA: 0.9mg’kg (not >90mg) 10% as bolus, rest over 1hrDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsStreptokinase: if have antistreptococcal ab’s ( fever, allergic reaction, therapeutic resistanceContraindicationsDrug interactionsPregnancyExamples Antiplatelet agents Action3 mechanisms of action: 1) Agents generated outside plt that interacts with plt membrane receptors: catecholamines, collagen, thrombin, prostacyclin 2) Agents generated inside plt that interact with membrane receptors: ADP, PGD2, PGE2, 5-HT 3) Agents generated in plt that act within plt: PG endoperoxides, thromboxane A2, cAMP, cGMP, Ca ion So can inhibit PG synthesis – aspirin inhibits formation of thromboxane A2 by irreversible acetylation of COX Inhibit ADP-induced plt aggregation – clopidogrel, ticlopidine irreversibly block ADP receptor on plts Block glycoprotein IIb/IIIa receptors on plts – abciximab, tirofiban, eptifibatide; receptors for vibronectin and von Willebrand factor which is final common pathway for plt aggregation Also dipyridamole – inhibits adenosine uptake and cGMP phosphodiesterase activity; used in combination with aspirin/warfarin Aspirin inhibits plt aggregration via inhibition of platelet COX (lasts 8-10 days) and decr production of thromboxane A2 Apirin also buffers and transports protons in mitochondria and induces formation of NO-radicals enabling WBC to fight infectionsIndicationTIA, stroke, MI, angina, ACSRoute of administrationIV for glycoprotein II/III blockersDoseAspirin: 1200 – 1500mg tid for analgesia; 325mg/day for prophylaxis of MI Ticlopidine: 250mg bd Clopidogrel: dose-dependent effects; effect within 5hrs of PO 300mg (80% plt activity inhibited); 75mg/day maintenanceDosing IntervalAbsorptionAspirin: peak level in 1-2hrsBioavailabilityAspirin: rapid and completeHalf lifeAspirin: 0.25hrs as rapidly hydrolysed; increases as dose increasesDuration of ActionClopidogrel: 7-10 daysDistributionMetabolismAspirin: hydrolysed to acetic acid and salicylate by esterases in tissue and bloodExcretionAspirin: <2% urinary excretion of unchanged drug; increases rate of excretion if alkalinsation of urineSide effectsAspirin: rashes, salicylism in high doses (vomiting, tinnitus, decr hearing, vertigo, hyperpnoea); toxicity ( resp alkalosis then metabolic acidosis, resp depression, cardiotoxicity, glu intolerance; incr bleeding in menstrual women; Reye’s syndrome in children (fatty degeneration of liver cells; high mortality rate), nephritis Ticlopidine: nausea, dyspepsia, diarrhoea; haemorrhage (5%), leucopenia (1%) monitor during 1st 3/12, TTP Clopidogrel: less SE than ticlopidine; TTPContraindicationsAspirin: haemophilia; GI bleeding with alcohol; displaces phenytoin, probenecid, valproic acid, methotrexate from protein binding sites; decr effect of spironolactoneDrug interactionsPregnancyExamples RESPIRATORY DRUGS Drugs Used in Asthma Pathogenesis of Asthma Non-specific bronchial hyperreactivity: tendancy to develop bronchospasm to stimuli that wouldn’t affect healthy lungs Foreign material provokes IgE ( IgE bind mast cells in airway mucosa. Reexposure to allergen ( Ag-ab interaction of surface of mast cells ( release of mediators stored in granules and synthesis of other mediators (histamine, tryptase, leukotrienes C4+D4, prostaglandin D2 ( muscle contraction, vascular leakage ( bronchoconstriction Late asthmatic response 2Y to influx of inflamm cells (eg. cytokines produced by TH2 cells – IL5,9,13 ( attract eosinophils, stimulate IgE production by B cells, stimulate mucus production by bronchial epithelial cells) into bronchial muscoa ( incr bronchial responsiveness lasting 7eral weeks. Neural pathways also thought to be involved in bronchoconstriction. Assessment: measure decr FEV1 ˛2-Selective Drugs ActionSalmeterol and formoterol  interact with inh corticosteroids to improve asthma Rapidly effective, safe, inexpensiveIndicationRoute of administrationINH, NEB (particles generated by nebs are larger than inh, so larger doses can be given ie. 2.5-5mg vs 100-400mcg BUT are no more effective and only for when people can’t co-ordinate for INH) PO – albuterol and terbutaline; no advantage over INH SC – terbutaline; for severe asthma in emergency treatmentDoseTerbutaline SC – 0.25mgDosing IntervalPRN; if required >2x/wk / if nocturnal symptoms >2x/month / if FEV1 <80% expected additional trt needed (ie. low dose inhaled corticosteroid)AbsorptionBioavailabilityHalf lifeDuration of ActionLong; max effect in 15-30mins; lasts 3-4hrs Salmeterol and formoterol – long-acting; 12+hrs due to high lipid solubility so can dissolve in SM cell membrane; known NOT to be effective in monotherapy so often combined in inhalers with corticosteroidsDistributionMetabolismExcretionSide effectsVasoD effect may incr perfusion of poorly ventilated lung units ( decr PaO2; giving supplemental O2 eliminates this Arrhythmias – unsubstantiated Tachyphylaxis - possible PO albuterol/turbutaline – tremor, nervousness, weaknessContraindicationsDrug interactionsPregnancyExamples Sympathomimetic Agents ActionRelax SM (despite no evidence of significant sym innervation, but much evidence that adrenoceptors are present) Inhibit release of bronchoconstricting mediators from mast cells Inhibit microvascular leakage Increase mucociliary transport by increasing ciliary activity Stimulate ˛2 receptors Stimulate adenylyl cyclase and incr levels of cAMP Epinephrine  incr HR and contractility via ˛1 receptor; also stimulates ą receptors; infrequently used for asthma Ephedrine  more pronounced central effects, lower potency; infrequently used for asthma Isoproterenol – potent; rarely used in asthma IndicationRoute of administrationINH – aerosol deposition depends on particle size, pattern of breathing (tidal vol and rate of airflow), geometry of airways; optimal size range 2-5mm; 80-90% will be deposited in mouth/pharynx; size 1-2źm will remain suspended and be exhaled SC  epinephrine PO - ephedrineDoseEpinephrine: SC: 0.4ml of 1:1000 solution; INH: 320mcg per puff Isoproterenol: 80-120mcg INHDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionEpinephrine: rapid action; max bronchoD 15mins post-inhalation; lasts 60-90mins Ephedrine: longer duration Isoproterenol: max effect in 5mins; 60-90min durationDistributionMetabolismExcretionSide effectsEpinephrine: tachycardia, arrhythmia, worsened angina (useful in vasoD and shock of anaphylaxis) Isopreterenol: cardiac arrhythmias Tachycardia, muscle tremorContraindicationsDrug interactionsPregnancyExamples Methylxanthines ActionInhibit phosphodiesterase family ( incr intracellular cAMP and cGMP ( stimulate cardiac function, relax SM, decr immune and inflamm action of specific cells (( decr release of cytokines and chemokines ( decr immune cell migration and activation); PDE4 seems to be most important Inhibit cell surface receptors for adenosine (which modulate adenylyl cyclase activity) ( prevent contraction of SM and histamine release from mast cells ( bronchoD; tolerance doesn’t develop Theophylline: 1,3-dimethylxanthine; most effective; not v soluble in H20 so delivered as a salt; can be used a sole trt or with steroids Theobromine: 3,7-dimethylxanthine Caffeine: 1,3,7-trimethylxanthine Aminopylline: a theophylline-etylenediamine complex Roflumilast. cilomilast, tofimilast: more specific for PDE4IndicationFor asthma where poorly controlled despite combined corticosteroid and ˛2-agonistRoute of administrationTheophylline: can be PODoseTheophylline: must measure levels as narrow therapeutic range; plasma conc 5-20mg/L; PO 3-4mg/kg 6hrly; takes 1-2 days to reach steady stateDosing IntervalAbsorptionTheophylline: good POBioavailabilityHalf lifeDuration of ActionTheophylline: SR versions availableDistributionMetabolismTheophylline: liverExcretionTheophylline: mean clearance is 0.69mL/kg/min (children faster; slower in neonates and young infants)Side effectsNausea and vomiting CNS: cortical arousal, nervousness, insomnia, tremor; high doses ( convulsions; headache, insomnia CV: +ive chonotropic and inotropic effects; due to inhibition of presynaptic adenosine receptors in sym nerves ( incr catecholamine release at nerve endings; may also be due to incr influx of Ca and impaired sequestration of Ca by SR; ( tachycardia, incr CO, incr PVR, incr BP; may ( arrhythmias; can decr blood viscosity ( improve blood flow (pentoxifylline used in IC) GI: stimulate secretion of gastric acid and enzymes; anorexia, nausea Renal: weak diuretics (incr GFR, decr tubular Na reabsorption) Skeletal muscle: improve contractility; reverse fatigue of diaphragm in COPDContraindicationsDrug interactionsTheophylline: induction of hepatic enzymes by smoking/diet incr clearancePregnancyExamples Antimuscarinic Agents Action Atropine is potent competitive inhibitor of Ach at post-ganglionic muscarinic receptors. In airways, Ach released from efferent endings of vagus nerve ( bronchoC and incr mucus secretion; has NO effect on nonmuscarinic stimulation, only effective on muscarinic portion of bronchoC, so limited usefulness and efficacy varies between individuals as degree of involvement of paraS pathways varies between people Slightly less effective than ˛-agonistsIndicationGreater value in COPD, or if intolerant to ˛2-agonistsRoute of administrationAtropine: IV Atropine, ipratropium bromide, tiotropium: INHDoseTiotropium: 18mcgDosing IntervalAbsorptionIpratropiom bromide: poor absorption when given INH, so less SEBioavailabilityHalf lifeDuration of ActionTiotropium: longer acting; 24hrDistributionMetabolismExcretionSide effectsContraindicationsDrug interactionsPregnancyExamples Corticosteroids in Asthma Action Anti-inflammatory action via inhibition of production of inflammatory cytokines; reduce bronchial reactivity; poss contraction of engorged vessels in bronchial mucosa; inhibition of lymphocytic, eosinophilic muscosal inflammation Beclomethasone, budesonide, flunisolde, fluticasone, mometasone, triamcinoloneIndicationIf severe (FEV <50% expected) – state with INH and PO corticosteroid then taper PO dose If standard inhaled dose doesn’t work can: double inhaled dose; or add in long-acting ˛2-agonistRoute of administrationPO: if needs urgent treatment; 30-60mg prednisone per day; discontinue in 7-10days; give mane after ACTH peak; give in late afternoon for noctural symptoms IV: 1mg/kg methyprednisolone every 6hrs INH: for regular treatment; avoid systemic effectsDoseBeclomethasone: 400mcg/day in 4 puffs bd is equivalent to 10-15mg/day PO predDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsOropharyngeal candidiasis – gargle water after each use Hoarseness Long term: OP, cataracts, glu intolerance, worsened hypertension, cushingoid changesContraindicationsDrug interactionsPregnancyExamples Cromolyn and Nedocromil Action Stable but insoluble salts ( as aerosols inhibit allergen, antigen and exercise induced asthma Have no effect on airway SM tone and ineffective in reversing asthmatic bronchospasm; only of use when taken prophylactically Not as potent or effective as corticosteroids; best in young pt’s Alter function of delayed Cl channels in cell membrane ( inhibit cell activation ( inhibit cough, inhibit mast cell response to Ag challenge, inhibit eosinophilic inflamm response Cromolyn sodium (disodium cromoglycate): Nedocromil sodium:IndicationAsthma Also useful for allergic rhinoconjunctivitis as nasal spray / eye dropsRoute of administrationINH onlyDoseDosing IntervalAbsorptionPoorBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsMinor as so poorly absorbed; throat irritation, cough, mouth dryness <2% - reversible dermatitis, myositis, gastroenteritis, pul infiltration with eosinophilia, anaphylaxisContraindicationsDrug interactionsPregnancyExamples Others Action Leukotriene Pathway Inhibitors: leukotrienes result from action of 5-lipoxygenase on arachidonic acid ( synthesized by inflamm cells in airways (incr eosinophils, mast cells, macrophages, basophils) ( leukotriene B4 is neutrophil chemoattractant, LTC4 and LTD4 known to be involved in asthma; block synthesis of these arachidonic acid derivatives Inhibition of 5-lipoocygenase prevents leukotriene synthesis (eg. zileuton) Inhibition of binding of LTD4 to target tissues prevents action (eg. zafirlukast, montelukast) Anti-IgE Monoclonal Antibodies (eg. omalizumab): inhibits binding of IgE to mast cells; inhibits IgE synthesis by B cellsIndicationLeukotriene pathway inhibitors – good for aspirin induced asthmaRoute of administrationDoseZileuton – 400-800mg bd-qid PO Zafirlukast 20mg bd Montelukast 10mg odDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsContraindicationsDrug interactionsPregnancyExamples Antitussives Opioid analgesics achieve this at doses lower than analgesic doses, act on different receptors Dextromethorphan, codeine, levopropoxyphene, nocapine: used; use with caution with monoamine oxide inhibitors Dextro – free if addictive properties; less constipation than codeine; 15-30mg 3-4x daily Levo – devoid of opioid effects, but does cause sedation Oxygen TO DO ANTIMICROBIAL AGENTS Bacteria Cell wall: surrounds cytoplasmic membrane, maintains cell shape and integrity, prevents cell lysis from high osmotic p Composed of peptidoglyccan (cross-linked polymer of polysaccharides and polypeptides) Contains aa’s N-acetylglucosamine N-acetylmuramic acid (which is linked to a 5-aa peptide terminating in D-alanyl-D-alanine, which is removed by penicillin-binding protein (PBP) to form cross-link with nearby peptides, giving wall structural rigidity) Classification of Bacteria G+ive Bacteria COCCIStaphAppear in clumps Produce catalase and coagulase Eg. Staph aureus Eg. Coag neg staph (which are resistant to drying)StrepAppear in chains Eg. ą-haemolytic (viridans) strep cause partial breakdown of blood (eg. strep pneumoniae ( pneumonia and meningitis Eg. ˛-haemolytic strep cause complete breakdown of blood (eg. strep pyogenes) Eg. Non-haemolytic strep – enterococci (eg. enterococcus faecalis)RODSAerobic sporingBacillus (eg. bacillus antracis, bacillus cereus ( food poisoning) Anaerobic sporingClostridium (eg. clostridium perfringens ( gangrene, clostridium tetani, clostridium botulinum ( food poisoning)Non-sporingListeria monocytogenes Lactobacilli (are coag neg) Corynebacterium diphtheriaeMycobacteriaHave v waxy cell wall and require Ziehl Neelson technique; are alcohol and acid fast bacilli Eg. Mycobacterium tuberculosis, mycobacteria leprae Suspected Pathogen1st ChoiceAlternativesG+ive COCCIStreptococcus pneumonaiePenicillinDoxycycline Ceftriaxone / cefuroxime Quinolone ErythromycinStreptococcus pyogenes (Grp A)Penicillin ClindamycinErythromycin 1st generation cephalosporinStreptococcus agalactiae (Grp B)PenicillinVancomycinStrep viridansPenicillin1st or 3rd generation cephalosporin VancomycinStaph aureus, beta-lactamase -Penicillin1st generation cephalosporin VancomycinStaph aureus, beta-lactamase +Penicillinase-resistant penicillinAs aboveMRSAVancomycinT-S (1:5 by the way!) DaptomycinEnterococcusPenicillin +/- aminoglycosideVancomycin + aminoglycosideG+ive RODSBacillusVancomycinImipenem Quinolone ClindamycinListeriaAmpicilin +/- aminoglycosideT-SNocardiaSulfadiazine T-SImipenemAnaerobesClostridia, actinomyces (anaerobe)Penicillin ClindamycinVancomycin ChloramphenicolC difficile (anaerobe)MetronidazoleVancomycinMycobacteriaM TBIsoniazid + rifampicin + ethambutol + pyrazinamideStreptomycin Quinolone EthionamideM lepraeDapsone + rifampicin + clofazimine G-ive Bacteria COCCIAerobicNeisseria (eg. neisseria meningitides ( meningitis; neisseria gonorrhoeae ( gonorrhoeaCOCCOBACILLIAerobicBordetella, Haemophilus, PasteurellaBACILLI / RODSEnterobacteriaceaeCan be aerobic/anaerobic Eg. Escerichia coli, Klebsiella, salmonella typhi, salmonella enteritidis, shigella dysenteriae, proteeae, proteusPseudomonasMake oxidase enzyme; aerobic Eg. Psuedomonas aeruginosaCurved G-ive rodsVibrio cholerae ( cholera Campylobacter Helicobacter pyloriOthersMoraxella, acinetobacter, legionella, bordetella pertussis (whooping cough) Bacteroides (anaerobic) Suspected Pathogen1st ChoiceAlternativesG-ive CocciMoraxella catarrhalisT-S 2nd or 3rd generation cephalosporinErythromycin / clarithryomycin / azithromycin QuinoloneNeisseria gonorrhoeaeCeftriaxone, cepodoximeSpectinomycin CefoxitinNeisseria meningitidesPenicillin GChloramphenicol 3rd generation cephalosporinG-ive RodsE Coli, Klebsiella, Proteus1st or 2nd generation cephalosporin T-SQuinolone AminoglycosideEnterobacter, citrobacter, serratiaT-S Quinolone CarbapenemPenicillin Aminoglycoside CefepimeShigellaQuinoloneT-S Ampicillin Azithromycin CeftriaxoneSalmonellaT-S Quinolone 3rd generation cephalosporinChloramphenicol AmpicillinCampylobacter jejuniErythromycin / azithromycinTetracycline Quinolone\BrucellaDoxycycline + rifampicin / aminoglycosideChloramphenicol + aminoglycoside / T-SH pyloriBismuth + metronidazole + tetracycline / amoxicillinPPI + amoxicillin / clarithromycinPseudomonas aeruginosaPenicillin + aminoglycosidePenicillin + quinolone Cefepime, ceftazidime Imipenem, meropenemLegionellaAzithromycin + rifampicin Quinolone + rifampicinClarithromycin / erythromycin DoxycyclineBacteroides fragilis (anaerobe)MetronidazoleChloramphenicol Carbapenems Beta-lactam plus beta-lactamase inhibitor Clindamycin Others Chlamydia (trachomatis, pneumoniae, psittaci): tetracycline and erythromycin preferred; can use clindamycin / clarithromycin / chloramphenicol Mycoplasma pneumoniae: tetracycline, erythromycin preferred; can use azithromycin / clarithromycin / quinolone CLINICAL USE OF ANTIMICROBIAL AGENTS Empiric: use of AB before MO is known; Formulate clinical diagnosis of microbial infection Obtain specimens for lab exam Formulate microbiologic diagnosis Determine necessity for empiric therapy – if serious risk of morbidity of therapy withheld until MO identified, if public health benefits (eg. STI) Institute trt Host factors: concomitant disease states (eg. AIDS, liver disease), prior adverse drug reactions, impaired elimination, age of pt, pregnancy status Pharmacologic factors: kinetics of absorption, distribution, elimination; ability of drug to be delivered to site of infection; potential toxicity of agent; pharmacokinetic/dynamic interactions with other drugs; cost Cultures: may fail due to Sample error (eg. cultures taken after AB given) Noncultivatable or slow-growing MO Infection actually due to virus / fungi Special media needed Tests measure: minimal inhibitory concentration (MIC) required to inhibit growth minimal bactericidal concentration (MBC) required to kill MO – used when required for eradication of infection (eg. meningitis, endocarditis, sepsis in neutropenia) Can do: beta-lactamase assay; synergy study (to see drug interactions) Therapeutic response: microbiologically – rpt cultures – find resistance/ superinfections clinically Duration of therapy: depends in pathogen, site of infection, host factors; if serious – 7-10/7 after pt afebrile Failure: rpt culture; look at drug dosing and absorption; look at immune function; ?abscess / FB Pharmacodynamics Pathogen susceptibility testing Drug synergism, antagonism Drug bactericidal vs bacteriostatic activity: if bacteriostatic, MIC lower; makes no difference in efficacy if immunocompetent, but use bactericidal if immunocompromised Bactericidal: generally cell wall active agents; can be concentration-dependent killing (aminoglycosides / quinlones) or independent (eg. beta-lactams, vancomycin) eg. aminoglycosides, beta-lactams, daptomycin, isoniazid, metronidazole, polymyxins, pyrazinamide, quinolones, rifampicin, vancomycin Bacteriostatic: generally inhibit protein synthesis; eg. chloramphenicol, clindamycin, ethambutol, macrolides, nitrofurantoin, sulfonamides, tetracyclines, trimetroprim Post-antibiotic effects: persistent suppression of growth after limited exposure to AB; reflects time required for bacteria to return to logarithmic growth; allows od dosing; due to Slow recovery after reversible nonlethal damage to cell structures Persistence of drug at binding site / in periplasmic space Need to synthesis new enzymes before growth can resume PAE = T (time required for viable count in culture to incr 10x above count observed immediately before drug removal) – C (time required for count in untreated culture to incr 10x) G+ive: most AB have PAE in vitro G-ive: aminoglycosides, carbapenems, chloramphenicol, quinolones, rifampicin, tetracyclines In vivo PAE > in vitro PAE due to postAB leukocyte enhancement and exposure of bacteria to subinhibitory AB concs Can be conc-dependent (eg. aminoglycosides, quinolones) so serum conc below MIC will still be effective (however if no PAE will need to keep conc above MIC between doses) Pharmacokinetics Route of administration: Similar PO/IV: tetracyclines, T-S, quinolones, chloramphenicol, metronidazole, clindamycin, rifampicin, fluconazole IV better if: critically ill, bacterial endocarditis/meningitis, N+V+gastrectomy+poor PO absorption, if AB has poor PO absorption Conditions that alter pharmacokinetics: Renal failure: acyclovir, amantadine, aminoglycosides, cephalosporins, clarithromycin, didanosine, ertapenem, ethambutol, famciclovir, fluconazole, ganciclovir, imipenem, lamivudine, meropenem, penicillins, quinolones, rimantadine, T-S, vancomycin, zidovudine Hepatic failure: amprenavir, chloramphenicol, clindamycin, erythromycin, indinavir, metronidazole, rimantadine Pt with burns, CF, trauma may need incr dosages; may alter in elderly, neonates, pregnancy Drug concs in body fluids: most do not penetrate uninflamed meninges well Measuring serum concs: eg. aminoglycosides, vancomycin; needed if There is a direct relationship between drug conc and efficacy/toxicity Substantial interpatient variability in serum concs on standard doses Small difference between therapeutic and toxic serum concs Clinical efficacy or toxicity of drug delayed or difficult to measure Accurate assay available Drug Reactions Cross-reactivity between penicilinns and cephalosporins is <10%, but avoid in hypersensitivity reactions Cross-reactivity between penicillins and carbapenems >50% Combination Therapy When unnecessary: incr toxicity and cost; drugs may have antagonistic effects Indicated: broad-spectrum empiric therapy in seriously ill patient polymicrobial infections (eg. intraabdo abscess) decr emergence of resistant strains decr dose-related toxicity by using decr dose of one/both drugs enhanced inhibition/killing Synergism: when inhibitory/killing effects greater than when drugs used alone; bacteriostatic drugs may become bacteriocidal (eg. penicillin + aminoglycoside); other eg.s are T+S, beta-lactamase inhibitors; may allow decr duration of trt; defined by 4x decr MIC/MBC; NB. antagonism is the exact opposite; synergism interaction expressed as: Fractional inhibitory conc index FICa/b = MIC of drug in combination / MIC of drug alone FICindex = FICa + FICb Mechanisms for synergism: Blockade of sequential steps in metabolic sequence (eg. T+S – 2 steps in folic acid pathway) Inhibition of enzymatic inactivation (eg. beta-lactam AB’s and beta-lactamase inhibitors) Enhancement of AB uptake (eg. cell wall active AB’s such as penicillins, incr uptake of aminoglycosides by bacteria – esp bacteria such as entercocci which have permeability barriers) Mechanisms for antagonism: Inhibition of cidal activity by static agents (eg. static agents such as tetracyclines and chloramphenicol can antagonize action of bactericidal cell wall active agents as the latter require bacteria to be actively growing and dividing) Induction of enzymatic inactivation (beta lactam AB’s can induce beta-lactamase production which may inactivate other beta-lactam AB’s) Antimicrobial Prophylaxis If efficacy demonstrated and benefits>risks; may beed to use vanc if MRSA; time and dose dependent on VOD, peak levels, clearance, protein binding, BA; IV at some time after 60mins before incision; may need to rpt dose if procedure >3-4hrs long; = principles: AB active against common surgical pathogens; avoid unnecessary broad spectrum AB AB has proved efficacy in clinical trials Shortest possible course of most effective and least toxic AB Reserve newer broad spectrum AB for resistant infections Least expensive AB should be used Type of OperationCommon PathogensDrug of ChoicewCardiacStaph, enteric G-ive rodsCefazolinThoracicStaph, strep, enteric G-ive rodsCefazolnVascularStaph, enteric G-ive rodsCefazolinNeurosurgStaphCefazolinOrthoStaphCefazolinHead and neckStaph aureus, oral floraCefazolinGastroduodenalStaph aureus, oral flora, enteric G-ive rodsCefazolinBiliaryStaph aureus, enterococci, enteric G-ive rodsCefazolinHysterectomyEnteric G-ive rods, anaerobes, enterococci, Grp B strepCefazolinC sectionAs aboveCefazolinColorectalEnteric G-ive tods, anaerobesCefoxitin, cefotetan, cefmetazole (or PO erythromycin + neomycin if elective)AppendicectomyEnteric G-ive rods, anaerobesCefoxitin, ceftizoxime, cefotetan, cefmetazole Non-surgical prophylaxis: InfectionDrug of ChoiceAnthraxCiprofloxacin, doxycyclineCholeraTetracyclineDiphtheriaPenicillin, erythromycinEndocarditisAmoxicillin, clindamycinGenital herpes simplexAcyclovirInfluenza BOsteltamivirGroup B strepAmpicillin, penicillinHibRifampicinHIVZidovudine, lamivudine, indinavirInfluenza AAmantadineMalariaCloroquine, mefloquineMeningococcalRifampicin, ciprofloxacin, ceftriaxoneOtitis mediaAmoxicillinPertussisErythromycinPlagueTetracyclinePCPT-SRheumatic feverBezathine penicillinToxoplasmosisT-SUTIT-S BETA-LACTAM AND OTHER CELL-WALL AND MEMBRANE-ACTIVE AB’s All act on bacterial cell wall synthesis BETA-LACTAM COMPOUNDS 1) Penicillins Action All are ˛-lactam compounds due to four-membered lactam ring Chemistry: all have: Thiazolidine ring attached to& ˛-lactam ring hat carries& (hydrolysis of this ring by bacterial ˛-lactamases ( penicilloic acid which has no antibacterial activity) 2Y amino group (RNH-) to which substituents can be attached Stuctural integrity of 6-aminopenicllanic acid nucleus vital for biologic activity Classification: properties altered by substituents of 6-aminopenicillanic acid moiety; within each group are compounds relatively stable to gastric acid and suitable for PO intake 1) Penicillins: Eg. penicillin G, penicillin V, benzathine and procaine penicillin ACTIVE AGAINST: G+ive rods and cocci, G-ive cocci and non-˛-lactamase producing anaerobes Penicillin G: strep, meningococci, enterococci, pneumococci, non-˛-lactamase producing staph, treponema pallidum, clostridium, actinomyces, other G+ive rods, non-˛-lactamase producing G-ive anaerobic MO s NOT ACTIVE AGAINST: G-ive rods SUSCEPTIBLE to hydrolysis by ˛-lactamases Antistaphylococcal penicillins (semisynthetic): Eg. Nafcillin, methicillin, isoxazolyl penicillins (eg. oxacillin, cloxacillin, dicloxacillin) – these are narrow-spectrum penicillinase resistant penicillins (note, penicillinase is a specific type of beta-lactamase specific for penicillin) ACTIVE AGAINST: staphylococci and streptococci NOT ACTIVE AGAINST: enterococci, anaerobic bacteria, G-ive cocci and rods, listeria RESISTANT to staphylococcal ˛-lactamases Extended-spectrium penicillins: Eg. Aminopenicillins (eg. ampicillin, amoxicillin), carboxypenicillins (eg. carbenicillin indanyl sodium, ticarcillin), ureidopenicillins (eg. piperacillinn, mezlocillin, azlocillin) ACTIVE AGAINST: improved activity against G-ive organisms as enhanced ability to penetrate outer membrane Amoxicillin: good for penicillin-resistant pneumococci Ampicillin: for shigellosis; for enterococci Ureidopenicillins: for G-ive bacilli (eg. Klebsiella pneumoniae) NOT ACTIVE AGAINST Ampicillin: many G-ive species produce ˛-lactamase and are now resistant, so not good for UTI, meningitis, typhoid fever; not for klebsiella, enterobacter, Pseudomonas aeruginosa, citrobacter, serratia, infole-positive proteus species, and other G-ive aerobes Ticarcillin: enterococci SUSCEPTIBLE to hydrolysis by ˛-lactamases Mechanism of action: inhibit bacterial growth by interfering with transpeptidation reaction of bacterial cell wall synthesis (ie. bind covalently to active site of PBP ( halting peptidoglycan synthesis); work only when cells actively growing Additional info: action was initially described in units; semisynthetic penicillins are prescribed in weight rather than units; minimum inhibitory concentration (MIC) of any penicillin given in mcg/mL; most dispensed as Na / K salt of acidIndicationRoute of administrationIM: irritation and local pain Benzathine penicillin and procaine penicillin G IM – low but prolonged drug levels PO: amoxicillin better absorbed PO than ampicillinDose1) Penicillin G: 4-24 million units/day in 4-6 doses Benzathine penicillin: 1.2 million units IM Banzathine penicillin G: 2.4million units IM 2) Isoxazoyl penicillin: 0.25-0.5g PO 4-6hrly Oxacillin/nafcillin: 8-12g/day 4-6hrly IV for serious systemic infection 3) Amoxicillin: 250-500mg tid Ampicillin: 4-12g/day IV for severe infection (eg. anaerobes, enterococci, Listeria monocytogenes, ˛-lactamase-negative strains of G-ive cocci, E coli, salmonellaDosing Interval1) Penicillin V: QIDAbsorptionVaries depending on drug s acid stability and protein binding Well absorbed PO: dicloxacillin, ampicillin, amoxicillin PO absorption impaired by food as bind with food proteins and inactivated by acid; administer 1-2hrs pre- or post-meal; 500mg ( 4-8mcg/mL serum conc IV: most absorption is rapid and complete; 1g ( 20-50mcg/mL serum conc Benzathine and procaine penicillins formulated to delay absorption ( prolonged concs (eg. >10days)Bioavailability1) Penicillin V: poor 2) ReasonableHalf life1) Penicillin G: 30mins (in renal failure may be 10hrs) Ampicillin: 1hrDuration of ActionDistributionOnly small amount of total drug in serum is free drug; amount determined by protein binding; becomes clinically relevant when protein binding is >95% Highly protein bound: nafcillin Lower protein bound: penicillin G, ampicillin Widely distributed in body fluids and itssues; tissue concs = serums concs; poor penetration into eye, prostate and CNS Polar so intracellular conc < extracellular concMetabolismExcretionRenal: 10% by glomerular filtration, 90% by tubular secretion; decr dose if poor CrCl; less efficient in newborns Small amounts by other routes Nafcillin: biliary Oxacillin, dicloxacillin, cloxacillin: biliary and renalSide effectsResistance: Inactivation of AB by ˛-lactamase  most common mechanism Can have narrow susbtrate specificity (ie. inactivate only penicillins) eg. Staph. aureus, Haemophilus, E. coli Can have wider substrate specificity (ie. inactivate penicilins and cephalosporins) eg. Pseudomonas aeruginosa, enterobacter Modification of target PBP – basis of methicillin resistance in staph, and of penicillin resistance in pneumococci and enterococci; PBP has low affinity for AB Impaired penetration of drug to target PBP – occur only in G-ive species due to impermeable outer cell wall membrane (absent in G+ive bacteria); AB’s cross this membrane via protein channels (porins) – absence or lack of this channel impairs drug entry to cell; usually alone this isn’t enough for resistance but in combination with 1) can be important Efflux – occur in G-ive species Hypersensitivity – all penicillins are cross-sensitive and cross-reacting; Ag is degradation product of penicillin (eg. penicilloic acid); ( anaphylaxis (0.05%), serum sickness reactions (rare, urticaria, joint swelling, angioneurotic oedema, pruritis, resp embarrassment 7-12 days after exposure), skin rashes Oral lesions, fever, interstitial nephritis, eosinophilia, hemolytic anaemia, vasculitis; GI upset Seizures in renal failure Nafcillin ( neutropenia Oxacillin ( hepatitis Methicillin ( interstitial nephritis Ampicillin ( pseudomembranous colitisContraindicationsDrug interactionsLevels raised by simultaneous administration of probenecid (500mg 6hrly – as impairs renal tubular secretion of weak acids) Ampicillin, amoxicillin, ticarcillin and piperacillin available in combination with ˛-lactamase inhibitors (eg. claulanic acid, sulbactam, tazobactam) extending spectrumPregnancyPenicillins are excreted into sputum and milk to levels 3-15% of serumExamples CEPHALOSPORINS AND CEPHAMYCINS Action Similar to penicillin but more stable to ˛-lactamases so have broader spectrum of activity Nucleus: 7-aminocephalosporanic acid (similar to 6-aminopenicillanic acid); attachment of R1 and R2 groups gives antimicrobial activity NOT ACTIVE AGAINST: strains of E coli and