Pathophysiology MCQ Eng. PDF

CIRCULATORY FAILURE. HEART FAILURE (Merey) 1. Circulatory failure occurs due to (4): A) Primary cardiac dysfunction + B) Peripheral circulatory disorders C) Vascular tone disturbances + D) Combined dysfunction of the heart and blood vessels + E) Hypovolemia + F) Compensatory myocardial hypertrophy 2. Align: 1.Chronic circulatory failure (CCF) degree I (1) 2.HNK II A degree (1) 3.HNK II B degree (1) CNC III degree (2) A) Tachycardia and shortness of breath appear during normal physical activity 1 B) Tachycardia and shortness of breath at rest 2 C) Significant cyanosis, severe shortness of breath, tachycardia at rest, congestion of blood in the systemic and pulmonary circulation 3 D) Cachexia 4 E) Irreversible dystrophic changes in organs and tissues 4 3. Heart failure is characterized by (4): A) Decreased myocardial contractility + B) As a rule, a decrease in stroke volume + C) As a rule, a decrease in cardiac output + D) Decrease in residual systolic blood volume E) Myogenic dilation of the heart cavities + 4. The causes of acute heart failure are (4): A) Myocardial infarction + B) Cardiosclerosis C) Acute myocarditis + D) Acute decompensation of hypertrophied myocardium + E) Attack of paroxysmal tachycardia + F) Sinus tachycardia 5. The causes of right ventricular failure may be (2): A) Arterial hypertension of the systemic circulation B) Arterial hypertension of the pulmonary circulation + C) Infarction of the anterior wall of the left ventricle of the heart D) Mitral valve insufficiency E) Chronic pneumonia + 6. Right ventricular failure is typical (4): A) Ascites + B) Cardiac asthma C) Swelling of the jugular veins + D) Swelling of the lower extremities + E) Hepatomegaly + F) Pulmonary edema 7. Cardiogenic pulmonary edema develops when (2): A) Right ventricular failure B) Left ventricular failure + C) Total heart failure + 8. The causes of left ventricular failure can be (3): A) Mitral valve insufficiency + B) Infarction of the anterior wall of the left ventricle + C) Hypertension of the pulmonary circulation D) Hypertension + E) Emphysema 9. Right ventricular heart failure manifests itself (3): A) Venous stagnation of blood in the systemic circulation + B) Venous stagnation of blood in the pulmonary circulation C) Pulmonary edema D) Ascites + E) Hepatomegaly + 10. Classification of heart failure by pathogenesis includes species (3): A) Overload + B) Myocardial + C) Mixed + D) Spicy E) Chronic F) Compensated G) Decompensated 11. An overload form of heart failure occurs due to (3): A) Hypervolemia + B) Myocardial ischemia C) Myocarditis D) Heart defects + E) Increase in total peripheral vascular resistance + 12. Overload of the heart with blood volume can develop with (2): A) Hypervolemia + B) Arterial hypertension C) Arterial hypotension D) Valve stenosis E) Heart valve insufficiency + 13. Overload of the heart with "resistance" develops when (3): A) Heart valve insufficiency B) Valvular stenosis + C) Arterial hypertension + D) Physical activity E) Coarctation of the aorta + 14. Urgent cardiac compensation mechanisms for hemodynamic disorders with increased load on the heart are (3): A) Bradycardia B) Tachycardia + C) Homeometric mechanism + D) Heterometric Frank-Starling mechanism + E) Myocardial hypertrophy 15. Cardiac mechanisms of heart failure compensation (5): A) Heterometric mechanism of increasing the force of heart contractions + B) Homeometric mechanism of increasing the force of heart contractions + C) Tachycardia + D) Myocardial hypertrophy + E) Increased adrenergic responsiveness of myocardium + F) Activation of the sympathoadrenal system G) Tachypnea H) Absolute erythrocytosis 16. Centralization of blood circulation during cardiogenic shock provides blood supply (2): A) Brain + B) Heart + C) Liver D) Kidneys E) Skeletal muscles 17. Compensation of heart functions is provided (4): A) Tachycardia + B) Myocardial hypertrophy + C) Heterometric mechanism of increasing contraction force + D) Homeometric mechanism for increasing contraction force + E) Cardiosclerosis 18. Align: 1.Stage of emergency cardiac hyperfunction (2) 2.Stage of completed hypertrophy and relatively stable hyperfunction (3) 3.Stage of progressive cardiosclerosis (3) A) Hyperfunction of non-hypertrophied myocardium 1 B) Increased energy production and protein biosynthesis per unit mass of myocardium 1 C) Hypertrophy of cardiomyocytes 2, 3 D) Proliferation of connective tissue 3 E) Tonogenic dilatation 2 F) Myogenic dilatation 3 G) Normalization of oxygen consumption, energy production, protein biosynthesis per unit myocardial mass 2 19. Intensity of functioning of hypertrophied cardiomyocytes in the phase of stable compensation (1): A) Increases to the maximum B) Decreases to normal + C) Progressively decreases 20. Sequence of Pathogenesis Stages in Pathological Cardiac Hyperfunction: A) Emergency hyperfunction of a non-hypertrophied heart 1 B) Hypertrophy and relatively stable hyperfunction 3 C) Decompensation of cardiac activity 7 D) Progressive cardiosclerosis with a sequential decline in function 6 E) Activation of a genetic program to increase protein synthesis 2 F) Ionic imbalance, structural disruption, energy deficits, and impaired regulation of cardiomyocytes 5 G) Mismatch between cardiomyocyte mass and their oxygen, substrate, and regulatory demands 4 21. Cardiosclerosis and myocardial function exhaustion in pathological hypertrophy develop due to (4): A) Mismatch between the surface area and mass of hypertrophied cardiomyocytes + B) Mismatch between the nucleus and cytoplasm of hypertrophied cardiomyocytes + C) Impaired neural trophism of hypertrophied cardiomyocytes + D) Adequate blood supply to hypertrophied cardiomyocytes E) Disrupted energy supply to hypertrophied cardiomyocytes + 22. The myocardial form of heart failure develops in cases of (3): A) Tricuspid valve insufficiency B) Vitamin B1 (thiamine) deficiency + C) Hypertension D) Septic conditions + E) Alcoholism + F) Hypervolemia G) Stenosis of cardiac valve openings 23. Match the following: 1. Myocardial failure of coronary origin (3) 2. Myocardial failure of non-coronary origin (6) A) Spasm of coronary vessels (1) B) Thrombosis or embolism of coronary vessels (1) C) Atherosclerosis of coronary vessels (1) D) Viruses, bacteria (2) E) Alcohol (2) F) Toxins (2) G) Heavy metal salts (2) H) Antibodies and immune complexes (2) I) Primary metabolic disturbances in the cardiac muscle (2) 24. Coronary insufficiency may result from (5): A) Stenosing coronary atherosclerosis + B) Accumulation of adenosine in the myocardium C) Paroxysmal tachycardia + D) Spasm of coronary arteries + E) Activation of β-adrenoreceptors of coronary vessels F) Infection G) Metabolic disturbances in the myocardium H) Thromboembolism of coronary arteries + I) Hyperproduction of adrenaline + 25. Coronary damage to the heart leads to (3): A) Angina pectoris + B) Myocardial infarction + C) Idiopathic cardiomyopathy D) Myocardial dystrophy + E) Pericarditis 26. Myocardial ischemia leads to (4): A) Decreased activity of oxidative phosphorylation + B) Intensification of glycolysis + C) Accumulation of lactic acid + D) Accumulation of glycogen in the myocardium E) Rapid depletion of ATP reserves + F) Increased concentration of potassium ions inside ischemic cells G) Increased concentration of creatine phosphate in cardiomyocytes 27. Hibernating myocardium refers to (3): A) Focal irreversible dysfunction of the myocardium B) Focal reversible dysfunction of the myocardium + C) A viable area with ischemic cardiomyocytes + D) Myocardium with reversible damage to cardiomyocytes + E) Central area of myocardial infarction 28. Reperfusion injury of the heart is characterized by (3): A) Incomplete diastolic relaxation of the myocardium + B) Increased inotropic function of the cardiac muscle C) Accumulation of calcium ions in cardiomyocytes + D) Accumulation of potassium ions in cardiomyocytes E) Decreased activity of sodium-calcium active transport + 29. Reperfusion syndrome is characterized by (3): A) Accumulation of calcium ions in the sarcoplasmic reticulum + B) Accumulation of calcium ions in the mitochondria of cardiomyocytes + C) Increased calcium ion levels in the cytoplasm of cardiomyocytes + D) Decreased exchange of intracellular sodium for extracellular calcium E) Activation of slow calcium channels 30. The cardiotoxic effect of post-ischemic reoxygenation includes (4): A) Acceptance of electrons by mitochondrial respiratory enzymes B) Transformation of respiratory chain enzymes into electron donors for oxygen + C) Formation of reactive oxygen species (radicals) + D) Free-radical damage to enzymes of energy-dependent ion transport in cardiomyocytes + E) Development of ionic imbalance + F) Overloading cardiomyocytes with potassium ions 31. Factors preventing restoration of microcirculation after myocardial reperfusion (5): A) Margination of leukocytes along the walls of microvessels + B) Production of reactive oxygen species and inflammatory mediators by leukocytes + C) Endothelial cell swelling + D) Microthrombosis + E) Damage to the walls of microvessels + F) Arterial hyperemia G) Development of stagnant stasis 32. Sudden cardiac death (3): A) Instantaneous, unexpected death + B) Develops within 1 hour after the first symptoms of acute coronary insufficiency + C) May be a consequence of asphyxia D) May be a consequence of ventricular fibrillation + 33. Idiopathic cardiomyopathies include (4): A) Ischemic B) Dilated + C) Hypertrophic + D) Hypertensive E) Inflammatory F) Restrictive + G) Arrhythmogenic right ventricular + H) Metabolic 34. Specific cardiomyopathy is defined as cardiomyopathy (5): A) Hypertrophic B) Associated with systemic diseases + C) Due to myocardial dystrophy + D) Caused by allergic heart damage + E) Metabolic + F) Inflammatory + G) Restrictive 35. Dilated cardiomyopathy is characterized by (4): A) Predominance of cardiac chamber dilation over hypertrophy + B) Systolic heart failure + C) More frequent occurrence in women D) Development of chronic heart failure + E) Formation of mural thrombi in cardiac chambers + 36. The pathogenesis of idiopathic dilated cardiomyopathy involves mutations in genes encoding the synthesis of (6): A) Actin + B) Heavy chains of beta-myosin + C) Alpha-tropomyosin + D) Light chains of myosin E) Troponin I F) Troponin T + G) Cytoskeletal proteins + H) Mitochondrial dehydrogenases + 37. Idiopathic hypertrophic cardiomyopathy is characterized by (5): A) Thickening of the left ventricular wall to more than 15 mm + B) Systolic heart failure C) Diastolic heart failure + D) High incidence of ventricular arrhythmias + E) Sudden death in 50% of cases + F) A decisive role of genetic factors (in 100% of cases) + G) A genetic factor contributing to disease development in 10% of cases 38. The pathogenesis of idiopathic hypertrophic cardiomyopathy involves mutations in genes encoding the synthesis of (7): A) Heavy chains of beta-myosin + B) Troponin T + C) Troponin I + D) Alpha-tropomyosin + E) Myosin-binding protein C + F) Actin + G) Light chains of myosin + H) Mitochondrial enzymes I) Cytoskeletal proteins 39. Restrictive cardiomyopathy is characterized by (4): A) Impaired diastolic function + B) Increased ventricular filling pressure + C) Decreased ventricular filling pressure D) Normal myocardial contractile function + E) Increased ventricular wall stiffness + F) Decreased size of the left atrium G) Increased size of ventricular chambers 40. Idiopathic restrictive cardiomyopathy develops in (2): A) Hemochromatosis B) Amyloidosis C) Glycogen storage diseases D) Scleroderma E) Endomyocardial fibrosis + F) Radiation-induced heart damage G) Eosinophilic endomyocardial disease (Löffler's endocarditis) + H) Drug intoxication 41. Molecular and cellular mechanisms of heart failure decompensation include (4): A) Ion imbalance in cardiomyocytes + B) Impaired energy production in cardiomyocytes + C) Dysregulation of cardiomyocyte function + D) Damage to membranes and enzymes of cardiomyocytes + E) Intracellular regeneration and hypertrophy 42. Ion imbalance in damaged cardiomyocytes is manifested by (3): A) Increased intracellular sodium concentration + B) Decreased intracellular calcium concentration C) Increased intracellular calcium concentration + D) Decreased intracellular sodium concentration