ŠĻą”±į>ž’ VXž’’’QRSTU’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’ģ„Į‘a šæ•ŃjbjbA]A] (¼+?+?Ļ­-’’’’’’ˆĪĪĪĪĪĪĪtųŹųŹųŹ80Ėd”Ėtq .¤Ņ¤ŅŗŅŗŅŗŅŗŅŗŅŗŅ\ ^ ^ ^ ^ ^ ^ ,Ÿ RńrŠ ”ĪŗŅŗŅŗŅŗŅŗŅŠ 8šĪĪŗŅŗŅ+ 8š8š8šŗŅŗĪŗŅĪŗŅ\ 8šā”vžĪĪĪĪŗŅ\ 8š8šĪĪ8š˜Ņ lÄųŹtļÄ8š8š$A 0q 8šc8šc8š8šĪtt„ĘųŹttųŹDrug Names/ClassesUsed for:ParasympathomimeticsIndirect ACh R AgonistsReversibleCarbamates (Physostigmine)Indicated for glaucoma. Antidote for atropine poisoning.Quarternary Alcohol (edrophonium)Diagnose Myasthenia GravisHorny Goat WeedIndicated for erectile dysfunctionIrreversible (Organo- Phosphates)Insecticide (malathione)Insects…Nerve Gas (Sarin)Lethal. Use atropine as antidote.Direct ACh R AgonistsCarbacholIndicated for glaucomaBethanecholIndicated for urinary retention.PilocarpineIndicated for GlaucomaParasympatholyticsmACh R BlockersAtropineCauses pupil dilation, increases HR (indicated for bradycardia), reduces bronchosecretion (for surgery) Antidote for organophosphate poisoning.ScopolamineIndicated for motion sickness; antiemetic drug delivered transdermallyPirenzipineIndicated for peptic ulcers; selectively blocks M1 Receptors, reduces gastric acid secretionnACh R BlocerksNon- DepolarizingTubocuraraine Poison; respiratory paralysis. Muscle relaxant. Competitive antagonistsPancuronium AtracuriumMuscle relaxants; competitive antagonistsDepolarizingSuccinylcholine/ SuxamethoniumMuscle relaxants nACh R agonists, but has parasympatholytic effect Cholinergic System Direct Parasympathomimetics – drugs that mimic ACh and mostly binds mAChR Indirect Parasympathomimetics – drugs that inhibit ACh-Esterase; raises [ACh] Muscarinic Parasympatholytics – competitive antagonists Nicotinic Parasympatholytics – neuromuscular junction blockers; muscle relaxants Non-Depolarizing – competitive antagonists; competes with ACh to prevent depolarization Depolarizing – nACh R agonist; initially mimics ACh causing depolarization but it is not hydrolyzed by ACh-Esterase so the depolarization is prolonged, inhibiting other signals Nicotine Low Concentration – acts as a direct nAChR agonist High Concentration – has an antagonistic effect on nAChR due to channel inactivation; similar to succinylcholine. nAChR = nicotinic acetylcholine receptor mAChR = muscarinic acetylcholine receptor Adrenergic System Drug Name/ClassUsed For:SympathomimeticsIndirect AgonistsMAO Inhibitors (Tranylcypromine, Moclobemide)Indicated for depression; inhibits metabolism of NE/E, DA, and 5HT; many side effectsEphedrineFound in diet pills; displaces NE from storage vesiclesAmphetamines Ritalin ( ADD Fenfluramine ( diet pillsDisplaces NE from storage, inhibits reuptake, inhibits MAODirect AgonistsNon-selectiveEpinephrine(Adrenaline)Indicated for anaphylactic shock and used as an adjuvant in local anesthetics. Dilates bronchii.Norepinephrine (Noradrenaline)Limited clinical use.Selective±1 Agonists (vasoconstrictor) Methoxamine  treats hypotension Phenylephrine  nasal decongestant Naphazoline  nasal decongestant±2 Agonists (sympatholytic!) Clonidine GuanfacineIndicated for hypertension. Presynaptic ±2 receptors are inhibitory, reduces sympathetic tone on cardiovascular system.²1 Agonists Dobutamine(+) inotropic & (+) chronotropic effect on heart Used in Dobutamine Stress Test²2 Agonists AlbuterolIndicated for asthma (inhaler). Dilates bronchiiSympatholytics±-receptor antagonistsNon-selective Blockers PhentolamineIndicated for pheocromocytoma. Blocking ±1 causes vasodilation; reducing BP Blocking ±2 removes inhibition, increasing NE action on ² receptors ( increasing HR and cardiac output Selective ±1 Blocker Prazosin, Terazosin, etc& Indicated for hypertension and urinary retention. Side effects: Reflex tachycardia and postural hypotension.Selective ±2 Blocker (sympathomimetic!) YohimibineIncreases sympathetic outpout. Used for male sexual dysfunction and as a weight loss drug.²-receptor antagonistsNoncardioselective ² blockers Propranolol-1st gen. drug, cross reaction w/ ²2 causes bronchoconstriction (side effect) -Labetalol also blocks ±1 receptors (strong antihypertensive drug) -same indications as cardioselective blockers (below)Cardioselective ² blockers Metoprolol, Atenolol& Newer drugs are more ²1 selective. Indicated for angina pectoris, hypertension, cardiac dysrhythmias, myocardial infarction, heart failure, and stage fright (anxiolytic). Drug/ClassMechanismSympathetic Nervous System Suppressors (sympatholytics)±2 Receptor Agonists - ClonidineElicits ±2 receptor s inhibitory effect on the sympathetic nervous system. Less NE binding to ±1 and ²1 receptors. ±1 Receptor Antagonists Prazosin, Terazosin, etc& Promotes peripheral vasodilation, reducing resistance, thereby reducing BP.