Klebsiella species that have extended spectrum ˛-lactamases; enterococci, L monocytogenes First Generation Cephalosporins: Eg. cefadroxil, cefazolin, cephalexin, cephalothin, cephapirin, cephradine ACTIVE AGAINST: G+ive cocci (eg. pneumococci, streptococci, staph); E. coli, Klebsiella pneumoniae, proteus mirabilis; usually works against anaerobic cocci NOT ACTIVE AGAINST: methicillin-resistant strains of staph, pseudomonas aeruginosa, enterobacter Second Generation Cephalosporins: Eg. cefaclor, cefuroxime, cefamandole, cefonicid, cefprozil, loracarbef, ceforanide, cefoxitin, cefmetazole, cefotetan a. ACTIVE AGAINST: same as 1st generation but with extra G-ive coverage; Klebsiella; ˛-lactamase- producing H influenzae and Moraxella catarrhalis Cefamandole, cefuroxime, cefonicid, ceforanide, cefaclor: H influenzae Cefoxitin, cefmetazole, cefotetan: B fragilis, serratia; anaerobes b. NOT ACTIVE AGAINST: enterococci, pseudomonas aeruginosa Cefamandole, cefuroxime, cefonicid, ceforanide, cefaclor: B fragilis, serratia Cefoxitin, cefmetazole, cefotetan: H influenzae Third Generation Cephalosporins: Eg. cefoperazone, cefotaxime, ceftazidime, ceftriaxone, ceftizoxime, cefixime, cefdinir, ceftibuten, moxalaxtam a. ACTIVE AGAINST: same as 2nd generation but with even more G-ive coverage; some able to cross BBB; citrobacter, S marcescens, providencia, ˛-lactamase-producing H influenzae and neisseria Ceftazidime and cefoperazone: pseudomonas aeruginosa Ceftizoxime and moxalactam: B fragilis b. NOT ACTIVE AGAINST: enterococci Cefixime and ceftibuten: pneumococci and S aureus Forth Generation Cephalosporins: cefepime a. ACTIVE AGAINST: more resistant to ˛-lactamases; penetrates BBB; good against pseudomonas aeruginosa, enterobacter, staph aureus and strep pneumoniae (penicillin-resistant strains), haemophilus, neisseriaIndication1) PO for UTI, cellulites; surgical prophylaxis; penicillin allergy 2) PO for sinusitis, otitis, LRTI; can be for peritonitis and diverticulitis 3) For serious infections caused by MO’s that are resistant to most other drugs (except when extended-spectrum ˛-lactamases expressed); NOT for enterobacter infections; ceftriaxone and cefotaxime for meningitis (except when caused by L monocytogenes and highly penicillin resistant strains of pneumococci); good in SUO in immunocompetent and immunocompromisedRoute of administration1) Cephalexin, cephradine, cefadroxil: PO Cefazolin IV / IM 2) Cefaclor, cefuroxime, cefprozil, loracarbef: PO 3) IV; cefixime can be PODose1) Cephalexin, cephradine, cefadroxil: PO; 500mg ( serum level 12-20mcg/ml; dose 0.25-0.5g QID Cefazolin IV 1g ( serum level 90-120mcg/ml; dose 0.5-2g 8hrky 2) Cefaclor, cefuroxime, cefprozil, loracarbef: PO 10-15mg/kg/day QID IV: 1g ( serum level 75-125mcg/ml 3) IV: 1g ( serum level 60-140mcg/ml Ceftriaxone: 15-50mg/kg/day 24hrly Cefoperazone: 25-100mg/kg/day 8-12hrly Others: 2-12g/day 6-8hrlyDosing IntervalAbsorptionBioavailabilityHalf lifeCeftriaxone: 7-8hrs Cefoperazone: 2hrs Other 3rd gen: 1-1.7hr Cefepime: 2hrsDuration of ActionDistribution1) Cefazolin penetrates well into most tissues; Doesn’t penetrate CNS, can’t be used for meningitis 3) Penetrate body fluid and tissue well, and can be used in meningitisMetabolismExcretion1) Glomerular filtration and tubular secretion; decr dose in impaired renal function 2) Renal 3) Cefoperazone, ceftriaxone: biliary; no dose change in renal impairment; others are renal 4) RenalSide effectsAllergy – similar to penicillin (anaphylaxis, fever, skin rash, nephritis, granulocytopenia, haemolytic anaemia); some people with penicillin allergy may tolerate cephalosporins; cross-reactivity 5-10% Thrombophlebitis; interstitial nephritis, tubular necrosis Some cause hypoprothrombinaemia and bleeding disorders Avoid alcohol ( disulfiram-like reactionContraindicationsDrug interactionsProbenecid increases serum levels by blocking tubular secretionPregnancyExamples OTHER BETA-LACTAM DRUGS 1) Monobactams: monocyclic ˛-lactam ring; tolerated in penicillin allergy; may cause incr AST/ALT ACTIVE AGAINST: G-ive rods (eg. pseudomonas) NOT ACTIVE AGAINST: G+ive bacteria / anaerobes RESISTANT to ˛-lactamases eg. aztreonam 1-2g IV 8hrly 2) ˛-lactamase Inhibitors: weak antibacterial action a) Most active against Ambler class A ˛-lactamases as produced by staph, H influenzae, N gonorrhoeae, salmonella, shigella, C coli and K pneumoniae b) No good against Ambler class C as produced by enterobacter, citrobacter, serratia, and pseudomonas c) Good against chromosomal ˛-lactamases produced by bacteroides and branhamella Eg. Clavulanic acid, sulbactam, tazobactam 3) Carbapenems: structurally related to ˛-lactam AB s; penetrate body tissue and fluids well inc CSF; renal clearance; for infections caused by MO s resistant to other drugs, or mixed anaerobe/aerobe infections; active against highly penicillin-resistant strains of pneumococci; drug of choice for enterobacter infections as resistant to ˛-lactamase eg. imipenem  ACTIVE AGAINST: G-ive rods (eg. pseudomonas), G+ive MO s, anaerobes NOT ACTIVE AGAINST: enterococcus faecium, methicillin-resistant strains of staph, clostridium difficile, Burkholderia cepacia RESISTANT to most ˛-lactamases Administer with cilastatin to prevent deactivation by kidneys; 0.25-0.5g IV 6-8hrly; half life 1hr eg. meropenem – ACTIVE AGAINST: more activity against G-ive aerobes NOT ACTIVE AGAINST: less activity against G+ive’s Doesn’t need cilastatin; 1g IV 8hrly eg. ertapenem – less active against pseudomonas; half life 4hrs; 1g IV od SE: N+V+D, skin rashes, seizures; may be cross-allergy with penicillin OTHER CELL WALL / MEMBRANE – ACTIVE AGENTS Vancomycin Action Produced by Streptococcus orientalis; water soluble; quite stable Active only against G+ive bacteria, esp staph in conc 0.5-10mcg/ml; kills slowly and only if cells are dividing Recommended peak 20-50mcg/ml, trough 10-15mcg/ml Resistant to ˛-lactamase Synergistic with gentamicin and streptomycin against enterococcus species Mechanism of action: inhibits cell wall synthesis by binding to D-Ala-D-Ala terminus of peptidoglycan pentapeptide ( inhibits transglycosylase ( prevent peptidoglycan cross-linking ( cell wall susceptible to lysis; cell membrane also damaged Resistance in enterococci / vanc resistant S aureus due to modification of D-Ala-D-Ala site so vancomycin isn’t able to bind to it with hydrogen bondIndicationSepsis; endocarditis caused by methicillin-resistant staph; in combination with gent for enterococcal endocarditis in penicillin allergy; in combination with cephalosporin for meningitis due to pneumococcus resistant to penicillin Not as effective as antistaphylococcal for MO that are sensitive to themRoute of administrationIVDoseIV over 1hr 1g ( serum level 15-30mcg/ml 30mg/kg/day in 2-3 doses – usually give 1g bdDosing IntervalAbsorptionPoor PO; PO only for treatment of enterocolitis caused by Clostridium difficile (0.125-1.25g 6hrly) – but metronidazole is preferredBioavailabilityHalf lifeDuration of ActionDistributionWidely distributed; 7-30% CSF levels if meningeal irritationMetabolismExcretion90% by glomerular filtration; accumulation in renal insufficiency; clearance directly proportional to CrClSide effectsIn 10% Phlebitis, chills. fever, red man syndrome (due to release of histamine, prevented by prolonging infusion time) Rare: ototoxicity, nephrotoxicityContraindicationsDrug interactionsPregnancyExamples Others Teicoplanin: similar to vancomycin; long half life (45-70hrs), can be given IM Daptomycin: similar to vancomycin; active against vanc-resistant strains of enterococci and S aureus; binds to and depolarizes cell membrane ( K efflux ( cell death; renal clearance; 4-6mg/kg od; SE – myopathy, monitor creatinine phophokinase; not to be used for trt of pneumonia Fosfomycin: inhibits v early stage of bacterial cell wall synthesis by being transported into bacterial cell and inhibiting cytoplasmic enzyme enolpyruvate trasnferase (blocking formation of UDP-N-acetylmuramic acid); active against G+ive and G-ive MO’s; PO/IV; PO bioavailability 40%; half life 4hrs; renal excretion of active drug Bacitracin: inhibits cell wall synthesis by interfering with dephosphorylation of lipid carrier that transfers peptidoglycan to growing cell wall; v nephrotoxic so only using TOP on skin and mucous membranes Cycloserine: inhibits G-ive and G+ive MO’s; used to treat TB; inhibits incorporation of D-alanine into pentapeptide by inhibiting alanine racemase (which converts L-alanine to D-alanine and D-alanyl-D-alanine ligase; widely distributed; active drug excreted in urine; 0.5-1g/day; CNS toxicity (headaches, tremors, acute psychosis, convulsions) TETRACYCLINES, MACROLIDES, CLINDAMYCIN, CHLORAMPHENICOL, STRETOGRAMINS All inhibit bacterial protein synthesis by binding to and interfering with ribosomes TETRACYCLINES Action Crystalline amphoteric substances; low solubility (available as acid hydrochlorides which are more soluble and stable) Broad-spectrum Bacteriostatic – enter by passive diffusion and AT ( drug concentrated intracellularily ( bind reversibly to 30S subunit of bavertial ribosome ( block binding of aminoacyl-tRNA to mRNA-ribosome complex ( prevents addition of aa to growing peptide Active against G+ive and G-ive inc anaerobes, rickettsiae, chlamydiae, mycoplasma, some protozoa (eg. amoebas) Note, tigecycline has v wide spectrum (inc. coag-neg staph, methicillin and vanc resistance staph, enterococci, G-ive rods, enterbacteraie). NOT ACTIVE AGAINST proteus or pseudomonasIndicationDrug of choice in mycoplasma pneumoniae, chlamydiae, rickettsiae, some spirochetes Used in H pylori, plague, tularemia, brucellosis, protozoa, acne, community-acquired pneumonia, Lyme disease, leptospirosis, mycobacterial infections No longer for gonorrhoea due to resistance Tigecycline good in skin and intraabdo infections; not good in urine infectionsRoute of administrationDosePO: 250-500mg 6hrly (20-40mg/kg/day in children) ( serum level 4-6mcg/ml 600mg daily for demeclocycline/methacycline 100mg od/bd for doxycycline 100mg bd for minocycline IV: 0.1-0.5mg every 6-12hrs ( serum level 2-4mcg/ml 100mg od/bd doxycycline Tigecycline IV 100mg loading ( 50mg 12hrlyDosing IntervalAbsorptionMainly occurs in upper SI Imparied by food (not so much for doxycycline), divalent cations (eg. Ca, Mg, Fe), dairy products, antacids, alkaline pH Chlortetracycline: 30% Tetracycline, Oxytetracycline, demeclocycline, methacycline: 60-70% Doxycycline, minocycline: 95-100% Tigecycline: v poor PO, must be given IVBioavailabilityHalf life6-8hrs – short acting (ie. chlortetracycline, tetracycline, oxytetracycline) 12hrs – intermediate acting (ie. demeclocycline, methacycline)\ 16-18hrs – long acting (ie. doxycycline, minocycline – almost complete absorption and slow excretion ( od dosing) 36hrs – tigecyclineDuration of ActionDistribution40-80% bound to serum proteins Large VOD except to CSF where conc is only 10-25% that of serumMetabolismExcretionA portion of PO dose will remain in gut lumen ( modify intestinal flora ( be excreted in faeces (10-40%) In bile (exhibits some enterohepatic circulation) – no dosage adjustment needed for renal failure on tigecycline In urine (10-50%) by glomerular filtration – except doxycycline and tigecycline are nonrenal and don’t accumulate in renal failureSide effectsResistance: (most important underlined) Efflux pumps (eg. Tet(AE) efflux pump – doesn’t work on tigecycline; Tet(K) pump – doesn’t work on doxycycline, minocycline or tigecycline) or impaired influx of drug; proteus and pseudomonas produce multidrug efflux pumps so are resistant to ALL tetracyclines) Ribosome protection (production of proteins that interfere with tetracycline binding to ribosome) Enzyme inactivation of drug (eg. Tet(M) ribosome protection protein – doesn’t work on tigecycline) Nausea (in 1/3), V, D due to direct local irritation – either give with food (which will decr absorption) or discontinue; modify normal gut flora – suppress coliform organisms, allow overgrowth of pseudomonas, proteus, staph, resistant coliforms, clostridia, candida ( anal pruritis, vaginal/PO candidiasis, enterocolitis Hypersensitivity reactions Bind Ca depositied in newly formed bone/deeth ( discolouration and enamel dysplasia, deformity or growth inhibition (avoid under age 8 and in pregnancy) Impair hepatic function; renal tubular acidosis; nitrogen retention if on diuretics Venous thrombosis on local injection; photosensitization; vestibular reactionsContraindicationsDrug interactionsHalf life shortened by carbamazepine, phenytoin, barbs, chronic alcohol ingestion – via induction of liver enzymesPregnancyCross placenta; reach milk; bind to and damage growing bones and teeth (avoid under age 8)Examples MACROLIDES Action Macrocyclic lactone ring to which deoxy sugars attached Erythromycin: poorly soluble in water but dissolves in organic solvents; lose activity in acid pH, enhanced in alkali pH; can be inhibitory / bactericidal; acts by binding to 50S ribosomal RNA ( blocks aminacyl translocation reaction and formation of initiation complexes ACTIVE AGAINST: G+ive MO’s (esp pneumococci, strep, staph, cornyebacteria); mycoplasma, legionella, Chlamydia, helicobacter, listeria, certain mycobacteria; some G-ive MO’s (eg. Neisseria, bordetella pertussis, bartonella, some rickettsia, treponema pallidum, campylobacter) NOT ACTIVE AGAINST: H influenzae Clarithromycin: addition of methyl group to erythromycin; same MOA as erythromycin ACTIVE AGAINST: same as above; BUT more active against mycobacterium avium and leprae and toxoplasma gondii Azithromycin: addition of methylated nitrogen into lactone ring; similar to clarithromycin ACTIVE AGAINST: H influenzae, chlamydia NOT ACTIVE AGAINST: staph and strep Ketolides (eg. telithromycin): substitution of 3-keto group for 1-cladinose ACTIVE AGAINST: Strep pyogenes/pneumoniae/aureus, H influenzae, Moraxella catarhalis, mycoplasmas, legionella, chlaymdia, H pylori, N gonorrhoea, B fragilis, T gondiiIndicationErythromycin: corynebacterial infections (eg. diphtheria); chlamydial infections; community acquired pneumonia (inc pneumococcus, mycoplasma, legionella); good for staph, strep and pneumococci in penicillin allergies; prophylaxis against endocarditis in dental proceduresRoute of administrationDoseErythromycin: 250-500mg 6hrly PO; 0.5-1g 6hrly IV; 20-40mg/kg/day IV in children Clarithromycin: 250-500mg bd (or 1g extended release od) Telithromycin: 800mg od Dosing IntervalAbsorptionDestroyed by stomach acid, must be given with enteric coating; food interferes with absorption Azithromycin: rapid PO absorption; Al ad Mg antacids delay absorptionBioavailabilityTelithromycin: 57%Half lifeErythromycin: 1.5hrs (5hrs if anuria – but no need to adjust for renal failure) Clarithromycin: 6hrs (bd dosing) Azithromycin: slowly released from tissue, so tissue half life 2-4 days; elimination half life 3 days (od dosing and shorter courses)Duration of ActionDistributionWidely distributed, except to CSFMetabolismTelithromycin: liverExcretionErythromycin: bile, faeces; only 5% in urine Telithromycin: bile and urineSide effectsResistance: cross-resistance is complete with macrolides; also occurs with clindamycin which shares same ribosomal binding site; note ketolides are more resistant to efflux pumps ERYTHROMYCIN: plasmid-encoded; 3 mechanisms (most important underlined) Decr permeability of cell membrane / active efflux Production of esterases that hydrolyse drug Modification of ribosomal binding site (ribosomal protection) by chromosomal mutation / methylase (which can be constitutional / induced by drug) Erythromycin: anorexia, N+V, diarrhoea; acute cholestatic hepatitis (reversible); fever, eosinophilia, rash Clarithromycin: lower incidence of GI upset Telithromycin: may prolong QTcContraindicationsDrug interactionsErythromycin and clar: can inhibit cP450 enzymes ( incr conc of theophyllie, warfarin, cyclosporine, methylprednisolone Incr bioavailability of digoxin Azithromycin: has no effect on cP450 enzymes, so no drug interactionsPregnancyErythromycin: crosses placentaExamples CLINDAMYCIN Action Inhibits protein synthesis by interfering with formation of initiation complexes and interferig with aminoacyl translocation reactions ACTIVE AGAINST: strep, staph, pneumococci; bacteroides and other anaerobes NOT ACTIVE AGAINST: enterococci; G-ive aerobic MO’sIndicationPreferred to clarithromycin for endocarditis prophylaxisRoute of administrationDosePO: 150-300mg 8hrly (10-20mg/kg/day children) IV: 600mg 8hrlyDosing IntervalAbsorptionBioavailabilityHalf lifeHalf life: 2.5hrs (6hrs with anuria – but no dosage adjustment needed in renal failure)Duration of ActionDistribution90% protein bound Good penetration into most tissue (except CSF)MetabolismHepaticExcretionActive drug and metabolites excreted in bile and urineSide effectsResistance: confers cross-resistance with macrolides Mutation of ribosomal receptor site Modification of receptor by constitutively expressed methylase Enzymatic inactivation of clindamycin Poor permeability of outer membrane (ie. in G-ive species) D + N; skin rashes; impaired liver function and neutropenia; may be severe diarrhoea with colitis due to Clostridium difficileContraindicationsDrug interactionsPregnancyExamples CHLORAMPHENICOL Action Soluble in alcohol but poorly soluble in H20 Chloramphenicol succinate (prodrug) used for IV is highly H20 soluble Chloramphenicol palmitate (prodrug) used PO Inhibitor of protein synthesis by binding reversible to 50S subunit of bacterial ribosome ( inhibits peptidyl transferase step of protein synthesis Bacteriostatic, broad-spectrum ACTIVE AGAINST: aerobic and anaerobic; G+ive and G-ive; ricketssiae; H influenzae, N meningitides, bacteroides NOT ACTIVE AGAINST: chlamydiaeIndicationRarely used; used in serious ricketssial infections (eg. typhus) and Rocky Mountain spotted fever; can used in meningococcal meningitis due to penicillin-resistant pneumococci Use top in eye infections as penetrates ocular tissues wellRoute of administrationDose50-100mg/kg/dayDosing IntervalAbsorptionPO: rapidly and completely absorbedBioavailabilityHalf lifeDuration of ActionDistributionWidely distributed (inc CSF)MetabolismInactivated by conjugation with glucuronic acid (liver) or reduction to inactive aryl aminesExcretionActive drug (10%) and inactive metabolites (90%) excreted renally Small amount of active drug in bile and faeces Don’t need to alter dose in renal insufficiency, but decr in hepatic failure Poorly cleared by neonates (lack effective glucuronic acid conjugation mechanism ( gray baby syndrome ( vomiting, flaccidity, hypothermia, gray colour, shock, collapse)Side effectsResistance: production of chloramphenicol acetyltransferase (enzyme that inactivates drug) N+V+D; PO and vaginal candidiasis Reversible suppression of RBC production; rarely aplastic anaemiaContraindicationsDrug interactionsInhibits hepatic microsomal enzymes ( prolong half life of phenytoin, tolbutamide, chlorpropamide, warfarinPregnancyExamples OTHERS Streptogramins: eg. quinupristin-dalfopristin Oxazolidinones: eg. linezolid AMINOGLYCOSIDES AND SPECTINOMYCIN Bactericidal inhibitors of protein synthesis that interfere with ribosomal function Mainly for aerobic G-ive MO’s AMINOGLYCOSIDES Action H20 soluble; stable; more active at alkaline than acid pH; highly polar and don’t enter cells readily Mechanism of action: irreversible inhibitors of protein synthesis; passive diffusion via porin channels across outer membrane ( AT across cell membrane into cytoplasm by O2-dependent process (coupled to proton pump; inhibited by low extracellular pH and anaerobic conditions; enhanced by cell wall-active drugs such as penicillin and vanc hence synergistic) ( bind to 30S-subunit ribosomal proteins ( interfere with initiation complex of peptide formation ( misread mRNA causing incorporation of incorrect aa into peptide ( nonfunctional protein ( breakup of polysomes into nonfunctional monosomes ( cell death ACTIVE AGAINST: G-ive enteric bacteria NOT ACTIVE AGAINST: anaerobes Streptomycin: resistance has emerged in most so not much use except as 2nd line agent for TB; also in plague, tularemia, brucellosis; plus penicillin for entercoccal or viridans endocarditis (largely replaced by gentamicin for this); still useful for treating entercoccal infections Gentamicin: against G+ive and G-ive; works on staphylococci and coliforms; synergistic with beta lactams against pseudomonas, proteus, enterobacter, klebsiella, serratua, other G-ive rods (be careful using as single agent as resistance develops quickly in some species or due to low penetration); used for severe infections caused by G-ive bacteria that are likely to be resistant to other drugs NOT ACTIVE AGAINST: streptococci, enterococci (cannot penetrate cell); combined with vanc / penicillin ( bactericidal effect due to enhanced uptake of drug due to inhibition of cell wall synthesis Tobramycin: similar to gent (with some cross-resistance) but more active against pseudomonas, less active against serratia; active against enterococcus faecalis Amikacin: resistant to many enzymes that inactive gent and tobra; also active agains streptomycin-resistant strains of M tuberulosis; works on G-ive enteric bacteria Netilmicin: similar to gent and tobra, but more reistant against enzymatic degradation Neomycin and kanamycin: active against G+ive and G-ive bacteria and some mycobacteria; not active against streptococci and pseudomonas; poorly absorbed from GI tract – will end up in faeces, but used as PO prep of GI tract prior to surgery / for hepatic coma to decr aerobic bowel flora (decr ammonia); usually for topical use; too toxic for IV IndicationUsed for G-ive enteric bacteria (esp sepsis or resistant strains) Usually used with beta lactam AB to extend spectrum to cover G+ive pathogens Used with vancomycin/penicillin for endocarditis Used for TBRoute of administrationCan be given IM Usually given IV in 30-60min infusion Gent can be given TOP for burns/wounds; intrathecal 1-10mg/day for meningitis Tobramycin can be given INH for pseudomonasDose5mg/kg over 30-60mins at CrCl 100ml/min (2mg/ml if <50ml/min) – check conc on 2nd-3rd day (trough) – aim for conc <1mcg/ml between 18-24hrs; measure at 2hrs and 12hrs and working out actual clearance, or measure at 8hrs (if at 8hrs 1.5-6mcg/ml, is OK) Alter dose by [5mg/kg dose] / [serum Cr level in mg/dL]; this equation doesn’t take into account age / gender – better method uses Cockcroft-Gault formula Work out daily dose by [max daily dose] x [ratio of estimated CrCl:normal CrCl] If bd dosing, peak 30-60mins post dose, and trough just before next dose Streptomycin: 0.5-1g/day (7.5-15mg/kg/day in children) IM/IV Gentamicin: 5-6mg/kg/day in 3 doses, but od can be used (target conc 5-10mcg/ml, with trough <1-2mcg/ml) Tobramycin: 5-6mg/kg IM/IV 8hrlyDosing IntervalUsually bd/tid; but can be od (concentration-dependent killing – incr conc kill more bacteria at higher rate; also have post-antibiotic effect – antibacterial effect exists beyond time in which measurable drug can be found)AbsorptionPoor PO absorption, almost all excreted in faecesBioavailabilityHalf life2-3hrs (incr to 24-48hrs in renal impairment)Duration of ActionDistributionGood (except CSF and eye) – in active inflamm may reach 20% in CSF, need intrathecal injection for higher levels; may reach 30% in bile, 50-90% in pleural/synovial fluidMetabolismExcretionRenal – excretion proportional to CrCl; usually glomerular filtration Only partially removed by renal/peritoneal dialysisSide effectsResistance: numerous mechanisms Production of transferase enzyme inactivates aminoglycoside by adenylyation / acetylation / phosphorylation – works for gent Impaired entry of aminoglycoside into cell (eg. mutation of porin protein) – works for gent Receptor protein on 30S ribosomal subunit deletered/altered Enterococcal production of enzyme (inactivates gent, amikacin, netilmicin, tobramycin) (another one inactivates streptomycin) Toxicity: time and conc dependent; trough conc of 2mcg/ml is toxic and time above this threshold is important; ototoxic and nephrotoxic; more likely when >5/7 trt, higher dose, elderly, renal insufficiency; worsened by concurrent use of loop diuretic or other nephrotoxic antimicrobial agents (eg. vanc, amphotericin) ( tinnitus, high-f hearing loss, vertigo, ataxia, loss of balance ( incr serum creatinine level, decr CrCl Nephrotoxicity worst with neomycin, tobramycin, gent – monitor renal function Ototoxicity worst with neomycin, kanamycin, amikacin Vestibulotoxicity worst with streptomycin, gent High doses ( curare-like effect with NM blockade ( resp paralysis (eg peritoneal absorption of kanamycin/tobramycin post-op); reversed with Ca gluconate or neostigmine Streptomycin: fever, skin rashes and other hypersensitivity reactions when prolonged exposure; pain at injection site; vestibular dysfunction is irreversible Gentamicin: nephrotoxicity is reversible and milkd, occurs in 5-25% receiving gent for 3-5/7; vestibulotoxicity is irreversible; can cause loss of hearing (in 1-5% receiving for 3-5/7) Tobramycin: ototoxic and nephrotoxicContraindicationsDrug interactionsPregnancyDeafness of newbornExamples Spectinomycin: active against many G-ive and G+ive MO’s, but only used in drug-resistant gonorrhoea SULFONAMIDES, TRIMETHOPRIM, QUINOLONES ANTIFOLATE DRUGS Sulfonamides Action Made by attaching substituents to amido/amino group of sulfanilamide nucleus; more soluble at alkaline pH Mechanism of action: MO’s cannot use exogenous folates but must synthesise it from PABA (p-aminobenzoic acid) to make purines and nucleic acids; sulfonamides inhibit dihydropteroate synthase and folate production as are structural analogs of PABA. ACTIVE AGAINST: G+ive and G-ive MO’s; nocardia, Chlamydia trachomatis, protozoa, E coli, klebsiella, salmonella, shigella, enterobacter NOT ACTIVE AGAINST: anaerobes; many meningococci, pneumococci, streptococci, staph and gonococci are now resistant PO, absorbable: sulfisoxazole (short, 6hrs / prompt absorption), sulfamethizole (short, 9hrs / prompt), sulfamethoxazole (intermediate, 10-12hrs / prompt), sulfadiazine (intermediate, 10-17hrs / slow absorption), sulfapyridine (intermediate, 17hrs / slow), sulfadoxine (long, 7-9 days / intermediate absorption) PO, non-absorbable: sulfasalazine TOP: sodium sulfacetamide, mafenide acetate, silver sulfadiazineIndicationRarely used as single agent 1) PO, absorbable: UTI Trimethoprim + sulfamethoxazole for Pneumocystis carinii, toxoplasmosis, nocardiosis Pyrimethamine + sulfadiazine for acute toxoplasmosis (sequential blockade of folate synthesis) 2)Sulfasalazine: for UC, enteritis 3) TOP: for bacterial conjunctivitis, trachoma, burnsRoute of administrationPO, absorbable – can have short, intermediate or long-acting halflives (see above) PO, nonabsorbable TOPDoseLevels peak 2-6hrs post PO administration Sulfisoxazole: 1g QID Sulfamethoxazole: 1g bd/tid Sulfadiazine: 1g QIDDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionWidely (inc CSF); protein binding 20-90%MetabolismA portion of PO drug acetylated / glucuronidated by liverExcretionDrug and inactive metabolite excreted renally (glomerular filtration); decr dose in renal failureSide effectsResistance: MO’s which lack enzymes for synthesis of folate from PABA gain it from endogenous sources Mutations causing overporuction of PABA Mutations causing production of folate acid-synthesising enzyme (eg. dihydropteroate synthase) that has low affinity for sulfonamides – often encoded on plasmid that is transmissible and disseminate rapidly Mutations that impair permeability to sulfonamide Cross-allergenic ( fever, skin rash, exfoliative dermatitis, photosensitivity, urticaria, N+V+D Crystalluria, haematuria ( may cause obstruction; trt by alkalinisation of urine and hydration Stevens-Johnson syndrome – uncommon Stomatitis, conjunctivitis, arthritis, hepatitis, PAN, psychosis Haematopoietic disturbances – haemolytic/aplastic anaemia, granulocytopenia, thrombocytopeniaContraindicationsDrug interactionsSynergistic action with trimethoprim / pyrimethamine due to sequential inhibition of folate synthesisPregnancyCross placenta to fetusExamples Trimethoprim and Trimethoprim-Sulfamethoxazole Mixtures Action Trimethoprim: selectively inhibits bacterial dihydrofolic acid reductase (which converts dihydrofolic acid to tetrahydrofolic acid ( synthesis of purines and DNA) Pyrimethamine: inhibits dihydrofolic acid reductase of protozoaIndicationTrimethoprim: UTI T-S combo: P jiroveci pneumonia, shigellosis, salmonella, UTI, prostatitis, nontuberculous mycobacterial, methicillin-resistance S aureus, pneumococcus, haemophilus, moraxella catarrhalis, Klebsiella pneumoniae IV can be used for G-ive bacterial sepsis (eg. enterobacter, serratis, shigellosis, typhoid fever) NOT ACTIVE AGAINST: mycoplasma pneumoniae; E coli and pneumococci are becoming resistant P-S combo: leishmaniasis, toxoplasmosis, falciparum malariaRoute of administrationPO, alone or in combination with sulfamethoxazole (combination can be IV)DosePO trimethoprim: 100mg bd PO T-S combo: 160mg T, 800mg S bd IV T-S combo: 80mg T, 400mg S diluted in 125ml 5% dextrose over 60-90minsDosing IntervalAbsorptionGood PO – trimethoprim is lipid soluble so wider than sulfaMBioavailabilityHalf lifeDuration of ActionDistributionWide (inc CSF); concentrates in prostatic and vaginal fluid so more active hereMetabolismExcretionRenal – decr dose if poor CrClSide effectsResistance: due to mutation or plasmid-encoded trimethoprim-resistant dihydrofolate reductases (rapid dissemination) Decr cell permeability Overproduction of dihydrofolate reductase Production of altered reductase with reduced drug binding Antifolate: megaloblastic anaemia, leucopenia, granulocytopenia N+V, drug fever, vasculitis, renal damageContraindicationsDrug interactionsSynergistic with sulfonamides ( bactericidal as opposed to bacteriostaticPregnancyExamples DNA GYRASE INHIBITORS Fluoroquinolones Action Analogs of nalidixic acid ACTIVE AGAINST: G-ive bacteria; atypical pneumonia (eg. mycoplasmas, chlamydias) and intracellular species (eg. legionella, M tuberculosis, M avium) NOT ACTIVE AGAINST: G+ive bacteria (although newer agents are better against G+ive cocci) Mechanism of action: block bacterial DNA synthesis by inhibiting: - bacterial topoisomerase II (DNA gyrase) ( prevents relaxation of supercoiled DNA for transcription and replication - topoisomerase IV ( interferes with separation of replicated chromosomal DNA into daughter cells during cell division 1) Norfloxacin: least active against G-ive and G+ive 2) Ciprofloxacin, enoxazin, lomefloxacin, levofloxacin, ofloxacin, pefloxacin: excellent G-ive; mod-good G+ive (except methicillin-resistant S aureus; not so good for streptococci and enterococci) Cipro: most active agent against G-ives (esp P aeruginosa) Levo: best against G+ive 3) Gatifloxacin, gemifloxacin, moxifloxacin: better against G+ive (esp S pneumoniae and staph); not as active against G-ive as cipro; moxi good for anaerobic; good against atypical pneumoniaIndicationUTI, bacterial diarrhoea (eg. shigella, salmonella, E coli, campylobacter); soft tissue/bone/joint/intra-abdo/resp infections; anthrax; gonococcal and chlamydia; occasionally for TBRoute of administrationDoseDosing IntervalAbsorptionBioavailability 80-95%; impaired by divalent cations (eg. antacids)BioavailabilityHalf life3-10hrs Long: levofloxacin, gemifloxacin, gatifloxacin, moxifloxacin ( odDuration of ActionDistributionWideMetabolismExcretionRenal (tubular secretion / glomerular filtration); alter dose if poor CrCl – except moxifloxacin which achieves low urinary levels and hence poor for UTISide effectsResistance: esp in staph, pseudomonas, serratia; cross-resistance exists Point mutation in quinolone binding region of target enzyme Change in permeability of MO Well tolerated N+V+D; headache, dizziness, insomnia, skin rash, abnormal LFT; damage growing cartilage ( arthropathy (avoid under 18yrs); tendonitis ( tendon rupture Lome + pe - photosensitivity Gati - hyperglycaemiaContraindicationsDrug interactionsProlonged QTc – be careful with type Ia / III antiarrhythmics, erythromycin, tricyclicsPregnancyExamples ANTIMYCOBACTERIAL DRUGS Mycobacteria are resistant to most drugs – slow growth, can lie dormant; lipid rich wall which can be impermeable; intracellular pathogens; can easily develop resistance So trt needs 2 drugs