E) Decreased intracellular potassium concentration + 43. Ion imbalance in cardiomyocytes leads to changes in (5): A) Excitability of the myocardium + B) Myocardial contractility + C) Rhythmogenesis + D) Conductivity + E) Cardiac automatism + 44. Decreased potassium concentration in damaged cardiomyocytes leads to (3): A) Depression of the ST segment on the electrocardiogram B) Development of arrhythmias + C) Reduction of the maximum diastolic potential + D) Increase in the maximum diastolic potential E) Reduction in action potential + F) Hypokalemia 45. Calcium accumulation in cardiomyocytes is accompanied by (3): A) Disruption of relaxation and contraction of myofibrils + B) Reduction of adrenergic reactivity of cardiomyocytes + C) Increase in adrenergic reactivity of cardiomyocytes D) Activation of membrane phospholipases + E) Activation of oxidative phosphorylation 46. Mechanisms contributing to increased sodium concentration in damaged cardiomyocytes (4): A) Decreased ATP levels in cardiomyocytes + B) Damage to cellular membranes + C) Reduced activity of sodium-potassium ATPase + D) Suppression of mitochondrial Ca²⁺-ATPase activity E) Excess accumulation of lipid hydroperoxides + 47. Mechanisms contributing to energy supply disruption in cardiomyocytes (4): A) Intensification of aerobic oxidation processes in the Krebs cycle B) Impaired transport function of the creatine phosphate system + C) Reduced accumulation of calcium ions in mitochondria D) Uncoupling of oxidation and phosphorylation + E) Disruption of energy utilization + F) Myocardial hypoxia + 48. Creatine phosphokinase activity during cardiomyocyte damage (1): A) Increased in cardiomyocytes and decreased in blood plasma B) Decreased in both cardiomyocytes and blood plasma C) Increased in both cardiomyocytes and blood plasma D) Decreased in cardiomyocytes and increased in blood plasma + 49. Factors in lipid peroxidation activation during coronary insufficiency (5): A) Increased content of pro-oxidants and substrates for lipid peroxidation in the myocardium + B) Reduced activity of antioxidants + C) Excess calcium in myocardial cells + D) Postischemic reperfusion + E) Excess catecholamines in the heart + F) Increased activity of superoxide dismutase and catalase in cardiomyocytes 50. Characteristics of the compensation stage of heart failure (4): A) Tonogenic dilatation + B) Dyspnea at rest C) Dyspnea during exertion D) Tachycardia + E) Myocardial hypertrophy + F) Myocardial contracture G) Myogenic dilatation H) Activation of sympathoadrenal system + 51. Mechanisms of dysfunctional regulation of cardiomyocyte function in decompensated heart failure (4): A) Decrease in myocardial adrenergic reactivity + B) Deficiency of norepinephrine in the myocardium + C) Impaired interaction of adrenaline and norepinephrine with receptors on damaged membranes + D) Disruption of the balance between cAMP and cGMP in cardiomyocytes + E) Increase in myocardial adrenergic reactivity 52. Changes during heart decompensation (5): A) Decrease in stroke volume + B) Myogenic dilatation + C) Reduction in blood flow velocity + D) Increase in venous pressure + E) Increase in residual blood volume in cardiac chambers + F) Increase in cardiac output 53. Intracardiac hemodynamics in myogenic dilatation (3): A) Increase in the rate of systolic blood ejection from ventricles B) Increase in diastolic blood volume in the ventricular chambers + C) Decrease in blood flow velocity D) Increase in end-systolic blood volume in the ventricular chambers + E) Decrease in blood pressure in the right atrium and openings of the vena cava F) Decrease in cardiac stroke volume + 54. Manifestations of chronic heart failure decompensation (6): A) Cyanosis + B) Pleuritis C) Hydrothorax + D) Orthopnea + E) Tachycardia + F) Rapid fatigue + G) Frequent arrhythmias, up to fibrillation + 55. Mechanisms of tachycardia in heart failure (4): A) Activation of the sympathoadrenal system + B) Bainbridge reflex + C) Hypervolemia + D) Hypocapnia E) Decrease in the rate of spontaneous depolarization of the sinus node F) Increased myocardial adrenergic reactivity + 56. Cyanosis in heart failure develops due to increased levels of (1): A) Deoxyhemoglobin + B) Carboxyhemoglobin C) Carbhemoglobin D) Methemoglobin E) Glycosylated hemoglobin 57. Factors contributing to increased deoxyhemoglobin in heart failure (5): A) Slowed blood flow velocity + B) Decreased blood oxygenation in the lungs + C) Increased oxygen utilization by tissues + D) Increase in blood oxygen capacity E) Rightward shift of the hemoglobin dissociation curve + F) Leftward shift of the hemoglobin dissociation curve G) Pulmonary blood congestion + H) Dyspnea 58. Initial mechanisms of dyspnea pathogenesis in heart failure (4): A) Stimulation of baroreceptors in vascular reflexogenic zones + B) Decreased blood flow velocity C) Stimulation of chemoreceptors in vascular reflexogenic zones by products of disturbed metabolism + D) Stimulation of pulmonary interstitial receptors + E) Hyperoxemia F) Stimulation of alveolar stretch receptors + G) Hypocapnia 59. Mechanisms of cardiac edema pathogenesis (7): A) Venous congestion + B) Increased secretion of aldosterone and ADH + C) Increased venous pressure + D) Decreased arterial blood flow delivery E) Activation of the renin-angiotensin system + F) Tissue hyperosmolarity + G) Increased lymphatic drainage to the venous system H) Hypoxic damage to membranes, including the vascular wall + I) Impaired liver and kidney function + CARDIAC ARRHYTHMIAS (Adi) 1. Heart arrhythmias occur due to disturbances in (3): A) Automaticity + B) Excitability + C) Conductivity + D) Elasticity E) Stretchability 2. Nomotopic disturbances in heart automaticity include (4): A) Sinus arrhythmia + B) Sinus tachycardia + C) Sinus bradycardia + D) Sick sinus syndrome + E) Paroxysmal tachycardia 3. Sinus tachycardia arises in cases of (4): A) Increased sympathetic influence on the heart + B) Increased parasympathetic influence on the heart C) Reduced sympathetic influence on the heart D) Elevated body temperature + E) Hyperoxia F) Stress + G) Acute arterial hypotension + 4. Sinus tachycardia is characterized by (3): A) Heart rate reaching 90–180 bpm + B) Heart rate exceeding 200 bpm C) Acceleration of spontaneous diastolic depolarization of the sinus node + D) Increased sinus node automaticity + E) Significant changes in P wave morphology 5. ECG in sinus tachycardia shows (2): A) Shortened R-R interval + B) Shortened T-P interval + C) Shortened P-Q interval D) Reduced conduction velocity in the myocardium E) Impulse conduction block in the heart's conduction system 6. Sinus bradycardia develops with (4): A) Lowered body temperature + B) Enhanced parasympathetic influence on the heart + C) Increased sympathetic nervous system tone D) Hypoxia E) Hypothyroidism + F) Cholemia + 7. The pathogenesis of sinus bradycardia involves (2): A) Slowing of spontaneous diastolic depolarization in the sinus node + B) Reduced sympathoadrenal effects on the heart + C) Appearance of injury currents D) Reduced excitation conduction velocity in the myocardium E) Conduction block in the heart's conduction system 8. ECG in sinus bradycardia is characterized by (2): A) Prolonged R-R interval + B) Prolonged T-P interval + C) Shortened P-Q interval D) Reduced conduction velocity in the myocardium E) Conduction block in the heart's conduction system 9. Sinus bradycardia is characterized by (3): A) Reduced sinus node automaticity + B) Heart rate below 60 bpm + C) Reduced depolarization rate of sinus node cell membranes + D) Shortened P-Q interval E) Deformed P wave 10. Uniform shortening of R-R and T-P intervals on ECG is characteristic of (1): A) Sinus tachycardia + B) Sinus arrhythmia C) Second-degree AV block D) Fourth-degree AV block E) Ventricular extrasystole 11. The pathogenesis of sinus (respiratory) arrhythmia involves (2): A) Formation of an ectopic focus of impulse generation B) Fluctuations in vagal tone + C) Conduction disturbances from atria to ventricles D) "Re-entry" mechanism E) Decrease in threshold potential of pacemaker cells 12. ECG in sinus arrhythmia is characterized by (2): A) Variations in T-P interval duration + B) Dropping of ventricular complexes C) Absence of the P wave D) Uneven R-R interval durations + E) Prolongation of P-Q interval 13. Extrasystole occurs due to (1): A) Slowing of impulses from the sinus node B) Prolongation of the absolute refractory period C) Formation of an ectopic focus of impulse generation + D) Slowing of impulse conduction E) Uneven sinus node impulses 14. The pathogenesis of extrasystole involves (4): A) Emergence of potential differences between adjacent cardiomyocytes + B) Formation of injury currents in the myocardium + C) Reduction of maximum diastolic transmembrane potential in cardiomyocytes to threshold + D) Electrical inhomogeneity of the myocardium + E) Impulse generation from the sinus node F) Conduction disturbances in the His bundle G) Decreased sinus node automaticity 15. The re-entry mechanism of excitation can cause (3): A) Atrial fibrillation + B) Paroxysmal tachycardia + C) Extrasystole + D) AV block E) Sinus arrhythmia 16. On ECG, atrial extrasystole is characterized by (2): A) Presence of a P wave before an early ventricular complex B) Deformation of the extrasystolic P wave + C) Reduction and deformation of the ventricular complex D) Incomplete compensatory pause + E) Complete compensatory pause 17. On ECG, extrasystole with an ectopic focus in the upper part of the AV node shows (1): A) Negative P wave before the QRS complex of the extrasystole + B) Negative P wave after the QRS complex of the extrasystole C) Overlapping of the P wave with the QRS complex of the extrasystole D) Absence of P wave in the extrasystolic contraction E) Prolongation of T-P interval before the extrasystole 18. On ECG, extrasystole with an ectopic focus in the middle part of the AV node shows (2): A) Negative P wave before the QRS complex B) Negative P wave after the QRS complex C) Overlapping of the P wave with the ventricular complex + D) Presence of a biphasic P wave E) Incomplete compensatory pause after the extrasystole + 19. On ECG, extrasystole with an ectopic focus in the lower part of the AV node shows (2): A) Negative P wave before the QRS complex of the extrasystolic contraction B) Negative P wave after the QRS complex of the extrasystole + C) Overlapping of the P wave with the QRS complex of the extrasystole D) Absence of P wave in the extrasystolic contraction E) Incomplete compensatory pause + 20. A negative P wave on ECG is characteristic of (1): A) Sinus extrasystole B) AV extrasystole + C) Left ventricular extrasystole D) Right ventricular extrasystole E) AV block 21. On ECG, ventricular extrasystole is characterized by (3): A) Complete compensatory pause + B) Deformed ventricular complex + C) Presence of an early ventricular complex + D) Presence of P wave before the extrasystolic contraction E) Absence of P wave before the extrasystole + 22. A prolonged episode of paroxysmal ventricular tachycardia manifests as (3): A) Increased cardiac output B) Decreased cardiac output + C) Decreased coronary blood flow + D) Increased systolic blood pressure E) Risk of progressing to ventricular fibrillation or flutter + 23. Transverse cardiac block refers to (1): A) Conduction disturbance in the right bundle of the His bundle B) Conduction disturbance in the left bundle of the His bundle C) Impulse conduction disturbance from atria to ventricles via the AV node + D) Conduction disturbance in the atria E) Conduction disturbance in Purkinje fibers 24. ECG characteristics of first-degree AV block (1): A) Appearance of an extra cardiac cycle B) Negative P wave C) Dropping of ventricular complexes D) Deformation of the ventricular complex E) Uniform prolongation of the P-Q interval in each cardiac cycle + 25. Wenckebach-Samoilov periods on ECG are characteristic of (1): A) First-degree AV block B) Second-degree AV block + C) Intra-atrial block D) Third-degree AV block E) Conduction disturbances in the atrial conduction system 26. Complete transverse heart block is characterized by (1): A) Tachycardia episodes B) Asynchronous contractions of atria and ventricles + C) Alternating periods of increased and decreased heart rates D) Irregular heartbeats E) Nomotopic heart