Pathophysiology

1. General Nosology (38)

1. What is the general aetiology ?

2. What factor serves as the endogene cause of disease?
3. What are the necessary conditions for diseases's appearance?
4. Which efect exert the favorable conditions for organism ?
5. Which efect exert the unfavorable conditions for organism ?
6. What are the endogenous conditions which influence diseases's appearance?
7. What is general pathogenesis?
8. What is the causes'diseases in the diseases's appearance?
9. What is the conditions's role in the diseases's appearance?
10. What is the cause's role in the disease's evolution?
11. What is the injury?
12. What is possible variant of acombination of general and local lessions in the disease?
13. What is pathogenetic factor?
14. What is the chain of causes-effects in the disease's pathogenesis ?
15. What is the main link of pathogenesis?
16. What is the aetiotropic therapy of disease?
17. What is the pathogenetic therapy of disease?
18. What is the symptomatic therapy of disease?
19. What is the specific prophylaxis of disease?
20. What is the unspecific prophylaxis of disease?
21. What is the charactheristic of organism's physiological reaction ?
22. What is the charactheristic of organism's pathological reaction ?
23. What is the adaptative reaction?
24. What is the compensatory reaction ?
25. What is the protective reaction ?
26. What is the reparative reaction ?
27. What is the first period of the disease?
28. What is the second period of the disease?
29. What is the third period of the disease?
30. What is the fourth period of the disease?
31. What is characteristic for latent period of the disease ?
32. What is characteristic for prodromal period of the disease ?
33. What is characteristic for comlet manifestations period of the disease?
34. What is characteristic for resolution period of the disease?
35. What is pathological process ?
36. What are the primary sanogenetic mechanisms ?
37. What are the secondary sanogenetic mechanisms?
38. What is the characteristic of vicious circle in pathogenesis?

2. Cell injuries (38)

1. What is the primary cellular injury ?
2. What is the secondary cellular injury?
3. What are the manifestations of nonspecific cellular injuries?
4. How changes enzyme spectrum of blood in liver cells injuries?
5. How changes enzyme spectrum of blood in pancreatic cells injuries?
6. How changes enzyme spectrum of blood in myocardial cells injuries?
7. How changes enzyme spectrum of blood in biliary ducts epithelial injuries?
8. What is the mechanical injury effect of cytoplasmic membrane ?
9. What is electric current effect on excitable cells?
10. What is the effect of continuously electric current on cells ?
11. Which one endogenous enzyme can cause lesions of cytoplasmic membrane ?
12. What is the direct action effect of high temperature on cell?
13. What is the direct action effect of low temperature on cell?
14. Which one extracellular dyshomeostasis causes cellular injuries?
15. What is the normal ratio of intracellular and extracellular K ions concentration?
16. What is the balancing effect of intracellular and extracellular K ions concentration?
17. What is the normal ratio of intracellular and extracellular sodium ions concentration?
18. What is the balancing effect of intracellular and extracellular potassium ions
concentration?
19. Which one process can cause decreased electrical resistance of cytoplasmic membrane?
20. Which one process can cause decreased electrical resistance of cytoplasmic membrane?
21. What is the normal ratio of Ca ions concentration in hyaloplasma and endoplasmic
reticulum ?
22. What intracellular enzymes are activated to increase hyaloplasma Ca concentration?
23. What is the nonspecific activation effect of intracellular ATP-ase ?
24. What is the nonspecific activation effect of cellular endonucleases ?
25. What is the nonspecific activation effect of cellular phospholipases ?
26. What is the nonspecific activation effect of cellular proteases ?
27. Which one reason causes cellular acidosis ?
28. Which is the consequence of decompensated cellular acidosis?
29. Which factor may decouple oxidation and phosphorylation processes in mitochondria?
30. Which is the decoupling effect of oxidation and phosphorylation processes?
31. Which is the consequence of cellular energy depletion ?
32. Which is the consequence of lysosomal membrane destabilization ?
33. Which is the destabilizing factor of lysosomal membranes ?
34. Which is the stabilizing factor of lysosomal membranes ?
35. What process leads to the generation of free radicals?
36. What substance refers to free radicals ?
37. What substance is part of endogenous antioxidant system?
38. What is the effect of free radicals action ?

3. Cellular pathological processes (17)

1. What is the general cause of cellular dystrophy?

2. Which intracellular pathological process causes dystrophy?
3. What are the specific manifestations of dystrophy?
4. What are the causes of parenchymal dyslipidoses ?
5. What are the consequences of cellular dystrophies ?
6. Which cells undergo apoptosis ?
7. What are the apoptosis's manifestations of initiation period ?
8. Which condition is necessary for development of apoptosis?
9. Which condition is necessary for final development of apoptosis?
10. What are the manifestations for medial period of apoptosis?
11. What is the final event of apoptosis ?
12. What is the necrosis ?
13. What is the necrosis main pathogenetic link of cytoplasmic membranes injuries ?
14. What is the necrosis main pathogenetic link of mitochondria injuries?
15. What is the necrosis main pathogenetic link due free radicals action ?
16. What are the necrosis consequences ?
17. What are the general consequences of necrosis?
 4.Tissue pathological processes (15)

1. What regenerative processes are possible at the molecular level?

2. What regenerative processes are possible at the organelles level?
3. What is pathological regeneration?
4. What is hyperplasia?
5. What is hypertrophy ?
6. What is the atrophy of organ ?
7. Which atrophy is physiological ?
8. Which atrophy is pathological ?
9. What is organ sclerosis?
10. Which factors cause sclerosis ?
11. What is the sclerosis pathogenesis ?
12. What are the reduction mechanisms for excess collagen in organ?
13. What pathological processes lead to progressive sclerosis ?
14. What are the sclerosis consequences ?
15. What are the principles of sclerosis pathogenetic correction?