²-receptor antagonists Propranolol, Metoprolol, Atenolol, etc²1 receptor activation causes an increase in HR and contractility. Blocking this receptor will reduce the HR and contractility (reduces stroke volume) leading to a drop in blood pressure.Direct Vasodilators Calcium channel blockers (Calcium antagonists) Dihydropyridines -Nifedipine, etc…Targets L-Type channels (no cardiac effects), blocking Ca2+ entry into the smooth muscle cell ( arterial vasodilation; decreases afterload ( reducing BP Side effects: Reflex tachycardia, postural hypotension, and peripheral edema.Potassium Channel Agonists MinoxidilIncreases membrane permeability to K+, K+ efflux causes membrane hyperpolarization, inhibiting voltage gated Ca2+ channels ( relaxation of smooth muscles ( vasodilation ( reduces BP Side effect: hair growth, marketed as Rogaine Last resort for unresponsive hypertension.NitroprussideDelivered thru iv only and is metabolized into NO which directly activates cGMP production ( vasodilation Review phosphodiesterase inhibitors (Caffeine & Viagra).Renin-Angiotensin-Aldosterone System Targeting DrugsACE-Inhibitors Captopril Enalapril Benazepril LisinoprilBy inhibiting the ACE enzyme, angiotensin I cannot be converted into the active peptide (ATII) -no aldosterone & ADH release ( no fluid retention -no sympathomimetic effects -no vasoconstriction Side effect – causes coughingAngiotensin II (ATII) Receptor Blocker -Losartan -Candesartan -etc…Inhibits the effect of AT II by blocking the receptor -usually used if patient cannot tolerate the cough caused by ACE inhibitorsAntihypertensive Drugs Other Cardiovascular Diseases Angina Pectoris – chest pain due to coronary heart disease; a symptom of myocardial ischemia (when heart doesn t get enough oxygen)Stable AnginaPredictable episodes; usually during/after physical exertion or stress Treatment: Nitrates & ²-Blockers (Propranolol, etc.)Unstable AnginaChest pain unexpected and usually occurs at rest Treatment: NitratesVariant AnginaChest pain almost always occurs at rest and does not follow physical exertion or stress. Due to coronary artery spasm. Treatment: Calcium channel blockers (Nifedipine, etc…)Nitrates Converted to nitric oxide (NO) ( guanylate cyclase ( cGMP ( smooth muscle relaxation ( vasodilationNitratesNitroglycerineDrug of choice for angina pectoris. Reduces cardiac workload (and its oxygen demand) by reducing venous return. Causes vasodilation primarily in veins. Many different forms of administration. Do NOT combine w/ other vasodilators (Viagra…).Isosorbide-dinitrate (ISDN)Longer lasting effect when compared to nitroglycerine. Tolerance may occur, give lowest dose. Do NOT combine w/ other vasodilators.NitroprussidePromotes peripheral vasodilation. IV only; rapid onset and short duration – allows for titration Cardiac Arrhythmias – abnormal rhythms of the heart that cause it to pump less effectively; abnormality in pacemaker cells, conduction pathway, or if other parts of the heart take over pacemaker.Class I: Sodium Channel BlockersSlows depolarization phase of AP. Procainamide – used for atrial & ventricular arrhythmias Lidocaine – used for acute ventricular arrhythmias Flecainide – used for chronic treatment of ventricular arrhythmiasClass II: ²-BlockersPropranolol -used for tachycardiaClass III: Potassium Channel BlockersProlongs repolarization by blocking potassium efflux. Bretylium & Amiodarone -used for intractable ventricular arrhythmiasClass IV: Calcium Channel BlockersProlongs repolarization by blocking calcium influx Verapamil – blocks both L & T Type calcium channels! Blocking T Type channels ( slows conduction (Blocking L Type channels ( coronary + arterial vasodilation) OthersAdenosine – for paroxysmal supraventricular tachycardia Digoxin – atrial fibrillation Epinephrine - bradycardia Other Cardiovascular Diseases Congestive Heart Failure – inadequate contractility; ventricles unable to expel blood ( rise in venous blood pressure. Caused by blocked coronary arteries, viral infections, hypertension, leaky heart vavles, myocardial infarctions… -Right sided failure – lower limb edema -Left sided failure – pulmonary edema & respiratory distressCardiac Glycosides (Digoxin)Slows heart rate and increases contractility. Mechanism: Inhibits Na/K ATPase, leading to an increase intracellular Na+ Increased Na+ slows Na/Ca exchanger, leading to an increase intracellular Ca++ Low therapeutic index. Potassium competes with digoxin in binding to Na/K ATPase -antidote for cardiac glycoside poisoning -increased potassium will reduce potency of digoxinACE inhibitors & ATII antagonistsCaptopril & Losartan (review RAAS) Effectively reducing cardiac workload (inhibits vasoconstriction, inhibits sodium/fluid retention, inhibits NE release…)VasodilatorsNitrates: Nitroglycerine, etc. (review Nitrates notes)DiureticsLoop Diuretics: Furosemide Thiazides: Hydrocholorothiazide K+ Sparring: Spironolactone  Diuretics Diuretics – increases urine output; indicated for hypertension & edema (except CA inhibitors) DrugsMechanismCarbonic Anhydrase Inhibitors Azetazolamide DorzolamideInhibits conversion of CO2 ( (H+) + (HCO3-); effectively blocking reabsorption of Na+ -primarily indicated for Glaucoma! Causes metabolic acidosis (lower HCO3-).Loop Diuretics (high ceiling) Furosemide TorasemideInhibits Na+/K+/2Cl- symporter @ ascending limb in the Loop of Henle; effectively blocking Na, K, Cl reabsorption -most potent diuretic -for severe/moderate hypertension & edema Causes hypokalemia Thiazide Diuretics Hydrochlorothiazide BenzthiazideInhibits Na+/Cl- symporter @ distal convoluted tube -for moderate hypertension & heart failure (edema) Causes hypokalemiaPotassium-Sparring Diuretics Spironolactone Amiloride Acts as distal portion of distal tube; enhances Na excretion & reduces K excretion (K sparring) Spironolactone – aldosterone receptor antagonist (slow) Amiloride – directly blocks Na/K channel (fast) Used in combo w/ other diurecticsOsmotic Diuretics Mannitol (iv only)Non-reabsorbable molecules that inhibit passive reabsorption of water (promoting water excretion w/ little Na excretion) -cannot