Слайд 6: Clinical features of hepatic failure
Jaundice Hypoalbuminemia Coagulopathy DIC Fetor hepaticus Increased serum levels of hepatic enzymes Gynecomastia Hepatic encephalopathy Hepatorenal syndrome
Слайд 7: Diseases of liver
The liver is vulnerable to a wide variety of metabolic, toxic, microbial, circulatory, and neoplastic insults. In some instances, the disease is primary to the liver, as in viral hepatitis and hepatocellular carcinoma. More often the hepatic involvement is secondary, often to some of the most often diseases in humans, such as cardiac decompensation, disseminated cancer, alcoholism, and extrahepatic infections.
Слайд 8: MORPHOLOGIC PATTERNS OF HEPATIC INJURY
Regardless of cause, five general reactions may occur: Necrosis. Degeneration. Inflammation. Regeneration. Fibrosis.
Слайд 11: Hepatoses – group of diseases characterized by dystrophy and necrosis of hepatocytes
Chronic Fatty degeneration Hepatoses Acute Massive progressive necrosis of the liver (toxic dystrophy of the liver)
Слайд 12: Massive progressive necrosis of liver
Etiology: exogenous factors-fungi, food toxins, arsenic. Endogenous-gestosis of pregnancy, thyrotoxicosis Pathogenesis-toxic substances affect the hepatocytes dire с tly, mainly in the central part of lobules.
Слайд 13: Massive progressive necrosis of the liver
Morphogenesis: Stage of yellow degeneration 1- 2 week Stage of red degeneration – 3 week
Слайд 20: Fatty hepatosis
Etiology: alcohol, medicines, metabolic disorders (diabetes mellitus, defective protein nutrition, excessive fat consumption), cardiac insufficiency, anemia. Morphology: in hepatocytes appear fat droplets, which can be small or big.
Слайд 21: Stages of development
Ordinary (simple) obesity Obesity in combination with the necroses of hepatocytes and mesenchymal-cellular reaction Obesity in combination with the reorganization of tissue Outcome: portal cirrhosis of the liver
Слайд 26: Viral hepatitis
Etiology: Viruses hepatitis A,B,C,D… Viral hepatitis is reserved for infection of the liver caused by a small (but growing) group of viruses having a particular affinity for the liver.
Hepatitis A Virus does not cause chronic hepatitis or a carrier state and only rarely causes fulminant hepatitis, and so the fatality rate associated with Hepatitis A Virus is about 0.1 %. Hepatitis В Virus can produce 1) acute hepatitis, 2) chronic nonprogressive hepatitis, 3) progressive chronic disease ending in cirrhosis, 4) fulminant hepatitis with massive liver necrosis, and 5) an asymptomatic carrier state with or without progressive disease. Furthermore, Hepatitis В Virus plays an important role in the development of hepatocellular carcinoma.
Transfusion, blood products, dialysis, needle-stick accidents among health care workers, intravenous drug abuse, and homosexual activity constitute primary risk categories for Hepatitis В Virus infection. Hepatitis С Virus has a high rate of progression to chronic disease and eventual cirrhosis, exceeding 50 %.
Слайд 29: Whatever the agent is, the disease is more or less the same and can be divided into four phases:
1) an incubation period, 2) a symptomatic preicteric phase, 3) a symptomatic icteric phase, and 4) convalescence.
Слайд 30: Forms of viral hepatitis
Cyclic icteric Non-icteric Cholestatic Necrotic Chronic (active and persistent)
Слайд 31: Morphological signs
Protein degeneration Proliferation of Kupffer cells Lymphohistiocytic infiltration Councilman bodies ( necrotic hepatocytes may be evident as fragmented, eosinophilic bodies о r may be phagocytosed, leading to the accumulaton of clumps of lymphocytes and macrophages.
