hepatitis and most cirrhosis Flashcards

1
Q

what viruses cause hepatitis? discuss types of HDV infection and the findings in window phase HBV infection

A

usually hepatitis virus, but EBV and CMV can do this too.
HDV: superinfection (when you are already infected with HBV and then get HDV) has a short incubation and a more severe presentation when compared with HDV/HBV coinfection
window phase: HBsAG NEGATIVE, IgM positive for HBcAB.

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2
Q

presentation of viral acute hepaptits; liver enzymes

A

jaundice: mixed CB and UCB with dark urine, fever, malaise, and nausea.
elevated liver enzymes with ALT > AST. symptoms last < 6 mo.

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3
Q

what is the histo in chronic viral hepatitis?

A

inflammation is mostly in the portal tracts.

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4
Q

how do you get hepatitis E? special features?

A

contaminated water or undercooked seafood. fecal-oral.

associated with fulminant hepatitis in pregnant women

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5
Q

What is cirrhosis?

A

end stage liver damage with disruption of parenchyma by broad bands of fibrosis that separate nodules of regenerative liver parenchyma.

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6
Q

What mediates liver cirrhosis?

A

stellate cells lie beneath endothelial cells that line the sinusoids and release TGF-beta, which mediates fibrosis

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7
Q

What are the clinical features of cirrhosis?

A
  1. portal HTN consequences: ascites, congestive splenomegaly, which can become hyperactive and begin to consume RBCs and platelets, portosystemic shunts, and hepatorenal syndrome (rapidly developing renal failure)
  2. decreased detoxification: mental status changes, asterixis, and eventual coma from increased serum ammonia; gynecomastia, spider angiomata, and palmar erythema from hypeerstrinism, and jaundice
  3. decreased protein synthesis: hypoalbuminemia with edema, coagulopathy d/t decreased synthesis of clotting factors (epoxide reductase loss?). We follow coagulopathy by following PT.
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8
Q

How can alcoholic liver disease present? Broad definition?

A
damage to hepatic parenchyma from consumption of alcohol.
may present as:
1. fatty liver disease
2. alcoholic hepatitis
3. cirrhosis
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9
Q

alcoholic fatty liver disease: clinical, gross, and histo features

A

accumulation of fat within the hepatocytes which results in a heavy, greasy liver. it is reversible with abstinence.

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10
Q

alcoholic hepatitis: what is it? what mediates the damage? features?

A

chemical injury to hepatocytes, often associated with binge drinking. acetaldehyde mediates the damage.
see SWELLING and BALLOONING of hepatocytes and MALLORY BODIES. mallory bodies are damaged intermediate filaments (like cytokeratin) within the hepatocytes.

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11
Q

How does alcoholic hepatitis present?

A

painful hepatomegaly and elevated liver enzymes (AST > ALT). AST is in the mitochondria, and EtOH is a mitochondrial toxin. this can result in death.

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12
Q

Nonalcoholic fatty liver disease

A

fatty change, hepatitis and/or cirrhosis that devolps without exposure to alcohol or other known insult. associated with OBESITY.
diagnosis of exclusion, though ALT is generally > than AST

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13
Q

hemochromatosis: definition. What causes damage?

A

excess body iron leads to deposition in tissues (hemosiderosis) and organ damage. damage is mediated by the generation of free radicals.

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14
Q

primary vs. seconday hemochromatosis: what causes both of these?

A

primary: enterocyte takes up basically all the iron in the gut, but will only pass it to the blood if the body needs it. this is the key regulatory step in the human body for iron.
in primary hemochromatosis, this regulation is disrupted- causes massive iron load. HFE gene mutations, usually the mutation C282Y (or H63D).
secondary usually from chronic transfusion therapy (ie. beta thalassemia major).

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15
Q

Presentation and lab findings in hemochromatosis

A

classic triad of cirrhosis, secondary diabetes mellitus (damage to the islets by iron deposits) and bronze skin (iron deposits in the skin). often also see cardiac arrhythmias/CHF (iron in heart) and gonadal dysfunction. it can cause HCC.
high ferritin, low TIBC, high serum iron, high percent saturation.

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16
Q

What are the histo findings with hemochromatosis?

A

brown pigment in hepatocytes (not specific- could be iron, or lipofuscin- wear and tear pigment).
prussian blue stain: turns iron blue but won’t mark lipofuscin.

17
Q

How do you treat hemochromatosis

A

repeated phelobotomy, deferasirox, deferoxamine

18
Q

What is Wilson’s disease?

A

autosomal recessive defect in ATP-mediated hepatocyte copper transport. results in alack of copper transporta into the bile and a lack of copper incorporation into ceruloplasmin (which normally carries copper around in the blood).
causes a buildup of copper in the liver, which eventually leaks out and deposits in other tissues like the brain, liver, kidneys, joints, cornea. copper causes free radical-mediated damage to those organs

19
Q

presentation of wilson’s disease

A

presents in childhood with cirrhosis, neurologic manifestations including chorea, dementia, behavior changes, and parkinson symptoms due to degeneration of the basal ganglia (esp. putamen).
also see kayser-fleisher rings in the cornea.

20
Q

treatment of wilson’s disease

A

penasillamine or trientine (copper chelating agents)

21
Q

labs for wilson’s disease

A

incr. urinary copper, decr. serum ceruloplasmin, and incr. copper on liver biopsy