cross blood-brain barrier; so water goes from brain to blood Used to reduce intracranial pressureMajor side effects of diuretics (except K-sparing) -Mainly Hypokalemia (loss of potassium) & hyponatremia & hypochloremia as well (may give extra potassium orally/iv) -Hypotension & dehydration Interaction w/ Cardiac Glycosides (digoxin) -cardiac glycosides are Na/K ATPase inhibitors as a competitive K antagonist -Hypokalemia secondary to diuresis increases digoxin potency -digoxin has a narrow therapeutic index; this may cause it to become toxic Uricosuric Agents Indicated for kidney stones and gouts. @ therapeutic dose: promotes excretion and inhibits reabsorption of uric acid @ sub-therapeutic dose: inhibits both excretion and reabsorption -possibly increase uric acid concentration Probenecid -strongly inhibits penicillin excretion!! May be beneficial when trying to elevate antibiotic plasma concentration Gastrointestinal Pharmacology AntacidsWeak Bases Tums, PeptoBismol, etc..Neutralizes stomach acid. Magnesium Hydroxide – causes diarrhea Aluminum hydroxide – causes constipation These are often combinedH2 Receptor Blockers Cimetidine Ranitidine-competitively inhibits binding of histamine to H2 receptors on parietal cells; thus reducing histamine stimulated gastric acid production (there are other signals that may stimulate acid production)Proton Pump Inhibitors Omeprazole Lansoprazole-irreversible inhibition of H+/K+ ATPase in parietal cells -only active at low pH (activity restricted to stomach) -inhibits acid production for 1-2days Note: prevents acid replenishment; does not neutralize acid already in the stomach (GERD is primarily treated w/ PPIs)Mucosal Protective Agents Misoprostol SucralfateMisoprostol – PGE analog; stimulates mucus and HCO3 production; used w/ NSAIDS Sucralfate – stabilizes mucus to inhibit H+ diffusion -not absorbedAntiemetic DrugsH1 Antagonists Diphenhydramine, Meclizine, etc Blocks H1 (histamine) receptors competitively.Muscarinic Receptor AntagonistsScopolamine (anticholernergic)BenzodiazepinesLorazempam; potentiates effects of GABA in CNSD2 (dopamine) Antagonists Metoclopramide Domperidone Competitively blocks C2 receptors in the CTZ Also increases gastric emptying Contraindicated in patients w/ Parkinson’s diseaseCannabinoids (marijuana)Synthetic cannabinoids: Nabilone & Dronabinol -acts as an agonists at cannabinoid receptors in the CNSPeptic Ulcers – ulcer formation in the stomach/duodenum due to insufficient mucus and/or bicarbonate and/or increased acid production (autodigestion of stomach/duodenal wall)Causes: H. pylori (majority) – breaks down mucus and triggers inflammation NSAIDS – inhibits PGE (needed for mucus/HCO3 production) Smoking – stimulates gastric acid production Treatment of H. pylori infection and peptic ulcer: Use a combo of antibiotics and PPI (or other mucosal protectant/enhancers & antacids) Antibiotics: Bismuth/Amoxicillin – disrupts cell wall Clarithromycin/Tetracyclin – inhibits protein synthesis Metronidazole – secondary agent, used when resistance develops or other agents are intolerated Gastrointestinal Pharmacology LaxativesBulk Laxatives – increases bowel content volume triggering stretch receptors causing reflex peristalsisBulkCarbohydrate Based -Vegetable Fibers -Bran (husk)-insoluble/non-absorbable -expands with water May cause constipation if not enough water.Osmotically Active -Epsom salt -Glauber’s salt-partially soluble/non-absrobable -potent and fast actingIrritant Laxatives – irritates enteric mucosa causing an increase secretion of water softening bowel content (stool); increased volume also triggers reflex peristalsisIrritantsRicinoleic acid (Castor Oil) -castor oil converted to ricinoleic acid -works in the small intestineAnthraquinones Diphenolmethanes Bisacodyl Sodium picosulfate-works in the large intestineLaxative Abuse: longer interval needed to refill colon, leads to constipation Loss of water/salts in gut leads to aldosterone release; causes excretion of K+ Hypokalemia reduces peristalsisAnti-diarrhealMuscarinic receptor antagonists and opiates can cause constipation but are not useful for treating diarrhea because of its effect on other parts of the body.Loperamide (Imodium)-opiod derivative that selectively acts in the GI tract (w/ no CNS activity). -directly acts on the intestinal muscles reducing motility -this increases water and electrolyte reabsorption Dimethicone – anti-gas agent that is often combined with anti-diarrheal drugs  Metabolic Disorders (Diabetes Mellitus) At low blood glucose levels (hypoglycemia); the body will increase blood glucose by: -Glucagon (secreted by ± pancreatic cells) promotes glycogenolysis & gluconeogenesis& -epinephrine also released by adrenal medulla ²-blockers will mask symptoms of hypoglycemic shock -cortisol (anti-insulin effects) is also released by the hypothalamus extended use of steroidal drugs may induce diabetes At high blood glucose levels (hyperglycemia); the body will decrease blood glucose by: -Insulin (secreted by ²- pancreatic cells) promotes glucose uptake & glycolysis & glycogenesis& Diabetes Mellitus Type 1 Diabetes  autoimmune disease; destruction of ² pancreatic cells Treatment requires exogenous insulin replacement to control hyperglycemia Type 2 Diabetes  hyperglycemia resulting from insulin resistance at target tissue or reduced insulin production by ² pancreatic cells Various