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Questions to prepare for examination 2015-16 1. The notion of "nosology", parts nosology. 2. The notions of "pathologic process", pathologic state", "pathologic reactions", "typical pathologic processes", "remission", “recurrence","complication". 3. Disease, definition. Principles used in classification of diseases. Stages of disease. 4. Etiology, definition. The nature and characteristics of pathogenic factors. Factors of diseases: environmental, genetic, social. The relation between causes and conditions in the development of diseases. 6. The notions of "pathogenesis", "vicious circles". 7. Reactivity of the body and its role in the development of disease. Forms and types of reactivity. 8. Arterial hyperemia: definition, causes, types (physiologic and pathologic), mechanisms (neurogenous, neuromyoparalytic and humoral) and consequences. Reactive hyperemia. Manifestations of arterial hyperemia and its mechanisms. 9. Venous hyperemia: definition, causes and consequences. Manifestations of venous hyperemia and their mechanisms. 10. Ischemia: definition, causes and consequences. Manifestations of ischemia and their mechanisms, factors that influence on the consequences of ischemia. 11 Stasis: types and causes. 12. Sludge syndrome: types, causes, and mechanisms. 13.Definition and significance of inflammation. Causes of inflammation. 14. Primary and secondary alteration in the focus of acute inflammation: causes, mechanisms of development, manifestation. Physico-chemical changes in the focus of inflammation. 15. Exudation. Definitions of an exudate and transudate. Sequence and mechanisms of vascular changes in acute inflammation. 16. Inflammatory mediators that influence on these processes. 17. Phagocytosis: stages. 18. Local and systemic signs of inflammation. 19. Nature and effects of inflammatory mediators: vasoactive amines, complement, kinin, and clotting systems, arachidonic acid metabolites, platelet-derived factor, cytokines and chemokines, nitric oxide, lysosomal constituents 20.General features of acute and chronic inflammation. 21. Typical forms of disordered immunologic reactivity. Principles of classification of immunodeficiency states. 22. Primary immunodeficiencies: classification and clinical manifestations. Forms of primary immunodeficiency (causes, mechanisms, clinical manifestations): a) B system-dependent: b) T system-dependent: с) combined. 23. Secondary (acquired) immunodeficiency states. AIDS 24. The notion of the "allergy". Types of allergens. Exogenous and endogenous allergens. 25. Stages of allergy. a) Immunologic stage. b) Pathochemical stage. c) Pathophysiological stage 26. Anaphylactic (I) type of allergy. The nature of allergen and antibody. Mediators of the anaphylactic reaction. 27. Type II hypersensitivity. The nature of allergen and antibody. Mechanisms and clinical examples of type II allergies. 28. Type III hypersensitivity. The nature of allergen and antibody. Mechanisms and clinical examples of type III allergies. Systemic and local immune complex disease. 29. Type IV hypersensitivity. The nature of allergen and antibody. 30. Definition of fever. Differences between fever and hyperthermia. Types of pyrogens. The biological significance of fever 31. Pathogenesis of fever. Features of thermoregulation at different stages of fever. 32. Types of fever: - based on the extent of temperature rise; - based on the circadian temperature fluctuations. 33. Exertional hyperthermia: causes, mechanisms 34. Definition of hypoxia and its classification 35. Exogenous hypoxia: causes, types and typical changes 36. Respiratory hypoxia: causes, types and typical changes in the given type of hypoxia 37. Anemic hypoxia: causes, types and typical changes 38. Circulatory hypoxia: causes, types and typical changes 39. Histotoxic and substrate types of hypoxia: causes, types and typical changes 40. Adaptive reactions in acute hypoxia. 41. Mechanisms of long-term adaptation to hypoxia. 42. Hypoglycemia: сauses and mechanisms. Hypoglycemic coma. 43. Hyperglycemia: causes and mechanisms. 44. Diabetes mellitus: characteristic features, classification, pathogenesis of type I and type II forms. 45. Metabolic disorders (carohydrate, protein, lipid) in diabetes mellitus. 46. Complications of diabetes mellitus (chronic and acute). Ketoacidotic coma. 47. The main classes of lipoproteins and their functions. Atherogenic and antiatherogenic lipoproteins. Mechanisms of hyperlipidemia. 48. Obesity: definition, diagnostic approaches, pathological significance. Types and pathogenesis of obesity. 49. Atherosclerosis: description and pathological features. Risk factors of atherosclerosis. Stages of atherogenesis: - initiation; - formation and evolution of atheroma; - complications. 50. Hypohydration: causes, types, mechanisms consequences, and pronciples of treatment. of development, manifestations, 51. Overhydration: causes, types, mechanisms consequences, and pronciples of treatment. of development, manifestations, 52. Edema: definition, types, the main factors of development, principles of treatment. 53. Edema during cradiac failure: etiology, pathogenesis, and manifestations. 54. Renal edema: etiology, pathogenesis, manifestations, and consequences. 55. Shock: characteristics, types, etiology, pathogenesis, manifestations, principles of treatment. 56. Coma: characteristics, types, etiology, general pathogenesis, manifestations, principles of treatment. 57. Definition of anemia and its classification. 58. Anemias of blood loss: types, causes, hematological signs. 59. Hemolytic anemias: types, common causes, manifestations, hematological signs. Hereditary spherocytosis: pathogenesis, manifestations, hematological signs. Sickle cell disease: pathogenesis, manifestations, hematological signs. Thalassemia syndromes: types, pathogenesis, manifestations, hematological signs. 60.B12 (Megaloblastic) anemia: causes, pathogenesis, manifestations, hematological signs. 61. Iron deficiency anemia: causes, pathogenesis, manifestations, hematological signs. 62. Aplastic anemia: causes and pathogenesis, hematological signs. 63. Erythrocytosis: causes and mechanisms 64. Leukopenia: definition and causes. General mechanisms of leukopenia. Patterns of shift to the right. 65. Leukocytosis: causes and mechanisms. Types of leukocytosis; patterns of shift to the left. 66. Leukemoid reactions: typical features, causes, mechanisms of development, physiologic significance. 67. The system of hemostasis: components and their function. Typical forms of pathology of the hemostatic system. 68. Thrombotic syndrome: its main causes, mechanisms of development, manifestations and consequences. 69. Hemorrhagic syndrome: causes, mechanisms of development, manifestations and consequences. 70. Causes and mechanisms of thrombocytopenia and thrombocytopathia. 71. Abnormalities in clotting factors. Hemophylias. 72. The syndrome of disseminated intravascular coagulation: stages, mechanisms of development, manifestations and consequences. 73. Definition of coronary insufficiency. The main cuases of coronary insufficiency. Adaptive mechanisms developing during acute and chronic coronary insufficiency. 74. The syndromes of coronary insufficiency: angina pectoris, myocardial infarction, chronic ischemic heart disease, sudden coronary death. 75. Definition, general causes and classification of heart failure. Myocardial and nonmyocardial cardiac insufficiency. 76. Adaptive reactions during acute and chronic heart failure: Frank-Starling mechanism, myocardial hypertrophy, redistribution of cardiac output, salt and water retention, activation of the sympathetic system. 77. Pathogenesis of the myocardium decompensation during hypertrophy. 78.Hemodynamic abnormalities in heart failure. Clinical features of heart failure: the syndromes of cardiac edema and cachexia. 79. Definition and principles of classification of arterial hypertension. 80. Renal arterial hypertension: pathogenesis of renovascular, renoprival, renal parenchymal hypertension. 81. Pathogenesis of endocrinogenic arterial hypertension. 82. Essential hypertension: etiology and pathogenesis. 83. Alveolar hyper- and hypoventilation: causes, mechanisms of development, consequences, and typical changes in breathing volumes. 84. Disorders of the neurogenic control of breathing. Pathological forms of breathing. 85. Types and consequences of perfusion disorders: pulmonary arterial hyper- and hypotension. 86. Types and mechanisms of ventilation-perfusion mismatch. 87. Abnormal diffusive capacity of the alveolar-capillary barrier. 88. Typical forms of functional pathology of the digestive tract: general etiology. 89. Disorders of appetite, taste, and initial treatment of food in the oral cavity. 90. Disorders of swallowing: dysphagia, achalasia, diffuse esophageal spasm. 91. Disorders of digestion in the stomach: disturbance of secretory and motor function. 92. Disorders of digestion in the intestine: disturbance of secretion, motor function, and absorption. 93. The syndrome of malabsorption: etiopathogenesis, manifestations and consequences. 94. Typical disorders of cavity digestion: causes, manifestations. 95. Typical disorders of parietal digestion: causes, manifestations. 96. Pathogenesis of peptic ulcer of the stomach and duodenum. 97. General causes of liver dysfunction. The syndrome of hepatic insufficiency Causes, types and pathogenesis of hepatic coma. 98. The syndrome of hepatic insufficiency. Typical disorders of carbohydrate, aminoacid, protein, and lipid metabolism in hepatic insufficiency; failure of detoxification function. 99. Hemolytic jaundice: causes, mechanisms, clinical and laboratory manifestations. 100. Obstructive jaundice: types, causes, mechanisms, clinical and laboratory manifestations, consequences. 101. Hepatocellular jaundice: causes, mechanisms, stages, clinical and laboratory manifestations. 102. General causes and mechanisms of kidneys dysfunction. Disorders of filtration, tubular reabsorption and excretion. 103. Syndromes of acute renal insufficiency: typical features, causes and manifestations 104. Syndromes of chronic renal insufficiency: typical features, causes and manifestations. Uremic coma. 105. Nephrotic and nefritic syndromes: typical features, causes and manifestations. 106. Pyelonephritis: characteristic features, causes and pathogenesis. 107. Nephrolitiasis: causes, mechanisms of development, consequences. 108. General etiology and pathogenesis of endocrine disorders. Typical forms of functional pathology of adenopituitary. Hypopituitarism: types, causes, mechanisms of development and manifestations 108. Hyperpituitarism: types, causes, mechanisms of development and manifestations. Acromegaly and gigantism. Typical forms of disorders of neurohypophysis. Diabetes insipidus 109. Typical forms of adrenals’ dysfunstion. Hypercortisolism: types, pathogenesis and manifestations. Cushing’s disease and syndrome, hyperaldosteronism. 110. Hypocortisolism: types, pathogenesis and manifestations. Acute adrenal failure and Addison’s disease, hypoaldosteronism, syndromes of adrenal androgen excess. 111. Disorders of adrenal’s medulla. Manifestations and consequences of phyochromocytoma. 112. Hypothyroidism: types, causes, mechanisms of development and clinical manifestations. Common hypothyroid states: myxedema, cretinism, endemic goiter. 