V.Voloshyn

(ILLUSTRATIONS: from FRANK Netter & http://library.med.utah.edu/WebPath/webpath.html)

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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

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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.

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Reasons of portal hypertension

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Liver infection diseases

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Liver infection diseases

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Echinococosis of Liver

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Schistosomosis of Liver

Liver Lipidosis and Chirrosis

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Pathogenesis of Haemosiderosis

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Hepatolenticular degeneration Willson-Konovalov

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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.

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MEMBERS AND CHARACTERISTICS OF THE HEPATITIS VIRUSES*

Name (Molecule)

Family Transmission

Incubation, weeks

Disease Carrier

Chronic

Cancer

HAV (ssRNA)

Picorna Enteral 2-6 Hepatitis, fulminant hepatitis 0 0 0

HBV (dsDNA)

Hepadna Parenteral 4-26 Hepatitis, fulminant hepatitis, cirrhosis

-1% -10% Yes

HCV (ssRNA)

Flavivirus Parenteral 2-26 Hepatitis, cirrhosis, extrahepatic disorders

-1% -50% Yes

HDV (ssRNA)

Subviral satellite (HBV helper)

Parenteral 4-7 (superinfection)

Hepatitis, fulminant hepatitis -10%

-5% 0

HEV (ssRNA)

Calicivirus Enteral 2-8 Hepatitis ? 0 0

HGV(ssRNA)

Flavivirus Parenteral ? Hepatitis, extrahepatic disorders in drug addicts

-2% 0 ?

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"councilman body"

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). 16

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Hepatitis

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Among all viral hepatitis the most dangerous are hepatitis C

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• viruses of hepatitis, especially B and C; • alcohol; • medicinal preparations; • autoimmune processes; • illness of Vil'sona; • α1-antytrepsin insufficiency.

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On histological principle chronic hepatitis is divided on:

• chronic recurrent hepatitis (CHRG); • chronic active hepatitis (CHAG).

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Chronic recurrent hepatitis

Chronic recurrent hepatitis is characterized: by limphocells infiltration only 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.

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

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is characterized:

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)

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

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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 a norm 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.

fatty dystrophy of hepatocells; acute hepatitis with Mellori hyaline

accummulated; violation of architectonics of liver: portal

primary, and than general cirrhosis of liver.

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Typical for acute alcoholic hepatitis are: Mallory's hyaline, neutrophils, necrosis of hepatocytes, collagen deposition, and fatty change.

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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.

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Clinical motion of Pankreatitis can be acute and chronic.

However necessary it is to know that patients with chronic one can have acute condition.

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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.

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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.

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Patients have sharp sudden painsharp sudden pain in an epigastria area, which is accompanied nausea and vomitnausea and vomit.

ShockShock can very quickly develop. A diagnosis is confirmed the

increase of amylaseincrease of amylase levellevel in blood.

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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.

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.

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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

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At hemorrhage prevailing they call – hemorrhage pancreatitis;

festering inflammation – acute festering pancreatitis;

necrotic changes – pancreonecrosis.

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Death of Patients comes from shock or from peritonitis more frequently

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

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chronic P. can develop after the clinical acute one and independently without any displays which are preceded.

alcoholism is the most frequent reason

chronic P. is the display of mucoviscidosis also.

rarely there is inherited chronic P.

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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.

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Thank you for attention!!!

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