levels of defect leading to resistance (receptor, signaling pathway, enzymes, glucose transporter& ) Treatment with exogenous insulin replacement or oral hypoglycemic agents Insulin TherapyRegular Insulin-unmodified; short acting -only insulin that can be administered thru ivInsulin Lispro (Humalog) -rapid onset (fastest) & short acting -used before a mealInsulin Lente (sc injection only)-insulin + zinc ( micro-precipitates (delayed absorption) -long lasting (UltraLente = longest lasting)NPH Insulin-insulin + protamine (delayed absorption -long lastingInsulin Glargine (Lantus)-synthetic insulin that is soluble at low pH, but becomes insoluble and forms precipitates at neutral pH after sc administration -long lasting (similar to Lente)Oral Hypoglycemic Agents (For Type II only)Sulfonylureas -Tolbutamide (1st gen.) -Glimepiridide -Glipizide Stimulates insulin release; useful for diabetes caused by low insulin levels where ²- pancreatic cells are still presentGlitazones -Rosiglitazone -Pioglitazone-Increases insulin sensitivity at target cells -Acts as a nuclear hormone receptor (PPAR³ agonist) increasing transcription of insulin receptor signaling components and glucose transportersBiguanides -Metformin-unknown mechanism -increase glucose uptake & inhibits gluconeogenesis -lowers LDL + VLDL (bad cholesterol) -suppresses appetite -no hypoglycemic effectsInsulin and oral hypoglycemic agents may cause hypoglycemia (except Metformin) Metabolic Disorders (Hyperlipidemia) “Statins” Lovastatin Atorvastatin (Lipitor)-Reversible HMG-CoA Reductase inhibitors. HMG-CoA reductase is the rate-limiting enzyme in the production of cholesterol. Inhibition effectively reduces de novo synthesis of cholesterol precursors. -Lower cholesterol levels upregulates LDL receptors in liver removing LDL from the bloodstream.Fibrates -Clofibrate -BenzafibratePPAR± agonists  stimulates ²-oxidation of fatty acids Promotes lipoprotein lipase activity Lowers VLDL (minor effect on LDL) Increases HDL levels Resins -Cholestyramine -ColestipolBile acid binding resins prevents reabsorption of bile acids in enterohepatic circulation. -The liver responds to this loss of bile acid by increasing cholesterol synthesis to make more bile acid (plasma cholesterol levels remain unchanged). -The liver will also upregulate LDL receptors to increase hepatic uptake of LDL (reducing plasma LDL). Resins are not absorbed into the blood. Steroid Drugs Corticosteriods (GC)  inhibits all phases of inflammation -inhibits NFŗB (a transcription regulator of proinflammatory mediators -upregulates lipocortin (lipocortin inhibits PLA2 ; no PT or LT synthesis) -promotes fetal lung development by increasing surfactantSide Effects-immune suppression -anti-insulin effects -“steroid diabetes” -increased glucose promotes lipogenesis (fat) -increased catabolism (muscle atrophy) -salt/water retention due to cross reactivity with mineralcorticoid (aldosterone) receptors -osteoporosis Prolonged use of GC therapy causes adrenal cortex atrophy, so it is important to phase out slowly to avoid flare ups due to cortisol insufficiency.Addison’s DiseaseAdrenal cortex failure – low cortisol levels -hypotension -weight loss -fatigue -abnormal glucose levels -inability to cope with stress -blotchy colored skin; w/o cortisol, corticotropin is unregulated and it increases melatonin (skin pigmentation)Cushing’s SyndromeAdrenal cortex tumor – high cortisol levels (symptoms similar to GC therapy) -hypertension -weight gain (upper body obesity, “buffalo hump”) -water retention -poor wound healingHydrocortison-equivalent to endogenous cortisol -indicated for adrenal insufficiency (Addison’s Disease) -mostly for topical application -cross-stimulation with mineralcorticoid receptors -have Na retaining effectsPrednisonePro-drug; converted to active form (prednisolone) PrednisoloneDrug of choice for systemic administration -lower Na retaining effectsTriamcinoloneStronger anti-inflammatory effect, 5x more potent than cortisol -no Na retaining effectsHalogenated GC (Betamethasone)30x more potent than cortisol -no Na or water retaining effects Steroid Drugs Female Sex SteriodsEstrogensEstradiolPrimary endogenous estrogen responsible for: -breast development -improving bone density -increase HDL -promotes uterus growth & supports endometrium development Rapidly metabolized by the liver and therefore not suitable as an oral drugEthinylestradiolStable derivative of estradiol Usually found as the estrogen component of birth control pillsMestranolOral contraceptive Similar to ethinylestradiol with an extra methyl group; prodrug -cleavage of the methyl group yields ethinylestradiolSelective Estrogen Receptor ModifierRaloxifene Indicated for postmenopausal osteoporosis SERM = selective estrogen receptor modifier -anti-estrogenic effect on breast and endometrium -reduces stimulation in these tissues to avoid tumorgenesis -estrogenic effect on bone and lipid metabolismTamoxifene (antiestrogen)Indicated for breast cancer -anti-estrogenic effect on breast tissue -weak effect on bone and lipid metabolismClomiphene (antiestrogen)Indicated for infertility -selectively inhibits estrogen binding in pituitary, effectively removing negative feedback -this causes an increase in LH ( ovulationProgesteroneRapidly metabolized by the liver Stable derivatives: Hydroxy/medroxy progesterone Testosterone derivatives: norethindrone norgestrel