and is over months Drugs Used To Treat Tuberculosis Action I + R are most active; will cure 95-98% in 9/12; I resistance is 10%’ I+R resistance is 3% Addition of P for 1st 2/12 decr course to 6/12 Use I+R+P+E/S Isoniazid: freely soluble in H20; bacteriacidal for growth bacteria; less effective against atypical mycobacterial species; active against intracellular and extracellular MO Prodrug activated by KatG (catalase-peroxidase of mycobacterium) ( forms covalent complex with acyl carrier protein (AcpM) and KasA (carrier protein synthase) ( blocks synthesis of mycolic acids which are used in cell wall ( cell death Rifampicin: active against G-ive and G+ive bacteria, some enteric bacteria, mycobacteria, chlamydia Binds to beta subunit of bavertial DNA+dependent RNA polymerase ( inhibits RNA synthsis ( bactericidal Ethambutol: water soluble Inhibits bacterial arabinosyl transferases encoded by embCAB gene (involved in polymerization reaction of arabinoglycan ( prevents cell wall synthesis) Pyrazinamide: active at acid pH when taken up by macrophages Converted to pyrazinoic acid (active) by mycobacterial pyrazinamidase (encoded by pncA)IndicationIsoniazid: can be used as single agent for trt of latent TB Rifampicin: for TB or leprosy; can be used as single agent for latent TB; can be used in Hib; can be used for serious strep infections (eg. osteomyelitis, prosthetic valve endocarditis)Route of administrationIsoniazid: usually PO; can be IV Rifampicin:DoseIsoniazid: 5-10mg/kg/day (eg. 300mg od); or 15mg/kg twice weekly Rifampicin: 600mg/day or twice weekely PO Ethambutol: 15-25mg/kg od; or 50mg/kg twice weekly Pyrazinamide: 40-50mg/kg 3x wkly (25-35mg/kg in renal failure) Dosing IntervalAbsorptionIsoniazid: good PO Rifampicin: good PO Ethambutol: good PO Pyrazinamide: good POBioavailabilityHalf lifePyrazinamide: 8-11hrsDuration of ActionDistributionIsoniazid: wide (inc CSF) Rifampicin: wide incr intracellular MO’s and those in abscesses/cavities; highly protein bound; good CSF level only in meningial inflammation Ethambutol: crosses BBB only in meningeal inflammation so 4-64% concs in CSF Pyrazinamide: wide inc inflamed meningesMetabolismIsoniazid: acetlylation by liver N-acetyltransferase (can be a rapid acetylator altering half life) Pyrazinamide: hepaticExcretionIsoniazid: metabolites and small amount unchanged drug excreted renally; don’t need to alter dose in renal failure Rifampicin: hepatic into bile ( enterohepatic circulation ( then metabolite excreted in faeces or urine; no need for dose adjustment in hepatic/renal failure Ethambutol: 20% in faeces, 50% in urine unchanged (accumulates in renal failure, dose alter) Pyrazinamide: renal excretion of metabolitesSide effectsIsoniazid resistance: Mutations causing overexpression of inhA (encodes NADH-dependent acyl carrier protein reductase) ( low level isoniazid resistance with cross-resistance to ethionamide Mutation / deletion of KatG gene ( high level isoniazid resistance without cross resistance to ethoniamide Mutation causing overexpression of ahpC (protects cell from oxidative stress) Mutation of kasA Isoniazid: fever and skin rash Hepatitis common (minor change in aminotransferases seen in 10-20%; loss of appetite, N+V, jaundice, RUQ pain in 1% (must stop drug promptly as hepatocellular damage and necrosis; greater risk in older and alcoholics) Peri neuropathy in 10-20% in higher doses; predisposed if malnutrition, alcoholism, DM, AIDs, uraemia; due to pyridoxine deficiency as isoniazid promotes pyridoxine excretion CNS toxicity – memory loss, psychosis, seizures Tinnitus, haematological abnormalities, GI discomfort Rifampicin resistance: 1) Mutations in rpoB (gene for RNA polymerase) ( decr binding of rifampicin to RNA polymerase Rifampicin: orange discolouration of urine, sweat, tears, contact lenses; rashes, thrombocytopenia, nephritis; occasional cholestatic jaundice and hepatitis; proteinuria commonly; can cuase fever, chills, myalgia, anaemia, thrombocytopenia and acute tubular necrosis Ethambutol resistance: Mutations causing overexpression of emb gene products Mutations within embB structural gene Ethambutol: hypersensitivity rare; retrobulbar neuritis Pyrazinamide resistance: Impaired uptake of pyrazinamide Mutations in pncA gene ( impair conversion to active form Pyrazinamide: hepatotoxicity (1-5%), N+V, drug fever, hyperuricaemia ( goutContraindicationsDrug interactionsPyridoxine: 25-50mg/day to prevent neuropathy caused by isoniazid Isoniazid: decr metabolism of phenytoin ( incr blood level and toxicity Rifampicin: strongly induces Cp450 ( incr elimination of methaone, anticoags, cyclosporine, anticonvulsants, OCPPregnancyIsoniazid: greater risk of hepatic SE’sExamples Other Drugs Used Streptomycin: used 15mg/kg/day IM/IV for several weeks ( 1-1.5g 2-3x weekly for several months; poor penetration of cells so only active against extracellular MO’s; crosses BBB; use when want to use IV as life-threatening or resistant strains 2nd line agents: if resistant to / adverse reaction to 1st line agents above Ethionamide: blocks synthesis of mycolic acids; only PO; metabolized by liver; good CSF penetration; GI irritation, hepatotoxic, neurological symptoms Capreomycin: can be given IM; nephrotoxic and ototoxic Cycloserine: prevents cell wall synthesis; renal clearance, alter dose; peri neuropathy, CNS dysfunction inc depression and psychosis Aminosalicylic acid: folate synthesis antagonist; good PO absorption; enters CSF; excreted renally (can cause crystalluria); peptic ulcers, hypersensitivity (inc hepatosplenomegaly, hepatitis, adenopathy, granulocytopenia) Kanamycin and amikacin: in streptomycin-resistant strains; active against atypical Fluoroquinolones: also active against atypical (esp cipro) Linezolid: good intracellular; may cause BM suppression, irreversible peri and optic neuropathy Rifabutin: cross-resistance with rifampicin; induces cP450 enzymes (ie. interact with antiretrovirals) Rifapentin: cross-resistance with rifampicin; induces cP450 enzymes For atypical mycobacteria: M Kansasii – use ciprofloxacin, clarithromycin, ethambutol, isoniazid, rifampicin, T-S M marinum – used amikacin, clarithromycin, ethambutol, doxycycline, minocycline, rifampicin, T-s M scrofulaceum – used amikacin, erythromycin, rifampicin, streptomycin M avium complex – use amikacin, azithromycin, clarithromycin, ciprofloxacin, ethambutol, rifabutin M chelonae – use amikacin, doxycycline, imipenem, macrolides, tobramycin M fortuitum – use amikacin, cefoxitin, cipro, doxy, ofloxacin, T-S M ulcerans – use isoniazid, streptomycin, rifampicin, minocycline For leprosy: Dapsone: inhibits folate synthesis; should be combined with rifampicin and clofazimine; good PO absorption; wide VOD; halflife 1-2days; excreted in bile with enterohepatic circulation then excreted urine; change dose in renal failure; may get haemolysis, methaemoglobinaemia, GI intolerance, fever, pruritis, rashes, erythema nodosum Rifampin: give with dapsone Clofazimine: alternative to dapsone ANTIFUNGAL AGENTS Systemic Drugs for Systemic Infections Amphotericin B Action Nearly insoluble in H20 so delivered as colloidal suspension with sodium desoxycholate for IV injection Ergosterol is found in cell membrane of fungi; cholesterol is in cell membrane of humans – toxicity due to small amount of binding with human sterols Binds to ergosterol and associates with H20 molecules on hydroxyl-rich side of cell membrane ( alters permeability of cell by forming pores in cell membrane ( leakage of intracellular ions and macromolecules ( cell deathIndicationBroad spectrum ACTIVE AGAINST: yeasts (candida albicans. Cryptococcus neoformans), endemic mycoses, pathogenic moulds Good in all life-threatening mycotic infections as induction agent, then later replaced by a newer azole drug; used longer or easier if immunocompromisedRoute of administrationIV Can be given intrathecal / TOPDoseSlow IV infusion 0.5-1mg/kg/day – give until 1-2g has been givenDosing IntervalAbsorptionPoor PO – so only effective on lumen of GI tractBioavailabilityHalf life15 daysDuration of ActionDistribution>90% bound to proteins Wide (poor in CSF however)MetabolismExcretionSome active drug excreted in urine No dose adjustment needed in hepatic/renal impairmentSide effectsResistance: 1) Impaired binding with ergosterol due to decr membrane conc of ergosterol or modifying sterol target molecule and decr its affinity for drug Infusion related toxicity: fever, chills, rigors, muscle spasms, vomiting, headache, hypotension; may need to premedicate / slow infusion Cumulative toxicity: renal damage (reversible due to prerenal failure; irreversible due to renal tubular injury and occurs with prolonged administration) ( renal tubular acidosis, K and Mg wasting; abnormal LFT’s, anaemia due to decr erythpoietin Intrathecal ( seizures, chemical arachidonitisContraindicationsDrug interactionsPregnancyExamples Flucytosine: narrower spectrum than amphotericin B; give 100-150mg/kg/day PO; >90% absorbed; poorly protein bound; wide VOD (inc CSF); eliminated by glomerular filtration; half life 3-4hrs; alter dose in renal impairment; synergistic with amphotericin due to pores in cells so rarely used as single agent ACTIVE AGAINST: Cryptococcus neoformans, candida, some moulds Taken up by fungal cells via cytosine permease ( converted intracellularily to 5-FU then 5- fluorodeoxyuridine monophosphate and fluorouridine triphosphate ( inhibit DNA and RNA synthesis Resistance due to altered metabolism of flucytosine Metabolised to toxic fluorouracil ( BM toxicity (anaemia, leucopenia, thrombocytopenia), deranged LFT’s, toxic enterocolitis; risk of toxicity at high doses due to narrow therapeutic window Azoles Action Classified as imidazoles or triazoles depending on number of N atoms in 5-membered azole ring; imidazoles less specific for fungal cP450 than triazoles so higher amount of drug interaction and SE’s Mechanism of action: reduction of erhosterol synthesis via inhibition of fungal cP450 enzymes (greater affinity for fungal than human)IndicationBroad spectrum – candida, Crytptococcus neoformans, endemic mycoses, dermatophytes, aspergillusRoute of administrationDoseItraconazole: 100-400mg/day PO/IV Fluconazole: 100-800mg/day PO/IV Voriconazole: 400mg/day PO/IVDosing IntervalAbsorptionItraconazole: incr absorption by food and low gastric pH Voriconazole: good POBioavailabilityK+I: low Fluconazole: high Voriconazole: >90%Half lifeDuration of ActionDistributionK+I: Poor availability to CSF Fluconazole: good penetration to CSF (used for candidiasis but not active against aspergillus)MetabolismVoriconazole: hepaticExcretionSide effectsNon-toxic; minor GI upset; abnormal LFT’s; rarely hepatitisContraindicationsDrug interactionsAffect cP450 ( drug interactions Ketoconazole: inhibit cP450 a lot Itraconazoole: less inhibition; rifampicin decreases bioavailability Fluconazole: least inhibition Voriconazole: lowPregnancyExamples Echinocandins (eg. caspofungin, micafungin, anidulafungin): active against candida, aspergillus and Cryptococcus neoformans; only IV; metabolites excreted renally and via GI tract; adjust dose in hepatic failure; act on fungal cell wall inhibiting synthesis of beta-glucan ( cell death; well tolerated (GI SE, flushing, minor elevation of LFT’s) Systemic Drugs for Mucucutaneous Infections Griseofulvin: 1g/day; better absorption with fatty foods; deposited in new skin protecting it from infection so must be given for 2-6/52; can cause serum-sickness, hepatitis, interact with warfarin/Phenobarbital Terbinafine: 250mg/day; works by interfering with ergosterol biosynthesis by inhibiting fungal enzyme squalene epoxidase (not cP450) ( accumulation of squalene which is toxic to MO; causes GI upset and headache Topical Therapy Nystatin: too toxic for systemic therapy; active against candida Topical azoles: clotrimazole and miconazole Topical allylamines: terbinafine and naftifine OTHER ANTIMICROBIAL AGENTS Metronidazole Action Antiprotozoal; reduction products responsible for AB action ACTIVE AGAINST: anaerobes (esp bacteroides and clostridium); also for amebiasis, giardiasis, trichomoniasisIndicationFor intra-abdo, vaginitis, C difficile colitis, brain abscessRoute of administrationGood absorption PO; also IV / PRDose500mg tid PO / IV (30mg/kg/day)Dosing IntervalAbsorptionBioavailabilityHalf life7.5hrsDuration of ActionDistributionWide VOD; good penetration CSF; low protein bindingMetabolismLiver metabolism; alter doseExcretionUrine (alter dose)Side effectsN+D, peri neuropathy; disulfiram-like effect; headache, dry mouth, metallic taste in mouth Less frequently: insomnia, weakness, dizziness, thrush, rash, dysuria, dark urine, vertigo, paraesthesia, neutropenia Take with meals to decr GI symptoms Rarely, pancreatitis and CNS toxicity (ataxia, encephalopathy, seizures)ContraindicationsDrug interactionsPotentiates anticoagulant effect Elimination increased by phenytoin and Phenobarbital; cimetidine decreases plasma clearance May precipitate lithium toxicityPregnancyAvoid in pregnancyExamples Mupirocin TOP for G+ive cocci (inc MRSA); inhibits Polymyxins (Eg. polymyxin B and E) ACTIVE AGAINST: G-ive bacteria NOT ACTIVE AGAINST: G+ive bacteria, proteus, neisseria Attach to and disrupt bacterial cell membrane; bind and inactive endotoxin TOP to skin lesions Urinary Antiseptics Little systemic antibacterial effect; for UTI Nitrofurantoin Action Bacteriostatic and bacteriocidal ACTIVE AGAINST: G+ive and G-ive NOT ACTIVE AGAINST: P aeruginosa, proteusIndicationLower UTIRoute of administrationDose100mg PO qidDosing IntervalAbsorptionGood POBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionRapid, so no systemic action; GF and TS; toxic in renal failure with low urine concsSide effectsAnorexia, N+V; hypersensitivity reactions (rashes, pul infiltration and fibrosis)ContraindicationsRenal insufficiencyDrug interactionsPregnancyExamples Methenamine mandelate / hippurate: same mechanism of action as above ANTIVIRAL AGENTS Viruses act by several steps: Attachment of virus to host cell Entry of virus through host cell membrane Uncoating of viral nucleic acid Synthesis of early regulatory proteins (eg. nucleic acid polymerases) Synthesis of RNA / DNA Synthesis of late, structural proteins Assembly of viral particles Release from cell TREATMENT OF HERPES SIMPLEX VIRUS / VARICELLA-ZOSTER VIRUS Acyclovir Action ACTIVE AGAINST: HSV-1, 2; VSV Mechanism of action: converted to monophosphate derivative by virus thymidine kinase ( converted to di- and triphosphate compounds by host cell enzymes. Active metabolite accumulates only in infected cells as step 1 requires virus. Acyclovir triphosphate inhibits viral DNA synthesis by: Competition with deoxyGTP for viral DNA polymerase ( binds DNA polymerase irreversible Chain termination following incorporation into viral DNAIndicationGenital herpes (may need longterm suppression of recurrence); varicella (less susceptible so higher doses needed) IV for herpes simplex encephalitis, neonatal HSV infection, immunocompromised with VZVRoute of administrationPO, IV, TOPDose400mg tid or 200mg 5x/day PO 5mg/kg 8hrly IV for severe 10-15mg/kg 8hrs IV for immunocompromised / herpes encephalitis / neonatalDosing IntervalAbsorptionUnaffected by foodBioavailabilityPO: 15-20%Half life3hrs (20hrs with anuria)Duration of ActionDistributionWide; 50% CSFMetabolismExcretionGlomerular filtration and tubular secretion; cleared by haemodialysisSide effectsResistance: Alteration of viral thymidine kinase – confers cross-resistance with other -cyclovirs Alteration of DNA polymerase Well tolerated; N+D, headache; reversible renal dysfunction due to crystal deposits; neurologic toxicity (seizures, tremors, delirium)ContraindicationsDrug interactionsPregnancyExamples Valacyclovir: rapidly converted to acyclovir after PO administration via intestinal and hepatic 1st pass metabolism; PO bioavailability 54%; CSF 50%; half life 2.5-3.3hrs; also good for CMV Famicyclovir: rapidly converted to penciclovir by 1st pass metabolism after PO administration; also for EBV abd HBV; similar action to above but doesn’t cause chain termination; lower affinity for DNA polymerase but achieves higher intracellular concs; resistance due to deficiency of thymidine kinase conferring cross-resistance; bioavailability 70%; half life 10-20hrs; excreted renally; Penciclovir: for TOP Docosanol: inhibits fusion between plasma membrane and HSV envelope preventing viral entry into cell and viral replication; given TOP Trifluridine: phophorylated intracellularily into active form by host cell enzymes then competes with thymidine triphosphate for incorporation by viral DNA polyermase; given TOP TREATMENT OF CMV Occur in advanced immunosuppression due to reactivation of latent infection; Ganciclovir: activation by triphosphorylation (catalysed by virus protein kinase phosphotransferase in CMV infected cells) ( inhibits viral DNA polymerase competitively ( termination of viral DNA elongation; active against CMV, HSV, VZV, EBV, HHV-6, KSHV; can be IV/PO; CSF 50%; intracellular half life 18hrs; clearance related to CrCl; poor PO bioavailability; resistance due to decr level of triphosphorylated drug, or altered DNA polymerase; SE is myelosuppression, N+D, rash, fever, headache, insomnia, peri neuropathy; rare: CNS toxicity (confusion, seizures), hepatotoxicity; can be carcinogenic and embryotoxic ( aspermatogenesis; levels increased by probenecid and trimethoprim Valganciclovir: well absorbed; metabolized in intestinal wall and liver to ganciclovir; bioavailability 60%; take with food; <2% plasma protein binding; renal elimination (glomerular filtration and tubular secretion) Foscarnet: active against HSV, VZV, CMV, EBV, HHV-6, KSHV, HIV-1; inhibits viral DNA polymerase, RNA polymerase and HIV reverse transcriptase; IV; CSF 43-67%; half life 3-6.8hrs but deposited in bone and there several months; renal clearance proportional to CrCl; resistance due to mutations in DNA polymerase gene and due to prolonged exposure to drug; SE are renal impairment (give with saline), low/high Ca/phos; low K/Mg; penile ulceration due to high level of drug in urine; N+V, anaemia, raised LFT’s, headache, hallucinations, seizures Cidofovir: active against CMV, HSV-1,2, VZV, EBV, HHV-6, KSHV, adenovirus, poxviruses, polyomaviruses, human papillomavirus; phosphorylation to active metabolite independent of viral enzymes; inhibits viral DNA polymerase competitively; resistance is rare; active metabolite has prolonged intracellular half life 17-65hrs; poor CSF penetration; elimination by renal tubular secretion – alter dose; given with probenecid which blocks active tubular secretion and decreases nephrotoxicity; other SE are uveitis, neutropenia, metabolic acidosis ANTIRETROVIRAL AGENTS Combination therapy decreases likelihood of emergence of resistance Nucleoside and Nucleotide Reverse Transcriptase Inhibitors (NRTI’s) Action Mechanism of action: competitive inhibition of HIV-1 reverse transcriptase; incorporate into growing viral SNA chain to cause termination; require intracytoplasmic activation via phosphorylation by cellular enzymes to triphosphate formIndicationRoute of administrationDoseAbacavir: 300mg bd / 600mg od Didanosine: 250-400mg od (Enteric coated); adjust in renal insufficiency Emtricitabine: 200mg od; adjust in renal insufficiency Lamivudine: 150mg bd / 300mg od; adjust in renal insufficiency Stabudine: 30-40mg bd immediate release; 75-100mg ER od; adjust in renal insufficiency Tenofovir: 300mg qid; adjust in renal insufficiency; take with food Zalcitabine: 0.75mg tid; adjust in renal insufficiency Zidovudine: 200mg tid / 300mg bd; adjust dose in renal insufficiencyDosing IntervalAbsorptionAbacavir: good (83%); not affected by foodBioavailabilityDidanosine: 30-40%, on empty stomach Emtricitabine: 93%, unaffected by food Lamivudine: >80%, unaffected by food Stavudine: 86%, unaffected by food Tenofovir: 39% when given with food Zalcitabine: >80%; do not give with food / antacids Zidovudine: goodHalf lifeAbacavir: intracellular 12-26hrs Didanosine: intracellular 20-24hrs Emtricitabine: intracellular >39hrs Lamivudine: intracellular 10.5-15.5hrs Stavudine: intracellular 3.5hrs Tenofovir: intacellular >60hrs Zalcitabine: intracellular 10hrs ZIdovudine: intracellular 3-7hrsDuration of ActionDistributionAbacavir: CSF 1/3 Didanosine: CSF 20% Emtricitabine: CSF low Stavudine: CSF 55% Zalcitabine: CSF 20% Zidovudine: wide, CSF 60-65%MetabolismLamivudine: mostly unchanged in urine Zidovudine: glucuronidation in liverExcretionDidanosine: glomerular filtration and tubular secretion; change dose in renal failure Emitric: glomerular filtration and tubular secretion Stavudine: glomerular filtration and tubular secretion Tenofovir: glomerular filtration and tubular secretion Zidovudine: renalSide effectsMitochondrial toxicity – due to inhibition of mitochondrial DNA polymerase gamma Lactic acidosis Disorders of lipid metabolism Abacavir: rash (50%), hypersensitivity (5%, fever, malaise, N+V+D, anorexia), dyspnoea, pharyngitis, cough; abnormal LFT’s Resistance: develops slowly Didanosine: peripheral neuropathy; dose-dependent pancreatitis, D+N, hyperuricaemia ((gout), hepatitis, oesophageal ulceration, cardiomyoopathy, CNS toxicity Emitrictabine: headache; D+N; skin hyperpigmentation Lamivudine: N, headache, fatigue Stavudine: peri neuropathy, lipodystrophy, hyperlipidaemia, NM weakness, pancreatitis, arthralgia, incr LFT’s, lactic acidosis Tenofovir: headache, D+N+V, flatulence, renal insufficiency Zalcitabine: peri neuropathy, PO ulcers, pancreatitis; headache, N, rash, arthralgias, cardiomyopathy Zidovudine: myelosuppression, macrocytic anaemia, neutropenia, N, headache, insomnia, thrombocytopenia, myopathyContraindicationsEmi: PO CI’ed in young children, pregnants, renal/hepatic failureDrug interactionsAbacavir: avoid alcohol Didanosine: avoid concurrent neuropathic drugs and alcohol; avoid with indinavir, dapsone and intraconazole as buffer in tablets interferes with absorption of them; tablets contain phenylalanine and sodium to careful on Na-restricted diet; don’t give at same time as fluoroquinolones and tetracyclines as decr AB conc due to chelation Emitricitabine: avoid disulifram and metronidazole; cross-resistance to lamibudine Lamivudine: synergistic with zidovudine and stavudine; incr bioavailability when given with T-S; should not be used with zalcitabine as they inhibit eachother’s intracellular phosphorylation Stavudine: avoid concurrent zidovudine and neuropathic drugs Tenofovir: avoid concurrent probenecid and didanosine Zalcitabine: avoid concurrent cimetidine and neuropathic drugs; amphoterecin B and aminoglycosides decr clearance and incr risk of toxicity Zidovudine: avoid concurrent myelosuppressant drugs; levels increased by probenecid, phenytoiin, methadone, fluconazole, valproic acid, lamivudine (inhibit first pass / decr clearance); zidovudine may decr phenytoin levelsPregnancyExamples Nonnucleoside Reverse Transcriptase Inhibitors (NNRTI) Action Bind to HIV-1 reverse transcriptase ( blockade of RNA and DNA-dependent DNA polymerase Don’t compete with nucleoside triphosphates, and don’t need phosphorylation to be active Resistance occurs rapidly with monotherapyIndicationRoute of administrationDoseDelviradine: 400mg tid Efavirenz: 600mg od, on empty stomach Nevirapine: 200mg bd; adjust dose in hepatic failureDosing IntervalAbsorptionBioavailabilityDelviradine: 85% Efavirenz: 45%; incr by high fat meal Nevirapine: 90%, unaffected by foodHalf lifeEfavirenz: 40-55hrs Nevirapine: 25-30hrsDuration of ActionDistributionDelviradine: 98% bound to plasma proteins; low CSF levels Efavirenz: 99% bound to albumin; CSF 0.3-1.2% Nevirapine: lipophilic, CSF 45%MetabolismEfavirenz: hepatic to inactive metabolites Nevirapine: hepatic to inactive metabolitesExcretionEfavirenz: in faeces as unchanged drug, and renal of inactive metabolites Nevirapine: renal of inactive metabolitesSide effectsGI intolerance Skin rash Delviradine: rash (18%; rarely Stevens-Johnson syndrome), incr LFT’s, headache, fatigue, N+D Efavirenz: CNS effects (up to 50%; dizziness, drowsiness, insomnia, headache, confusion, amnesia, agitation, delusions, depression, nightmares, euphoria), rash (28%), incr LFT’s, N+D+V, crystalluria, incr cholesterol Nevirapine: rash (17%; rarely Stevens-Johnson syndrome and TEN), hepatotoxicity (4%), N, headache, feverContraindicationsDrug interactionsMetabolised by CYP450 and CYP3A4 systems so multiple drug interactions Delviradine: metabolized by CYP3A and CYP2D6; inhibits CYP3A4 and CYP2C9; BA decreased by antacids and H2-blockers; inhibits liver enzymes Efavirenz: inducer and inhibitor of CYP3A4; avoid carbamazepine, itraconazole, ketoconazole, methadone, Phenobarbital, phenytoin, triazolam; inducer and inhibitor of liver enzymes Nevirapine: inducer pf CYP3A; avoid rifampicin, St John’s wort as they induce CYP3A and decr levels of nev; avoid fluconazole, ketoconazole and clarithromycin as they inhibit CYP3A and incr levels of nev; induces hepatic enzymes ( decr levels of methadone, other -avirsPregnancyDelviradine: avoid pregnancy Efavirenz: avoid pregnancyExamples Protease Inhibitors Action During last stages of HIV growth cycle, Gag and Gag-Pol gene products are translated ( protease cleaves these precursor molecules to produce structural protein; these drug cause immature, noninfectious viral particles Resistance common so avoid monotherapy Lopinavir/ritonavir: subtherapeutic dose of ritonavir inhibits CYP3A-mediated metabolism of lopinavir Rotinavir: inhibits HIV-1 and 2 proteasesIndicationRoute of administrationDoseAmprenavir: 1400mg bd; adjust in hepatic insufficiency; avoid high fat meals as decr absorption Atazanavir: 400mg od; adjust in hepatic insufficiency; with food; separate from acid-reducing drugs Darunavir: 600mg bd, with food Fosamprenavir: 1400mg bd; adjust in hepatic insufficiency Indinavir: 800mg tid; adjust in hepatic insufficiency, on empty stomach, drink plenthy H20 Nelfinavir: 750mg tid / 1250mg bd, with food Ritonavir: 600mg bd, with food Saquinavir: varies depending on tablet Tipranavir: 500mg bd, avoid anatacids Ritonavir/lopinavir: enhanced by foodDosing IntervalAbsorptionAmprenavir: readilyBioavailabilityAtazanavir: 60-68%; needs acid medium for absorption Indinavir: 65% Rotinavir: 75%, incr with food Saquinavir: 4%; incr with fatty food Tipranavir: poor; incr with fatty foodHalf lifeAmprenavir: 7-10.6hrs Atazanavir: 6-7hrs Indinavir: 1.5-2hrs Nelfinavir: 3.5-5hrs Saquinavir: 12hrsDuration of ActionDistributionAtazanavir: penetrates CSF Indinavir: CSF 76% Saquinavir: wide, poor CSFMetabolismFosamprenavir: hydrolysed in intestinal epithelium to amprenavir Lopinavir:CYP3A (alter in hepatic impairment) Nelfinavir: CYP3A Rotinavir: CYP3A and CYP2D6 (alter in hepatic impairment) Saquinavir: extensive 1st pass by CYP3A4 Tipranavir: liver microsomal enzyme system (avoid in hepatic impairment)ExcretionAtazanavir: biliary Indinavir: fecal Nelfinavir: fecal Rotinavir: fecal Saquinavir: fecalSide effectsRedistribution and accumulation of body fat ( central obesity, buffalo hump, cushingoid appearance, breast enlargement Incr triglyceride and LDL; glu intolerance and insulin resistance Amprenavir: N+V+D; rash (inc SJS); headache; oral paraesthesia; incr LFT’s Atazanavir: N+V+D, abdo pain, headache, peri neuropathy, rash, hyperbilirubinaemia, prolonged PR/QTc; doesn’t affect triglycerides/fat distribution Darunavir: D+N, headache, rash, hyperlipidaemia, incr LFT’s Fosamprenavir: N+V+D, rash, headache, oral paraesthesdias, incr LFT’s Indinavir: renal stones (10-20%), N, hyperbilirubinaemia, headache, blurred vision, thrombocytopenia, insulin resistance (3-5%), acute haemolytic anaemia Nelfinavir: D+N, flatulence Ritonavir: N+D, paraesthesia, hepatitis, altered taste, hypertriglyceridaemia Saquinavir: N+D, rhinitis, abdo pain, dyspepsia, rash Tipranavir: D+N+V, abdo pain, rash, incr LFT’s (may be life-threatening), hypercholesterolaemia, hypertriglyceridaemia; poss incr intracranial haemorrhage, decr WCC Lopinavir: D+N+V, abdo painContraindicationsTipranavir: avoid in sulphur allergyDrug interactionsAll are inhibitors of CYP3A4; some are inducers of other CYP’s (such interactions can be used to boost levels of other antiretrovirals) Amprenavir: metabolized by CYP3A4 (inducer and inhibitor); avoid cimetidine; avoid alcohol, disulfiram. metronidazole as PO drug contains propylene glycol; avoid vit E as drug contains high levels; contains sulphur Atazanavir: inhibits CYP3A4 and CYP2C9; omeprazole decreases levels; avoid Ca channel blockers as prolong QTc Fosamprenavir: avoid cimetidine, disulfiram, metronidazole, vit E, alcohol Indinavir: inhibits CYP3A4 Nelfinavir: inhibits CYP3A Rotinavir: inhibits CYP3A4; incr digoxin and theophylline levels; lower therapeutic doses given to incr levels of other antiretrovirals Saquinavir: inhibits CYP3A4 Tipranavir: inhibit and induce CYP3A4; also induced P-glycoprotein transporter ( alter disposition of other drugsPregnancyNelfinavir: safeExamples Fusion Inhibitors Enfuviritde: blocks entry into cell by binding gp41 subunit of viral envelope glycoprotein ( prevent fusion of viral and cellular membranes; SC; metabolism by proteolytic hydrolysis; HL 3.8hrs; SE local irritation, hypersensitivity Contraindicated Drugs Usually anti-arrhythmics (eg. flecainiade), antihistamines, sedative-hypnotics (eg. diazepam, midazolam, triazolam), neuroleptics, HMG CoA reductase inhibitors (eg. atorvastatic, simvastatin), anticonvulsants (eg. Phenobarbital, phenytoin), OCP, rifampicin, St John’s wort Caution with amiodarone, quinidine, lidocaine, nifedipine, sildenafil, warfarin, levodopa, cyclosporine, itraconazole, ketoconazole, carbamazepine, dezamethasone, methadone, omperazole, lansoprazole ANTIHEPATITIS AGENTS Interferon Alpha Action Host cytokines; induction of intracellular signals ( bind specific cell membrane receptors ( inhibition of viral penetration, translation, transcription, protein processing, maturation, release; incr expression of MHC antigens, enhanced phagocytic activity of macrophages, incr proliferation and survival of cytotoxic T cells ACTIVE AGAINST: HBV, HCVIndicationRoute of administrationSC/IV (alfa 2a and 2b); SC (alfacon-1)DoseDosing IntervalAbsorptionBioavailabilityHalf life2a,2b: 2-5hrs Alfacon-1: 6-10hrs Pegylated forms: longer, better efficacyDuration of ActionDistributionMetabolismExcretionGlomerular filtration ( proteolytic degradation during tubular reabsorption (30%) – adjust in renal failure Liver metabolism (minor) Biliary excretion (minor)Side effectsFlu-like syndrome within 6hrs in 30%, which resolves; incr LFT’s; neurotoxicity (mood disorder, depression, confusion, seizure); myelosuppression, fatigue, weight loss, rash, cough, myalgia, tinnitus, hearing loss, retinopathy, pneumonitis, cardiotoxicity; induction of autoantibodiesContraindicationsCI: hepatic decompensation, autoimmune disease, arrhythmia, epilepsy, thyroid disease, psych, IHD, severe renal insufficiency, pregnancyDrug InteractionsIncr theophylline and methadone levels; NRTI ( hepatic failure Trt of Hep B Success = seroconversion from HBeAg +ive to –ive, suppression of HBV DNA to undetectable Trt (NRTI) suppresses HBV replication, doesn’t eradicate virus; ccDNA will remain in cell as reservoir and may reactivate Lamivudine: 17-19hr half life in HBV infected cells (longer than HIV) so lower dose and less f; suppression to undetectable in 44%, seroconversion in 17% Adefovir dipivoxil: phosphorylated by cellular kinases to active diphosphate metabolite ( competitively inhibits HBV DNA polymerase; BA 59%; half life 7.5hrs; excreted by GF and ATS; can be given in liver disease; seroconversion 23%; may be renal toxicity, headache, diarrhoea, abdo pain Entecavir: BA 100%, half life 15hrs; GF and TS elimination; SE headache, fatigue, dizziness, N Trt of Hep C Sustained viral response = absence of detectable viraemia for 6/12 after completion of trt; generally use IFa (once weekly) + ribavirin PO Ribavirin: phosphorylated intracellularily by host enzymes ( interfere with synthesis of GTP, inhibit capping of viral mRNA, inhibit viral RNA-dependent polymerase ( inhibit replication; also active against influenza A+B, parainfluenza, RSV, HIV-1; BA 64%; eliminated renally; SE haemolytic anaemia, depression, fatigue, rash, cough, Anti-Influenza Drugs ANTI-INFLUENZAL DRUGS Amantadine and rimantadine: block M2 protein ion channel of virus particle ( block uncoating of viral RNA in infected host cells; influenza A only; 100mg bd/200mg od; resistance due to altered M2 protein; SE N, nervousness, dizziness, peri oedema; incr SE when used with antihistamines, anticholinergics, T-S; avoid in preg A: excreted unchanged in urine; dose adjust in R failure R: extensive hydroxylation, conjugation, glucuronidation ( urinary excretion; dose adjust in R+H failure Zanamivir and oseltamivir: neuraminidase inhibitors; interfere with release of virus from host cells in resp tract; flu A+B; resistance rare Z: INH; 5-15% absorbed and excreted renally; SE: cough, bronchospasm, decr PFT O: PO; activated by hepatic esterases; HL 6-10hrs; excretion renal (alter dose); SE: N+V+D, abdo pain, headache, fatigue insomnia, N, pruritis; CI renal failure, preg Can be given INH for RSV ANTISEPTICS Disinfectants: Inhibit/kill MO; can be chemical / ionizing radiation / heat / steam Antiseptics: as above but low toxicity so can be used on skin / wounds Sterilants: kill vegetative cells and spores Antisepsis: application of agent to living tissue to prevent infection Decontamination: destruction / marked reduction in no / activity of MO Disinfection: chemical / physical trt that destroys most vegetative microbes / viruses (not spores) in /on inanimate surfaces Sanitsation: decr microbial load on inanimate surface to acceptable level Sterilisation: kill MO (inc spores and viruses) or remove to low probability of survival Pasteurisation: kills non-sporulating MO by hot water / steam at 65-100C NB. May have biocidal activity, accumulate in environment / body, interfere with wound healing ON SKIN: Alcohols: ACTIVE AGAINST: G+ive, G-ive, acid fast, lipophilic viruses, fungi NOT ACTIVE AGAINST: spores, prions; spores of C difficile eg. ethanol, isopropanol; act by denaturation of proteins; not sterilants Chlorhexidine: ACTIVE AGAINST: G+ive, G-ive (less active); mod against fungi and viruses NOT ACTIVE AGAINST: acid fast, spores, prions Adsorbs to bacterial membranes causing leakage of molecules and precipitation of cytoplasmic proteins; has more residual activity than alcohol as alcohol evaporates away; inhibits spore germination Halogens: iodine ACTIVE AGAINST: G+ive, G-ive, acid fast, spores, lipophilic viruses, fungi NOT ACTIVE AGAINST: hydrophilic viruses, prions may cause hypersensitivity iodophors contain iodine (for bacteria, mycobacteria, fungi, lipophilic viruses, may be sporocidal) chlorine ACTIVE AGAINST: all; not used on skin ON EQUIPMENT: Phenolics: ACTIVE AGAINST: G+ive, G-ive, acid fasy, lipophilic viruses, fungi NOT ACTIVE AGAINST: spores, hydrophilic viruses, prions Phenol too corrosive/toxic/carcinogenic to be used; can use o-phenylphenol etc… but still some skin irritation; disrupt cell walls and membranes, precipitate proteins, inactive enzymes Quaternary ammonium compounds: as phenols; inactivation of E-producing enzymes, denaturation of proteins, disruption of cell membrane; bacteriostatic, fungistatic, sporistati; inhibit algae; eg. banzalkonium chloride Aldehydes: ACTIVE AGAINST: all except prions; eg. formaldehyde, glutaraldehyde; for sterilization of equipment; alkylation of chemical groups; work on lipophilic and hydrophilic viruses Peroxygen compounds: eg. hydrogen peroxide, peracetic acid; broad spectrum incr spores Heavy metals: eg. mercury, silver; rarely used; silver nitrate and sulfadiazine used on skin Sterilants: eg. stea Superoxidised water: non-toxic and non-irritating Preservatives: benzoic acid, parabens, sorbic acid, phenolic compounds, quaternary ammonium compounds, alcohols ANTIPARASITIC DRUGS 3 major targets: 1) Unique essential enzymes found only in parasite – only possible in a few parasites; may develop drug resistance a) Sulfones/sulfonamides: inhibit enzymes for dihydropteroate synthesis Nitromidazoles: inhibits pyruvate:forrodoxin oxidoreductase Allopurinol riboside and formycin B: inibit trypanothione reductase and peroxidase 2) Similar enzymes found in host and parasite, but indispensable only in parasite due to metabolic deficiencies of parasites a) Azoles (eg. Ketoconazole): inhibit lanosterol C-14alpha demethylase Allopurinol: inhibit pruine phosphoribosyl transferase Diamidines: inhibits S-Adenosylemthionine decarboxylase 3) Common biochemical function found in host and parasite but with different pharmacologic properties (eg. Transporter, receptor, cellular structural component, nervous synaptic transmission etc…) ANTIPROTOZOAL DRUGS Treatment of Malaria Anopheline mosquito inoculates plasmodium sporozoites to initiate human infection ( sporozoites invade liver cells ( exoerthrocytic tissue schizonts mature in liver ( merozoites released from liver ( invade erythrocytes ( clinical illness ( gametocytes in erythrocytes, taken up by mosquitos ( infective sporozoites P falciparium and P malariae: one stage of liver cell invasion; liver infection ceases in <4/52; elimination of erythrocytic parasites will cure infection P vivax and P ovale: dormant hepatic stage (hypnozoite) can cause relapses; elimination of erthrocytic and hepatic parasite required to cure infection Tissue schizonticides: eliminate liver forms of parasite Blood schizonticides: eliminiate erythrocytic parasites Gametocides: kill sexual stage parasites Causal prophylactic drugs: prevent erythrocyte infection; use chloroquine in sensitive areas, mefloquine in other malarious areas, doxycycline where v high prevalence of multi-drug resistant falciparium Summary: Nonfalciparum infection / falciparum in areas without known resistance: give chloroquine Vivax / ovale: also primaquine to eradicate liver forms Falciparum: PO quinine / IV quinidine + doxycycline (or clindamycin in children); also effective against resistant falciparum are mefloquine, halofantrine May be given drugs to self-trt if no medical help available: given quinine; don’t recommend routine primaquine for dormant hepatic stage 4-aminoquinolines: Action Chloroquine: Mechanism of action: concentrates in parasite food vacuoles ( prevents polymerization of heme into hemozolin ( parasite toxicity due to buildup of free heme Blood schizontocite: v effective Gametocytes: mod. effectiveness in vivax, ovale and malariae, but not falciparum Hepatic stage: not effective; so primaquine must be added for these infections Amiodiaquine: same MOA and resistance; low cost, limited toxicity Primaquine (8-aminoquinolone): for P vivax and ovale Hepatic stage: active against; only available drug for this Gametocytes: active Blood schizontocite: low activityIndicationChloroquine: Drug of choice in sensitive falciparum and other species for trt; clears parasitaemia in 48-72hrs Preferred for chemoprophylaxis in areas without resistant falciparum Reaches high liver concs and can be used to trt amoebic abscesses that fail to respond to metronidazole Amiodiaquine: may be effective against chloroquine-resistant falciparum Primaquine: acute vivax / ovale malaria; needed in prophylaxis to prevent relapseRoute of administrationChloroquine: PO preferred, but can give IV infusion Primaquine: never IV (( hypotension)DoseChloroquine: 500mg once weekly Primaquine: 26.3mg od for 14/7Dosing IntervalAbsorptionChloroquine: Rapid and complete PO; max plasma concs in 3hrs Primaquine: good PO; max plasma level in 1-2hrsBioavailabilityHalf lifeChloroquine: Terminal elimination half flife 1-2/12 Primaquine: 3-8hrsDuration of ActionDistributionChloroquine: Large VOD (100-1000L/kg) Primaquine: wideMetabolismPrimaquine: rapidExcretionChloroquine: Renal Primaquine: renalSide effectsChloroquine: Resistance: v common among P falciparum (due to mutations in putative transporter, PfCRT); uncommon but increasing in P vivax Usually well tolerated – pruritis; N+V, abdo pain, headache, anorexia, malaise, blurred vision, urticaria; rarely impaired hearing, psychosis, confusion, seizures, agranulocytosis, alopecia, hypotension, wide QRS, T wave abnormalities; long tern can cause irreversible ototoxicity, retinopathy, myopathy, peri neuropathy Amiodiaquine: agranulocytosis, aplastic anaemia, hepatotoxicity; toxic in longterm so can’t be used for prophylaxis Primaquine: Resistance: some strains show resistance, for which rpted courses required Well tolerated; N, epigastric pain, abdo pain, headache; rare is leucopenia, agranulocytosis, leukocytosis, cardiac arrhythmia; haemolysis, methemoglobianaemiaContraindicationsChloroquine: Psoriasis, porphyria – may cause attack; avoid if retinal/visual field abnormalities, myopathy; caution in liver disease, neurologic/haematologic disorders Primaquine: avoid in granulocytopenia, methaemoglobiaemia, myelosuppressive drugs; disorders causing myelosuppressionDrug interactionsChloroquine: Ca and Mg antacids interfere with absorptionPregnancyChloroquine: safeExamples Quinoline Methanol Action Quinine and Quinidine Blood schizontocide: v effective Gametocytes: vivax and ovale; not falciparum Hepatic stage: not effective Mefloquine Blood schizontocide: v effective against falciparum and vivax Gametocytes: not effective Hepatic stage: no effectiveIndicationQuinine: first line for falciparum unless the area is sensitive to chloroquine; resistance is uncommon but increasing Quinidine: first line for falciparum; IV for severe infections Not used for prophylaxis due to toxicity Mefloquine: effective against chloroquine-resistant falciparum; used for chemoprophylaxis and trt; effective for most falciparum malaria, but not if severe/complicated as quinine is more effectiveRoute of administrationQuinine: slow IV / IM for severe; PO Quinidine: IV with a loading dose with cardiac monitoring for severe Mefloquine: PO onlyDoseMefloquine: 250mg weeklyDosing IntervalMefloquine: weeklyAbsorptionQuinine: rapid PO; peak plasma level in 1-3hrs esp if use loading dose; those with malaria achieve higher levels and longer half life Mefloquine: good PO; peak plasma concs in 18hrsBioavailabilityHalf lifeQuinine: 18hr in infected person, 11hrs in healthy Quinidine: shorter due to decr protein binding Mefloquine: 20 daysDuration of ActionDistributionQuinine: wide VOD Mefloquine: highly protein bound; wide VODMetabolismQuinine: liverExcretionQuinine: renal Mefloquine: slow, drug and metabolites, in faecesSide effectsQuinine and Quinidine Resistance: common in SE Asia Common: tinnitus, headache, nausea, dizziness, flushing, visual disturbances (cinchonism) Hypersensitivity: skin rash, urticaria, angioedema, bronchospasm Haematologic abnormalities: haemolysis (if severe, blackwater fever due to haemoglobinuria), leucopenia, agranulocytosis, thrombocytopenia Hypoglycemia Cardiac toxicity – prolonged QT; caution if underlying cardiac abnormality Mefloquine Resistance: in SE Asia N+V+D, dizziness, sleep disturbance, abdo pain, headache, rash; leukocytosis, thrombocytopenia, incr LFT’s; neuropsychiatric toxicitiesContraindicationsMefloquine: history of epilepsy, psychiatric disorders, arrhythmia, cardiac conduction defectsDrug interactionsQuinine and Quinidine Often used with anther drug (eg. Doxycycline or clindamycin) to shorten trt duration and limit toxicity Don’t give with mefloquine Al antacids block absorption Incr levels of warfarin and digoxin Meflaquine: don’t give with quinidine/quininePregnancyQuinine: Can cause uterine contractions in 3rd trimesterExamples Inhibitors of Folate Synthesis Action Proguanil: a prodrug Pyrimethamine: related to trimethoprim (also used in toxoplasmosis when combined with sulfadiazine) Blood schizontocide: effective Hepatic stage: proguanil has some action, but not very good Gametocyte: no activity Mechanism of action: inhibit plasmodial dihydrofolate reductase (enzyme in synthesis of folate) Fansidar: sulfadoxine (sulfonamide) + pyrimethamine; not reliable in vivax; for trt of some with chloroquine-resistant falc Malarone: atovaquone (quinone) + proguanil Chlorporguanil + dapsone: for multidrug resistant falciparum in Africa Chloroquine + proguanil – alternative to mefloquine as less toxicIndicationProguanil: od for prophylaxis with chloroquine Pyrimethamine: weekly for prophylaxis Effective in combination, rarely used alone Fansidar: for uncomplicated falciparum; low rates of drug resistance and toxicity, cheap; not for severe as slow-acting; can be used with quinine to shorten course; can be used for presumptive trt in travellersRoute of administrationPODoseMalarone: 250mg atovaquone, 100mg proguanilDosing IntervalAbsorptionProguanil and pyrimethamine: slowly adequate PO absorption; peak levels in 2-6hrs for pyri, 5hrs for progBioavailabilityHalf lifePyrimethamine: 3.5 days Proguanil: 16hrs Sulfadoxide: 170hrsDuration of ActionDistributionMetabolismPyrimethamine: extensivelyExcretionRenalSide effectsResistance: due to mutations in dihydrofolate reductase and dihydropteroate synthase; most common in falciparum Well tolerated; GI symptoms, rashes, itching, mouth ulcers, alopecia; rarely erythema multiforme, SJS and TEN; rarely hematologic, GI, CNS, derm and renal toxicity Maloprim ( agranulocytosisContraindicationsBeware in hepatic / renal failureDrug interactionsPregnancySafe with folate supplementationExamples Others Action Halofantrine (phenanthrene-methanol): for erythrocytic stage; active against chloroquine-resistant falciparum Lumefantrine (amyl alcohol): for falciparum in combination with artemisinin Atovaquone (quinone) + proguanil (named Malarone) Artemisinin (sesquiterpene lactone endoperoxidase): insoluble; artesunate is H20-soluble version for IV/IM/PR/PO use; artemether is lipid-soluble version for PO/IM/PR use; used in combination with methloquine for highly resistant malaria Blood schizonts: rapidly active; resistance rare so good in multi-drug resistant forms Hepatic stage: no effect Tetracycline and doxycycline: for blood schizonts; when combined with quinine to shorten dosing time Clindamycin: for blood schizonts; again can be used with quinineIndicationHalofantrine: not used as prophylaxis due to toxicity concerns Malarone: for trt and prophylaxis of falciparum; can also be used for P jiroveci infectionRoute of administrationArtemesisin: only PODoseDoxycycline: 100mg odDosing IntervalAbsorptionHalofantrine: increased by food so be careful as may cause toxicity Artemisinin: rapidBioavailabilityAtovaquone: low; absorption increased by fatty foods Lumefantrine: also variableHalf lifeHalofantrine: 4 days Lumefantrine: 4.5hrs Atovaquone: 2-3days Artemisinin: 1-3hrs, so limited efficacy esp in chemoprophylaxisDuration of ActionDistributionMetabolismArtemisinin: metabolized to active metabolite dihydroartemisininExcretionHalofantrine: in faeces Atovaquone: unchanged in faecesSide effectsHalofantrine: cardiac toxicity (prolonged QT and PR); abdo pain, D+V, cough, rash, headache, prirotos, incr LFT’s Atovaquone: feverm rasgm N+V+D, headache, insomnia Artemesinin: well tolerated; N+V+DContraindicationsHalofantrine: cardiac conduction defectsDrug interactionsPregnancyHalofantrine: contra-indicated Artemisinin: contra-indicated due to teratogen effectsExamples Chloroquine sensitive falciparum and malariae: chloroquine 1g followed by 500mg at 4, 24 and 48hrs P vivax and ovale: chloroquine as above, then primaquine 26.3mg od for 14/7 Chloroquine-resistant falciparum infections: quinine 650mg tds for 3-7/7 plus doxycycline 100mg bd for 1/52 or clindamycin 100mg bd for 1/52 or fansidar 3 tabs once Alternatives: malarone, mefloquine, artesunate, artemether, coartem Severe/complicated falciparum: quinidine 10mg/kg IV over 1-2hrs, then 0.02mg/kg/IV/min; alternative atersunate or artemether Treatment of Amebiasis (Entamoeba Histolytica) ( colitis, liver abscess Luminal ambecides: for trt in nonendemic areas to eradicate carriage Diloxanide furoate: splits into diloxanide (90% absorbed and conjugated to form the glucuronide which is excreted in urine; 10% is active) and furoic acid; no serious SE but causes flatulence, N and abdo cramps Iodoquinol: often used with metronidazole; 90% retained in intestine and excreted in faeces ( rest enter circ, HL 11-14hrs ( excreted in urine; not effective against trophozoites in gut wall; SE: D+N+V, abdo pain (take with meals to avoid), headache, rash, pruritis, neurotoxicity; CI: optic neuropathy, renal, thyroid disease Paromomycin: aminoglycoside AB; poorly absorbed; absorbed stuff is excreted renally by GF (may accumulate in renal insufficiency); SE: abdo pain and D Tissue ambecides: for amebic colitis, extraintestinal infections Metronidazole and tinidazole – kill trophozoites but not cysts; tindinazole has better toxicity profile; see above Tetracyclines and erythromycin Other Antiprotozoals Action Pentamidine: trypanosomatid protozoa and P jiroveci Sodium stibogluconate: 1st line for leishmaniasis Nitazoxanide: Giardia lamblia, Cryptosporidium parvum; active metabolite tizoxamide inhibits pyruvate:ferredoxin oxidoreductase pathway; good for metronidazole resistant strains Suramin: trypanosomiasis Melarsoprol: trypansomiasis Eflornithine, nifurtimox, benzindazole, amphotericinc, miltefosineIndicationPentamidine: pneumocystosis (although 1st choice is T-S), trypanosome brucei ( African trypanosomiasis; leishmaniasisRoute of administrationPentamidine: IV, NEB Sodium stibogluconate: IV/IM Suramin: IVDoseDosing IntervalAbsorptionNitazoxanide: rapid, with conversion to tizoxanideBioavailabilityHalf lifePentamidine: 6hrs, but accumulates due to slow excretion ( 12 days Suramin: terminal of 50 daysDuration of ActionDistributionPentamidine: poor penetration of CNS Suramin: poor entry to CNS so not in advanced diseaseMetabolismExcretionPentamidine: urine Sodium stibogluconate: short phase over 2 hrs, then longer phase >24hrs, so 2 half lives Nitazoxanide: metabolites excreted in urine and faeces Suramin: slow renal excretionSide effectsPentamidine: highly toxic; severe hypotension, incr HR, dizziness, dyspnoea when IV; pancreatic toxicity, hypoglycaemia; renal insufficiency; rash, metallic taste, fever, GI symptoms, incr LFT’s, hypoCa, thrombocytopenia, hallucinations, cardiac arrhythmia Sodium stibogluconate: incr toxicity if longer therapy; GI symproms, fever, headache, myalgias, arthralgias, rash; T wave changes and QT prolongation; hemolytic aneamia, liver, renal and cardiac effects Suramin: fatigue, N+V, seizures, shock; fever, reash, headache, paraesthesias, neuropathies, proteinuria, haemolytic anaemia, agranulocytosisContraindicationsDrug interactionsPregnancyExamples ANTHELMINTIC DRUGS Albendazole Broad spectrum; drug of choice for hydatid disease and cystercosis; also for pinworm and hookworm, ascariasis, trichuriasis, neurocysticercosis; PO absorption erratically ( 1st pass metabolism in liver ( metabolite albendazole sulfoxide; HL 8-12hrs; protein bound, high VOD entering bile, CSF and hydatid cysts; excreted in urine; inhibit microtubule synthesis; took work on luminal, give on empty stomach, to work on tissue, give with fatty meal; SE: epigastric pain, D+N, headache, dizziness, lassitude, insomnia; long term ( abdo pain, headaches, fever, fatigue, alopecia, incr LFT, pancytopenia Bithionol: For sheep liver fluke (fascioliasis) and paragonimiasis; renal excretion; PO; SE: D+N+V+AP; dizziness, headache, skin rashes Diethylcarbamazine citrate: for filiarsis, loiasis, tropical eosinophilia; rapid PO absorption; HL 2-3hrs (longer if alkaline urine); large VOD except in fat; renal excretion as unchanged frug and N-oxide metabolite; alters surface structure and immoblises microfilariae ( destruction by host mechanisms; SE: headache, malaise, anorexia, weakness, N+V, dizziness; reaction to dying MO ( fever, malaise, popular rash, headache, GI symptoms, cough, chest pain, myalgia, arthalgia, proteinuria; may get lymphangitis, wheals, papules in area of infection Doxycycline: for W bancrofti by killing intracellular symbiont of filarial parasites (Wolbachia) Invermectin: strongylodiasis and onchocerciasis; PO; rapid absorption; wide VOD (50L); HL 16hrs; excretion in faeces; paralyses MO by intensifying GABA-mediated transmission of signals in peripheral nerves; SE: fatigue, dizziness, N+V+AP, rash; killing of MO ( Mazotti reaction (see above); severe reaction ( high fever, low BP, bronchospasm (need corticosteroids); may get corneal opacities Mebendazole: wide spectrum (ascariasis, trichuriasis, hookwork, pinworm); <10% PO absorbed (incr with fatty meal) ( >90% protein bound ( rapid conversion to inactive metabolites during 1st pass in liver; HL 2-6hrs; excreted in urine and bile; inhibits microtubule synthesis; SE: mild N+V+D+AP; rarely hypersensitivity reactions, agranulocytosis, alopecia, incr LFT’s; CI in pregnancy; levels may be decreased by carbamazepine and phenytoin, increased by cimetidine; caution in cirrhosis Metrifonate: Schistosoma haemoatobium; PO; rapid absorption; HL 1.5hrs; clearance by nonenzymatic transformation to dichlorvos; high VOD; eliminated in 24-48hrs; works by cholinesterase inhibition ( paralyses adult worms ( encased by immune system and die; SE: cholinergic symptoms, N+V+D+AP, bronchospasm, headache, sweating, fatigue, weakness, dizziness, vertigo Niclosamide: tapeworm; poor PO absorption; inhibit oxidative phophorylation or stimulation of ATPase activity; SE: mild N+V+D+AP; avoid alcohol Oxyamniquine: S mansoni; well PO absorbed ( HL 2.5hrs ( metabolized to inactive metabolite ( renal excretion; contraction and detachement of worms then transit to liver where they die; SE: CNS (dizziness, headache, drowsiness); N+V+D+AP, pruritis, urticaria, fever, proteinuria, haematuria; caution in epilepsy Piperazine: ascariasis; good PO absorption ( unchanged excretion in urine; paralyses by blocking Ach at myoneural junction; SE: N+V+D+AP, dizzinss, headache; CI: pregnancy, renal and hepatic disease, epilepsy Praziquantel: schistosomiasis, clonorchiasis, opistorchiasis, paragonimiasis, taeniasis, neurocysticercosis, hydatid disease etc…; rapid PO absorption (BA 80%) ( CSF levels 14-20%, 80% bound to p proteins ( rapidly metabolized to inactive product after 1st pass in liver, HL 0.8-1.5hrs ( excretion renally (60-80%) and in bile (15-35%); phenytoin and carbamazepine and corticosteroids decr BA; work by incr permeability of cell membrane to Ca ( paralysis, dislodgement and death; SE: headache, dizziness, drowsiness, N+V+AP+D, pruritis, urticaria, arthralgia, myalgia, low grade fever; may get neurological abnormalities due to inflamm reaction around dying parasite, so give corticosteroids; can’t give in ocular cystercosis as will cause irreversible damage; avoid in pregnancy Pyrantel pamoate: broad spectrum; pinworm, ascaris, hookworm; poor PO absorption so for luminal MO; >50% eliminated unchanged in faeces; work as NM blocking agent ( causes release of Ach and inhibition of cholinesterase ( paralysis and expulsion of worm; SE: N+V+D+AP, dizziness, drowsiness, headache, rash, fever, weakness; careful in liver disease Thiabendazole: strongyloidiasis, cutaneous larva migrans; good PO absorption; HL 1.2hrs; metabolized in liver to 5-hydroxy form; 90% excreted in urine; SE: more toxic; N+V+AP; dizziness, anorezia, pruritis, headache, neuropsych probs, liver failure, SJS CNS DRUGS Ion Channels Nerve cell membranes contain channels (NB. Can be affected by toxins from various insects etc…) Voltage-gated: concentrated in initial segment and axon and responsible for fast AP from cell body to nerve terminal; for K and Ca; act slowly Ligand-gated (Ionotropic) receptors: by binding of NT’s; act fast for brief opening; for fast synaptic transmission Metabotropic receptors: G-protein coupled receptors which modulate voltage-gated channels (usually Ca and K); can have longer effects; in diffuse neuronal systems in CNS Membrane delimited pathway: directly act on channels in membrane; inhibit Ca channels presynaptically, activate K channels postsynaptically (( slow postsynaptic inhibition) Diffusable second messengers: eg. Beta-adrenoceptor ( generates cAMP via activation of adenylyl cyclase Synapses AP in presynapic fibre ( Activates voltage gated Ca channels in nerve terminal (can be blocked by marine toxins and metal ions) ( Ca enters terminal ( fusion of synaptic vesicles with presynaptic membrane ( NT enters synaptic cleft, diffuses to postS membrane (delay 0.5s – mostly due to opening of Ca channels) ( change in permeability to ions in postS membrane; NT either degraded or reuptook Excitatory postsynaptic potential (EPSP): excitatory NT acting on ionotropic receptor ( incr Na and K permeability; when enough excitatory fibres activated ( depolarizes to threshold ( all- or-none AP propogated Inhibitory postsynaptic potential (IPSP): opening of Cl channels ( hyperpolarized, with more leaky membrane so changes in membrane potential harder to achieve Pre-synaptic inhibition: axoaxonic synapses decreasing amount of NT released from terminals; occurs mainly in spinal cord Sites of Drug Action Mostly work by modifying a step in synaptic pathway Presynaptic: alter synthesis, storage, metabolism and release of NT’s Eg. Reserpine – interfere with intracellular storage of monoamines Eg. Amphetamine – induces release of catecholamine from adrenergic synapses Eg. Capsaicin – release of peptide substance P from sensory neurons Eg. Tetanus toxin – blocks release of NT’s Eg. Cocaine – blocks uptake of catecholamines at adrenergic synapses Eg. Anticholinesterases – block degradation of Ach Postsynaptic: can act as NT agonists (eg. Opioids mimic action of enkephalin) or block receptor function (eg. Strychnine blocks receptor for inhibitory NT glycine ( seizures); can directly act on ion channels (eg. Barbs enter/block channel of excitatory ionotropic receptors); can act downstream of metabotropic receptors (eg. Methylxanthines work on cAMP) Cellular Organisation of Brain 1) Hierarchial systems: all pathways involved in sensory perception and motor control; large, myelinated fibres that conduct >50m/s in bursts of AP’s; info processed sequentially at each relay nucleus; 2 types of cells: relay/projection neurons – form interconnecting pathways to transmit signals over long distances; large cell bodies; collaterals extensively; excitatory with short lived responses; release glutamate Local circuit neurons – smaller; axons more local; inhibitory; release GABA/glycine; synapse on dendrites of projection neurons; form recurrent feedback pathways and feed-forward pathways; involved in axoaxonix synapses on sensory axons Blocking GABAa receptors with picrotoxin ( generalized convulsions (ie. Nonspecific effect) Limited no. of NT’s used so easy to affect systems 2) Nonspecific/Diffuse Neuronal Systems: eg. Monoamines (eg. NE, dopamine, 5-HT). Differences: a) Noradrenergic cell bodies found in compact group (locus ceruleus) in caudal pontine gray matter b) Axons fine and unmyelinated; slow conduction 0.5m/s; axons branch repeatedly ( tangents so an effect large areas of cortex; axons studded with periodic enlargements called varicosities containing large no’s of vesicles c) Targets determined by site of receptors rather than location of release sites d) Most NT’s work on metabotropic receptors (rather than ionotropic above) so have longer acting effects e) Not involved in conveying topographical specific info, more acting on vast areas of CNS – sleeping, waking, attention, appetite, emotion Central NT’s: see physiology notes Sedative-Hypnotic Drugs Sedative: decr anxiety, calming; aim for minimum CNS depression Hypnotic: produce drowsiness, encourage sleep; depressive on CNS Have dose-dependent CNS depression; older barbs and alcohols have linear (high doses cause resp and vasomotor depression); more curvy for benzo’s and newer hypnotics Mechanism of action: bind GABAa receptor in CNS (Cl ion channel; inhibitory; benzo’s and barbs bind in different sites; zolpidem, zaleplon and eszopiclone bind only to GABAa receptors with ą1 subunits) (thought that ą1 subunits for sedation, amnesia, antiseizure; ą2 subunits for anxiolytic and muscle-relaxing, ą5 for memory impairment) Benzos ( potentiate GABAergic inhibition at all levels by increasing effiency at synapses (do not directly open channels or activate receptors, but aid GABA to incr frequency of channel opening); 3 types on interactions reported Agonists: facilitate GABA Antagonists: flumezanil (doesn’t antagonize barbs/meprobamate/ethanol/opioids/GA); competitivel; acts rapidly but HL 0.7-1.3hrs (duration of action <90mins) due to rapid hepatic clearance; SE: agitation, confusion, dizziness, nausea; may cause a withdrawal syndrome; used to accelerate recovery when used in anaesthesia Inverse agonists: can produce anxiety and seizures (eg. ˛-carbolines) Barbs ( facilitate GABA by incrasing duration of channel opening; at high concs may directly open Cl channels; less selective than benzos (also depress actions of excitatory NT’s, other nonsynaptic membrane effects) – hence more pronounced CNS depressant effects Note GABAa can also be bound by alcohol, etomidate, propofol, volatile anaesthetics, gabapentin; blocked by picrotoxin and bicuclline ( convulsions Effects: Sedation: usually some effects on psychomotor and cognitive functions; euphoria, impaired judgement, loss of self control, anterograde amnesia Hypnosis: all induce at high enough dose; Benzo’s and older sedative-hypnotics: decr time to fall asleep, incr duration of stage 2 NREM sleep, decr duration of REM sleep, decr duration of stage 4 NREM slow-wave sleep; zolpidem has minimal effect on slow-wave sleep; zalepon has little effect on total sleep time, NREM or REM; decr REM may cause irritability and anxiety; may get rebound insomnia when stop drug; tolerance can develop after 2-3/52; daytime sedation more common when slow elimination rate (eg. Lorazepam) or biotransformed into active metabolites (eg. Flurazepam, quazepam); zolpidem etc… good for rapid onset with less hangover next day Anaesthesia: high doses reach stage III general anaesthesia; from barbs – thiopental and methohexital lipid-soluble and penetrate BBB rapidly so good for induction, short duration of action due to rapid redistribution and elimination; from benzos – beware of long HL and active metabolites Anticonvulsants: benzos; of barbs – Phenobarbital and metharbital; NOT in zolpidem, zaleplon and eszopiclone as more selective binding Muscle relaxation: inhibit polysynaptic reflexes and may depress NMJ; NOT in zolpidem, zaleplon, eszopiclone Resp and CV function: effects are dose-related; CV effects in pt already with heart failure or in high doses due to effect on medullary vasomotor centres (decr contractility and vascular tone) Tolerance: decr responsiveness on repeated exposure; common; cross-tolerance with ETOH; may be due to incr drug metabolism (metabolic tolerance) for barbs, changes in responsiveness of CNS (Eg. Downregulation of brain receptors) (pharmacodynamic tolerance) for sedative-hypnotics Psychologic dependence Physiologic dependence: need drug to prevent withdrawal syndrome (anxiety, insomnia, CNS excitability, weakness, restlessness, low BP, hyperreflexia, seizures); depends on dose, HL (worse if short – eg. Triazolam gives daytime anxiety); occurs less with zaleplon etc… For trt: high therapeutic index, flumezanil must reverese, low risk of drug interaction due to liver enzymes, minimal effect of CV and autonomic functions SE: CNS depression ( impaired judgement, drowsy, decr motor skills; anterograde amnesia; affect cognitive processes (eg. Learning); hangover; significant effects in elderly; breathing probs in COPD; CV depression; disinhibition with aggression; occasional hypersensitivity reactions; caution in pregnancy In OD: Benzo’s better in OD as have flatter dose-response curves (alprazolam is most toxic in OD of benzos); may need +ive inotrope (eg. Dopamine) to conserve renal blood flow; use flumezanil to reverse (variable effect on resp depression, short HL, may cause withdrawal) Drug interactions: additive effects with ETOH, opioids, anticonvulsants, phenothiazines, antihistamines, antihypertensives, tricyclics Benzodiazepines Action See aboveIndicationAlprazolam: v good for panic disorder To stop seizures (diazepam, lorazepam); IV diaz to max 20-30mg for status epilepticus; lorazepam is slightly longer acting Clonazepam and nitrazepam: used for myoclonic seizures, infantile spasms Clorazepate dipotassium: for complex partial seizures Diazepam, lorazepam and midazolam: used for pre-medication; slow onset of CNS depressant effects which reach plateau at depth of sedation