- •30. Pathophysiology of digestion.
- •30.1. What is deficiency of digestion?
- •30.2. How is deficiency of digestion is classified?
- •30.3. What factors can cause digestion deficiency?
- •30.4. What principles do they use in experimental modulating of digestion deficiency?
- •30.5. With what influences into nervous system do they modulate indigestion?
- •30.6. What disorders of humoral regulation do they use for modeling of indigestion?
- •30.7. What syndromes characterize digestion deficiency?
- •30.8. With what symptoms is dyspeptical syndrome manifestated?
- •30.9. What is anorexia? When does it appear?
- •30.10. What is heartburn? What is its mechanism?
- •30.11. What is belch? What are its mechanisms?
- •30.12. What is nausea and vomiting? What are its mechanisms?
- •30.13. What is constipation? When does it happen?
- •30.14. What is altered bowel sounds? When does it arise?
- •30.15. What is diarrhea? By what can it be caused?
- •30.16. What can be reason of dehydration of organism?
- •30.17. What disorders of pH condition are symptoms of disorders of digestion?
- •30.18. What causes intestinal autointoxication in case of disorder of digestion?
- •30.19. What mechanisms can cause pain syndrome in case of injuries of digestive system?
- •30.20. What disorders of motorical, secretory and absorption function of digestive system can cause disorders of digestion?
- •30.21. What reasons can cause disorders of chewing? What inportance for digestion have these disorders?
- •30.22. What is caries of teeth?
- •30.23. How pathogenesis of caries is nowadays understood?
- •30.24. What is periodontitis? What factors can cause it?
- •30.25. What are the reasons and importance of hypersalivation?
- •30.26. What are the reasons of and importance of hyposalivation?
- •30.27. What is dysphagy? name its reasons and influence.
- •30.28. What is gastric dyskinesia? What are its variants?
- •30.28. Name reasons and importance of hyperkynetic dyskinesia of stomach.
- •30.30. What is pylorospasm?
- •30.31. Name reasons and importance of hypotonic dyskinesia of stomach
- •30.32. There are some types of pathologic gastric secretion:
- •30.33. How is gastric hypersecretion manifestated? What is its importance?
- •30.34. How can gastric hypersecretion be modelated in experiment?
- •30.35. What is ulcer disease? What is its etiology?
- •30.36. What are theories of pathogenesis of ulcer disease?
- •30.37. What pathogenic variants of gastric ulcer do they distinguish nowadays?
- •30.38. What is exogenous gastric ulcer? What can be its reason?
- •30.39. What is peptic ulcer? How is it modelated in experiment?
- •30.40. What is trophic ulcers of stomach? How is it reproduced in experiment?
- •30.41. What is hyporegeneratory ulcers of stomach? What can cause it?
- •30.42. What is the manifestation of gastric hyposecretion? What is its importance?
- •30.43. How can gastric hyposecretion be modelated in experiment?
- •30.44. What are the reasons of pancreatic hypersecretion? How it can manifestate?
- •30.45. What is acute pancreatitis? What is its etiology?
- •30.46. What is main link of pathogenesis of acute pancreatitis? What pathogenic variants of this disease do they distinguish?
- •30.47. What is the characteristic for primary alterative variant of development of acute pancreatitis?
- •30.48. What can cause development of hypertensive variant of acute pancreatitis?
- •30.49. What conditions cause refluxe variant of pancreatitis?
- •30.50. Describe pathogenesis of local changes in case of acute pancreatitis.
- •30.51. What mechanisms can cause pancreatic shock?
- •30.52. With what symptoms is pancreatic shock manifestated?
- •30.53. What reasons can cause development of pancreatic hyposecretion? What is its importance?
- •30.54. What is maldigestion syndrome? What symptoms is its manifestation?
- •30.55. What is intestinal dyskinesia? What are its variants?
- •30.57. How are hypokynetical diskynesies of intestines manfestated? What is its importance?