113. Hyperthyroidism: types, causes, mechanisms of development and clinical manifestations. Pathogenesis and manifestations of Grave’s disease, Hashimoto’s thyroiditis. 114. General etiology, pathogenesis, and typical forms of pathology of the nervous system. 115. Disorders of locomotion: manifestations of the upper (central) and lower (peripheral) motor neuron damage. 116. Hypokinetic and hyperkinetic movement disorders: types, etiology and pathogenesis. 117. Disorders of sensation: general etiology and classification.Hypo- and hypersthesia, dysesthesia: types and mechanisms of disorders. HYPOXIA 3. Urgent compensatory reaction at acute hypoxia (reduced pO2 in air): tachypnoe stimulation of erythropoesis redistribution of blood tachycardia increase blood supply in liver spasm vessels into internal organs 4. Choose the reasons of hypoxie hypoxia: mountain sickness increased pO2 in air emphysema reduced pO2 in air poisoning by aniline 5. Choose the reasons of blood type hypoxia: poisoning by charcoal gaze mountain sickness reduced pO2 in air anemia poisoning by methemoglobin-complexes presence into closed space 6.Which changes in cells яге adaptive in the case of hypoxia? inhibition of glycolysis r e d u c e d act ivity of Na/K t and Ca2+ ATP-enzymes activation of' glycolysis mobilization of kreatinphosphate mobilization of glycogen from depot activation of peroxidative oxidation of lipids increased concentration of Sodium into cells 7. Which factor can promote oxygenic capacity of blood at hypoxia? tachypnoe mobilization of blood from depot tachycardia stimulation of erythropoesis into bone marrow activation of erythropoietins increased cardiac output 8. Choose clinical signs of long-time adaptation to hypoxia: hypertrophy of lungs tachypnoe hypertrophy of myocardium tachycardia increased number of mitochondria into cells stimulation of erythropoesis mobilization of blood from depot 9. Choose the reason of blood type hypoxia: poisoning by CO (charcoal gaze) vit. D deficiency vit. В12 deficiency shperocytosis gaseous embolism 10. Choose the reason of blood type hypoxia: hemoglobinosis S reduced activity of respiratory enzymes in tissues poisoning by cyanides poisoning by nitrates chronic blood loss 11. Choose the reasons of tissue type hypoxia: vit. A deficiency poisoning by methemoglobin-complexes poisoning by cyanides acute blood loss increased formation of prostaglandins E1 12. Choose cases when hemoglobin affinity to oxygen is reduced? metabolic acidosis sickle-cells disease metabolic alkalosis reduced activity 2,3-diphosphoglycerate in red blood cells reduced body temperature increased body temperature hypocapnia 13. Choose cases when hemoglobin affinity to oxygen is increased? metabolic acidosis sickle-cells disease metabolic alkalosis reduced activity 2,3-diphosphoglycerate in red blood cells reduced body temperature increased body temperature hypocapnia 14. Choose changes in human body at long presence in mountains: increased activity 2,3-diphosphoglycerate in red blood cells increased hematocrit hypertrophy of myocardium hypoventilation in lungs reduced activity of respiratory enzymes in cells inhibition of nucleonic acids' synthesis increased concentration of endogenous opiates increased vascularisation in peripheral organs and tissues increased basal metabolism 15. Choose the reasons of respiratory hypoxia: anemia pneumonia poisoning by nitrates lung's collapse poisoning by charcoal gaze pneumothorax 17.Choose the reasons of tissue type hypoxia: poisoning by charcoal gaze poisoning by cyanides poisoning by aniline poisoning by monoiodineacetate poisoning by barbiturates 18. Choose the signs of circulatory hypoxia: increased arterio-venous difference of oxygen reduction of linear blood velocity respiratory acidosis -hypertension braducardia reduction of volumetric blood velocity into capillaries reduced arterio-venous difference of oxygen. 19.Choose the mechanisms of long-time adaptation to hypoxia: mobilization of blood from depot increased number of capillaries increased number of mitochondria dyspnea hyperplasia of bone marrow tachycardia hypertrophy of myocardium 20. Choose the mechanisms of circulatory hypoxia: reduction of oxygen transport to tissues reduction of oxygen utilization in tissues reduced activity of respiratory enzymes in tissues chronic heart insufficiency increased consumption of oxygen at physical loading 21. Choose the reasons of respiratory hypoxia: emphysema pneumonia collapse lung's collapse chronic heart insufficiency pneumothorax reduction of blood volume 22. Choose clinical signs for circulatory hypoxia: hypotension decreased arterio-venous difference of oxygen reduced concentration of oxygen into arterial blood reduction of volumetric blood velocity into capillaries tachycardia 23. Choose reaction in organism at hyperoxia: inhibition of chemo-receptors into vessels dyspnea suppression of heart rate and rhythm of respiration activation of chemo-receptors into vessels reduced cardiac output tachycardia DISORDERS OF MICROCIRCULATIOIN 1. Give types of venous hyperemia due to pathogenesis: myoparalytic obstructive cardiogenic (at heart failure) compressive neuroparalytic 2. Which factors can increase permeability of vascular wall? increased blood velocity in capillaries increased viscosity of blood products of must cells degranulation acidosis leucopenia activation of hydroiyzes in interstitial liquid 3. Give types of arterial hyperemia due to pathogenesis: neurotonic obstructive neuroparalytic myoparalytic comprcssive 4. Which changes of microcirculation are characteristic for ischemia? increased arlerio-venous difference into vessels reduction of hydrostatic pressure in arterioles and pre-capillaries incretled linear blood velocity increased reabsorption of liquid from tissues into capillaries reduced number of capillaries with blood 5. Which factors can promote development of thrombosis? reduction of blood velocity increased blood velocity reduced number of platelets aggregation of platelets exudation atherosclerosis 6. "Sludge" phenomenon is: the first stage of cloth formation vital aggregation of red blood cells into microcirculatory vessels at increased blood viscosity and separation of blood formation of thrombo-leucocytic aggregates on the vessel's wall separation of btood on cells and plasma coagulation of blood 7. "Sludge" phenomenon can develop at the next types pathology: acute heart failure massive burn shock massive blood loss hypervolemia (increased blood volume) hyperhydratation 8. Which factors can promote development of thrombosis? damages of vascular wall decreased blood velocity activation of coagulation increased blood viscosity activation of anti-coagulant system vit. К deficiency excess of epinephrine in blood 9. Choose the normal level of hydrostatic pressure into arterial part of capillaries: 15 mm of Mercury 25 mm of Mercury 35 mm of Mercury 55 mm of Mercury 10. Which changes can develop in the focus of ischemia? necrosis acidosis hypofunction hyperfunction excess of K+ into cells deficiency of Na+ into cells excess of Си++ into cells 11. Stasis is: complete stop of blood circulation into vessels increased blood supply in organs or tissues due to dilatation of arterioles decreased blood supply in organs or tissues due to spasm of arterioles 12. True stasis is: increased blood supply in organs or tissue due to reduced blood outflow local spot of blood circulation due to increased blood viscosity 13. Choose pathogenic factors of neuroparalytie arterial hyperemia: activation of parasympathetic system irritation of cholinergic system blockade of adrenergic system activation of histamine and serotonin system activation of vegetative system 14. Heat in the focus of arterial hyperemia can be explained by: increased inflow of arterial blood activation of oxidative processes excessive formation of lymph increased number of capillaries with blood 15. Choose the reasons of true (capillary) stasis: compression of arteries by scar-tissue direct action temperature on vascular wall damages of tissues by acid and alkaline thromboembolism spasm of peripheral vessels actions of toxins on organism 16. Rheological state of blood depends on: cardiac output concentration of proteins in plasma ratio between blood cells and plasma deformation's properties of red blood cells functions of collateral vessels 17. Which changes of microcirculation are characteristic for arterial hyperemia? increased number of capillaries with blood reduction of hydrostatic pressure in capillaries increased blood velocity in capillaries increased outflow of lymph increased filtration of liquid from vessels into tissues 18. Choose the sequences of venous hyperemia: infarction embolism atrophy hemorrhage into tissues thrombosis stasis sclerosis 19. Choose the sequences of venous hyperemia: growth of connective tissue increased function of organs dystrophy of tissues hemorrhage into tissues 20. Which changes of microcirculation are characteristic for venous hyperemia? decreased blood velocity in small arteries, capillaries and veins pendulum-like circulation increased outflow of lymph reduced number of capillaries with blood 21. Filtrative pressure is: difference between oncotic pressure in blood and in tissues difference between hydrostatic arterial and hydrostatic venous pressure difference between hydrostatic presuure and oncotic pressure in blood oncotic pressure and osmotic pressure in blood 22. Venous hyperemia can localize focus of inflammation: yes no 23. Physiologic arterial hyperemia is: arterial hyperemia in the focus if inflammation post-ischemic arterial hyperemia activation of thyroid gland function action of turpentine on skin Choose the types of endogenous embolism: fatty air tissue gaze thromboembolism embolism by foreign bodies embolism by amniotic water parasite 25. Give characteristics of microcirculation for arterial hyperemia: increased hydrostatic pressure in capillaries reduced number of capillaries with blood increased number of capillaries with blood increased reapsorption of liquid from tissues into capillaries decreased linear and volumetric blood velocity increased linear and volumetric blood velocity reduced outflow of lymph 26. Choose correct sentences: thrombus, foreign bodies, tissues, fat, bubbles of air, parasites can be embolus arterial embolus can stay in lung's vessels, but venous embolus can stay in any organ embolus of pulmonary vessels, coronary vessels and cerebral vessels are dangerous 27 Choose я possible reasons of gaseous embolism: rapid increasing of barometric pressure wounding of big veins rapid change of barometric pressure from increased level to normal level inspiration of inert gazes sudden change of barometric pressure from normal level to reduced level 28 Which substances can cause arterial hyperemia? acetylcholine epinephrine histamine bradykinin thromboxane A2 29 Which pathogenic factors can cause arterial hyperemia? cutting of peripheral nerves mechanical irritation of tissues and organs. remove of ligature occlusion of arteries by cloth action of mustard plaster on skin compression of veins by tumor V 30 Which substances can cause ischemia? histamine epinephrine acetylcholine bradykinin thromboxane A2 31. Which pathogenic factors can cause venous hyperemia? cutting of peripheral nerves increased pressure into big veins thrombosis of veins at insufficient collaterals compression of veins at