Progesterone is important for the formation of secretory endometrium and the establishment of pregnancy.Mifepristone (RU486) (anti-progesterone)Induce medical abortions (<49days) Combine w/ PG analogue (Misoprostol) to increase uterine contraction Steroid Drugs Male Sex Steroids/Others AndrogensTestosteroneResponsible for both anabolic and androgenic effects Rapidly metabolized by the liver. -ester derivatives increases its half-lifeNandrolone (banned)Strong anabolic effects. Injection only.Stanozolol (banned)Strong anabolic effects. (Not a ² blocker despite  -olol ending) Oral.DHEADehydroepiandrosterone. Marketed as an anabolic steroid. This is misleading because it s a precursor for both testosterone and estrogen. High levels of DHEA may lead to elevated levels of testosterone as well as estrogen.Anti-AndrogensFlutamideIndicated for prostate cancer Competitive androgen receptor antagonist -blocks testosterone’s stimulating effectsFinasterideIndicated for prostate gland enlargement and baldness -blocks the conversion of testosterone to DHT -DHT is a testosterone metabolite that is much more potent Note: bald men have elevated levels of DHTGnRH Modifiers/AnalogusDanazolIndicated for endometriosis (growth of endometrium outside of the uterus) Inhibits GnRH release (no LH/FSH production) and consequently no steroid productionSynthetic GnRH -Gonadorelin -BuserelinGiven in pulses (s.c.) ( induced ovulation (stimulates LH/FSH) Given continuously ( medical castration (desensitize GnRH receptors)  Steroid Drugs “Oral Contraceptives” General Mechanism-Estrogen inhibits FSH; suppressing follicle development -Progesterone inhibits LH; inhibiting ovulation & increases mucus viscosity (prevents sperm penetration) -Both steroids alter endometrium, preventing implantationCombination PillsHighly effective Estrogen component: Ethinylestradiol Progesterone component: varies 29 day cycle (includes 7 day break to induce withdrawal bleeding) Biphasic preparation – includes progesterone break after 7 day break Monophasic preparation – no progesterone break (but [progesterone] varies through-out cycle)Mini PillLess reliable than combination pills Contains only progesterone (used when estrogen is contraindicated) Contraception mechanism relies mainly on increased mucus viscosity. -mucolytic agents (usually found in cough medications) may cause contraception failureMorning After Pill -LevonorgestrelHigh dose of progesterone Must be taken within 72 hours.Oral contraception failures: 1. Mucolytic agents 2. Barbituates. Barbituates or other P450 inducing drugs may cause failure because steroids are metabolized by P450 enzymes 3. Diarrhea or laxatives. Due to poor absorption of the drug. Allergy Drugs Allergy Mediators Allergen ( activates mast cells 1. Mast cell degranulation. Rapid release of histamine and other inflammatory agents 2. Activation of PLA2; producing leukotrienes and prostaglandins. Late stage response. 3. Stimulates cytokine transcription. Late stage inflammatory response. Review histamine and leukotriene actions (receptor specific) from lecture slides. H1 Recptor Antagonists1st Generation Drugs (Sedating)EthanolaminesDephenhydramine (Benadryl)Indicated for seasonal and skin allergies Dimenhydrinate (Dramamine)Used as an anti-emetic (for motion sickness) Also blocks mAChRs.Doxyamine (Nyquil)Most potent OTC sedative (better than barbiturates) Same efficacy as diphenhydramine in terms of anti-allergies.Chlorpheniramine Anti-allergy Anti-depressant (also blocks serotonin re-uptake) (Alklyamines)Piperazines Meclizine (Dramamine II)Anti-emetic (but less drowsy)Hydroxyzine (Atarax)Pro-Drug, anti-allergy effect from metabolite Certirizine2nd Gen. (Non-Sedating)Certirizine (Zyrtec)Hydroxyzine metabolite. (also a Piperazine)PiperidinesLoratadine (Claritin)No drowsiness. Active metabolite = desloratadineDesloratadine (Clarinex)Long half-lifeFexofenadine (Allegra)Highly selective for H1-receptorMast Cell Stabilizers -Cromolyn -NedcromilOnly preventative; acts by preventing mediator release from mast cells. Useless if histamine or other mediators are already released. Prophylactic agent for asthma and other allergy symptomsLeukotriene Receptor Blockers -Montelukast (Singulair)Prevents exercise and aspirin-induced asthma Antagonist of LTD4 at cysteinyl LT receptor5-Lipoxygenase Inhibitor -Zileuton (Zyflo)Prevents production of all leukotrienes Not useful for treatment of attacks. CNS Drugs Hypnotics/Anxiolytics Barbiturates -phenobarbital (long acting) -thiopental (short acting)General inhibition of the CNS w/ sedative-hypnotic actions. Mechanism: Augments GABA responses (by potentiating GABA signal) and mimics GABA (by opening Cl-channels in the absence of GABA). Keeps Cl channels open longer, hyperpolarizing the cell preventing further excitation. Also blocks excitatory glutamate receptors. Indications: -epilepsy (phenobarbital) and anesthesia induction (thiopental) (not a first line drug due to many side effects) Side effects/Risks -high risk of dependence (severe/lethal withdrawal symptoms) -may lead to cardio-respiratory depression -potent inducers of P450 enzymes; drug interactions (contraceptives, etc.)Benzodiazepines -Diazepam (Valium) -Lorazepam - Alprazolam - MidazolamMechanism: Benzodiazepines enhance the effects of GABA by increasing GABA affinity for the GABA receptor (by selectively binding to benzodiazepine receptors which are coupled