- •30.58. What is intestinal impassability? How is it classified?
- •30.59. Which changes in organism are the manifestation of intestinal impassability? What is its pathogenesis?
- •30.60. What reasons can cause disorders of defecation? How does such disorders manifestate?
- •30.61. What is malabsorption syndrome? What reasons can cause the disorders of absorption?
- •30.62. What reasons can cause the disorders of absorption in intestines?
- •30.63. What is intestinal enzymopathy? How can it be manifestate?
- •30.64. What enterocytic disorders can cause malabsorption syndrome?
- •30.65. What postenterocytic disorders can cause disorders of absorption of substances in intestines?
30.50. Describe pathogenesis of local changes in case of acute pancreatitis.
Premature activation of enzymes of pancreatic juice causes autodigestion of glandular tissue. Because of influence of tripsine and chemotripsine tissue proteins and protein components of cells are denatured. Elastase causes denaturation of elastine - component of basal membrane of vessels. Phospholipase causes disorder of barrier function of phospholipides through its fission , lipase causes disorders in fatty tissue.
Prostaglandines form from released arachidonic acid. Kallikreinogen and α2-globulines enter into tissue from blood. Under influence of tripsinogen and tripsine activation of kallikrein takes place, kinines form.
Active enzymes of pancreatic juice, prostaglandines, kinines cause secondary alteration of pancreatic tissue, increasing of permeability of vessels with development of edema, hemorrhages, arising of pain. Acute inflammation, which has many peculiarities develops. It is generalized stage of alteration, is very obstacle, vascular changes are very characterized.
30.51. What mechanisms can cause pancreatic shock?
Pancreatic shock is hard general manifestation of acute pancreatitis and it is characterized by disorders of general blood circulation (decreasing of arterial pressure) and general disorders of microcirculation.
Pathogenesis of pancreatic shock has two main mechanisms:
Acute pain which arise at pancreatitis is caused by edema of pancreas (pressure on solar plexus),influence on biological active digestive enzymes (tripsine, phospholipase) into neural extremities of gland) Intensive pain causes excitement, and then overlimit braking in important for life centers. It causes oppression of external respiration and disorders of system blood circulation- pain shock develops
Humoral mechanism. Entering into blood of active pancreatic enzymes causes it. Enzymes that entered into blood are inactivated by nature inhibitors of proteases (α1-inhibitor of proteases, antitrombine III, α2-macroglobuline, α2-antiplasmine, α-inhibitor of tripsine and others). But if there is deficiency of its power, all entered enzymes can’t be inactivated, and activation of all blood systems caused by tripsine takes place. Kallikrein-kinine, blood coagulation and fibrinolytic systems are activated. Formed kinines cause general widening of vessels , that cause decreasing of peripheral resistance, and permeability of vessels increase, that causes transfusion of fluid from blood into tissues (plasmorhagy) and blood circulation volume decreases. It causes decreasing of arterial pressure. Activation of coagulate and fibrinolytic systems cause DIC-syndrome, and disorders of microcirculation.
30.52. With what symptoms is pancreatic shock manifestated?
Acute arterial hypotension (collapse). It is caused by widening of vessels (peripheral resistance decreases) and decreasing of blood circulation volume (minute volume of heart decreases)
DVC-syndrome. Is caused by activation of coagulative and fibrinoytic systems, and permeability of blood vessels
Hypotonical syndrome. It is caused by:
circulatory hypoxia: disorder of general hemodynamics (decreasing of arterial pressure) and microcirculation (DVC-syndrome)
respiratory hypoxia - oppression of activities of respiratory center of (overlimit braking of important for life centres in case of strong pain syndrome)
hematic hypoxy ,which arises as a result of hemolysis of erythrocytes by pancreatic phospholipase
Intoxication syndrome. Entering of products of autolytic destruction of tissue of pancreas into the blood causes it.