ࡱ> HKABCDEFG[QbjbjΐΐZ3DDDDDXXX8$X&&.&&&((($+D)}("())DD&&GZcZcZc)D&D&Zc)ZcZc&*XHl|]0[Dd(0("Zc( )(((bv((())))(((((((((( :INDEX Theme 16: PATHOLOGY OF ENERGY METABOLISM. (SELF WORK OF THE STUDENTS) Theme 17: PATHOLOGY OF CARBOHYDRATE METABOLISM Theme 18: VIOLATION LIPID METABOLISM. "heme ! 19: DISORDERS OF PROTEIN METABOLISM. "heme ! 19: DISORDERS OF VITAMINE METABOLISM. (SELF WORK OF THE STUDENTS). Theme 21: VIOLATION of WATER-ELECTROLYTE METABOLISM. Theme 23: VIOLATION OF THE ACID-BASIC BALANCE. Theme 16: Pathology of ENERGY METABOLISM. (SELF WORK OF THE STUDENTS) Actuality of the theme. Energy metabolism disorders underlies in functional and organic violations of organs and tissues. It can occur at all stages of the energy transformations due to the absence or lack of substrate, changing the number or activity of enzymes in connection with genetic defects, enzyme inhibitors, insufficient intake into the body of essential aminoacids, fatty acids, vitamins, microelements and other substances necessary for metabolic processes or regulatory systems damaged. Between the intracellular mechanisms related with genetic information, and neuro-hormonal regulation of metabolism there is a close relationship and the violation of any of can causes pathology development. Understanding of the reasons and mechanisms of main disorders and energy metabolism, understanding of preventive measures has undeniable value. General purpose of the lesson Learn reasons and mechanisms of development of the energy metabolism disorders. For this it is necessary to know: To expose the typical forms of the energy metabolism disorders. To explain intercommunication between disorders of energy and carbohydrate metabolism. For realization of purpose of lesson it is necessary to have the base knowledges-skills. Role of energy metabolism in the human organism (department of normal physiology) Intercommunication between energy, carbohydrate, lipid and protein metabolism (department of biochemistry). Neurohumoral regulation of energy metabolism (department of normal physiology) Theoretical questions, at the base of which the execution of purpose types of activity is possible. 1. Energy needs of the body. Energy balance, negative and positive, causes and mechanisms of development. 2. Basal metabolism as a factor of influence on energy balance. Pathological changes in basal metabolism: etiology, pathogenesis. 3. Violation of cell energysupply. Violation transport nutrients through cell membranes, disturbances of intracellular catabolic pathways. 4. Violation of cellular respiration, the effect of separation of oxidation and phosphorylation, their mechanisms. 5. The value of energy metabolism disorders in the cell cycle, organs, organism. The role of energy disorders in development of cell damage. Literature. 1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. 2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005. Theme 17: PATHOLOGY OF CARBOHYDRATE METABOLISM Actuality of the theme. Violation of carbohydrate metabolism is the leading link in pathogenesis of many diseases (nervous, cardio- vascular systems, liver). Most frequent and the most heavy form of pathology of carbohydrate metabolism is diabetes mellitus. Diabetes mellitus - one of the most widespread diseases with steady tendency to growth. From data of WHO, frequency of him on the average hesitates from 1,5 to 3-4%, considerably growing in the developed countries of the world (to 5-6%). Growth of morbidity, heavy invalidization consequences and high lethality, especially among capable of working population develops due to diabetes mellitus and it complications. Fight against diabetes mellitus is delivered to the medico-social problems. Understanding of reasons which influence on growth of morbidity on diabetes finding out of thin mechanisms of its development, understanding of prophylactic, sanitary educational measures on morbidity of population of Ukraine on diabetes mellitus, has an irrefutable value. General purpose of the lesson Learn reasons and mechanisms of development of basic types hypo- and hyperglycemia. To study etiology, pathogenesis, mechanism of development of basic displays of diabetes mellitus, its pathogenic treatment. For this it is necessary to know: To expose the typical forms of violations of carbohydrate metabolism. Modern classification by WHO of diabetes melitus; To explain the modern views of reasons and pathogenesis of diabetes mellitus. The value if inherited factors and surrounding environment; To expose metabolism violations at pathogenesis of different types (I and II types)of diabetus mellitus; To analyze cause-effect relationship in the pathogenesis and their role in the pathogenesis of the main types sof diabetus melittus (type 1,type 2) and its complications; For this it is necessary to know: To expose the typical forms of violations of carbohydrate metabolism. To define reasons and mechanisms of hypo- and hyperglycemia development. To expose reasons and mechanisms of hypo- and hyperglycemia development at the children of different age, value of these changes for child's organism. To explain the modern views of reasons and pathogenesis of diabetes mellitus. To explain intercommunication between disorders of metabolism and basic functional violations at diabetus mellitus. To expose features, which is typical for diabetes mellitus at children. Transfer the base moments of the first aid during hypo- and hyperglycemic states. For realization of purpose of lesson it is necessary to have the base knowledges-skills. Role of carbohydrates in an organism (department of biochemistry). Intercommunication between carbohydrate, lipid and protein metabolism (department of biochemistry). Neurohumoral regulation of carbohydrate metabolism (department of normal physiology) The checking of primary level of knowledges. Give the answer to the followings questions: Name hormones which take part in regulation of carbohydrate metabolism. Participation of the nervous system in the carbohydrate metabolism regulation. Name the contrinsular hormones. Where is insulin made? What is hyperglycemia? Kinds. What is hypoglycemia? Kinds. What is glycosuria? What is a kidney threshold for glucose? Why is it evened? What is diabetes mellitus? Definition. Name the types of diabetes mellitus. Commas which arise up at diabetes mellitus, mechanisms of their development Ketoacidotic coma, reasons. Hyperosmolar coma, reasons. Name the reasons of hypoglycemic coma development at diabetes mellitus? What are consequences of hypoglycemia? What are complications of diabetes mellitus? What are the experimental models of diabetes mellitus? Theoretical questions, at the base of which the execution of purpose types of activity is possible. 1. Disorders of carbohydrates absorbtion and glycogen deposition, transport of carbohydrates in cells. Violation of the nervous and hormonal regulation of carbohydrate metabolism. 2. Hyperglycemia, kinds, reasons of origin, mechanisms of development. Value for organism. 3. Hypoglycemia, reasons of origin, mechanisms of development. Value for an organism. 4. Diabetes mellitus. Modern view of etiology and pathogenesis. Classification. Basic experimental models of diabetes mellitus. 5. Etiology and pathogenesis of diabetes mellitus type 1. The role of hereditary factors and environmental factors in its occurrence and development. Pathogenesis of absolute insulin deficiency and its manifestations and consequences: The violation of energy, protein, carbohydrate, fat, water and electrolyte exchange, acid-base balance. 6. Etiology and pathogenesis of diabetes mellitus type 2. The role of hereditary factors and environmental factors in its occurrence and development. Variations of relative insulin deficiency at diabetes mellitus type 2. Manifestations and consequences of relative insulin deficiency. The concept of metabolic syndrome. 7. Complications of the diabetus mellitus Coma, determination of concept. Pathogenesis of basic types of comas which can arise at diabetes mellitus, pathogenic treatment. Long-term complications (macro-microangiopathy, neuropathy, fetopathy et al.), their overall characteristic. V440;5=V CA:;04=5==O (<0:@>-, <V:@>0=3V>?0BVW, =59@>?0BVW, D5B>?0BVW B0 V=.), WE 7030;L=0 E0@0:B5@8AB8:0. 8. Prophylaxis of diabetes mellitus development. Principles of therapy of diabetes mellitus. Prevention of complications. Literature is necessary for theoretical questions . Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005. Nota bene! Glycated hemoglobin - (21A) - contains glucose, attached to terminal valin in every chain. It is permanent index of the compensative state of diabetes mellitus. The concentration of it is increased in patients with decompensate diabetes mellitus. Normal index of 21A in blood: 5-7% from the general level of hemoglobin. THEMES of reports for individual work of students: 1. Modern view in mechanisms of development of microangiopathy at diabetes mellitus. 2. Modern view in mechanisms of development of macroangiopathy at diabetes mellitus. 3. Modern view in mechanisms of development of diabetic coma. Pathogenetic treatment. 