3. Viral and Non-viral Liver Disease Flashcards
LO1: Acute Hepatitis (1-length of dz, and labs, 2-causes)
1) < 6mo of systemic dz and lab evidence of hepatocyte injury
2) causes- acute viral hepatitis and drug injury
LO1: Chronic Hepatitis(1-duration, 2c-causes)
1) Long, ongoing hepatocyte injury and inflamm >6mo
2) Causes
a) Chronic viral hepatitis
b) autoimmune hepatitis
c) drug injury
LO2: Histo Patterns of Liver Injury (4)
1) Cytoplasmice accumulations
2) Degeneration, necrosis, and apoptosis
3) Inflamm
4) Regeneration, fibrosis, and cirrhosis
LO3: Hep A - Type, mode, risk of chronicity, path, and serology (5)
1) ssRNA
2) Fecal-oral
3) Never ->chronic
4) Serum IgM Ab
5) Acute hepatitis only
LO3: Hep B - Type, mode, risk of chronicity, path, serology, relationship to genome, histo (7)
1) partially dsDNA
2) parenteral, sexual contact, perinatal
3) 10% -> chronic liver dz
4) HBsAG or HBcAb
5) Major cause of chronic liver dz worldwide
6) Can integrate into genome
Histo
7) Ground glass hepatocytes
8) Sanded nucleus
LO3: Hep C - Type, mode, risk of chronicity, path, serology, genetics (6)
1) ssRNA
2) Parenteral; intranasal cocaine-risk factor
3) 80% -> chronic liver dz
4) PCR for HCV RNA, 3rd generation ELISA for Ab
5) Major cause of chronic liver dz in US
6) Genetically unstable
LO3: Hep D - Type, mode, risk of chronicity, path, serology, HBV relationship (9)
1) ssRNA
2) parenteral
3) 5% alone; <70% w/ Hep B superinfxn
4) IgM and IgG Ab
5) HDV RNA serum
6) HDAg in liver
7) Potentiate and dependent HBV
8) Increased risk of fulminant hepatitis
9) Faster progression to end stage liver dz
LO4: Grade of dz in chronic hepatitis
Based on amount of inflamm and injury
LO4: Stage of dz in chronic hepatitis
Amount of fibrous tissue deposition
LO5: HCC in chronic liver dz. Prognosis?
Dismal long term survival
LO6: Primary Biliary Cirrhosis (1)
1) Immune mediated attack of intrahepatic small caliber bile ducts
LO6: Primary Sclerosing cholangitis (1)
1) Immune mediated? obliterative fibrosis of intrahepatic and extrahepatic bile ducts
LO7: Autoimmune Hepatitis, presentation (2-4) (4)
1) Immune-mediated attack directed at hepatocytes Presentation 2) F>M 3) Other autoimmune association 4) variable course
LO8: Drug induced Liver Injury, how common, pattern of injury, intrinsic or extrinsic (4)
1) Relatively common
2) Patterns of injury-cholestasis, bile ducts, auto-immune, steatosis, acute or chronic hepatitis
3) Intrinsic -dose related
4) Idiosyncratic
LO8: Acetaminophen Toxicity, stats, intrinsic or extrinsic, necrosis where? (3)
1) Major cause of acute liver failure -> liver transplant
2) Intrinsic hepatotoxin
3) Centrilobular necrosis -Zone 3
LO9: Steatosis, causes (4)
1) Accumulation of fat in hepatocytes
2) metabolic derangement of hepatocytes
3) causes- metabolic syndrome, ETOH, drug effect, Wilson, viral
4) Lipid influx> lipid clearance
LO10: Benign Liver Tumors (3)
1) Hemangioma
2) Focal Nodular Hyperplasia
3) Hepatocellular adenoma
LO10: Malignant Liver Tumors (2)
1) Hepatocellular carcinoma
2) Cholangiocarcinoma
Hepatitis Inflammation Associations, lymphs, neutrophils, eosinophils, plasma cells (4)
1) Lymphs - viral hepatitides
2) Neutrophils - steatohepatitis
3) Eosinophils - common in drug injury
4) Plasma Cells - Autoimmune hepatitis
