Acute Hepatitis Flashcards

1
Q

What suggests ACUTE hepatitis?

A

less than 6 months

previously normal lab values

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2
Q

Why is alcoholic hepatitis not in the differential of true acute hepatitis?

A

it is the result of an acute exacerbation of underlying CHRONIC liver dz

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3
Q

Which antibody tests are used to look for autoimmune hepatitis?

A

anti smooth muscle antibody (SMA)
anti nuclear antibody (ANA)
LKM1

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4
Q

What is the initial management approach to patients with mild acute hepatitis?

A

watchful waiting

if abnormalities persist - evaluate like severe dz

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5
Q

Which causes of hepatitis are unlikely to present as acute and mild?

A

ischemia and obstruction

genetic liver diseases

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6
Q

What happens in acute self-limited hepatic injury?

A

if inciting agent IDed and removed - enzymes back to normal (ALT slower than AST)
common following ischemia, choledocholithiasis, acetaminophen toxicity

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7
Q

Which causes of hepatitis typically have slow returns of enzyme levels to normal?

A

viral hepatitis

drug hepatotoxicity

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8
Q

What are the basics of the urea cycle?

A

metabolism of dietary AAs and excess ammonia forms urea - major source of enzymes in liver
urea cycle defects lead to ammonia accumulation

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9
Q

What does acute liver failure cause in the brain?

A

hepatic encephalopathy - not seen in chronic

cerebral edema and intra-cranial HTN from excess ammonia and glutamine

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10
Q

What is the most common etiology of acute liver failure in developed countries?

A

acetaminophen - level between 4-24 hrs after ingestion predicts hepatotoxicity

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11
Q

How is acetaminophen metabolized by the liver?

A

3 pathways
glucoronidation and sulfation –> innocuous metabolites
third catalyzed by p450 –> potentially toxic NAPQ1
Glutathione transferase promotes NAPQ1 binding to glutathione = innocuous - less glutathione = toxicity

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12
Q

What can provide a source for glutathione?

A

therapy with N-acetyl cysteine

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13
Q

What factors can increase flux through the toxic pathway of acetaminophen metabolism?

A

ones that decrease glucoronidation - Gilbert’s and fasting

ones that induce p450s - alcohol, some meds

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14
Q

What is the histologic hallmark of acetaminophen toxicity?

A

centrilobular necrosis (also in ischemic, heat stroke, and cocaine)

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15
Q

What clinical features suggest hepatic encephalopathy?

A
disturbances of consciousness
impaired intellectual function
asterixis (hand flap)
constructional apraxia (can't sign name)
coma or delirium
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16
Q

What is the requisite lab finding for the diagnosis of ACUTE liver failure?

A

prolonged PTT and INR - coagulopathy (coagulation factors have short half lives) THEN elevated ATs
prolonged INR seen first in acetaminophen overdose
prolonged, rather than spontaneous, bleeding

17
Q

What findings can differentiate a non-hepatic cause of encephalopathy?

A

arterial ammonia levels normal except in renal failure (modest increase)
lack of coagulopathy or evidence of hepatic injury

18
Q

What is the management of acute liver failure?

A

prevent problems while waiting for regeneration or transplant - IV glucose, head elevation/hyperventilation/diuretics/drug-induced coma, avoid hyperthermia, hyperglycemia, hyponatremia and hypercapnia

19
Q

What is the management of hepatic encephalopathy?

A

cathartic agents - lactulose - to decrease ammonia
aggressively treat infection, electrolyte abnormalities, GI bleeding
limit dietary protein