5. Organs pathological processes (42)

1. What are the cellular sources of inflammatory mediators ?

2. What are the effects of mast cell tryptase in inflammation?
3. Which chymiotactic factors are released by mast cells?
4. What are the required enzymes for prostaglandins synthesis ?
5. What are the required enzymes for leukotrienes synthesis ?
6. What are the biological effects of prostaglandins in inflammatory site?
7. What are the biological effects of thromboxane into inflammatory site?
8. What are the biological effects of prostacyclin into inflammatory site ?
9. What are the biological effects of leucotrienes into inflammatory site ?
10. What are the general effects of interleukin IL-1?
11. What effects has interleukin (IL-1) into inflammatory site ?
12. Which cell-derived mediators originated from neutrophils leukocytes?
13. What oxygen –depending bactericidal factors are generated by neutrophils leukocytes ?
14. What bacteriostatic factors are generated by neutrophils leukocytes ?
15. Which cell-derived mediators originated from eosinophils ?
16. Which cell-derived mediators originated from platelets?
17. Which cell-derived mediators originated from lymphocytes ?
18. Which active biologic factors are formed from complement activation?
19. What are C3a and C5a effects into inflammatory site ?
20. What are the effects of activated Hageman contact factor?
21. What are the effects of kinines into inflammatory site ?
22. What is the sequence of vascular reactions into inflammatory site?
23. What mediators cause inflammatory arterial hyperemia?
24. What are the peculiarities of inflammatory arterial hyperemia ?
25. What is the pathogenesis of increase in vascular permeability in inflammation?
26. What is the pathogenesis of inflammatory venous hyperemia?
27. What is the biological importance of venous hyperemia and inflammatory stasis?
28. What is exudates pathogenesis into inflammatory focus?
29. What is the hallmark of serous exudates?
30. What is the hallmark of fibrinous exudates ?
31. What is the hallmark of purulent exudates?
32. What is the hallmark of hemorragic exudates?
33. What are the leukocyte emigration mechanisms into inflammatory focus?
34. What is the biological important of neutrophils leukocyte migration into inflammatory
focus?
35. What is the biological important of eosinophils leukocyte migration into inflammatory
focus?
36. What is the biological important of monocytes leukocyte migration into inflammatory
focus?
37. What are the sources of cell proliferation into inflammatory focus?
38. What processes include physiological regeneration into inflammatory focus?
39. What is the biological important of proliferation into inflammatory focus?
40. What processes include physiological regeneration into inflammatory focus?
41. What are the organism general manifestations into inflammatory focus?
42. Which hormone has anti-inflammatory direct action?

6. Fever. Stress (26)

1. What are the infectious exogenous pyrogenic factors?
2. What are the non-infectious exogenous pyrogenic factors?
3. Which are the primary endogenous pyrogenic factors?
4. Which are the secondary endogenous pyrogenic factors?
5. What is the ratio of thermo genesis and thermo lysis during I period of fever?
6. What are the activated mechanisms of thermo genesis in fever?
7. What are the mechanisms that ensure increased thermo genesis in fever?
8. What are the mechanisms of reduced thermo lysis in I period of fever ?
9. What body's temperature remains in low grade fever ?
10. What body's temperature remains in hyper pyretic reactions?
11. What temperature in fever is hazardous for the body?
12. How changes endocrine glands secretion during state period of fever?
13. How changes the function of cardio-vascular system in second period of fever?
14. How changes the function of cardio-vascular system in third period of fever?
15. How changes the function of digestive system in fever?
16. What are the beneficial effects of fever?
17. What is the stress?
18. What is the SNC reaction in shock phase of stress ?
19. What is cardiovascular system reaction in shock phase of stress?
20. What is the metabolic reaction in shock phase of stress ?
21. What is the SNC reaction in anti- shock phase of stress?
22. What is endocrine system reaction in anti- shock phase of stress?
23. What is endocrine system reaction in stress resistance stage ?
24. How changes blood biochemical properties in stress resistance stage ?
25. What are the manifestations of exhaustion stage of stress?
26. Which complications are possible in exhaustion stage of stress?

7. Allergy (37)

1. What immunological processes underlying immediate- type allergic reactions?

2. What immunological processes underlying delayed- type allergic reactions?
3. What is characteristic for type I (anaphylactic) allergic reactions ?
4. What is characteristic for type II (antibody-mediated) allergic reactions ?
5. What is characteristic for type III (Arthus) allergic reactions?
6. What is characteristic for type IV (delayed) allergic reactions?
7. What is characteristic for type V (stimulatory) allergic reactions?
8. How lasts the latent period of anaphylactic reaction after first contact with allergen?
9. How much time maintains anaphylaxis situation in active sensibility?
10. Which antigens cause anaphylactic allergic reactions?
11. Which cell makes anaphylactic allergic reactions?
12. What immunoglobulins participate in anaphylactic allergic reactions?
13. Where are localized IgE in anaphylactic allergic reactions?
14. What mediators are stored into mast cells ?
15. What mediators are synthesized in mast cells through cyclooxygenase pathway?
16. What mediators are synthesized in mast cells through lipoxygenase pathway?
17. What are the path physiological local processes in anaphylactic allergic reactions?
18. What path physiological processes involve in lungs during anaphylactic allergic
reactions?
19. What path physiological processes involve in cardiovascular system in anaphylactic
allergic reactions?
20. What path physiological processes involve in digestive system in anaphylactic allergic
reactions?
21. How much time lasts hypo-sensibility period after anaphylactic shock?
22. What antigens participate in type II (antibody-mediated) allergic reactions ?
23. Which is cell destruction mechanism in type II (antibody-mediated) allergic reactions ?
24. What are the clinical manifestations of type II (antibody-mediated) allergic reactions?
25. What antigens initiate type III, immune complex-mediated disorders?
26. What conditions occur type III, immune complex-mediated disorders, in?
27. What are the mediators of type III, immune complex-mediated disorders ?
28. What structures are afected in type III, immune complex-mediated disorders ?
29. What cells are frequently included in type V, antibody-mediated cellular dysfunction?
30. What are the mediators of pathochemical fase in type IV, cell-mediated hypersensitivity
disorders ?
31. What are the finaly manifestations of type IV, cell-mediated hypersensitivity disorders ?
32. What is non-specific hyper sensibility?
33. What processes include the non-specific hyper sensibility?
34. What is the cause of autoimmune reactions ?
35. What is the consequince of antibodies directed against thyroid-stimulating hormone?
36. What is the consequince of antibodies directed against intrinsec anti-anaemic factor?
37. What are the consequences of antibodies directed against acetylcholine receptors?

