Cirrhosis of the Liver

  1. Explain the vicious cycle of portal HTN
    • Cirrhosis blocks the flow through the portal vein
    • Pressure is increased and albumin is decreased (d/t blocked flow, decreased NO (vasodilator), and increased endothelin (vasoconstrictor))
    • This leads to acites (d/t incr hydrostatic pressure and lower oncotic pressure b/c of lower albumin)
    • This leads to decreased intravascular volume. CO is down, so renal perfusion is lower.
    • Kidneys turn on the RAAS which leads to retention of sodium and excretion of potassium (H2O retention)
    • More H2O leads to more pressure and less effective intravascular volume and kidneys keep producing more and more renin
  2. General series of events leading to portal hypertension
    inflammation -> fibrosis -> cirrhosis -> impaired blood flow -> portal HTN
  3. Etiology of hepatic encephalopathy
    • Cirrhotic liver can't detox ammonia and other CNS depressants like mercaptans
    • Pt becomes increasingly confused then sedated/asterixis, then goes into coma
  4. What is asterixis?
    • sign of too much ammonia and hepatic encephalopathy
    • cannot hold hand up in stop motion - hand flops down
  5. Treatment of hepatic encephalopathy
    • Make sure we're not making it worse - remove sedating drugs, treat any infx, limit dietary protein, treat GI bleed and constipation, make sure we are not overdiuresing the pt
    • DOC: lactulose
    • Can substitute neomycin or use in combo with lactulose
    • Another option is rifamixin
  6. MOA of lactulose
    metabolized to lactic, acetic, and formic acids which interact with ammonia in colon (donate a H+) to form ammonium ion
  7. MOA of neomycin for hepatic encephalopathy and AEs
    • Kills urea splitting bacteria (so ammonia is not formed)
    • Leads to nephro and oto toxicity - be esp careful in renal impairment
  8. Monitoring for lactulose and neomycin
    • it is an osmotic laxative - diarrhea is SE and therapeutic goal
    • want hepatic encephalopathy pts to have 2-4 loose stools per day
    • Efficacy monitoring - mental status and connect the number
    • Monitor renal function for neomycin
  9. Treatment of esophageal varices
    • DOC is octreotide. It has vasoconstrictive properties. For acute treatment.
    • Also vasopressin. Reserved for treatment failures. More SEs like decr CO, ischemia, gangrene.

    Interventional treatment includes balloon tamponade and portosystemic shunt. Last line.
  10. Prevention of esophageal varices
    • DOC is propranolol. MOA - decr pressure and CO.
    • Isosorbide mononitrate. MOA - vasodilation.
    • Combo of propranolol and isosorbide mononitrate
    • Variceal ligation - banding
  11. Monitoring for esophageal varices treatment
    • BP
    • bleeds
    • decr. CO
    • ischemia, gangrene with vasopressin and balloon tamponade
  12. What types of pressure lead to/cause acites?
    • increased hydrostatic pressure
    • decreased plasma oncotic pressure d/t decr in albumin
  13. Acites treatment. MOA, AEs.
    • Spironolactone is DOC (eplerinone is alternative)
    • MOA - inhibits aldosterone which is responsible for Na/K exchange. If too much aldosterone, Na and H2O retained and K is excreted.
    • Spironolactone can cause gynecomastia (possibly irreversible) - eplerenone doesn't
    • Can use furosemide to get more fluid loss, but be careful. Ratio is 100 mg spironolactone to 40 mg furosemide.
    • Overdiuresis can lead to hepatorenal syndrome to kidney failure to death.
  14. What is the goal for net loss with spironolactone treatment of acites?
    • if peripheral edema, want 1 L net loss per day
    • if no peripheral edema, want 0.5 L loss
  15. What is the significance of the spot urine sodium test in ascites treatment monitoring?
    • We know the drugs are maximized when the spot urine sodium EQUALS the spot urine potassium (want 1:1 ratio).
    • When pt is hyperaldosterone-ic the Na:K ratio is less than 1.
  16. Monitoring of furosemide in ascites treatment
    • Monitor weight and BUN/creatinine ratio
    • Use baseline BUN as starting point because the pt is not making urea very well to start with.
  17. What is the rationale for large volume paracentesis to treat ascites?
    • controversial
    • infuse 6-8 g albumin per L of fluid removed
    • Rationale: treats ascites, prevent renal failure, improve mortality even if pt has spontaneous bacterial peritonitis
  18. Define and give risk factors for hepatorenal syndrome and ways to minimize the risk
    • It is a bunch of organ dysfunctions caused by severe cirrhosis - very high mortality
    • Risk factors: organ dysfxn
    • Avoid overdiuresis of pt
  19. What is the lab value used to diagnose spontaneous bacterial peritonitis?
    • if PMNs are >/= 250
    • (cultures are usually negative)
  20. Treatment and prophylaxis of spontaneous bacterial peritonitis
    • Treatment: cover anaerobes and G(-) organisms with Abx like AG or FQ + metronidazole or piperacillin/tazobactam
    • Prophylaxis: Norfloxacin or Bactrim
  21. Liver Lab tests to be monitored in all cirrhosis pts
    • Transaminases - AST/ALT (ALT is sufficient for screening b/c AST won't go up unless ALT does except with ethanol). Will be normal in end stage cirrhosis.
    • Alkaline Phosphatase (goes up with liver obstruction)
    • Bilirubin - conjugated and unconjugated
    • Liver Function - Poor liver fxn is indicated by low albumin level. Incr INR is best indicator of liver fxn d/t impaired ability of anti-platelets to be metabolized.
  22. At what ALT level do we adjust med doses for hepatic failure? In what case would it go above 500?
    • when ALT is 3x baseline (so, at 120, which is 3 x 40)
    • it doesn't go above 500 except in viral hepatitis - can go up to 2000-3000
Card Set
Cirrhosis of the Liver
Cirrhosis of the Liver Therapeutics Exam6 Jameson