Слайд 36: Acute hepatitis with secondary submassive necrosis (NECROTIC FORM) Nodule formation reflects regenerative activity
Слайд 37: Hepatitis B virus infection Hepatitis B virus produces intranuclear inclusions
Слайд 39: CHRONIC HEPATITIS
Symptomatic, biochemical or serologic evidence of continuing or relapsing hepatic disease for more than 6 months, optimally with histologically documented inflammation and necrosis, is taken to mean chronic hepatitis.
Слайд 40: etiologic forms of hepatitis
Hepatitis A Virus: Extremely rare. Hepatitis В Virus: Develops in more than 90% of infected neonates and 5 % of infected adults, of whom one-fourth progresses to cirrhosis. Hepatitis С Virus: Develops in more than 50 % of infected patients, of whom half progresses to cirrhosis. Hepatitis D Virus: Rare in acute Hepatitis D Virus/ Hepatitis В Virus coinfection; a more severe chronic hepatitis is the most frequent outcome of Hepatitis D Virus superinfection. Hepatitis E Virus: Does not produce chronic hepatitis.
Слайд 41: Since 1968, chronic hepatitis has been classified according to the extent of inflammation:
1. Chronic persistent hepatitis, in which inflammation is confined to the portal tracts. 2. Chronic active hepatitis, in which portal tract inflammation spills into the parenchyma and surrounding regions of necrotic hepatocytes. 3. Chronic lobular hepatitis, in which persistent inflammation is confined to the lobule.
Слайд 42: Chronic active hepatitis Liver shows significant collapse indicative of progression to cirrhosis
Слайд 44: Chronic active hepatitis The limiting plate regions are blurred due to an inflammatory infiltrate
Слайд 45: Chronic persistent hepatitis Chronic viral hepatitis manifests as a portal inflammatory infiltrate
Слайд 49: Markers of AH
Fatty dystrophy and necrosis of hepatocytes Alcoholic hyaline ( Mallory bodies ) Prevalence of neutrophils in the infiltrate
Слайд 54: Cirrhosis
Is chronic disease of liver which is characterized by hepatic failure due to structural reorganization of liver. Cirrhosis is among the top ten causes of death in the world, largely the result of alcohol abuse, chronic hepatitis and biliary disease.
Слайд 55: This end stage of liver disease is defined by three characteristics:
- Fibrosis is present in the form of delicate bands or broad scars replacing multiple adjacent lobules. - The parenchymal architecture of the entire liver is disruptured by interconnecting fibrous scars. - Parenchymal nodules are created by regeneration of hepatocytes, The nodules may vary from micronodules (less than 3 mm in diameter) to macronodules (3 mm to several centimeters in diameter).
Слайд 60: Micronodular cirrhosis with portal hypertension and esophageal varices
Слайд 65: Primary biliary cirrhosis Inflamed and destroyed bile ducts are characteristic of this disorder
Слайд 66: Portal areas contain an extensive scarring process obliterating vascular channels as well as bile ducts
Слайд 67: Several features should be understood:
- The parenchymal injury and consequent fibrosis are diffuse, extending throughout the liver; focal injury with scarring does not constitute cirrhosis. - Nodularity is requisite for the diagnosis and reflects the balance between regenerative activity and constrictive scarring.
Слайд 68: Several features should be understood:
- Fibrosis, once developed, is generally irreversible - Vascular architecture is recognized by parenchymal damage and scarring, with formation of abnormal interconnections between vascular inflow and hepatic vein outflow.
Слайд 69: The ultimate mechanism of most cirrhotic deaths is :
1) progressive liver failure, 2) a complication related to portal hypertension, 3) the development of hepatocellular carcinoma.
Слайд 70: The four major clinical consequences are :
1) ascites, 2) the formation of portosystemic venous shunts, 3 ) congestive splenomegaly, 4) hepatic ehcephalopathy.
Слайд 73: Chronic cholestasis Accumulation of bile salts and their deposition in skin leads to a strong itching stimulus
Слайд 78: Histological forms
Hepatocellular carcinoma Cholangiocellular carcinoma