-
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
-
General series of events leading to portal hypertension
inflammation -> fibrosis -> cirrhosis -> impaired blood flow -> portal HTN
-
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
-
What is asterixis?
- sign of too much ammonia and hepatic encephalopathy
- cannot hold hand up in stop motion - hand flops down
-
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
-
MOA of lactulose
metabolized to lactic, acetic, and formic acids which interact with ammonia in colon (donate a H+) to form ammonium ion
-
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
-
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
-
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.
-
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
-
Monitoring for esophageal varices treatment
- BP
- bleeds
- decr. CO
- ischemia, gangrene with vasopressin and balloon tamponade
-
What types of pressure lead to/cause acites?
- increased hydrostatic pressure
- decreased plasma oncotic pressure d/t decr in albumin
-
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.
-
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
-
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.
-
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.
-
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
-
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
-
What is the lab value used to diagnose spontaneous bacterial peritonitis?
- if PMNs are >/= 250
- (cultures are usually negative)
-
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
-
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.
-
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
|
|
