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57 Cards in this Set

  • Front
  • Back
what are complications of CLD
esophageal varicies
hepatic encephalopathy
spontaneous bacterial perotinitis
hepatorenal syndrome
bleeding disorders
ascites
hepatocellular carcinoma
at what hepatic venous pressure gradient do esophageal varices form
> 8-10 mmHg
what is the pathophysiological cause of esophageal varicies
increase resistance in portal vein causing back up of blood
what kind of bleed is it when esophageal varicies rupture
GI bleed

high mortality when ruptures occur
what is the done to prevent Variceal bleeding
non selective Beta blockers (propranolol, nodolol)

endoscopic therapies (sclerosing, band ligation)

TIPS

combo therapy
how do propranolol, nodolol help prevent variceal bleeding
decrease hepatic blood flow so you have less blood going to the liver (constriction of mesenteric vein)

B2 blockage decreases blood going into protal vein
what are the endoscopic therapies and what do they do
sclerosis - inject something into blood vessels to die off so no longer at risk for rupturing

band ligation - wrap band around blood vessels so it shrivels up and dies so no longer at risk for rupturing
what are TIPS
go in via jugular vein feed catheter down into liver and SET UP SHUNT FROM PORTAL VEIN TO IVC

so instead of blood going through the liver and out the hepatic vein, blood will flow out of the portal vein also and through the IVC giving another outlet for blood which will decrease the pressure in the portal vein
what are the issues with TIPS
make encephalopathy worse b/c since you're shunting blood away from the liver it won't get a chance to detoxify blood so you have a build up of things liver should metabolize

they get clogged up/occluded and therefore don't last forever
when are routine endoscopies done
when pt diagnosed with cirrhosis
what are the treatment options for Variceal bleeding
manage fluid loss (give enough Na to maintain intravascular volume) and correct bleeding disorder (vit K, platelets, plasma)

manage bleeding
prevent rebleeding
treat SBP unless ruled out
how do you manage variceal bleeding
somatostatin or octreotide
endoscopic therapies (sclerosing, band ligation)
combination therapy
salvage therapy (TIPS, ballon tamponade, surgery)
how does somatostatin/octreotide work
cause constriction of mesenteric vein resulting in a decrease in the amount of blood reaching the portal vein therefore decrease portal pressure
aside from somatostatin/octreotide what can be used to treat variceal bleeding
vasopressin + nitroglycerin

works at mesenteric vein as well, only issue is VASOPRESSIN INCREASES BP THEREFORE GIVEN W/ NITROGLYCERIN
in treating variceal bleeding why would you put a pt on drugs before conducting an endoscopy
the drugs would decrease the amount of bleeding occuring allowing you to find the varicies with the endoscope
what is balloon tamponade
place balloon in pt esophagous which will put pressure on the varices decreasing the amount of blood coming out
what is the main treatment for variceal bleeding
octreotide + endoscopic therapy
why is it crucial to treat SBP unless it is ruled out
pt with SBP tend to go down hill
what is the pathophysiology of ascites
resistance to hepatic blood flow
decrease oncotic pressure (decrease albumin)
increase Na retention
how can resistance to hepatic blood flow result in ascites
serous fluid oozes out of the blood vessels into the abdomen
what are some things that can cause increase Na retention
decrease aldosterone metabolism
decrease renal blood flow
systemic vasodilation
what is the volume status of pt with ascites
volume overloaded but intravascularly volume depleted
how do you treat ascites
Na retention +/- fluid retention
spironolacton + furosemide
paracentesis
TIPS or surgical shunt
how does spironolactone help ascites and why is it given with furosemide
spironolactone is an aldosterone Rc antagonist and one of the causes of ascites is increased Na retention due to decreased aldosterone metabolism