rhythm 27. The pacemaker for ventricles in complete AV block is located (1): A) In the sinus node B) In the atria C) In the His bundle + D) In the left branch of the His bundle E) In the right branch of the His bundle 28. Complete transverse heart block is accompanied by (5): A) Decreased cardiac output (CO) + B) Tachycardia C) Bradycardia + D) Decreased blood pressure + E) Development of Morgagni-Adams-Stokes syndrome + F) Increased venous pressure + G) Decreased venous pressure 29. The pathogenesis of atrial fibrillation involves (5): A) Shortened refractory period of cardiomyocytes + B) Increased excitability of cardiomyocytes + C) Uneven impulse generation from the sinus node D) Re-entry mechanism + E) Electrical inhomogeneity of the myocardium + F) Decreased extracellular potassium ion concentration G) Reduced pH in cardiomyocytes + 30. Severe hemodynamic disturbances occur in (2): A) Sinus tachycardia B) Sinus arrhythmia C) Paroxysmal tachycardia + D) Extrasystole E) Ventricular fibrillation + F) First-degree AV block 31. The pathogenetic treatment method for ventricular fibrillation is (1): A) Defibrillation + B) Administration of cardiac glycosides C) Use of hypotensive agents D) Use of sedatives E) Use of central analeptics 32. The treatment method for complete transverse heart block is (1): A) Administration of cardiac glycosides B) Administration of atropine C) Defibrillation D) Use of antiarrhythmic drugs E) Implantation of a pacemaker + 33. Match the following: 1. Sinus tachycardia (2) 2. Atrial fibrillation (3) A) Belongs to nomotopic arrhythmias 1 B) Belongs to heterotopic arrhythmias 2 C) Appearance of "f" waves on ECG 2 D) Regular ventricular contraction rhythm 1 E) Irregular ventricular contraction rhythm 2 34. Increased extracellular potassium leading to paroxysmal tachycardia and fibrillation occurs due to (3): A) ATP deficiency in cardiomyocytes + B) Creatine phosphate deficiency in cardiomyocytes + C) Reduced activity of Na⁺/K⁺ ATPase in the plasma membrane + D) Disruption of the lipid membrane layer of cardiomyocytes + E) Activation of anaerobic glycolysis in cardiomyocytes F) Activation of the pentose phosphate pathway G) Activation of oxidative phosphorylation in cardiomyocytes 35. Hyperkalemia in myocardial interstitium induces paroxysmal tachycardia, fibrillation, and flutter due to (3): A) Reduced excitability threshold of cardiomyocytes + B) Accelerated impulse conduction C) Decreased arrhythmogenic vulnerability period D) Decreased maximal diastolic potential + E) Emergence of injury currents in micro-areas of the myocardium + F) Prolonged refractory period VASCULAR TONE DISORDERS. ATHEROSCLEROSIS (Olzhas) 1. Match the following: 1. Basal vascular tone (2) 2. Vasomotor vascular tone (3) A) Ability of vascular muscles to contract in response to vasomotor nerve influences (2) B) A phylogenetically young and fast-acting mechanism (2) C) Response to sympathetic alpha-adrenergic influences (2) D) Ability of smooth muscle cells in vascular walls to exhibit spontaneous activity and propagate excitation (1) E) Ability to maintain vascular wall tension in the absence of external (neural or humoral) influences (1) 2. Match the following: 1. Hypotension (1) 2. Hypotonia (1) A) Decrease in arterial pressure (1) B) Decrease in vascular tone (2) 3. Increased peripheral vascular resistance and hypertension are caused by: A) Bradykinin B) Angiotensin II+ C) Vasopressin (ADH)+ D) Nitric oxide E) Endothelins+ 4. Decreased peripheral vascular resistance and hypotension are caused by: A) Catecholamines B) Bradykinin+ C) Angiotensin II D) Adenosine+ E) Nitric oxide+ 5. After administering a drug, the patient’s arterial pressure increased, but total peripheral resistance decreased. This drug likely caused: A) Vasoconstriction and decreased cardiac output B) Vasodilation and increased cardiac output+ C) Vasoconstriction and increased cardiac output D) Vasodilation and decreased cardiac output 6. Primary arterial hypertension may result from: A) Frequent negative psycho-emotional stressors+ B) Hereditary defects in membrane ion pumps+ C) Stenosing atherosclerosis of renal arteries D) Adrenal cortex hyperplasia E) Excessive salt intake+ 7. Risk factors for essential arterial hypertension include: A) Excess body weight+ B) Frequent negative emotional stress+ C) High salt intake in the diet+ D) Physical inactivity+ E) Noise+ F) Environmental pollution with lead and cadmium+ G) Harmful habits (alcohol, smoking)+ H) Hyperactivity of the sympathoadrenal system+ I) Hyperactivity of the parasympathetic nervous system J) Physical labor 8. Mechanisms of arterial hypertension development include: A) Activation of the renin-angiotensin system+ B) Activation of the kallikrein-kinin system C) Reduced afferent impulses from baroreceptors in the aorta and carotid sinuses through depressor nerves+ D) Excessive production of glucocorticoids+ E) Excessive production of mineralocorticoids+ 9. The pathogenesis of hypertension involves: A) Persistent increased excitability of sympathetic nerve centers+ B) Chronic excitation of emotional centers+ C) Reduced inhibitory effects of the cerebral cortex on the vasomotor center+ D) Hereditary defects in ion pumps of vascular smooth muscle cells+ E) Adrenal cortex dysfunction F) Hypernatremia+ 10. The pathogenesis of hypertension due to hereditary defects in cell membrane ion pumps includes: A) Reduced excretion of sodium and water by the kidneys+ B) Accumulation of sodium and calcium in vascular smooth muscle cells+ C) Increased sodium and water content in the body+ D) Increased sensitivity of vascular smooth muscle cells to catecholamines+ E) Genetically increased production of angiotensinogen+ F) Decreased circulating blood volume G) Reduced antidiuretic hormone levels in the blood H) Hyperparathyroidism 11. Genetic defects in vascular smooth muscle cell membranes lead to hypertension through: A) Increased calcium content in the cytoplasm of cells+ B) Increased electrical potential of cell membranes C) Increased reuptake rate of neurotransmitters by nerve endings D) Suppression of myosin ATPase activity E) Shortened action time of neurotransmitters on vascular walls 12. Primary arterial hypertension is characterized by: A) Persistent increase in arteriolar tone+ B) Adrenal insufficiency C) Reduced renin production D) Increased cardiac output+ E) Hypervolemia+ 13. During the stabilization period of primary arterial hypertension, the following are characteristic: A) Reduced nitric oxide production+ B) Increased renin secretion by the kidneys+ C) Activation of the kallikrein-kinin system D) Increased production of natriuretic hormone E) Increased renal production of prostaglandins E1 and E2 14. Symptomatic arterial hypertension includes: A) Renal hypertension+ B) Endocrine hypertension+ C) Essential hypertension D) Hypertension in pheochromocytoma+ E) Hypertension in hyperthyroidism+ F) Portal hypertension G) Pulmonary hypertension 15. Secondary (symptomatic) arterial hypertension is a symptom of: A) Myocardium diseases B) Gastrointestinal diseases C) Kidney diseases+ D) Spleen diseases E) Endocrine system diseases+ F) Lung diseases 16. Secondary arterial hypertension is a symptom of: A) Chronic adrenal insufficiency B) Peptic ulcer disease C) Primary aldosteronism.+ D) Hypocorticism E) Intestinal autointoxication 17. The most common type of symptomatic arterial hypertension is: A) Endocrine B) Renal.+ C) Neurogenic, central origin D) Neurogenic, reflex origin E) Hemodynamic 18. The pathogenesis of renovascular hypertension includes: A) Activation of the renin-angiotensin-aldosterone system.+ B) Decreased renal blood flow.+ C) Reduced production of depressor substances in the kidneys D) Increased secretion of renal kinins E) Decreased sodium reabsorption in the kidneys 19. The pathogenesis of renoparenchymal hypertension involves: A) Activation of the renin-angiotensin-aldosterone system B) Reduced erythropoietin secretion C) Increased water reabsorption in the kidneys D) Reduced secretion of renal kinins and prostaglandins.+ E) Increased sodium reabsorption in the kidneys 20. Pathogenesis of hypertension in nephrosclerosis is explained by: A) Loss of vasodilatory effects of bradykinin and kallidin.+ B) Reduced influence of prostaglandins.+ C) Increased renin production D) Increased angiotensin formation E) Decreased aldosterone production by the adrenal glands 21. Hypertension caused by brain injury is classified as: A) Essential arterial hypertension B) Neurogenic hypertension.+ C) Endocrine hypertension D) Drug-induced hypertension E) Renal hypertension 22. Pathogenesis of hypertension associated with activation of the renin-angiotensin system involves: A) Contraction of arterial smooth muscles.+ B) Increased release of catecholamines from sympathetic neurons.+ C) Increased sensitivity of vascular smooth muscle cells to catecholamines.+ D) Reduced influence of aldosterone E) Increased renal blood flow 23. Endocrine hypertension may result from hyperproduction of: A) Mineralocorticoids.+ B) Adrenaline.+ C) Glucocorticoids.+ D) Corticotropin (ACTH).+ E) Glucagon F) Parathyroid hormone.+ 24. Endocrine hypertension occurs in cases of: A) Hypofunction of the adenohypophysis B) Hyperfunction of the adrenal medulla.+ C) Hyperfunction of the glomerular zone of the adrenal cortex.+ D) Hyperfunction of the parathyroid glands.+ E) Hyperfunction of the thyroid gland.+ F) Hypofunction of the fascicular zone of the adrenal cortex G) Hypofunction of the pituitary gland 25. Pathogenesis of hypertension in aldosteronism (Conn’s syndrome) includes: A) Increased sodium reabsorption in renal tubules.+ B) Water retention in the body by the kidneys.+ C) Increased total peripheral vascular resistance.+ D) Increased sensitivity of the vascular wall to vasodilators E) Increased cardiac output.+ F) Suppressed activity of vascular sodium-potassium ATPase 26. Hypertension associated with hypernatremia is due to: A) Hypersecretion of renin B) Development of hypervolemia.+ C) Swelling of vascular endothelium.+ D) Blood thickening E) Activation of prostacyclin synthesis by endothelial cells 27. Hypertension in pheochromocytoma is caused by: A) Spasm of peripheral vessels due to β-adrenergic receptor stimulation B) Positive chrono- and inotropic effects of catecholamines on the heart.+ C) Increased cardiac output.+ D) Activation of the renin-angiotensin system.+ E) Increased thyroxine production 28. Hypertension due to hyperproduction of ADH is linked to: A) Decreased water reabsorption in renal tubules B) Increased circulating blood volume (CBV).+ C) Increased cardiac output.+ D) Constriction of peripheral vessels.+ E) Increased sodium reabsorption in renal tubules 29. Hypertension associated with excessive ACTH production is caused by: A) Stimulation of the fascicular and reticular zones of the adrenal cortex.+ B) Reduced effect of catecholamines C) Decreased glucocorticoid production D) Increased production of angiotensinogen and angiotensin-converting enzyme.+ E) Increased catecholamine production by the adrenal glands F) Increased circulating blood volume (CBV).+ 30. The missing link in the pathogenesis of arterial hypertension: Stress → Increased corticosteroids → Increased synthesis of angiotensinogen and angiotensin-converting enzyme → ? → Vascular spasm → Increased TPR → Arterial hypertension: A) Increased water reabsorption in the kidneys B) Increased sensitivity of vascular smooth muscle cells to catecholamines C) Increased formation of angiotensin II.+ D) Increased total peripheral resistance E) Increased aldosterone secretion 31. Methods of modeling arterial hypertension include: A) Bilateral transection of Ludwig-Cyon and Hering "depressor" nerves.+ B) Removal of both adrenal glands C) Removal of one kidney and ligation of the artery of the other.+ D) Electrical stimulation of depressor nerves E) Neurosis modeling.+ 32. Match the following: I. Renovascular model of arterial hypertension (3) II. Renoparenchymal model of arterial hypertension (3) A) Goldblatt (1) B) Grollman (2) C) Activation of the renin-angiotensin-aldosterone system (1) D) Reduced synthesis of depressor substances in the kidneys (2) E) Placement of narrowing rings on renal arteries (1) F) Bilateral nephrectomy (2) 33. Match the following: I. Central-ischemic model of arterial hypertension (2) II. Disinhibition model of arterial hypertension (1) A) Ligation of carotid artery branches (1) B) Introduction of kaolin suspension into the brain's large cistern (1) C) Disruption of excitatory and inhibitory processes D) Transection of depressor nerves (2) E) Formation of conditioned reflex 34. Antihypertensive systems include: A) Angiotensin II B) Catecholamines C) Prostacyclin.