Cirrhosis of the Liver
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Cirrhosis of the Liver
Cirrhosis of the Liver Therapeutics Exam6 Jameson
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
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
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?
infuse 6-8 g albumin per L of fluid removed
: 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
: 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
: cover anaerobes and G(-) organisms with Abx like AG or FQ + metronidazole or piperacillin/tazobactam
: 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