pregnancy increased concentration of epinephrine in blood mechanical irritation of organs 32. Aggregation of erythrocytes can be promoted by: increased concentration of globulins in blood decreased concentration of fibrinogen in blood change of electrical charge in red blood cells damages of small vessels reduction of arterial pressure extra-cellular dehydration 33. Choose the types of stasis: hyperemia congestive ischemic true 34. Give characteristics of microcirculation for ischemia: primary dilatation of arteries and secondary dilatation of veins and capillaries spasm capillaries and veins after occlusion in arteries increased linear and volumetric blood velocity decreased linear and volumetric blood velocity increased temperature of organs and tissues decreased temperature of organs and tissues 35. "Sludge-phenomenon" is a main mechanism of: arterial hyperemia venous hyperemia thrombosis stasis ischemia 36. Choose clinical symptoms of venous hyperemia: redness of organs and tissues paleness cyanosis edema increased turgor increased temperature of organ or tissue 3. INFLAMMATION 1. Mechanisms of glucocorticoids effects at inflammation: increase permeability of vascular wall decrease permeability of vascular wall inhibit of kinins production stabilizeof lysosomal membranes inhibit growth of connective tissue 2. Intra-vascular factors of exudation: ncreased viscosity of blood hyperosmia in the focus of inflammation hyperoncm of tissues in the focus of inflammation margination of leucocytes 3. Choose properties of activated components of complement system: provide lyses of foreign cells play role of chemo-attractive substances for neutrophiles and monocytes can activate phagocytosis can cause degranulation of must cells can reduce permeability of vascular wall 4. Choose characteristics of neutrophiles: can recognize and neutralize host dead cells participate in acute inflammation can produce mediators of inflammation can form giant multi-nuclear cells in the focus of inflammation present in the focus of inflammation about 1-2 days 5. Which pathogenic factors can promote transformation arterial hyperemia into venous hyperemia in the focus of acute inflammation? increased permeability of vascular wall increased blood viscosity increased adhesion of endothelium and blood cells 6. Which biological active neutrophiles? C3a-component of complement C5a- component of complement substances play role of chemo-attractive substances for eukotriens B4 prostaglandins E2 7 Enzyme systems of macrophages which have direct bacteriostatic and bacteriolytic effects? katalaze neutral proteazes myeloperoxidaze katepsines 8. Which from listed substances are contained in neutrophiles? lyoscim myeloperoxidaze serotonin prostaglandins 9. Which mediators are produced from phospholipids of cellular membranes? prostaglandins leucotriens factor of platelet's activation bradykinin 10. Which cells play main role in chronic inflammation? micro-phages tissue macrophages macrophages (monocytes) 11. Inflammation is a specific response of organism on injury: yes no 12. Which substance will be loss at cell's destruction: Potassium Sodium Calcium 13. Permeability of vascular wall at alteration is: reduced not changed ncreased 14. Inflammation is developed in three stages: yes no . 15. Which physical-chemical changes in tissues are characteristic for acute inflammation? H+-hyperionia hyperoncia K+-hyperionia hypooncia hyperosmia hypoosmia 16. Which from listed substances are contained in granules of neutrophiles? bradykinin prostaglandins lactoferrin kationic proteins 17. Mediators (stimulators) of proliferation: histamin serotonin polyamines keylones platelet's growth factor 18. Which biological active substances have chemo-attractive properties for neutrophiles? kallidin rkujlicrein histamin Cl-component of complement 19. Which substances can cause pain at inflammation? histamine Sodium ions epinephrine Potassium ions bradykinin prostaglandins 20. Which pathogenic factors can promote transformation of arterial hyperemia into venous hyperemia? dilatation of venules exudation margination of leucocytes aggregation of platelets V 21. Effects of glucocorticoids on inflammation: stimulate proliferation of connective tissue activate histaminaze inhibit of antibodies production cause edemas 22. Primary mediators of inflammation: complement system (C) biogenic amines elasthaze bradykinin serotonin 23. Choose effects of kinins: fibrinolysis activation of all components in guard system of blood pain alteration of cellular membranes spasin of smooth muscles hemostasis chemotaxis of leucocytes 24. Mediators of late (steadfast) exudation: serotonin leucotriens histamine factor of platelet's activation bradykinin 25. Local reactions at inflammation: heat fever redness edema general adaptive syndrome increased RSE 26. Choose cellular mediators of inflammation: kinins ysosomal enzymes vaso-active amines components of complement (C) lymphokins 27. Choose mediators - inhibitors of proliferation: monokins keylones immunoglobulins endothelial factor of chemotaxis prostaglandins filldin 28. Factors of exudation are linked with intra-vascular changes in the focus of inflammation: aggregation of fed blood cells increased hydrostatic pressure into vessels increased viscosity of blood inter-cellular edema of endolhelium destruction of desmosomes 29. Enervation of tissues at inflammation can cause the next effects: activation of energy metabolism inhibition of energy metabolism immune depression immune stimulation activation of proliferation inhibition of proliferation 30. Choose hormones which have anti-inflammatory effects: mineralocotricoids giucocorticoids thyroxin epinephrine ACTH TSH 31. Effects of activated components in complements system: stimulation of histamine's releasing from must cells destruction of attacked cells activation of leucocytes activation of pain terminals 32. Which processes can cause adhesion of leucocytes on the surface of endothelial cells at acute inflammation? neutralization of negative charge in leucocytes and endothelium by positive ions and kationinc proteins reduction of blood supply in venous vessels exposition of P-selectines on the surface of endothelium arterial hyperemia ischemia 33. Acute inflammatory response is characterized by: formation of inflammatory granules increased permeability in micro-circulatory vessels accumulation of giant poly-nuclear cells accumulation of neutrophiles in the focus of inflammation 34. Which processes can be stimulated by neutrophiles at inflammation: chemotaxis of monocytes degranulation of must cells reduced permeability of vascular wall destruction of cells 35. Choose effects of bradykinin: increased arterial pressure in aorta spasm of smooth muscles in organs increase permeability of vascular wall irritate pain terminals reduce permeability of vascular wall 36. Adhesion of leucocytes to endothelium primary develops in: arterioles capillaries post-capillary venules 37. Choose characteristics for histamine: belongs to preformed mediators of inflammation can cause dilatation of micro-circulatory vessels can cause late vascular permeability at acute inflammation irritate pain terminals 38. Which types of exudates are more often at pericarditis? purulent serous hemorrhagic fibrinous 39. Choose obligate (professional) phagocytes: neutrophiles monocytes lymphocytes eosinophiles 40. Which cells can produce mediators at inflammation? basophiles platelets smooth muscles endothelium 41. Choose characteristics for histamine: belong to a new-formed mediators of inflammation can cause immediate permeability of vascular wall at acute inflammation can cause degranulation of must cells product of histidin decarboxilation 42. Choose characteristics for neutrophiles: belong to obligate (professional) phagocytes can produce free radicals have myeloperoxidaze activity contain azurophilic granules can differentiate into focus of inflammation 43. Which substances can activate phagocytosis? IgG IgE prostagiandins E2 fragment C3b of complement system 44. Aspirin inhibits cyclic-oxygenize and suppress the next mediators of inflammation: prostaglandin E2 factor of platelet's aggregation *prostaglandin D2 thromboxane A2 45. Which cells participate in chronic inflammation? macrophages lymphocytes epithelial cells must cells 46. Which factors promote exudates formation at acute inflammation? difficulties of venous outflow reduction of hydrostatic pressure into micro-circulatory vessels retraction of endothelial cells in post-capillary venules destruction of basal membrane in micro-circulatory vessels by enzymes of leucocytes 47. Which cells can produce mediators of inflammation? must cells red blood cells monocytes lymphocytes 48. Choose mechanisms of anti-inflammatory effects of glucocorticoids: inhibit activity of phospholipaze A2 reduce permeability in vessels inhibit of interleukins inhibit of complement system 49. Choose effects of complement system at inflammation: chernotaxis increase permeability in vessels dilatation of vessels 50. Choose correct sequence of leucocyte's emigration in the focus of acute inflammation: 1 .monocytes 2.lymphocytes 3.neutrophiles 3-1-2 1-2-3 2-3-1 4. PATHOPHYSIOLOGY OF THERMOREGULATION. FEVER 1. Choose negative sequences of fever: renal failure vascular failure heart failure hyperthermia damages of liver 2. Effects of endogenous pyrogens on center of thermoregulation: increased production of 1L-1 increased activity of cold-sensitive receptors increased activity of warm-sensitive receptors decreased production of prostaglandins E increased production of prostaglandins E 3. Heat-stroke can develop at the next body temperature: 39°C 40°C 41°C 42°C 4. Which changes of metabolism cam develop at fever? hypoglycemia positive nitrogen balance metabolic acidosis activation of lipolysis inhibition of glycolysis 5. Adaptive reactions of organism to cold temperature: shivering hypertonus of muscles increased sweating decreased excitability of cold-sensitive receptors reduction of respiratory rhythm increased affinity receptors to epinephrine hyperglycemia dilatation of peripheral vessels 6. Choose substances with pyrogenic activity: histamine prostaglandins E lypopolysachrids 1L-1 IL-2 1L-6 kinins factor of platelet's aggregation . 