8. Microcirculation (26)
1. What is the main pathogenetic link of arterial hyperemia?
2. What is the correlation between inflow and outflow in arterial hyperemia?
3. What is the pathogenetic mechanism of neurotonic arterial hyperemia?
4. What is the pathogenetic mechanism of neuro paralytic arterial hyperemia?
5. What is the pathogenetic mechanism of neuro-myo- paralytic arterial hyperemia?
6. What is the pathogenetic mechanism of functional arterial hyperemia?
7. What are the manifestations of arterial hyperemia?
8. What is venous hyperemia?
9. What are the causes of venous hyperemia?
10. What is the main pathogenetic link of venous hyperemia?
11. What are the external manifestations of venous hyperemia?
12. What is the cause of enlargement organ volume in venous hyperemia?
13. What is the cause of shrinking due to local temperature in venous hyperemia?
14. What are the consequences of venous hyperemia?
15. What are the local pathogenetic mechanisms of ischemia?
16. How changes local hemodynamic in ischemia?
17. How changes cellular metabolism in ischemia?
18. What are the external external manifestations of ischemia?
19. Which organs the collaterals are absolutely functionally insufficiency in ?
20. Which emboli is endogenous?
21. Which emboli is exogenous ?
22. The trauma of which vessels cause air emboli?
23. Which states occur gas emboli in?
24. What vessels are obturated with amniotic liquid in emboli state?
25. What are the consequences of artery emboli?
26. What factors damaged the rheological properties of the blood ?

10. Physiopathology of metabolisms (57)

1. What product is formed by bacterial fermentation of carbohydrates in the digestive tract?

2. What condition favor bacterial fermentation of carbohydrates in the stomach?
3. What are the consequences of bacterial fermentation of carbohydrates in the stomach?
4. What are the causes of saccharides maldigestion?
5. In which cases is increasing bacterial fermentation of carbohydrates in the large intestine?
6. What are the consequences cellulose deficiency in the diet?
7. What are the causes of monosaccharides malabsorption in the small intestine?
8. How is changing the nutrient content of the liver in carbohydrate starvation?
9. How is changing the nutrient content of the blood in carbohydrate starvation?
10. What are compensatory reactions for maintaining normal blood glucose in long-term
starvation?
11. How to change the endocrine glands function in carbohydrate starvation?
12. From what sources is kept blood sugar level compatible with lifelong starvation?
13. What are the sources of endogenous glucose in long lasting carbohydrate starvation?
14. What are the mechanisms of protein usage for gluconeogenesis in starvation?
15. Proteins of which organs are subjected to carbohydrate catabolism in starvation?
16. What are the possible consequences of increasing gluconeogenesis from endogenous
proteins?
17. What are endocrine responses to excessive consumption of carbohydrates?
18. What are the homeostatic responses in hyperglycemia?
19. What are the mechanisms of glycosuria at excessive consumption of carbohydrates?
20. What are the causes of hypoglycemia?
21. What are the compensatory responses in hypoglycemia?
22. What are the possible consequences of hypoglycemia?
23. How to change lipidemia in hypoglycemia?
24. How to change the content of lipids and glycogen in the liver during hypoglycemia?
25. What kind of liver dystrophy is possible in prolonged hypoglycemia?
26. What are the possible consequences of alimentary hyperglycemia?
27. What are the possible consequences of diabetic hyperglycemia?
28. What are the possible causes of galactosemia?
29. What are the possible causes of galactosemia in newborns?
30. How to change the composition of blood in fatty food consumption?
31. What are the metabolic consequences of excessive consumption of fat?
32. What are the consequences of lipid starvation?
33. What causes of lipid’s maldigestion?
34. What consequences of lipid’s maldigestion?
35. How changes the blood lipid fractions in maldigestion of lipids?
36. To what lipoproteins are transported the lipids absorbed from the small intestine?
37. To what lipoproteins are transported the lipids synthesized in liver?
38. In what form are transported the lipids mobilized from adipose tissue?
39. In what form is transported cholesterol to organs?
40. In which form cholesterol is transported from the organs to the liver?
41. What are the causes of retention hyperlipidemia?
42. What are the consequences of alimentary hyperlipidemia?
43. What are the consequences of native alimentary protein absorption from GUT?
44. How to change the protein spectrum of blood in liver failure?
45. What disturbances of GUT functions could lead to protein maldigestion?
46. How to change the protein metabolism in protein maldigestion?
47. How to modify the digestive processes in the large intestine in protein maldigestion?
48. What pathological processes are accompanied by hypoproteinemia?
49. To what leads hypoproteinemia?
50. In what pathological processes hyperproteinemia is installed?
51. What substances are excessively formed by increase catabolism of nucleoproteins?
52. In which cases is found negative nitrogen balance?
53. In which cases is found positive nitrogen balance?
54. To what leads excessive protein food consumption?
55. What substances are formed in intestine from protein putrefaction?
56. What toxic substances cause intestinal autointoxication?
57. What pathological processes provoke intestinal autointoxication?

11. Electrolytic imbalances (26)

1. What is hypernatremia?
2. In what pathological processes meets hypernatremia?
3. What are the causes of absolute hypernatremia?
4. What are the causes of relative hypernatremia?
5. What are the compensatory mechanisms of absolute hypernatremia?
6. What are the final consequences of hypernatremia for the cells?
7. How to modify the electrolyte concentration in primary aldosteronism?
8. What are the pathogenesis of edema in primary hyperaldosteronism?
9. In what pathological processes meets secondary hyperaldosteronism?
10. At which concentration of Na begins hyponatremia?
11. What are the causes of absolute hyponatremia?
12. What are the causes of relative hyponatremia?
13. What hormones are involved in maintaining of potassium homeostasis in the body?
14. What minimum value of potassium indicates hyperkalemia?
15. What pathological processes are associated by absolute hyperkalemia?
16. How to modify the cardiovascular functions hyperkalemia?
17. Which minimum value of potassium concentration shows hypokalemia?
18. What are the pathogenetic mechanisms of hypokalemia in chronic liver disease?
19. By what mechanisms parathyroid hormone regulates calcium homeostasis?
20. By what mechanisms thyreocalcitonin regulates calcium homeostasis?
21. Ce complcaţii grave provoacă hipocalcemia la copii?
22. What are the causes of secondary hypercalcemia?
23. What are the pathogenetic mechanisms of hypercalcemia?
24. What are the causes of hypocalcemia?
25. What are the pathogenetic mechanisms of hypocalcemia?
26. What are the mechanisms of hypocalcemia in lack of bile in intestine?
12.Physiopathology of acid-base imbalance. Hypoxia (40)
1. Which endogenous substances could lead to acidosis?
2. What is the criterion of acidosis?
3. What is the criterion of alkalosis?
4. What is compensated acidosis?
5. What is decompensated alkalosis?
6. In what process respiratory acidosis occurs?
7. In what process respiratory alkalosis occurs?
8. In what process excretory acidosis occurs?
9. What are the pathogenetic factors of excretory acidosis?
10. What are the pathogenetic factors of metabolic acidosis?
11. What are the pathogenetic factors of alkalosis?
12. What are the renal compensatory reactions in acidosis?
13. What are the respiratory compensatory reactions in acidosis?
14. What is the consequence of acidosis?
15. What are the compensatory reactions in alkalosis?
16. What is hypoxia?
17. What is hypoxemia?
18. What determines the vulnerability of different organs to hypoxia?
19. What is the vulnerability of different organs to hypoxia (in decreasing order)?
20. What type of hypoxia develops in Alpine disease?
21. What type of hypoxia develops in disorders of intracellular processes of oxygen usage?
22. What is the pathogenesis of hemic hypoxia in nitrites poisoning?
23. What is the pathogenesis of hemic hypoxia in hemoglobinopathies?
24. What is the pathogenesis of hemic hypoxia in hemorrhage?
25. What is the pathogenesis of hemic hypoxia carbon monoxide?
26. In what cases is developing histotoxic hypoxia?
27. In what states oxyhemoglobin dissociation curve deviates to the right?
28. In what states oxyhemoglobin dissociation curve deviates to the left?
29. How does is manifested brain hypoxia?
30. What pathological processes develop in the brain by decreasing of partial pressure of O2
in arterial blood below 20 mmHg?
31. What is hyperoxia?
32. Under what conditions increase the rate of O2 dissolved in blood?
33. In what processes is developed hyperdynamic hyperoxia?
34. By which is characterized hyperdynamic hypoxia?
35. What is dysmetabolic hyperoxia?
36. What is the oxygen pressure applied for therapeutic purposes?
37. In what diseases is contraindicated therapeutic application of oxygen?
38. What are the harmful effects of hyperoxia?
39. What are the mechanisms of CO2 accumulation in hyperoxia?
40. How to modify the acid-base balance in hyperoxia?

