Cirrhosis Flashcards
top two causes
chronic alcohol abuse
chronic hep C
5 complications
portal hypertension esophageal and gastric varices with risk of variceal bleeding ascites spontaneous bacterial peritonitis hepatic encephalopathy
what is portal hypertension
increased BP in the portal venous system
hepatic venous pressure gradient >5mmHG
how does portal hypertension develop
scarring of liver causes mechanical obstruction of blood flow from portal vein to liver
splanchnic arterial vasodilation and decreased response to vasoconstrictors increases blood flow to portal vein
what causes varices
portal hypertension with HVPG>10mmHg
small veins in lower esophagus and stomach become distended as blood is redirected
what is ascites
accumulation of fluid in the peritoneal cavity
what causes ascites
increased nitric oxide causes vasodilation
decreased arterial blood volume activates RAAS = sodium retention therefore fluid pushes out on the wall
low serum albumin to push back on the wall and keep it in
fluid leaks into peritoneal cavity
definition of spontaneous bacterial peritonitis
infection of ascitic fluid without an obvious surgically treatable source
how does spontaneous bacterial peritonitis occur
bacteria from GI tract end up in ascitic fluid
exact mechanism not know
common bacteria in SBP
ecoli
kpneumoniae
pneumococci
how does hepatic encephalopathy occur
decreased liver function and shunting of blood around the liver causes neurotoxins to accumulate, affects brain function
most commonly ammonia
diagnosing cirrhosis
signs and symptoms
lab values, endoscopy, radiographic tests
biopsy not necessary
symptoms of cirrhosis
weight loss fatigue anorexia jaundice impotence abdominal distention confusion pruitis GI bleed dark colored urine
physical signs of cirrhosis
hepatomegaly splenomegaly spider angiomata caput medusa digital clubbing gynecomastia jaundice asterix - hand flap ascites fector hepaticus - sweet smelling breath
lab indicating alcoholic liver disease
AST:ALT 2:1
labs that can be abnormal in cirrhosis
elevated aminotransferase elevated alkaline phosphatase with GGT rise decreased serum albumin elevated INR hyperbilitubinemia increased serum creatinine hyponatremia thrombocytopenia, leukopenia
abnormal radiographic tests
ultrasonography - detects hepatic nodules, ascites
CT, MRI - detect hepatic nodules, ascites, varices
child pugh classification used for
recommending drug dosage adjustments
model for end stage liver disease score used for
allocation of liver transplants
predicts 3 month mortality
grade A child pugh
<7points
grade B child pugh
7-9 points
grade C child pugh
> 9 points
treat patients with no varices or small varices with no risk factors ?
no
what are risk factors for variceal hemorrhage
red wales
child pugh score C
treat small varices with risk factors for variceal hemorrhage?
yes with non selective beta blocker
treat medium to large varices with no bleeding?
yes with non selective beta blocker
what to treat varices with if have asthma or diabetes (beta blocker intolerant)
endoscopic variceal ligation - banding
non selective beta blocker options
propranolol 20mg BID
nadolol 20mg daily
carvediol 6.25 BID
monitoring of non selective beta blockers
titrate every 3 days to HR 55-6o bbp
when do you stop beta blocker therapy for varices
when in end stage liver disease
beta blocker MOA
decrease portal venous inflow by decreasing cardiac output - beta1
decreasing splanchnic blood flow - beta2
treatment of acute variceal bleeding
maintain BP with fluids, control bleeding
octreotide asap
endoscopic variceal ligation
prophylaxis for SBP
what to do if still bleeding after octreotide and EVL
transjugular intrahepatic portosystemic shunt
octreotide dosing
50mcg IV then 50mcg/hr IV continuous x 3-5days
octreotide mechanism
inhibits vasodilatory glucagon and has local splanchnic vasoconstrictive effect
prophylaxis treatment for SBP durign acute variceal bleeding
cipro or ceftriaxone for 7 days
what is a transjugular intrahepatic portosystemic shunt
shunt that bypasses the liver
secondary prophylaxis of varices to prevent rebleed
non selective beta blocker + chronic EVL
if had TIPS possible liver transplant candidate
things to do for diagnosing of ascites
measure cell count, ascitic fluid total protein, ascitic fluid cultures
calculate serum asciteis albumin gradient (serum albumin - ascitic fluid albumin)
diagnosis of ascites
SAAG >11g/L
treatment of ascites
furosemide 40 + spironolactone 100
non pharm for ascites
restrict salt <2g/day
fluid too if hyponatremia
avoid nsaids, acei
monitoring of ascites treament
titrate diuretics up every 3-5 days for 0.5kg weight loss daily
monitor potassium and serum creatinine
treatment for ascites resistent to diuretics
therapeutic paracentesis
presentation of SBP
fever, ab pain, encephalopathy, confusion, renal failure
diagnoses of SBP
PMN >250cells/mm3 and positive ascitic fluid bacterial cultures
when to treat SBP
treat empirically (before culture back) if PMN >250 or signs/sx of infection
treatment of SBP
3rd generation cephalosporins perferred
quinolone second line
why cefotaxime is preferred over ceftriaxone
less bound to proteins in the blood and more easily passed into acidic fluid
cefotaxime treatment SBP dosing
2g IV q8h
5 day treatment course
long term prophylaxis after SBP episode
septra lower dosing than standard treatment
ex septra DS 5x a week
precipitating factors for hepatic encephalopathy
electrolyte abnormalities - dehydration, diuretic overuse
infection
GI bleeding
constipation
mainstay of hepatic encephalopathy treatment
reduce ammonia levels
first line for hepatic encephalopathy
lactulose - non absorbable disaccharide
how often to give lactulose and preferred route
q1hr
oral
mechanism of lactulose lowering ammonia
laxative effect - less time for systemic ammonia absorption from gut
decreased pH so charged NH4+ cations trapped in acidic colon
titration for lactulose
3 soft stools daily
monitoring for lactulose
3 soft stools dialy
improved mental status
rifaximin MOA
porrly absorbed antibiotic
reduces ammonia producing bacteria in the gut
when to use rifaximin
with lactulose in recurrent HR not responding to max tolerated lactulose
why arent neomycin and metro use anymore
higher risk of side effects