which is inadequate; in high doses, unacceptable post-anaesthetic recovery period with much antergrade amnesiaRoute of administrationMidazolam is H20-soluble and is benzo of choice for IV; rapid onset with steep dose-response curveDoseFor sedation: Alprazolam: 0.25-0.5mg bd/tid Diazepam: 5mg bd Lorazepam: 1-2mg od/bd Oxazepam: 15-30mg tid/qid Chlordiazepoxide: 10-20mg bd/tid For hypnosis: Estazolam: 500-1000mg Lorazepam: 2-4mg Temazepam: 7.5-30mgDosing IntervalAbsorptionVariable, but generally good Triazolam: v rapid (as lipid soluble) Diazepam: quite rapid Temazepam: slow Alprazolam: activeBioavailabilityHalf lifeLong HL’s can cause cumulative effects Short: estazolam, oxazepam, lorazepam – as metabolized to inactive glucuronides Triazolam: 2-3hrs Alprazolam: 12-15hrs Chlordiazepoxide: 15-40hrs (long) Diazepam: 20-80hrs (long) Lorazepam: 10-12hrs Oxazepam: 10-20hrs Temazepam: 10-40hrs Midazolam: 2-4hrs Duration of ActionDistributionGenerally wide Diazepam and lorazepam: rapid and extensiveMetabolismGenerally extensively metabolized, with many active metabolites Must be transformed to H20-soluble metabolite for excretion, liver – determines elimination HL Usually undergo microsomal oxidation (phase I reaction), inc N-dealkylation and aliphatic hydroxylation catalysed by cytochrome P450 enzymes (esp CYP3A4) (some of these metabolites are active with long HL’s – such as desmethyldiazepam for diazepam, chlordiazepoxide, prazepam, clorazepate - 40hrs) ( metabolites conjugated to form glucuronides (phase II reaction) Oxazepam, lorazepam: no active metabolites Flurazepam: metabolites with long HL’s Diazepam: active metabolitesExcretionH20-soluble metabolites excreted in urine; change in renal function has little effectSide effectsSedation; children may have paradoxical hyperactivity; toleranceContraindicationsElimination HL increased by hepatc dysfunction; elderly; inducers/inhibitors of enzymesDrug interactionsDiazepam, midazolam, triazolam affected by inhibitors/inducers of hepatic P450 isoenzymesPregnancyAll cross uterus and milkExamples Barbiturates: Action Enhances inhibitory processes (potentiates effect on GABAa); decr excitatory transmission (blocks action of glutamate at AMPA receptor); may selectively suppress abnormal neurons in epilepsy (at high conc acts like phenytoin ( suppresses Na conductance preventing high-f AP firing; also blocks Ca currentsIndicationPhenobarbital: for epilepsy in infants; partial and generalized TC seizures Primidone: partial and generalized TC seizures Thiopental: used in anaesthesiaRoute of administrationDoseFor sedation: Phenobarbital: 15-30mg bd/tid For hypnosis: Secobarbital: 100-200mg Phenobarbital: therapeutic level in epilepsy 10-40mcg/mL; 100-200mg IV for status epilepticus (beware resp depression) Primidone: therapeutic level in epilepsy 8-12mcg/mLDosing IntervalAbsorptionGenerally rapid Primidone: complete, peak in 3hrsBioavailabilityHalf lifeCan range from 18-48hrs in different people Phenobarbital: 4-5/7 Primidone: 6-8hrs due to faster clearanceDuration of ActionDistributionNote, for Phenobarbital, pKA is important and slight flucturation in pH will alter ratio of ionized:non-ionised Primidone: in body water, 0.6L/kg; only 30% bound to p proteins Thiopental: rapidly crosses BBB (plasma:brain equilibrium in <1min due to high lipid solubility) ( LOC; redistributed rapidly to muscle and fat so LOC briefMetabolismMust be transformed to H20-soluble metabolite for excretion,liver – determines elimination HL; usually slow metabolism Undergo oxidation by hepatic enzymes to form alcohols / acids / ketones Then conjugated to glucuronides Primidone: oxidised to Phenobarbital (which accumulates slowly to reach therapeutic levels) and phenylethylmalonamide (PEMA) (minimal contribution, HL 8-12hrs) – all 3 are anticonvulsants; primidone and phenobartbial undergo conjugation and excretion. Primidone reaches SS after 30-40hrs, Phenobarbital takes 20 days Thiopental: metabolized at 12-16% per hourExcretionH20-soluble metabolites excreted in urine; change in renal function has little effect NB. Phenobarbital 20-30% is excreted unchanged in urine; incr elimination with alkalinisation of urine Thiopental: <1% excreted unchanged renallySide effectsPhenobarbital toxic >40 Multiple dosing can cause cumulative effects GI complaints Thiopental: Dose-dependent decr MAP, SV, CO due to myocardial depressant effect and incr venous capacitance Resp depressant ( apnoea, decr sensitivity of medullary resp centre to CO2 Decr cerebral metabolism and O2 utilisation; decr cerebral blood flow; but DOESN’T incr ICp so can be used with cerebral swelling Decr hepatic blood flow and GFR, but no adverse effect on hepatic/renal function Can exacerbate acute intermittent porphyriaContraindicationsElimination HL increased by hepatc dysfunction; elderly; inducers/inhibitors of enzymes Absolutely CI in porphyria as can enhance porphyrin synthesisDrug interactionsNote Phenobarbital can induce liver enzymes, increasing own metabolism and that of other drugsPregnancyAll cross uterus and milkExamplesFor sedation/hypnosis - Phenobarbital, secobarbital, pentobarbital For epilepsy – Phenobarbital, mephobarbital, metharbital (latter 2 have decr SE), primidone For anaesthesia - Methohexital is shorter acting; can cause central excitation so useful in ablation of seizure foci Hypnotics: Action Eg. Zolpidem, zaleplon, eszopicloneIndicationRoute of administrationDoseFor hypnosis: Eszopiclone: 1-3mg Zaleplon: 5-20mg Zolpidem: 5-10mgDosing IntervalAbsorptionGenerally rapid; lipid-solubility makes more fastBioavailabilityHalf lifeZolpidem: 1hr Eszopiclone: 6hrs Zaleplon: 1-2hrsDuration of ActionDistributionMetabolismMust be transformed to H20-soluble metabolite for excretion,liver – determines elimination HL Zolpidem: rapidly metabolized to inactive metabolites via oxidation and hydroxylation by hepatic cP450 (inc CYP3A4) Eszopiclone: metabolized by p450 enzymes to inactive N-oxide derivative and weakly active desmethyleszopicloneExcretionH20-soluble metabolites excreted in urine; change in renal function has little effectSide effectsContraindicationsElimination HL increased by hepatc dysfunction; elderly; inducers/inhibitors of enzymesDrug interactionsCimetidine inhibits aldehyde dehydrogenase and CYP3A4; incr level of zaleplon Ketoconazole inhibits CYP3A4, ripampicin induces itPregnancyAll cross uterus and milkExamples Others Action Buspirone: relieves anxiety without sedative/hypnotic/euphoric/anticonvulsant/muscle relaxant effects; doesn’t interact with GABAergic systems; affinity for brain 5-HT1A and D2 receptors; effects take >1/52 to kick inIndicationRoute of administrationDoseDosing IntervalAbsorptionBuspirone: rapid POBioavailabilityHalf lifeBuspirone: 2-4hrsDuration of ActionDistributionMetabolismBuspirone: extensive 1st pass via hydroxylation and dealkylation ( active metabolites (eg. 1-2-pyrimidyl-piperazine); slower clearance in liver dysfunctionExcretionSide effectsBuspirone: no rebound anxiety/withdrawal signs; low abuse liability; less psychomotor impairment; can cause tachycardia, palpitations, nervousness, GI distress, paraesthesias, pupillary constrictionContraindicationsDrug interactionsBuspirone: rifampicin decreases HLby inducing cytochrome P450; incr plasma levels by inhibitors of CYP3A$ (eg. Erythromycin, ketoconazole)PregnancyExamples The Alcohols Alcohol abuse: unable to limit ETOH consumption Alcoholism: drink in spite of adverse medical or social consequences Ethanol Action Acute effects: CNS: BAL 50-100 ( sedation, slower reaction times BAL 100-200 ( impaired motor function, slurred speech, ataxia BAL 200-300 ( emesis, stupor BAL 300-400 ( coma BAL >500 ( resp depression, death Develop tolerance after few hrs drinking; effects many membrane proteins in signaling pathways (eg. NT receptors, N/K ATPase, adenylyl cyclase, PLC, ion channels), enhances GABA at GABAa; inhibits glutamate’s ability to open NMDA (important in memory) Heart: decr contractility and vasomotor centre SM: vasoD via vasomotor centre and direct action on SM of acetaldehyde; may cause hypothermiaIndicationRoute of administrationDoseLow potency so needs higher doseDosing IntervalAbsorptionH20 soluble; rapid PO; peak in 30mins; absorption delayed by food in gutBioavailabilityHalf lifeDuration of ActionDistributionRapid; VOD is body water = 0.5-0.7L/kg; readily crosses BBB and high blood supply to brain so quickly reaches CNSMetabolism90% oxidized in liver (zero-order kinetics – rate of oxidation independent of time and conc of drug); typically can metabolized 7-10g alcohol per hour (ie. One measure). 2 pathways: Alcohol dehydrogenase pathway: cytosolic enzyme converts ETOH to ACETALDEHYDE; in liver, brain and stomach (more in stomach in men); during reaction H transferred from ETOH to NAD forming NADH ( XS reduction equivalents in liver ( metabolic disturbances Microsomal ethanol oxidisng system (MEOS): NADPH used to metabolise ETOH to ACETALDEHYDE; needs cP450 2E1, 1A2 and 3A4; this system contributes little until BAL >100mg/dL when system 1) saturated due to depletion of NAD; MEOS activity induced during chronic alcoholism ( affects metabolism of other drugs with generation of toxic byproducts 3) Final common pathway: acetaldehyde metabolism: oxidized in liver, catalysed by mitochondrial NAD-dependent ALDEHYDE DEHYDROGENASE (ALDH), ACETALDEHYDE ( ACETATE ( CO2 and H20; oxidation inhibited by disulfiram ( acetaldehyde accumulates ( facial flushing, N+V, dizziness, headache; disulfiram-like effect from metronidazole, trimethoprimExcretion10% that isn’t oxidized, excreted by lungs and renalSide effectsChronic alcohol consumption: Tissue damage: due to direct effect of ETOH and metabolic consequences of metabolizing large amount of drug; incr oxidative stress, depletion of glutathione, damage to mitochondria, GF dysregulation, potentiation of cytokine-induced injury Liver disease: alcoholic fatty liver ( alcoholic hepatitis ( cirrhosis and liver failure Due to metabolic repercussions of ETOH oxidation in liver dysregulation of fatty acid oxidation and synthesis activation of innate immune system (eg. TNF-alpha) via direct effects of ETOH and metabolites and bacterial endotoxins that reach liver via changes in intestinal flora GI tract: chronic pancreatitis (direct toxic effect, alters epithelial permeability ( protein plugs and CaCO3-containing stones) Gastritis SI damage ( diarrhoea, weight loss, vit def; malabsorption CNS: tolerance (maybe due to upregulation of enzyme pathway, adaptive responses of NT’s, receptors, ion channel) withdrawal ( hyperexcitability, seizures, toxic psychosis, DT’s (possibly due to upregulation of NMDA and voltage sensitive Ca-channels ( seizures; downregulation of GABAa); begins 6-8hrs after ETOH stopped; lasts 1-2/7; trt- restore K, Mg and PO balance, thiamine, long-acting sedative-hypnotic drug (eg. Chlordiazepoxide, diazepam) – beware of accumulation, used short-acting if poor liver function (eg. Lorazepam, oxazepam) peri neuropathy, ataxia, dementia, demyelinating disease, impaired visual acuity, optic nerve degeneration Wernike-Korsakoff syndrome (eye paralysis, ataxia, confusion due to thiamine deficiency) Korsakoff’s psychosis (memory impairment) CV: dilated cardiomyopathy with V hypertrophy and fibrosis (membrane disruption, decr function of mitochondria and SR, intracellular accumulation of phospholipids and fa, upregulation of voltage dependent Ca channels) A and V arrhythmias (in withdrawal, abnormality of K and Mg, enhanced release of catecholamines), seizures, syncope, sudden death hypertension XS ( IHD; mod amounts decr CAD and incr HDL, inhibit inflamm processes of atherosclerosis, antioxidants Blood: inhibit bone marrow due to metabolic and nutritional effects ( folic acid def ( anaemia Endocrine and electrolyte: deranged steroid hormones (( gynaecomastia, testicular atrophy); ascites, oedema, effusions; V+D ( low K; 2Y aldosteronism ( muscle weakness; impaired hepatic gluconeogenesis ( hypoG Fetal alcohol syndrome: IUGR, microcephaly, poor coordination, underdeveloped midfacial region, minor joint anomalies; congenital heart defects, mental retardation; ETOH rapidly crosses placenta, fetal liver has poor alcohol dehydrogenase activity so fetus relies on maternal enzymes to eliminate ETOH ( apoptotic neurodegenerationm with aberrant neuronal and glial migration Immune system: inhibited in some tissues (eg. Lung – suppressed alveolar macrophages, inhibited chemotaxis of granulocytes, decr no and function of T cells); triggered in others (eg. Liver – Kupffer and hepatic stellate cells, pancreas); incr risk of pneumonia Incr risk of Ca: mouth, pharynx, larynx, oesophagus, liver, breast; acetaldehyde and reactive O2 species from cP450 activity damage DNA; change in folate metabolism, chronic inflammation Trt of alcoholism: Naltrexone: PO; ź opioid receptor antagonist; decr craving and decr relapse; 50mg od; do not use with disulfiram as both are hepatotoxins; if pt dependent on opioids ( withdrawal / decr painkilling response Acamprosate: weak NMDA antagonist and GABAa activator; decr relapse rate; 333-666mg tid; poor absorption; wide VOD; renal elimination; SE: GI Disulfiram: flushing, headache, N+V, sweating, hypotension, confusion when drink; inihibits aldehyde dehydrogenase; rapid complete absorption; slow elimination so will stay several days; inhibits metabolism of phenytoin, PO anticoagulation and isoniazid; compliance generally poorContraindicationsDrug interactionsIncr metabolism of drugs via induction of cP450 enzymes – eg. Paracetamol Acute alcohol use may inhibit metabolism due to decr enzyme activity and decr liver blood flow (eg. Phenothiazines, tricyclics, sedative-hypnotics) Additive effect with sedative-hypnotics, vasoD and hypoG’sPregnancyExamples Methanol: absorbed from skin/GI tract; eliminiated by oxidation to FORMALDEHYDE ( FORMIC ACID ( CO2 and H20 (this step is folate dependent); formate is the toxic metabolite; visual disturbances (like snowstorm), blurred vision (may be delay of 30hrs before symptoms); bradycardia, seixures, coma, acidosis (elevated anion gap and osmolar gap), decr HCO3; level >50mg/dL is absolute indication for haemodialysis; support respiration; can trt in 4 ways Suppress metabolism by alcohol dehydrogenase to toxic formate – ETOH has higher affinity than methanol so saturating enzyme decr formation of formatel fomepizole is alcohol dehydrogenase inhibitors Haemodialysis to enhance removal of methanol and formate – beware if trting with ETOH as will also remove ETOH Alkalinisation to counteract metabolic acidosis – HCO3 Give folic acid – to encourage last step Ethylene Glycol: in antifreeze; metabolized to toxic aldehydes and oxalate; transient excitation ( CNS depression ( severe metabolic acidosis after 4-12hrs due to accumulation of metabolites and lactic acid ( deposition of oxalate in tubules causes renal insufficiency; anion gap acidosis, osmolar gap, oxalate crystals in urine; trt with ETOH and haemodialysis, fomepizole prevents toxic metabolites and renal inj Antiseizure Drugs Partial seizures: localized onset Simple partial seizures: no LOC, pt aware of seizure Complex partial seizures: localized onset but spread of excitation ( altered consciousness; automatisms Phenytoin, carbamazepine, lamotrigine Partial seizures, 2Yily generalized: becomes TC Phenytoin, carbamazepine, lamotrigine Generalised seizures: no evidence of localized onset Generalised TC: phenytoin, carbamazepine, lamotrigine, valproate Absence (petit mal): altered LOC; automatisms, postural tone changes, autonomic phenomena Ethosuximide and valproate; clonazepam, lamotrigine Exacerbated by phenytoin and carbamazepine Tonic seizures Atonic seizures: valproate and lamotrigine, benzos Clonic and myoclonic seizures: valproate, benzos Infantile spasms: benzos Absorption: usually good (80-100%) Distribution: usually not highly protein bound; distributed into body water Metabolism: converted to active metabolites by liver Excretion: slow, so most longer acting Teratogenicity: 2x incr risk of congenital malformations; fetal hydantoin syndrome from phenytoin; 1-2% risk of spina bifida in valproate Withdrawal: rebound seizures more in partial/generalized TC seizures OD: resp depression DRUGS IN GENERALISED TC AND PARTIAL SEIZURES Phenytoin Action Non-sedative Alters Na permeability (binds inactive receptors and prevents action ( blocks sustained high-f repetitive firing of AP’s) K permeability Ca permeability (decr permeability ( decr influx ( inhibits Ca-dependent secretory processes eg. Of NT’s, hormones) Alters membrane potentials Alters conc of aa’s and NT’s (NE, Ach, incr GABA, decr glutamate) Causes paradoxical excitation in some neuronsIndicationPartial seizures, generalized TC seizures IV 13-18mg/kg for status epilepticus; max rate 50mg/min; cardiac monitor (cardiotoxicity for phenytoin and propylene glycol in which phenytoin dissolved)Route of administrationFosphenytoin: more soluble version for IV use; converted to phenytoin in plasmaDoseStart at 300mg/day; may need higher doseDosing IntervalAbsorptionDependent on formulation; PO good; IM unpredictable with some precipitation in muscle (fosphenytoin good)BioavailabilityHalf life12-36hrs (ave 24hrs); incr at higher concsDuration of ActionDistribution90% bound to p proteins; CSF level proportionate to free plasma level; accumulates in brain, liver, muscle and fat 5-7 days to SS – aim for 10-20mcg/mL; can give loading dose; most common cause of low levels is poor complianceMetabolismMetabolised to inactive metabolitesExcretionInactive metabolites excreted in urine; only v small amount excreted unchanged Dose-dependent kinetics: At low blood levels – 1st order kinetics At high blood levels – max ability of liver to metabolise reached ( further incr dose causes large rise in conc ( incr HL ( toxicitySide effectsDecr protein binding in renal disease Toxicity (>20) ( nystagmus, loss of smooth pursuit movements, diplopia, ataxia, sedation at high doses; gingival hyperplasia, hirsutism; long term ( coarsening of facial features, peri neuropathy, decr deep tendon reflexes, abnormal vit D metabolism (( osteomalacia), decr folate levels, megaloblastic anaemia Rare: hypersensitivity rash, fever, skin lesions; agranulocytosisContraindicationsDrug interactionsDue to protein binding – phenylbutazone and sulfonamides can displace phenytoin from proteins ( incr free drug Due to metabolism – phenytoin induces enzymes ( altered metabolism of many other drugs Phenobarbital and carbamazepine ( induce hepatic microsomal enzymes ( decr phenytoin conc Isoniazid ( inhibits metabolism ( incr phenytoin concPregnancyExamplesVersions: mephenytoin (SE worse), ethotoin (less SE than phenytoin), phenacemide Carbamazepine Action Tricyclic compound closely related to imipramine; non-sedative Similar mechanism of action to phenytoin: blocks Na channels ( prevent repetitive AP; presynaptically decreases synaptic transmissionIndicationPartial seizures, generalized TC seizures; trigeminal neuralgia; bipolar disorderRoute of administrationPODose15mg/kg/day in children; 1-2g/day (need extended release preps for bd dosing); therapeutic level 4-8mcg/mLDosing IntervalAbsorptionVaries; peaks levels in 6-8hrsBioavailabilityHalf life36hrs; will decr to 8-12hrs when on continuous trtDuration of ActionDistributionSlow; VOD 1L/kg/dayMetabolismMetabolised to several derivatives (eg. Carbamazepine 10,11-epoxide) which have anticonvulsant activityExcretionSide effectsToxic >8 Diplopia, ataxia; mild GI upset, unsteadiness, drowsiness, water intoxication, hypoNa Idiosyncratic blood dyscrasias (inc aplastic anaemia, agranulocytosis)ContraindicationsDrug interactionsInduces microsomal enzymes ( can decr own concs; incr metabolism of phenytoin, primidone, ethosuximide, valproic acid, clonazepam Other drugs inhibit carbamazepine clearance (eg. Valproic acid) ( incr conc Other drug induce enzymes (eg. Phenytoin, Phenobarbital) ( decr conc of carbamazepine No protein binding interactionsPregnancyExamplesClosely related – oxcarbazepine – halflife 1-2hrs but active metabolite 10-hydroxy version HL 8-12hrs; excreted as glucuronide of metabolite; less potent than carbamazepine; less SE’s with less induction of hepatic enzymes Barbiturates (eg. Phenobarbital: see above Others Action Vigabatrin: irreversible inhibitor fo GABA aminotransferase (GABA-T) which is responsible for degradation of GABA ( incr GABA released at synaptic sites Lamotrigine: inactivates Na channels as phenytoin; also active on voltage-gated Ca channels; decr release of glutamate Felbamate: causes aplastic anaemia and hepatitis so is 3rd line; blocks NMDA receptor, incr GABAa responses Gabapentin: analog of GABA; modifies release of GABA ( incr brain conc; bind to voltage-gated Ca channels ( decr presynaptic Ca entry ( decr release of glutamate; pregabalin is similar drug in every way Levetiracetam: for parital seizures Tiagabine: adjunct for partial seizures Topiramate: likely works via Na channels; potentiates GABA; inhibits glutamate receptors Zonisamide: partial and generalized TC seizuresIndicationVigabatrin: partial seizures Lamotrigine: partial seizures in adults; focal epilepsy; 1Y generalized seizures in children inc absences Gabapentin: partial seizures; generalized TC seizures; generally used as adjunct; also used as analgesic for neuropathic pain Topiramate: partial and generalized TC seizures; absences; trt of migraineRoute of administrationDoseVigabatrin:start at 500mg bd ( aim for 2-3g/day Lamotrigine: 100-300mg/day; aim for 3mcg/mLDosing IntervalGabapentin: bd/tidAbsorptionLamotrigine: good Gabapentin: dose-dependent Topiramate: rapidBioavailabilityTopiramate: 80%Half lifeVigabatrin: 6-8hrs Lamotrigine: 24hrs Gabapentin: 5-8hrs Topiramate: 20-30hrsDuration of ActionDistributionLamotrigine: VOD 1-1.4L/kg; protein binding 55% Gabapentin: not bound to p proteins Topiramate: protein binding 15%MetabolismLamotrigine: linear kinetics; metabolized by glucuronidation to 2-N-glucuronide Gabapentin: NOT metabolized; NO effect on hepatic enzymes Topiramate: 20-50% metabolized with no active metabolitesExcretionLamotrigine: metabolite excreted in urine Gabapentin: linear; renal excretion of unchanged drug Topiramate: excreted unchanged in urineSide effectsVigabatrin: drowsiness, dizziness, weight gain; agitation, confusion, psychosis; visual field defects in 1/3 in longterm Lamotrigine: dizziness, headache, diplopia, nausea, somnolence, skin rash; severe dermatitis in 1-2% paeds Gabapentin: somnolence, dizziness, ataxia, headache, tremor Topiramate: somnolence, fatigue, dizziness, paraethesia, nervousness, confusion; myopia and glaucomaContraindicationsDrug interactionsLamotrigine: valproate causes 2X incr HL of lamotrigine Gabapentin: none really Topiramate: may decr effectiveness of OCPPregnancyExamples DRUGS IN GENERALISED SEIZURES Valproate Action Affect Na channels as phenytoin Blocks NMDA receptor Incr level of GABA (possibly due to helping glutamic acid decarboxylase (GAD) – enzyme which forms GABA; possibly due to inhibition of GAT-1 (GABA transporter); at high concs blocks GABA transaminase (breaks down GABA)) Inhibits histone deacetylase ( altered gene transcriptionIndicationAbsences; preferred if pt has abscences + generalized TC seizures; some myoclonic seizures, some atonic attacksRoute of administrationDoseLevels seem to have little correlation with clinical effect 25-30mg/kg/day; therapeutic level 50-100mcg/mLDosing IntervalAbsorptionGood; peak in 2hrs; delayed by foodBioavailability>80%Half life9-18hrsDuration of ActionDistributionFully ionized at body pH so valproate ion is effective ingredient, regardless of whether salt or acid given 90% bound to p proteins Distribution in extracellular H20 – 0.15L/kgMetabolismExcretionLow clearance – dose-dependent; 20% excreted as direct conjugate of valproateSide effectsToxic >100 Hepatotoxicity may be severe – usually within 4/12 of commencement; monitor LFT’s Thrombocytopenia N+V+AP; weight gain, incr appetite, hair lossContraindicationsDrug interactionsValproate displaces phenytoin from p proteins Inhibits metabolism of Phenobarbital (resulting in toxicity and sedation), phenytoin, carbamazepinePregnancyCan cause incr spina bifida; incr CV, orofacial and digital abnormalitiesExamples Ethosuxamide Action Safe and efficacious Decr T-type Ca current (responsible for pacemaker current in thalamic neurons responsible for generating rhythmical cortical discharge of an absence attack)IndicationAbsences -1st choiceRoute of administrationDose750-1500mg/day; aim levels 60-100mcg/mL; linear relationship between dose and SS levelsDosing IntervalAbsorptionComplete, peak in 3-7hrsBioavailabilityHalf life40hrsDuration of ActionDistributionNo protein bindingMetabolismComplete – by hydroxylation to inactive metabolitesExcretionSlow clearanceSide effectsToxic >100 GI SE (AP+N+V); otherwise well tolerated; lethargy, headache, dizziness, hiccup, euphoria, SJSContraindicationsDrug interactionsValproic acid decreases clearance and inhibits metabolismPregnancyExamplesMethsuximide (more toxic; for partial seizures) and phensuximide (less effective) are similar Trimethadione: was 1st choice in absences until ethosuximide; rarely used now; effects Ca thalamic currents as above OTHER DRUGS USED Benzodiazepines: see above General Anaesthetics Analgesia, amnesia, LOC, inhibition of sensory and autonomic reflexes, SM relaxation Stages of Anaesthesia Analgesia: analgesia without amnesia ( analgesia with amnesia Excitement: delirious and vocalizes, but is amnesiac; irregular vol and r of resp; will retch and vomit if stimulated; ends with re-establishment of regular breathing Surgical anesthesia: recurrence of regular breathing ( cessation of breathing; can be further subclassified according to eyes; indicated by loss of response to noxious stimuli and reestablishment of normal resp pattern Medullary depression: deep; severe depression of vasomotor and resp centre; death occurs without circulatory and resp support INHALED ANAESTHETICS Action Mechanism of Action: Depress spontaneous and evoked activity of neurons in brain; modification of ion currents due to direct interactions with specific nerve membrane components (ligand-gated) 1) GABAa receptor-Cl channel (made of combinations of ą˛ł subunits)  mediator of inhibitory synaptic transmission; either act by directly activating GABAa channel (bind at sites on ąand ˛ subunits, esp at ą2 subunit, NOT at GABA-binding site; in contrast to benzos which cannot directly activate GABA channels) or potentiating effect of GABA 2) NMDA (N-methyl-D-aspartate) receptor: antagonize glutamic acid; may be target for NO and ketamine 3) Activation of K channels: ( hyperpolarisation of membrane; some channels linked to NT’s (Ach, dopamine, NE, 5-HT) 4) Decr duration of opening of nicotinic receptor-activated cation channels: decr excitatory effect of Ach 5) Glycine channel: ligand-gated ion channel; cause channel opening Stages of anaesthesia 2Y to differences in sensitivity of certain pathways Substantia gelatinosa in dorsal horn of SC: v sensitive; decr transmission of nociceptive stimuli Complex actions wih blockade of inhibitory neurons and facilitation of excitatory ( stage 2 Reticular activating system, decr spinal reflex activity ( stage 3 Resp and vasomotor centres of medulla depressed at high concs ( cardioresp collapse ( stage 4 Effects: 1) CV: dose-dependent decr MAP (prevented by hypercapnia which causes release of catecholamines) Halothane and enflurane ( decr CO; isoflurane, desflurane and sevoflurane ( decr SVR Altered HR Halothane ( bradycardia due to direct vagal stimulation Enflurance, sevoflurane ( little effect on HR Desflurane, isoflurane ( tachycardia Incr RAp due to depression of myocardial function – enflurane and halothane have greater depressant effect; decr myocardial O2 consumption; NO has least depressant effect so if used in conjuction with other anaesthetics can help 2) RS: dose-dependent decr tidal vol and incr RR , with overall decr minute ventilation (except NO) resp depressant effect with decr response to CO2 (isoflurane and enflurane most depressant) incr apnoeic threshold (paCO2 below which apnoea occurs due to lack of CO2-driven respiration), decr ventilatory response to hypoxia – overcome by mechanically assisting ventilation and counteracted by surgical stimulation decr mucociliary function ( atelectasis and post-op infections bronchodilation – useful in status asthmaticus and induction of COPD airway irriation – with desflurane 3)NS: decr metabolic r of brain incr cerebral blood flow due to decr cerebral vascular resistance (undesirable in raised ICp; NO is least likely to do this; occurs less with desflurane and secoflurane; minimized by hyperventilating patient) high doses enflurane ( cerebral irritation ( muscle twitching 4) Renal: decr GFR, decr renal b/flow; incr filtration fraction; impaired autoregulation 5) Hepatic: decr hepatic blood flow 6) Uterus: halogenated anaesthetics ( profound uterine relaxation; useful in manual extraction of placenta / IU fetal manipulationIndicationRoute of administrationDoseEstimate of anaesthetic potency can be obtained using quantal dose-response principles pp in brain = pp in lung @ SS Anaesthetic conc = % alveolar gas mixture (pp anaesthetic as % of 760mmHg (atmospheric p at sea level) Minimum alveolar anaesthetic conc (MAC) = median conc that results in immobility in 50% patients when exposed to noxious stimulus (ie. ED50 on dose/response curve) A dose of 1 MAC of any anaesthetic ( no movement in 50% pts on surgical incision this gives no info on slope of dose-response curve – usually STEEP so 1.1 MAC may enough for 95% peeps not to response to stimulus NO >100% - indicates it is LEAST potent ie. It cannot achieve full surgical anaesthesia even at pp 760mmHg MAC decreased by elderly / hypothermia / concomitant drugs (eg. Opiates, sedative, sympatholytics); not affected by sex, height or weight MAC values are additive so can produce 40% MAC with NO, then use 70% of another drug’s MAC to achieve 110% MAC for surgical anaethesiaDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionRate at which therapeutic conc in brain achieved depends on 1) Solubility properties of anaesthetic: useful index is blood:gas partition coefficient (relative affinity of anaesthetic for blood compared to inspired gas) Low (volatile anaesthetics) = relatively insoluble in blood = desflurane, NO; when anaesthetic with low blood solubility enters arterial blood from lung ( arterial tension rises quickly as few particles required to raise pp ( rapid equilibration with brain, fast onset of action High = soluble in blood = halothane, enflurane, isoflurane = more molecules dissolve as pp raises less rapidly ( slower induction of anaethesia 2) Conc of anaesthetic in inhaled air: conc of inhaled anaesthetic in mixture of gases ą partial pressure (tension); incr inspired conc ( incr r of transfer into blood according to Fick s law ( incr r of induction of anaesthesia 3) Vol of pulmonary ventilation: r of rise of anaesthetic gas tension in arterial blood ą r and depth of ventilation; incr ventilation will have big effect on arterial conc of highly soluble agent, but less effect of low soluble agents (related to blood:gas partition coefficient); depression of resp by opioids will slow induction in some if not being manually ventilated 4) Pulmonary blood flow: incr pul b/flow ( slows r of rise of arterial tension (esp. if high solubility), incr vol of blood exposed to gas so incr blood capacity; if in shock ( decr pul blood flow and incr ventilation ( faster induction of anaesthesia with soluble agents 5) Parital pressure gradient between arterial and mixed venous blood anaesthetic concs (ie. AV conc gradient): dependent on uptake of anaesthetic by tissues; greater if more taken up; the greater the difference, the longer it takes to achieve equilibrium with brain; depends on tissue:blood partition coefficients, r of blood flow to tissues, conc gradients; during induction phase, most important tissues are highly perfused (eg. Liver, brain, heart, kidneys, spleen); if blood highly soluble in highly perfused tissue, AV gradient high and equilibrium achieved slowly; drug less likely to accumulate in muscle and fat as these are not highly perfusedMetabolismMethoxyflurane > halothane > enflurane > sevoflurane > isoflurane > desflurane > NO Methoxyflurane 70% metabolized ( Fl which can cause nephrotoxicity Halothane 40% metabolized (oxidative) hepatically ( trifluoroacetic acid, bromide, Cl (may cause halothane hepatitis) Enflurane (10%) and sevoflurane ( FlExcretionRate of elimination determines time til recovery. Factors same as above, but in reverse Blood:gas partition coefficient: low coefficient = insoluble in blood and brain ( faster elimination Duration of exposure to anaesthetic: esp if soluble; accumulation in muscle, skin and fat incr if prolonged inhalation ( longer recovery period Metabolism in liver: can incr speed of recovery Pul blood flow, magnitude of ventilation, tissue solubility of anaestheticSide effectsHepatotoxicity: if re-exposed to halothane following prev exposure; most susceptible in obese; no trt; thought to be due to reactive metabolites causing direct damange or immune-mediated responses Nephrotoxicity: methoxyflurane/enflurane metabolized intrarenally (eg. renal ˛-lyase) ( Fl production intrarenally sevoflurane can be degraded by CO2 absorbant in machine ( compound A ( metabolized by renal ˛-lyase to thioacylhalide ( renal damage in high concs Malignant hyperthermia: AD genetic disorder of skeletal muscle (mutation of skeletal muscle ryanodine receptor (RyRl) which is Ca release channel from SR; or of skeletal muscle dihydropyridine-senstive L-type voltage-dependent Ca channel) ( incr HR and incr BP, muscle rigidity, hyperthermia, hyperkalaemia, acidosis; due to incr free Ca conc in skeletal muscle cells; trt with dantrolene (to decr Ca release from SR) Halothane and isoflurane sensitise myocardium to catecholamines ( may incr risk of ventricular arrhythmias (esp. if anxious, has received epinephrine-containing LA, on sympathomimetics drug); less soluble drugs are less arrhytmogenicContraindicationsDrug interactionsPregnancyExamplesDesflurane, sevoflurane, isoflurane and NO most commonly used; rapid onset and offset drugs being used more as day surgery cases increase AnaestheticBlood:gas partition coefficientBrain:blood partition coefficientMinimal alveolar conc (%)Metabolism (%)CommentNO0.471.1>1000Rapid onset and recovery; incomplete anaestheticDesflurane0.421.36-7<0.05Low volatility; poor induction agent; rapid recoverySevoflurane0.691.722-5Rapid onset and recoveryIsoflurane1.42.61.4<2Med onset and recoveryEnflurane1.81.41.78Med onset and recoveryHalothane2.32.90.75>40Med onset and recoveryMethoxyflurane122.00.16>70Slow onset and recovery IV ANAESTHETICS Barbiturates (eg. Thiopental): see above; rapid onset and recovery; CV depression Benzos (eg. Midazolam): see above; slow onset and recovery; CV stability; rarely used for induction, but pre-anaesthetic for anxiolysis, sedation and amnesia; in balanced anasethesia and conscious sedation Opioid analgesics: esp if doing cardiac surgery and circulatory reserve is limited; allow periop analgesia; can get awareness during anaesthesia; can make post-op analgesia difficult due to acute tolerance; can use as premedication or co-induction agents with benzos Fentanyl 100-150mcg/kg: slow onset and recovery; marked analgesia Sufentanil 0.25-0.5mcg/kg Remifentanyl and alfentanyl: v short acting with rapid onset, as rapidly metabolized to esterases in blood and muscle Propofol Action Rapid onset and recovery; less post-op N+V Dosre-related depression of central ventilatory drive and apnoeaIndicationInduction and maintenance of anaesthesia; can be used prolonged in ICU – beware of cumulative effects delaying arousalRoute of administrationDoseDosing IntervalAbsorptionBioavailabilityHalf lifeDistribution HL 2-8mins; redistribution HL 30-60minsDuration of ActionDistributionMetabolismRapid hepatic metabolism – glucuronide and sulfate Must also be some extrahepatic metabolismExcretionRenal excretion of metabolites; <1% excreted unchangedSide effectsMARKED decr BP during induction via decr PVR and venoD Marked –ive inotropic effects Prolonged ( incr serum lipid levels, muscle movements, hypotonus, tremors Pain on injection Severe acidosis in children, with prolonged neurological sequelae on withdrawalContraindicationsDrug interactionsPregnancyExamples Etomidate Action Rapid LOC and mod fast recovery; slower recovery than propofol Note – no analgesic effect so will need opiatesIndicationFor induction in pt with limited CV reserve with minimal CV and resp depression – good in elderly; HR unchanged; incidence of apnoea low Has CV stabilityRoute of administrationDoseDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionRapid; initial distribution 3 mins; intermediate 29mins Short duration of effect due to redistribution from brain to highly perfused tissuesMetabolismExtensive, hepatic and plasma ( inactive metabolitesExcretionOnly 2% unchanged drug excreted in urineSide effectsPain on injection; myoclonic activity; post-op N+V May cause adrenocortical suppression Prolonged infusion in critically ill ( hypotension, electrolyte imbalance, oligura (due to adrenal suppression)ContraindicationsDrug interactionsPregnancyExamples Ketamine Action Mod onset and recovery Produces dissociative anaesthetic state with catatonia, amnesia, analgesia, maybe LOC Blockade of effects of glutamate at NMDA receptor Dose-related CV STIMULATION ( incr HR, BP, CO (peak at 2-4mins, return to normal over 10-20mins) by stimulating central SNS and inhibiting reuptake of NEIndicationCan be used as adjunct to volative agent instead of opioid to decr resp depression Good for elderly and shocked pt due to CV support Children OP proceduresRoute of administrationDoseDosing IntervalAbsorptionBioavailabilityHalf lifeDuration of ActionDistributionHighly lipophilic so rapidly distributed to well-perfused organs (eg. Brain, liver, kidney) followed by redistribution to less well perfused tissuesMetabolismHepaticExcretionUrinary and biliarySide effectsMarked incr cerebral blood flow, O2 consumption and ICp so dangerous in incr ICp Decr RR Post-op disorientation, sensory and perceptual illusions, vivid dreams – decr by benzosContraindicationsDrug interactionsPregnancyExamples Local Anaesthetics Reversibly block impulse conduction along nerve axons and other excitable membranes that used Na channels to generate AP’s Action Weak bases; as salts to incr solubility and stability ( in body exist as uncharged base / cation (proportions governed by pKa and pH of body fluids according to Henderson-Hasselbach equation) Log cationic form = pKa – pH Uncharged form pKa most LA’s is 8-9: most drug in cationic form at normal body pH more drug in uncharged from in infected tissues due to decr pH Cationic form is more active at receptors; uncharged form important for penetration of biologic membranes in order to reach receptor; LA less effective when injected into infected tissue as cannot diffuse across membrane; rpted injections ( tachyphylaxis due to decr pH as buffering capacities of tissue exhausted (as LA sol is acidic) The smaller and more lipophilic the LA the faster the r of interaction with Na channels (though substance must have enough H20 solubility to diffuse through cell membrane); onset of action accelerated by adding NaHCO3 to LA sol ( incr drug in lipid-soluble form Mechanism of action: blockade of voltage-gated Na channels on nerve axons (RMP -60 to -90mV) with no change in RMP at min dose ( Na channels open on excitation ( Na influx which depolarizes membrane towards +40mV (Na equilibrium potential) ( Na channels close as depolarization occurs ( K channels open ( K efflux and repolarisation toward -95mV (K EP) ( Na channels return to rested state. Bind Na channels near intracellular end ( incr threshold for excitation ( slowed impulse conduction ( decr r of rise of AP ( decr size AP ( finally no AP (progressive effects due binding of LA to more and more Na channels). Block channel in time-dependent: a proportion of channels will recover between each AP; but lengthened refractory period Factors affecting action: Fibre diameter: see below Firing frequency: Block is voltage-dependent: LA has higher affinity for channel in activated/inactivated state (at higher MP); lower affinity for channel in resting state (at lower MP); so more effective on rapidly firing axons than resting fibres (NB. Sensory (pain) fibres A´ and C have high firing rate and long AP duration so block easier; motor fibres Aą slower) Fibres position in nerve bundle: motor nerves located circumferentially in NV bundle, so in large mixed nerves as exposed to LA first ( motor block may appear 1st; in peripheral nerves, prox sensory fibres are outer and affected 1st, distal sensory fibres innerIndicationRoute of administrationSC / TOP / epidural / IV regional IV lidocaine and PO mexiletine/tocainide can be used for neuropathic pain syndromes due to rapid uncontrolled sensory fibre firingDoseDosing IntervalAbsorptionNot important for onset of effect; important for offset. Systemic absorption depends on Dosage Site of injection Drug-tissue binding Local blood flow: incr b/flow ( faster absorption ( higher blood levels; intercostal > caudal > epidural > brachial plexus > sciatic nerve Use of vasoC’s: decr systemic absorption, enhanced local neuronal uptake; prolong duration of action; when used during spinal anaesthesia, enhances anaesthesia by acting on ą2-adrenoceptors ( inhibit release od substance P ( decr sensory neuron firing; can prolong anaesthetic effecy by up to 50%; less effective on lipid-soluble, long-acting drugs (eg. Bupivicaine, ropivacaine) as molecules highly tissue bound Physiochemical properties of drugBioavailabilityHalf lifeProcaine, chloroprocaine: <1min due to rapid hydrolysis in plasma Bupivacaine: 3.5hr Lidocaine: 1.6hr Mepivacaine: 1.9hr Prilocaine: 1.5hr Ropivacaine: 4.2hr Lidocaine, mepivacaine, prilocaine: intermediate acting Tetracaine, bupivacaine, levobupivacaine and ropivacaine: long actingDuration of ActionDistributionNot important for onset of effect; important for offset; sequestration can occur in lipophilic storage sites (eg. Fat) On IV ( rapid initial distribution phase (to brain, liver, kidney, heart) ( slower phase (to mod perfused organs, eg. Muscle, GI) Half-time of distriubution (min): bupivacaine 28, lidocaine 10, mepivacaine 7, prilocaine 5, ropivacaine 23 VOD: bupivacaine 72, lidocaine 91, mepivacaine 84, prilocaine 261, ropivacaine 47 H20 soluble: lidocaine, procarine, mepivacaine Lipid soluble: tetracaine, bupivacaine, ropivacaine ( more potent, longer duration of action, bind more to p proteinsMetabolismAmides converted in liver (hydrolysed by cP450 isoenzymes; prilocaine (fastest) > lidocaine > mepivacaine > ropivacaine > bupivacaine and levobupivacaine) Esters in plasma (hydrolysed by butyrylcholinesterase) ( H20-soluble inactive metabolitesExcretionMetabolites excreted in urine; little excretion of uncharged form as they readily diffuse through membranesSide effectsSystemic effects due to absorption of LA from site of administration CNS: Sleepiness, dizziness, visual and auditory disturbance, restlessness 1st sign of toxicity = circumoral and tongue numbness, metallic taste ( nystagmus, muscular twitching ( TC convulsions (depression of cortical inhibitory pathways ( unopposed excitatory pathways; can avoid by pre-medicating with benzo’s; important to prevent acidosis as will decr seizure threshold so hyperventilate ( incr pH, decr extracellular K to hyperpolarize axons, so more rested Na channels, decr toxicity) ( generalized CNS depression Autonomic nerve blockade ( hypotension, urinary retention CV: Direct effect on cardiac and SM – block cardiac Na channels ( depress abnormal pacemaker activity, excitability and conduction; high concs block Ca channels ( decr contractility, decr PVR; bupivacaine is most cardiotoxic (( slow rhythm with broad QRS ( HB) NB. Cocaine blocks NE reuptake ( vasoC and hypterT, cardiac arrhythmias Indirect effect on autonomic NS Haematologic: Prilocaine ( accumulation of metabolite o-toluidine which can convert Hb to methHb ( pt appears cyanotic with chocolate coloured blood Direct neurotoxicity when given close to spinal cord / major nerve trunks Chlorprocaine and lidocaine most neurotoxic ( transient radicular irritation due to pooling of LA in cauda equina Toxicity from amides in liver disease Allergic reaction to esters more common than amides due to metabolitesContraindicationsDrug interactionsIncr extracellular Ca antagonizes LA due to incr RMP ( more channels in resting state ( decr effect of LA Incr extracellular K depolarized MP ( more channels in activated state ( enhance affect of LAPregnancyIncr risk of toxicity, decr dose needed for blockade; risk of cardiac arrest on epiduralExamplesEsters: procaine, chloroprocaine Amides: prilocaine, lidocaine, mepivacaine, ropivacaine, bupivacaine, levobupivacaine Fibre TypeFunctionDiameterMyelinationConduction Velocity (m/s)Sensitivity to BlockType AAlphaProprioception (sensory muscle spindles, golgi tendon organ), motor12-20 (L)Heavy70-120 (F)+ (motor function last to be blocked)BetaTouch, pressure5-12 (M)Heavy30-70 (M)++GammaMuscle spindles (motor)3-6 (S)Heavy15-30 (M)++DeltaPain, temp2-5 (S)Heavy12-30 (M)+++ (for myelinated nerves, at least 2-3 successive nodes must be blocked; the larger the neuron, the further apart the nodes)Type BPreganglionic autonomic<3 (S)Light3-15 (M)++++ (blocked before C, as myelinated nerves tend to be blocked before unmyelinated if same size)Type CDorsal rootPain, reflexes0.4-1.2 (S)None0.5-2.3 (S)++++SympatheticPostganglionic0.3-1.3 (S)None0.7-2.3 (S)++++ (smaller fibres blocked first) Effect of toxins: Batrachotoxin, aconitine, vertridine, scorpion venom: bind Na channel preventing inactivation ( prolonged influx of Na ( depolarization of RMP Tetrodotoxin, saxitotoxin: block Na channel ( block conduction with no change in RMP Skeletal Muscle Relaxants Normal: influx of Ca ( release Ach ( nicotinic receptor (composed of 1 beta, 1 gamma, 1 delta and 2 alpha peptides; binding of 2 Ach on alpha-beta and delta-alpha ( opens channel) ( Na and K movement ( depolarization of end plate membrane, if large enough, propogation ( excitation/contraction coupling ( acetylcholinesterase degrades 1 presynaptic Ach receptor ( activation mobilizes more Ach by moving vesicles to synaptic membrane 1 Ach receptor on perijunctional cells, not normally involved, but may proliferate in prolonged immobilization / burns Monitoring effect of NM drug: nerve stimulator Single-twitch stimulation: single supramaximal stimulus (0.1-1Hz) Train-of-four stimulation: 4 successive supramaximal stimuli at intervals of 0.5secs; TOF ratio is magnitude of 4th twitch : 1st twitch Depolarising block (succ): all 4 twitches reduced proportional to dose; if fade develops, phase II block has occured Non-depolarising block (roc): decr TOF ratio (fades), inversely proportional to dose; during recovery fade decreases and TOF ratio approaches 1 Tetanic stimulation: rapid (30-100Hz) stimuli over several secs Depolarising block (succ): Non-depolarising block (roc): response not sustained and fade noted; degree of fade depends on degree of blockade; during partial blockade tetanic stimulation will be followed by incr posttetanic twitch responses (post-tetanic facilitation); in high degree of blockade will get no response to tetanic or post-tetanic stimulation NM blocking drugs Action Interfere with transmission at NMJ; no CNS activity; all related to Ach Nondepolarising (Antagonist) NM blocking drugs: ring structure Act at nicotinic receptor site by competing with Ach ( prevent depolarization (eg. D-tubocurarine is prototypic drug); action can be REVERSED by acetylcholinesterase inhibitors, which cause incr Ach at NMJ In large doses can enter pore of ion channel ( intense motor blockade, with DECREASED ABILITY of acetylcholinesterase inhibitors (eg. Neostigmine, edrophonium, pyridostigmine) Can block prejunctional Na channels ( interfere with mobilization of Ach at nerve ending Tetanic stimulation ( incr Ach ( transient posttetanic facilitation of twitch strength with non-sustained (fade) twitch response to tetanic stimulus Rate of recovery: 30-60mins Larger muscles more resistant (eg. Abdo, trunk, diaphragm) and recover more rapidly that small muscles Eg. Isoquinolone derivatives: atracurium (intermediate acting), cisatracurium, doaxcurium, metocurine, mivacurium (short acting), Tubocurarine Eg. Steroid derivatives: pancuronium, pipecuronium (longer acting), rocuronium, vecuronium (short acting) Depolarising (agonist) NM blocking drugs: linear structure Phase 1 (depolarizing) block: reacts with nicotinic receptors ( opens channel causing depolarization ( contraction of muscle motor units due to prolonged flickering of ion conductances (resulting in FASCICULATIONS within 30secs); not metabolized well at synapse so longer depolarization ( unresponsive to subsequent impulses As excitation-contraction coupling needs end plate repolarisation (repriming) and repetitive firing to maintain muscle contraction ( flaccid paralysis; this block is AUGMENTED by acetylcholinesterase inhibitors Get sustained (non-fade) response to tetanic stimulus, with no posttetanic facilitation Rate of recovery: 4-8mins Phase 2 (desensitizing) block: with continued exposure, end plate depolarization decreases ( membrane becomes repolarised, but cannot be depolarized as is is desensitized ( channels behave in prolonged closed state; channel block more important than agonist action Similar blockade to nondepolarising, so nonsustained (fade) twitch response to tetanic stimulation with posttetanic facilitation of twitch response; which can be REVERSED by aceytlcholiesterase inhibitors Rate of recovery: >20mins Eg. Succinylcholine IndicationSurgery; tracheal intubation; decr chest wall resistance in control of ventilation; occasionally used in seizuresRoute of administrationDoseNon-depolarising: Tubocurarine: 0.1-0.4mg/kg IV Depolarising: Succinycholine: 0.75-1.5mg/kg IVDosing IntervalAbsorptionInactive PO; highly polar; must be given IVBioavailabilityHalf lifeNon-depolarising: Strongly correlates with action Renally excreted usually have longer duration of action (>60mins) than hepatically eliminated Onset of action: rocuronium: fastest DOA: atracurium: 20-35mins Mivacurium: 10-20mins Cisatracurium: 25-44mins Tubocurarine: >35mins (usually 45-60mins) Metocurine: >35 mins Depolarising: (ie. Succ) Onset of action: <90 secs DOA: <10mins (due to rapid hydrolysis by plasma and liver cholinesterase)Duration of ActionDistributionHighly ionized, do not easily cross cell membranes; VOD only slightly larger than blood vol (80-140mL/kg) Non-depolarising: Rapid initial distribution phase ( slower elimination phaseMetabolismNon-depolarising: Steroidal muscle relaxants metabolized to 3-hydroxy (40-80% potency), 17-hydroxy or 3,17-dihydroxy products in liver – normally metabolites don’t have significant effect, but if given longterm 3-hydroxy metabolite accumulates ( paralysis with longer half-life than parent compound Atacurium: also undergoes Hofmann elimianation (spontaneous breakdown ( laudanosine, which has no NM blocking properties, and has long elimination HL) Mivacurium: by plasma cholinesterase; rapid and independent of liver or kidney Depolarising: Rapid hydrolysis by cholinesterases (eg. Butyrylcholinestease, pseudocholinesterase) in liver and plasma Succinylcholine metabolized quicker than mivacurium, so shorter duration of action ( succinylmonocholine ( broken down to succinic acid and choline. Only small % IV dose reaches NMJ ( as little cholinesterase at NMJ, succinylcholine blockade terminated by diffusion away from end plate. Duration of action influenced by circulating levels of plasma cholinesterase.ExcretionNon-depolarising: Dependent on biliary excretion or hepatic metabolism Atracurium, cisatracurium: spontaneous Daxacurium, metocurine, tubocurarine: kidney Mivacurium: plasma cholinesterase Pancuronium: kidney Rocuronium, vecuronium, pipecuronium: liver and kidney Depolarising: Succinylocholine: plasma cholinesteraseSide effectsCV: vecuronium, pipecuronium, doxacuronium, cisatracurium, rocuronium: minimal Pancuronium: incr HR and CO due to vagolytic action and release of NE Tubocurarine, metocurine, mivacurium, atracurium: hypotension and bronchospasm due to histamine release (premedicate with antihistamines); may get ganglionic blockade Succinylcholine: stimulation of autonomic cholinoceptors ( -ive inotrope and chonotrope, and direct myocardial effects (eg. Incr muscarinic stimulation) ( bradycardia; prevent with anticholingergic drug (eg. Atropine) Hyperkalaemia: with burns, nerve damage, NM disease, closed HI, trauma; with succinycholine Incr IOp: with succ; may be due to tonic contraction of myofibrils or transient dilation of ocular choroidal BV’s Incr intragastric p: with succ; due to fasciculations ( aspiration Muscle pain: with succ; due to fasciculations; can be prevented by giving small dose of non-depolarising before giving succ Atacurium: if laudanosine accumulates (long term therapy) ( readily crosses BBB ( seiures, incr volatile anaesthetic requirement. Cisatracurium is form of atacurium which relies less of hepatic inactivation and forms less laudanosine For reversal: cholinesterase inhibitors; effectively inhibit nondepolarising drugs Eg. Neostigmine, pyridostigmine: increase Ach by inhibition of acetylcholinesterase; also incr release of Ach Eg. Edrophonium: only inhibits acetylcholinesterase, so is less effective Residual block: may result in hypoventilation, apnoea NB. Since mivacurium is metabolized by plasma cholinesterase, interaction with reversal drugs less predictable NB. Another reversal agent – sugammadex – forms inactive complex with steroidal drugs ( excreted in urineContraindicationsMivacurium, succinylcholine: prolonged action in genetic variants of plasma cholinesterase; ability to metabolise measured by dibucaine number MG: enhances NM blockade Liver/renal probs / elderly: enhanced Severe burns, UMND: resistant to nondepolarising muscle relaxants, due to incr extrajunctional receptors so incr dose neededDrug interactionsVolatile anaesthetics agument effect on nondepolarising agents: isoflurane > sevoflurane > desflurane > enflurane > halothane > NO; due to CNS effects, incr muscle blood flow (due to peri dilation), der sensitivity of postjunctional membrane to depolarization Succ + volatile: rarely causes malignant hyperthermia due to release of Ca Succ + halothane: cardia arrhythmia AB’s: augment NM blockade, possibly due to decr release of AchPregnancyExamples Spasmolytic drugs Spasticity = incr tonic stretch reflexes, flexor muscle spasms (incr basal muscle tone), muscle weakness; due to abnormal stretch reflex arc and CNS probs with damage of descending pathways ( hyperexcitability of alpha motoneurons Action Aim to decr activity of Ia fibres that excite 1Y motoneuron Enhance activity of inhibitory internuncial neurons Diazepam: facilitate action of GABA in CNS at GABAa synapses ( acts centrally and in spinal cord Baclofen: works on GABAb receptors ( hyperpolarisation due to incr K conductance ( presynaptic inhibition due to decr Ca influx, decr relase of excitatory NT in brain and SC; decr pain due to inhibition of relase of substance P in SC; less sedation than diazepam with less effect on muscle strength Alpha agonists (eg. Tizanidine): alpha2; pre and postsynaptic inhibition in SC; inhibition of nociceptive transmission Gabapentin: centrally acting Dantrolene: interferes with excitation-contraction coupling in muscle fibres; binds rayanodine receptor channel on SR preventing release of Ca from stores; more sensitive on rapidly contracting motor units so cardiac muscle and SM spared as the RyR channel is different Botulinum toxin:IndicationDantrolene: used in malignant hyperthermia (impaired ability to sequester Ca in SR; volatile anaesthetics and succ ( muscle contraction, lactic acid production, body temp)Route of administrationBaclofen: PO; can be given intrathecallyDoseBaclofen: 15mg bd, incr as tolerated Dantrolene: 25mg od, incr as tolerated; 1mg/kg IVDosing IntervalAbsorptionBaclofen: rapid and complete PO Dantrolene: only 1/3 absorbedBioavailabilityHalf lifeBaclofen: 3-4hrs Dantrolene: 8hrsDuration of ActionDistributionMetabolismExcretionSide effectsBaclofen: drowsiness, incr seizure activity Alpha agonists: drowsiness, hypotension, dry mouth Dantrolene: muscle weakness, sedation, hepatitisContraindicationsDrug interactionsPregnancyExamples Antiparkinsonism Agents Parkinsons: due to decr effect of dopamine in basal ganglia due to loss of dopaminergic neurons in substantia nigra that normally inhibit GABAergic cells in corpus striatum; aim to inr dopamine or decr Ach Drug induced parkinsonism: reserpine ( depletes monoamines from storage sites Haloperiodol and phenothiazines ( block D receptors; give antimuscarinics NB. Dopamine doesn’t cross BBB, so peri administration has no effect D1 receptor: in zona compacta of substantia nigra; found presynaptically on striatal axon comes from cortical neurons and dopaminergic cells in substantia nigra D2 receptor: postsynaptically on striatal neurons, and presynaptically on basal ganglia neuron axons in substantia nigra Levodopa Action 3-(3,4-dihydroxyphenyl)-l-alanine Metabolic precursor of dopamine and NE – enters brain via L-amino acid transporter ( decarboxylated to dopamine ( stimulate D2 receptors (but some D1 receptor stimulation needed for max benefit) Responsiveness to drug lost over time (3-4yrs) Drug holiday: 3-21/7; may temporarily incr responsiveness; risk of severe immobility during holiday; not recommenededIndicationRoute of administrationDoseLarge amount needed when used alone (ie. Without inhibitor) Sinemet = carbidopa 25mg, levodopa 100mg tid ( incr to 25/250 or add in dopamine agonistDosing IntervalAbsorptionRapid PO; depends on rate of gastric emptying and pH; food delays absorption; peak 1-2hrs after administrationBioavailabilityHalf life1-3hrsDuration of ActionDistributionOnly 1-3% enters brain unalteredMetabolism97% metabolized extracerebally, by decarboxylation to dopamine which can’t pass through BBB; give with dopa decarboxylase inhibitor (carbidopa) to decr peri metabolism ( longer halflife, higher plasma levelsExcretionMetabolites in urine (3-methoxy-4-hydroxyphenyl acetic acid (homovanillic acid, HVA) and dihydroxyphenylacetic acid (DOPAC)Side effectsDose must be decreased over time to prevent SE’s GI: anorexia, N+V (stimulation of chemoreceptor trigger zone which is outwith BBB); less when given with carbidopa; will develop tolerance to this CV: incr HR, V extrasystoles, AF, incr BP; due to incr NE formation peripherally; less with carbidopa Dyskinesias: in 80% if longterm; often choreoathetosis of face and distal extremities Behaviour: depression, anxiety, agitation, insomnia, confusion, delusions, halluncinations; more common with carbidopa; antipsychotic agents may help End-of-dose akinesia On-off phenomenon: akinesia / improved mobility but dyskinesia Mydriasis, blood dyscrasias, gout, brown discoloration of secretions, deranged LFT’sContraindicationsPsychosis; angle-closure glaucoma; active PUD; cardiac disease; malignant melanoma (precursor of melanin)Drug interactionsPyridoxine: enhances peri metabolism MAOI A – cause hypertensive crisisPregnancyExamples Dopamine Receptor Agonists Action Don’t require conversion to active metabolite Have no toxic metabolites Don’t compete with other substances for AT across BBB Less SE’s than above – less response fluctuations and dyskinesias; can help end-of-dose akinesia and on-off effect Bromocriptine: D2 agonist Pergolide: D1 and D2 agonist; more effective than bromocriptine Pramipexole: D3 agonist; may have neuroprotective effect by scavenging H peroxide Ropinirole: D2 agonistIndicationRoute of administrationDoseBuild up gradually Bromocriptine: 7.5-30mg Pramipexole: 0.5-1.5mg tid Ropinirole: 2-8mg tidDosing IntervalAbsorptionBromocriptine: variable from GI; peak in 1-2hrs Pramipexole: rapid, peak in 2hrsBioavailabilityHalf lifeDuration of ActionDistributionMetabolismRopinirole: CYP1A2ExcretionBromocriptine: in bile and faeces Pramipexole: unchanged in urineSide effectsGI:N+V, constipation, dyspepsia, PUD CV: postural hypotension; cardiac arrhythmias; peripheral oedema Dyskinesias Mental disturbances: confusion, hallucinations, delusion Others: headache, nasal congestion, incr arousal, pul infiltrates, pleural fibrosis, erythromelalgia Pergolide: valvular heart diseaseContraindicationsPsychotic illness, recent MI, PUD, PVDDrug interactionsPregnancyExamples Amantadine: Unknown MOA; peak in 1-4hrs; HL 2-4hrs; excreted unchanged in urine; benefits may only last few wks; 100mg bd-tid SE: restlessness, depression, agitation, insomnia, hallucinations, confusion, livedo reticularis, peri oedema, headache, heart faulyre, postural hypoT, urinary retention; toxicity ( convulsions and psychosis Monoamine Oxidase Inhbitors: MAO A: metabolises NE and 5-HT MAO B: metabolise dopamine Eg. Selegiline: irreversible, selective MAO B inhibitor; 5mg bd; serotonin syndrome if given with SSRI or tricyclics Eg. Rasagiline: more potent Catechol-O-Methyltransferase (COMT) Inhibitors: Inhibition of dopa decarboxylase (by pyridoxine) causes activation of catechol-O-M (COMT) which is another pathway for levodopa metabolism ( incr levels of 3-O-methyldopa (3OMD) which competes with levodopa for transport across BBB; COMT inhibitor prevents formation of this metabolite and prevents peri metabolism of levodopa ( incr BA Eg. Tolcapone: central and peri effects; slightly more potent with longer DOA; 100mg tid; assoc with hepatotoxicity Eg. Entacapone: only peri effect; 200mg 5x day Both rapidly absorbed; both bound to p proteins; both metabolized then excreted; both HL 2hrs SE: dyskinesia, N+D+AP, confusion, orthostatic hypotension; may need to lower dose of levodopa Apomorphone: Potent dopamine agonist; given SC; for temporary relief of periods of akinesia; onset of effect in 10mins; lasts 2hrs; max 10mg SE: N, dyskinesia, drowsiness, sweating, hypotension Ach Blocking Drugs (Antimuscarinic) Surgical Procedures: thalamic stimulation, dopaminergic tissue transplant Other Movement Disorders Tremor: postural thought to be due to beta-2 receptors so prevented by propanolol; essential thought to be duet o beta-1 so improved by metoprolol and propanolol; no satisfactory trt of intention tremor; can be caused by bronchoD’s, lithium, tricyclics and valproate; can try primidone, topiramate, alprazolam Huntingtons: loss of cholinergic neurons and GABAergic cells in corpus striatum ( imbalance of dopamine (incr), Ach (decr choline acetyltransferase for synthesis), GABA (decr glutamic acid decarboxylase for synthesis) in basal ganglia; chorea due to overactivity of dopamine in nigrostriatal pathway; AD on C4; can give risperpine/tetrabenzine ( decr dopamine by interfering with intraneuronal storage, phenothiazines/butyrophenones ( block D receptors; same trt indicated for tardive dyskinesias caused by neuroleptics Tics: haloperidol Drug induced Dyskinesias: benzotropine, diphenhydramine, biperiden (antimuscarinics) Antipsychotic Agents (Neuroleptics) Dopaminergic systems: Mesolimbic-mesocortical pathway: from cell bodies near substantia nighra to limbic system and neocortex; antipsychotics work here Nigrostriatal system: from substantia nigra to caudate and putamen; for co-ordination of voluntary movement; antiparkinsonian drugs work here Tuberoinfundibular system: from arcuate nuclei and periventricular neurons to hypothalamus and PPG; dopamine inhibits PL secretion (hence SE of hyperPL with antipsychotics) Medullary-Periventricular pathway: from motor nucleus of vagus; involved in eating Incertohypothalamic pathway: from medial zona incerta to hypothalamus and amygdale; involved in sex Dopamine receptors: antipsychotics work on D2 receptors – agonists worsen schizo, blockers are antipsychotics; antipsychotics also block 5-HT and other receptors D1-like: D1: incr cAMP by Gs-coupled activation of adenylyl cyclase; found in putamen, nucleus accumbens, olfactory tubercle D5: incr cAMP; found in hippocampus and hypothalamus D2-like: D2: decr cAM|P by Gi-coupled inhibition of adenylyl cyclase; inhibits Ca channels, opens K channels; found in caudate-putamen, nucleus accumbens, olfactory tubercle D3: decr cAMP; in frontal cortex, medulla, midbrain D4: decr cAMP Action Phenothiazine Derivatives: less potent than haloperidol Aliphatic: chlorpromazine (ą1 = 5-HT2a > D2 > D1); many SE esp autonomic (eg. Antimuscarinic) Piperidine: thioridazine; more potent and selective; cardiotoxic Piperazine: fluphenazine; depot available Thioxanthene derivatives: thiothixene; less potent than above; parental form available Butyrophenone derivatives: haloperidol (D2 > ą1 > D4 > 5-HT2a > D1 > H1); more potent; less autonomic SE s; more extrapyramidal SE s; parental form available Misc: newer better than old for negative symptoms, with less extrapyramidal SE s and tardive dyskinesia pimozide, molindone, loxapine, ziprasidone, aripiprazole clozapine (D4 = ą1 > 5-HT2a > D2 = D1; reserved for trt-resistant people, risk of agranulocytosis in 2% - weekly blood tests for 1st 6/12, then every 3/52 thereafter lowered seizure threshold) olanzapine (5-HT2a > H1 > D4 > D2 > ą1 > D1; good against negative symptoms, little extrapyramidal SE s; weight gain, decr seizure threshold) quetiapine (H1 > ą1> M1,3 > D2 > 5-HT2a; short HL) risperidone (broad efficacy, little extrapyramidal SE’s) Mechanism of action: block dopamine, alpha adrenoceptor, muscarinic, H1, 5-HT2 receptorsIndicationSchizophrenia; manic-depression; Tourettes; Alzheimer’s dementia; psychotic depressionRoute of administrationParenteral: fluphenazine and haloperidolDoseBroad effective doses Chlorpromazine: 100-1000mg Thioridazine: 100-800mg Fluphenazine: 2-60mg Thiothixene: 2-120mg Haloperidol: 2-60mg Clozapine: 300-600mg Olanzapine: 10-30mg Quetiapine: 150-800mg Risperidone: 4-16mgDosing IntervalOD at nightAbsorptionReadily but incompletelyBioavailabilityPhenothiazines: 25-35% Haloperidol: 65%Half lifeLonger DOA than expected from HL as lipid soluble with high affinity for NT receptors, remaining bound to receptors for up to weeksDuration of ActionDistributionHighly lipid soluble and protein bound (92-99%); VOD >7L/kg)MetabolismSignificant 1st pass; completely metabolized; some metabolites have activity but not clinically significant (except mesoidazine from thioridazine which is more potent than parent compound)ExcretionPolar metabolites excretedSide effectsANS: Ach blockade ( loss of accommodation, dry mouth, urinary hesitancy, constipation ą blockade ( orthostatic hypotension, impotence, delayed ejaculation CNS: D blockade ( extrapyramidal SE s (parkinsonism, akathesia, dystonias)  give anticholinergics Incr sensitivity of D receptors ( tardive dyskinesia (due to relative cholinergic deficiency 2Y to supersensitivity of D receptors; in 20-40% chronically treated with older agents) Ach blockade ( toxic-confusional state Endocrine: D blockade ( incr PL ( amenorrhoea, galactorrhoea, infertililty, impotence, gynaecomastia; may be incr peri conversion of androgens to oestrogen Other: H1 and 5-HT2 blockade ( weight gain (esp clozapine and olanzapine); deposits in ant eye (chlorpromazine), retinal deposits (thioradazine) CV: high resting HR, decr SV, decr MAP, decr PVR; prolonged QT, abnormal ST and T (esp with thioradazine) Neuroleptic malignant syndrome: muscle rigidity, fever, leukocytosis, autonomic instability (BP, HR), incr creatinine kinase; due to rapid blockade of D receptors ( severe extrapyramidal SE’s; can give diazepam, dantrolene (muscle relaxant), bromocriptine (D agonist)ContraindicationsDrug interactionsPregnancySome teratogenicityExamplesOD: rarely fatal; drowsy ( coma, convulsions; decr deep tendon reflexes, miosis, decr temp, decr BP; thioridazine and mesoridazine more important as arrthymias Mood Stabilising Drugs Lithium Action Cation (closely related to Na – can substitute with Na in generating AP and exchange across membranes) MOA: unsure NT: enhances 5-HT; also effect on NE and D (decr turnover; block D supersensitivity) and Ach (incr) Enzymes: inhibits inositol monophosphate (IP2(1) and inositol polyphosphate 1-phosphatase ( decr phosphatidylinositol- 4,5-biphosphate (PIP2) which is substrate for IP3 formation (important messenger in ą-adrenergic and muscarinic transmission); may cause altered PKC signaling ( long term neuroplastic events Also inhibits biphosphate nucleotidase (may cause nephrogenic diabetes insipidus), glycogen synthase kinase-3 Inhibits NE-sensitive adenylyl cyclase May uncouple G proteins from their receptors IndicationBipolar disorder; used in combination with above, often continued as maintenance therapy; may be used in schizoaffective disorder; may be used in trt resistant depressionRoute of administrationDoseTarget conc 0.6-1.4mEq/L – take trough level 10-12hrs post-dose; SS achieved in 5/7 Dose 0.5 mEq/kg/dayDosing IntervalAbsorptionAlmost complete in 6-8hrs; peak in 0.5-2hrsBioavailabilityHalf life20hrsDuration of ActionDistributionIn total body H20; VOD 0.5-0.9L/kg (rises when reaches intracellular compartment); some sequestration in bone; no protein bindingMetabolismNONEExcretionIn urine – clearance decreased by diuretics and NSAIDSide effectsNS: tremor alleviated by beta-blockers; choreoathetosis, motor hyperactivity, ataxia, dysarthria, aphasia Thyroid: decr function Nephrogenic diabetes insipidus: loss of responsiveness to ADH; responds to amiloride; may cause chronic interstitial nephritis, minimal change glomerulopathy and nephrotic syndrome Oedema: common; causes Na retention Weight gain Cardiac: T wave flattening Causes leukocytosisContraindicationsSick sinus syndrome: depresses sinus nodeDrug interactionsIncreases likelihood of extrapryramidal SE’s with antipsychoticsPregnancyIncr clearance during pregnancy so may get toxic postpartum Toxicity in newborn ( lethargy, cyanosis, poor suck reflex Relatively low teratogenicityExamplesOD: over 2mEq/L; can be dialysed easily as is a small ion Valproic acid: usually 1500-2000mg/day Carbamazepine: usually 800-1200mg/day; beware blood dyscrasias Antidepressants Affect NT’s in synapses (generally incr) ( decr cAMP, and down-regulation and pre- and post-synaptic receptors; common effect is incr serotonergic transmission even without incr synaptic 5-HT; long-term intracellular changes with phosphorylation of elements Tricyclic Antidepressants Action Block amine uptake pumps (for NE and 5-HT, NERT and SERT) Imipramine (mod sedative; mod antimuscarinic) Amitriptyline (high sedative; high antimuscarinic) (doxepin also has high antimuscarinic and sedative) Nortriptyline Doxepin ClomipramineIndicationUseful in chronic pain; better for severe depressionRoute of administrationDoseA: 75-200mg I: 75-200mgDosing IntervalAbsorptionIncompletely absorbedBioavailabilityAmitriptyline: 31-61% Imipramine: 29-77%Half lifeAmitriptyline: 31-46hrs Imipramine: 9-24hrsDuration of ActionDistributionHigh lipid solubility Protein binding: A: 82-96% (high) I: 76-95% (high) VOD: A: 5-10L/kg (high) I: 15-30 L/kg (high)MetabolismSignificant 1st pass; transformation of tricyclic nucleus and alteration of aliphatic side chain; monodemethylation ( active metabolites Amitriptyline: has active metabolite nortriptyline Imipramine: active metabolite desipramineExcretionSide effectsAntimuscarinic: blurred vision, urinary hesitancy, dry mouth, constipation ą-blocking: postural hypotension, conduction defects, arrhythmia Sedation: sleepiness Sympathomimetic (incr NE): tremor, insomnia NS: seizures Metabolic: weight gain, sexual disturbanceContraindicationsDrug interactionsCombination with alcohol may impair driving due to sedative effectPregnancyExamplesDangerous in OD 2nd generation and 3rd generation agents: Action Similar pharmacokinetics as tricyclics; some have active metabolites 2nd: Amoxapine (mod sedative, mod antimuscarinic; blocks reuptake of NE > D = 5HT; dangerous in OD) Maprotiline (mod sedative, mod antimuscarinic; blocks reuptake of NE; dangerous in OD) Trazodone (high sedative; blocks reuptake of 5-HT) Bupropion (blocks reuptake of NE; relatively free of SE’s) 3rd: Venlafaxine (blocks reuptake of 5-HT > NE > D; behaves like SSRI at low doses and relatively free of SE’s) Mirtazapine (high sedative; blocks H and ą2 receptors) Nefazodone (mod sedative, high antimuscarinic; blocks reuptake of 5-HT) Duloxetine (blocks reuptake of 5-HT > NE; relatively free of SE s) Note: trazodone, nefazodone and mirtazapine  antagonize 5-HT2a and 5-HT2c receptorIndicationRoute of administrationDoseAmoxapine: 150-300mg Venlafaxine: 75-225mg Maprotiline: 75-300mg Mirtaz: 15-60mg Trazadone: 50-600mg Nef: 200-600mgDosing IntervalAbsorptionIncompletely absorbedBioavailabilityHalf lifeTrazodone: 4-9hrs (short) Venlafaxine: 4-10hrs (short) Mirtazapine: 20-40hrs (long)Duration of ActionDistributionProtein binding: V: 27-30%MetabolismTrazodone: active metabolite m-chloro-phenyl-piperazine Venlafaxine: active metabolite O-desmethyl Mirtazapine: active metabolite desmethylExcretionSide effectsAmoxapine, maprotiline: similar to tricyclics Mirtazapine: somnolence, incr appetite, weight gain, dizziness Trazodone: drowsiness, dizziness, insomnia, N, agitation Venlafaxine: N, somnolence, sweating, dizziness, anxiety, sex disturbance, hypertension Bupropion: dizziness, dry mouth, sweating, retmor, seizuresContraindicationsNefazodone: inhibits CYP3A4Drug interactionsPregnancyExamplesOD amoxapine ( severe neurotoxicity, seizures OD maprotiline ( seizures, cardiotoxicity SSRI’s Action Fluoxetine (slight sedation, slight antimuscarinic; blocks reuptake of 5-HT > NE = D) Sertraline (slight sedation; blocks reuptake of 5-HT) Paroxetine (slight sedation; blocks reuptake of 5-HT) Citalopram (blocks reuptake of 5-HT)IndicationUniquely effective in OCDRoute of administrationDoseF: 10-60mg S: 50-200mg C: 20-60mg P: 20-50mgDosing IntervalAbsorptionBioavailabilityFluoxetine: 70% Citalopram: 51-93%Half lifeFluoxetine: 24-96hrs (long half life of active metabolite) Sertraline: 22-35hrs Paroxetine: 24hrs Citalopram: 23-75hrsDuration of ActionDistributionProtein binding: F: 94% S: 98% P: 95% C: 70-80% VOD: F: 12-97 L/kg S: 20 L/kg P: 28-31 L/kg C: 12-16 L/kgMetabolismFluoxetine: active metabolite norfluoxetine (half life 7-9/7 at SS) Sertraline: active metabolite desmethyl Paroxetine: no active metabolite Citalopram: active metabolite desmethylExcretionSide effectsTransient nausea; decr libido; anxiety, insomnia, GIContraindicationsDrug interactionsParoxetine: possible teratogen Paroxetine and fluoxetine are potent inhibitors of P450 2D6 (effect nortriptyline, flecainide)PregnancyExamplesOD: high VOD rules out removal by dialysis, supportive trt only MAOI’s Action Non-selective inhibitors of MAO A (for NE, 5-HT and tyramine) and B (for dopamine) Inhibition of MAO persists after drug has been eliminated Hydrazides: phenelzine, isocarboxazid; combine irreversibly with MAO A and B; effects persist for 2-3/52 Non-hydrazides:tranylcypromine – has some sympathomimetic characteristics; doesn’t bind irreverisibly but has longer DOA; effects persist for 1/52 Must have failed on other trt to receiveIndicationRoute of administrationDosePhenelzine: 45-75mg Tran: 10-30mgDosing IntervalAbsorptionReadily absorbedBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsAccumulation of tyramine with irreversible blockers Headache, drowsiness, dry mouth, weight gain, postural hypoT, sex disturbanceContraindicationsDrug interactionsIncr NE ( sensitive to sympathomimetics (eg. Tyramine, and drugs) When combined with SSRI may cause serotonin syndrome ( hyperthermia, muscle rigidity, myoclonus, altered mental statusPregnancyExamplesOD: agitation, delirium, NM excitability ( decr LOC, shock, hyperthermia, seizures NB. MAOI, bupropion, fluoxetine, sertraline, paroxetine, citalopram and venlfaxine given mane as may cause insomnia. Others given nocte as cause drowsiness. Will not get full response to trt for 8/52. Need to be on maintenance for at least 6/12. Response may take >3/52 TOXICOLOGY Drugs of Abuse Dependence: physical Tolerance: can be pharmacokinetic – decr conc of drug or shorter DOA Pharmacodynamic – change in receptor function (eg. Desensitization, receptor internalization) Other adaptive mechanisms – eg. Altered intercellular enzymes (eg. Adenylyl cyclase ( altered levels of cAMP) May not occur to SE’s therefore dangerous Withdrawal: when drug withdrawed, adaptive mechanisms become evident Addiction: psychological; high motivation to use drug despite negative consequences; relapse in certain circumstances or re-exposure thought to be due to synaptic plasticity (eg. Long-term potentiation), stimulation on mesolimbic dopamine system ( strong learning signal; likelihood of addiction to certain drugs can be inherited Dopaminergic mesolimbic system is prime target (involves nucleus accumbens, amygdale and prefrontal cortex; dopamine important in reward processing); dopamine thought to be only assoc with unexpected rewards, as opposed to conditioned rewards; giving drug causes incr dopamine causing inappropriate learning signal, pathologic reinforcement. All addictive drugs incr dopamine. Drugs split into 3 groups: Binds Gio-coupled receptors ( inhibit neurons through postsynaptic hyperpolarisation and presynaptic regulation of NT release – in ventral tegmental area (in mesolimbic system) this occurs on inhibitory GABA interneurons Opioids: work on 3 G protein-coupled receptors (źş´; coupled to Gi ( inhibit adenylyl cyclase; have different effects as ź is on (and inhibits) GABA (inhibitory) neurons ( incr dopamine, whereas ş is on (and inhibits) dopamine neurons, so former causes euphoria, latter causes dysphoria); ź opioids are morphine, heroin, codeine, oxycodone, meperidine ( tolerance and dependence Withdrawal: dysphoria, N+V, muscle aches, lacrimation, rhinorrhoea, mydriasis, piloerection, sweating, diarrhoea, yawning, fever lasting few days Trt: give methadone (longer halflife) od Cannabinoids: active substances inc ”9-tetrahydrocannabinol; causes disinhibition of dopaminergic neurons by presynaptic inhibition of GABA in VTA (HL 4hrs, max effect 1-2hrs Withdrawal: short lived; restlessness, irritability, agitation, insomnia, N, cramping ł-hydroxybutyric acid: binds as weak agonist to GABAb so effectively inhibits it (at high doses will bind dopaminergic neurons also, so inhibit them); max conc in 20-30mins, HL 30mins; has been used in date rape LSD, mescaline, psilocybin: hallucinogens; flashbacks several years later; induce neither dependence nor addiction, but can get tolerance; no effect on dopamine; incr release of glutamate in cortex; act on 5-HT2a receptor ( coupled to Gq ( incr IP3 ( incr intracellular Ca Interacts with ionotropic receptors ( combined effects on dopamine and GABA neurons ( enhanced dopamine release Nicotine: agonist of nicotinic Ach receptor (nAChR, ą2˛2 form) which have role in cognitive processes; in VTA this receptor found on dopamine neurons ( D release in nucleus accumbens and prefrontal cortex Withdrawal: irritable, sleeplessness Benzo’s: act on GABAa receptors on inhibitory interneurons ( disinhibition of dopaminergic neurons Withdrawal: within days (irritable, insomnia, phonophobia, photophobia, depression, muscle cramps, seizures), last 1-2wks Alcohol: alters function of several receptors; ENT1 receptor involved in dependence (via accumulation of adenosine, stimulation of adenosine A2 receptors, enhanced CREB signaling) Withdrawal: 6-12hrs after cessation; tremor, N+V, sweating, agitation, anxiety; hallucinations after 12-24hrs, seizures after 24-48hrs, DT s after 48-72hrs (inc autonomic instability) Treatment: disulfiram (inhibits acetaldehyde dehydrogenase ( N+V, dysphoria); naltrexone (antagonist at ź opioid receptor ( decr craving); top%ôú  E [ \ m ş Ë " - = x y  ť ź Đ I K r t Ź ­ Ž Ţ ń  4 L ł Ă –—˛ĚćřőěäěäŮěäËőěäěäŔőä¸ě丯§¸ž¸–¸––Ŕ––––‚–v–v–hß_ƒhÄ.\>*CJaJhÄ.\hÄ.\CJaJhÄ.\6CJaJhÄ.\CJaJhp™6CJaJhß_ƒCJaJhß_ƒ6CJaJhp™CJaJhÄ.\5>*CJaJhv&$hv&$5>*CJaJhv&$hv&$CJaJhv&$CJaJhv&$6CJaJhv&$5>*CJaJ. 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FWgdG?Z\ŘÚ<x<y<z<†<Œ<–<==H=e=f=g=Ś=§=Á=Č=ţ=˙=Â>Ă>ä>ĺ>f?g?h?i?s?Ĺ?ü?ý?4@5@d@ňęňęčęŕÔČÔČęŔÔ´ŔŚŔŚŔš’„’„’„’Ŕęxš’pbpbp jŕđh 9kh 9kCJaJh 9kCJaJhóh"ž>*CJaJ jŕđh"žh"žCJaJh"žCJaJhóhB'>*CJaJ jŕđhB'hB'CJaJhÄRühB'6CJaJhB'CJaJhč`#hB'>*CJaJhč`#hč`#>*CJaJhG?CJaJUhč`#CJaJ jŕđhč`#hč`#CJaJ&iramate (facilitates GABA function, antagonizes glutamate receptors, decr dopamine release after alcohol, decr cravings) Phencyclidine (PCP), ketamine: non-competitive antagonism of NMDA receptor; no dependence or addiction, but can cause long-lasting psychosis Inhalants: nitrates, ketones, aliphatic and aromatic hydrocarbons Targets monoamine trasporters ( block reuptake, or stimulate nonvesicular release of dopamine ( accumulation of dopamine Cocaine: H20-soluble salt (inject / absorbed via m membrane) ( when dissolved in alkaline solution is transformed into free base which can be smoked which is freely absorbed by lungs with rapid penetration of brain; in CNS blocks reuptake of D, NE and 5-HT ( incr D in nucleus accumbens; NE ( incr BP, incr HR, V arrhythmia, decr appetite, hyperactive, less sleep’ incr risk of intracranial haemorrhage, CVA, MI, seizures Amphetamine: cause release of amines (eg. D and NE) by reversing action of amine transporters, also use these transporters to be taken up into cell ( interfere with vesicular monoamine transporter (VMAT) ( deplete synaptic vesicles of their NT content ( incr D in cytoplasm ( release into synapse via reversed action transporter (incr nonvesicular release, decr vesicular release); incr NE+E ( arousal, decr sleep; incr D ( euphoria, abnormal mvmt, psychosis; incr 5-HT ( anorexia, hallucinations; may cause hypertensive crisis and stroke; neurotoxic Withdrawal: dysphoria, drowsiness, irritability Ecstasy: contains methylenedioxymethamphetamine (MDMA) which causes release of biogenic amines by reversing acion of transporters (SERT>DAT, NET); risk of hyperthermia and dehydration, serotonin syndrome, seizures ( XS water causing water intoxication with low Na, seizures and death Withdrawal: depression, aggression Non-addictive: hallucinogenics and dissociative anaesthetics; that alter perception without sensation of reward/euphoria; target cortical/thalamic areas Carbon Monoxide Byproduct of incomplete combustion; combines irreversibly with O2-binding sites of Hb (220x more affinity for Hb than O2) ( COHb which cannot transport O2 and interferes with dissociation of O2 from HbO, so decr transfer to tissues Non-smoking adult: <1% saturation (endogenous formation of CO from heme catabolism) Smoker: 5-10% Symptoms: rarely <15%; collapse and syncope at 40%, death >60% Due to hypoxia: psychomotor impairment ( headache and tight temporal area ( confusion, loss of visual acuity ( incr HR and RR, syncope, coma ( deep coma, shock, convulsions, resp failure; damage brain and myocardium, may be delayed neuropsychiatric impairment; note PO2 measures only O2 in plasma and not total blood O2 content so may appear normal Trt: O2 antagonises CO; elimination HL 230mins at room air, 80mins at 100% O2, 20mins with hyperbaric O2 Organophosphates (cholinesterase inhibitors) DUMBELS Stimulation of muscarinic receptors ( sweating, XS salivation, lacrimation, abdo cramps, urination, diarrhoea, incr bronchial secretions, miosis, bronchospasm Stimulation of nicotinic receptors ( ganglionic activation ( hypertension, either incr/decr HR; muscle twitching, fasciculations ( weakness and resp muscle paralysis Agitation, confusion, seizures, excitation Trt: supportive; can try atropine which competes at muscarinic site (not nicotinic); pralidoxime given early restores cholinesterase activity Insecticides: Organochlorine insecticides: DDT (chlorophenothane), benzene hexachlorides, cyclodienes, toxaphenes; can be absorbed through skin, inhaled, PO; interfere with inactivation for Na channel in excitable membranes ( repetitive firing in most neurons; inhibit Ca transport; enhance excitability of neurons; tremor ( convulsions; mng is symptomatic; stable and may take a long time to break down in enviro Organophosphorus Insecticides: azinphos-methyl, malathione etc…; can be used in humans as antiparasitics; rapid biotransformation; inhibit acetylcholinesterase through phosphorylation ( accum of Ach; altered neurologic and cognitive function, psychologic symptoms; some agents phosphorylate neuropathy target esterase (enzyme in neural tissue) ( delayed neurotoxicity with polyneuropathy (sensory and motor, ataxia); unstable and breakdown quickly in environment Carbamate insecticides: inhibit acetylcholinesterase by carbamoylation; shorter effect than above; nonstable Botanical insecticides: derived from natural sources (eg. Nicotine, rotenone) Herbicides Chlorophenoxy herbicides: 2,4-D (causes coma and muscle hypotonia) and 2,4,5-T (causes coma); liver and kidney dysfunction Bipyridyl herbicides: paraquat accumulates in lung ( oedema, alveolitis, fibrosis; GI irritation (haematemesis and bloody stools); delayed resp distress, congestive haemorrhagic pul oedema; may take several weeks until death from ingestion; prompt gastric lavage, adsorbants, cathartics; O2 may aggravate pul lesions Solvents Halogenated Aliphatic hydrocarbons: industrial solvents, degreasing agents, cleaning agents; caron tetrachloride, chloroform (most potent), trichlororethylene etc…; cause CNS depression, liver and kidney damage, cardiotoxicity; may cause impaired memory and peri neuropathy after chronic exposure; carcinogenicity Aromatic hydrocarbons: benzene (CNS depression; vertigo, drowsiness, headache, N ( euphoria, N, locomotor problems, coma; chronic ( BM injury ( aplastic anaemia, leucopenia, pancytopenia, thrombocytopenia); toluene / methylbenzene (CNS depressant; severe fatigue and ataxia ( LOC) ?environmental pollutants Management of Poisoned Patient Toxicokinetics: adsorption, distribution, excretion, metabolism; toxic doses and metabolites VOD: apparent vol into which substance is distributed; large (>5 L/kg): implies drug is not readily accessible to measures aimed at purifying blood (eg. Antidepressants, antipsychotics, antimalarials, narcotics, propanolol, verapamil); small (<1 L/kg): salicylate, ethanol, Phenobarbital, lithium, valproic acid, phenytoin Clearance: measure of vol of plasma that is cleared of drug in unit time (sum of clearance by kidney and metabolism by liver); important in planning detoxification strategy; OD may alter pharmacokinetics (eg. Drug may damage gastric lining and incr absorption, capacity of liver to metabolise drug overcome, protein binding exceeded); most drugs eliminate by 1st order kinetics (proportionate to plasma conc), if normal metabolise exceeded may become 0 order Toxicodynamics: injurious effects of substances; depends on dose-response curve (linear – 10x dose cause 10x lethal effect, in curve with plateau – may need 100x dose 10x lethal effect); for benzo’s toxic effect is same as therapeutic effect but for others toxic effect is different Symptoms: Hypertension and incr HR: amphetamines, cocaine, antimuscarinics Hypotension and decr HR: Ca channel blockers, beta blockers, clonidine, sedative hypnotics Hypotension and incr HR: tricyclics, trazodone, quetiapine, vasoD, beta agonists Incr RR: salicylates, CO, metabolic acidosis Hyperthermia: sympathomimetics, anticholinergics, salicyclates Hypothermia: CNS depressants Miosis: opioids, clonidine, phenothiazines, cholinesterase inhibitors (eg. Organophosphates) Mydriasis: amphetamines, cocaine, LSD, atropine, antimuscarinics Horizontal nystagmus: phenytoin, alcohol, barbs, sedatives Vertical and horizontal nystagmus: phencyclidine Ptosis and opthalmoplegia: botulism Cyanide: bitter almond smell Hot, flushed, dry skin: antimuscarinics Sweating: organophosphates, nicotine, sympathomimetics Ileus: antimuscarinic, opioid, sedative Hyperactive bowel: organophosphates, arsenic, theophylline Nystagmus, dysarthria, ataxia: phenytoin, carbamazepin, alcohol, sedatives Muscle hyperactivity: antimuscarinics, cocaine, sympathomimetics Muscular rigidity: haloperidol, antipsychotics, serotonin syndrome, strynine Seizures: antidepressants, cocaine, amphetamines, theophylline, isoniazid, diphenhydramine Biochem:Elevated anion gap (due to unmeasured anions in plasma): aspirin, metformin, methanol, ethylene glycol, isoniazid, iron, valproic acid, cyanide, CO, ibuprofen Hyperkalaemia: beta blockers, digitalis, K-sparing diuretics, fluoride Hypokalaemia: barius, beta agibsts, caffeine, theophylline, thiazide and loop diuretics Incr serum osmolality: ethanol, methanol, isopropanolol, ethylene glycol ECG: Wide QRS: tricyclics, quinidine Prolonged QTc: quinidine, tricyclics, other antidepressant and antipsychotics, lithium, arsenic AV blocks and other arrhythmias: digoxin Decontamination: Emesis: ipecac syrup; not to be used if suspected poison is corrosive / petroleum distillate / rapidly acting convulsant Gastric lavage: usually N saline at body temp Activated charcoal: adsorbs drugs due to large SA; give 10x weight of toxin; NOT for iron, lithium, K, alcohol, cyanide, corrosive acids/alkali; repeated dose may enhance systemic elimination of some drugs (eg. Carbamazepine, dapsone, theophylline) via ‘gut dialysis’ Cathartics (laxative): decr absorption; whole bowel irrigation with GoLYTELY for Fe, enteric-coated medicines, illicit drug-filled paclets, foreign bodies; 1-2L/hr for several hours until rectal effluent clear Haemodialysis: assists correction of fluid and electrolyte imbalance; enhance removal of toxic metabolites (eg. Formate in methanol, oxalate/glycolate in ethylene glycol); efficacy depends on molecular weight, water solubility, protein binding, distribution; good for carbamazepine, lithium, methanol, metformin, Phenobarbital, salicylate, theophylline, valproic acid Alter urinary pH: alkalinisation for salicylate; acidification for phencyclidine, amphetamines Acetaminophen: ingestion of 7g (150-200mg/kg) is potentially toxic; liver produces toxic metabolite; if serum level >150-200mg/L at 4hrs, at risk; if liver enzymes induced >100mg/L ( mild GI upset ( 24-36hrs: incr LFT’s, hypoprothrombinaemia, fluminant liver failure, hepatic encephalopathy and death, renal failure Antidote: acetylcysteine; acts as glutathione substitute, binding toxic metabolite; should be given within 8-10hrs Stimulants: prolonged muscle hyperactivity ( dehydration, hpotension, hyperthermia (brain damage, hypotension, coagulopathy, renal failure), rhabdo; trt supportive, may need to be paralysed Anticholingergics: in mushrooms too; flushed skin, hot, dry m membranes, no sweating, blurred vision, cycloplegia, confusion, delirium; incr HR, mydriasis, agitation, muscle twitching, urinary retention; supportive trt Antidote: physostigmine 0.5-1mg IV – beware can cause bradycardia and seizures; do not give in tricyclics as can aggravate cardiotoxicity ( HB and asystole Antidepressants: Tricyclics (>1g, or 15-20mg/kg) – competitive antagonists at muscarinic cholingergic receptors ( tachycardia, mydriasis, dry mouth; may be alpha-blocker ( vasoD; agitation and seizures ( depression and hypotension; wide QRS and depressed contractility ( arrhythmias; supportive trt Antidote: for hypotension can give NE; for cardiac toxicity give NaHCO3 (50-100mEq) to incr extracellular Na to overcome Na blockade; DO NOT USE PHYSOSTIGMINE MAOI: severe hypertensive reaction SSRI: seizures, prolonged QTc, torsades de pointes; serotonin syndrome (agitation, muscle hyperactivity, hyperthermia) Antipsychotics: CNS depression, seizures, hypotension, prolonged QT; dystonic reaction due to D2 blockade; neuroleptic malignant syndrome (lead pipe rigidity, hyperthermia, autonomic instability) Aspirin: >200mg/kg; uncoupling of oxidative phosphorylation and disruption of normal cellular metabolism ( hyperventilation, resp alkalosis due to medullary stimulation ( metabolic acidosis with INCREASED ANION GAP from accumulation of lactate and excretion of HCO3 (so mixed resp alkalosis and met acidosis); hot due to uncoupling of oxidative phsophorylation; vomiting; fluid loss and dehydration ( severe: profound metabolic acidosis, seizures, coma, pul oedema, CV collapse Trt: supportive, aggressive gut decontamination; maybe alkalinsation of urine or haemodialysis Beta-blockers: selectivity is lost at high doses so block beta1 and 2; propanolol toxic at only 2-3x dose (Na channel blocking, lipophilic so enters CNS) ( bradycardia, hypotension; partial agonists (eg. Pindolol) may cause tachy and hyper; seizures, cardiac conduction block Trt: supportive Antidote: glucagons – raises cAMP in cardiac cells through stimulation of glucagon receptors; 5- 20mg IV Ca channel blockers: serious with small overdose; depress sinus node automaticity and slow AVN conduction Trt: supportive; as may be SR, can try whole bowel irrigation or activated charcoal Antidote: Ca 2-10g IV; good to counter decr contractility, but less for block or peri vasc collapse; can try glucagons, vasopressin, E, insulin plus glucose Digoxin: may accumulate in renal insufficiency ( vomiting, hyperK, sinus brady, AV block, atrial tachy, accelerated junctional rhythm, premature ventricular beats, VT Trt: supportive, atropine Antidote: digoxin ab’s; takes 30-60mins to work Ethanol and sedatives: >300mg/dL ( coma; resp depression, hypothermia Antidote: flumazenil for benzo’s Ethylene glycol and methanol: highly toxic metabolites (formic, hippuric, oxalic and glycolic acid) ( anion gap metabolic acidosis, hyperV, altered mental status ( coma, blindness, renal failure Antidote: alcohol, blocks alcohol dehydrogease; aim for 100mg/dL level; fomepizole does same Iron and metals: important OD Opioids: see earlier Theophylline: incr HR, tremor, vomiting, hypotension, hypoK, hyperglycaemia, cardiac arrhythmia, seizures; supportive trt, aggressive gut decontamination PHARMACOLOGY IN EXTREMES OF AGE Drugs in Pregnancy Most drugs cross placenta Pharmacokinetics: Physicochemical properties of drug Rate at which drug crosses placenta Lipid solubility: lipophilic diffuse readily and hence transfer is dependent on blood flow (as pass SO rapidly) Degree of drug ionization: highly ionized pass slowly, but will still pass if high enough gradient NB. Even though aspirin is highly ionized (ie. Polar) it still crosses placenta as the small amount that is non-ionised is highly lipid soluble Molecular weight: 250-500 cross readily; >1000 v poorly; heparin is good choice of anticoagulant as v large; avoid warfarin Placental transporters: may pump drugs back into maternal circulation Protein binding: v lipid soluble drugs aren’t affected by protein binding; phenytoin, barbs and LA show more protein binding in maternal than fetal tissues due to lower affinity for fetal proteins Placental metabolism: aromatic oxidation reactions occur in placental tissue; may result in toxic metabolites ( augment toxicity (eg. Of ethanol) 40-60% blood in umbilical vein enters fetal liver where is metabolised, rest goes to general circ; umbilical artery may shunt back to umbilical vein and through liver again Duration of exposure to drug Distribution characteristics in different fetal tissues Stage of placental and fetal development Effects of drugs used in combination Pharmacodynamics: Maternal drug actions: effect of drug on reproductive tissues altered by endocrine enviro; effect on other tissues not changed much; physiology (eg. CO, renal blood flow) may be changed Therapeutic drug actions in fetus: eg. Corticosteroids for fetal lung maturation, Phenobarbital given to induce liver enzymes required for glucuronidation of bilirubin decreasing incidence of newborn jaundice, zidovudine for HIV Toxic drugs actions of fetus: opioids ( dependence in fetus; ACEi ( renal damage in fetus Teratogenic drug actions: affect tissues undergoing rapid development at that time; may interfere with passage of O2 through placenta so affect rapidly metabolizing fetal tissues at that time; vit A may alter processes of differentiation; folic acid deficiency causes neural tube defects; to be teratogenic a substance must: Cause a characteristic set of malformations, hence selective for certain target organs Exert effect a particular stage of fetal development Show dose-dependence incidence TrimesterDrugEffectFirstCarbamazepineNeural tube defectsCyclophosphamideVariousLithiumEbstein’s anomalyMetronidazoleOrganic solventsVariousThalidomidePhocomeliaWarfarinHypoplastic nasal bridge, chondrodysplasiaSecondWarfarinCNS malformationsThirdWarfarinBleedingTricyclicsNeonatal withdrawalAllACEiRenal damageAmphetaminesBarbsNeonatal dependenceCocaineSpontaneous abortion, placental abruption, premature labour, neonatal cerebral infarctionDiazepamNeonatal dependenceEthanolFASHeroinNeonatal dependenceMethadoneNeonatal dependencePhenytoinFetal