+ D) Cortisol E) Bradykinin.+ F) Nitric oxide.+ G) Endothelins H) Natriuretic hormone.+ 35. Acute arterial hypotension occurs in: A) Acute blood loss.+ B) Hypercortisolism C) Shock.+ D) Myxedema E) Addison's disease F) Collapse.+ G) Fainting.+ 36. Fainting is characterized by: A) Acute hypotension.+ B) Transient arterial hypotension and brain ischemia.+ C) Reduced vascular tone.+ D) Occurs during strong emotions, fear, or pain.+ E) Occurs during intense physical activity F) More common in men 37. Types of collapse by origin include: A) Renal B) Toxic-infectious.+ C) Pulmonary D) Hemorrhagic.+ E) Pancreatic.+ F) Hyperoxic G) Anoxic.+ H) Gravitational I) Orthostatic.+ 38. Toxic-infectious collapse can develop in: A) Tuberculosis B) Dysentery.+ C) Intensive antibacterial therapy for intestinal infections.+ D) Effects of toxins suppressing the respiratory center E) Significant reduction of liver barrier function F) Foodborne toxic infections.+ 39. Hemorrhagic collapse is possible due to: A) Significant bradycardia B) Action of sympatholytics or ganglioblockers C) Increased sweating D) Acute massive hemorrhage.+ E) Gravitational overloads 40. Pancreatic collapse is possible in: A) Acute and chronic adrenal insufficiency B) Hyperthermia C) Abdominal trauma with pancreatic injury.+ D) Diabetes mellitus E) Acute pancreatitis.+ F) Exposure to bacterial endotoxins 41. The main link in the pathogenesis of collapse is: A) Dysfunction of the nervous system B) Dysfunction of the cardiovascular system.+ C) Impaired gas exchange in the lungs D) Dysfunction of renal excretory functions E) Blood and hemostatic disorders 42. Mechanisms of collapse development include: A) Decreased tone of arterioles and venules.+ B) Primary reduction in cardiac output C) Decreased tone of capacitance vessels.+ D) Reduced ability to mobilize blood from depots E) Rapid decrease in circulating blood volume (CBV) without adequate compensation.+ 43. Collapse is characterized by: A) Increased tone of arterioles and venules B) Acute decrease in CBV.+ C) Increased venous blood return to the heart D) Reduced cardiac output.+ E) Decreased arterial pressure.+ F) Decreased systolic pressure.+ G) Increased diastolic pressure 44. Collapse is accompanied by: A) Pathological blood deposition.+ B) Venous hyperemia C) Chronic arterial hypotension D) Decrease in circulating blood volume.+ E) Increased capillary permeability.+ F) Plasma leakage (plasmorrhagia).+ G) Hemic hypoxia 45. Orthostatic collapse occurs: A) After massive blood loss B) Pancreatic trauma C) Rapid reduction in oxygen in inspired air D) Intestinal infections E) Abrupt transition from horizontal to vertical position.+ F) After prolonged bed rest.+ 46. Primary chronic arterial hypotension is: A) Hypotension in endocrine diseases B) Hypotension due to starvation C) Hypotonic disease.+ D) Hypotension in peptic ulcer disease E) Hypotension after chronic blood loss 47. Primary arterial hypotension occurs with: A) Congenital heart defects B) Acquired heart defects C) Chronic pneumonia or hepatitis D) Mental disorders E) Dysfunction of higher centers of vasomotor regulation.+ F) Endocrine insufficiency 48. Primary arterial hypotension is characterized by: A) Persistent decrease in total peripheral vascular resistance.+ B) Reduced cardiac output.+ C) Slight but persistent reduction in CBV.+ D) Increased cerebral blood flow velocity E) Elevated venous pressure 49. Symptomatic arterial hypotension is observed in: A) Anemia.+ B) Pheochromocytoma C) Hyperaldosteronism D) Acute diffuse glomerulonephritis E) Cushing's disease 50. Symptomatic arterial hypotension is observed in: A) Cholemia.+ B) Pheochromocytoma C) Hyperaldosteronism D) Acute diffuse glomerulonephritis E) Cushing's disease 51. Atherosclerosis is defined as: A) Vascular wall damage by autoantibodies and connective tissue overgrowth B) Plasma protein infiltration of vascular walls, development of hyalinosis, and subsequent sclerosis C) Chronic focal damage to elastic and muscular-elastic arteries with thickening of the inner layer due to lipid deposits and fibrous tissue formation.+ D) Calcium salt deposition in the middle layer of the vessel, leading to reactive inflammation and surrounding tissue sclerosis E) A type of arteriosclerosis.+ 52. The first signs of atherogenesis appear at: A) 9–10 years.+ B) 10–15 years C) 25 years D) 30–40 years E) 50–60 years 53. Morphogenetic stages of atherosclerosis include: A) Immune disorders B) Complicated lesions.+ C) Fibrous plaque.+ D) Fatty streak.+ E) Structural-cellular disruptions 54. Key stages of atherogenesis include: A) Formation of an atheroma.+ B) Development of fibroatheroma.+ C) Progression of atherogenesis.+ D) Initiation of atherogenesis.+ E) Release of atheroma contents into the arterial lumen 55. Factors contributing to atherosclerosis include: A) Predominance of plant-based foods in the diet B) High dietary fiber content C) Vegetables rich in carotenoids D) Predominance of animal fats in the diet.+ E) Fruits with high carbohydrate content 56. Risk factors for atherosclerosis include: A) Obesity.+ B) Smoking.+ C) Lack of animal fats and cholesterol in the diet D) Age over 30–40 years.+ E) Female sex F) Male sex.+ G) Hereditary hypercholesterolemia.+ 57. Risk factors for atherosclerosis include: A) Diabetes insipidus B) Diabetes mellitus.+ C) Hypothyroidism.+ D) Hyperthyroidism E) Gout.+ F) Hypotension G) Hypertension.+ 58. Genes involved in atherosclerosis development encode: A) LDL receptors.+ B) HDL receptors C) Cholesteryl ester transfer protein (CETP).+ D) Superoxide dismutase.+ E) Histamine (H1) receptor 59. The most atherogenic lipoproteins are: A) Low-density lipoproteins (LDL).+ B) Very low-density lipoproteins (VLDL) C) High-density lipoproteins (HDL) D) Chylomicrons E) Intermediate-density lipoproteins (IDL) 60. Antiatherogenic properties are attributed to: A) LDL B) VLDL C) HDL.+ D) Chylomicrons E) IDL 61. Lipid accumulation in the intima of vessels and monocytes is due to: A) Activation of lysosomal enzymes that break down esterified cholesterol B) Uptake of atherogenic lipoproteins via nonspecific endocytosis.+ C) Suppression of lecithin-cholesterol acyltransferase (LCAT) activity D) Incorporation of esterified cholesterol into the phospholipid layer of membranes E) Activation of lipoprotein lipase 62. The first theory of atherosclerosis was: A) Peroxidative B) Cholesterol.+ C) Monoclonal D) Membrane E) Autoimmune 63. The autoimmune theory of atherosclerosis is based on: A) Formation of antibodies (Abs) to LDL.+ B) Formation of antibodies to HDL C) Formation of LDL-Ab complexes in antigen excess.+ D) Formation of LDL-Ab complexes in antigen deficiency E) Interaction of LDL-Ab complexes with arterial wall cells.+ 64. Macrophages with abundant lipids in their cytoplasm are called: A) Labrocytes B) Microphages C) Foam cells.+ D) Dendritic cells E) Mast cells 65. Formation of "foam cells" is associated with lipid accumulation in: A) Neutrophils B) Macrophages.+ C) Lymphocytes D) Smooth muscle cells.+ E) Endothelial cells 66. The fibrous plaque contains the following cells: A) Neutrophils B) Lymphocytes.+ C) Macrophages.+ D) Eosinophils E) Smooth muscle cells.+ 67. Complications of atherosclerosis include: A) Arterial thrombosis.+ B) Venous thrombosis C) Thromboembolism.+ D) Mitral valve insufficiency E) Coronary artery disease.+ 68. Atherosclerosis can lead to: A) Arterial hyperemia B) Venous hyperemia C) Ischemia.+ D) True capillary stasis E) Development of aortic aneurysm.+ F) Stroke.+ G) Myocardial infarction.+ PATHOPHYSIOLOGY OF EXTERNAL RESPIRATION (Aknur) 1. External respiratory insufficiency is defined as a condition in which (1): A) The normal gas composition of arterial blood is not maintained. + B) Blood delivery to tissues is impaired. C) The oxygen capacity of blood is reduced. D) Biological oxidation is primarily disrupted. E) The normal gas composition of venous blood is not maintained. 2. External respiratory insufficiency is accompanied by (1): A) Increased partial pressures of oxygen (pO₂) and carbon dioxide (pCO₂) in arterial blood. B) Decreased pO₂ and pCO₂ in arterial blood. C) Decreased pO₂ and increased pCO₂ in venous blood. D) Increased pO₂ and normal pCO₂ in blood. E) Decreased pO₂ and normal pCO₂ in blood. F) Decreased pO₂ and increased pCO₂ in arterial blood. + 3. Consequences of external respiratory insufficiency include (3): A) Exogenous hypoxia. B) Hypocapnia. C) Hypoxemia. + D) Hypercapnia. + E) Reduced deoxyhemoglobin in the blood. F) Respiratory hypoxia. + 4. Alveolar hypoventilation leads to (2): A) Hypoxemia, hypocapnia, and acidosis. B) Hypoxemia, hypocapnia, and alkalosis. C) Hypoxemia, hypercapnia, and acidosis. + D) Hypoxemia, hypercapnia, and alkalosis. E) Respiratory acidosis. + F) Non-respiratory acidosis. 5. Classifications of respiratory insufficiency by pathogenesis include (4): A) Ventilatory. + B) Diffusion-related. + C) Perfusion-related. + D) Mixed. + E) Chronic. F) Exogenous. G) Acquired. 6. Obstructive ventilation disorders of the lungs can occur due to (2): A) Reduction of the total bronchial lumen. + B) Restriction of lung expansion during breathing. C) Reduction of pulmonary surface area. D) Decreased lung elasticity. + E) Increased lung rigidity. 7. Restrictive ventilation disorders of the lungs include (3): A) Reduction of the total bronchial lumen. B) Restriction of lung expansion during breathing. + C) Reduction of pulmonary surface area. + D) Narrowing of the tracheal lumen. E) Decreased lung compliance. + 8. Obstructive hypoventilation of the lungs arises in cases of (2): A) Impaired airway patency. + B) Dysfunction of respiratory muscles. C) Bronchospasm. + D) Reduced pulmonary surface area. E) Depression of respiratory center function. 9. A valvular mechanism of bronchial obstruction can occur in (1): A) Pulmonary emphysema. + B) Pneumonia. C) Surfactant deficiency. D) Resection of a lung lobe. E) Pulmonary edema. 10. Extrathoracic obstruction (in the neck area) of the upper respiratory tract is characterized by (2): A) Stridor breathing. + B) Rapid, shallow breathing. C) Breathing with difficulty during the expiratory phase. D) Cheyne-Stokes breathing. E) Breathing with difficulty during the inspiratory phase. + 11. Intrathoracic obstruction of the airways is characterized by (1): A) Stridor breathing. B) Rapid, shallow breathing. C) Difficulty in the expiratory phase. + D) Cheyne-Stokes breathing. E) Difficulty in the inspiratory phase. 12. Laryngeal stenosis is characterized by (1): A) Rapid, shallow breathing (tachypnea). B) Rapid, deep breathing (hyperpnea). C) Slow, deep breathing with difficulty in exhalation. D) Slow, deep breathing with difficulty in inhalation. + E) Biot’s respiration. 13. The pathogenesis of stridor breathing involves (1): A) Reduced excitability of the respiratory center. B) Increased excitability of the respiratory center. C) Accelerated Hering-Breuer reflex. D) Delayed Hering-Breuer reflex. + E) Activation of the Bainbridge reflex. F) The Euler-Liljestrand reflex. 14. Obstruction of the lower airways is associated with (3): A) Difficulty in the expiratory phase. + B) Difficulty in the inspiratory phase. C) Stridor breathing. D) Increased residual lung volume (RLV). + E) Reduced RLV. F) Increased Tiffeneau-Pinelli index. G) Reduced Tiffeneau-Pinelli index. + 15. Restrictive hypoventilation of the lungs occurs in (3): A) Bronchial mucosal edema. B) Surfactant deficiency. + C) Pulmonary edema. + D) Bronchospasm. E) Lung atelectasis. + 16. Restrictive ventilation disorders of the lungs develop in (4): A) Intercostal myositis. + B) Bronchitis. C) Bilateral pneumothorax. + D) Dry pleuritis. + E) Lung atelectasis. + F) Bronchial asthma. G) Laryngospasm. 