7. Exogenous pyrogens can influence on: cerebral cortex hypothalamus peripheral thermoreceptors neutrophiles monocytes B-lymphocytes red blood cells V 8. Adaptive reactions of organism to cold temperature: increased activity of metabolic processes «muscular shivering» hyperventilation +hypoventilation reduction of basal metabolism spasm of peripheral vessels dilatation of peripheral vessels reduction of sweating increased sweating 9. Choose mechanisms of physical thermoregulation: production of primary heat production of secondary heat («muscular shivering») increased circulation into superficial tissues spasm of peripheral vessels sweating convection V 10. Choose symptoms of the 1Ststage of fever: shivering heat intensive perspiration spasm of peripheral vessels hyperemia into superficial tissues prevalence heat-loss over heat-production prevalence heat-production over heat-loss 11. Choose signs of overheating: activity of termoregulative center is saved depends on environmental temperature absence of shivering anti-pyretic therapy is effective 12. Choose signs of overheating: is caused by pyrogens disorders of thermoregulation active regulation of body temperature 13. Choose mediators with pyrogenic activity: L-1 IL-2 IL-6 G-colony-stimulating factor *factor of tumor necrosis alpha (TNF) IL-8 14. Defense-adaptive reaction at exogenous hyperthermia: shivering intensive perspiration dryness of skin paleness of skin hyperemia of skin dyspnea 15. Mechanisms of urgent adaptation to cold: spasm of peripheral vessels stimulation of fatty tissues «muscular shivering» morphologic-functional changes into muscles increased activity of metabolic processes increased sensitivity of receptors to epinephrine 16. Which action on CNS can promote fever: injection of psychostimulators (phenamin, caffeine) deep narcosis bilateral decortication injection of sedative and neuroleptics (bromides, aminazin) 17. Choose inductors of IL-1: bacterial lipopolysacharides IL-2 IL-1 IL-6 factor of tumor necrosis alpha (TNF) G-colony-stimulating factor 18. Choose effects of IL-6: induction of IL-1 synthesis induction of TNF synthesis fever neurtophilia induction of stress-reaction 19. Choose clinical symptoms of compensatory stage in the case of hyperthermia: tachycardia bradycardia dyspnea suppression of respiration dilatation of peripheral vessels dilatation of vessels in internal organs hemodilution hemoconcentration 20. Choose clinical symptoms of non-compensatory stage in the case of hyperthermia: tachycardia bradycardia dyspnea dilatation of peripheral vessels dilatation of vessels in internal organs + suppression of respiration * hemodilution hemoconcentration 21. Successful reanimation is possible at the next body temperature: 24°C 25°C 26°С 27°С 28°С 22. Which protein's concentration is increased at response of acute phase? C-reactive protein transferrin fibrinogen alpha-2-macroglobu 1 in serum amyloid A 23. Neurtophilia at response of acute phase is caused by: IL-1 IL-6 IL-2 TNF alpha IL-8 24 Which proteins of acute phase have anti-inflammatory effects: C-reactive protein alpha-2-macroglobulin alpha-1 -antitripsin cerulloplasmin fibrinogen crotisol alpha-1 -chemotripsin 25. Choose effects of IL-6: fever activation of T-lymphocytes activation of B-lymphocytes stimulation of immunoglobulins synthesis synthesis of proteins acute phase in liver anorexia activation of endothelial cells 26. Which cytokine can cause synthesis of proteins acute phase in liver? IL-1 TNF alpha 11-6 26 27. Choose urgent adaptive reactions at hypothermia: spasm of peripheral vessels dilatation of peripheral vessels reduction of metabolism activation of glycogenolysis into liver and muscles increased perspiration muscular shivering dyspnea 28. Choose clinical symptoms for non-compensatory stage of hypothermia: reduction of basal metabolism activation of basal metabolism spasm of peripheral vessels dilatation of peripheral vessels arterial hypotension arterial hypertension tachycardia bradycardia 29. Choose the main mechanism of sun-stroke: hyperemia of skin covers dilatation of cerebral vessels dyspnea increasing of arterial pressure reduction of inter-cerebral pressure 30. Endogenous hyperthermia is caused by endogenous pyrogens: yes no 31. Choose correct sentences: pyrogenic activity of microbes is not equal their pathogenic properties only endotoxins have pyrogenic activity components of bacterial membranes have pyrogenic activity nucleonic acids of phagocytes have direct pyrogenic activity 5. ALLERGY 1. Give definition of "hypoergia": State of organism with abnormal (deviated) reactivity and resistance State of organism with reduced non-specific reactivity and resistance State of organism with increased specific reactivity and reduced resistance 2. Give characteristics for phase sensibilization of delayed type allergy: antigen presentation by macrophages reduced number of T-helpers increased number of T-helpers production of 1L-2 increased number of T-suppressors activation of B-lymphocytes formation of sensibilizeted T-lymphocytes synthesis of antibodies by B-lymphocytes (Ig) 3. Target-cells of the 1st order at reaginic type of allergy: monocytes must cells eosinophiles neutrophiles lymphocytes basophiles smooth muscles 4. Choose clinical manifestation of Arthus' phenomenon: periodical edema and blisters into skin, mucous membranes, itch, fever periodical conjunctivitis, rhinitis caused by pollen ocal inflammatory-necrotic reaction in skin and subcutaneous tissue caused by multiply injection of alien proteins 5. Is it correct that medicinal allergy can develop due to the II and the IV types of allergic reactions? yes no 6. Choose allergic reaction of III type: Arthus' phenomenon pollen allergy medicinal agranulocytosis (leucopenia) allergic orhitis acute glomerulonephritis Hashimoto' thyroiditis rhesus-conflict between mother and fetus 7. Choose allergic reactions of the III type: anaphylactic shock reaction of transplantation rejection serum sickness bronchial asthma urticaria contact dermatitis 8. Is it possible to release mediators from must cells without complement participation? yes no 9. Choose allergic reaction of the IV type: Arthus' phenomenon pollen allergy medicinal agranulocytosis (leucopenia) allergic orhitis acute glomerulonephritis Hashimoto' thyroiditis rhesus-conflict between mother and fetus 10. Choose allergic reactions of the IV type: anaphylactic shock reaction of transplantation rejection serum sickness bronchial asthma urticaria contact dermatitis 11. Mechanism of tissue injury at reaginic type of allergy: excess formation super-oxide anion-radicals activation of complement-depended cytotoxity activation of antibody-depended cytotoxity degranulation of must cells and releasing of mediators 12. Mechanism of tissue injury at reaginic type of allergy: releasing of mediators from eosinophiles, platelets, neutrophiles releasing of lymphokins activation of complement fragments C3, C5, C8, C9 activation of к in in system activation of phagocytes and effects of lysosomal enzymes 13. Methods of desinsibilizaton at delayed type allergy: injection of anti-histamine medicine injection of glucocorticoids gradual injection of allergens blockade of kinin system activation of adenylatecyclaze inhibition of phosphodiesthraze inhibition of lymphokins inhibition of 1L-2 14. Primary mediators of anaphylaxia: serotonin interleucins factor causing stimulation of neutropiles migration histamine prostaglandins E, F factor causing inhibition of macrophage's migration 15. Primary mediators of anaphylaxia: kinins heparin histamin interferon eosiniphilic factor of chemotaxis lysosomal enzymes 16. Is it correct sentence "specific degranulation of must cells is accompanied by their destruction"? yes no 17. Red blood cells destruction at autoimmune hemolytic anemia is a result interaction between allergen and fixed on their surface antibodies: yes no 18. Main role in pathogenesis of the IV type allergy belongs to mediators released from must cells: yes no 19. Can allergic diseases develop due to different mechanism of tissue injury? yes no 20. Is specific hyposensibilization effective at atopias? yes no 21. Is specific hyposensibilization effective at the IV type of allergy? yes no 22. Choose characteristics of complete antigen: molecular mass less than 1000 Dalton molecular.mass more than 50000 Dalton has 1-2 antigenic determinants has more than 5-10 antigenic determinants can induce formation of specific antibodies and sensibilizated lymphocytes directly receives immunogenic properties after combination with host proteins can interact with antibodies and sensibilizated lymphocytes 23. Production which factors can reduce tissue injury at allergy: factor of platelets activation histamin arylsulfataze histaminaze hosphodiesthraze cGMP leucotriens 24. Choose allergic reaction of immediate type: Quinke edema Hashimoto's thyroiditis urticaria bronchial asthma rheumatic myocarditis acute glomerulonephritis 25. Choose allergic reaction of immediate type: anaphylaxia serum sickness tuberculin test contact dermatitis pollen allergy medicinal allergy 26. Which from listed allergens can cause atopies? domestic dust bacterial toxins viruses bacteria micro-anthraces epidermal allergens pollen spores cow' milk 27. Which from listed allergens can cause pollen allergy? domestic dust cereal's pollen micro-anthraces tree's pollen flower's pollen antibiotics spores 28. Choose allergic disease of the I type immune injury: urticaria myasthenia gravis «pollen» bronchial asthma anaphylactic shock Qunke's edema serum sickness pollen allergy insect allergy 29. Which from listed diseases are atopies? pollen allergy urticaria Qunke's edema serum sickness 30. Choose allergic reactions of the II type immune injury: serum sickness immune agranulocytosis autoimmune hemolytic allergy 31. Choose allergic reactions of the I II type immune injury: serum sickness local reactions (Arthus' phenomenon) immune agranulocytosis allergic alveolitis acute glomerulonephritis autoimmune hemolytic anemia 32. Choose allergic reactions of the IV type immune injury: contact dermatitis Arthus' phenomenon bacterial allergy food allergy transplantation rejection Hashimoto's thyroiditis 33. Choose autoimmune diseases: Hashimoto's thyroiditis Arthus' phenomenon rheumatoid arthritis myasthenia gravis immune agranulocytosis lupus erythrematous autoimmune-hemolytic anemia 34. Choose allergic reactions of the II type immune injury: thyroiditis tuberculin test contact dermatitis acute glomerulonephritis autoimmune hemolytic anemia 35.Which allergic diseases have been need for diagnostics of skin test with allergen? allergic rhinitis medicinal allergy bronchial asthma pollen allergy immune agranulocytosis tuberculosis of lung brucellosis 36. Choose characteristics for the I (reaginic) type immune injury: main role in pathogenesis play Ig E clinical manifestations develop in a 15-20 minutes after repeated contact with allergen clinical manifestations develop in a 6-8 hrs after repeated contact with allergen histamine, kinins, leucotriens, factor of platelet's aggregation participate in this type immune injury lymphokins play main role in this type immune tissue injury 37. Choose time of appearance clinical manifestation of the 1 type immune tissue injury after repeated injection allergen: 15-30 minutes 6-8 hrs 24-48 hrs 10-14 days 38. Choose types of Ig which participate in the I type allergic reactions: IgGl IgO4 IgE IgA IgM 39. Choose correct sentences: the 1st stage of allergic reaction starts after primary contact with allergen the 1st stage of allergic reaction starts after secondary contact with allergen specific antibodies or sensibilizated lymphocytes are produced during the 1st stage of allergic reaction mediators are produced during the 2nd stage of allergic reaction the 3rd stage of allergic reaction is characterized by clinical manifestations 40. Choose events for the 1st stage allergic reaction reaginic type: cooperation of T-, B-lymphocytes and macrophages cooperation of must cells, neutrophiles and eosinophiles formation of plasmatic cells clone formation of specific T-effectors clone synthesis and accumulation of antibodies activation of must cells 41. Choose cells which play main role in the I type of immune tissue injury: B-lymphocytes T-lymphocytes macrophages eosinophiles neutrophiles must cells plasmatic cells 42. Choose processes which play main role in the II type of immune tissue injury: interaction circulated antibodies (igG, IgM) with