to the GABA receptors). While barbiturates increase the length of time Cl channels stay open, benzodiazepines increases the frequency of GABA binding (opening of Cl channels). Indications: Anxiolytic, anticonvulsant (anti-epilepsy), anesthesia induction, etc… -all forms of anxieties -epilepsy (Clonazepam) -depression (Alprazolam) -anesthesia induction (Midazolam) Side effects/Risks: -anterogade amnesia (date rape drug) -much fewer side effects than barbituratesBoth barbiturates and benzodiazepines have an inhibitory effect on the CNS by modulating GABA signals (hyperpolarizing cells to prevent further excitation). While both classes of drugs enhance GABA signals, barbiturates can also open Cl channels even in the absence of GABA. CNS Drugs Antidepressants “Amine hypothesis of depression” – functional decrease in NE or serotonin causes depression (over-simplified…) MAO Inhibitors -TranylcypramineMechanism: Inhibits the metabolism of serotonin (as well as NE/E and dopamine); effectively increasing serotonin levels. Side Effects: -may cause fatal hypertension (due to increase sympathetic input (NE)) -Food-Drug interaction: “cheese-reaction” Increased levels of tyramine which is usually metabolized by MAO may displace NE from storage vesicles, further increasing NE signals ( hypertensive crisis Only used if resistant to all other treatments.Tricyclic Antidepressants (TCAs) -Imipramine -AmitriptylineMechanism: Prevents reuptake of NE and serotonin into pre-synaptic terminal thereby potentiating the effect of the neurotransmitters at the post-synaptic neurons. Side Effects -sedation (also binds H1 receptors) -strong interaction with alcoholSelective Serotonin Reuptake Inhibitors (SSRIs) -Fluoxetine (Prozac) -Paroxetine (Paxil) -Sertraline (Zoloft)Mechanism: Specifically prevents serotonin reuptake thereby potentiating its effect on post-synaptic neurons Same efficacy as TCAs but fewer side effects possibly due to its specificity for serotonin Side Effects -rare: may cause violence and aggression -inhibits sexual climaxThese antidepressants produce a functional increase in serotonin levels in the CNS. Supports the “amine hypothesis of depression.” CNS Drugs Neuroleptics (anti-psychotics) “Dopamine hypothesis of schizophrenia” – functional increase in CNS dopamine causes schizophrenia. Serotonin may also be involved in modulating dopamine responses. (over-simplified) Typical/Classical Neuroleptics Phenothiazines -Chlorpromazine Butyrophenones -haloperidol Mechanism: Blocks D2 receptors on post-synaptic neuron preventing receptor activation by dopamine. Side Effects Extrapyramidal Effects: Due to dopamine blockage in striatum -Acute dystonia: motor impairment (around face, neck); -immediate onset, reversible -Akatheisa: “pseudo-Parkinsonism,” tremor/rigidity -occurs days/months after treatment, reversible -Tardive Dyskinesia: involuntary movements of most body parts -occurs after extended treatment; irreversible -Sedation (blocks H1 receptor) -Dry mouth, constipation, and urinary retention -blocks mACh receptors and ±-adrenergic receptors -lactation (dopamine is needed to inhibit prolactin) -strong interaction with alcoholAtypical Neruoleptics Clozapine Olanzapine RisperidoneMechanism: Blocks both dopamine and serotonin receptors preventing receptor activation by dopamine and serotonin. Acts more specifically in the limbic system (fewer extrapyramidal effects) Clozapine – causes agranulocytosis (decrease in white blood cells) Note: Cocaine and amphetamines both causes an increase in dopamine levels in the CNS, which mimics schizophrenia symptoms. CNS Drugs Parkinson’s Disease Pathology -Loss of dopaminergic suppression of excitatory cholinergic neurons in the striatum -Cholinergic neurons causes an increase in GABA output suppressing the thalamus which reduces signaling to the motor cortex…causing movement disorder Refer to lecture slide. Dopamine ReplacementL-Dopa & CarbidopaL-Dopa – dopamine precursor that can cross the blood brain barrier (dopamine cannot cross the blood brain barrier) -L-Dopa can be converted to dopamine in the periphery leading to many side effects… Combine with Carbidopa! Carbidopa – dopamine decarboxylase inhibitor -Since it cannot cross the blood brain barrier, it exerts its effect in the periphery by inhibiting the conversion of L-dopa to dopamine -this means more L-dopa will reach the CNSDopamine AgonistBromocriptineActions similar to L-Dopa. Potent agonist of D2 receptor. (suppresses prolactin; was used to treat galactorrhoea) SelegilineIndirect agonist. Specifically inhibits MAO-B in the CNS, extending dopamine’s half-life. MAO-B is responsible for the metabolism of dopamine.AtropineMuscarinic acetylcholine receptor antagonist. Reduces cholinergic signals in the CNS which is responsible for stimulating GABA output suppressing the thalamus. No longer used for Parkinson’s disease.Antipsychotics used to treat schizophrenia may induce symptoms similar to Parkinson’s disease due to its dopamine lowering effect. CNS Drugs Epilepsy (seizures) Pathology Excessive excitability of neurons in the CNS, causing seizures Enhancement of GABA: Augment inhibitory effect of GABA to counter excessive excitation. Only useful for generalized and partial convulsive disorders (not for absence seizures)Carbamazepine (benzodiazepine)Increases Cl- influx in response to GABA, counteracts depolarization, (elevating seizure