DISEASES of the LIVER, GALLBLADDER AND PANCREAS

1. DISEASES of the LIVER, GALLBLADDER AND PANCREAS V.Voloshyn (Frank Netter’s illustrations)

2. Pankreatitis • Clinical motion of Pankreatitis can be acute (sharp) and chronic. • However necessary it is to know that patients with chronic one can have acutecondition.

3. Acute Pancreatitis • Etiology. Acute Pancreatitis can develop at: • obstructions of pancreas duct; • reflux of bile; • alcoholism; • violation of blood circulation (for example, at shock); • defeat by parotitis virus; • hyperparathyroidism; • hypothermia; • trauma.

4. In many cases Pancreatitis is poorly expressed, but is a heavy disease which is characterized by high lethality. Pancreatitis of adults is observed more frequent than children’s one. A defeat develops difficultly& characterized by massive activation of pancreatic enzymes, which, in acute cases, may cause life-threatening autodigestion and shock. • In addition, these enzymes damage surrounding tissues & finishes by their dissolution.

5. Clinical displays: • Patients have sharp sudden pain in an epigastria area, which is accompanied nausea and vomit. • Shock can very quickly develop. • A diagnosis is confirmed the increase of amylaselevelin blood.

6. Pathogeny: • the initial stage depends on reasons: • at the obstruction of pancreas channel by a stone or at bile reflux there is a damage of epithelium pancreatic duct canaliculuses, especially if a bile is infected or contains activated. • A damage spreads after it on glands, that results in liberation and activating of proteolytic and other enzymes.

7. Pathogeny 2: • At a violation of blood circulation peripheries pancreas acinuses suffer primary (they are disconnected from blood supplying first). • After it rapid and widespread destruction of gland develops by proteolytic enzymes.

8. Morphology: • a gland swelling • seat of hemorrhages as a result of destruction of blood vessels • fatty necrosis in grate omentum and hypodermic cellulose (very often with skin colour change in epigastrium area (Grey-Terner's symptom) • fat acids link the ions of calcium→ calcium concentration decreas→ tetanus • insular apparatus destruct→hyperglycemia • abscesses and cysts in pancreas & neighbors tissues

11. PANCREATITIS KINDS • At hemorrhage prevailing they call – hemorrhage pancreatitis; • festering inflammation – acute festering pancreatitis; • necrotic changes – pancreonecrosis.

12. Death of Patients comes from shock or from peritonitis more frequently

13. Chronic pancreatitis • cause extensive destruction of pancreatic parenchyma with fibrosis and loss of enzymatic activities • which can develop after the clinical acute one and independently without any displays

14. Etiology: • chronic P. can develop after the clinical acute one and independently without any displays which are preceded. • alcoholismisthe most frequent reason • chronic P. is the display of mucoviscidosis also. • rarely there is inherited chronic P.

18. Pathoanatomical description. • Chronic P. is more frequent observed for adults, than for children • At X-ray examination – calcification areas as a result of preceding fatty necrosis. • Exocrine parts of gland transformed in to fibrosis tissue • Endocrine part mainly is not damaged.

20. The liver maintains the physiologic and metabolic balance of the body. Therefore, disease of the liver may have numerous effects throughout the body: it may cause disturbances in carbohydrate, lipid, amino acid, and vitamin metabolism and interfere with protein synthesis, blood clotting, and detoxification of endogenous and exogenous substances

21. LIVER ILLNESSES • Illnesses of liver are various and can be primary and secondary (at other diseases). • Chronic hepatitis is an inflammatory disease of liver, which lasts more than 6 months without the signs of recovery.

22. Acute Viral Hepatitis • an inflammatory disease of the hepatic parenchyma, is caused most frequently by the hepatitis viruses (HVs) and less frequently by other viruses. In the Western world, HBV and HBC are most prevalent.

23. MEMBERS AND CHARACTERISTICS OF THE HEPATITIS VIRUSES*

35. Disease symptoms develop between 2 and 26 weeks after the onset of immune reactions against virus/virus-infected cells. The pathogenesis of liver injury in viral hepatitis is not completely clear, although a cytotoxic T-lymphocyte reaction against hepatocytes presenting viral antigens seems to be the key reaction. Histology shows many lymphocytes invading the liver parenchyma from portal triads, which causes adjacent hepatocellular necroses (piecemeal necroses). Infected hepatocytes change to a ground-glass appearance. In more severe disease, infected hepatocytes show ballooning degeneration. In addition, there are single or multiple hepatocellular coagulation necroses of virus-infected hepatocytes (Councilman bodies) or lytic necroses (dropout necroses).

37. Etiology.Reason of chronic hepatitis can be different factors. Most frequent is: • • viruses of hepatitis, especially B and C; • • alcohol; • • medicinal preparations; • • autoimmune processes; • • illness of Vil'sona; • • α1-antytrepsin insufficiency.

38. Classification. On histological principle chronic hepatitis is divided on: • • chronic recurrent hepatitis (CHRG); • • chronic active hepatitis (CHAG).

39. Chronic hepatitis is the unspecific display of many chronic diseases of liver

40. Chronic recurrent hepatitis Chronic recurrent hepatitis is characterized: • by limphocells infiltrationonly of portal tracts; • saving of normal architectonics of liver; • by absence or rare necrosis of liver cells; • by a favourable prognosis. Mostly at chronic recurrent hepatitis there is convalescence even without specific treatment.

41. Chronic active hepatitis is characterized: • by boundary (for peripheries of particle on a border with portal highways) (necrosis of two particles is with involvement of portal highway which lies between them) necrosises; • by infiltration of portal highways and parenchyma of liver; • by the high risk of development of liver cirrhosis

42. Histologically • boundary necrosises • decrease of hepatocells quantity • violation of normal architectonics • sometimes specific signs which specify on reason of hepatitis:(for example: Mellori's gialin at alcoholism)

45. Alcoholic hepatitis • An alcohol (ethyl spirit) is the most frequent reason of acute and chronic damage of liver.

46. The defeat of liver takes a place as a result of the followings mechanisms: • the cells of liver begin to take away energy from more accessible source – alcohol (the oxidization processes of fat acids which are the source of energy in anorm are stopped, as a result of their accumulation in a cells, that fatty dystrophy develops; • an alcohol is poison & accumulat in a cells, results in its damage, an inflammatory reaction develops round their; • an alcohol stimulates the synthesis of collagen →fibrosis in portal highways primary.

47. Markers of biopsy changes • fatty dystrophy of hepatocells; • acute hepatitis with Mellori hyaline accummulated; • violation of architectonics of liver: portal primary, and than general cirrhosis of liver.

49. Chronic diseases of liverTo them belong: • overload of liver by iron (haemokhromatozis); • illness of Vil'sona (hepatic lentikular degeneration); • insufficiency of α1-antitripsinum; • autoimmune disease • autoimmune ("lyupoid") hepatitis; • primary bile cirrhosis.

50. THE END