antigen fixed on the surface target-cells a.t participation complement, phagocytes and NIC-cells interaction circulated antibodies (IgG, IgM) with antigen at formation soluble immune complexes with complement participation interaction sensibilizated lymphocytes with antigen interaction antibodies fixed on the surface target-cells (IgG, IgM) with antigen without complement participation 43. Choose processes which play main, role in the IV type of immune tissue injury: interaction circulated antibodies (IgG, IgM) with antigen fixed on the surface target-cells at participation complement, phagocytes and NK-cells; interaction circulated antibodies (IgG, IgM) with antigen at formation soluble immune complexes with complement participation; interaction sensibilizated lymphocytes with antigen interaction antibodies fixed on the surface target-cells antigen without complement participation; 44. Which mediators and enzymes can produced by activated must cells? histamine eucotrins C4, D4 prostaglandins (IgG, IgM) with arylsulfateze histaminaze oxidants lysosomal enzymes factor of platelet's activation 45. Can Iodine, Gold, Platinum, Cobalt cause state of sensibjlization? yes no 46. Which from listed allergens can be more frequent reason of atopies? domestic dust bacterial toxins viruses microbes micro-anth races epidermal allergens pollen mycosis spores 47. Choose correct sentences: reagines and skin-sensibilizating antibodies are produced at atopia IgG] and IgG2 are produced at atopia antibodies have cellular affinity at atopia reagines can cause cell's destruction after fixation on the surface of target-cells; main role in pathogenesis of atopia play oxidants, anaphylotoxins and lysosomal enzymes; 48. Which events develop in the 1 s t stage of rcaginic type? formation of complexes Ag+Ab cooperation of T-,B-lymphocytes and macrophages cooperation of must cells,neutrophiles and eosinophiles contact of antigen (allergen) with specific antibodies activation of must cells 47. Can serum sickness develop: at primary injection of small dozes alien serum at primary injection of large dozes alien serum at repeated injection of large dozes alien serum 48. Can complement participates in the IV type allergy: yes no 49. Main role in pathogenesis of the I type of allergy belongs to Jg E: yes no 50. Main role in pathogenesis of the I type of allergy belongs to Jg M: yes no 51. Fixed antigens present: 1 type П type Ш type IV type 52. Activation of complement system (C) due to classic way is caused by: super-oxide anion-radical immune complex bacterial lipopolysacharides endogenous enzymes (plasmin, trypsin, kallikrein) 53. Alternative way activation of complement system (C): activation of fragments C5-C9 activation of C1 activation of C3 54. Activation of complement system (c) is accompanied by: lysis of target-cells reduction of vascular permeability destruction of cellular membranes and releasing of lysosomal enzymes stabilization of cellular membranes and inhibition of lysosomal enzymes activation of kinin system inhibition of chemotaxis activation of chemotaxis 55. Choose correct sentences: allergy and immune response can be caused by the same antigens allergy and immune response can't be caused by the same antigens allergy unlike immune response can't be caused by physical factors immune response unlike allergy can't be caused by chemical factors allergy is reduction, but immune response is activation resistance to antigen allergy is increasing, but immune response is reduction of resistance to antigen 56. Reactivity is: state of organism which characterized by resistance to different pathogenic factors; state of organism which characterized by inadequate reactions on ordinary factors and predisposition to action of pathogenic factors; ability of organism to response on environmental actions 57. Types of reactivity: biological (primary) individual pathological age sexual 58. Primary mechanisms of tissue injury at allergic reactions of the IV type: complex AB+AG which can activate complement (C) sesibilizated T-lymphocytes (effectors) lymphokins lysomal enzymes of macrophages lysosomal enzymes of neutrophiles mediators which released after formation complex (AG+lgE) on the surface of cells 59. Which cells can produce iminunoglobulins: B-lymphocytes macrophages plasmatic cells T-helpers T-inductors 60. Mechanisms of ig E-depended allergic reactions: action of 1L-4 presentation of antigen by B-lymphocytes deficiency of T-helpers excess of T-helpers excess of cytotoxic T-effectors prevalence of T-helpers 61. Choose tissues isolated from immune system during embryogenesis (primary endogenous allergens): heart kidney lens of eye adrenal glands thyroid gland testicules myelin of neurons liver 62. Clinical-physiological manifestation of sensibilization: reduction of arterial pressure urticaria leukocytosis absence of clinical symptoms fever local edemas increased concentration of specific Ig increased number of T-lymphocytes 6. PATHOPHYSIOLOGY OF TISSUE'S GROWTH. TUMORS 1. Choose endogenous cancerogenes: a) estrogens, b) aniline, c)cholic acid, d) litocholic acid, e)methylcholantren, Oderivates of triptophane a, b, с b, c, d c, d, e a, d, f 2. Choose functions of oncoproteins: stimulate of neoplastic progression stimulate of tissue respiration inhibit of glycolysis stimulate of neoplastic transformation 3. Which cells can produce TNF (tumor necrotic factor)? neutrophiles eosinophiles monocytes platelets red blood cells tissue macrophages 4. Give the mechanisms of growth and differentiation at neoplastic transformation: excessive activity of cGMP excessive activity of с AMP reduced activity of tyrosine-dependent proteinkinazes increased activity of tyrosine-dependent proteinkinazes hyper-activity of Ca- dependent proteinkinazes presence of proteins which phosphorilated by tyrosine increased concentration of phosphotirosines 5. which "host" factors can kill the tumors? T-kiIlers blocking antibodies allogenic inhibition NK. (natural kiilers) phagocytosis antigenic simplification masking of antigenic structures 6. Which metabolites can be endogenous cancerogenes cholesterol galactose cholic acid tryptophane estradiol acorbinic acid (vit. C) 7. Which effects belong to morphologic atypism? a) negative Pasteur's effect, b) reduced number of nexuses, c) reduced number of mitochondria, d) defective receptors, e) increased synthesis of P-proteins a, b, с a, c, d b, c, d b, d, e 8. Choose the possible reasons of tumor's return: suppression of local immunity reduced activity of anti-cellular mechanisms anti-tumor resistance surviving of tumor's cells after their extraction or destruction insert of DNA tumor cells into genome of normal cells 9. Which effects belong to functional atypism? loss of specific functions aerobic glycolysis reduced number of nexuses infiltrative growth utilization of substrates at low concentration reduced number of mitochondria antigenic transformation metastasis 10. Choose oncogenes of initiation stage at tumor process: a) c-rnyc, b) c-fos, c) c-sis, d)c-jin, e)c-erb a, b, d a, c, d c, d b, d, e 11. Choose typical forms of pathology in tissue growth: necrosis pathologic hypertrophy pathologic hyperplasia sarcoma hyperplasia of mitochondria dysplasia carcinoma 12. Choose functions of oncoproteins: inductors of oxidative phosphorilation inductors of protein's phosphorilation by tyrosine inductors of cGMP inductors of cAMP hormones - growth factors receptors to growth factors receptors to steroid hormones homologies to growth factors 13. Choose features of carbohydrate metabolism in tumors: ability to utilize glucose in low concentration excessive activity of oxidative phosphorilation excessive activity of glycolysis positive Pasteur's effect negative Pasteur's effect 14. Which metabolites can be endogenous cancerogenes: thyroxin fcorticosterone estradiole epinephrine growth hormone insulin 15. Choose the signs of benign tumors: metastasis expansive growth return (relapse) formation of blocking antibodies high level of neoplastic progression absence of contact breaking infiltrative growth high level of proliferation block of cellular maturation 16. Absence of Haiflik's limit presence at: normal regeneration of tissue low regeneration of tissue high regeneration of tissue stage of "initiation" stage of "transformation" equilibrium between growth and differentiation in tissues 17. Choose correct definition for "pathological hypertrophy of tissue": increase mass and size of structural elements in tissue increase mass and size of structural elements after excessive physical load increasing mass and size of structural elements in tissue inadequate to their function 18. Choose the main mechanism of dysplasia: disorders in mitosis disorders in meiosis disorders of metabolic regulation extra-cellular acidosis disorders in cellular differentiation acute hypoglycemia disorders in genetic program of cells 19. Choose factors which can cause cell's division: cAMP keylones reduction of superficial stretching growth factors cGMP V 20. Malignant tumors after ionizing radiation develop more in the next organs: lungs breast stomach bone marrow skin hemopoetic tissue 21. Choose states with increased risk of tumor's development: acute inflammation chronic inflammation old age onizing radiation immune deficiency vaccination 22. Choose the signs of malignant tumors: absence of contact breaking in tissue increased concentration of keylones ctivation of anaerobic glycolysis inhibition of protein's phosphorilation by tyrosine presence of factors which stimulate angiogenesis in tissues nhibition of cell's differentiation 23. Which cellular structure is target for chemical cancerogenes? cytoplasmatic membranes lysosomes sarcoplasmatic reticulum inter-cellular matrix mitochondria DNA 24. Choose the signs of neoplastic progression: anaplasia loss of autonomy invasive growth infiltrative growth terminal differentiation is saved antigenic stimulation of organism by tumors inability to metastasis 25. Choose effects of TNF (tumor necrotic factor): cahexia activation of cytotoxic function of macrophages nduction of terminal differentiation in tumor cells reduce antigenic abilities in tumor cells activation of natural killers increase activity of lipoproteinlipaze in tissues 26. Choose virues which contain DNA: virus of Raus's sarcoma Epstein-Barr's virus вирус папилломы шейки матки virus of adult T-leukemia virus of Showp's papiloma virus of mouse leukemia Brittner's virus 1. PATHOPHYSIOLOGY OF RED BLOOD 1.Picture of blood at B12-folic deficiency anemia: anisocytosis anulocytosis poikilocytose microcytosis target-cell macrocytosis megalocytes with Jolly's bodies megalocytes with Kebot's rings 2.Reasons of inherited hemolytic anemias: action of biological poisons transfusion of incompatible blood group enzyme's deficiency (glucose-6-phsphate dehydrogenaze) ATP deficiency in erythrocytes action of drugs abnormal hemoglobin presence 3.Reasons of congenital hemolytic anemia: action of biological poisons transfusion of incompatible blood group enzyme's deficiency (glucose-6-phsphate dehydrogenaze) ATP deficiency in erythrocytes action of drugs abnormal hemoglobin presence 4.Erythrocytosis is observer at: mountain sickness poisoning with charcoal gas inborn defect of heart hemoglobinopathy 5.Reasons autoimmune hemolytic anemias are: transfusion of incompatible blood group systemic diseases of