14. Shock. Terminal states (34)

1. What is the main pathogenetic link of shock of any etiology?

2. How does the activity of CNS change in compensated shock?
3. How does the endocrine activity change in compensated shock?
4. How does the cardiovascular function change in compensated shock?
5. What pathological processes are developed in kidney in compensated shock?
6. How does the activity of RAA system change in compensated shock?
7. How do are modifying the glomerular filtration and reabsorption canallicular in
compensated shock?
8. How does the diuresis change during the compensated shock?
9. What are the pathogenetic factors of shock at the level of tissue?
10. What changes of microcirculation occur in compensated shocks in the kidneys and
abdominal organs?
11. What respiratory disorders occur in late stages of shock?
12. What is the urine output resulting in renal failure in shock?
13. How does the biochemistry of blood changes in shock associated with renal failure?
14. What is the main pathogenetic link of hepatic failure in shock?
15. What biochemical changes of blood occurs during shock associated with hepatic failure?
16. What are the manifestations of blood-intestinal barrier injury in shock?
17. What are the manifestations of pancreatic injury in shock?
18. What is the main pathogenetic link of myocardial injury in shock?
19. What are the manifestations of myocardial injury in shock?
20. What amount of glucose is incompatible with the normal activity of the brain?
21. What amount of oxygen is incompatible with the normal activity of the brain?
22. What value of blood plasma osmolality is incompatible with the normal activity of the
brain?
23. What value of body temperature is incompatible with the normal activity of the brain?
24. What electrolyte imbalance can lead to cardiac arrest?
25. What is the sequence of terminal states?
26. What is the minimum cerebral perfusion enough for cardio-pulmonary resuscitation?
27. Disruption of which nervous structure can lead to agony?
28. What is the clinical sign which characterizes agony?
29. What are the signs of clinical death?
30. What factors determine the duration of clinical death?
31. How much longer after clinical death appear the first functional disorders of cortical
neurons?
32. How much longer since the establishment of anoxia appears the cortical neurons
necrosis?
33. How much time the subcortical structures resist to anoxia?
34. What is the mechanism of clinical death extending in hypothermia?

Central nervous system (45)

1. What is the measure of cell excitability?

2. What is the threshold of excitation in excitable cell?
3. How does cell excitability changes by decreasing of resting potential?
4. How does cell excitability changes by increasing of resting potential?
5. What processes enhance the cell excitability ?
6. How does excitable cell resting potential changes at cessation of membrane pumps Na,
K?
7. How does intracellular concentration of electrolytes changes at cessation of membrane
pumps Na, K?
8. How does cessation of membrane pumps Ca2+, Mg2+ act on intracellular Ca2+
homeostasis?
9. What are the mechanisms of action of excitable mediators?
10. What are the mechanisms of action of inhibitory mediators?
11. What are the mechanisms of increasing cell excitability under condition of hypoxia?
12. What are the mechanisms of increasing cell excitability under condition of
hyponutrition?
13. What are the effects of postsynaptic receptor blockade?
14. What are the effects of exhaustion of mediator reserves in nerve endings?
15. What are the effects of norepinephrine reserves exhaustion in postsynaptic sympathetic
nerve endings?
16. What are the effects of dopamine reserves exhaustion in extrapyramidal nerve centers?
17. Injury of which structures lead to spastic paralysis?
18. Injury of which structures lead to flaccid paralysis?
19. What are the characteristics of spastic paralysis?
20. What are the characteristics of flaccid paralysis?
21. What are the characteristics of physiological pain?
22. What are the characteristics of pathological pain?
23. What are the mechanisms of pain in anoxia?
24. What are the mechanisms of pain at spastic contraction of smooth muscles of internal
organs?
25. What are the mechanisms of pain in organ’s inflammation?
26. What is the suprasegmental responce to the pain?
27. What is the cardiovascular responce to the pain?
28. What is the endocrine responce to the pain?
29. What are the functions of antinociceptive system ?
30. What are the effects of autonomic sympathetic system activation on carbohydrate
metabolism?
31. What are the effects of autonomic sympathetic system activation on lipids metabolism?
32. What are the effects of autonomic sympathetic system on the endocrine glands ?
33. What are the effects of autonomic sympathetic system on the cardiovascular system ?
34. What are the effects of autonomic sympathetic system on the endocrine glands ?
35. What are the effects of autonomic sympathetic system on the GUT ?
36. What are the effects of autonomic sympathetic system on the bronchial tree ?
37. What are the sympathetic system effects on the coronary blood vessels ?
38. What are the sympathetic system effects on the blood vessels of the abdominal organs?
39. What are the sympathetic system effects on the external sexual organs?
40. What are the sympathetic system effects on the eye ?
41. What are the sympathetic system effects on the on skin vessels and derivatives? ?
42. What are the effects of autonomic parasympathetic system on the cardiovascular
system ?
43. What are the effects of autonomic parasympathetic system on the GUT ?
44. What are the effects of autonomic parasympathetic system on the bronchial tree ?
45. What are the parasympathetic system effects on the external sexual organs?
46. What are the effects of parasympathetic system on the eye ?