4. Modern view in mechanisms of development of hyperosmolar coma. Pathogenetic treatment. Practical work: PATHOLOGY OF CARBOHYDRATE METABOLISM Object of work: to model experimental hypoglicemia for a rabbit. Content of work: determination of glucose concentration in condition of insulin intoxication. EXPERIMENT 1. Students work as brigades. The first brigade carries out the test on determination of glucose in the control samples; the other one carries out the test in experimental samples: before and after insulin introduction. Insulin is entered to the rabbit which was not fed by 24 hours in an amount 10 ME on the 1 kg of weight under the skin of the back. First test is carried out in 15 minutes after insulin introduction, than in 30 min., in 1 hour, in 1,5 hour. Blood for the test in an amount 0,1 ml is taken from an ear regional vein. After taking the blood the 10-15 ml of 30% glucose solution is entered to the rabbit throw the ear regional vein or through the mouth with the purpose to remove of insulin hypoglicemia. COURSE OF ANALYSIS: Fill in two test tubes by 1 ml of decinormal solution of caustic soda and 5 ml of 0,45% solution of sulfuric zinc. Add to one of test tubes 0,1 ml of blood, wash a pipette by solution from a test tube 2-3 times. The second test tube remains the control. Put both test tubes on an water bath on 3 min. Filter the maintenance of test tube through the sterile cotton wool in glass. Wash test tubes twice by 3 ml of the distilled water which is poured on a filter. At the end of filtration the filter is levitated on an edge of bailer. Wait while all liquid will flow from it. Take away the filter from the bailer and shake off the drops of liquid which remained in the bailer in glass. Add to the filtrate 2 ml K3[Fe(CN) 6] 1: 200. Boil on an water bath during 15 min. Cool glasses and add to each 2 ml of mixture of salts. Add to each glasses 2 ml of 3 % to solution of !3!. Add 2-3 drops of 1 % to solution of starch. Titrate the maintenance of glasses by hyposulphite 1:200 till discolouring. Find the maintenance of glucose at the table by the amounts of hyposulphite which we used for titration. Find the maintenance of glucose in the control tube at the table by the amounts of hyposulphite which we used for titration. Find a difference in the maintenance of glucose in an experimental test tube, take away an error, determine the maintenance of glucose in blood in mg % . For the translation of the got result in mmol/l (international unit) use the coefficient - 0,05. An initial maintenance of glucose in the blood before the introduction of insulin is___________mmol/l, after the introduction of insulin : in 15 min. - _________mmol/l, in 30 min. - _________ mmol/l in 90 min. - _________ mmol/l  in 120 min.- _________ mmol/l Conclusion ______________________________________________________________ _______________________________________________________________ _______________________________________________________________ _______________________________________________________________ _______________________________________________________________ _______________________________________________________________ "5AB8 7 10=:C 40=8E  @>:-1 Tests of an open database (2011) 1. On the empty stomach in the patients blood glucose level was 5,65 mmol/L, in an hour after usage of sugar it was 8,55 mmol/L, in a 2 hours - 4,95 mmol/L. Such indicators are typical for: A Healthy person B Patient with hidden diabetes mellitus C Patient with insulin-dependent diabetes mellitus D Patient with non-insulin dependent diabetes mellitus E Patient with tireotoxicosis 2. Patient with diabetes mellitus experienced loss of consciousness and convulsions after injection of insulin. What is the result of biochemical blood analysis for concentration of the sugar? A 1,5 mmol/L B 8,0 mmol/L C 10,0 mmol/L D 3,3 mmol/L E 5,5 mmol/L 3. A patient was delivered to the hospital by an emergency team. Objectively: grave condition, unconscious, adynamy. Cutaneous surfaces are dry, eyes are sunken, face is cyanotic. There is tachycardia and smell of acetone from the mouth. Analysis results: blood glucose - 20,1 micromole/l (standard is 3,3-5,5 micromole/l), urine glucose - 3,5\% (standard is - 0). What is the most probable diagnosis? A Hyperglycemic coma B Hypoglycemic coma C Acute heart failure D Acute alcoholic intoxication E Anaphylactic shock 4. A patient is ill with diabetes mellitus that is accompanied by hyperglycemia of over 7,2 millimole/l on an empty stomach. The level of what blood plasma protein allows to estimate the glycemia rate retrospectively (4-8 weeks before examination)? A Glycated hemoglobin B Albumin C Fibrinogen D C-reactive protein E Ceruloplasmin 5. A child's blood presents high content of galactose, glucose concentration is low. There are such presentations as cataract, mental deficiency, adipose degeneration of liver. What disease is it? A Galactosemia B Diabetes mellitus C Lactosemia D Steroid diabetes E Fructosemia 6. The B cells of endocrine portion of pancreas are selectively damaged by alloxan poisoning. How will it be reflected in blood plasma? A The content of sugar increases B The content of fibrinogen decrease C The level of sugar decreases D The content of globulins decreases E The content of albumins decreases 7. A patient with insulin-dependent diabetes had an insulin injection. Some time later he felt weakness, irritability, excessive sweating. What is the main reason of these disorders? A Carbohydrate starvation of brain B Intensified glycogenolysis C Intensified ketogenesis D Intensified lypogenesis E Reduced glyconeogenesis 8. After recovering from epidemic parotiditis a patient began to lose weight, he was permanently thirsty, drank a lot of water, had frequent urination, voracious appetite. Now he has complaints of skin itch, weakness, furunculosis. His blood contains: glucose - 16 mmole/L, ketone bodies - 100 mcmole/L; glucosuria. What disease has developed? A Insulin-dependent diabetes B Insulin-independent diabetes C Steroid diabetes D Diabetes insipidus E Malnutrition diabetes 9. A patient has been suffering from diabetes mellitus for 5 years. As a result of not keeping to a diet the patient passed into a comatose state. Emergency doctor injected him glucose. The patients state got better. What is the most probable type of coma in this case? Hypoglycemic Acidotic Hepaatic Hyperglycemic Hypothyreoid 9. Prophylactic examination of a patient revealed hyperglycemia, ketonuria, polyuria, glycosuria. What form of acid-base balance disorder is the case? Metabolic acidosis Gaseous alkalosis Metabolic alkalosis Gaseous acidosis Nongaseous acidosis 2010 1. Prophylactic examination of a patient revealed hyperglycemia, ketonuria, polyuria, glycosuria. What form of acid-base balance disorder is the case? Metabolic acidosis Gaseous alkalosis Metabolic alkalosis Gaseous acidosis Nongaseous acidosis 2. It is known that patients with diabetes mellitus are more subject to inflammative processes, they have low regeneration and slower wound healing. What is the reason for this? Decrease in lipolysis Itensification of catabolism Accelerated gluconeogenesis Increase in lipolysis dEcrease in protheosynthesis 3. Glucose concentration in a patients blood is 15 millimole/l (reabsorption threshold is 10 millimolel/l). What effect can be expected? Reduced glucose reabsorption Reduced vasopressin secretion Diuresis reduction Reduced aldosterone secretion Glucosuria 4. A patient has been suffering from diabetes mellitus for 5 years. As a result of not keeping to a diet the patient passed into a comatose state. Emergency doctor injected him glucose. The patients state got better. What is the most probable type of coma in this case? Hypoglycemic Acidotic Hepaatic Hyperglycemic Hypothyreoid Algorithm for skills passing "Analyses of the glucose-tolerance test indexes at the patients with diabetes mellitus" 1. Name the reasons for the GTT Standard answer: - Capillary blood glucose on an empty stomach - more than 5.5 mmol / l - Presence of a diabetes mellitus at the family - Presens of the paradVabetes symptoms (itching of the skin and mucous membranes, often purulent disease, candidiasis) 2. Name the main stages of the GTT Standard answer: - Weigh the patient - Determination of the concentration of glucose in the capillary blood - Peroral entrance of glucose at a rate of 1g/kg of body weight - Determination of the glucose concentration in capillary blood of patient after 2 hours 3. Appraise the results of GTT in this patient in accordance with the diagnostic criterias of diabetes mellitus and other categories of hyperglycaemia. Standard answer: ConclusionConcentration of glucose in the capillary blood on an empty stomachconcentration of glucose in capillary blood after 2 hours after the glucose loadingDiabetes mellitusMore than 6.1 mmol/lMore than or equal to 11.1mmol/LDisordered glucose toleranceLess than 6.1 mmol/l7,8 - 11.1 mmol/lDisordered blood glucose 5.6 - 6.1 mmol/lLess than 7.8 mmol/l Situational tasks. 1. 52 years old patient went to the dentist with complaints about dryness of the mouth, thirst (water intake up to 5l per day), increased appetite. The doctor suspected a pathology of carbohydrate metabolism and prescribed to the patient examination (blood and urine). 1.What disease can be suspected in this case ? ________________________________________________________________________________________________________________________________________ 2.What changes can be found in the analysys of the urine and blood? Explain mechanism of their origin. ________________________________________________________________________________________________________________________________________ What reasons can cause this disease? ________________________________________________________________________________________________________________________________________ What does it mean tolerance for carbohydrates? How it can be find out? Describe it in the case of diabetes mellitus. ________________________________________________________________________________________________________________________________________ ________________________________________________________________________________________________________________________________________ 2. During examination of the patient A was find out hyperglycemia, glucosuria, ketonemia. Diabetus mellitus of II type was diagnosed. 1. Determination of the diabetes melitus. ________________________________________________________________________________________________________________________________________ 2. What are the possible reasons of the diabetes mellitus in this case? ________________________________________________________________________________________________________________________________________ 3. What kind of lipid metabolism changes wiil be observed in this case? ________________________________________________________________________________________________________________________________________ 3 . 10 years old child began to lose weigth and fell thirst after carried epidemic parotiditis. At the examination glucose blood plasma level 19 mmol/, glucosuria. 