PANCE Blueprint GI and Nutrition (8%)

60-year-old with a distended abdomen

Patient will present as → a 63-year-old white male with a chief complaint of blood in his stool. He is accompanied by his wife, who also reports weight gain, abdominal distension, and swelling of his legs. Physical exam reveals a healthy-appearing male with 3+ bilateral lower extremity edema and distended abdomen with evidence of shifting dullness. You also note several skin changes seen here. The patient is hemoccult positive and has blood on his urine dipstick. He denies tobacco and illicit drug use but admits to drinking 1-2 times per week and has about 6 beers on each occasion.

Cirrhosis is a late stage of hepatic fibrosis that has resulted in a widespread distortion of normal hepatic architecture

• Characterized by regenerative nodules surrounded by dense fibrotic tissue
• The liver is unable to regenerate due to large amounts of scar tissue
• Cirrhosis is a leading cause of death worldwide and is the ninth leading cause of death among U.S. adults

The most common cause of cirrhosis in the United States is now MASLD/MASH, followed by chronic alcohol abuse, with other causes including viral hepatitis B and C, autoimmune hepatitis, and inherited metabolic disorders.

• MASLD/MASH (25–30%): History of diabetes mellitus or metabolic syndrome. Diagnosis may be suspected by abnormal liver biochemical tests and hepatic imaging showing fatty infiltration and is confirmed by liver biopsy
• Alcohol liver disease (20–25%): History of alcohol abuse
• Chronic Hepatitis C (15–20%): ELISA assay for anti-HCV with PCR for HCV RNA if a confirmatory test is necessary
• Hepatitis B + hepatitis D infection (5–10%): HBsAg and HBeAg and, in some cases, HBV DNA by hybridization or bDNA assay
• Wilson's disease: ↑ Copper, ↓ Ceruloplasmin + family history

Physical exam may be normal until end-stage disease:

• Hepatomegaly (small, fibrotic liver in end-stage disease)
• Terry’s nails (white nail beds)
• Splenomegaly (if portal hypertension)
• Central obesity
• Abdominal fluid wave, shifting dullness (ascites)
• Gynecomastia
• Esophageal varices
• Pulmonary edema/effusion

Classical skin changes: spider angiomata, palmar erythema, jaundice, scleral icterus, ecchymoses, caput medusae, hyperpigmentation

Hepatic encephalopathy:

• Asterixis (flapping tremor), dysarthria, delirium, coma

Progressive cirrhosis

• Elevated ammonia level; BUN, sodium, and potassium
• α-fetoprotein level at diagnosis to screen for hepatocellular carcinoma (HCC)
• Abdominal ultrasound every 6 months to screen for hepatocellular carcinoma
• All patients with cirrhosis should undergo esophagogastroduodenoscopy (EGD) to exclude esophageal varices
• MRI is the best follow-up test for HCC if α-fetoprotein elevated and/or liver mass found on ultrasound
• Noninvasive modalities, such as elastography, are being researched as an alternative to liver biopsy
• Update necessary immunizations and focus on the treatment of the underlying cause of cirrhosis (hepatitis C, alcohol abuse, etc.)
• Fever and abdominal pain in a patient with cirrhosis think spontaneous bacterial peritonitis
• Hepatocellular carcinoma: Monitor AFP
• Budd Chiari (hepatic vein thrombosis) triad of abdominal pain, ascites, and hepatomegaly

Labs: typically, AST > ALT, ↑ the risk for hepatocellular carcinoma: monitor AFP

• AST/ALT: mildly elevated ⇒ Typically AST > ALT. Enzymes normalize as cirrhosis progresses
• ↑ ALP and ↑ GGT
• Anemia from hemolysis, folate deficiency, and splenomegaly
• Decreased platelet count from portal hypertension with splenomegaly
• Decreased bilirubin conjugation by the liver ⇒ ↑ unconjugated bilirubin ⇒ jaundice
• Decreased albumin production by the liver ⇒ Hypoalbuminemia
• Decreased clotting factor production by the liver ⇒ Prolonged prothrombin (PT), international normalized ratio (INR), partial thromboplastin time (PTT). Vitamin K–dependent clotting factors
• Ultrasound: helpful to determine the liver size and evaluate for hepatocellular carcinoma
  • Current guidelines recommend performing an abdominal ultrasound every 6 months in patients with cirrhosis to allow for early detection and treatment of HCC. AFP testing can be added to US screening - however, the trade-off is an increase in false positives when using AFP with ultrasound compared to ultrasound alone
• Liver biopsy is invasive and is subject to sampling error, but it remains the gold standard for the diagnosis of cirrhosis
• All patients with cirrhosis should undergo esophagogastroduodenoscopy (EGD) ⇒ Exclude esophageal varices

Child-Pugh Score for Cirrhosis Mortality

• Class A (5–6 points): one-year survival 100%, two-year survival 85%
• Class B (7–9 points): one-year survival 81%, two-year survival 57%
• Class C (10–15 points): one-year survival 45%, two-year survival 35%

Generally, scarring from cirrhosis is irreversible ⇒ Prevent further damage by identifying and treating the underlying cause

• Stop alcohol
• Antiviral treatment for Hepatitis C
• Corticosteroids for autoimmune hepatitis
• Chelation therapy (e.g., penicillamine) for Wilson's disease
• Diuretics, antibiotics, laxatives, enemas, thiamine, steroids, acetylcysteine, pentoxifylline for decompensation
• Nonselective beta-blockers (nadolol and propranolol) for primary prophylaxis against variceal hemorrhage or esophageal variceal ligation (EVL)
• For advanced cirrhosis ⇒ liver transplant may be necessary
• Encephalopathy ⇒ lactulose + neomycin
• Ascites ⇒ sodium restriction, paracentesis
• Pruritus: ⇒ cholestyramine

Spontaneous bacterial peritonitis is suspected in cases of unexplained fever and abdominal pain