furosemide is given also due to spironolactone being a subpar diuretic
what is the reason we diures pt with ascites and why is it critical when treating ascites that we don't diures too fast
diuresis is done b/c we remove fluids from BV so fluid from the abdomen can replace it, only issue is that EASY TO TAKE FLUID OUT OF VASCULATURE BUT IT TAKES TIME FOR FLUID TO MOVE FROM ABDOMEN TO BV
what is paracentes
use needle to drain fluid out of the abdomen
how much fluid would you have to take off to require albumin administration with paracentesis and what is a major draw back of paracentesis
albumin administration done when you take off >5L of fluid
-albumin given just to maintain IV volume but only temporary fix b/c albumin t1/2 in BV is 24hrs

major drawback is that the fluid reaccumulates
what will increase your risk of SBP infection
ascites
what is spontaneous bacterial peritonitis
infection of ascites fluid
what are some of the causative organisms of SBP
enterobacteriaceae
pneumococcus
enterococcus
anaerobes
what is the clinical presentation of SBP
pt more confused
ascites gets worse
variceal bleeding
when is prophylaxis given in SBP
after first attack since it has a high reoccurance and mortality
what is given for acute SBP therapy
ceftriaxone, cefotaxime
beta latams, beta lactamase inhibitors
ertapenem
fluoroquinolone
short term IV albumin to decrease risk of renal failure
what is given for prophylaxis in SBP therapy
Trimethoprim/Sulfamethoxazole (Bactrim) 5 times a week

or

large dose of ciprofloxacin weekly
what is seen in Hepatic encephalopathy
alteration of mental status due to accummulation of metabolites or alteration in BBB

asterixis
what is asterixis
flapping of the hands due to false NT being present due to lack of liver detox
encephalopathy from liver disease leans towards?
somnolence
what is hepatic encephalopathy often associated with
increased ammonia levels

but ammonia levels don't correlate with severity of encephalopathy
what are the precipitating factors of hepatic encephalopathy
excess dietary protein
constipation
azotemia
SBP
GI hemorrhage
electrolyte disturbances
shunts
CNS depressants
what electrolyte disturbance predisposes pt to encephalopathy
hypokalemia
what precipitating factor is a major cause of encephalopathy and why
constipation (due to increased nitrogen load)

causes altered mental status

GI contents sitting in colon giving body more chance to absorb ammonia
why do shunts lead to encephalopathy
move blood from portal vein to IVC thereby bypass livers ability to detox
how do you treat hepatic encephalopathy
dietary protein restriction (1g/kg/day)
lactulose (osmotic laxative)
rifaximin
flumazenil
Zn
how does lactulose treat encephalopathy
prevents and tx constipation
decrease bowel pH (therefore ammonia and other substances not absorbed)
how does rifaximin work
inhibits bacteria that break down protein into smaller absorbable components therefore it keeps protein waste products out of blood
how does flumazenil work
BZD antagonist
if you give flumazenil to a pt and they wake up what does that mean
that the metabolic waste products are acting on the BZD Rc
what are coagulopathies
reduced production of clotting factors and decrease platelet production and function
what are some things that can cause a decrease in clot factors or decrease in platletts
decrease in clotting factors due to decreased synthesis by liver

decrease in platelets due to splenomegally storing platelets or consuming alcohol w/ liver disease
what can cause hepatorenal syndrome
vasoconstriction and decrease perfusion (bleeding/hypovolemia) or infection (SBP this is why you give albumin to maintain IV volume), nephrotoxic drugs (AVOID AT ALL COST AMINOGLYCOSIDES, NSAIDS, BECAREFUL W/ ACE-I/ARB AND DIURETICS)
what type of hepatorenal syndrome will you see a double in SCr within 2 weeks
TYPE 1 - this has a high mortality rate
what is the only definitive treatment for hepatorenal syndrome
transplant
when do you worry about hepatocellular carcinoma
once pt develops cirrhosis

fatal without transplantation
what is the SCr in pt with liver disease
its lower than it should be but you must be careful not to over estimate it in pt with ESLD
what are other antibiotics you can use to tx Encephalopathy
neomycin
metronidazole
what are SE of neomycin
ototoxicity
nephortoxcity
what are SE of metronidazole
disulfram reaction
metalic taste
peripheral neuropathy