1. What pathology can be suspected in this case? ________________________________________________________________________________________________________________________________________ 2.Describe two types of this pathology? ________________________________________________________________________________________________________________________________________ 3. What is it kidneys threshold for glucose? ________________________________________________________________________________________________________________________________________ 4. What kind of protein metabolism changes wiil be observed in this case? ________________________________________________________________________________________________________________________________________ 5. Which substances belongs to the ketonic bodies and how will be changed in this case? ________________________________________________________________________________________________________________________________________ 4. Patient who suffers from diabetes mellitus was hospitalized in the grave condition. At the examination patient with out consciousness, blood gucose level 35 mmol/l. 1.Which disease can be suspected in this case? ________________________________________________________________________________________________________________________________________ 2. What is the main mechanism of its development? ________________________________________________________________________________________________________________________________________ 5. Patient was hospitalized in the comatose state. Breathing is deep, noisy. Acetone smail from mouth. Blood glucose level 17 mmol/l. Urine reaction for acetone is positive. How this type of breathing is called?. ________________________________________________________________________________________________________________________________________ Explain mechanism of glucosuria`? ________________________________________________________________________________________________________________________________________3. Explain mechanism of acetone appearing in the urine? ____________________________________________________________________ ____________________________________________________________________ 4. What does it mean coma? Explain mechanism of its development. ________________________________________________________________________________________________________________________________________ 6. Patient with diabetes mellitus was hospitalized with complaints of general weaknees, dizziness, hunger, cold sweat, convulsions. BP -80/50 <<hg., glucose blood level  2 mmol/l. 1. What possible complication of the diabetes mellitus can be in this case. ________________________________________________________________________________________________________________________________________ 2. Explain mechanism of these symptoms development. ________________________________________________________________________________________________________________________________________ 7. Damage of the pancreas -cell (adenoma) takes. Place in the patient. 1. How level of the blood glucose level wiil be changed in this case? ________________________________________________________________________________________________________________________________________ 2. Specify contrainsulin hormones? Explain mechanism of their action. ________________________________________________________________________________________________________________________________________ 8. 60 years old patient suufer from diabetes mellitus during last 20 years. Glucose level changes from 7 to 12 mmol/l. The patient marks decrising of the vision. 1. What type of the diabetes mellitus takes place in this case? ____________________________________________________________________ ____________________________________________________________________2. Explain derising of the vision. ____________________________________________________________________ ____________________________________________________________________ 3. Specify other complication in the case of diabetes mellitus. ________________________________________________________________________________________________________________________________________ 9. After physical loading level of blood glucose of the sportman was -2 mmol/l. 1. How is called decreasinf of the glucose level? ________________________________________________________________________________________________________________________________________2. What kinds of complications can be in this case? ____________________________________________________________________ ____________________________________________________________________3. Which types if glucose level decreasing do you now? ____________________________________________________________________ ____________________________________________________________________ 10. After glucose loading at the patient initial level of glucose - 6,66 mmol/l, after 2 hours after loading 8 mmol/l. About what test data testify? ________________________________________________________________________________________________________________________________________ Describe data of this test at healthy person. ________________________________________________________________________________________________________________________________________3. Pracrical value of this test ____________________________________________________________________ ____________________________________________________________________ Theme 18: VIOLATION LIPID METABOLISM. Actuality of the theme. Metabolic disturbances can appear at all levels of biological organization from molecular and cellular to the organism level. These changes can be investigation of violation of nervous hormonal mechanisms, changes of genetic information, action of pathogenic factors. A primary metabolic disturbance lies in the basis of many diseases, f. ex. diabetes mellitus, obesity, gout and other. The secondary violations accompany the most pathological processes. The studies of reasons, mechanisms of development, displays of metabolic disturbance at different levels, their diagnostics, treatment and prophylactic have great significance in preparation of future doctor. General purpose of the lesson: To learn the basic stages of violations of lipid metabolism. For this it is necessary to know: To expose the typical forms of violations of protein and lipid metabolism. To expose main forms of lipid metabolism violations. To analyze cause-effect relationship in the pathogenesis of the typical disorders of lipid and characterized pathological and the adaptive-compensatory changes; To analyze the methods of experimental modeling of typical metabolic processes and to determine the causes and mechanisms of their development. For realization of purpose of lesson it is necessary to have the base knowledges-skills. 1. Value of lipid for an organism (department of biochemistry). 2. Regulation of lipid metabolism (department of normal physiology). 3. A concept about lipoproteid (department of biochemistry). The checking of primary level of knowledges Give the answer to the followings questions: What is obesity? Name the types of obesity. What is the secondary obesity? Make examples. Name the basic classes of blood plasma lipoproteids. What are the modificated lipoproteids? Make examples. Make examples of hormonal obesity. Theoretical questions, at the base of which the execution of purpose types of activity is possible. 1. Disorders of the digestion and absorption of the lVpVds. Hyper-,hypo, dislVpoproteinemVa. 2. Dependence of dislipoproteinemia from environmental factors (diet), heredity, and associated diseases. 3. Modern classifications of dislipoproteinemia (primary and secondary; by phenotype, with high or low risk of atherosclerosis), the criteria for hypercholesterolemia, hypertriglyceridemia, low levels of HDL. 4. Etiology and pathogenesis of primary (hereditary, family) and secondary (with food disorders, obesity, diabetes, kidney disease, hypothyroidism, liver cirrhosis, AIDS, under the influence of drugs) dislipoproteinemia. 5. Effects / Complicationsof the dislipoproteinemia. Principles and purposes for the restoration of normal lipid composition of blood. 6. Obesity, determination. Reasons and mechanisms of obesity different forms development. 7. Etiology and pathogenesis of obesity. Mechanisms of fatty dystrophy. 8. Characteristics of the medical problems associated with obesity. Literature. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005. THEMES of reports for individual work of students: 1. Pathogenesis of obesity. 2. Modern pictures of pathogenesis of atherosclerosis. !8BC0FV9=V 7040GV 1. 60 years old patient suffers from atherosclerosis of lower extremities, ischemic heart disease. At examination hyperlipidemia was revealed. 1. Which class of lipoproteins of blood plasma will be increased raised? ________________________________________________________________________________________________________________________________________2. Specify classes of lipoproteins. Discribe them. ____________________________________________________________________ ____________________________________________________________________3. Explain meaning of hyperlipoprotenemia? ____________________________________________________________________ ____________________________________________________________________ 4. How hyperlipoprotenemia can be classyfied? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 2. The patient in a coma state was hospitalised. In the anamnesis - diabetes melitus of II type during 5 years. At examination: noisy, deep breathing with odor of acetone. What kind of lipid metabolism changes can be in this case? ________________________________________________________________________________________________________________________________________2. For what complication this symptoms is typical? ____________________________________________________________________ ____________________________________________________________________ 3.%2>@89 ?>ABC?82 2 ;V:0@=N 7 4V03=>7>< 045=><0 >AB@V2FV2 0=35@30=A0. %0@0:B5@=5 28@065=5 >68@V==O. The patient was hospitalised to the hospital with a diagnosis of adenoma of islets of Langerhans. Obesity is observed. 1. What is the reason of obesity in this case? ________________________________________________________________________________________________________________________________________2. Which types of obesity do you know? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 3. What type of obesity is observed in this case? ________________________________________________________________________________________________________________________________________ "5<0! 