hydantoin syndromeStreptomycinVIII toxicitySmokingIUGR, prematurity, SIDSTamoxifenSpontaneous abortionTetracyclinesDiscolouration of teeth, altered bone growthValproic acidNeural tube defects, cardiac and limb malformations Drugs in Lactation Most drugs excreted into breast milk in doses too small to adversely affect neonatal health; take drug 30-60mins post-nursing and 3-4hrs pre-nursing Significant effect: chloramphenicol (possibly cause BM suppression) Diazepam (sedation) Heroin (neonatal dependence) Methadone Lithium Moderate effect: Ethanol (only when large amount drunk by mum) Phenobarbital (sedation) Prednisone (avoid >15mg/day) Tetracycline (staining of developing teeth) Drugs in Paediatrics Drug Absorption: Blood flow at site of administration: irregular and difficult to predict in ill preterm on IM administration as decr peri blood flow and low muscle mass; may be slow then unexpectantly become high on improved blood flow GI function: in preterm, secretion of gastric acid occurs slowly and peaks on day 4, so avoid drugs that are inactivated at low pH; neonates have prolonged gastric emptying time – therapeutic effect delayed if drug absorbed in SI; decr peristalsis causes incr drug absorbed; decr GI enzyme activity; decr conc of bile acids and lipase ( decr absorption of lipid soluble drugs Drug Distribution: H20: neonate is 70-75% H20 (50-60% adult; 85% preterm); extracellular H20 is 40% body weight in neonate (20% adult); important for H20 soluble drugs Fat: total body fat in neonate is 15% body weight (1% in preterm) Protein binding: decr protein binding in neonates ( incr conc of free drug; some drugs compete with bilirubin for binding to albumin; drugs given to jaundiced neonate displaced bilirubin from albumin ( kernicterus OR bilirubin displaces drug ( incr free drug Drug Metabolism: decr activity of P450 and conjugating enzymes (50-70% adult values) ( slowed clearance and prolonged half life; beware of induction of fetal hepatic enzymes by drugs administered to mother in pregnancy Drug Excretion: decr GFR in neonates (30-40% adult value) ( incr by 50% in 1st wk ( reaches adult value at 6-12/12; note toddlers may actually have HIGHER GFR Estimating Paediatric Dose: By age: Young’s rule: Dose = adult dose x age (years) / (age + 12) By weight: Clark’s rule: Dose = adult dose x weight (kg) / 70 Drugs in Geriatrics Pharmacokinetic changes: Absorption: little change; altered nutritional habits, changes in gastic emptying (slower) Distribution: decr lean body mass, decr body water, incr fat, decr serum albumin (binds weak acids), incr serum orosomucoid (binds basic drugs) Metabolism: liver doesn’t alter much (greatest change is in stage I reactions); some drugs affected (eg. Alprazolam, barbs, chlormethiazole, diazepam, imipramine, meperidine, nortriptyline, propanolol, quinine, theophylline); heart failure can dramatically affect ability of liver to metabolise; hepatic blood flow v important; nutritional deficiencies may effect liver Elimination: age related decr CrCl (use Cockcroft-Gault formula to calculate); prolonged half life; may be worsened by dehydration; resp excretion of volatile agents Pharmacodynamic changes: far less important; MAY be some incr sensitivity to benzos and analgesics, possibly decr responiveness to beta agonists; note altered homeostatic mechanisms CNS drugs: Sedative-hypnotics: HL incr; note that often metabolites are active; may incr VOD for some of drugs; more sensitive pharmacodynamically Analgesics: more sensitive to resp effect due to decr resp function Antipsychotic / antidepressants: use haloperidol if trying to avoid sedation (beware extrapyramidal toxicity); beware postural hypotension due to alpha-blocking; may have incr HL; note lithium is cleared renally Alzheimer’s: may be v sensitive to antimuscarinics (ie. Worsen Alzheimer’s); trt with cholinomimetics (eg. Tacrine – cholinesterase inhibitor, incr release of Ach from cholinergic nerve endings, inhibit MAO, decr release of GABA; donepezil, rivastigmine, galantamine) CV: Antihypertensives: thiazides are first step at low dose (beware hypoK, hyperG, hyperU), Ca channel blockers effective and safe; beta-blockers can be hazardous in COPD; ACEi’s not v good +ive inotropes: v dangerous as more susceptible to arrhythmias; decr clearance of digoxin with incr HL (even though decr VOD), check renal function; toxicity occurs more Antiarrhythmics: incr HL of quinidine, lidocaine and procainamide; may be more sensitive to toxic effects Antimicrobial: decr host defences, altered T cells, altered mucociliary clearance; more are excreted renally (esp important for aminoglycosides) Anti-inflammatory: care of toxicities inc GI erosion and renal damage; will accumulate more readily ( viscious circle; consider Ca if getting corticosteroids to avoid OP Adverse drug reactions: polypharmacy Cimetidine inhibits metabolism of phenytoin, warfarin, beta-blockers ( elevated levels ENDOCRINE DRUGS Hypothalamic and Pituitary Growth Hormone (somatotropin) Recombinant human GH used – somatropin and somatrem used; HL 20-25mins (endogenous); cleared by liver; given SC 3-6x/wk, active in blood for 36hrs; used in GH def, short stature in chronic renal failure, Prader Willi syndrome, Turner syndrome; improve metabolic state, incr lean body mass in GH def in adults and wasted people with AIDS and short bowel syndrome SE: intracranial hypertension ( vision changes, headache, N+V; pancreatitis, gynaecomastia, nevus growth; peri oedema, myalgia, arthalgia; induce CP450 Mecasermin: for trt of IGF-1 def GH antagonists: incr GH when adenomas ( acromegaly Octreotide: somatostatin analogue ( decr production GH; more potent than endogenous somatostatin at inhibits GH release, but less reduction of insulin secretion; HL 80mins; SC 8hrly – can get longer acting forms; SE N+V+AP, flatulence, steatorrhoea, gallstones, sinus brady Bromocriptine: dopamine receptor antagonist ( decr production GH Pegvisomant: decr GH activating receptor – prevents signal transduction after dimerisation FSH and LH: not done GRH: not done PL: not done Dopamine Agonists: not done Oxytocin: involved in labour and delivery; causes milk ejection; causes uterine contraction (via GPCR and phosphoinositide-Ca 2nd messenger system) – given IV to initiate and augment labour, given IM to prevent postpartum bleeding; HL 5mins; no p protein binding; eliminated by liver and kidneys SE: XS uterine contraction ( fetal distress, placental abruption, uterine rupture; high concs activate vasopressin receptors ( fluid retention, hypoN, CCF, seizures, death; hypoT Oxytocin Antagonist: atosiban, for preterm labour Vasopressin: acts via GPCR – V1 on vascular SM ( vasoC, V2 on renal tubule cells ( incr H20 permeability and resorption of CD; desmopressin acetate is a long-acting synthetic analogue; given IV/IM (not PO as inactivated by digestive enzymes; desm can be PO and nasally); HL 15mins (1.5-2/5hrs for desm); renal and hepatic metabolism; given for diabetes insipidus, occasionally for variceal and colonic diverticular bleeding SE: headache, N+AP, agitation, hypoN, seizures Thyroid Drugs NB. In myxoedema coma, all drugs given IV as poor PO absorption; caution with IV fluids NB. In thyroid storm, slow IV 1-2mg propanolol or PO 40-80mg (diltiazem if CI’ed); give K iodide and prop/meth NB. In ophthalmopathy – may need steroids Thyroxine: Action Synthetic: levothyroxine (T4), liothyronine (T3), liotrix Animal origin: desiccated thyroid – never used Aim to keep TSH 0.5-2.5mU/L; 6-8/52 til SSIndicationRoute of administrationPO, IVDose12.5 – 25mcg/day increasing until eithyroid IV loading 300-400mcg levothyroxine in myxoedema coma ( 50-100mcg dailylllllllllllllllllllllllllDosing IntervalLevothyroxine: od Liothyronine: multiple dailyAbsorptionThyroxine: best from SI; may be poor in severe hypothyroidism; depends in interactions with foods so give on empty stomachBioavailabilityThyroxine: 80% PO T3: 95% POHalf lifeLevothyroxine: 7/7 Liothyronine: 1/7Duration of ActionDistributionMetabolismClearance and metabolism faster in hyperthyroidism, slower in hypoExcretionSide effectsCardiotoxicity with T3 Restlessness, insomnia, nervous, heat inteolerance, palpitations, weight lossContraindicationsLow does in elderly, long standing hypothyroidism, cardiac diseaseDrug interactionsDopamine, CS’s, somatostatin, metformin, levodopa ( inhibit TRH/TSH secretion but little effect on T levels Iodides (eg. Amiodarone), lithium ( inhibits T synthesis/release ( hypothyroid Oestrogens, tamoxifen, heroin, methadone ( incr TBG Androgens, GC’s ( decr TBG Salicylates, mefenamic acid, frusemide ( displace T from TBG ( transient hyperthyroidism Inducers (eg. Rifampicin, Phenobarbital, carbamazepine, phenytoin) incr metabolism Hyperthyroidism ( lower warfarin doses needed Hyperthyroidism ( incr hepatic glu production ( glu intolerance Hyperthyroidism ( higher digoxin doses needed Hyperthyroidism ( sedatives and analgesics less effectivePregnancyPregnancy ( incr TBG sites ( incr bound hormone ( hypothyroidism causes slowed elimination ( incr bound, normal unbound levels; may aim to keep levels at upper range of normal so need incr thyroxine doseExamples Antithyroid Agents: Action Thioamides: methimazole, propylthiouracil, carbimazole; onset of action can take 3-4/52; given for 12-18/12 with 50-68% relapse rate ( prevent hormone synthesis by inhibitng thyroid peroxidase-catalysed reactions and blocking iodine organification, block coupling of iodotyrosines, inhibit peri deiodination of T4 and T3, prevents conversion of T4 to T3 (prop) Anion in hibitors: perchlorate, pertecgnetate, thiocyanate; rarely used Block uptake of iodide by gland through competitive inhibition of iodide transport; useful in hyperthyroidism is amiodarone induced Iodides: rarely used; K iodide; rapid onset of action (2-7/7) so good in thyroid storm; good pre-op Inhibit organification and hormone release (?due to inhibition fo TG proteolysis); decr size and vascularity of gland Iodinated contrast media: diatrizoate PO, iohexol PO/IV Inhibit conversion of T3(T4 in liver, kidney, pituitaryand brain; prolonged effect Radioactive iodine: 131I; PO ( rapid absorption ( conc in thyroid and encorporated into storage follicles; cheap and painless; pretreat with antithyroid drugs until pt euthyroid; 6-12/52 until effect; results in hypothyroidism in 80%IndicationRoute of administrationDoseProp: 100-150mg 6-8hrly ( od maintenance Meth: 20-40mg od ( 5-15mg maintenanceDosing IntervalProp: tid Meth: odAbsorptionPropylthiouracil: rapid Methimazole: complete, variable ratesBioavailabilityPropylthiouracil: 50-80%Half lifePropylthiouracil: 1.5hrs – but duration of action longer as accumulates in thyroid Methimazole: 6hrs – “ “Duration of ActionDistributionPropylthiouracil and methimazole: VOD = TBW (42L); accumulates in thyroid Prop: more strongly protein boundMetabolismExcretionPropylthiouracil: inactive glucuronide excreted by kidney Methimazole: slower excretionSide effectsThioamides: N+AP, altered sense of taste and smell, maculopapular pruritic rash, fever, vasculitis, lymphadenopathy, dermatitis, hepatitis, cholestatic jaundice; agranulocytosis (0.1-0.5%) – heralded by sore throat and fever, usually reversible of discontinuing Iodides: incr conc of I in gland so delays onset of action of thioamines (start them 1st) and makes radioactive iodine trt useless; gland will escape block in 6-8/52 so don’t use alone; ( acneiform rash, swollen salivary glands, mm ulcers, conjunctivitis, rhinorrhoea, metallic tasteContraindicationsDrug interactionsPregnancyCross placenta, caution ( fetal hypothyroidism; meth ( congenital malformation; use propExamples STEROID DRUGS Steroids Action Short-med acting: hydrocortisone; cortisone, prednisone (converted to prednisolone in body), prednisolone, methylprednisolone, meprednisone Intermediate acting: tramcinolone, paramethasone, fluprednisolone Long acting: betamethasone (used for fetal lung maturation; has lower maternal protein binding and placental metabolism so incr transfer across to fetus), dexamethasone (v. potent) Mineralocorticoids: fludrocortisone (GC and MC activity), desoxycorticosterone acetateIndicationRoute of administrationDoseHydrocortisone – 20-30mg PO maintenance; 100mg IV 8hrly in acute crisis Betamethasone – 12mg IM @ 34/40 gestation Prednisone: autoimmune conditions: 1mg/kg/day May get less side effects with high doses every 2/7Dosing IntervalAbsorptionRapid and complete POBioavailabilityHalf lifeDuration of ActionDistributionMetabolismExcretionSide effectsInsomnia, behavioural disturbance, PUD, pancreatitis Iatrogenic Cushing’s syndrome; protein catabolism; gluconeogenesis; weight gain; hyperG; OP; diabetes; impaired wound healing Masks symptoms of bacterial infection; psychosis; depression, cataracts; glaucoma; benign intracranial hypertension; growth retardation in children; Na and H20 retention, hypoK ( hypoK hypoCl alkalosis, incr BP, oedema, CCF Adrenal suppression – takes 2-12/12 for things to return to normal (if stop too quickly ( anorexia, weight loss, lethargy, headache, fever, myalgia, arthralgia, postural hypoTContraindicationsCaution: PUD, heart disease, hypertension, infection, psychosis, diabetes, OP, glaucomaDrug interactionsPregnancyExamples Steroid Antagonists Action Metyrapone: inhibits steroid synthesis; inhibits 11-hydroxylation ( prevents cortisol and corticosterone synthesis; will get incr ACTH and adrenal 11-deoxycortisol secretion Aminoglutethimide: blocks conversion of chol to pregnenolone Ketoconazole: inhibits adrenal and gonadal steroid synthesis in high doses Miepristone: GC receptor antagonist Spirinolactone: lasts 2-3/7; also an androgen antagonist so can be used in hirsutism Eplerenone: aldosterone antagonistIndicationRoute of administrationDoseMetyrapone: 0.25mg bd – 1g qidDosing IntervalAbsorptionBioavailabilityHalf lifeMifepristone: 20hrsDuration of ActionDistributionMifepristone: strong p protein bindingMetabolismExcretionSide effectsMetyrapone: dizziness, GI; Na and H20 retention, hirsutism (11-deoxycortisol precursor becomes DOC and androgen)ContraindicationsDrug interactionsPregnancyMetyrapone: safeExamples Oestrogens and Progesterones GnRH in pulses (decr by stress) ( FSH and LH ( oestrogen ( breast development, growth spurt, altered fat distribution ( after a year endometrial changes. Follicles enlarge in response to FSH ( dominant follicle ( LH causes follicle to releae oestrogen ( oestrogen inhibits FSH release ( granulose cells begin to secrete progesterone ( brief surge of LH and FSH ( ovulation ( cavity of ruptured follicle becomes corpus haemorrhagicum ( theca and granulose cells form corpus luteum which releases oestrogen and progesterone ( ceases hormone release, corpus albicans ( period Oestrogens Etradiol (E2) from ovary – in ovarian follicle by theca and granulose cells before ovulation; from luteinised granulose and thece cells of corpus luteum after ovulation; from fetoplacental unit during pregnancy; binds to ą2 globulin (SHBG) and albumin in circ, only free fraction is physiologically active; converted by liver and other tissues to below Estrone (E1) mostly from liver formed from estradiol, or from peri tissues from androstenedione and other androgens; low affinity for oestrogen receptor Estriol (E3) mostly from liver formed from estradiol, or from peri tissues from androstenedione and other androgens; low affinity for oestrogen receptor Estrone and estriol conjugated ( excreted in bile ( may be hydrolysed in intestine back to active reabsorbable compounds (EH circ) Mechanism of action: dissociate from SHBG ( bind receptor in nucleus ( receptor released from stabilizing proteins (eg. Hsp90) ( complex binds oestrogen response elements (ERE) in genes Effects: ( stimulate development of vagina, uterus, uterine tubes, 2Y sex characteristics ( stimulate growth, closure of epiphyses ( proliferation of endometrial lining ( decr r of resorption of bone by causing apoptosis of osteoclasts ( stimulate adipose tissue production of leptin ( incr levels of CBG, TBG (incr total levels T4), SHBG (decr level of free androgens), transferring, renin, fibrinogen ( incr HDL, decr LDL and chol ( incr CF’s, decr antithrombin III ( modulate SNS control of SM, sense of wellbeing, decr plasma vol Progesterone Made in ovary (made by CL), testis and adrenal from chol; precursor for oestrogens, androgens and adrenocortical steroids Mechanism of action: progestins enter cell ( bind receptors in cytoplasm ( complex binds PRE ( gene transcription Effects: ( favour fat deposition ( incr basal insulin levels and insulin response to glu; glycogen storage, ketogenesis ( can compete for aldosterone at receptor ( incr levels aldosterone ( incr body temp ( incr ventilatory response to CO2 ( causes changes in endometrium seen after ovulation ( involved in breast development Action Synthetic progesterones: hydroxyprogesterone, medroxyprogesterone, megestrol, dimethisterone, desogestrel, gestodene, norgestimate; progestin only good for hepatic disease, hypertension, psychosis, prior TE Inhibition of ovulation, change in cervical mucus, change in uterine endometrium, change in motility and secretion in uterine tubes; depresses ovarian function (( decr follicular development); after prolonged use may get hypertrophy and polyp formation in uterus OCP: decr ovarian cysts, ovarian and endometrial Ca, benign breast disease, ectopic pregnancies, RAIndicationRoute of administrationPV: avoids 1st pass through liver, so higher ratio of peri: liver effects (liver effects inc effect on levels of CBG, SHBG and other live proteins) P: when PO, must be in high dose Depot injection: medroxyprogesterone acetate (DPMA), every 3/12 – ovulation suppressed for 14/52; can persist for 18/12 after stopping trt SC implant: progestin – last 2-4yrs; low levels of drug so little effect on carb metabolism / BPDoseHRT: 0.625mg conjugated oestrogens, 2.5mg medroxyprogesterone OCP: usuall 0.02-0.035mg ethinyl estradiol amd a progestinDosing IntervalAbsorptionProgesterone: rapidBioavailabilityHalf lifeP: 5minsDuration of ActionDistributionMetabolismP: on 1st passage through liver, almost complete metabolism to inactive metabolites (( pregnanediol ( conjugated with glucuronic acid ( excreted in urine)ExcretionSide effectsIncr risk of endometrial Ca – risk decreased with medroxyprogesterone given during last days, take lowest dose possible of oestrogen; incr risk in HRT, not in OCP ? incr risk of breast Ca (no protective effect from adding in progesterone); may get breast enlargement, suppress lactation N, breast tenderness,, oedema – can prevent by slight decr dose oestrogen Breakthrough bleeding (change to bisphasic/triphasic; more common with P only) Weight gain – change to less progestin effect form Acne – change to less progestin effect form Hirsutism – use nonandrogenic progestin form Vaginal infections Amenorrhoea – 95% will return to normal after cessation Abnormal bleeding – high incidence in progestin only Hyperpigmentation, Migraines – if present, incr risk CVA ( discontinue Cholestasis (incr proportion of cholic acid in bile; due to progestin) Incr clotting (incr factors VII, VIII, IX, X; decr antithrombin III) – 3x incr risk; due to oestrogen; also due to decr venous blood flow, endothelial proliferation in veins and arteries; slight incr risk of MI esp if smoker (due to decr glu tolerance, decr levels HDL, incr LDL level, incr plt aggreagation); incr risk of CVA and haemorrhagic Depression Decr rate absorption of carbs from GI tract Hypertension – incr CO, SBP and DBPContraindicationsEndometrial Ca, high risk of breast Ca; liver disease, thromboembolic disorder, heavy smokers Caution in liver disease, asthma, eczema, migraine, diabetes, hypertension, optic neuritis Incr growth fibroids – use lowest poss dose of oestrogenDrug interactionsPhenytoin, rifampicin ( decr efficacy of OCP AB – if altered flora, altered EH cycling, so less efficacy of OCPPregnancyExamples Drugs Used in Trt of Diabetes Insulin Action Rapid-acting: fast onset, short duration; insulin lispro (humalog), aspart (novolog) and glulisine (aventis) – mimic prandial release Short-acting: rapid onset; novolin, humulin Intermediate acting: NPH (neutral protamine Hagedorn, isophane) insulin Long acting: slow onset; glargine and detemirIndicationRoute of administrationIV: can only be short-acting used SC; SC infusion pump; INHDoseDosing IntervalShort acting: before meal times Intermediate acting: qid Long acting: od/bdAbsorptionRapid-acting: rapid absorption; OOA 5-15mins, peak 1hr Short-acting: OOA 30mins, peak 2-3hrs, lasts 5-8hrs – delayed absorption as hexamers must be broken down into dimers and monomers for absorption ( 3 rates of absorption; inject 30-45mins before meal Intermediate-acting: NPH – combined insulin and protamine (isophane) ( after injection, tissue enzymes degrade protamine ( absorption of insulin; OOA 2-5hrs, DOA 4-12hrs Long acting: peakless; glargine – inslin molecules slowly dissolve away from crystalline depot; OOA 1-1.5hrs, peak at 4-6hrs, DOA 11-24hrs; detemir – incr aggregation in subC tissue and albumin binding; OOA 1-2hrs, DOA >24hrsBioavailabilityHalf lifeDuration of ActionRapid-acting: 3-5hrsDistributionMetabolismExcretionSide effectsHypoG – if can’t eat, give 20-50ml of 50% glu over 2-3mins, 1mg glucagons IM/SC Allergy: rare; local / systemic urticaria from histamine release from tissue mast cells Insulin resistance: v rare; due to IgG ab Lipodystrophy: v rareContraindicationsDrug interactionsGlargine: as acidic pH, can’t mix with other insulins Detemir: cannot be mixed NPH can be mixed with lispro, aspart and glulisine acutely Intermediate acting can be premixed with lispro and aspartPregnancyExamples Oral Agents Action Insulin secretogogues: Sulphonylureas: bind sulphonylurea receptor ( inhibits efflux of K through B cell ATP-sensitive K channel ( depolarization ( opens voltage-gated Ca channel ( Ca influx ( release of insulin; long term use reduces glucagon levels 1st generation: tolbutamide; chlorpropamide, tolazamide 2nd generation: used more often as less SE and drug interactions; glyburide, glipizide, glimepiride Meglitidnides: repaglinide – regulate K efflux D-phenylalanine derivatives – nateglinide; regulates K channel Biguanides: metformin; euglycaemic; doesn’t need functioning B cells; v low risk of hypoG; decr hepatic and renal gluconeogenesis, slow glu absorption from GI tract, incr glu to lactate conversion by enterocytes, stimulation of glycolysis in tissues ( incr glu removal from blood, decr plasma glucagon levels; decr macro and microvascular risks Thiazolidinediones: pioglitazone, rosiglitazone; euglycaemic; decr insulin resistance; regulation of genes involved in glu and lipid metabolism and adipocyte differentiation via peroxisome proliferators-activated receptor-gamma; promotes glu uptake and utilization, modulates release of hormones and cytokines used in E regulation; decr macrovascular events; slow onset and offset; v low risk of hypoG ą-glucosidase inhibitors: rarely used; acarbose, miglitol; inhibit intestinal ą-glucosidases (eg. Sucrase, maltase, glycoamylase, dextranase) ( decr absorption of starch and disaccharides NB. Pramlintide: analog of amylin; given SC when insulin alone not working; dec glucagons release, delays gastric emptying; peak 20mins, DOA 150mins, renal metabolism and excretionIndicationRoute of administrationDoseChlorproamide: 250mg od Glipizide: start at 5mg/day, to max 15mg/day in divided doses Glimepiride: 1-8mg od Metformin: 500mg od – tid Pioglitazone: 15-30mg Rosiglitazone: 4-8mg over 2 doses Acarbose / miglitol: 25-100mg tidDosing IntervalAbsorptionTolbutamide: well absorbed Tolazamide: slower, delayed OOA Glipizide: give 30mins before breakfast as delayed absorption with food Pioglitazone: within 2hrs Rosiglitazone: rapidBioavailabilityHalf lifeDuration of ActionDistributionMetabolismTolbutamide: rapid; DOA short, HL 4-5hrs – this is good for elderly diabetics Chlorproamide: HL 32hrs, slow metabolism in liver to products that hae some biologic activity – may get prolonged hypoG in elderly Tolazamide: potent as C, but shorter DOA, HL 7hrs; metabolism to active products Glyburide: metabolized to lowly active products in liver Glipizide: HL 2-4hrs – less likely to cause problematic hypoG Glimepiride: HL 5hrs Repaglinide: fas onset of action; peak 1hr Metformin: HL 1.5-3hrs; not bound to p proteins, NOT metabolized Pioglitazone: by CYP3C8 and CYP3A4 to ACTIVE metabolites Rosiglitazone: highly protein bound; metabolized in liver by CYP2C8 and CYP2C9 to minimally active metabolites Alpha-glu’s: flatulence, D+AP; hypoG; hepatic enzyme elevationExcretionChlorproamide: 20-30% excreted unchanged in urine Metformin: excreted by kidneys as active compound Alpha-g’s: renalSide effectsChlorproamide: leucopenia / thrombocytopenia in <1%; flushing on drinking ETOH Glyburide: flushing with ETOH Metformin: may impair hepatic metabolism of lactic acid due to block of gluconeogenesis (risk of lactic acidosis in renal failure); anorexia, N+V+AP+D, decr absorption B12 Tzd’s: fluid retention, anaemia, weight gain 2Y failure: loss of effect over time; possible due to decr B cell mass, decr lean body mass, incr ectopic fat depositionContraindicationsChlorproamide, glyburide: renal/hepatic insufficiency Metformin: renal failure, alcoholism, hepatic disase – incr risk of lactic acidosisDrug interactionsPregnancyExamples Agents in Bone Mineral Homeostasis Bisphosphonates: etidronate, pamidronate, alendronate, risedronate, tiluronate, ibandronate, zoledronate; decr formation and dissolution of hydroxyapatite crystals in skeletal system, inhibit bone resorption – exact mechanism unknown (also inhibit 1,25 formation, inhibit intestinal Ca transport, inhibit glycolysis, inhibit cell growth); give on empty stomach as food decr absorption; cause gastric irritation, renal problems; excreted unchanged in urine; CI: decr renal function, oesophageal motility disorder, PUD For hyperCa of malignancy (pamidronate 60-90mg IV infusion over 2-4hrs), pagets, OP Calcitonin: for hyperCa; can be given at high doses as non-toxic Gallium nitrate: for hyperCa; inhibits bone 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„˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()„ „˜ţĆ ^„ `„˜ţo()‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()„ „˜ţĆ ^„ `„˜ţo(.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ6o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ6o() „ „˜ţĆ ^„ `„˜ţ‡hˆH.„$ „˜ţĆ$ ^„$ `„˜ţo()€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.„$ „˜ţĆ$ ^„$ `„˜ţo()€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţCJOJQJo(ˇđ€„ „˜ţĆ ^„ `„˜ţCJOJQJo(o€„p„˜ţĆp^„p`„˜ţCJOJQJo(§đ€„@ „˜ţĆ@ ^„@ `„˜ţCJOJQJo(§đ€„„˜ţĆ^„`„˜ţCJOJQJo(§đ€„ŕ„˜ţĆŕ^„ŕ`„˜ţCJOJQJo(§đ€„°„˜ţĆ°^„°`„˜ţCJOJQJo(§đ€„€„˜ţĆ€^„€`„˜ţCJOJQJo(§đ€„P„˜ţĆP^„P`„˜ţCJOJQJo(§đ„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„„˜ţĆ^„`„˜ţo()€ „ě„˜ţĆě^„ě`„˜ţ‡hˆH.‚ „ź„L˙Ćź^„ź`„L˙‡hˆH.€ „Œ „˜ţĆŒ ^„Œ `„˜ţ‡hˆH.€ „\ „˜ţĆ\ ^„\ `„˜ţ‡hˆH.‚ „,„L˙Ć,^„,`„L˙‡hˆH.€ „ü„˜ţĆü^„ü`„˜ţ‡hˆH.€ „Ě„˜ţĆĚ^„Ě`„˜ţ‡hˆH.‚ „œ„L˙Ćœ^„œ`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH. „p„L˙Ćp^„p`„L˙‡hˆH. „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH. „„˜ţĆ^„`„˜ţ‡hˆH. „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH. „°„˜ţĆ°^„°`„˜ţ‡hˆH. „€„˜ţĆ€^„€`„˜ţ‡hˆH. „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ6o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ6o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„8„˜ţĆ8^„8`„˜ţo()€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „Ř „L˙ĆŘ ^„Ř `„L˙‡hˆH.€ „¨ „˜ţƨ ^„¨ `„˜ţ‡hˆH.€ „x„˜ţĆx^„x`„˜ţ‡hˆH.‚ „H„L˙ĆH^„H`„L˙‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.€ „č„˜ţĆč^„č`„˜ţ‡hˆH.‚ „¸„L˙Ƹ^„¸`„L˙‡hˆH.h„Đ„˜ţĆĐ^„Đ`„˜ţOJQJo(‡hˆHˇđh„ „˜ţĆ ^„ `„˜ţOJQJ^Jo(‡hˆHoh„p„˜ţĆp^„p`„˜ţOJQJo(‡hˆH§đh„@ „˜ţĆ@ ^„@ `„˜ţOJQJo(‡hˆHˇđh„„˜ţĆ^„`„˜ţOJQJ^Jo(‡hˆHoh„ŕ„˜ţĆŕ^„ŕ`„˜ţOJQJo(‡hˆH§đh„°„˜ţĆ°^„°`„˜ţOJQJo(‡hˆHˇđh„€„˜ţĆ€^„€`„˜ţOJQJ^Jo(‡hˆHoh„P„˜ţĆP^„P`„˜ţOJQJo(‡hˆH§đ„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţCJOJQJo(ˇđ€„ „˜ţĆ ^„ `„˜ţCJOJQJo(o€„p„˜ţĆp^„p`„˜ţCJOJQJo(§đ€„@ „˜ţĆ@ ^„@ `„˜ţCJOJQJo(§đ€„„˜ţĆ^„`„˜ţCJOJQJo(§đ€„ŕ„˜ţĆŕ^„ŕ`„˜ţCJOJQJo(§đ€„°„˜ţĆ°^„°`„˜ţCJOJQJo(§đ€„€„˜ţĆ€^„€`„˜ţCJOJQJo(§đ€„P„˜ţĆP^„P`„˜ţCJOJQJo(§đ„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„8„˜ţĆ8^„8`„˜ţo() „„˜ţĆ^„`„˜ţ‡hˆH.‚ „Ř „L˙ĆŘ ^„Ř `„L˙‡hˆH.€ „¨ „˜ţƨ ^„¨ `„˜ţ‡hˆH.€ „x„˜ţĆx^„x`„˜ţ‡hˆH.‚ „H„L˙ĆH^„H`„L˙‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.€ „č„˜ţĆč^„č`„˜ţ‡hˆH.‚ „¸„L˙Ƹ^„¸`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ5o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„8„˜ţĆ8^„8`„˜ţo()€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „Ř „L˙ĆŘ ^„Ř `„L˙‡hˆH.€ „¨ „˜ţƨ ^„¨ `„˜ţ‡hˆH.€ „x„˜ţĆx^„x`„˜ţ‡hˆH.‚ „H„L˙ĆH^„H`„L˙‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.€ „č„˜ţĆč^„č`„˜ţ‡hˆH.‚ „¸„L˙Ƹ^„¸`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()„ „˜ţĆ ^„ `„˜ţo()‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„h„˜ţĆh^„h`„˜ţo()€ „8„˜ţĆ8^„8`„˜ţ‡hˆH.‚ „„L˙Ć^„`„L˙‡hˆH.€ „Ř „˜ţĆŘ ^„Ř `„˜ţ‡hˆH.€ „¨ „˜ţƨ ^„¨ `„˜ţ‡hˆH.‚ „x„L˙Ćx^„x`„L˙‡hˆH.€ „H„˜ţĆH^„H`„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „č„L˙Ćč^„č`„L˙‡hˆH.„I„˜ţĆI^„I`„˜ţo()€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „é„L˙Ćé^„é`„L˙‡hˆH.€ „š „˜ţĆš ^„š `„˜ţ‡hˆH.€ „‰ „˜ţƉ ^„‰ `„˜ţ‡hˆH.‚ „Y„L˙ĆY^„Y`„L˙‡hˆH.€ „)„˜ţĆ)^„)`„˜ţ‡hˆH.€ „ů„˜ţĆů^„ů`„˜ţ‡hˆH.‚ „É„L˙ĆÉ^„É`„L˙‡hˆH.h„Đ„˜ţĆĐ^„Đ`„˜ţOJQJo(‡hˆHˇđh„ „˜ţĆ ^„ `„˜ţOJQJ^Jo(‡hˆHoh„p„˜ţĆp^„p`„˜ţOJQJo(‡hˆH§đh„@ „˜ţĆ@ ^„@ `„˜ţOJQJo(‡hˆHˇđh„„˜ţĆ^„`„˜ţOJQJ^Jo(‡hˆHoh„ŕ„˜ţĆŕ^„ŕ`„˜ţOJQJo(‡hˆH§đh„°„˜ţĆ°^„°`„˜ţOJQJo(‡hˆHˇđh„€„˜ţĆ€^„€`„˜ţOJQJ^Jo(‡hˆHoh„P„˜ţĆP^„P`„˜ţOJQJo(‡hˆH§đ„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţCJOJQJo(ˇđ€„ „˜ţĆ ^„ `„˜ţCJOJQJo(o€„p„˜ţĆp^„p`„˜ţCJOJQJo(§đ€„@ „˜ţĆ@ ^„@ `„˜ţCJOJQJo(§đ€„„˜ţĆ^„`„˜ţCJOJQJo(§đ€„ŕ„˜ţĆŕ^„ŕ`„˜ţCJOJQJo(§đ€„°„˜ţĆ°^„°`„˜ţCJOJQJo(§đ€„€„˜ţĆ€^„€`„˜ţCJOJQJo(§đ€„P„˜ţĆP^„P`„˜ţCJOJQJo(§đ„8„˜ţĆ8^„8`„˜ţo()€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „Ř „L˙ĆŘ ^„Ř `„L˙‡hˆH.€ „¨ „˜ţƨ ^„¨ `„˜ţ‡hˆH.€ „x„˜ţĆx^„x`„˜ţ‡hˆH.‚ „H„L˙ĆH^„H`„L˙‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.€ „č„˜ţĆč^„č`„˜ţ‡hˆH.‚ „¸„L˙Ƹ^„¸`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ6o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ5o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ6o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH. „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţCJOJQJo(ˇđ€„ „˜ţĆ ^„ `„˜ţCJOJQJo(o€„p„˜ţĆp^„p`„˜ţCJOJQJo(§đ€„@ „˜ţĆ@ ^„@ `„˜ţCJOJQJo(§đ€„„˜ţĆ^„`„˜ţCJOJQJo(§đ€„ŕ„˜ţĆŕ^„ŕ`„˜ţCJOJQJo(§đ€„°„˜ţĆ°^„°`„˜ţCJOJQJo(§đ€„€„˜ţĆ€^„€`„˜ţCJOJQJo(§đ€„P„˜ţĆP^„P`„˜ţCJOJQJo(§đ„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH. „p„L˙Ćp^„p`„L˙‡hˆH. „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH. „„˜ţĆ^„`„˜ţ‡hˆH. „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH. „°„˜ţĆ°^„°`„˜ţ‡hˆH. „€„˜ţĆ€^„€`„˜ţ‡hˆH. „P„L˙ĆP^„P`„L˙‡hˆH.h„Đ„˜ţĆĐ^„Đ`„˜ţOJQJo(‡hˆHˇđh„ „˜ţĆ ^„ `„˜ţOJQJ^Jo(‡hˆHoh„p„˜ţĆp^„p`„˜ţOJQJo(‡hˆH§đh„@ „˜ţĆ@ ^„@ `„˜ţOJQJo(‡hˆHˇđh„„˜ţĆ^„`„˜ţOJQJ^Jo(‡hˆHoh„ŕ„˜ţĆŕ^„ŕ`„˜ţOJQJo(‡hˆH§đh„°„˜ţĆ°^„°`„˜ţOJQJo(‡hˆHˇđh„€„˜ţĆ€^„€`„˜ţOJQJ^Jo(‡hˆHoh„P„˜ţĆP^„P`„˜ţOJQJo(‡hˆH§đ„Đ„˜ţĆĐ^„Đ`„˜ţ6o() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo() „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()„ „˜ţĆ ^„ `„˜ţo()‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.`/KŤ\8f4w7‹fj]Żr„zncG@ YH`˙pţ˜h$<ÍpĆţÂ^ =lRHię 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" # $ % & ' ( ) * + , - . / 0 1 2 3 4 5 6 7 8 9 : ; < = > ? @ A B C D E F G H I J K L M N O P Q R S T U V W X Y Z [ \ ] ^ _ ` a b c d e f g h i j k l m n o p q r s t u v w x y z { | } ~  €  ‚ ƒ „ … † ‡ ˆ ‰ Š ‹ Œ  Ž   ‘ ’ “ ” • – — ˜ ™ š › œ  ž Ÿ   Ą ˘ Ł ¤ Ľ Ś § ¨ Š Ş Ť Ź ­ Ž Ż ° ą ˛ ł ´ ľ ś ˇ ¸ š ş ť ź ˝ ž ż Ŕ Á Â Ă Ä Ĺ Ć Ç Č É Ę Ë Ě Í Î Ď Đ Ń Ň Ó Ô Ő Ö × Ř Ů Ú Ű Ü Ý Ţ ß ŕ á â ă ä ĺ ć ç č é ę ë ě í î ď đ ń ň ó ô ő ö ÷ ř ů ú ű ü ý ţ ˙                           ! " # $ % & ' ( ) * + , - . / 0 1 2 3 4 5 6 7 8 9 : ; < = > ? @ A B C D E F G H I J K L M N O P Q R S T U V W X Y Z [ \ ] ^ _ ` a b c d e f g h i j k l m n o p q r s t u v w x y z { | } ~  €  ‚ ƒ „ … † ‡ ˆ ‰ Š ‹ Œ  Ž   ‘ ’ “ ” • – — ˜ ™ š › œ  ž Ÿ   Ą ˘ Ł ¤ Ľ Ś § ¨ Š Ş Ť Ź ­ Ž Ż ° ą ˛ ł ´ ľ ś ˇ ¸ š ş ť ź ˝ ž ż Ŕ Á Â Ă Ä Ĺ Ć Ç Č É Ę Ë Ě Í Î Ď Đ Ń Ň Ó Ô Ő Ö × Ř Ů Ú Ű Ü Ý Ţ ß ŕ á â ă ä ĺ ć ç č é ę ë ě í î ď đ ń ň ó ô ő ö ÷ ř ů ú ű ü ý ţ ˙                           ! 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