threshold.)TiagabinPrevents GABA reuptake.Phenytoin Mechanism: Blocks voltage gated Na channels that are in the inactivated state, preferentially blocks high frequency discharges. “use-dependent inhibition” (does not elevate seizure threshold, but rather, limits the propagation and spread of seizure.) -eliminated by 0th order kinetics -Indicated for convulsive seizures, not absence seizures Side Effect: hyperplasia (gum enlargement)EthosuximideMechanism: Blocks T-type calcium channels; (elevates seizure threshold thru depression of nerve transmission) -good for absence seizuresValproateMechanism: unknown; thought to be GABA-mediated -useful for both convulsive and absence seizures Side Effects -hepatotoxicity -teratogenicStrychnine – a toxin that induces strong convulsions by blocking Glycine receptors -Glycine is an inhibitor NT that is similar to GABA -Glycine also binds NMDA receptor as a co-activator (with Glutamate) where it has excitatory functions (not strychnine sensitive) Antedotes: anticonvulsants (benzodiazepines) and muscle relaxants (nACh R blockers) Alcoholism Review lecture slides on effects of alcohol. Disulfuram – inhibits aldehyde dehydrogenase; leading to acetylaldehyde accumulation causing “hang-over” -also blocks the conversion of dopamine to NE, rise in dopamine levels causes schizophrenic symptoms Naltrexone – opiod receptor antagonist; inhibiting the reward response that normally results for alcohol consumption Pain Killers General Anesthesia -unconciousness, analgesia, amnesia, and muscle relaxation -induced by intravenous anesthetics and maintained by inhalation anesthetics -inhalation anesthetics are generally removed simply by exhalation of unchanged gas Intravenous Anesthetics Thiopental (barbiturate)Rapid onset with high lipid solubility (accumulates in fat); slow recovery Narrow therapeutic range No analgesic effectPropofolRapidly metabolized for quick recovery. Used for same-day surgeryKetaminePhencyclidine (PCP) analogue; may cause hallucinations during recovery Have both anesthetic and analgesic properties -often used in veterinarian medicine and in tranqulizersMidazolamBenzodiazepine. Very short-acting. Have all benzodiazepine properties, often used for anesthesia inductionInhalation AnestheticsSpeed and Potency Solubility in blood – speed of onset is inversely correlated w/ degree of solubility in blood -blood acts as a drug reservoir (need to saturate the blood first, to achieve effect) -more soluble = slower onset Solubility in lipid – potency is directly correlated w/ lipid solubility -more lipophillic = more potentEtherObsolete. Slow onset and recovery.Nitrous OxideLow potency (must be combined with other agents to achieve anesthesia) Rapid induction and recovery Have both anesthetic and analgesic properties.HaloethanesHigh potency anesthetic; combined w/ N2O No analgesic properties. Some hepatic metabolism occurs; repeated use causes hepatoxicity Also causes hypotension (thru vasodilation and cardiac suppression)-Enfluran -Isofluran -DesfluranHigh potency anesthetic; similar to haloethanes Fewer side effects because less metabolized by liver.Example1. Pre-medication-Diazepam (anxiolytic, benzodiazepam) -Fantanyl (analgesis, opiod) -Atropine (autonomic stabilization, mACh R blocker)2. Anesthesia Induction-Midazolam (benzodiazepine) or Thiopental (barbiturate) -Succinylcholine (muscle relaxant, nACh R blocker)3. Anesthesia Maintenance-Haloethane (anesthesia) -Nitrous Oxide (analgesia & anesthesia) -Pancuronium (muscle relaxant, nACh R blocker)4. Recovery-Neostygmine (reversing neuromuscular block) ACh R agonist) Pain Killers Opioid Analgesics Analgesic Mechanisms 1. Spinal Analgesia – Activation of pre-synaptic opioid receptors decreases Substance P release -Decreasing pain signal transmission from nocireceptors 2. Supraspinal Analgesia – Activation of post-synaptic opioid receptors causes hyperpolarization -Inhibition of neurons in the pain pathway MorphineCNS – sedation, nausea, and cough suppression Respiratory System – reducing frequency and depth of breathing GI Tract – increases segmentation and decreases peristalsis (constipation) Eyes – papillary constriction (due to parasympathetic activation) Withdrawal symptoms -autonomic hyperactivity due to tolerance (elevated levels of cAMP in response to adenylyl cyclase upregulation) -diarrhea, vomiting, pain, etc…CodeinePro-drug, that is converted into morphine by CYP2D6. -CYP2D6 inhibitors (like Fluoxetine) may reduce codeine efficacy -Genetic polymorphism may also explain codeine resistance (lacking this enzyme) Little euphoric effect, so low risk for addiction. Used as an anti-tussive (cough suppressant) -may still cause constipation and respiratory suppressionDextromethrophanSynthetic morphine derivative that does not act thru opioid receptors. Same efficacy as codeine -no GI or analgesic effectHeroinDiamorphine; diacylated-morphine is more lipophilic than morphine so it crosses the blood-brain barrier more rapidly producing a greater rush. -2x more potent than morphineHydrocodoneVicodin; often combined w/ NSAIDs for synergistic effectOxycodoneIndicated for chronic pain. -Addicts chew thru the slow release formulation to obtain immediate release to mimic heroin rushMeperidineSimilar to morphine, but shorter duration. Used during labor.MethadoneSimilar to morphine, but much longer duration. Used to treat morphine/heroin