17. Intrapulmonary restrictive ventilation disorders can occur with (1): A) Changes in the pleura and mediastinum. B) Chest deformity. C) Ossification of costal cartilage. D) Ascites. E) Diffuse pulmonary fibrosis. + 18. Extrapulmonary restrictive ventilation disorders can occur in (2): A) Hydrothorax. + B) Lung tumors. C) Lung atelectasis. D) Pneumoconiosis. E) Exudative pleuritis. + 19. Match the following: I. Intrapulmonary causes of restrictive hypoventilation (4) II. Extrapulmonary causes of restrictive hypoventilation (4) A) Pneumonia → I B) Hydrothorax → II C) Atelectasis → I D) Rib fracture → II E) Lung tumors → I F) Intercostal myositis → II G) Surfactant deficiency → I H) Ascites → II 20. Restrictive hypoventilation is characterized by (3): A) Tachypnea. + B) Bradypnea. C) Reduced vital lung capacity (VLC). + D) Increased VLC. E) Increased residual lung volume (RLV). F) Reduced total lung capacity (TLC). + 21. Match the following: I. Obstructive-type ventilation disorders (4) II. Restrictive-type ventilation disorders (2) A) Forced expiratory volume in one second (FEV1) reduced → I B) Inspiratory reserve volume (IRV) always reduced → I C) FEV1 unchanged → II D) Maximum expiratory flow rate decreased → I E) Tiffeneau index reduced → I F) Tiffeneau index unchanged → II 22. Lobar pneumonia is characterized by (1): A) Frequent deep breathing (hyperpnea) B) Rare deep breathing C) Biot's respiration D) Frequent shallow breathing (tachypnea) + E) Kussmaul's respiration 23. Respiratory surface of the lungs decreases with (3): A) Intense physical activity B) Pneumothorax + C) Lobar pneumonia + D) Significant blood loss E) Lung atelectasis + 24. Suppression of the respiratory center causes (2): A) Diffusion-type respiratory failure B) Ventilation-type respiratory failure + C) Perfusion-type respiratory failure D) Obstructive ventilation disorder E) Restrictive ventilation disorder + 25. Pathogenesis of respiratory center dysfunction includes (3): A) Direct damage to the respiratory center by pathogenic factors + B) Deficiency of excitatory afferentation + C) Excessive excitatory afferentation + D) Excessive inhibitory afferentation + E) Impairment of efferent stimulation of respiratory muscles 26. Central hypoventilation is observed in (4): A) Encephalitis + B) Cerebrovascular disorders + C) Narcotic poisoning + D) Low sensitivity of central and peripheral chemoreceptors + E) Intense irritation of the mucosal receptors of the upper airways + F) Administration of analeptics 27. Diffusion-type external respiratory failure occurs in (4): A) Increased alveolar thickness + B) Increased interstitial fluid volume + C) Thickening of capillary basal membrane + D) Blood stasis in the pulmonary circulation + E) Narrowing of lower airways F) Restrictive external respiratory disorders G) Pulmonary edema + 28. Diffusion impairment through the alveolar-capillary membrane is observed in (3): A) Interstitial pulmonary edema + B) Pleurisy C) Bronchial asthma D) Laryngeal edema E) Silicosis + F) Diffuse pulmonary fibrosis + 29. Perfusion-type respiratory failure results from (4): A) Arterial hypertension B) Shock + C) Hypervolemia D) Pulmonary artery branch embolism + E) Reduced myocardial contractility + F) Dehydration + G) Right-to-left blood shunting in heart defects + 30. Perfusion-type external respiratory failure is observed in (4): A) Reduced circulating blood volume + B) Right-sided heart failure + C) Left-sided heart failure + D) Alveolar hypoventilation E) Arterial hypotension + 31. Match the following: I. Causes of pulmonary hypertension (4) II. Causes of pulmonary hypotension (5) A) Pulmonary artery embolism → I B) Acute blood loss → II C) Reduced alveolar oxygen pressure → I D) Compression of pulmonary capillaries → I E) Dehydration → II F) Shock, collapse → II G) Left-sided heart failure → I H) Right-sided heart failure → II I) Tetralogy of Fallot → II 32. External respiratory efficiency is impaired at ventilation-perfusion ratios of (2): A) V̇A/Q̇ = 0.8–1.0 (V̇A = alveolar ventilation; Q̇ = cardiac output) B) V̇A/Q̇ < 1 + C) V̇A/Q̇ > 1 + 33. If V̇A = 3 L/min and Q̇ = 5 L/min, the ventilation-perfusion ratio (1): A) Decreases + B) Increases C) Remains unchanged 34. Match the following: I. V̇A/Q̇ > 1 (2) II. V̇A/Q̇ < 1 (3) A) Bronchospasm → II B) Fluid accumulation in alveoli → II C) Lung atelectasis → II D) Pulmonary arteriole spasm → I E) Blood stasis in the pulmonary circulation → I 35. Manifestations of respiratory failure include (3): A) Shortness of breath + B) Anemia C) Cyanosis + D) Changes in partial pressure of O₂ and CO₂ in venous blood E) Altered acid-base balance + 36. Shortness of breath is defined as (1): A) Frequent deep breathing B) Frequent shallow breathing C) Rare deep breathing D) Rare shallow breathing E) A feeling of air hunger accompanied by changes in breathing patterns + 37. The primary mechanism in the pathogenesis of shortness of breath is (1): A) Persistent stimulation of inspiratory neurons in the respiratory center + B) Persistent stimulation of expiratory neurons in the respiratory center 38. Initial stages in the pathogenesis of shortness of breath may involve stimulation of the respiratory center due to irritation of (3): A) Lung interstitial receptors + B) Respiratory muscle receptors + C) Vascular zone chemoreceptors by oxygen excess D) Airway receptors + E) Vascular zone chemoreceptors during hypocapnia F) Vascular chemoreceptors during alkalosis 39. Inspiratory shortness of breath is characterized by (1): A) Difficulty and prolongation of inhalation + B) Difficulty and prolongation of exhalation C) Difficulty and shortening of inhalation D) Difficulty and shortening of exhalation E) Increased breathing movements 40. Expiratory shortness of breath is characterized by (1): A) Difficulty and prolongation of inhalation B) Difficulty and shortening of exhalation C) Difficulty and shortening of inhalation D) Difficulty and prolongation of exhalation + E) Increased breathing movements 41. Inspiratory dyspnea is observed in (2): A) Pulmonary emphysema B) Narrowing of the tracheal lumen + C) Bronchial asthma D) Pleurisy E) Laryngeal edema + 42. In the pathogenesis of inspiratory dyspnea, the following factors are significant (2): A) Delay in the Hering-Breuer reflex + B) Increased tone of inspiratory respiratory muscles + C) Increased tone of expiratory respiratory muscles D) Decreased tone of expiratory respiratory muscles E) Acceleration of the Hering-Breuer reflex 43. Expiratory dyspnea is observed in (2): A) Bronchial asthma + B) Pulmonary emphysema + C) Pleurisy D) The first stage of asphyxia E) Laryngeal edema 44. Match the following: I. Pathogenesis of inspiratory dyspnea (2) II. Pathogenesis of expiratory dyspnea (2) A) Delay in the Hering-Breuer reflex → I B) Acceleration of the Hering-Breuer reflex C) Reduced elasticity of lung tissue → II D) Increased resistance to airflow in the lower airways → II E) Increased resistance to airflow in the upper airways → I 45. Match the following: I. Inspiratory dyspnea (4) II. Expiratory dyspnea (3) A) Pulmonary emphysema → II B) Bronchial asthma attack → II C) Narrowing of the tracheal lumen → I D) Laryngeal edema → I E) The first stage of asphyxia → I F) Compression of the trachea by an enlarged thyroid gland → I G) The second stage of asphyxia → II 46. Periodic breathing is characterized by (1): A) Breathing with an altered ratio between inhalation and exhalation B) Alternation of breathing periods with apnea + C) Rapid breathing D) Breathing with variable amplitude E) Cessation of breathing 47. In the pathogenesis of periodic breathing, the following factors are significant (2): A) Decreased sensitivity of the respiratory center to carbon dioxide + B) Increased sensitivity of the respiratory center to carbon dioxide C) Overstimulation of the respiratory center D) Constant stimulation of inspiratory neurons in the respiratory center E) Delayed response of central chemoreceptors to stimulation + 48. Cheyne-Stokes breathing is characterized by (1): A) Alternation of apnea with breathing movements that gradually increase in depth and then decrease + B) Alternation of apnea with breathing movements of uniform frequency and depth C) Deep, rare breathing movements D) Breathing movements that decrease in intensity E) Breathing movements that increase in intensity 49. Biot’s breathing is characterized by (1): A) Alternation of apnea with breathing movements that gradually increase in depth and then decrease B) Alternation of apnea with breathing movements of uniform frequency and depth + C) Deep, rare breathing movements D) Breathing movements that decrease in intensity E) Breathing movements that increase in intensity 50. Kussmaul breathing is characterized by (1): A) Alternation of apnea with breathing movements that gradually increase in depth and then decrease B) Alternation of apnea with breathing movements of uniform frequency and depth C) Deep, rare breathing movements + D) Breathing movements that decrease in intensity E) Breathing movements that increase in intensity 51. Terminal types of breathing include (3): A) Kussmaul breathing + B) Apneustic breathing + C) Tachypnea D) Bradypnea E) Gasping respiration + 52. Match the following: I. Kussmaul breathing (1) II. Apneustic breathing (1) III. Gasping respiration (1) A) Deep, rare breathing movements → I B) Prolonged convulsive inhalation, occasionally interrupted by exhalation → II C) Single, rare, weakening “sighs” → III 53. Match the following: I. Kussmaul breathing (1) II. Apneustic breathing (1) III. Gasping respiration (1) A) Stimulation of neurons in the caudal part of the medulla oblongata → III B) Overstimulation of the respiratory center → I C) Regulation of breathing through stimulation of apneustic center neurons, occasionally interrupted by impulses from the pneumotaxic center → II 54. Hyperpnea is (1): A) Rare breathing B) Frequent breathing C) Frequent, deep breathing + D) Frequent, shallow breathing E) Deep, rare breathing 55. Hyperpnea is observed in (2): A) Altitude sickness + B) Increased blood pressure C) Pneumonia D) Effects of narcotics E) Hysteria + 56. Bradypnea is (1): A) Rare breathing + B) Frequent breathing C) Frequent, shallow breathing D) Deep breathing E) Cessation of breathing 57. Bradypnea is observed in (3): A) Increased blood pressure + B) Suppression of the respiratory center + C) Brain tumors + D) Prolonged hypoxia E) Pneumonia 58. Tachypnea is (1): A) Frequent, shallow breathing + B) Frequent, deep breathing C) Rare breathing D) Deep, rare breathing E) Rare, shallow breathing 59. Tachypnea is observed in (1): A) Narcotic poisoning B) Pneumonia + C) Laryngeal edema D) Bronchial asthma E) Increased blood pressure 60. Asphyxia is defined as (1): A) Temporary cessation of breathing B) Difficulty and prolongation of inhalation accompanied by pronounced dyspnea C) Difficulty and prolongation of exhalation in an unconscious state D) Hyperventilation of the lungs due to intense stimulation of the respiratory center E) An acute or subacute condition of significant hypoxemia and hypercapnia + 61. Asphyxia occurs in (4): A) Anemia B) Entry of foreign bodies into major airways + C) Chest pain D) Hyperoxia E) Pulmonary emphysema F) Bilateral pneumothorax + G) A sharp decrease in oxygen in inhaled air + H) Paralysis of respiratory muscles + 62. The first stage of asphyxia is characterized by (4): A) Increased blood pressure + B) Bradycardia C) Expiratory breathing D) Tachycardia + E) Inspiratory dyspnea + F) Increased tone of the sympathetic nervous system + G) Rapid breathing 63. The second stage of asphyxia is characterized by (4): A) Decreased blood pressure + B) Increased blood pressure C) Pulmonary hypertension D) Bradycardia + E) Tachycardia F) Expiratory dyspnea + G) Increased tone of the parasympathetic nervous system + H) Excitation of the respiratory center 64. The pathogenesis of asphyxia involves (3): A) Hypercapnia + B) Non-gaseous alkalosis C) Hypoxemia + D) Gaseous acidosis + E) Hypocapnia F) Gaseous alkalosis 65. Acute respiratory failure is observed in (4): A) Severe bronchospasm attack + B) Pulmonary emphysema C) Pulmonary artery thromboembolism + D) Bronchiectasis E) Adult respiratory distress syndrome (ARDS) + F) Spontaneous pneumothorax + 66. ARDS (Adult Respiratory Distress Syndrome) may result from (5): A) Disseminated intravascular coagulation (DIC) syndrome + B) Surfactant deficiency + C) Sepsis + D) Pulmonary emphysema E) Atypical pneumonia + F) Exposure to toxic gases + 67. The main pathogenic factor in ARDS is (1): A) Increased hydrostatic pressure in the microvessels of the alveolar walls B) Decreased hydrostatic pressure in the microvessels of the alveolar walls C) Significant increase in arterial pressure levels D) Generalized damage to lung capillaries and alveolocytes + E) Interstitial pulmonary edema F) Cardiogenic pulmonary edema G) Development of hyalinosis in the alveolar walls 68. In the pathogenesis of diffuse damage to alveolocytes and capillaries in ARDS, the following factors are significant (5): A) Interleukins + B) Tumor necrosis factor (TNF) + C) Oxygen radicals + D) Antiproteases E) Platelet-activating factor + F) Leukotrienes + 69. The main pathogenic factor in neonatal respiratory distress syndrome (RDS) is (1): A) Deposition of hyaline in the alveolar walls B) Surfactant deficiency + C) Decreased compliance (elasticity) of lung tissue D) Upper airway obstruction E) Spasm of small bronchi PATHOPHYSIOLOGY OF THE DIGESTIVE SYSTEM (Munisa) 1. Consequences of digestive insufficiency (4): A) Positive nitrogen balance B) Hypovitaminosis + C) Body exhaustion + D) Edema + E) Reduced nonspecific resistance + 2. Pathological increase in appetite is called (1): A) Hyperrexia + B) Polyphagia C) Dysphagia D) Aphagia E) Xerostomia 3. Anorexia is (1): A) Lack of appetite + B) Inability to swallow C) Excessively increased appetite D) Increased food intake E) Lack of salivation 4. Bulimia is (1): A) Lack of appetite B) Inability to swallow C) Excessively increased appetite + D) Increased food intake E) Increased salivation 5. Polyphagia is (1): A) Lack of appetite B) Inability to swallow C) Excessively increased appetite D) Increased food intake + E) Chewing disorder 6. Dysphagia is (1): A) Lack of appetite B) Inability to swallow C) Excessively increased appetite D) Increased food intake E) Difficulty swallowing + 7. Hyporexia is caused by (4): A) Intoxication + B) Intestinal infection + C) Stress + D) Irritation of ventromedial hypothalamic nuclei + E) Irritation of ventrolateral hypothalamic nuclei 8. Neurotic anorexia is observed in (1): A) Intestinal infections B) Diabetes mellitus C) Negative emotions + D) Intoxications E) Pain 9. Nervous anorexia is observed in (1): A) Intense cortical excitation B) Obsessive idea of excessive weight + C) Reciprocal inhibition of the food center D) Pain syndrome E) Intoxication 10. Intoxication anorexia is observed in (1): A) Conditional-reflex inhibition of appetite due to pain B) Intense cortical excitation C) Obsessive idea of excessive weight D) Poisoning + E) Dysfunction of digestive tract receptors 11. Hyperrexia is observed in (1): A) Diabetes mellitus + B) Intoxication C) Pain syndrome D) Suppression of the food center E) Destruction of ventrolateral hypothalamic nuclei 12. Parorexia is (1): A) Perversion of appetite + B) Rapid satiety C) Swallowing disorder D) Increased appetite E) Decreased appetite 13. Chewing is impaired in (4): A) Trigeminal nerve damage + B) Tetanus + C) Periodontal disease + D) Hypersalivation E) Tooth decay + 14. Chewing disorders are caused by (4): A) Tooth prosthetics + B) Pulpitis + C) Gingivitis + D) Irritation of ventromedial hypothalamic nuclei E) Damage to the temporomandibular joint + 15. Consequences of poor food chewing are (3): A) Reduced gastric juice secretion + B) Increased pancreatic juice secretion C) Reduced pancreatic juice secretion + D) Increased gastric juice secretion E) Mechanical damage to the esophageal and stomach mucosa + 16. Swallowing is impaired in (3): A) Tongue paralysis + B) Stomach tumors C) Tonsillitis + D) Hypersalivation E) Chewing disorders + 17. Swallowing disorders are caused by (4): A) Botulism + B) Esophageal obstruction (achalasia) + C) Collagen diseases (scleroderma) + D) Parkinson’s disease + E) Hypochlorhydria 18. Consequences of swallowing disorders are (4): A) Hydrophobia + B) Aspiration pneumonia + C) Body exhaustion + D) Dehydration + E) Hyperchlorhydria 19. Hyposalivation is observed in (4): A) Salivary gland tumors + B) Sialolithiasis + C) Increased vagal tone D) Reduced vagal tone + E) Strong emotions + 20. Hyposalivation is characterized by (3): A) Tongue paresis B) Xerostomia + C) Gum hyperplasia D) Difficulty swallowing + E) Multiple tooth decay + 21. Hyposalivation leads to (3): A) Increased gastric juice production B) Xerostomia + C) Multiple tooth decay + D) Development of inflammatory processes in the oral cavity + E) Ptyalism (salivation) 22. Hypersalivation is observed in (4): A) Effect of atropine B) Stomatitis + C) Helminthiasis + D) Sialolithiasis E) Bulbar paralysis + F) Pregnancy toxicosis (gestosis) + 23. Hypersalivation is accompanied by (3): A) Gum bleeding B) Salivation + C) Atrophy of oral mucosa D) Skin maceration + E) Neutralization of gastric acid + 24. With uncontrollable vomiting, the following occur (4): A) Hyperkalemia B) Hyponatremia + C) Hypochloremia + D) Metabolic alkalosis + E) Convulsions + 25. Causes of reduced gastric juice secretion (3): A) Excessive parasympathetic stimulation of the stomach B) Excess secretin production + C) Reduced gastrin secretion + D) Increased histamine secretion E) Stomach mucosa atrophy + 26. Reduced stomach acidity leads to (4): A) Reduced bactericidal action of hydrochloric acid + B) Fermentation and decay in the stomach + C) Difficulty evacuating food masses from the stomach D) Rapid neutralization of food masses by duodenal contents + E) Diarrhea + 27. Achlorhydria leads to (4): A) Pyloric gaping + B) Constipation C) Reduced protein digestion + D) Accelerated evacuation of food masses from the stomach to the intestine + E) Rapid neutralization of food masses by duodenal contents + 28. Gastric achilia is (1): A) Absence of hydrochloric acid in gastric juice B) Absence of bile in the intestine C) Increased enzyme production in gastric juice D) Almost complete absence of gastric secretion (hydrochloric acid and enzymes) + E) Absence of intestinal juice secretion 29. Hyperchlorhydria is (1): A) Increased hydrochloric acid production by gastric parietal cells + B) Increased pepsin production by chief cells C) Increased mucin production by accessory cells D) Increased chloride content in the blood E) Increased hydrochloric acid production by chief cells 30. Excessive parasympathetic nerve tone leads to (3): A) Reduced hydrochloric acid production B) Increased gastric juice secretion + C) Reduced histamine secretion D) Increased histamine secretion + E) Hypersecretion of hydrochloric acid + 31. Hyperchlorhydria is caused by (4): A) Increased gastrin production + B) Increased number of parietal gastric cells + C) Increased vagal tone + D) Atrophic gastritis E) Somatostatin deficiency + 32. Hyperchlorhydria of gastric juice is associated with (3): A) Pyloric spasm + B) Food retention in the stomach + C) Diarrhea D) Acidic belching, sometimes vomiting + E) Pyloric gaping 33. The pathogenesis of heartburn involves (4): A) Cardiac gaping + B) Gastroesophageal reflux + C) Esophageal spasm and antiperistalsis + D) Reduced gastric acid content E) Increased organic acid content in the stomach + 34. Hyperchlorhydria is compensated by (4): A) Reduced production of mucous alkaline secretion rich in bicarbonate B) Neutralization of hydrogen ions by saliva entering the stomach + C) Gastrin secretion inhibition + D) Hydrogen ion sorption by mucus + E) Increased production of mucous alkaline secretion in the stomach + 35. Hyperchlorhydria and hypersecretion of gastric juice lead to (5): A) Food retention in the stomach + B) Accelerated evacuation of food from the stomach to the duodenum C) Reduced pancreatic juice secretion D) Constipation + E) Diarrhea F) Increased pepsin activity + G) Pyloric spasm + H) Pyloric gaping I) Reduced gastric motility + 36. Lead to the formation of gastric mucosal ulcers (4): A) Increased acidity of gastric juice + B) Helicobacter pylori + C) Presence of the mucosal barrier D) High pepsin activity + E) Good blood supply to the gastric mucosa F) Rapid regeneration of the gastric mucosa G) Disruption of the mucosal barrier + 37. Contribute to the development of gastric ulcer disease (7): A) Blood group I + B) Asthenic constitution + C) Hypokinesia + D) Nervous and psychological stress + E) Rapid regeneration of the gastric mucosa F) Increased tone of parasympathetic nerves + G) Increased mucus production in the stomach H) Increased tone of sympathetic nerves + I) Decreased synthesis of DNA, RNA, and proteins + 38. "Aggression factors" in the pathogenesis of gastric and duodenal ulcer disease (4): A) Helicobacter pylori + B) Hyperproduction of hydrochloric acid and pepsin + C) Gastroduodenal dysmotility + D) Prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs) + E) High concentration of prostaglandins 39. "Defense factors" in the pathogenesis of gastric and duodenal ulcer disease (4): A) Secretion of mucus and bicarbonates + B) Hypercortisolism C) Active secretion of prostaglandins + D) Adequate blood supply + E) Active regeneration of the mucosa + 40. Gastric ulcers are reproduced experimentally by (6): A) Ligating the pylorus while maintaining its patency + B) Damaging the gastric mucosa with physical or chemical irritants + C) Ligation of the gastric wall vessels + D) Modeling neurosis with additional administration of gastric juice + E) Prolonged stimulation of the vagus nerve + F) Prolonged administration of M-cholinomimetics + G) Administration of M-cholinolytics 41. Cavitary digestion is disrupted by (5): A) Hypochlorhydria + B) Achylia + C) Dystrophic changes in intestinal cells + D) Acholia + E) Disruption of the glycocalyx structure of microvilli in the small intestine F) Insufficient secretion of pancreatic juice + 42. Causes of impaired membrane digestion (6): A) Diseases of the liver and pancreas leading to impaired cavitary digestion + B) Disruption of the structure of villi and microvilli in the small intestine + C) Disruption of the enzyme layer on the intestinal wall surface + D) Parorexia E) Disruption of the motor and excretory functions of the small intestine + F) Atrophy of the small intestinal mucosa + G) Intestinal motility disorders + 43. Manifestations of impaired cavitary digestion (5): A) Hyporexia + B) Hyperrexia C) Flatulence + D) Profuse diarrhea + E) Colicky abdominal pain + F) Steatorrhea + G) Constipation 44. Malabsorption syndrome is a syndrome characterized by (1): A) Increased bile flow into the intestine B) Impaired endocrine function of the pancreas C) Increased absorption of maltose D) Impaired absorption of nutrients in the small intestine + E) Increased absorption processes in the stomach 45. Causes of primary malabsorption (2): A) Hereditary lactase deficiency + B) Hypocholia C) Pancreatitis D) Hereditary peptidase deficiency + E) Gastritis 46. Secondary malabsorption is associated with (6): A) Achlorhydria + B) Subtotal gastrectomy + C) Hereditary gluten digestion disorder (celiac disease) D) Chronic pancreatitis + E) Chronic hepatitis + F) Enteritis + G) Dysbiosis + 47. Manifestations of malabsorption include (6): A) Weight loss + B) Non-gaseous alkalosis C) Hypovitaminosis + D) Absolute hyperproteinemia E) Flatulence + F) Polyfecalia with undigested food residues + G) Steatorrhea + H) Osmotic diarrhea + 48. Reduced secretion of pancreatic juice occurs in (6): A) Excessive production of secretin B) Neurogenic inhibition of pancreatic function + C) Autoallergic damage to the pancreas + D) Destruction of the pancreas by a tumor + E) Obstruction or compression of the pancreatic duct + F) Duodenitis + G) Pancreatitis + H) Increased secretion of cholecystokinin 49. Pathogenesis of acute pancreatitis involves (7): A) Autodigestion of pancreatic tissue by proteolytic enzymes + B) Exhaustion of trypsin inhibitors in the pancreas + C) Stimulation of secretin release by alcohol + D) Arterial hypertension E) Activation of the kallikrein-kinin system + F) Development of collapse + G) Reflux of bile into the pancreatic duct in gallstone disease + H) Obstruction of the pancreatic duct + 50. Steatorrhea develops in (2): A) Pancreatic insufficiency + B) Hypersecretion of gastric juice C) High activity of intestinal lipases D) Acholia + E) Impaired intestinal motility F) Excessive protein intake 51. Factors that enhance intestinal peristalsis (3): A) Achylia + B) Reduced excitability of the vagus nerve center C) Increased excitability of intestinal