15. Endocrine system (89)

1. What are the causes of pituitary gland impairment?
2. What are causes of ADH hypersecretion?
3. What are the mechanisms of ADH hyposecretion in pituitary pediculus trauma?
4. What are the manifestations of ADH hypersecretion?
5. What are the causes of prolactine hypersecretion?
6. What are the hallmarks of prolactine hypersecretion in women?
7. What are the hallmarks of prolactine hypersecretion in men?
8. What are the mechanisms of lactotrop hormone hypersecretion in trauma of pituitary
foot?
9. What are the causes of STH hypersecretion?
10. What are the causes of STH hyposecretion?
11. How does carbochydrates metabolism changes in STH hypersecretion in children?
12. How does proteins metabolism changes in STH hypersecretion?
13. How does blood biochemistry changes in STH hypersecretion?
14. What are the somatic manifestations of STH hypersecretion in children?
15. What are the somatic manifestations of STH hypersecretion in adults?
16. What are the somatic manifestations of STH hyposecretion in adults?
17. What are the somatic manifestations of STH hyposecretion in children?
18. What are the posible causes of tertiar hypercorticism?
19. What are the posible causes of secondary hypercorticism?
20. What are the posible causes of primary hypercorticism?
21. What are the posible causes of tertiar hypocorticism?
22. What are the posible causes of secondary hypocorticism?
23. What are the posible causes of primary hypocorticism?
24. What are the mechanisms of adrenal hyposecretion by prolonged administration of high
doses of glucocorticosteroids?
25. What are the mechanisms of Leydig cells atrophy by prolonged administration of high
doses of androgens?
26. What are the mechanisms of Sertoli cells atrophy by prolonged administration of high
doses of androgens?
27. What are the mechanisms of testosterone hyposecretion by prolonged administration of
high doses of androgens?
28. What are the manifestation of glucocortiocoids hypersecretion?
29. What are the metabolic effects of glucocorticoids?
30. What are the manifestation of glucocortiocoids hypersecretion?
31. What are the manifestation of glucocortiocoids hyposecretion?
32. What are the causes of primary hyperaldosteronism?
33. What are the causes of secondary hyperaldosteronism?
34. How does hyperaldosteronism is manifested?
35. How does hypoaldosteronism is manifested?
36. What is the biological significance of glucocorticoids in stress reaction?
37. What are the metabolic effects of glucocorticoids?
38. What are the metabolic effects of glucocorticoids on the organs?
39. What are the significance of glucocorticoids in prenatal ontogenesis of lungs?
40. What are the significance of glucocorticoids in prenatal ontogenesis of thyroid glands?
41. What are the significance of glucocorticoids in prenatal ontogenesis of GUT?
42. What are the significance of glucocorticoids in prenatal ontogenesis of eyes?
43. What are the role of glucocorticoids hormones in developement of inflammatory
reaction?
44. How do glucocorticoids act on the vascular reactions during inflammation?
45. How do glucocorticoids act on process of exudation in inflammatory reaction?
46. How do glucocorticoids act on process of leucocyte emigration in inflammatory reaction?
47. What is the pathogenesis of tertiar hyperthyroidism?
48. What is the pathogenesis of secondary hyperthyroidism?
49. What is the pathogenesis of primary hyperthyroidism?
50. How does blood hormones concentration change in tertiar hyperthyroidism?
 51. How does blood hormones concentration change in secondary hyperthyroidism?
52. How does blood hormones concentration change in primary hyperthyroidism?
53. What are the causes of tertiar hypothyroidism?
54. What are the causes of secondary hypothyroidism?
55. What are the cause of primary hypothyroidism?
56. How does blood hormones concentration change in secondary hypothyroidism?
57. How does blood hormones concentration change in primary hypothyroidism?
58. How does the energy metabolism change in hypothyroidism?
59. How does the thermoregulation change in hypothyroidism?
60. How does organism with hypothyroidism can adapt to ambient temperature?
61. How does the lipid metabolism change in hypothyroidism?
62. What are the cardiac effects in hypothyroidism?
63. How does urine output change in diabetes mellitus type I?
64. What is the pathogenesis of polyuria in diabetes mellirus type I?
65. What is the cause of hyperstenuria in diabetes mellitus type I?
66. What is the cause of polydypsia in diabetes mellitus type I?
67. What is the cause of increased appetite in DM type I?
68. How does body’s weight changes in DM type I?
69. How do metaboic processes change in DM typeI?
70. How does the skeletal muscles weight change in DM type I?
71. Which cells have Glut insulindependent receptors?
72. What conditions ensure glucose using by neuron in lack of insulun?
73. What cells have insulindependent hexokinase?
74. What is the pathogenesis of hyperglicemia in DM type I?
75. What is the ccause of muscular atrophy in DM type I?
76. What is the cause of erectile dysfunction in men in type I diabetes?
77. What is the cause of coronary failure in type I diabetes?
78. What are the causes of visual impairment in type I diabetes?
79. What is the cause of predisposition to pyrogenic infections in patients with type I
diabetes?
80. What is the cause of phagocytes bactericide activity decreasing in patients with type I
diabetes?
81. What is the cause of slowly wounds regeneration in patients with type I diabetes?
82. How does lipidogramme change in type I diabetes patients?
83. How does acid-base balance change in type I diabetes patients?
84. Storage of which acids develope acidosis in type I diabetes patients?
85. How does proteins metabolism change in type I diabetes patients?
86. What is the pathogenesis of negative nitrogen balance in type I diabetes?
87. What is the mechanism of glucosuria in type I diabetes patients?
88. What is the glucose urine level for glucosuria in type I diabetes patients?
89. What is the mechanism of albuminuria in type I diabetes patients?

