Acute Hepatitis Flashcards Preview

Block 7 - GI > Acute Hepatitis > Flashcards

Flashcards in Acute Hepatitis Deck (19):
1

What suggests ACUTE hepatitis?

less than 6 months
previously normal lab values

2

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

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

3

Which antibody tests are used to look for autoimmune hepatitis?

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

4

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

watchful waiting
if abnormalities persist - evaluate like severe dz

5

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

ischemia and obstruction
genetic liver diseases

6

What happens in acute self-limited hepatic injury?

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

7

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

viral hepatitis
drug hepatotoxicity

8

What are the basics of the urea cycle?

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

9

What does acute liver failure cause in the brain?

hepatic encephalopathy - not seen in chronic
cerebral edema and intra-cranial HTN from excess ammonia and glutamine

10

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

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

11

How is acetaminophen metabolized by the liver?

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

12

What can provide a source for glutathione?

therapy with N-acetyl cysteine

13

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

ones that decrease glucoronidation - Gilbert's and fasting
ones that induce p450s - alcohol, some meds

14

What is the histologic hallmark of acetaminophen toxicity?

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

15

What clinical features suggest hepatic encephalopathy?

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

16

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

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

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

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

18

What is the management of acute liver failure?

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

19

What is the management of hepatic encephalopathy?

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