connective tissue hemoglobinuria due to decreased temperature action hemoglobinopathy action of drugs 7.Signs of aplastic anemia: blood volume is increased (hypervolemia) reticulocytes are decreased secondary infection erythropoetins are increased megaloblastosis 8.Etiology of aplastic anemia: ionizing radiation vitamin's deficiency drugs (cytostatic) protein's deficiency 9. lmportant role in pathogenesis B12-deficiency anemia play next factors: insufficient erythrocyte saturation by hemoglobin disorders of DNA synthesis in nucleus of erythroblasts period of erythrocyte's life is decreased 10.Common sings of anemia: pain tachycardia dyspnea hypertension paleness 11.What reasons can cause hypo-aplastic anemia: stomach resection ionizing radiation chronic kidney failure toxic mania vitamin B12 deficiency 12.Syroptoms B12-folic acid deficiency anemia are: jaundice polyneuritis normoblastosis megaloblastosis airophy of mucous in stomach splenomegaly 13.Erythrocyte's shape at thalassemia: target-liked cells sickle-liked cells microspherocytes 14.Bilirubinemia presence at: sideroachristic anemia hemoglobinopathy hemolytic disease at newborns aplastic anemia 15.Reasons of iron deficiency anemia: hypoacidic gastritis tumor acute hemorrhage chronic hemorrhage 16.Urgent compensative mechanisms at hemorrhage: spasm peripheral vessels tachycardia hyperpnoea increased blood coagulation increased hemopoesis (increased hemopoetic activity of bone marrow) increased protein's synthesis in liver intratissue liquid comes in vessels 17.Factors can cause iron-deficiency anemia: deficiency intrinsic Castle's factor non-compensated loss of iron suppression HCL secretion in stomach disorders of folic acid activation vitamin В12 deficiency decreased erythropoetin's production increased expenditure of iron exhaustion of iron's depot 18.Choose factors which can cause megaloblastic anemia: hypoxia of myeloid tissue chronic iron deficiency vitamin В12 deficiency in food disorders of folic acid activation deficiency of intrinsic Castle's factor inherited disorders of hemoglobin's synthesis competitive consumption of vitamin В12 disorders of vitamin В12 utilization in bone marrow 19. At what case iron deficiency anemia can develop? chronic blood loss rhesus conflict folic acid deficiency stomach resection acute blood loss chronic enteritis 20. At what case hemolytic anemia can develop? hemophilia rhesus conflict protein starvation gastromucoprotein's deficiency hemoglobinopathy malaria 21.Hematoiogicai signs of hypoplastic anemia are: hypochromia of red cells neutrophilia normochromia of red cells relative lymphocytosis neutrophile's number is decreased in peripheral blood latent ability of iron's consumption is decreased in blood 22.Hematoiogicai signs of hypo-aplastic anemia are: non-effective erythropoesis is increased period of erythrocyte's life is decreased neutrophile's number is decreased in peripheral blood hyperchromia of red cells norm-megaloblastic type of hemopoesis latent ability of iron's consumption is increased in blood 23.Моге often reasons of iron deficiency anemia are: chronic blood loss inborn deficiency of Castle's factor ionizing radiation folic acid's deficiency in meal chronic enteritis hypo-acidic gastritis 24.Hematological signs of chronic post hemorrhage anemia are: iron's level is increased in blood iron's level is decreased in blood coefficient of transferrin' saturation is increased coefficient of transferrin' saturation is decreased sideroblast's number is increased in bone marrow sideroblast's number is decreased in bone marrow 25.Choose anemias with megaloblastic type of hemopoesis: post hemorrhage anemia anemia at folic acid's deficiency inherited hemolytic anemia anemia at worm invasion Addison-Birmer's anemia 26.Reasons of hypo-aplastic anemia: stomach' resection leukemia ionizingradiation toxin'and poison'action vitamin В12 deficiency in meal 27.Factors, which can cause iron deficiency anemia more often: acute blood loss immunodepressants chronic blood loss chronic enteritis tiredness at training hypoacidic gastritis folic acid's deficiency 28.Choose more often reasons of iron deficiency anemia: iron' deficiency in meal inherited deficiency of transferrin chronic blood loss kidney diseases pregnancy and lactation disease of gastro-intestinal tract 2. PATHOPHYSIOLOGY OF WHITE BLOOD 1.Which changes in peripheral blood are characteristic for neutrophilic leukocytosis: percentage concentration of lymphocytes is decreased leukocyte's number is increased presence of myeloblasts percentage concentration of stabs neutrophiles is increased percentage concentration of juvenile neutrophiles is increased percentage concentration of eosinophiles and basophiles is increased 2.Which changes in peripheral blood are characteristic for chronic myeloleukemia at flare: percentage concentration of lymphocytes is decreased leukocyte's number is increased presence of myeloblasts percentage concentration of stabs neutrophiles is increased percentage concentration of juvenile neutrophiles is increased percentage concentration of eosinophiles and basophiles is increased 3.Which leukemia is accompanied acute disorders of maturation ("leukemic gap"): myeloblasts leukemia erythremia lympholeukemia monocytic leukemia myeloleukemia monoblastic leukemia lymphoblastic leukemia 4.More possible reasons of agranulocytosis: vitamin В12 deficiency viral infection lupus erythematosus acute infection fungal intoxication 5.More possible reason of patient's death with agranulocytosis is: uremia secondary infection acute heart failure hypoxia acidosis 6.More possible reason of patient's death at leukemia: hypoglycemia hemorrhage in brain acute heart failure hypoxia edema of brain 7.Which changes in peripheral blood are characteristic for acute myeloblasts leukemia? all type myeloid cell presence in peripheral blood (from myeloblasts to granulocytes) "leukemic gap" absence of pre-matured cells anemia thrombocytopenia 8.Which changes in peripheral blood are characteristic for chronic myeloleukemia: presence of all cell's types (from myeloblasts up to granulocytes) absence of pre-matured cells - "leukemic gap" anemia thrombocytopenia 9.Clinical symptoms arc characteristic for leukemia: anemia, leukocytosis, jaundice hemolytic anemia, splenomegaly, jaundice megaloblastic anemia, polyneropathy, atrophy of stomach' mucosa metaplastic anemia, secondary infections, thrombocytopenia aplastic anemia, leucopenia, thrombocytopenia 10.Which reasons can cause physiological leukocytosis: glucocorticoid's abuse infarction of myocardium infection newborn state+meal loading 11.Which reasons can cause "pathological" leukocytosis: glucocorticoid's abuse infection infarction of myocardium newborn state meal loading physical loading mental loading 12.Which disorders of hemostasis accompany chronic leukemia? bleeding due lo fibrinogen's deficiency bleeding due to thrombocyte's deficiency bleeding due to vitamin С deficiency physical loading+mental loading bleeding due to vitamin К deficiency 3. PATHOPHYSIOLOGV OF HEMOSTASIS 1.Which diseases are coagulopathy? Shonlein-Henoch disease afibrinogenemia hemophilia vitamin С deficiency vitamin К deficiency 2.Which mechanisms are thrombocyte's factor of hemostasis: thrombocyte's adhesion cloth's retraction active thromboplastin's formation adhesive molecule's formation vessel's spasm white agglutinative thrombus's formation thrombin's formation contact factor's activation 3.Which mechanisms are vascular factors of hemostasis: thrombocyte's adhesion cloth's retraction active thromboplastin's formation adhesive molecule's formation vessel's spasm white agglutinative thrombus's formation thrombin's formation contact factor's activation 4.Which mechanisms are coagulative factors of hemostasis: thrombocyte's adhesion cloth's retraction active thromboplastin's formation adhesive molecule's formation vessel's spasm white agglutinative thrombus's formation thrombin's formation contact factor's activation 5.Factors of coagulation system: heparin antithromboplastin antithrombin tissue thromboplastin fibrinogen plasmin 6.Factors of anti-coagulation system: heparin antithromboplaslin antithrombin tissue thromboplastin fibrinogen plasmin 7.Hemorrhagic diathesis linked with vascular disorders: vitamin С deficiency Shonlein-Henoch disease hemophilia Werlgoff disease Rendu-Osler disease (angiotelectasia) afibrinogenemia 8.Which mechanisms can cause activation of coagulation at DIC-syndrome? decreased blood viscosity increased tissue thromboplastin in blood disseminated damages of vessel's wall decreased thrombocyte's number increased blood viscosity intensive inter-vascular aggregation of blood cells 9.Reasons of coagulopathies: absence of anti-hemophilic globulins thrombocytopenia vitamin С deficiency obturative jaundice vitamin К deficiency afibrinogenemia 10.Which plasma factor is absence at hemophilia A? Hagemann' factor anti-hemophilic globulin С (Rosental' factor) anti-hemophilic globulin В (Christmas' factor) VIII factor 11.Reasons of DIC-syndrome: sepsis lupus erythrematosis hey fever bronchial asthma vitamin С deficiency cardiogenic shock trauma with tissue damages 12.Factors promoted of thrombus formation: reduced thrombocyte's number vessel's wall damages decreased blood velocity change of endothelium's charge from negative on positive decreased coagulants activity 13.Thrombocylopathy is: changes of physiological function of thrombocytes independently from their number changes of physiological function of thrombocytes obligatory combined with changed thrombocyte's number changes of physiological function of thrombocytes obligatory combined with decreased thrombocyte's number 14.Reasons of DIC-syndrome: sepsis shock damages of placenta acute leukemia 15.Vascular-thrombocytic hemostasis is changed at: decreased of thrombocyte's number disorders of thrombocyte's function inherited angiopathy deficiency VIII factor deficiency of Willebrand's factor expression on the surface of thrombocytes receptors to fibrinogen absence on the surface of thrombocytes receptors to Willebrand's factor 16.Hemorrhagic syndrome is result: increased vessel's permeability decreased activity of plasminogen system deficiency of procoagulants functional disorders of thrombocytes increased activity of plasmin system decreased of thrombocyte's number increased concentration of fibrinolysis's inhibitors 17.Choose clinical signs characteristic for thrombocytopenic purpura (Werlgoff's disease): increased of thrombopoetin's production disorders of vessel's wall short time of capillary bleeding short time of thrombocyte's life disorders of cloth's retraction +petechial type of bleeding hematomic type of bleeding increased of anti-thrombocytic antibodies in plasma (IgG3) 18.Choose changes characteristic for hemophilia: long time of capillary bleeding decreased procoagulant activity of VIII factor long time of coagulation disorders in synthesis of VIII factor positive ligature test deficiency of Willebrand's factor 19.Choose disorders characteristic for thrombocytopathy: decreased synthesis of thromboxan A2 deficiency of thrombostenin in thrombocytes absence of thrombocyte's aggregation defreased releasing from thrombocytes ADP and serotonin +decreased cloth's retraction 20.Choose factors which can cause thrombocytopenia: suppression of megacariocyte's proliferation suppression of megacariocyte's