16. Physiopathology of the blood (50)

1. What are parameters of normocythemic normovolemia?

2. In what situation can be attested simple hypovolemia?
3. What are parameters of oligocythemic hypovolemia?
4. In what situation can be attested oligocythemic hypovolemia?
5. What are parameters of polycythemic hypovolemia?
6. In what situation can be found polycythemic hypovolemia?
7. What are parameters of oligocythemic hypervolemia?
8. In what states can be found oligocythemic hypervolemia?
9. What are parameters of polycythemic hypervolemia?
10. In what states can be found polycythemic hypervolemia?
11. What are signs that reflect disorders of cell differentiation in erythroblast lineage?
12. What are changes in the myelogram in red marrow hyperproliferation?
13. What are hemogram changes in red marrow hyperproliferation?
14. What are signs of erythrocytes hypochromia?
15. What are signs of erythrocytes hypochromia?
16. What are signs of erythrocytes macrocytosis?
17. What are signs of primary erythrocytosis (erythremia)?
18. In what cases can be found primary erythrocytosis?
19. What are signs of secondary absolute erythrocytosis?
20. In what situation can be found absolute secondary erythrocytosis?
21. What are signs of relative secondary erythrocytosis?
22. In what states can be attested relative secondary erythrocytosis?
23. What processes are disturbed in hypo/aplastic anemia?
24. How hemogram is changed in hypo/aplastic anemia?
25. What is pancytopenia?
26. What processes are disturbed in hemolytic anemias?
27. What are signs of intracellular hemolysis?
28. What are signs of severe intravascular hemolysis?
29. What processes are disturbed in iron deficiency anemia?
30. How the hemogram is changed in iron deficiency anemia?
31. In what anemias is attested microcytosis?
32. What processes are disturbed in B12 deficiency anemia?
33. What are hemogram changes in B12 deficiency anemia?
34. In what anemias is attested megaloblastic erythropoiesis?
35. What are signs of absolute leucocytosis?
36. What are signs of relative leucocytosis?
37. What leucocytosis can be considered physiological?
38. What are causes of neutrophilia?
39. In what diseases is attested neutrophilia?
40. What represents “nuclear left shift”?
41. In what cases is attested hyperregenerative neutrophilia?
42. In what states is attested eosinophilia?
43. In what diseases is found lymphocytosis?
44. In what states is attested monocytosis?
45. What represent agranulocytosis?
46. In what states is attested agranulocytosis?
47. What processes are disturbed in erythroblast leucosis?
48. What are main hematologic signs of myeloid subleukemic leucosis?
49. What are main hematologic signs of myeloid leucocytopenic leucosis?
50. What are main hematologic signs of myeloid aleukemic leucosis?

17. Physiopathology of systemic circulation (42)

1. In what diseases can be attested resistance heart overload?

2. In what diseases can be attested volume heart overload?
3. In what diseases develop dysmetabolic heart failure?
4. What are possible causes of right heart failure?
5. What are possible causes of left heart failure?
6. What are characteristic manifestations of left cardiac failure?
7. What are characteristic manifestations of right cardiac failure?
8. What are emergent cardiac compensatory mechanisms in heart diseases?
9. What are late cardiac compensatory mechanisms in heart disorders?
10. What are emergent extracardiac compensatory mechanisms in heart diseases?
11. What are late extracardiac compensatory mechanisms in heart diseases?
12. How homeometric myocardium hyperfunction is realised?
13. How heterometric myocardium hyperfunction is realised?
14. For what heart vices is characteristic homeometric hyperfunction?
15. For what heart vices is characteristic heterometric hyperfunction?
16. How myocardium structure is changed in case of hypertrophy?
17. What are mechanisms of functional exhaustion and cardiosclerosis in hypertrophied
myocardium?
18. What is the cause of relative hypoxia in hypertrophied myocardium?
19. How systolic output and circulatory blood volume are changed in cardiac failure?
20. What are causes of hypervolemia in chronic cardiac failure?
21. What are consequences of venous stasis in circulatory failure?
22. In what anatomical areas develop venous stasis in case of left ventricular failure?
23. What are consequences of venous stasis in the liver?
24. What are causes of portal hypertension in liver cirrhosis?
25. What are consequences of portal hypertension?
26. In what diseases can develop venous stasis in the liver?
27. In what cases porto-caval anastomoses develop?
28. What are pathogenetic factors of cardiac edemas?
29. What is the role of kidneys hypoperfusion in pathogenesis of edemas?
30. What is pathogeny of secondary hyperaldosteronism in circulatory failure?
31. How metabolism in the myocardium is changed in the first stage of hypertrophy?
32. How arterial pressure and venous pressure are changed in cardiac failure?
33. How systolic output and end-diastolic volume are changed in cardiac failure?
34. By what manifest intracardiac conductibility disorders?
35. For what affection is characteristic sinus bradycardia?
36. For what extrasystole is characteristic complete compensatory pause?
37. By what manifest excitability disorders of the heart?
38. By what manifest disorders of cardiac automatism?
39. What are causes of sinus bradycardia?
40. What is pathogeny of arterial hypertension in some renal disorders?
41. Hyperfunction of what heart compartment happen in hypertensive disease?
42. In what endocrine disorders develop secondary arterial hypertension?

18. PATHOPHYSIOLOGY OF EXTERNAL RESPIRATION(45)

1. What is hyperpnea?
2. What is polypnea?
3. What is bradypnea?
4. What is hyperventilation?
5. What is hypoventilation?
6. What changes in the composition of alveolar air occur in hyperventilation?
7. What changes in the composition of alveolar air occur in hypoventilation?
8. What gaseous changes of arterial blood can be found in hyperventilation?
9. What gaseous changes of arterial blood can be found in hypoventilation?
10. What changes in the acido-base equilibrium can be found in hyperventilation?
11. What changes in the acido-base equilibrium can be found in hypoventilation?
12. What changes of lung ventilatory parameters can be attested in hyperventilation?
13. What changes of lung ventilatory parameters can be attested in hypoventilation?
14. How intrathoracic pressure and venous return to heart are changed in profound and
accelerated respiration?
15. How intrathoracic pressure and venous return to heart are changed in superficial
respiration?
16. What is characteristic for dyspnea?
17. What is inspiratory dyspnea?
18. What is respiratory dyspnea?
19. What physical parameters of alveolar air slow the diffusion through alveolo-capillary
barrier?
20. What conditions diminishes gaseous diffusion through alveolo-capillary barrier?
21. What factors decrease oxygenic capacity of the blood?
22. What hemoglobin compounds reduce oxygenic capacity of the blood?
23. What physicochemical parameters impede association of oxygen with hemoglobin at the
level of pulmonary circulation?
24. What physicochemical parameters impede oxyhemoglobin dissociation at the level of
systemic circulation?
25. What processes lead to extraparenchymatous pulmonary restriction?
26. What is intraparenchymatous pulmonary restriction?
27. What is pulmonary obstruction?
28. What factors can lead to upper airways obstruction?
29. What factors can lead to inferior airways obstruction?
30. In what cases can be found profound and accelerated breathing*
31. In what cases can be attested superficial and frequent breathing?
32. In what cases can be found rare and profound breathing?
33. In what cases can be attested expiratory dyspnea?
34. What biological active substances have bronchoconstrictor effect?
35. What biological active substances have bronchodilator effect?
36. What biological active substances increase pressure in the pulmonary circulation?
37. What biological active substances reduce pressure at the level of pulmonary circulation?
38. What factors induce adult pulmonary distress syndrome?
39. What is the pathogeny of adult acute respiratory distress syndrome?
40. What is pulmonary edema?
41. What factors lead to pulmonary edema?
42. What is pulmonary emphysema?
43. What is the main pathogenetic loop in pulmonary emphysema?
44. What are sources of proteolytic enzymes which damage the pulmonary alveolae?
45. What are characteristics of pulmonary emphysema?