Cytoplasmic Accumulation Associations, fat, bile, iron, copper, viral particles (5)
1) Fat - steatosis
2) Bile - cholestasis
3) Iron - Hemosiderosis/ genetic hemochromatosis
4) Copper -Wilson Dz/chronic cholestasis
5) Viral particles -viral hepatitis
LO1: Acute Hepatitis Micro, inflammation where? (4)
1) lobular disarray
2) marked inflamm throughout
3) widespread hepatocyte injury
4) No fibrosis
LO1: Chronic Hepatitis Micro, Inflammation where? (3)
1) Less prominent inflamm and injury
2) Portal-tract based inflamm
3) fibrosis
HCV Outcomes (4)
1) Resolution
2) Stable dz
3) Stable cirrhosis
4) Death
HBV Outcomes (3)
1) Recovery
2) 0.5% fulminant hepatitis
3) 5% Chronic hepatitis -> Cirrhosis ->HCC
LO3: Hep E, acute or chronic, mode, who’s at risk (3)
1) Acute hepatitis only
2) Fecal-oral
3) Higher mortality in pregnant women
LO6: PSC Presentation (3)
1) M>F
2) Asymptomatic w/ persistent Alk phos elevation
3) Progressive fatigue, pruritis, and jaundice
LO6: PSC Dx (1)
1) cholangiography -alternating biliary strictures and dilations (beads on a string)
2) No specific serology
LO6: PSC Prognosis + Histo (4)
1) Variable
2) Increased risk for cholangiocarcinoma
Histo:
3) Periductal “onion-skin” fibrosis
4) Fibrous obliteration of bile ducts
LO6: PBC Presentation (3)
1) Insidious onset w/ pruritis before jaundice
2) Middle aged women
3) Cholestatic LFT (elevated ALP, GGT, bilirubin)
LO6: PBC Serology, prognosis, and histo (4)
1) Anti-mitochondrial Ab (90%)
2) Elevated IgM
Prognosis
3) 25% w/ liver failure @ 10 yrs
4) Ductopenia
LO7: Autoimmune Hepatitis (1)
1) Anti-ANA, Anti-ASMA, Anti-LKMB, elevated IgG
LO9: Steatohepatitis (3)
1) Hepatocellular injury w/ steatosis +/- overt inflamm
2) Causes-ETOH, metabolic syndrome, drug injury
3) Often chronic and can lead to fibrosis and cirrhosis
LO9: Steatohepatitis Histo (4)
1) Ballooning degeneration
2) Inflamm
3) Steatosis
4) Pericentral, pericellular fibrosis
LO9: Alcoholic Steatosis/steatohepatitis (2)
1) Neutrophil infiltrate
2) Mallory bodies - hyaline
LO9: Non-alcoholic steatosis/steatohepatitis (1)
1) Fatty liver dz w/ obesity, DM2, Hypertriglyceridemia
LO9: Hereditary Hemochromatosis (5)
1) Genetic iron overload throughout body
2) Manifests as liver dz, DM2, HF
3) AR inheritance
4) HFE gene mutation
5) Iron Deposits
Wilson Dz (3)
1) Genetic Cu overload throughout body
2) Liver dz and neuropsych problems
3) ATP7B mutation - transporter involved in bile excretion of Cu
LO9: Alpha-1-Antitrypsin Deficiency (5)
1) Genetic decreased production of alpha-1-antitrypsin
2) Alpha-1-antitrypsin -protease inhibitor
3) AR
4) PiZZ genotype- most have emphysema
5) PASD stain - pink globules
HCC (2)
1) Most common malignant liver tumor
2) Mostly in chronic liver dz (HCV, HBV, ETOH) and cirrhosis
Cholangiocarcinoma (2)
1) Malignant-effects the bile ducts - intra or extrahepatic
2) Major risk - PSC
Hemangioma (4)
1) Benign - dilated vascular spaces
2) Most common primary hepatic tumor
3) small and asymptomatic
4) Vague RUQ pn, early satiety, n/v
Focal Nodular Hyperplasia (3)
1) Benign mass-like proliferation of hepatocytes
2) Due to local vascular flow anomaly
3) 2nd most common benign
Hepatocellular adenoma (4)
1) Benign -hepatocytes
2) Women of child bearing age-OC use
3) Asymptomatic or RUQ pn
4) Extremely low risk of malignant transformation