locus by tumor cells at leukemia activation of Leukocytic locus in bone marrow at inflammation increased "consumption" of thrombocytes at thrombopoesis immune damages of thrombocytes large doze of ionizing radiation leukolysis 21.Reasons of long-time coagulation: excess of anticoagulants activation of fibrinolytic system inhibition of fibrinolysis deficiency of procoagulants decreased activity of natural coagulants increased concentration of procoagulants in blood 4. PATHOPHYSIOLOGY OF CARDIO-VASCULAR SYSTHEM 1.Clinical manifestation of right-ventricular cardiac insufficiency: portal hypertension tachycardia lung's edema circulatory hypoxia-gaseous acidosis cyanosis ascites 2.Which from listed mechanisms is initial for cardiac edema: decreased of sodium and water reabsorption in kidney increased vessel's permeability venous congestion decreased oncotic pressure in blood decreased cardiac output 3.Mixed hyperfunction of myocardium develops at next diseases: essential hypertension thyreotoxicosis emphysema of lungs infarction of myocardium combined aortal defect mitral stenosis 4.Inter-cardiac reasons of cardiac insufficiency: stenosis of aorta lung's emphysema essential hypertension renal hypertension myocarditis 5.Extra-cardiac reasons of cardiac insufficiency: myocarditis thyreotoxicosis myocardiodystrophy renal hypertension endocarditis 6.Which diseases can cause isometric hyperfunction of myocardium: defect of inter-atrial septum caorctation (narrowing) of aorta essential hypertension infarction of myocardium 7.Choose inter-cardiac reasons of cardiac insufficiency: thyreotoxicosis pericarditis myocarditis ischemic disease of heat essential hypertension endocarditis 8.Choose possible reasons of right ventricle cardiac insufficiency: infarction of forward wall left ventricle thyreotoxicosis exudative pericarditis lung's emphysema essential hypertension 9.How blood velocity change in coronary vessels at chronic coronary insufficiency: doesn't change is decreased non-significantly is decreased significantly is increased 10.Which states can cause myocardium's over-loading by pressure: anemia insufficiency of aortal valve general atherosclerosis insufficiency of mitral valve arterial hypertension aortal stenosis 11.Choose reasons can cause myocardium's overloading by volume: aortal valve insufficiency diabetes mellitus excessive production of norepinephrine arterial hypertension stenosis of left atrio-ventricular foramen mitral valve insufficiency 12.Clinical manifestation at left ventricular cardiac insufficiency: edema on legs decreased cardiac output dyspnea hepatomegaly tachycardia bubbly sounds in basal fields of lungs angiotelectasis 13.Coronary insufficiency is result of: paroxysmal tachycardia endocarditis spasm of coronary arteries hypercapnia adenosine cumulation in myocardium stenotic coronarosclerosis 14.Choose events and factors at increased epinephrine's concentration causing myocardium's damages: oxygen's consumption by myocardium is decreased oxygen's transport to myocardium is decreased absolutely oxygen's transport to myocardium is decreased relatively phosphorilation and aerobic oxidation in cardiomyocytes are decreased phosphorilation and aerobic oxidation in cardiomyocytes are increased glycogen's storage is decreased in cardiomyocytes 15.Which diseases can cause right-ventricular cardiac insufficiency: lung's emphysema defect of inter-ventricular septum thyreotoxicosis caorctation (narrowing) of aorta acute myocarditis 16.What events are characteristic for renin-depended hypertension: increased tonus of peripheral vessels at the expense of adrenoreceptor's sensitivity increased tonus peripheral vessel is result activation RAAS significant increasing of blood volume increased excretion Na+ and water by kidney decreased excretion Na+ and water by kidney activation of JGZ 17.Mechanism of arterial hypertension: cardiac work is decreased blood volume is decreased blood volume is increased vessel's tonus is decreased 18.Choose secondary (symptomatic) arterial hypertension: hypovolemic (blood volume is decreased) pituitary renal reflexogenic thyroid adrenal essential portal 19.Choose main differences between essential hypertension and secondary hypertension: increased arterial pressure develops without organic damages internal organs develops as result primary renal disorders inherited predisposition has important role develops as result adrenal glands disorders develops as result primary damages of aortal receptors important role have hypothalamic disorders (vaso-motor center) 20.Risk factors at hypertension: obesity decreased activity of sympathetic system weight loss increased activity of sympathetic system diabetes mellitus hyperthyroidism 21.Mechanisms of reno-vascular hypertension is: activation of RAAS insufficiency of prostaglandin and kinin system in kidney insufficiency of RAAS 22.Which substances produced in kidney can cause direct vasodilatation: renin prostaglandin F2alpha bradikinin callidin prostaglandins A, E 23.Endocrine hypertensions develop at: total hypofunction of adrenal cortex hyperfunction of adrenal cortex (zone glomeruloza) hyperfunction of adrenal medulla hypophyseal cachexia hypofunction of thyroid gland thyreotoxicosis 24.Complications at hypertonic disease: acute renal failure extrasystoles chronic renal failure lung's edema cardiac asthma atrio-ventricular block 1st degree fibrillar palpitation 25.Which disorders can develop at acute arterial hypotension: blood type of hypoxia disorders of microcirculation circulatory hypoxia cardiac insufficiency coronary insufficiency syncope anuria PATHOPHYSIOLOGY OF LIVER 1.Which signs characteristic for physiological jaundice of newborns: increased concentration of indirect bilirubin in blood increased concentration of direct bilirubin in blood yellow color of skin and mucous feces is normal color feces is black color presence of biliary pigments in urine 2.Which symptoms characteristic for aholia: increased arterial pressure diarrhea steatorrhea constipation disorders of vitamin resorption disorders of intestinal digestion bleeding meteorism tachycardia 3.What variant of symptom complex characteristic for mechanical jaundice: result of hepatocyte's damages at infections or intoxication, direct and indirect bilirubin in blood, decreased urobilin in urine, biliary acids and pigments, decreased stercobilin in feces result of hemolysis, increased indirect bilirubin in blood, negative urobilin in urine, absence of biliary acids, increased stercobilin in feces result of bile congestion, direct and indirect bilirubin in blood, decreased urobilin in urine, positive biliary acids and pigments, decreased stercobilin in feces 4.CIinical signs characteristic for mechanical jaundice: cholemia increased concentration indirect and direct bilirubin in blood increased concentration indirect bilirubin in blood acholia hypercholia bradycardia yellow color skin, mucous and while of the eye itch 5.At what types of jaundice indirect bilirubin is in urine? mechanical with one of listed hemolytic parenchial 6.Mechanism of bradycardia at cholemia: increased of n. vagus activity direct action of bile acids on sinus nodes decreased activity of adrenoreceptors 7.Which from listed signs are characteristic for total hepatic failure? hyperglycemia without meal loading bilirubin in blood hypoglycemia without meal loading decreased oncotic pressure of blood increased oncotic pressure of blood 8.Which from listed signs are characteristic for cholemia? tachycardia skin itch bradycardia hyporeflexia arterial hypertension hyperrreflexia arterial hypotension 9.Choose signs characteristic for pre-hepatic (hemolytic) jaundice: increased non-conjugated bilirubin in blood increased reticulocyte's number in blood increased conjugated bilirubin in blood foamy urine bilirubin in urine hypoxia urobilin in urine decreased arterial pressure tachycardia 10.Syndrome cholestasis is characteristic for next jaundice : pre-hepatic (hemolytic) hepatic (parenhial) post-hepatic (mechanical) 11.Reasons of hepatic (parenhial) jaundice: viral hepatitis hypoxia hemolytic anemia rheumatism toxic hepatitis intoxication of hemolytic poisons cirrhosis of liver cancer of liver sepsis pneumonia GASTROINTESTINAL TRACKT PATHOPHYSIOLOGY 1.Achilia: deficiency of bile absence of pepsin in stomach juice absence of HC1 and pepsin in stomach juice absence of tripsin in intestine juice absence of HC1 in stomach juice 2.Disorders of digestion can cause: starvation auto-allergic diseases autointoxication psycho-emotional stress chronic cardiac failure dyspeptic disorders chronic renal insufficiency 3.Which states can cause functional disorders of parietal digestion? stress cholera changes in composition and structure of enzymes in surface of intestine spry ionizing radiation action of antibiotics 4.Complications of ulcer disease: decreased of blood supply in coronary vessels chronic adrenal cortex insufficiency hyperchromic anemia penetration cancer (malignant tumor) peritonitis decreased blood volume 5.Choose possible mechanisms of hyposecretion in stomach: excessive parasympathetic stimulation of stomach excessive sympathetic stimulation of stomach decreased production and secretion of histamine decreased production and secretion of secretin increased formation of enterogastron decreased secretion of cholecystokinin 6.Which factors play role in ulcers development of stomach and duodenum? infection excessive glucocorticoid's production increased mucosa production increased parasympathetic stimulation increased sympathetic stimulation duodenal reflex 7.Mechanisms resistance of Helicobacter pylori to bactericide action of stomach juice: adaptation to inhabit under mucosa of stomach ability to decompose of urea adaptation to inhabit in mucosa of stomach decreased catalyze activity 8.Factors play role in pathogenesis of "aspirin" ulcers in stomach: decreased synthesis of prostaglandins E decreasing inverse diffusion H+ in mucous of stomach increased synthesis of prostaglandins E increasing inverse diffusion H+ in mucous of stomach increased production of mucus decreased production of mucus 9.Choose characteristic signs for increased secretion of stomach juice: rapid evacuation meal from stomach slow evacuation meal from stomach increased secretion of stomach juice before meal absence of pepsin activity long-time spasm of pylorus heartburn decreased production of pancreatic juice increased motility of intestine, diarrhea 10.Which diseases can cause disorders of parietal digestion? mechanical jaundice lactaze insufficiency chronic pancreatitis duodenitis 11.Choose sequences of acholia: bile absence in duodenum increased rotting in intestine decreased pH in duodenum fatty diarrhea absence of lipase disorders of fatty acids absorption decreased lipaze activity absence of lipids decomposition disorders of lipids emulgation 12.Symptoms at malabsorption: meteorism vitamin В12 deficiency diarrhea vitamins A, D, E, K deficiency constipation fatty diarrhea weight loss decreased ammonia in blood decreased oncotic pressure of blood 13.Choose reasons of decreased intestinal absorption: inflammation caused by infection inflammation caused by toxins action (diabetes, uremia) resection 25% of small intestine resection 50% of small intestine resection 75% of small intestine atrophy of mucous in small intestine RESPIRATORY SYSTHEM PATHOPHYSIOLOGY 1.What