19: DISORDERS OF PROTEIN METABOLISM. DISORDERS OF PURINE AND PYRIMIDINE BASES. Actuality of the theme. Metabolic disturbances can appear at all levels of biological organization from molecular and cellular to the organism level. These changes can be investigation of violation of nervous hormonal mechanisms, changes of genetic information, action of pathogenic factors. A primary metabolic disturbance lies in the basis of many diseases, f. ex. diabetes mellitus, obesity, gout and other. The secondary violations accompany the most pathological processes. The studies of reasons, mechanisms of development, displays of metabolic disturbance at different levels, their diagnostics, treatment and prophylactic have great significance in preparation of future doctor. General purpose of the lesson: To learn the basic stages of violations of protein metabolism. For this it is necessary to know: To expose the typical forms of violations of protein metabolism. To expose main forms of protein metabolism violations. To analyze cause-effect relationship in the pathogenesis of the typical disorders of protein and characterized pathological and the adaptive-compensatory changes; To analyze the methods of experimental modeling of typical metabolic processes and to determine the causes and mechanisms of their development. For realization of purpose of lesson it is necessary to have the base knowledges-skills. 1. Value of proteins for an organism (department of biochemistry). 2. Regulation of protein metabolism (department of normal physiology). 3. Negative and positive nitrous balance (department of biochemistry). 4. Protein composition of blood (department of normal physiology). The checking of primary level of knowledges Give the answer to the followings questions: What is positive nitrous balance? What is negative nitrous balance? Name the reasons which lead to the origin of negative nitrous balance? Name the reasons which lead to the origin of positive nitrous balance? What is hypoproteinemia? Make examples. What is hyperproteinemia? Make examples. What is dysproteinemia? Make examples. What is hypernitrogenemia? Make examples. What is products hypernitrogenemia? Make examples. What is retentional hypernitrogenemia? Make examples. What is phenylketonuria? What type of its inheritance? What is alcaptonuria? What type of its inheritance? Gout, mechanisms of development. What acid does accumulate in blood at a gout? Theoretical questions, at the base of which the execution of purpose types of activity is possible. 1. Conception about positive and negative nitrous balance. 2. Disorders of the main stages of protein metabolism. 3. Hypernitrogenemia, productive and retentional. 4. Violation of protein composition of blood plasma: hypo-, hyper, dysproteinemia, paraproteinemia. 5. Disorders of the serum protein transport function. >=D>@<0FV9=V 7<V=8 1V;:>28E <>;5:C;, ?>@CH5==O 453@040FVW 1V;:V2 2 ;V7>A><0E V ?@>B5>A><0E, WE @>;L C ?0B>;>3VW. Conformational changes of protein molecules, degradation of proteins in lysosoms and proteosoms and their role in pathology. 6. Hereditary disorders of aminoacid metabolism. 7. Gout. Reasons and mechanisms of development. Basic pathophysiologycal principles of treatment. Literature. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005. THEMES of reports for individual work of students: Inherited disorders of metabolism of amino acid. Gout. Role of eczo- and endogenous factors in its origin. Mechanisms of development. Pathogenic treatment. Tests of an open database (2011) 1. Nappies of a newborn have dark spots that witness of formation of homogentisic acid. Metabolic imbalance of which substance is it connected with? A Thyrosine B Galactose C Methionine D Cholesterine E Tryptophane 2. A 1,5-year-old child presents with both mental and physical lag, decolorizing of skin and hair, decrease in catecholamine concentration in blood. When a few drops of 5% solution of trichloroacetic iron had been added to the childs urine it turned olive green. Such alteration are typical for the following pathology of the amino acid metabolism: A Phenylketonuria B Alkaptonuria C Tyrosinosis D Albinism E Xanthinuria 3. Albinos can't stand sun impact - they don't aquire sun-tan but get sunburns. Disturbed metabolism of what aminoacid underlies this phenomenon? A Phenilalanine B Methionine C Tryptophan D Glutamic acid E Histidine 4. A13-year-old boy complains of general weakness, dizziness, tiredness. He is mentally retarded. Increased level of valine, isoleucine, leucine is in the blood and urine. Urine has specific smell. What is the diagnosis? A Maple syrup urine disease B Addison's disease C Tyrosinosis D Histidinemia E Graves' disease 5. A 48 year old patient complained about intense pain, slight swelling and reddening of skin over the joints, temperature rise up to $38^oC$. Blood analysis revealed high concentration of urates. This condition might be caused by disturbed metabolism of: A Purines B Collagen C Cholesterol D Pyrimidines E Carbohydrates 6. The concentration of albumins in human blood sample is lower than normal. This leads to edema of tissues. What blood function is damaged? A Maintaining the oncotic blood pressure B Maintaining the Ph level C Maintaining the body temperature D Maintaining the blood sedimentation system E All answers are correct 2010 1. Examination of a patient with chronic renal insufficiency revealed an increase in residual nitrogen concentration in blood up to 35 millimole/l, more than half of which is urea. What type of hyperazotemia is it? Hepatic Combined Residual Retentional Productional 2. A 13-year-old patient complains of general weakness, dizziness, fatiguability. Mental retardation is also observed. Examination revealed high concentration of valine, isoleucine and leucine in blood and urine. The patients urine has a specific smell. What is the likely cause of such condition? Basedows disease Histidinemia Addisons disease Tyrosinosi Maple surup urine disease 3. A patient who has been treated for viral hepatitis B developed symptoms of hepatic insufficiency. What changes indicating disorder in protein metabolism are likely to be observed in this case? Absolute hyperalbuminemia Absolute hypoalbuminemia Protein rate in blood will stay unchanged Absolute hyperglobulinemia Absolute hyperfibrinogenemia 4. A patient has been diagnosed with alkaptonuria. This pathology is caused by deficiency of the following enzyme: Pyruvate dehydrogenase Phenylalanine hydroxylase Glutumate dehydrogenase Oxidase of homogentisis acid DOPA decarboxylase 5. A patient has high sunlight sensitivity of skin. During standing his urine turns dark-brown. What is the most probable cause of this condition? Albinism Alkaptonuria Porphyria Haemolytic jaundice Pellagra Situational tasks 1. At the examination of the child with kvashiorkor defects of teeth, loosening of teeth, gum atrophy were revealed. 1. What is the reason of these disorders? ________________________________________________________________________________________________________________________________________2. Specify all changes which may occur at kvashiorkor? ____________________________________________________________________ ____________________________________________________________________ 3. What is the prevention and treatment of this pathology. ________________________________________________________________________________________________________________________________________ 2. A child age two months to plot the nose, cheeks, on the sclera and ears were dark spots. Urine while standing in the air turns black. 1. Accumulation of which substance in blood and urine can cause it? ________________________________________________________________________________________________________________________________________2. How that pathology is called? ____________________________________________________________________ ____________________________________________________________________ 3. What type of inheritance has this disease? ________________________________________________________________________________________________________________________________________ 3. 5 month old child has high level of homogentisic acid. 1. What diseases is typical for ? ____________________________________________________________________ ____________________________________________________________________ 2. Which enzymes defect takes place in this pathology? ____________________________________________________________________ ____________________________________________________________________ 3. What type of inheritance has this disease? ________________________________________________________________________________________________________________________________________ 4. 9 month old child has blond hair (parents - dark haired), very fair skin and blue eyes. There is a physical and mental development lag. Felinha test (with 3% trichloroacetic iron) is positive. 1. Which aminoacids level should be defined? ____________________________________________________________________ ____________________________________________________________________2. Which enzymes defect takes place in this pathology? ________________________________________________________________________________________________________________________________________ 3. What type of inheritance has this disease? ____________________________________________________________________ ____________________________________________________________________ ____________________________________________________________________ 4. Explain mechanism of this disease development. ____________________________________________________________________ ____________________________________________________________________ 5. Prophylaxis of this disease. ____________________________________________________________________ ____________________________________________________________________ 5. The patient complaints of pains in the small joints of arms and legs. At the examination there are incresing of the joints and their deformation. Increased amount of urate was found. 1. What disease is it? ____________________________________________________________________ ____________________________________________________________________2. What is the mechanism of changes which occurred at the patient? