Final: Liver Flashcards
Response in liver disease
degeneration and intracellular accumulation, necrosis and apoptosis, inflammation, regeneration, fibrosis
Degeneration
- ballooning degeneration (hepatocytes enlarge)
- At later stage hepatocytes shrinks down to eosinophilia “Councilman body”
fibrosis
- generally moving towards irreversible changes
- deposit of collagen; continued deposition will result in cirrhosis
hepatitis
- usually caused by hepatrotropic viruses. In US –>C; worldwide–>B
- Also d/t alcohol or infection from other organisms
Hep A
- Fecal-oral
- NO chronic state
- rare to cause fulminant hep
Hep B
- chronic state possible
- May lead to LV CA (hepatocellular carcinoma)
- Only DNA virus. body fluid transmission; neonatal transmission usually leads to lifelong carrier status
Hep C
- most common chronic blood-borne infxn in US
- perinatal transmission lower than w/ Hep B. Both acute and chronic states; however most people develop chronic unlike B.
- Complications: cirrhosis and hepatocellular carcinoma
Hep D
- RNA virus that requires Hep B to replicate
- IV drug abuse
- co-infection w/ HBV usually not too serious; but SUPERINFECTION w/ pre-existing Hep B often SEVERE
Hep E
- fecal-oral. No chronicity
- PREGNANT WOMEN at risk
Hep G
innocent bystander virus
Chronic hepatitis
> 6 months
-causes: Hep C/B, chronic alcoholism, Wilson’s disease, alpha-1 antitrypsin deficiency
ground glass hepatocytes
CHRONIC HEP B (not pathognomic but characteristic)
Acetaminophen poisoning
HIGHEST levels of AST/ALT especially w/ concomitant ETOH abuse
fulminant hepatitis
sx progress to hepatic encephalopathy within 2-3 weeks (when d/t viral–>usu hep B)
ETOH/acetaminophen injury
depletion of GSH and induction of CYP enzymes results in increased amounts of NAPQI and inability to remove it
ETOH
- leading cause of LV disease in western countries
- liver changes: hepatic steatosis, alcoholic hepatitis, cirrhosis
- MALLORY bodies seen: not pathognomic but characteristic (also see w/ NASH, PBC, Wilson’s and hepatocellular tumors)
- AST:ALT 2:1
cirrhosis
- insidious. Starts fatty and yellow and enlarged then over years liver shrinks and becomes cirrhotic.
- complications: portal HTN (and subsequent splenomegaly), gastric varices
- stigmata of cirrhosis: distended abdomen, wasted extremities, Caput medusae
NAFLD
- resembles ETOH liver disease but not d/t ETOH
- AST:ALT ratio
NASH
- intermediate form of LV damage
- Shows steatosis, Mallory bodies, elevated enzymes
- cirrhosis can occur
hemochromatosis
- primary: genetic cause; excessive iron absorption
- secondary: iron supplementation/transfusions
- bronze diabetes: iron deposition in skin plus diabetes d/t deposition of iron in pancreas
Wilson’s disease
- autosomal recessive w/ copper deposition
- liver, brain and eyes
- mimicks acute viral hepatitis except for accompanying fatty changes that are also seen
- Kayser- Fleischer rings PATHOGNOMIC
alpha-1 antitrypsin def
- autosomal recessive; low levels of protease inhibitor
- signifcant liver damage
PBC
- AI destruction of bile ducts of liver. Granulomatous destruction of medium sized intrahepatic bile ducts
- cirrhosis, jaundice and severe pruritus
- POSITIVE anti-mitochondrial Ab test. F>M.
PSC
- AI but no known ab
- segmental stricture and dilatation of bile ducts. BEADED appearance w/barium
- COEXISTANCE W/ UC
- onion skinning fibrosis