19. PHYSIOPATHOLOGY OF DIGESTIVE SYSTEM AND LIVER(44)

1. What pathological processes disturb digestion in the mouth?
2. What are digestive disorders in case of salivatory amylase lack?
3. What can be causes of pathologic hypersalivation?
4. What are pathologic consequences of sialorrhea?
5. What are causes of pathologic hyposalivation?
6. What exogenous factors induce stomachal hypersecretion?
7. What endogenous factors induce stomachal hypersecretion?
8. How evacuation function of the stomach is affected in hypersecretion and hyperacidity?
9. How intestinal transit is changed in case of stomachal hypersecretion and hyperacidity?
10. What can be causes of achlorhydria?
11. What are consequences of HCl lack in gastric juice?
12. What can be causes of incoercible vomiting?
13. What are causes of exocrine pancreatic secretion insufficiency?
14. What are digestive consequences in pancreatic secretion insufficiency?
15. What represent steatorrhea?
16. What can be causes of steatorrhea?
17. What represent acholia?
18. What factors lead to intestinal maldigestion?
19. What can be consequences of disaccharide maldigestion?
20. What can be consequences of protein maldigestion?
21. What can be consequences of lipid maldigestion?
22. What are causes of intestinal autointoxication?
23. What are manifestations of intestinal autointoxication?
24. How the gastric tonus and motility is changed in hypochlorhydria?
25. How the gastric tonus and motility is changed in hyperchlorhydria?
26. What changes in gastric digestion are attested in hypochlorhydria?
27. What changes in gastric digestion are attested in hyperchlorhydria?
28. What digestive changes can be found in exocrine insufficiency of the pancreas?
29. What digestive changes are attested in bile insufficiency?
30. What digestive changes are found in affections of small intestine mucosa?
31. Absorbtion of what nutritive substances are disturbed in affection of small intestine
mucosa?
32. What processes are disturbed in affections of large intestine mucosa?
33. Absorbtion of what substances is disturbed in affections of large intestine mucosa?
34. How carbohydrate metabolism is changed in hepatic failure?
35. How protein metabolism is changed in hepatic failure?
36. How lipid metabolism is changed in hepatic failure?
37. How blood biochemistry is changed in hepatic failure?
38. How blood biochemistry is changed in cholestasis?
39. What are consequences of bile duct obstruction?
40. What are consequences of hepatic duct obstruction?
41. What processes of bilirubin metabolism are changed in premicrosomial hepatic jaundice?
42. What processes of bilirubin metabolism are changed in microsomial hepatic jaundice?
43. What processes of bilirubin metabolism are changed in postmicrosomial hepatic
jaundice?
44. What processes of bilirubin metabolism are changed in intrahepatic mechanic jaundice?

7. KYDNEYS (28)

1. What is pathogenetic mechanism of glomerular hematuria?

2. In what affections can be found leucocyturia?
3. In what affections can be found lipiduria?
4. What factors decrease water reabsorbtion at the level of proximal renal tubes?
5. What factors decrease water reabsorbtion at the level of distal and collector tubes?
6. What factors decrease proximal reabsorbtion of Na ions?
7. What factors decrease distal reabsorbtion of Na ions?
8. The result of what affection can be tubular proteinuria?
9. What factors decrease glucose reabsorbtion?
10. What disorders lead to aminoaciduria?
11. In what diseases can be found hypostenuria?
12. In what disorders can be found hyperstenuria?
13. In what cases can be found isostenuria?
 14. What disorders involve nephrotic syndrome?
15. What disorders involve nephrotic syndrome?
16. What factors induce proximal canalicular acidosis?
17. What processes induce distal canalicular acidosis?
18. What factors stimulate renin synthesis?
19. What are endocrine functions of the kidneys?
20. What are pre-renal causes of acute renal failure?
21. What are causes of intrinsic acute renal failure?
22. What are causes of post-renal acute renal failure?
23. What are main syndromes in acute renal failure?
24. What are manifestations of urinary syndrome in acute renal failure?
25. What are manifestations of humoral syndrome in acute renal failure?
26. What are manifestations of clinical syndrome in acute renal failure?
27. What are causes of chronic renal failure?
28. What is evolution sequence in acute renal failure?

Pathophysiology examination questions “Practical skills”

Medicine faculty, 2016-2017 year

The questions are formulated according to skills at Pathophysiology and contain the exposed material in:
Didactic films demonstrated at practical lessons
Compendium “Pathophysiology”. Practical lessons
Pathophysiology . Collection of review exercises.