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 3. Prophylaxis of this disease. ____________________________________________________________________ ____________________________________________________________________ 4. Specify risk factors for this disease. ____________________________________________________________________ ____________________________________________________________________ 6. The patient at the hematology department has diagnosis of multiple myeloma. Complains of pain in the area of the chest and spine, fractions of the ribs. Serum protein - 130g / l 1. What is the basis of disease? ________________________________________________________________________________________________________________________________________2. What is the normal level of serum protein? Reason of the serum protein increasing and how is called? ____________________________________________________________________ ____________________________________________________________________3. How protein at this pathology is called? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 7. Stportman was preparing for competitions. Over the past three days intensively trained. During the examination revealed the changes of protein composition of blood? 1. What changes protein composition of blood were found at the sportman? ________________________________________________________________________________________________________________________________________2. Explain the mechanism of their development. ____________________________________________________________________ ____________________________________________________________________3. What other changes in protein composition of blood do you know. Their characteristics. ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 8. At the patien after the removing significant segment of small intestine serum protein level was 3.5 g/l. 1. How changes of the protein composition can be classified? ________________________________________________________________________________________________________________________________________2. Which the hereditary forms of serum protein composition disorders you know. Their characteristics. ____________________________________________________________________ ____________________________________________________________________ "opic ! 19: DISORDERS OF VITAMINE METABOLISM. (SELF WORK OF THE STUDENTS). Actuality of the theme. Vitamins are biologically active substances needed for a the normal living organism. They promote proper metabolism, increase efficiency, resistance to infectious agents. Also, vitamins are catalysts of enzymes and hormones. Changes in content of vitamins in the body is accompanied by many pathological processes.The studies of reasons, mechanisms of development, displays of metabolic disturbance at different levels, their diagnostics, treatment and prophylactic have great significance in preparation of future doctor. General purpose of the lesson: To learn the basic stages of violations of vitamine metabolism. For this it is necessary to know: To expose the typical forms of violations of vitamine metabolism. To expose main forms of vitamine metabolism violations. To analyze cause-effect relationship in the pathogenesis of the typical disorders of vitamines and characterized pathological and the adaptive-compensatory changes; To analyze the methods of experimental modeling of typical metabolic processes and to determine the causes and mechanisms of their development. For realization of purpose of lesson it is necessary to have the base knowledges-skills. 1. Value of vitamines for an organism and regulation of protein metabolism (department of normal physiology). Theoretical questions, at the base of which the execution of purpose types of activity is possible. Types of hypo- and hypervitaminosis, their etiology, pathogenesis. Mechanism of the main clinical signs development. Principles of the vitamine insufficiency correction. Tests of an open database (2011) 1. A clinic observes a 49 year old patient with significant prolongation of coagulation time, gastrointestinal haemorrhages, subcutaneous hematomas. These symptoms might be explained by the deficiency of the following vitamin: A K B B1 C B6 D H E E 2. Examination of a patient with frequent hemorrhages from internals and mucous membranes revealed proline and lysine being a part of collagene fibers. What vitamin absence caused disturbance of their hydroxylation? A Vitamin C B Vitamin K C Vitamin A D Thiamine E Vitamin E 3. There is observed inhibited fibrillation in the patients with bile ducts obstruction, bleeding due to low level of absorbtion of some vitamin. What vitamin is in deficit? A  B  C D D  E Carotene 4. Treatment of many diseases involves use of cocarboxylase (thiamine pyrophosphate) for supplying cells with energy. What metabolic process is activated in this case? A Oxidizing decarboxylation of pyruvate B Glutamate deamination C Amino acids decarboxylation D Decarboxylation of biogenic amines E Detoxication of harmful substances in liver 5. What vitamin deficiency leads to both disorder of reproductive function and distrophy of skeletal muscles? A Vitamin E B Vitamin A C Vitamin K D Vitamin D E Vitamin B1 Theme 21: VIOLATION of WATER-ELECTROLYTE METABOLISM. Actuality of the theme. The changes of water and electrolytes maintenance in the organism and their redistribution between the separate sectors of water violate such major parameters of homeostasis, constancy of volume, osmotic and ionic composition of blood, extracellular and intracellular liquid. It can cause violation of blood circulation, retraction of heart function, edema, changes of acid basic balance and other. Violations of water-electrolyte metabolism can be the result not only external influencing but also internal disorders. A lot of diseases and the pathological states accompanied with the changes of water-electrolyte homeostasis parameters which complicates their course. The effective correction of water-electrolyte homeostasis changes is possible only on condition of etiology and mechanisms of their development knowledge. General purpose of the lesson To learn violation of water-electrolyte metabolism, reason for origin and mechanisms of their development. Learn reasons and mechanisms of edema development. For this it is necessary to know: To select principal reasons for violations of water-electrolyte metabolism. To explain the mechanisms of their development. To modulate different pathogenetic forms of edema, to be able to explain the mechanisms of their development. For realization of purpose of lesson it is necessary to have the base knowledges-skills. Metabolism of water between blood and tissues after Starling (department of normal physiology). Contents of electrolytes in blood plasma in a norm (department of normal physiology). Regulation of water-electrolyte metabolism (department of normal physiology) Information that is necessary for addition to knowledges-abilities of bases on these questions, can be found in the followings textbooks: Materials from normal physiology course. For this it is necessary to know: To expose the typical forms of violations of water -salt metabolism. To expose main forms of water-salt metabolism violations. To analyze cause-effect relationship in the pathogenesis of the typical water-salt disorders and characterized pathological and the adaptive-compensatory changes; To analyze the methods of experimental modeling of typical metabolic processes and to determine the causes and mechanisms of their development. The checking of primary level of knowledges Give the answer to the followings questions: What is positive water balance? What is negative water balance? Name hormones which take part in regulation of water-electrolyte metabolism. What is dehydration? Name the types of dehydration. What is isoosmolar dehydration? What reasons for isoosmolar dehydration origin? What is hypoosmolar dehydration? Name reasons for hypoosmolar dehydration origin. What is hyperosmolar dehydration? Name reasons for hyperosmolar dehydration origin. What is hyperhydration? Name types for hyperhydration. What is isoosmolar hyperhydration? Name reasons for isoosmolar hyperhydration origin. What is hypoosmolar hyperhydration? Name reasons for hypoosmolar hyperhydration origin. What is hyperosmolar hyperhydration? Name reasons for hyperoosmolar hyperhydration origin. What is edema? What is dropsy? Name the types of edema after pathogenesis. Explain the development of oncotic edema. Explain the development of osmotic edema. Explain the development of hydrostatical edema. Explain development of membranogenic edema. Explain development of lymphatic edema. Name the quantity of sodium in blood plasma in a norm. Name the quantity of potassium in blood plasma in a norm. Name the quantity of calcium in blood plasma in a norm. Name the quantity of phosphorus in blood plasma in a norm. Standards of answers: It is the state at which entering of fluid in organism exceeds its excreting. It is the state at which excreting of fluid from an organism exceeds its receipt. Aldosteron, vasopresin (antidiuretic hormone), atrial Na-uretic factor. Diminishing of volume of extracellular fluid. ) Isoosmolar B) Hypoosmolar C) Hyperosmolar It is a type of dehydration in case of which osmotic pressure of extracellular liquid does not change. ) Polyuria B) Diarrhea C) First hours after hemorragia. It is a type of dehydration, with exceed loss of salts, which is accompanied the decrease of osmotic pressure of extracellular liquid. ) Vomiting B) Diarrhea C) Sweating It is a type of dehydration, with exceed loss of water which is accompanied the increase of osmotic pressure of extracellular liquid. ) Hyperventilation B) Increased sweating C) Hypersalivation D) Diarrhea E) Vomiting Increasing of volume of extracellular liquid. ) Isoosmolar B) Hypoosmolar ) Hyperosmolar It is a type of hypergidration, in case of which osmotic pressure of extracellular fluid does not change. Surplus introduction of isotonic solutions. It is a type of hypergidration, in case of which osmotic pressure of extracellular fluid is decreased. ) Reflectory anuria B) Acute kidney insufficiency It is a type of hypergidration, in case of which osmotic pressure of extracellular fluid is increased. The use for drink of sea water. It is a surplus accumulation of liquid in intercellular space as a result of water metabolism violation between blood and tissues. It is an accumulation of liquid in cavities. ) Oncotic B) Osmotic C) Hydrostatic D) Membranogenic E) Lymphogenic ) In the condition of reduced blood plasma oncotic pressure (the deficiency of proteins in organism at starvation, violation of liver protein syntesis function, loss of albumens with urine at pathology of kidney) B) In the condition of promoted oncotic pressure in tissues (output of albumens in the tissues in case of increased permeability of vascular wall, at the damage of cell) In the condition of increased osmotic pressure in the tissues. In the condition of increased venous hydrostatical pressure. In the condition of increased permeability of vascular wall (action of biologically active substances, endo- and exotoxins on a vascular wall). In the condition of lymphostasis. 