Liver Pathology Flashcards
Cirrhosis
Chronic end stage liver disease with diffuse fibrosis, diffuse loss of lobular architecture, diffuse formation or regenerative nodules
Cirrhosis etiology
Liver damage by excess alcohol
Liver damage by viruses ( HBV, HCV, HBV+D)
Biliary disease
Congenital diseases ( Wilson’s disease, a-1 anti trypsin deficiency, galactoseMia,tyrosinosis)
Drugs ( a-methyl dopa, anti cancer ).
Cryptogenic
Fibrosis in cirrhosis
Irréversible
Bundles of portal portal , portal central , central , broad bands, that replace adjacent lobules
Loss of architecture in cirrhosis
Done by diffuse scars
Nodules formation in cirrhosis
Micronodular (less than 3mm)
Macronodular (more than 3mm)
Mixed nodular cirrhosis
Pathogenesis of cirrhosis
Causative agent
Fibrosis by type 1&3 collagen in space of disse and lobules
Impaired nutrients and solutes diffusion
Loss of fenestrations in sinusoids
Mpaired transfer of products (albumin, lipoproteins, clotting factors) hepatocytes into blood
Fibrous tissue by ito cells due to cytokines Etc
Portal hypertension due to increased resistance in sinusoids caused by narrowing, nodules and fibrosis compressing portal vein
Complications of portal hypertension
Ascites
Portosystemic shunt
Congestive splenomegaly
Hepatic encephalopathy
Pathogenesis of ascites in cirrhosis
Sinusoidal hypertension
Hypoproteinemia
Low peritoneal reabsorption of fluid
interstitial leakage from capillaries due to portal hypertension
renal retention of sodium and water from secondary hyperaldosteronism
Hepatocellular failure
Progressive
Loss of function over 80% to see failure symptoms.
70-95% mortality
Features of hepatic failure
Jaundice hypoalbuminemia coagulation defects Hyperammonemia Fetor hepaticus High hepatic enzyme in serum Gynecomastia Testicular atrophy Male hypogonadism Palmar erythema Spider angiomas Muscle wasting Hypoglycemia Hepatic encephalopathy
Hepatic encephalopathy
Metabolites normally processed and eliminated by the liver gain entrance to the brain
Brain edema , severe loss of hepatic function, neurological signs , hyper reflexia, seizures, asterixis
Hepatorenal syndrome
Appear like renal failure with no intrinsic morphologic or functional causes for renal failure
Drop in renal output Rising bun and creatinine Hyperosmolar urine with no protein Abnormal sediment Low sodium
Complications of cirrhosis
Portal HPT (ascites, haemorrhoids, varices, splenomegaly)
Hepatocellular failure p
Hepatocellular ca
IInfections pneumonia duodenal ulcers TB
Circulatory disturbances- clubbing of fingers, cyanosis, peripheral vasodilation
Anorexia and wasting
Hypothermia
Hepatic adenoma
Benign tumors of hepatocytes that occur mostly in women ( because of oral pill)
Focal nodular hyperplasia
Nodular lesion that resembles cirrhosis
5 to 15 cm
Can protrude and can be pedunculated
Has central scar where fibrous septa radiate
Most common tumor of the liver
Hepatic hemangioma’s
Hepatic hemangioma incidence
All ages
both sexes
What type of tumor is more common primary or secondary
Secondary
Type of malignant tumor
Hepatocellular carcinoma’s( to hepatitis , mostly HBV)
Hepatoblastoma ( young childhood)
Angiosarcoma (vinyl chloride ..)
Main primary malignant tumors of liver
Hepatocellular carcinoma (90%)
Cholangiocarcinomas(10%)
Cholangiocarcinoma linked to
Thorotrast and opistorchis infections
Hepatocellular carcinoma pathogenesis
HBV or HCV repeated cycles of replication
Accumulation of mutations
HBV x protein disrupt growth mechanism control
Aflatoxins activated and form mutagenic DNA adducts
Etiology of hepatocellular carcinoma
HBV HCV Cirrhosis Haematochromatosis Tyrosinosis Drugs Chemicals
Morphology of hepatocellular carcinoma
Enlarged liver
Paler
Yellowish necrotic areas
Areas of hemorrhage
Variant fibrolamellar type
Good prognosis Not associated to HBV or cirrhosis Affects young male and females in 20-40 Well differentiated hepatocytes Fibrous stroma
Steatosis
Accumulation of fat in hepatocytes
Cholestasis
Accumulation of bilirubin in hepatocytes
Most severe consequence of liver disease
Liver failure
Acute liver disease
Sudden and massive hepatic destruction
Encephalopathy and coagulopathy that occurs within 26weeks of initial liver injury
Chronic liver failure
Progressive and insidious liver injury over decades leading to hepatic failure