addictionFentanylHigh potency. Can be used transdermally. Short-lasting. Used in anesthesia and patient controlled infusions.Opiate AntagonistsNaloxoneShort-acting competitive antagonist used to rapidly reverse opioid induced analgesia and respiratory suppression.NaltrexoneLong-acting competitive antagonist Used to protect detoxified addicts from relapsing. Pain Killers Local Anesthetics Mechanism Reversibly inhibits Na channels (cytoplasmic side) that are activated to block generation of action potentials. “Use dependent” Note: Phenytoin (antiepileptic) specifically blocks inactivated Na channels All are weak bases that exist mainly in its ionized form. Passes thru the plasma membrane in its unionized form, but exerts its effect in its ionized form intracellularly. Cocaine-contains ester bond; rapidly metabolized by non-specific esterases in the plasma -cocaine’s CNS effects are independent from its analgesic effect (blocks reuptake of DA, 5-HT, NE)Lidocaine-contains amide bond; longer acting compared to local anesthetics w/ ester bondsLocal anesthetics often combined with vasoconstrictors (epinephrine) to extend duration of action and to minimize bleeding. Pain Killers NSAIDS (non-steroidal anti-inflammatory drugs) Mechanism: Inhibits cyclooxygenase (COX), preventing prostaglandin synthesis. Prostaglandins do not cause pain themselves, but sensitize nocireceptors to pain Note: COX1 – constitutively expressed; “house-keeping functions” COX2 – induced by pro-inflammatory factors (TNF & IL-1…) Classical NSAIDs – inhibits both COX1 and COX2 -inhibition of COX1 reduces overall “house-keeping” PGs ( side effects (gastric ulcers)Aspirin The only known irreversible COX inhibitor -have cardioprotective effects (low dose aspirin) PGIs – anticoagulating effects; found in endothelial cells w/ nucleus. They can renew COX transcriptionally after aspirin is elminated TXa – coagulating effect; found in thrombocytes w/o nucleus. They cannot renew COX even after aspirin is elminated. Low dose aspirin shifts PG synthesis to PGI. Side Effects -Reyes syndrome in children, do not use in children! -high doses may cause tinnitus and nauseaAcetaminophen (Tylenol)Indicated for analgesic and antipyretic property. Easily crosses blood-brain barrier. Have little side effects but a very narrow therapeutic index. Overdose ( fatal hepatoxicity Acetaminophen can be converted into a toxic metabolite that requires glutathione conjugation. OD of acetaminophen will deplete glutathione and lead to accumulation of the toxic metabolite ( hepatic necrosisCOX-2 Specific NSAIDs – inhibits only COX 2 -supposedly fewer side effects -recent studies show that they increase the risk of cardiovascular diseases!!! -Reofecoxib (Vioxx) -Celecoxib (Celebrex) Antibiotics (overview)Cell Wall Synthesis Inhibitors²- Lactam AntibioticsGeneral Mechanism: Inhibit transpeptidase required for cross-linking of peptidoglycan chains for bacterial cell wall synthesis. Also inactivates autolytic enzyme inhibitor.PenicillinsClassifications: -Narrow Spectrum: active against gram (+) only -Broad or Extended Spectrum: active against gram (+) & gram (-) & some others -increased range is due to the addition of amino or carboxy group -²-Lactamase sensitive vs. ²-Lactamase resistant -antibiotics that are inactivated by ²-Lactamase are said to be ²-Lactamase sensitve²-Lactamase Inhibitor -Clavulanic Acid -sulbactam-inhibits ²-Lactamase produced by the bacteria -allows ²-Lactamase sensitive antibiotics to become resistantCephalosporinsSame mechanism as penicillins There are 4 generations. The newer generations have: broader spectrum, increased resistance to ²-Lactamase, and increased ability to reach CSF.Vancomycin (polypeptides) Bacitracin (polypeptides)Other cell wall inhibitors that operate thru a different mechanism (different than ²- Lactam Antibiotics) Protein Synthesis InhibitorsGeneral Mechanism  Inhibit either 30s or 50s ribosomal subunit (which differ from mammalian cells). Since they operate intracellularly, they must be able to penetrate the cell wall and/or membrane. Entry inhibition would be a point of drug resistance.Aminoglycosides -Gentamycin-O2 dependent transport to enter cells -ineffective against anaerobes Tetracyclines-oral absorption impaired by Ca2+ and Mg2+Macrolides -Azithromycin (long t1/2)-good alternative to penicillin -once daily dosing of Azithromycin increases complianceChloramphenicol-very broad spectrum -reserved for resistant cases; severe side effectsClindamycin-used to treat penicillin-resistant cocciFolate AntagonistsGeneral Mechanism – block folate synthesis (folate is required for nucleotide synthesis) Bacteria cannot take up folic acid and must make it from PABA. Folate Metabolism: PABA ( Folate ( Tetrathydrofolate ( DNASulfonamides -structurally similar to PABA; competes with PABA in the folate pathway (interferes with PABA ( folate)Trimethoprim-interferes with the folate ( tetrahydrofolate step -often combined with sulfonamidesQuinolonesCiprofloxain Levofloxain Etc…Mechanism – inhibitor of bacterial DNA gyrase (enzyme that is involved in the winding/unwinding of DNA. This results in inhibition of DNA synthesis/transcription -very broad spectrum-Focus on knowing the general mechanism and the classifications (cell wall synthesis inhibitors, protein synthesis inhibitors, folate antagonists, and quinolones).     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