135 - 155 mmol/L 3,5 - 5,5 mmol/L 2,1 - 3,1 mmol/L 0,9 - 1,2 mmol/L Theoretical questions which implementation of having a special purpose types of activity is possible on the basis of: Positive and negative water balance. Dehydration: extracellular and intracellular, hypo-, iso-, hiperosmola. Causes and mechanisms of their development. Protective and compensatory mechanisms. Hypo-, iso-and hyperosmolar hyperhidration, causes and mechanisms of development, protective, compensatory response. Extra-and intracellular hyperhydration. Definition of edema. Reasons and mechanisms of edema. The Starling theory of the edema pathogenesis. Edema caused by changes in oncotic pressure of blood and tissue fluid. The role of vascular wall permeability and lymph outflow in the pathogenesis of edema. Edema caused by sodium retention and / or water in the body. Myxedema. Principles of edema treatment. Violation of sodium metabolism. Reasons for origin, mechanisms of development, consequences. Violation of potassium metabolism. Reasons for origin, mechanism of development, consequences. Violation of phosphate-calcium exchange. Violation of hormonal regulation of calcium-phosphate metabolism: hyper-and hypoparathyreosis, hypo-and hypervitaminosis D, calcitonin secretion violation. Hypocalcium states: causes, mechanisms of development, manifestations. Rickets: Causes and mechanisms of development, clinical manifestations. The principles of prevention and treatment of rickets. Forms of rickets, resistant to vitamin D. Osteodystrophy. Hypercalcium conditions, reasons and mechanisms of development. Calcification of soft tissues: metastatic, dystrophic and metabolic mechanisms. Hyper-and hypo-phosphatemia. Reasons and mechanisms of development. Value of systeme violations of phosphoric-calcium metabolism in the development of dental diseases. Disorders of microelements metabolism. Etiology and pathogenesis. Literature: Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005. Practical work: EXPERIMENTAL EDEMA Object of work: to show formation of frog back arms edema at the passing through the vascular net of solution of lactic acid; to show development of lungs edema at a white rat after intraperitoneal introduction of adrenalin. EXPERIMENT ! 1. Prepare preparation of back arms of frog. Dissect an abdominal region by the longitudinal slit, extract internals. Place ligature under an aorta, incise an aorta, insert into a glass cannula and fix it by ligature. The upperparts of trunk is chopped off. Fill a cannula by Ringers solution for cool-blooded animals and unite it with the apparatus which consists of two Marriotts tubes connected with a T-joint by rubber tubing with pressed-on clamps. Fill one burette by solution of Ringer and another one by lactic acid solution painted by methylene-blue. At first pass Ringers solution through the preparation of arms vessels and count up the amount of drops. Close the clamp of burette with Ringers solution and open the clamp of burette with lactic acid solution. Count up the amount of drops. Pass a few times by turns Ringer s solution and lactic acid solution. Look after development of frog back arms edema. !Amount Ringer s solution dropsAmount lactic acid solution drops1234  Conclusion:__________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________ Tests of an open database (2011) 1. After a surgery a 36-year-old woman was given an intravenous injection of concentrated albumin solution. This has induced intensified water movement in the following direction: A From the intercellular fluid to the capillaries B From the intercellular fluid to the cells C From the cells to the intercellular fluid D From the capillaries to the intercellular fluid E No changes of water movement will be observed 2. Atria of an experimental animal were superdistended by blood that resulted in decreased reabsorption of Na+ and water in renal tubules. This can be explained by the influence of the following factor upon kidneys: A Natriuretic hormone B Aldosterone C Renin D Angiotensin E Vasopressin 3. A 4 y.o. child with signs of durative proteinic starvation was admitted to the hospital. The signs were as follows: growth inhibition, anemia, edemata, mental deficiency. Choose a cause of edemata development: A Reduced synthesis of albumins B Reduced synthesis of globulins C Reduced synthesis of hemoglobin D Reduced synthesis of lipoproteins E Reduced synthesis of glycoproteins 4. A hypertensive glucose solution was introduced to a patient. It will intensify water movement: A From the cells to the intercellular liquid B From the intercellular liquid to the capillaries C From the intercellular liquid to the cells D From the capillaries to the intercellular liquid E There will be no changes of water movement 5. Toxic pulmonary edema was reproduced on a laboratory rat by means of ammonium chloride solution. What is the leading pathogenetic factor of this edema? A Increased permeability of capillars B Increase of venous outflow C Decrease of colloid osmotic pressure D Disorder of neural and humoral regulation E Increase of lymph outflow 2010 1. A woman with intractable vomiting was admitted to the infectious disease ward. What changes of water-salt metabolism are likely to be observed? Hyperosmolar dehydration Hypo-osmolar hyperdehydration Hyper-osmolar huperdehydration Hypo-osmolar dehydration Iso-osmolar dehydration 2. A 49-year-old woman spent a lot of time standing. As a result of it she got leg edema. What is the most likely cause of the edema? Increase in oncotic pressure of blood plasma Decrease in hydrostatic pressure of blood in arteries Decrease in hydrostatic pressure of blood in veins Increase in systemic arterial pressure Increase in hydrostatic pressure of blood in veins 3. Examination of experimental rats that have been getting only carbohydrate feed for a long time revealed accumulation of water in tissues. What is the leading pathogenetic mechanism of edema development? Membranogenic Lymphogenous Dysregulatory Hypooncotic Hypersmolar 4. A patient was admitted to the infectious diseases department. His skin was dry, with low turgor; he had rice-water stool. The patient was diagnosed with cholera. This disease is ordinarily accompanied by the following disorder of water-electrolytic balance: Hypoosmotic hypohydration Hypoosmotic hyperhydration Isoosmotic hypohydration Hyperosmonic hyperhydration Hyperosmotic hypohydration 5. An experimental rat got intra-abdominal injection of 10 ml of 40% glucose solution. 60 minutes later the rat passed into a comatose state as a result of dehydratation. What is the mechanism of development of this state? Acid-base disbalance Reduction of vasopressin secretion Rise of osmotic pressure of extracellular fluid Rise of oncotic pressure of extracellular fluid Loss of salts and water Situational tasks 1. The patient has tumor of the medulla oblingata whuch accompanied by a pronounced hypersalivation (6-7 l per day). 1. What disorder of the water-salt metabolism can be at the patients? ____________________________________________________________________ ____________________________________________________________________2. What types of this disorder you know? ____________________________________________________________________ ____________________________________________________________________3. What reasons can lead to them? ________________________________________________________________________________________________________________________________________ 4. What changes will occur at the organism? ________________________________________________________________________________________________________________________________________ 2. The newborn child has vomiting, excessive dryness of the skin and mucous membranes. At the examination pilorostenosis was found. 1. What disorder of the water-salt metabolism can be at the patients? ____________________________________________________________________ ____________________________________________________________________2. Clasification of the water-salt metabolism disorders? ____________________________________________________________________ ____________________________________________________________________ 3. Operation of malignant tumor of the upper jaw removing was done to the patient. Operation complicated by massive bleeding. During two days after this the patient was injected plenty of fluids. (Daily diuresis did not control) .. 1. What disorder of the water-salt metabolism can be at the patients? ____________________________________________________________________ ____________________________________________________________________2. How this disorder can be classified according to the osmotic pressure? ____________________________________________________________________ ____________________________________________________________________3. Reasons of its origin? ________________________________________________________________________________________________________________________________________ 4. During examination of the children from carpathian village in many of them multiple caries was found. 1. Inssuficiency of which mineral in food can cause development of caries? ____________________________________________________________________ ____________________________________________________________________2. What other reasons could lead to its origin. ____________________________________________________________________ ____________________________________________________________________3. Prophylaxis of this disease? ________________________________________________________________________________________________________________________________________ 5. Development of the sialolithiasis (chronic inflammation of the salivary gland, accompanied by the formation of calculus in its channel) can be in the case mineral metabolism disorder. 