Review Question - QID 215111

The presentation of coffee-ground emesis in a patient with a long history of alcohol abuse is consistent with esophageal variceal bleeding secondary to portal hypertension. The concomitant presence of peripheral edema, hypotension, ascites (i.e., shifting dullness and fluid wave), AST/ALT ratio > 2, elevated PT, and low platelet count are concerning for alcoholic cirrhosis, which manifests with decreased plasma oncotic pressure and increased portal hydrostatic pressure, renin, and ADH.

Alcoholic cirrhosis should be suspected in a patient with chronic alcohol abuse who presents with stigmata of chronic liver disease such as portal hypertension (e.g., esophageal varices and/or caput medusae), signs of hyper-estrinism (e.g., palmar erythema, spider telangiectasias, and/or gynecomastia), and/or evidence of liver biosynthetic dysfunction (e.g., elevated PT/international normalized ratio [INR] and/or low platelet count). In cirrhosis, reduced liver biosynthetic function results in decreased liver synthesis of albumin, which is the primary determinant of plasma oncotic pressure. The consequent reduction in plasma oncotic pressure drives fluid extravasation, leading to edema, ascites, ADH release, and activation of the renin-angiotensin-aldosterone system. Cirrhosis also causes fibrosis of the liver, which increases hepatic vascular resistance and leads to increased hydrostatic pressure in the portal venous system. Over time, portal hypertension causes dilation of veins at the site of porto-systemic anastomoses, which can slowly ooze blood or rupture into the gastrointestinal tract. Liver cirrhosis can be diagnosed on the basis of clinical, laboratory, and imaging (i.e., abdominal ultrasound) findings, although the gold standard is a liver biopsy.

Figure A is a table displaying the answer choices.

Incorrect Answers:
Answer 1: Decreased plasma oncotic pressure, increased portal hydrostatic pressure, increased renin, and decreased ADH is incorrect because ADH increases in cirrhosis. Patients with a history of hypertension commonly become hypotensive after cirrhosis develops due to fluid extravasation (e.g., peripheral edema and ascites) and the regulatory response to portal hypertension that results in systemic vasodilation. Decreased systemic blood pressure stimulates ADH release from the posterior pituitary as a homeostatic response.

Answer 3: Decreased plasma oncotic pressure, decreased portal hydrostatic pressure, increased renin, and increased ADH is incorrect because portal hydrostatic pressure increases in cirrhosis. The fibrotic remodeling of the liver that occurs in cirrhosis results in extensive scar tissue that increases hepatic vascular resistance. The back pressure is then transmitted through the portal venous system.

Answer 4: Decreased plasma oncotic pressure, increased portal hydrostatic pressure, normal renin, and increased ADH is incorrect because renin increases in cirrhosis. Decreased liver biosynthesis of albumin causes fluid extravasation and hypotension, leading to activation of the renin-angiotensin-aldosterone system as the body responds to low renal perfusion pressures.

Answer 5: Normal plasma oncotic pressure, increased portal hydrostatic pressure, increased renin, and increased ADH is incorrect because plasma oncotic pressure decreases in cirrhosis. One of the hallmarks of cirrhosis is reduced liver synthesis of proteins, including albumin, which causes a decrease in the plasma oncotic pressure.

Bullet Summary:
Liver cirrhosis is characterized by decreased plasma oncotic pressure, increased portal hydrostatic pressure, increased renin, and increased ADH due to portal hypertension, systemic vasodilation, and reduced liver biosynthetic function.