1. Model of alteration in the focus of inflammation. Pathogenesis of primary and secondary

alteration.
2. Model of acute inflammation (Conheim experience). Pathogenesis of vascular reactions into inflammatory
focus.
3. Model of acute inflammation (Conheim experience). Pathogenetic role of inflammatory
mediators.
4. Composition of the following types of inflammatory exudates: serous, fibrinous,
hemorrhagic, purulent. Biological role of exudate. Consequences. Diagnostical
importance.
5. Types of fever patterns. Diagnostic importance.
6. Model of algic shock. Pathogenesis. Neuro-vegetative and metabolic disorders.
7. Model of anaphylactic shock. Aetiology. Pathogenesis. Local and systemic anaphylactic
reactions.
8. Model of arterial hyperemia. Aetiology. Pathogenetic classification. Manifestations.. Consequences.
9. Model of venous hyperemia. Pathological processes with venous hyperemia. Pathogenesis. Functional and
metabolic manifestations.
10. Model of ischemia. Aetiology. Pathogenesis. Manifestations. Consequences.
11. Model of lipid embolism. Pathological processes with lipid embolism. Pathogenesis. Manifestations.
Consequences.
12. Model of white thrombus. Causes. Pathogenesis. Consequences.
13. Model of red thrombus. Causes. Pathogenesis.Consequences.
14. Model of hyperthyroidism. Aetiology. Pathogenesis. Functional and metabolic manifestations.
15. Model of hypothyroidism. Aetiology. Pathogenesis. Functional and metabolic manifestations.
16. Model of hypercathecholemia. Pathological processes with hypercathecholemia. Vegetative and metabolic
manifestations.
17. Model of plethora (hyper volemia). Pathological processes with plethora. Compensatory
reactions. Hemodynamics disorders. Consequences.
18. Interpretation of patient's BCC with acute bleeding in early period. Emergent
compensatory reactions. Hemodynamics disorders.
19. Model of acute bleeding. Immediate and delated compensatory mechanisms.
Hemodynamics disorders.
20. Interpretation of patient's BCC with acute bleeding (24 h after untreated bleeding).
Immediate compensatory mechanisms.
21. Interpretation of patient's BCC with chronic bleeding. Metabolic disorders. Clinical manifestations.
22. Interpretation of patient's BCC with hyporegeneration of erythroblasts series. Aetiology. Pathogenesis.
Consequences.
23. Interpretation of patient's BCC with iron-deficiency anemia. Pathogenesis.
Consequences.
24. Interpretation of patient's BCC with B12 vitamin deficiency anemia. Pathogenesis. Peripheral blood smear.
Metabolic and gastrointestinal manifestations.
25. Interpretation of patient's BCC with folic acid deficiency. Aetiology. Pathogenesis. Peripheral blood smear.
Manifestations.
26. Interpretation of patient's BCC and biochemical indices of blood with intracellular
hemolysis. Pathological processes with intracellular hemolysis. Pathogenesis. Disorders
of bile metabolism.
27. Interpretation of patient's BCC and biochemical indices of blood with intravascular
hemolysis. Aetiology. Pathogenesis. Disorders of bile metabolism.
28. Interpretation of patient's BCC with autoimmune hemolytic anemia. Pathogenesis. Disorders of bilirubin.
29. Interpretation of patient's BCC with decompensated congenital heart vice. Clinical manifestations.
Pathogenesis. Compensatory reactions. Consequences.
30. Interpretation of patient's BCC with deep diarrhea. Pathogenesis. Hemodynamics disorders. Consequences.
31. Interpretation of patient's BCC with erythromyeloblast acute leucosis. Pathogenesis. Consequences.
32. Interpretation of patient's BCC with lymphoid leukemia. Pathogenesis. Peripheral blood
smear.
33. Interpretation of patient's BCC with coccal acute infection. Diagnostic importance. Biological importance
of neutrophils.
34. Interpretation of patient's BCC with tuberculosis. Pathogenesis. Biological role of
lymphocytes.
35. Interpretation of patient's BCC with parasitic invasion. Diagnostic importance. Biological
role of eosinophils.
36. Interpretation of patient's BCC with agranulocytosis. Aetiology. Manifestations. Biological role of
granulocytic cells.
37. Model of cardiac work overload with volume. Pathological processes with work overload with volume.
Pathogenesis. Consequences.
38. Model of toxic myocarditis. Pathogenesis. Compensatory reactions and hemodynamics
disorders.
39. Interpretation of electrocardiographic changes in patients with sinus bradycardia.
Pathogenesis. Hemodynamics disorders. Consequences.
40. Interpretation of electrocardiographic changes in patients with sinus tachycardia.
Hemodynamics disorders. Consequences.
41. Interpretation of electrocardiographic changes in patients with supra-ventricular
arrhythmias. Aetiology. Pathogenesis. Hemodynamics disorders. Consequences.
42. Interpretation of electrocardiographic changes in patients with ventricular arrhythmias. Aetiology.
Pathogenesis. Hemodynamics disorders. Consequences.
43. Interpretation of electrocardiographic changes in patients with atrial fibrillation. Aetiology. Pathogenesis.
Hemodynamics disorders.Complications.
44. Interpretation of electrocardiographic changes in patients with ventricular fibrillation. Pathogenesis.
Consequences.
45. Interpretation of electrocardiographic changes in patients with incomplete first-degree AV block.
Pathogenesis. Hemodynamics disorders. Consequences.
46. Interpretation of electrocardiographic changes in patients with incomplete second-degree
AV block. Aetiology. Pathogenesis. Hemodynamics disorders.
 47. Interpretation of electrocardiographic changes in patients with complete AV Block.
Hemodynamics disorders.
48. Model of deep and accelerated respiration. Pathological processes with deep and accelerated respiration.
Pathogenesis. Physiological importance. Consequences.
49. Model of stenotic breathing. Aetiology. Pathogenesis. Consequences.
50. Model of Kreichimer protective reflex. Pathogenesis. Biological importance.
51. Model of asphyxia. Asphyxia in pathological processes. Manifestations. Consequences.
52. Model of gastrointestinal intoxication. Pathogenesis. Consequences.
53. Model of bile toxic action on the heart. Pathological processes with cholemia.
Pathogenesis. Manifestations.
54. Model of bile toxic action on respiratory center. Pathogenesis. Manifestations.
55. Model of bile toxic action on spinal cord reflexes. Pathogenesis. Manifestations.
56. Model of tubules necrosis. Aetiology. Manifestations. Biochemical changes of urine.
Consequences.
57. Model of glucosuria. Physiological and pathological glucosuria. Pathogenesis.
Consequences.
58. Model of nephritic syndrome. Manifestations. Consequences.
59. Model of hydremia. Pathological processes with hydremia. Aetiology. Pathogenesis.
Compensatory reactions and hemodynamics disorders. Consequences.
60. Model of metabolic acidosis. Pathological processes with metabolic acidosis. Pathogenesis. Compensatory
reactions. Consequences.
61. Model of metabolic alkalosis. Pathological processes with alkalosis. Compensatory reactions.
Consequences.
62. Model of vasopresin hypersecretion. Pathological processes with vasopresin hypersecretion. Pathogenesis.
Manifestations.Consequences.

Head of department,
M.D., professor V. Lutan