1. Which mineral metabolism disturbances can be in this case? ________________________________________________________________ ____________________________________________________________________2. Characteristic of the sialolithiasis? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 6. The patient has edem of the left half face, acute toothache. The doctor diagnosed acute pulpitis. 1. Explain mechanism of edema formation at the patient. ____________________________________________________________________ ____________________________________________________________________2. How edema can be classified by pathogenesis? ____________________________________________________________________ ____________________________________________________________________3. Treatment tactic ________________________________________________________________________________________________________________________________________ 7. A few days after the flu patient began to complain of decreasing of diuresis (5-6L), a thirst (polydipsia), takes place nicturia. In the analysis of urine specific gravity 1004. 1. Which disease nakes place in this case? ____________________________________________________________________ ____________________________________________________________________2. Explain reasons of this edema formation. ________________________________________________________________________________________________________________________________________3. Treatment tactic ____________________________________________________________________ ____________________________________________________________________ 8. Edema of the the face and upper extremities developed at the child after strowberry eating . 1. Explain the main mechanism of this edema origin. ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 2. How edema can be classified by pathogenesis? ________________________________________________________________________________________________________________________________________3. What does it mean hidden edama? ____________________________________________________________________ ____________________________________________________________________ 9. Young woman just eat plant food. The number of calories per day 1000 Kkal. A month after this "diet" edema began to develop at this woman. 1. Explain the main mechanism of this edema origin. ___________________________________________________________________ ____________________________________________________________________2. Explain reasons of this edema formation. ____________________________________________________________________ ____________________________________________________________________________________________________________________________________________________________________________________________________________ 10. The patient was hospitalized with a diagnosis congestive heart failure in a state of decompensation. Complains of shortness of breath, tachycardia, edema of lower extremities, ascites. 1. Expalin mechanism of edema formation in this patient? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 2. Expalin their localization. ________________________________________________________________________________________________________________________________________ 3. Definition of "dropsy" and "edema". Give examples of dropsy. ____________________________________________________________________________________________________________________________________________________________________________________________________________ Theme 23: VIOLATION OF THE ACID-BASIC BALANCE. Actuality of the theme. Constancy of pH of internal environment is the necessary condition of existence of higher organisms. It is provide certain correlation of acids and bases (acid-basic balance - ABB) in biological environments, at violation of which an organism perishes. Violations of ABB are observed at many diseases and complicate their course. Knowledge of indemnification mechanisms of ABB violations and their support is one of major steps in the prophylaxis of many diseases complications. General purpose of the lesson. To learn reasons and mechanisms of basic acid-basic state (ABS) violations development, and also indexes which characterize these violations. For this it is necessary to know: To select main reasons which result in the origin of ABB. To expose the mechanisms of ABB violations development. To explain compensate possibilities of organism which are included at the different forms of ABB violations. To design violation of the ABB. For realization of purpose of lesson it is necessary to have the base knowledges-skills: Concept about the buffer systems. (department of normal physiology); Concept about blood pH (department of normal physiology). Information that is necessary for addition to knowledges-abilities of bases on these questions can be found in the followings textbooks: Materials from normal physiology course For this it is necessary to know: To expose the typical forms of violations of acid base balance metabolism. To expose main forms of acid base balance metabolism violations. To analyze cause-effect relationship in the pathogenesis of the typical acid base balance disorders and characterized pathological and the adaptive-compensatory changes; To analyze the methods of experimental modeling of typical metabolic processes and to determine the causes and mechanisms of their development. The checking of primary level of knowledges Give the answer to the followings questions: Give determination of the acid-basic balance. What index of blood active reaction and what is it evened? Name the chemical buffer systems of organism. What physiological systems take part in supportion of ABB? How does the system of the external breathing take part in regulation of ABB? How does the kidney take part in regulation of ABB? What is acidogenesis? What is amoniogenesis? Name the basic forms of ABB violation. Give definition to acidosis. Give definition to alkalosis. How does divide acidosis and alkalosis depending on the pH changes? How does divide acidosis and alkalosis after the mechanisms of development? Name main reasons for gas acidosis origin. Name main reasons for gas alkalosis origin. Name the types for nongas acidosis. Name the types fon nongas alkalosis. What reasons of metabolic acidosis origin? What are the reasons for exogenous acidosis origin? What are the reasons for excretory acidosis origin? What are the reasons for hypochloremic alkalosis origin? What are the reasons for hypokaliemic alkalosis origin? What are the reasons for exogenous alkalosis origin? Standards of answers. It is permanent correlation between hydrogen and OH ions in the internal environment of organism. pH = 7,36 - 7,44 ) Hydrocarbonatic B) Phosphatic C) Hemoglobin D) Protein ) System of the external breathing B) Kidney C) Digestive system Supports pressure of CO2 in arterial blood. ) Acidogenesis B) Amoniogenesis C) Reabsorbtion of hydrocarbonat Synthesis and secretion in the kidney tubules H+ ions. Synthesis and secretion in the kidney tubules the ammonium ion. ) Acidosis B) Alkalosis It is an absolute or relative accumulation of acids in the internal environment of organism. It is an absolute or relative accumulation of bases in the internal environment of organism. ) Compensated (if pH keeps in physiological norm) B) Uncompensated (if pH goes outside physiological norm) ) Gas (caused the primary changes of CO2 pressure in blood) B) Non gas (caused an accumulation in the organism of non-flying products of acid or alkaline character) ) Hypoventilation of lungs, that is accompanied violation of CO2 destroying from the organism B) Breathing in air with high maintenance of !2 ) Hyperventilation of lungs B) Incorrectly guided artificial respiration ) Metabolic B) Excretory C) Exogenous ) Excretory (hypochloremic, hypokaliemic) B) Exogenous (hypernatriemic) An accumulation in the organism of non-flying acids as a result of metabolic disturbances: lactatatsidosis, ketoacidosis. Hit in the organism of exogenous non-flying acids. Loss of hydrocarbonat by an organism at kidney function violation and digestive disorders. Repeating vomit which is accompanied the loss of Cl-. Hyperaldosteronism, that is accompanied the loss of potassium ions with urine. Hit in the organism of exogenous bases (for example, introduction of hydrocarbonat during wrong correction of nongas acidosis). Theoretical questions, at the base of which the execution of purpose types of activity is possible. Classification of ABB violations. Acidosis, definition of concept. Kinds. Reasons and mechanisms of development. Gas acidosis: causes and mechanisms of development, clinical manifestations. Non gas acidosis (metabolic, excretory, exogenous): causes and mechanisms of development, the relationship between ABB and electrolyte exchange disorders. Compensation and violation of functions at acidosis. Alkalosis, determination of concept. Kinds. Reasons and mechanisms of development. Gas acidosis: causes and mechanisms of development, clinical manifestations. Non gas acidosis (excretory, exogenous): causes and mechanisms of development. Violation of functions and compensation of the different types of alkalosis. Main indexes of the acid-basic state. Changes of indexes at different ABB violations. Role of blood buffer systems, ion exchange, respiratory system and kidney in mechanisms of compensation and correction of violations of ABB. Prynciples of the pathogenetic therapy of acidosis and alkalosis. Literature: Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005. Practical work: VIOLATION of the ACID-BASIC STATE Object of work: to define titratable acidity of urine at acidosis and alkalosis. EXPERIMENT ! 1. Take 5 ml of urine, add 2 drops of phenolphthalein. Titrate by the drops of decinormal solution of NaOH till the colour of solution become to rose. Titratable acidity  it s the amount of alkali (ml), which we use for neutralization of 1 liter of urine acidic products. In a norm this index is equal 200-400 ml. For titration of 5 ml of urine we used ______ ml of alkali. 5 ml of urine - _______ ml of alkali 1000 ml of urine X ml of alkali X = ____________________________ ml Conclusion:____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________ Tests of an open database (2011) . 