wall receptors + D) Acute enteritis + E) Constant consumption of low-fiber foods 52. Secretory diarrhea develops in (2): A) Increased production of vasoactive intestinal polypeptide (VIP) + B) Increased secretion of water and electrolytes into the intestinal lumen + C) Increased osmotic pressure of intestinal contents D) Disruption of cavitary and membrane digestion E) Increased intestinal peristalsis F) Hyperthyroidism G) Stress 53. Hyperkinetic diarrhea develops in (3): A) Increased production of vasoactive intestinal polypeptide (VIP) B) Increased secretion of water and electrolytes into the intestinal lumen C) Increased osmotic pressure of intestinal contents D) Increased intestinal peristalsis + E) Hyperthyroidism + F) Stress + 54. Osmotic diarrhea develops in (2): A) Increased production of vasoactive intestinal polypeptide (VIP) B) Increased secretion of water and electrolytes into the intestinal lumen C) Increased osmotic pressure of intestinal contents + D) Disruption of cavitary and membrane digestion + E) Increased intestinal peristalsis F) Hyperthyroidism G) Stress 55. Spastic (hyperkinetic) constipation occurs in (2): A) Dysentery B) Achlorhydria C) Intestinal spasms + D) Achylia E) Hypersecretion of gastric juice + 56. Atonic (hypokinetic) constipation occurs in (3): A) Intestinal paresis in the postoperative period + B) Intestinal spasms C) Lead intoxication D) Hypokinesia + E) Decreased acetylcholine synthesis + 57. Dietary constipation occurs in (1): A) Lack of fiber in the diet + B) Disruption of the conditioned reflex for bowel emptying C) Diseases of the anorectal region (anal fissures, paraproctitis, hemorrhoids) D) Mercury or lead poisoning, or drug effects E) Hypothyroidism F) Hirschsprung's disease (megacolon) 58. Habitual constipation occurs in (1): A) Lack of fiber in the diet B) Disruption of the conditioned reflex for bowel emptying + C) Diseases of the anorectal region (anal fissures, paraproctitis, hemorrhoids) D) Mercury or lead poisoning, or drug effects E) Hypothyroidism F) Hirschsprung's disease (megacolon) 59. Proctogenic constipation occurs in (1): A) Lack of fiber in the diet B) Disruption of the conditioned reflex for bowel emptying C) Diseases of the anorectal region (anal fissures, paraproctitis, hemorrhoids) + D) Mercury or lead poisoning, or drug effects E) Hypothyroidism F) Hirschsprung's disease (megacolon) 60. Toxic constipation occurs in (1): A) Lack of fiber in the diet B) Disruption of the conditioned reflex for bowel emptying C) Diseases of the anorectal region (anal fissures, paraproctitis, hemorrhoids) D) Mercury or lead poisoning + E) Hypothyroidism F) Hirschsprung's disease (megacolon) 61. Mechanical intestinal obstruction occurs in (3): A) Adhesive disease + B) Intestinal diverticula + C) Obstruction of the intestinal lumen by a tumor, helminths, or fecal masses + D) Intestinal spasms E) Intestinal muscle atony 62. Dynamic intestinal obstruction occurs in (2): A) Adhesive disease B) Intestinal diverticula C) Obstruction of the intestinal lumen by a tumor, helminths, or fecal masses D) Intestinal spasms + E) Intestinal muscle atony + 63. The pathogenesis of intestinal obstruction involves (5): A) Increased intraintestinal pressure + B) Proliferation of pathogenic bacterial flora + C) Intestinal autointoxication + D) Hypervolemia E) Loss of fluid and electrolytes + F) Blood thickening + 64. Intestinal autointoxication is caused by the toxic effects of (2): A) Products of protein putrefaction in the intestines + B) Biogenic amines + C) Indirect bilirubin D) Ketone bodies E) Bile acids 65. Acute intestinal autointoxication is characterized by (4): A) Increased blood pressure B) Decreased pain sensitivity + C) Decreased blood pressure + D) Disturbed breathing rhythm + E) Deep inhibition of cerebral cortex functions + PATHOPHYSIOLOGY OF THE LIVER (Karina and Zhaukhar) 1. Primary liver failure develops in (2): A) Heart failure B) Shock C) Renal failure D) Viral liver damage + E) Exposure to carbon tetrachloride + 2. Secondary liver failure develops in (2): A) Exposure to carbon tetrachloride B) Circulatory insufficiency + C) Phosphorus intoxication D) Diabetes mellitus + E) Chronic alcohol intoxication 3. Match the following: I. Primary liver failure (5): A) Chloroform → 1 B) Mechanical trauma → 1 C) Hepatitis viruses A, B, C, D, E → 1 D) Fungal toxins → 1 E) Echinococcosis of the liver → 1 II. Secondary liver failure (1): F) Leukemias → 2 4. Are all liver functions necessarily impaired in liver failure? (1): A) Yes B) No + 5. Hepatocytes are damaged under the influence of (4): A) Damaging environmental factors + B) Bile components in case of impaired bile excretion + C) Circulatory disorders + D) Autoimmune mechanisms + E) Increased blood supply 6. Pathogenesis of hepatocyte damage involves (4): A) Destabilization of hepatocyte membranes + B) Activation of lipid peroxidation + C) Increased activity of phospholipases + D) Formation of autoantibodies to hepatocyte antigens + E) Increased formation of conjugated bilirubin 7. Carbohydrate metabolism disorders in liver failure are characterized by (3): A) Increased glycogen content in the liver B) Decreased glycogen content in the liver + C) Hyperlactacidemia + D) Tendency to hypoglycemia between meals + E) Activation of gluconeogenesis 8. Protein metabolism disorders in liver failure are characterized by (4): A) Hyperproteinemia B) Hyperazotemia + C) Hypoprothrombinemia + D) Dysproteinemia + E) Hyperaminoacidemia + 9. Metabolic disorders in liver failure manifest as (4): A) Edema + B) Changes in blood pH + C) Increased urea synthesis D) Increased blood ammonia levels + E) Bleeding tendency + 10. Liver failure manifests as (4): A) Increased blood ammonia levels + B) Hypoproteinemia + C) Increased ALT and AST activity in the blood + D) Bleeding tendency + E) Dehydration of the body 11. Hemorrhagic syndrome in liver failure is caused by (4): A) Impaired synthesis of prothrombin + B) Impaired synthesis of fibrinogen + C) Impaired synthesis of proteins C and S D) Impaired synthesis of clotting factors V, VII, IX, X, XII, XIII + E) Congenital deficiency of factor VIII 12. Lipid metabolism disorders in liver failure are characterized by (4): A) Impaired synthesis of lipoproteins + B) Decreased synthesis of phospholipids + C) Decreased oxidation of free fatty acids + D) Increased synthesis of esterified cholesterol E) Fat infiltration of the liver + 13. The pathogenesis of liver fat infiltration involves (4): A) Increased fat inflow to the liver + B) Reduced synthesis of phospholipids and increased formation of triacylglycerols from fatty acids + C) Reduced lipolysis and fatty acid oxidation in the liver + D) Decreased synthesis of apolipoproteins for lipoproteins + E) Increased synthesis of lipoproteins 14. Vitamin metabolism disorders in liver failure are characterized by (5): A) Reduced absorption of fat-soluble vitamins in the intestine + B) Decreased ability of hepatocytes to convert provitamins into active vitamin forms + C) Inhibition of coenzyme formation from vitamins + D) Impaired storage of vitamin B12 + E) Impaired formation of active vitamin D + F) Impaired absorption of water-soluble vitamins 15. Hormonal metabolism disorders in liver failure are characterized by (3): A) Reduced hormone inactivation + B) Development of primary aldosteronism C) Development of secondary aldosteronism + D) Reduced hormone synthesis E) Development of gynecomastia + 16. The liver neutralizes (4): A) Biogenic amines (cadaverine, putrescine) + B) Ammonia + C) Unconjugated bilirubin + D) Phenolic aromatic compounds + E) Urea 17. Experimental methods for studying liver function (6): A) Direct Eck fistula + B) Complete liver removal + C) Partial liver removal + D) Angiostomy by E.S. London + E) Perfusion of isolated liver + F) Reverse Eck-Pavlov fistula + G) Application of vasoconstrictor rings by Goldblatt 18. A direct Eck fistula is (1): A) Anastomosis between the portal and inferior vena cava with ligation of the inferior vena cava above the junction B) Anastomosis between the portal and inferior vena cava with ligation of the portal vein above the junction + C) Anastomosis between the portal and superior vena cava with ligation of the portal vein below the junction 19. A direct Eck fistula is used to study liver functions (2): A) Metabolic B) Urea-forming + C) Barrier, detoxification + D) Bile formation E) Bile excretion 20. Creating a direct Eck fistula in animals and feeding them meat leads to (3): A) Encephalopathy + B) Increased levels of indole, skatole, putrescine, cadaverine in the blood + C) Increased blood urea levels D) Increased blood ammonia levels + E) Hyperalbuminemia 21. A reverse Eck-Pavlov fistula is (1): A) Anastomosis between the portal and inferior vena cava with ligation of the inferior vena cava above the junction + B) Anastomosis between the portal and inferior vena cava with ligation of the portal vein above the junction C) Anastomosis between the portal and superior vena cava with ligation of the portal vein below the junction 22. Substances with pronounced toxic effects on the body include (2): A) Conjugated bilirubin B) Unconjugated bilirubin + C) Bile acids + D) Urobilinogen E) Stercobilinogen 23. Missing link in the pathogenesis of hepatic coma after creating a direct Eck fistula (4): Reduced blood flow to the liver via the portal vein → Blood enters the systemic circulation bypassing the liver → Intoxication with substances → ? → Coma. A) NH₃ (Ammonia) + B) Phenols + C) Cadaverine + D) Unconjugated bilirubin + E) Conjugated bilirubin 24. The first step in the operation of complete liver removal is (1): A) Creation of a direct Eck fistula B) Creation of a reverse Eck-Pavlov fistula + C) Performing angiostomy by London D) Introduction of toxic substances into the body E) Partial liver removal 25. Angiostomy by E.S. London is performed by (1): A) Anastomosis between the portal and inferior vena cava with ligation of the inferior vena cava above the junction B) Suturing metal cannulas to the walls of the portal and hepatic veins, followed by externalizing their free ends through the anterior abdominal wall + C) Anastomosis between the portal and inferior vena cava with ligation of the portal vein above the junction D) Anastomosis between the portal and superior vena cava with ligation of the portal vein below the junction E) Creation of a bile fistula 26. The angiostomy method by E.S. London is used to study liver functions (4): A) Bile formation and bile excretion B) Urea-forming + C) Detoxification + D) Barrier + E) Protein-synthetic + 27. Partial liver removal allows studying (1): A) Barrier function of the liver B) Protective function of the liver C) Urea-forming function of the liver D) Regenerative capacity of the liver + E) Liver involvement in metabolism 28. The detoxification function of the liver is studied experimentally by (2): A) Ligation of the hepatic artery B) Creating a direct Eck fistula + C) Angiostomy by E.S. London + D) Ligation of the hepatic vein 29. Types of hepatic coma by pathogenesis (3): A) Hepatocellular coma B) Shunt (portosystemic) coma C) Mixed hepatic coma 30. Missing link in the pathogenesis of shunt hepatic coma: Liver cirrhosis → ? → Development of portocaval and cavocaval anastomoses → Bypassing part of the blood from the liver into the systemic circulation → Intoxication with intestinal toxins and metabolic products. A) Portal hypertension + B) Massive necrosis of the liver parenchyma C) Impaired bile formation 31. Factors involved in the pathogenesis of hepatic coma (4): A) Hypoglycemia + B) Acidosis + C) Auto-intoxication of the body + D) Hyperbilirubinemia + E) Alkalosis 32. Hypokalemia in hepatocellular coma develops due to (2): A) Primary aldosteronism B) Secondary aldosteronism + C) Impaired potassium absorption in the intestine D) Increased potassium excretion by the kidneys + E) Decreased synthesis of parathyroid hormone 33. The development of coma in liver failure is slowed down by dietary restriction of (1): A) Carbohydrates B) Trace elements C) Proteins + D) Fluids E) Salts 34. Direct bilirubin is bilirubin that (3): A) Is conjugated with glucuronic acid + B) Is unconjugated with glucuronic acid C) Is free D) Is bound + E) Gives a direct van den Bergh reaction with Ehrlich's diazo reagent + F) Gives an indirect