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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
Key points
- ALD ranges from reversible steatosis to hepatitis, cirrhosis, and acute-on-chronic liver failure
- AST:ALT ratio >2 with values usually <300 is classic
- Severe alcohol-associated hepatitis has jaundice and coagulopathy; use Maddrey DF or MELD
- Treatment foundation is abstinence, nutrition, thiamine, and AUD therapy
- Selected severe hepatitis may receive corticosteroids after infection and GI bleeding are excluded
Overview
Alcohol-associated liver disease results from toxic ethanol metabolism, oxidative stress, gut permeability, inflammation, and malnutrition. Alcohol-associated hepatitis presents with recent heavy alcohol use, jaundice, tender hepatomegaly, systemic inflammation, and impaired synthetic function.
Epidemiology
ALD is a major cause of cirrhosis and liver-related mortality in the United States. Risk depends on exposure amount/duration, sex, genetics, obesity, viral hepatitis, and metabolic risk.
Clinical Features
Symptoms
Fatigue, anorexia, nausea, weight loss
RUQ pain and tender hepatomegaly
Jaundice developing over weeks
Ascites, GI bleeding, confusion
Fever can occur but infection must be excluded
Signs
Hepatomegaly, jaundice, fever
Spider angiomas, palmar erythema, gynecomastia
Ascites, edema, muscle wasting
Asterixis or altered mental status
Investigations
First-line
AST/ALT, bilirubin, INR, albumin, CBCAST:ALT >2, macrocytosis, thrombocytopenia, synthetic dysfunction
Viral hepatitis testingExclude concurrent HBV/HCV
UltrasoundSteatosis, cirrhosis morphology, ascites, obstruction
Second-line
Maddrey DF or MELDRisk stratifies severe alcoholic hepatitis
Diagnostic paracentesisAny ascites with hospitalization or deterioration
Cultures/chest X-ray/urinalysisExclude infection before corticosteroids
Specialist
HCC surveillanceUltrasound with or without AFP every 6 months when indicated
Transplant/hepatology evaluationAdvanced fibrosis, decompensation, or early HCC
1
Core treatment
- Complete alcohol abstinence and AUD medications when safe
- Thiamine before glucose if malnourished or withdrawal risk
- High-calorie, high-protein nutrition
2
Alcohol-associated hepatitis
- Hospitalize severe jaundice/coagulopathy or renal injury
- Prednisolone for selected severe cases after excluding infection/GI bleed
- Assess response with Lille score at 7 days
3
Cirrhosis care
- Manage ascites, varices, encephalopathy, SBP risk, HCC surveillance
- Early transplant referral for decompensation
- Long-term addiction medicine support
Complications
- Cirrhosis/portal hypertension: Ascites, varices, encephalopathy.
- HCC: Risk rises with cirrhosis and chronic HBV.
- Acute liver failure: Severe hepatitis can cause coagulopathy and encephalopathy.
- Extrahepatic disease: Vasculitis, renal disease, metabolic complications depending on etiology.
USMLE Step 2 CK Exam Tips
- 1AST:ALT >2 suggests alcohol-associated liver injury
- 2AST and ALT usually not in the thousands
- 3Alcoholic hepatitis can cause fever and leukocytosis — still rule out infection
- 4Give thiamine before glucose
- 5Maddrey DF >=32 or high MELD indicates severe disease
- 6Prednisolone only for selected severe cases
- 7Abstinence is the most important intervention
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