1. Patients who suffer from severe diabetes and don't receive insulin have metabolic acidosis. This is caused by increased concentration of the following metabolites: A Ketone bodies B Fatty acids C Unsaturated fatty acids D Triacylglycerols E Cholesterol 2. An infant has apparent diarrhea resulting from improper feeding. One of the main diarrhea effects is plentiful excretion of sodium bicarbonate. What form of acid-base balance disorder is the case? A Metabolic acidosis B Metabolic alkalosis C Respiratory acidosis D Respiratory alkalosis E No disorders of acid-base balance will be observed 3. Diabetes mellitus causes ketosis as a result of activated oxidation of fatty acids. What disorders of acid-base equilibrium may be caused by excessive accumulation of ketone bodies in blood? A Metabolic acidosis B Metabolic alcalosis C Any changes woun't happen D Respiratory acidosis E Respiratory alcalosis 4. The patient with diabetes mellitus has been delivered in hospital in the state of unconsciousness. Arterial pressure is low. The patient has acidosis. Point substances, which accumulation in the blood results in these manifestations: A Ketone bodies B Amino acids C Monosaccharides D High fatty acids E Cholesterol esters 5. A pregnant woman had been having toxicosis with severe repeated vomiting for 24 hours. In the end of the day there appeared tetanic convulsions and fluid loss. What shift of acid-base state caused these changes? A Excretory alkalosis B Gaseous alkalosis C Gaseous acidosis D Metabolic acidosis E Excretory acidosis 6. A newborn child ill with pylorostenosis has frequent vomiting accompanied by apathy, weakness, muscular hypertonia, sometimes convulsions. What form of acid-base balance disorder has developed? A Nongaseous alkalosis B Gaseous alkalosis C Gaseous acidosis D Metabolic acidosis E Excretory acidosis 7. A patient has disorder of airways patency at the level of small and middle bronchs. What changes of acid-base balance may take place? A Respiratory acidosis B Respiratory akcalosis C Metabolic acidosis D Metabolic alkalosis E Acid-base balance won't change 2009-2010 1. A man is in the state of rest. He was been forcing himself to breath deeply and frequently for 3-4 minutes. What effect will it have upon acid-bace balance of the organism? Respiratory acidosis Respiratory alkalosis There will be no change in acid-base balance Metabolic alkalosis Metabolic acidosis 2. As a result of improper feeding an infant got full-blown diarrher. One of its main consequences is excretion of large amount of sodium bicarbonate. What form of acid-base balance disturbance is it? 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The patient has severe inflammation of the gums which caused hypersalivation (3-4 l of saliva during the day) What kind of ABB violations can be at the patient? ________________________________________________________________________________________________________________________________________ 2. What data of ABB will be changed at the patient? ________________________________________________________________________________________________________________________________________3. Explain role of physiological buffers in this case. ________________________________________________________________________________________________________________________________________ 2. The pregnant woman has toxicosis, which accompanied by prolonged vomiting =0 ?@>BO7V 4>18. Convulsions and xerostomia take place. 1. What kind of ABB violations can be at the patient? ________________________________________________________________________________________________________________________________________2. What possible violations can arise up from the side of different organs and systems? ________________________________________________________________________________________________________________________________________3. How ABB can be corrected at the patient? ________________________________________________________________________________________________________________________________________ 3. Diarrhea arised up at the patient after receiving poor quality food. At the next day arterial hypotension, tachycardia, extrasystoles apeared. Blood-pH 7, 20 1. What kind of ABB violations can be at the patient?? Blood @ in the norm? ____________________________________________________________________________________________________________________________________________________________________________________________________________2. Value of physiological buffer? ________________________________________________________________________________________________________________________________________3. In what does consist compensation of functions? ____________________________________________________________________________________________________________________________________________________________________________________________________________ 4. What possible violations can arise up from the side of different organs and systems? ____________________________________________________________________________________________________________________________________________________________________________________________________________ 4. Patient with diabetes mellitus has diabetic coma with violation of acid-basic state. 1. What kind of ABB violations can be at the patient? ________________________________________________________________________________________________________________________________________ 2. What data of ABB will be changed at the patient? ________________________________________________________________________________________________________________________________________ 3. Classification ABB disorders? ________________________________________________________________________________________________________________________________________ 4. What reasons can lead to different disorders of ABB? ________________________________________________________________________________________________________________________________________ 5. What compansatory reactions can take place at the ABB disorders? ________________________________________________________________________________________________________________________________________ 5. The patient suffered with bronchial asthma characterized by frequent attacks. There is a pronounced spasm of the bronchius and difficult exhalation (expiratory dyspnea). 1. What kind of ABB violations can be at the patient? ____________________________________________________________________________________________________________________________________________________________________________________________________________2. In what does consist compensation of functions? ________________________________________________________________________________________________________________________________________3. What is the main data of compensation? ________________________________________________________________________________________________________________________________________4. What possible violations can arise up from the side of different organs and systems? ____________________________________________________________________ ________________________________________________________________________________________________________________________________________ 6. Patient A. was hospitalized in the neurosurgical department with brain concussion accompanied by repeated vomiting, shortness of breath expressed. In a surveyAt examination next data of ABB pH = 7.56;pSO2 = 30 mm Hg; SB = 28 mmol / l BB = 50 mmol / l, RE = 5 mmol / liter. 1. What kind of ABB violations can be at the patient? ________________________________________________________________________________________________________________________________________2.What is the possible reason of its origin ________________________________________________________________________________________________________________________________________3. What possible violations can arise up from the side of different organs and systems? ________________________________________________________________________________________________________________________________________4. How ABB can be corrected at the patient? ________________________________________________________________________________________________________________________________________ 7. A pregnant woman has toxicosis, which accompanied by prolonged vomiting. Data of her biochemical analyses show: pH of blood 7.38, pCO2 of arterial blood 46 mmHg, SB 38 mmol/L, BE (+ 6 mmol/L). 1) What type of ABB violation does take place in this patient? ________________________________________________________________ 2) In what does consist of compensation of functions? ________________________________________________________________________________________________________________________________________________________________________________________________________ 3) What possible violations can arise up? ________________________________________________________________________________________________________________________________________________________________________________________________________ 4) How does to correct ABB violation in a patient? ________________________________________________________________________________________________________________________________________________________________________________________________________ 8. Patient with diabetes mellitus has violation of acid-basic state, which developed as a result of keton bodies accumulation. Blood pH 7,32. 1) What type of ABB violation does take place in this patient? ________________________________________________________________ 2) What possible violations can arise up from the side of different organs and systems? ________________________________________________________________________________________________________________________________________________________________________________________________________ 3) How does to correct ABB violation in a patient? ________________________________________________________________________________________________________________________________________________________________________________________________________ 9. A 58-years-old patient was admitted to the hospital in severe state. 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