van den Bergh reaction with Ehrlich's diazo reagent 35. Indirect bilirubin is bilirubin that (3): A) Is conjugated with glucuronic acid B) Is unconjugated with glucuronic acid + C) Is free + D) Is bound E) Gives a direct van den Bergh reaction with Ehrlich's diazo reagent F) Gives an indirect van den Bergh reaction with Ehrlich's diazo reagent + 36. Direct bilirubin (2): A) Is water-soluble + B) Is water-insoluble C) Is toxic D) Is non-toxic + 37. Indirect bilirubin (3): A) Is water-soluble B) Is water-insoluble + C) Is toxic + D) Is non-toxic E) Is absent in normal urine + F) Is excreted in urine 38. Bile formation function of the liver increases with (4): A) Stimulation of the vagus nerve + B) Excess secretion of secretin, cholecystokinin, gastrin + C) Consumption of fatty foods + D) Consumption of egg yolk + E) Activation of the sympathetic nervous system 39. Bile formation function of the liver decreases with (4): A) Inhibition of the vagus nerve + B) Liver cirrhosis + C) Hepatitis + D) Hypoxia + E) Excess secretion of secretin and gastrin 40. The bile excretory function of the liver is impaired in (4): A) Biliary dyskinesia + B) Insufficient secretion of secretin, cholecystokinin, motilin + C) Obstruction of bile ducts by stones or helminths + D) Compression of bile ducts by a tumor + E) Impaired conversion of unconjugated bilirubin to conjugated bilirubin 41. Hyperbilirubinemia corresponds to a total bilirubin level in the blood (1): A) 1–3 μmol/L B) 4–5 μmol/L C) 5–6 μmol/L D) 8–20 μmol/L E) 20–30 μmol/L + 42. Causes of prehepatic jaundice (4): A) Exposure to hemolytic toxins + B) Rh incompatibility between mother and fetus + C) Transfusion of incompatible blood + D) Erythroenzymopathies + E) Biliary dyskinesia 43. Hemolytic jaundice is observed in (3): A) Viral hepatitis B) Toxic hepatitis C) Sepsis + D) Poisoning with hemolytic toxins + E) Malaria + 44. The key link in the pathogenesis of prehepatic jaundice (1): A) Dehydration of the body B) Heart failure C) Insulin deficiency D) Impaired bile flow E) Increased hemolysis of erythrocytes + 45. Hemolytic jaundice is characterized by (2): A) Increased unconjugated bilirubin in the blood + B) Increased conjugated bilirubin in the blood C) Discoloration of stool D) Impaired digestion in the intestine E) Urobilinuria + 46. Stool color in hemolytic jaundice (1): A) Unchanged B) Intensely colored + C) Discolored D) Black 47. Hemolytic jaundice is associated with (4): A) Intensely colored stool + B) Dark urine due to increased stercobilin and urobilin + C) Impaired central nervous system function + D) Lemon-yellow skin and mucous membranes + E) Cholemia and acholia 48. In hemolytic jaundice (2): A) Increased conjugated bilirubin in the blood B) Increased unconjugated bilirubin in the blood + C) Hypercholic stool + D) Increased both conjugated and unconjugated bilirubin in the blood E) Acholia 49. Yellow coloration of the skin and mucous membranes in hemolytic jaundice is caused by (1): A) Excess conjugated bilirubin in the blood B) Excess unconjugated bilirubin in the blood + C) Presence of bile acids in the blood D) Increased cholesterol in the blood 50. Prehepatic jaundice is characterized by (3): A) Increased unconjugated bilirubin in the blood + B) Increased conjugated bilirubin in the blood C) Bilirubinuria D) Increased stercobilin in urine + E) Increased hemolysis of erythrocytes + 51. The dark color of urine in a patient with suprahepatic jaundice is caused by (2): A) Conjugated bilirubin B) Unconjugated bilirubin C) Urobilin + D) Stercobilin + 52. Parenchymal jaundice is observed in (3): A) Viral hepatitis + B) Toxic hepatitis + C) Sepsis + D) Poisoning with hemolytic toxins E) Malaria 53. Hepatotropic toxins include (4): A) Alcohol + B) Carbon tetrachloride + C) Phosphorus compounds + D) Arsenic preparations + E) Glucuronic acid 54. The leading link in the pathogenesis of hepatic jaundice (1): A) Enhanced hemolysis of erythrocytes B) Impaired bile outflow C) Damage to hepatocytes + 55. Parenchymal jaundice is characterized by (4): A) Urobilinogenemia + B) Increased AST and ALT activity in the blood + C) Cholemia + D) Hyperglycemia E) Hypocholia + 56. Stool color in hepatic jaundice (1): A) Normal B) Dark C) Light + 57. Clinically expressed parenchymal jaundice is characterized by (4): A) Increased direct bilirubin in the blood + B) Increased indirect bilirubin in the blood + C) Presence of direct bilirubin in urine + D) Increased stercobilin in stool and urine E) Cholemia + 58. In parenchymal jaundice (3): A) Only direct bilirubin increases in the blood B) Hemorrhages are possible + C) Hypercholic stool D) Dark, foamy urine + E) Both direct and indirect bilirubin increase in the blood + 59. Cholemia is characterized by (4): A) Lowered blood pressure + B) Skin itching + C) Bradycardia + D) Tachycardia E) Hyperbilirubinemia + 60. Cholemia is accompanied by (3): A) Arterial hypertension B) Arterial hypotension + C) Hyporeflexia + D) Tachycardia E) Skin itching + 61. Symptoms of cholemia are caused by the pathogenic action of (1): A) Cholesterol B) Indirect bilirubin C) Fatty acids D) Bile acids + 62. The mechanism of bradycardia in cholemia is due to (2): A) Activation of parasympathetic effects on the heart + B) Blockade of impulse conduction through the cardiac conduction system C) Direct action of bile acids on the sinoatrial node + D) Activation of the re-entry mechanism in the sinoatrial node 63. The leading link in the pathogenesis of subhepatic jaundice is (1): A) Damage to hepatocytes B) Sialolithiasis C) Urolithiasis D) Enhanced hemolysis of erythrocytes E) Impaired bile outflow + 64. Obstructive jaundice is characterized by (5): A) Hyperbilirubinemia + B) Acholia + C) Cholemia + D) Bilirubinuria + E) Steatorrhea + F) Urobilinogenuria 65. In obstructive jaundice (4): A) Direct bilirubin increases in the blood + B) Direct bilirubin appears in urine + C) Urobilinogen appears in urine D) Urobilinogen is absent in urine + E) Stool is discolored + 66. Acholia is accompanied by (4): A) Impaired fat emulsification in the intestine + B) Impaired absorption of fat-soluble vitamins + C) Impaired fat digestion and absorption + D) Steatorrhea + E) Dark stool color 67. Acholia is characterized by (3): A) Increased absorption of vitamin K B) Decreased blood clotting + C) Increased blood clotting D) Increased putrefaction and fermentation in the intestine + E) Flatulence + 68. As a result of bile flow cessation into the intestine (3): A) Intestinal motility weakens + B) Absorption of vitamins A, D, E, K decreases + C) Absorption of B-group vitamins and vitamin C decreases D) Enhanced parietal fat breakdown E) Enhanced protein putrefaction in the intestine + 69. Steatorrhea in obstructive jaundice is caused by (1): A) Impaired fat absorption in the intestine + B) Activation of pancreatic lipase C) Inherited enzymopathy D) Activation of gluconeogenesis 70. Bleeding in obstructive jaundice is caused by (2): A) Deficiency of von Willebrand factor B) Thrombocytopenia C) Excess anticoagulants D) Impaired synthesis of prothrombin complex factors + E) Impaired absorption of vitamin K in the intestine + 71. In obstructive jaundice (2): A) Tachycardia B) Bradycardia + C) Increased blood pressure D) Decreased blood pressure + 72. In obstructive jaundice (2): A) Hypervitaminosis of vitamin K B) Hypovitaminosis of vitamin A + C) Hypervitaminosis of vitamin E D) Hypovitaminosis of vitamin K + E) Hypovitaminosis of vitamin C 73. The dark color of urine in subhepatic jaundice is caused by (1): A) Conjugated bilirubin + B) Unconjugated bilirubin C) Urobilin D) Stercobilin 74. Indirect bilirubin increases in the blood in (3): A) Hemolytic anemia + B) Impaired uptake of bilirubin by hepatocytes + C) Hepatocyte damage + D) Impaired bile outflow E) Biliary dyskinesia 75. Direct bilirubin increases in the blood in (3): A) Hemolytic anemia B) Impaired uptake of bilirubin by hepatocytes C) Hepatocyte damage + D) Impaired bile outflow + E) Impaired bilirubin excretion from hepatocytes into bile ducts + 76. The appearance of indirect bilirubin in urine is observed in (1): A) Hemolytic jaundice B) Parenchymal jaundice C) Obstructive jaundice D) Not observed in any type of jaundice + E) Observed in all types of jaundice 77. An increase in ALT levels in the blood is most characteristic of (1): A) Enzymopathic jaundice B) Any type of jaundice C) Hepatocellular jaundice + D) Hemolytic jaundice 78. Cholemia is characteristic of (2): A) Hemolytic jaundice B) Parenchymal jaundice + C) Obstructive jaundice + 79. The development of hypotension in liver failure is influenced by (2): A) Reduced synthesis of angiotensinogen by the liver + B) Increased synthesis of angiotensinogen by the liver C) Decreased tone of the parasympathetic nervous system D) Reduced production of ferritin by the liver E) Cholemia + 80. Causes of hepatitis include (4): A) Viruses + B) Alcohol + C) Carbon tetrachloride + D) Excessive carbohydrate intake E) Medications + 81. Hepatitis leads to the development of (4): A) Asthenovegetative syndrome + B) Obesity C) Hemorrhagic syndrome + D) Hepatomegaly + E) Dyspeptic syndrome + 82. Portal hypertension can arise due to (2): A) Left ventricular heart failure B) Right ventricular heart failure + C) Blood loss D) Liver cirrhosis + E) Hypovolemia 83. Ascites in liver cirrhosis is caused by (3): A) Hypoalbuminemia + B) Hyperalbuminemia C) Secondary hyperaldosteronism + D) Hypovitaminosis of A, D, E, K E) Portal hypertension + 84. In liver cirrhosis, the following occur (4): A) Activation of glycogenesis B) Activation of fibrogenesis + C) Proliferation of undamaged cells + D) Impaired microcirculation in the liver + E) Hypoxia of liver cells + 85. Cirrhosis leads to the development of (3): A) Portal hypertension + B) Right ventricular heart failure C) Pulmonary edema D) Encephalopathy + E) Ascites + 86. The pathogenesis of ascites involves (4): A) Hypoalbuminemia + B) Hyperalbuminemia C) Increased hydrostatic pressure in the portal vein system + D) Obstruction of lymphatic outflow + E) Increased aldosterone levels + 87. Dyscholia is (1): A) Acholia B) Hypocholia C) Hypercholia D) A change in bile composition making it lithogenic + 88. The pathogenesis of gallstone disease involves (4): A) Inflammation of the bile ducts + B) Bile stasis + C) Infection + D) Decrease in the cholate/cholesterol ratio, leading to a reduction in bile acids and an increase in cholesterol in bile + E) Increase in the cholate/cholesterol ratio, leading to a rise in bile acids and a reduction in cholesterol 89. Clinical symptoms of cholestasis include (4): A) Skin itching + B) Discolored stool + C) Dark stool D) Dark brown urine + E) Normal urine color F) Increased blood alkaline phosphatase activity + 90. Causes leading to gallstone formation (3): A) Dysbacteriosis + B) Reduced bile acid production in the liver + C) Increased bile acid absorption by the inflamed gallbladder wall + D) Decreased cholesterol in bile E) Reduced dietary cholesterol intake 91. Increase cholesterol solubility in bile (2): A) Bile acids + B) Gastrin C) Insulin D) Lecithin + E) Hydrochloric acid 92. Contribute to the formation of gallstones (4): A) Inflammation of the bile ducts + B) Bile stasis + C) Shift of bile reaction to the acidic side + D) Shift of bile reaction to the alkaline side E) Decrease in the cholate-cholesterol ratio + 93. Obstruction of bile ducts by a stone leads to (1): A) Parenchymal jaundice B) Obstructive jaundice + C) Hemolytic jaundice PATHOPHYSIOLOGY OF THE KIDNEYS (Daniyor) 1. Pre-renal causes of impaired kidney function include (4): A) Prostate adenoma B) Systemic circulation disorders + C) Neuro-psychological disorders + D) Hyperparathyroidism + E) Primary aldosteronism + 2. Renal causes of impaired kidney function include (3): A) Heavy metal salts + B) Hemolytic streptococcus + C) Systemic circulation disorders D) Autoimmune processes + E) Hypertension 3. Post-renal causes of impaired kidney function include (2): A) Shock B) Ureteral obstruction by a stone + C) Glomerulonephritis D) Cadmium poisoning E) Urethral stricture + 4. Impaired glomerular function is accompanied by (1): A) Decreased filtration + B) Disturbance in hydrogen ion excretion C) Disturbance in kidney concentration ability D) Disturbance in

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