cirrhosis, vitamins/minerals, nutrition Flashcards
what is cirrhosis
cell injury in liver, death of hepatocytes
hepatocytes: functional unit of liver
causes of cirrhosis
- # 1 cause: alcohol use (severe amounts of drinking)
- hepatitis C
- fatty liver disease (obesity)
continual hepatocyte damage –> no time for hepatocytes to recover –> death > regeneration –> organ failure
cirrhosis s/s
- ascitic belly
- altered mental status
cirrhosis labs to look at – 4 main ones
- jaundice / high bilirubin
- low platelets
- low albumin
- high PT/INR (low clotting factors, dec clotting)
bc liver makes: platelets, albumin, clotting factors
other labs to look at for cirrhosis
LTFs: ALT, AST –> released by liver when cell damage occuring
- acute damage: LFT inc –> bc there are hepatocytes that can release LFTs and regenerate
- chronic damage: LFT dec –> bc no more hepatocytes around to release LFTs
cirrhosis complications in order of progression
- ascites
- portal HTN
- variceal bleeding
- spontaneous bacterial peritonitis (SBP)
- hepatic encephalopathy
- hepatorenal syndrome
ascites Dx
step 1: abdominal ultrasound** –> look for fluid
step 2: parcentesis
step 3: compare albumin in serum to albumin in ascitis fluid with SAAG –> portal HTN
paracentesis
put a needle in the ascitic belly and remove the fluid accumulated
SAAG
serum ascites albumin gradient
SAAG = serum albumin - ascitic albumin
if SAAG >/= 1.1 –> portal HTN
sodium restriction MoA
sodium will cause further fluid retention – do not want more fluid retention when already a bunch of fluid in peritoneal
DO NOT FLUID RESTRICT – already dehydrated bc alcoholic
aldosterone antagonist MoA
aldosterone drive:
not enough blood through liver –> not enough blood volume to heart –> low cardiac output –> trigger a inc HR, kidney water retention, direct blood away from peripheral to central –> BUT when fluid gets to GI, will go into extravascular space bc portal HTN–> STILL low cardiac output –> will continue to rev up this drive
aldosterone antagonist: inhibit this process
what is a more potent diuretic in cirrhosis? loops or aldosterone antagonists
aldosterone antagonists!!
therefore always do spironolactone over furosemide if need to pick one!
midodrine MoA
alpha activity –> inc BP
**allows toleration of other two diuretics
large volume paracentesis MoA
remove all the fluid from the extravascular space
** if > 5L: the intravascular fluid will rush back into the extravascular space when the fluid is removed, therefore dropping BP –> therefore need IV albumin
IV albumin MoA
hypertonic, therefore will keep fluid in the intervascular space instead of it rushing back into the extravascular space after LVP –> prevents the drop in BP that would occur
aldosterone antagonist AE
inc K
loop diuretic AE
dec K
what diuretic ratio do you need to optimize diuresis and keep K normal
40mg furosemide : 100mg spironolactone
**THESE ARE DAILY AMOUNTS – CAREFUL OF BID!
benefit of IV albumin with LVP
may dec mortality !
cons of IV albumin with LVP
- expensive
- short circulating half life (hours)
- short term solution to help with the transition
TIPS procedure MoA
put in a shunt from the portal vein to the hepatic vein –> bypass the liver –> this bypasses the highly pressurized area that will prevent fluid from getting through/prevents backups
TIPS AE and therefore CIs
AE: hepatic encephalopathy
**bc ammonia in blood no longer going through liver –> ammonia not detoxified by liver –> ammonia goes to CNS –> mental changes
CI: pts with refractory hepatic encephalopathy
pts with history of hepatic encephalopathy
what to avoid in acities
thiazide diuretics (HCTZ)
- will dec Na (Na is already low)
ACEi/ARB
- will lower bowman capsule pressure –> WILL CAUSE AKI
fluid restricition
- patients are already drhydrated
if do TIPS, what do you need to do
START HEPATIC ENCEPHALOPATHY PROPHYLAXIS
- bc such a high risk of it