CM- Acute Hepatitis Flashcards Preview

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Flashcards in CM- Acute Hepatitis Deck (25):

When is hepatotoxicity dose-related?
What is an example of this type of drug?

when every individual ingesting a sufficient amount manifests hepatotoxicity

Ex. acetaminophen


What is hepatic injury dependent on in idiosyncratic drug-induced liver injury?

Host factors.
Genetics: gender, metabolizing enzymes, differences in immune responsiveness
Acquired: nutritional status, concomitant conditions, other medications, alcohol


What determines the clinical presentation of drug induced hepatitis?

The pattern of enzyme change:
1. hepatocellular
2. cholestatic
3 .mixed


What are the 3 major etiologic categories for MILD acute hepatitis?

1. Early stages of Hep A-E, CMV, EBV
2. drugs and toxins
3. autoimmune


Why is alchohol not included in the differential diagnosis of true acute hepatitis?

It is an acute exacerbation of underlying chronic liver disease


How is the etiology of acute hepatitis determined?

1. History (look for risk factors, travel, etc)
2. serological tests (autoimmune, viral)
3. imaging (gallstones, secondary dilation)


Viral serologic tests for acute hepatitis are appropriate unless there is evidence of what lab finding?

Elevated LD equal to AST. This is a sign of ischemia (cocaine, heart failure, hyperthermia)


When serologic studies are negative what test should you consider?

US to check for gallstones and secondary dilation


If the viral serologic test are all negative and the sonogram shows no obstructions, what is the next thing you want to consider?

Look for :
SMA, ANA and LKM1 antibodies


If a patient has mild acute hepatitis (asymptomatic with slightly elevated liver enzymes) what do you do?

"watchful waiting" - confirm the findings before trying to figure out the etiology.


What stimuli are going to have asymptomatic or mild liver disease? Which are going to have more severe acute disease?
What are unlikely to present as an acute process?

Asymptomatic/Mild: viruses, drugs/toxins, autoimmune

Severe: obstruction, ischemia

Chronic: genetic disorder (A1AT, Wilson, hemochromatosis), alcohol


How long does it take for AST and ALT to return to normal after ischemia, choledolithiasis, and acetaminophen toxicity stimuli are removed?

How long does it take for AST and ALT to return to normal after viral hepatitis?

Ischemia, choledolithiasis, acetaminophen toxicity return quickly (half life of the enzymes)

Viral takes longer because it is the immune response, not the virus itself causing the damage


How does severe liver damage cause hepatic encephalopathy?

Portal venous blood enters systemic circulation directly without passing through the liver.

The unaltered metabolites like ammonia and glutamine change the brain osmolarity and water content, neurotransmitter levels and energy metabolism


Are you more likely to get cerebral edema and intra-cranial hypertension in acute or chronic liver disease?

Acute - this is because of degree, not mechanism

Also in acute, ammonia clearance and metabolism is compromised. Glutamine also accumulates.

A rapid change will cause brain shrinkage quickly


What drug is the most common etiology for acute liver failure? What determines the hepatotoxicity?


The level between 4 and 24 hours after ingestion predicts hepatotoxicity


What are the 3 pathways by which acetaminophen is metabolized?

1. Glucuronidation (same as bilirubin)
2. Sulfation

3. p450s produce NAPQI (radical toxic metabolite)
Glutathione S-transferase (GSH) can take NAPQI to make it innoculous but if glutathione is depleted, NAPQI will form a hepatotoxic covalent adduct


What decreases glucuronidation of acetaminophen?
What else can increase the flux down the hepatotoxic pathway?

Environmental factors - fasting
Genetic - Gilbert's
Factors that induce p450s (alcohol, meds) will increase NAPQI production


How is acetaminophen toxicity treated?

N-acetyl cysteine to help make glutathione to push NAPQI to mecapturic acid instead of the toxic adduct


What is the histologic hallmark of acetaminophen toxicity?
How does it differ from ischemic and viral injuries?
How does it differ from acute fatty liver of pregnancy?

centrilobular necrosis (same as ischemic injury)

Viral has massive hepatic necrosis but no centrilobar demarcation

Acute fatty liver of pregnancy has microvesicular fat


What is the requisite clinical finding for the diagnosis of fulminant hepatic failure?

hepatic encephalopathy in less than 8 weeks from the onset of symptoms


A patient comes in with disturbances of consciousness, impaired intellectual fuction and asterixis. You ask them to sign their name and they are unable to do so. What is it likely they have?

hepatic encephalopathy


What is the first laboratory finding for the diagnosis of acute liver failure?

Coagulopathy (prolonged PT and INR)
It is the first lab detected in acetaminophen OD because of the centrilobular bleeding pattern.

clotting factors have short half lives so they quickly demonstrate liver injury


What is the differential diagnosis of acute liver failure?

1. decompensation of underlying chronic liver disease (alcohol)
2. non-hepatic causes of encephalopathy:
- metabolic (uremia, hypoxia, hyponatremia, hyper/hypoglycemia, sepsis, delerium tremens)
- ischemia, toxins, vit, def, endocrine probs


What differentiates non-hepatic causes of encephalopathy from hepatic?

The ammonia will not be elevated (except in rena and a genetic disorderl) and the there will be a lack of coagulopathy


What is the treatment for fulminant liver failure?

1. autologous replacement
2. allogenic replacement (transplant)

While waiting for new liver to grow, you must
- give IV glucose to maintain levels
- head elevation, hyperventilation,diuretics to lower pressure
- avoid HYPER capnia, glycemia, thermia and HYPOnatremia because they increase pressure