Flashcards in 117b Complications of cirrhosis Deck (22):
complications of cirrhosis
ascites and hepatic hydrothorax (through diaphragm via holes)
HPS and HRS
Varices --> bleeding
where does cirrhosis damage occur in the liver that leads to portal HTN? What else contributes to ascites?
scarring in sinusoids --> portal HTN
arterial splanchnic vasodilation leads to blood pooling
stellate cells - location and role in cirrhosis
space of disse
lay down collagen from hepatic injury --> fibrosis --> cirrhosis
ascites development - pathogenesis and timeline of fluid build up
portal HTN -->
systemic + splanchnic vasodilation via NO -->
lowers renal perfusion --> increased RAAS, SNS, ADH --> retain salt and water --> fluid oozes from abdominal organs
fluid build up quickly
ascites and hepatic hydrothorax - what labs confirm that its from portal HTN?
-high SAAG (serum ascites albumin gradient) = serum albumin - ascites albumin
-lower protein (<2.5)
Ascites and Hepatic Hydrothorax - treatment + what should never be used?
1) salt < 2 g/day (usually not fluid restriction unless hyponatremic in late stages)
2) diuretics - lasix (furosemide) and aldactone (spironolactone)
3) paracentesis as needed
4) prophylaxis against SBP (spont bact peritonitis) in some patients
5) Use TIPS.
Never put in a chest tube OR drainage catheter in abdomen -- high risk of infection without benefit
when should prophylaxis for SBP be considered?
Hostpialized patient (protein <1.5)
TIPS and what it does
Transjugular intrahepatic portosystemic shunt
bypasses liver sinusoids - reduces ascites by reducing portal HTN
hepatopulmonary syndrome - what happens in the lungs? what does this lead to?
intrapulmonary vascular dilations (IPVD) from NO at base of lung --> hypoxia due to ventilation/perfusion mismatch
HPS patient symptoms/findings and treatment
1) spider angiomata
2) orthodeoxia playpnea - sit up and get short of breath and deoxygenated
treatment - supplemental O2 and transplant (curative)
hepatorenal syndrome - pathogenesis and outcomes
cirrhosis --> portal HTN --> splanchnic and systemic vasodilation --> low effective circulating volume --> heart pumps harder (high output heart failure) + increased Na/water retention + kidney vasoconstriction
high risk of death
1) hold diuretics
2) volume replacement with albumin -> increases kidney perfusion
3) if 48 hrs w/out improvement -> use cocktail
octreotide (reduces splanchnic vasodilation)
midodrine (a-agonist - systemic vasoconstrictor)
portal HTN - varices locations
varices treatment goal and specific agents/procedures
goal is to reduce risk of bleeding
1) nonselective B-blockers (propran, nad, carved _olol) "PROPer CARVED NADs"
highest dose tolerable
B1+B2 (2=unopposed alpha reduces inflow via vasoconstriction, 1=slows heart and CO)
2) band ligation
variceal bleeding treatment
octreotide - reduces portal HTN via splan vasodilat
TIPS for recurrent
hepatic encephalophaty - what substances cause it and why does it occur?
ammonia + toxins from bacteria in intestines
bypass liver via shunts (TIPS increases) AND bad liver function
what type of patient gets hepatic encepahlopathy? what occurs in the brain? treatment?
acute liver failure; edema and herniation; use dialysis
brain adapts to chronic liver cirrhosis
hepatic encephalopahty presentation
3) asterixis - flapping when hand is up with wrist flexed back
treatment of hepatic encephalopathy
1) reduce gut bacteria --> rifaximin
2) trap ammonia --> lactulose (ionizes), zinc
3) never protein restrict
what type of blood supply does HCC have? does it occur with or without cirrhosis ?
arterial - can be diagnostic w/out biopsy AND used to treat
always occurs with cirrhosis
how often should cirrhosis get imaged for HCC?
every 6 months with advanced fibrosis and cirrhosis