type of respiration is characteristic for pneumonia? frequent deep respiration (hyperpnoe) Kussmaul' respiration deep редкое respiration frequent superficial respiration (polipnoe) Biot' respiration 2.What types of respiration can develop at suppression of respiratory center? polipnoe hyperpnoe Chain-Stocks' respiration Kussmaul' respiration Biot' respiration oligopnoe 3.Kussmaul' respiration takes place at patients with: respiratory alkalosis metabolic acidosis metabolic alkalosis respiratory acidosis 4.Inspiratory dyspnea develops at next diseases: 1st stage of asphyxia closed pneumothorax pulmonary emphysema trachea stenosis lагуnх edema attack of bronchial asthma 5.Chose possible reasons of respiratory insufficiency obstructive type: spasm of bronchus pleuritis pneumothorax collapse of bronchioles increased intrapulmonary pressure decreased surfactant production bronchial asthma 6.Chose possible reasons of respiratory insufficiency restrictive type: inflammatory damage of bronchioles pneumofibrosis diffuse fibrous alveolitis spasm of bronchioles massive pulmonary inflammation collapse of lung 7.Disorders of diffusion in alveolar-capillary membrane plays main role in development of respiratory insufficiency at: bronchial asthma decreased surfactant production larynx edema silicosis interstitial edema of lungs 8.Disorder of perfusion plays main role in development of respiratory insufficiency at next pathological states: bronchial asthma Fallow' tetrad larynx edema left-ventricular cardiac insufficiency tuberculosis blood loss myasthenia hysteria 9.Which from listed diseases and pathological states can cause development of respiratory insufficiency? bronchial asthma emphysema asphyxia acute renal failure anemia 10.Mechanisms disorders of gases exchange at emphysema: increased air in pulmonary tissue decreased respiratory surface decreased oxygen in alveolar air increased perfusion in pulmonary vessels 11.Which from listed diseases develop due to disorders of perfusion? emphysema pulmonary collapse embolism of pulmonary vessels pneumothorax 12.Which reasons can cause pulmonary collapse? cardiac insufficiency chronic bronchitis chronic renal insufficiency pneumofibrosis surfactant insufficiency 13.Respiratory insufficiency is characterized by: dyspnea hypoxia tachycardia cyanosis changes of 02 and CO2 levels in blood anemia changes of acid-base balance 14.Reasons of restrictive disorders of ventilation: chronic bronchitis intercostals myositis closed pneumothorax 15.Internal respiration is process of gases exchange between: environmental air and tissue blood and tissue alveolar air and blood 16.Dyspnea is: increased frequency and deepness of respiration, accompanied with sensation of air deficiency increased frequency and deepness of respiration sensation of air deficiency Pathophysiology of endocrine system 1.Diseases are accompanied with disorders of ADH (antidiuretic hormone) production: -diabetes insipidus - acromegaly - somatomegaly (gigantism) - Cushng's disease - pituitary dwarfism - hypothyroidism 2.Diseases are accompanied with disorders of GH (growth hormone): - diabetes insipidus - acromegaly - eunuchoidism - somatomegaly (gigantism) - Cushng's disease - hyperthyroidism - early (premature) sexual development -pituitary dwarfism 3.At what disorders of adrenal cortex can develop next syndromes and diseases: - Conn's syndrome -Addison's disease - Cushing's syndrome - adreno-genital syndrome - Simmond's disease - pheohromocytoma 4.Choose main effects of thyroid hormones: -increase of protein anabolism (in physiological concentration) - permissive action on catecholamines - increase of oxygen's consumption by tissues - mobilization of lipids from depot - activation of lipogenesis - activation of glycogenosis - bradycardia - activation heat-production 5.Signs, characteristic for Cushing's syndrome: -hypotension -hypertension -local obesity -dehydration -increase of sodium's concentration in blood -decrease of sodium's concentration in blood -hyperglycemia -hypoglycemia -secondary infection 6.Manifestation of hyperthyroidism, causing by direct action of TTH: -increase of base metabolism -exophthalmos -tachycardia -goiter -tremor -increase of body's temperature -increase of protein's decomposition 7.Pathological states, appear at excessive production ACTH: - adrenogenital syndrome - gigantism - Cushing's disease - hyperthyroidism - acromegaly 8.Manifestation of primary aldosteronism: -increase of potassium in blood -normal level of potassium in blood -increase of sodium in blood -normal level of sodium in blood -polyuria -edema -increase of renin secretion -decrease of renin secretion 9.Manifestation of increased function of adrenal cortex: - increase of ACTH production - decrease of ACTH production - hypoglycemia - decrease of sodium in blood - hyperglycemia - increase of sodium in blood - hypotension - hypertension - increase of MSH production - increase of calcium in blood 10.Which changes characteristic for Addison's disease? - decrease blood volume and dehydration - decreased arterial pressure - muscular weakness - edema - cumulation of Na+ and loss of K+ - hypoglycemia - tachycardia III. Pathophysiology of carbohydrate metabolism 1.Which form listed states are complication of diabetes mellitus: -ascites -neuropathy -retinopathy -cellular jaundice -hypertension -mixedema -nephropathy 2.Reasons can cause functional hyperglycemia: -emotional stress -the 1st period complete starvation -gigantism -Cushing's syndrome -meal loading -hyperthyroidism 3.Which from listed states are accompanied with increased base metabolism: -hyperthyroidism -Cushing's syndrome -Addison's disease -physical loading -heart insufficiency -iron-deficiency anemia -emotional stress -the 2nd period of complete starvation 4.Which from listed states are accompanied with alimentary hyperglycemia (hyperglycemia after meal): -atherosclerosis -diabetes mellitus -spleen extraction -starvation -pheochromocytoma -decrease of heparin production 5.Which states lead to relative insufficiency of insulin: -pancreatitis -increase of glucocorticoids production -increase of insulinaze activity -cumulation of anti-bodies to insulin -decrease of receptors number on target-cells -multicystosis of pancreas 6.Which mechanisms are main in pathogenesis of diabetic coma: -disorders of carbohydrate metabolism, lipid metabolism, protein metabolism lead to disorders of energy metabolism in brain and other tissues, water-electrolyte disorders and intoxication -disorders of water-electrolyte balance causing increased osmotic pressure in blood, intra-cellular hypohydration - disorders of carbohydrate metabolism, lipid metabolism, protein metabolism lead to disorders of energy metabolism in central nervous system causing substrate and oxygen starvation of brain 7.Which symptoms are characteristic for diabetic coma: -acute beginning -giddiness, entangled consciousness, feeling of hunger -periodical respiration type Kussmaul -decrease of arterial pressure -smell of acetone -cramps -hyperemia of skin -eyeballs are firm at palpation 8.Which hormones excess can cause hyperglycemia? -epinephrine -thyroid hormones (ТЗ, Т4) -glucocorticoids -growth hormone -insulin -vasopressin -ADH -glucagone 9.Which type of lipids excess plays atherogenic role? -cholesterol -lipoproteins high density -lipoproteins very low density -lipoproteins low density -phosphoproteins 10Development of atherosclerosis is promoted: -decreased activity of lipoproteinlipaze -deficiency of receptors to lipoproteins low density -excess of receptors to lipoproteins low density -increased heparin concentration in blood 11.Choose the risk factors for atherosclerosis: -decreased insulin concentration -hyperlipidemia -obesity -local infiltrative sclerosis of arterioles -fibromucular hypertrophy of vessels wall -endarteritis -phlebitis 12.Which factors promote atherosclerosis development at obesity? -arterial hypertension -hypercholesterolemia -hyperglycemia -polyuria -polydipsia -hypertriglycerolemia -dyslipoproteinemia ^ 13.More frequent complications of atherosclerosis: -aneurysm of aorta and/or other big arteries -hemophilia A -hemophilia В -insult of brain -thrombosis of arteries -thrombosis, of veins -thromboembolism -schemia of myocardium 14.Choose factors promote development of diabetic angiopathy: -excessive glycosy lation of proteins -hyperlipoproteinemia -dyslipoproteinemia -sorbite formation -activation of gluconeogenesis 15.Choose the complications of diabetes mellitus: -immunodeficiency states -rapid development or atherosclerosis -decreased resistance to infection -decreased anti-tumor resistance -hypothyroidism -nephropathy -arterial hypotension Pathophysiology of kidney 1.Exogenous reasons of nephrolitiasis are: -inherited diseases of aminoacids metabolism -hypercalciuria -work in metallurgical factory -infection of urinary tract -disorders in mechanisms of urine elimination 2.Endogenous reasons of nephrolitiasis are: -disorders of aminoacids reabsorption -vitamin В deficiency -drinking water saturated with calcium -endocrine disorders (hyperparathyroidsm) -diseases of metabolism 3.Uremic stage chronic renal insufficiency is characterized by: -pleuritis and pericarditis -eliminative acidosis -delay of sodium in organism -decreasing of creatinine's clearance -metabolic alkalosis -gastroenteritis -nitrogenemia -disorders of parathyroid glands function 4.Which symptoms are characteristic for decompensative stage of chronic renal insufficiency: -oligouria -acidosis -hypercalciumemia -polyuria -hypersodiumemia -hypocaiciumemia -increasing of nitrogen in urine -pericarditis, pleuritis, gastroenteritis -decreasing of creatinine's clearance 5.Which from listed states characterize functional proteinuria: -nephrotic syndrome -glomerulonephritis -proteinuria at physical loading -pyelonephritis -dehydration -proteinuria after meal loading -ortostatic proteinuria 6.Which reasons can cause primary nephrotic syndrome: -poisoning with heavy metals -rejection of kidney transplantant -disorders of blood supply in kidney -inherited diseases of lipid metabolism -penetration specific antibodies to kidney through placenta -glomerulonephritis -serum sickness 7.Which reasons of acute renal failure are included in group post-renal: -shock -collapse -dehydration -acute glomerulonephritis -sepsis -pyelonephritis -toxicosis at pregnancy -tumor in urinary tract -thrombus in renal vessels -nephrolithiasis 8.Choose main mechanism promote renal hypertension -activation of rennin-angiotensin-aldosterone system -activation of kallikrein-kinin system - activation of symphato-adrenal system -delay of sodium in organism -rennin synthesis is decreased -synthesis of kidney Prostaglandines is decreased 9.Which from listed symptoms and syndromes can develop in oligo-anuric stage of acute renal failure? -immunodeficient state -hypervolumia (increased blood volume) -dehydration of organism -edema of brain -acidotic coma 10.Mechanisms can cause increased glomerular filtration: -increased tonus afferent arteria -decreased tonus afferent arteria -increased tonus efferent arteria -increased oncotic pressure of blood -decreased oncotic pressure of blood -increased intra-renal pressure -decreased intra-renal pressure 11.Choose pathological components of urine renal nature: -urobilin -bilirubin -stercobilin -keton bodies -erythrocytes (changed) -protein -cylinders -bile acids