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Fatty Liver Disease for USMLE Step 2

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Fatty Liver Disease for the USMLE Step 2
Overview
  • Fatty liver disease encompasses Non-Alcoholic Fatty Liver Disease (NAFLD) and Alcoholic Liver Disease (ALD), both characterized by the accumulation of fat in hepatocytes.
  • NAFLD occurs in individuals with minimal alcohol intake, while ALD results from chronic alcohol consumption.
Non-Alcoholic Fatty Liver Disease (NAFLD)
Pathophysiology
  • NAFLD is strongly associated with insulin resistance and metabolic syndrome, including obesity, dyslipidemia, and type 2 diabetes mellitus (T2DM).
    • Simple steatosis: Fat accumulation without significant inflammation or fibrosis.
    • Non-Alcoholic Steatohepatitis (NASH): Fat accumulation with inflammation and hepatocyte damage, potentially progressing to fibrosis and cirrhosis.
  • Oxidative stress and lipotoxicity lead to hepatocyte injury, contributing to NASH.
Risk Factors
  • Obesity: Visceral obesity is a significant predictor.
  • Type 2 diabetes mellitus (T2DM): Increased risk of fibrosis and cirrhosis in NASH.
  • Dyslipidemia: Elevated triglycerides and low HDL cholesterol.
  • Metabolic syndrome: Central obesity, hypertension, hyperglycemia, and dyslipidemia increase the likelihood of NAFLD.
Clinical Presentation
  • NAFLD is often asymptomatic; patients are frequently diagnosed after incidental findings of elevated liver enzymes or imaging.
  • When symptomatic, patients may report fatigue, right upper quadrant (RUQ) discomfort, or nonspecific abdominal pain.
Diagnosis
  • Imaging:
    • Ultrasound: Common first-line test showing increased liver echogenicity.
    • Transient elastography (FibroScan): Measures liver stiffness and can estimate fibrosis.
  • Laboratory tests:
    • Elevated ALT and AST levels, usually with an AST:ALT ratio <1.
    • Gamma-glutamyl transferase (GGT) may also be mildly elevated.
  • Liver biopsy: Gold standard to distinguish between simple steatosis and NASH, especially if there is concern for advanced fibrosis.
Fatty Liver Progression Fibrosis
Complications
  • NASH may progress to cirrhosis and increases the risk of hepatocellular carcinoma (HCC).
  • Cardiovascular disease is the leading cause of death in NAFLD patients, driven by underlying metabolic risk factors.
Management
  • Lifestyle modification:
    • Weight loss: A reduction of 7–10% of body weight is recommended to improve steatosis and NASH.
    • Diet: A low-calorie, low-carbohydrate diet like the Mediterranean diet is beneficial.
  • Pharmacotherapy:
    • Pioglitazone: Improves liver histology in patients with NASH, particularly those with T2DM.
    • Vitamin E: Used in non-diabetic patients with NASH for its antioxidant properties.
    • Statins: Safe to use for dyslipidemia and cardiovascular risk management.
  • Bariatric surgery: Considered for morbidly obese patients who fail conservative measures.
Alcoholic Liver Disease (ALD)
Pathophysiology
  • Chronic alcohol consumption leads to fat accumulation in hepatocytes, hepatocyte damage from oxidative stress, and release of proinflammatory cytokines, resulting in inflammation and fibrosis.
  • The disease spectrum includes simple steatosis, alcoholic hepatitis, and cirrhosis.
Clinical Presentation
  • Early stages are often asymptomatic.
  • Alcoholic hepatitis presents with jaundice, fever, RUQ pain, and tender hepatomegaly.
  • Signs of advanced disease include ascites, spider angiomata, and palmar erythema.
Diagnosis
  • AST:ALT ratio >2 is characteristic of ALD.
  • Liver biopsy: Shows steatosis, Mallory bodies, and neutrophilic infiltration in alcoholic hepatitis.
Complications
  • Cirrhosis, leading to portal hypertension, hepatic encephalopathy, and an increased risk of hepatocellular carcinoma.
Management
  • Alcohol cessation is critical for preventing progression.
  • Corticosteroids: Used in severe alcoholic hepatitis to reduce inflammation and improve short-term survival.
  • Nutritional support: Often necessary, especially in malnourished patients.
Key Points
  • NAFLD is related to metabolic syndrome and can progress from simple steatosis to NASH, leading to cirrhosis and hepatocellular carcinoma (HCC).
  • ALD is caused by chronic alcohol intake and can progress from steatosis to alcoholic hepatitis and cirrhosis.
  • AST:ALT ratio >2 is suggestive of ALD, while NAFLD usually has an AST:ALT ratio <1.
  • Treatment for NAFLD focuses on lifestyle modification and weight loss, while ALD requires alcohol cessation and may include corticosteroids for severe alcoholic hepatitis.

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