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Clinical 2.0 winter > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

top two causes

A

chronic alcohol abuse

chronic hep C

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2
Q

5 complications

A 
portal hypertension
esophageal and gastric varices with risk of variceal bleeding
ascites
spontaneous bacterial peritonitis 
hepatic encephalopathy
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3
Q

what is portal hypertension

A

increased BP in the portal venous system

hepatic venous pressure gradient >5mmHG

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4
Q

how does portal hypertension develop

A

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

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5
Q

what causes varices

A

portal hypertension with HVPG>10mmHg

small veins in lower esophagus and stomach become distended as blood is redirected

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6
Q

what is ascites

A

accumulation of fluid in the peritoneal cavity

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7
Q

what causes ascites

A

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

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8
Q

definition of spontaneous bacterial peritonitis

A

infection of ascitic fluid without an obvious surgically treatable source

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9
Q

how does spontaneous bacterial peritonitis occur

A

bacteria from GI tract end up in ascitic fluid

exact mechanism not know

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10
Q

common bacteria in SBP

A

ecoli
kpneumoniae
pneumococci

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11
Q

how does hepatic encephalopathy occur

A

decreased liver function and shunting of blood around the liver causes neurotoxins to accumulate, affects brain function
most commonly ammonia

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12
Q

diagnosing cirrhosis

A

signs and symptoms
lab values, endoscopy, radiographic tests
biopsy not necessary

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13
Q

symptoms of cirrhosis

A 
weight loss
fatigue
anorexia
jaundice
impotence
abdominal distention
confusion 
pruitis
GI bleed
dark colored urine
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14
Q

physical signs of cirrhosis

A 
hepatomegaly
splenomegaly 
spider angiomata
caput medusa
digital clubbing
gynecomastia
jaundice
asterix - hand flap 
ascites 
fector hepaticus - sweet smelling breath
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15
Q

lab indicating alcoholic liver disease

A

AST:ALT 2:1

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16
Q

labs that can be abnormal in cirrhosis

A 
elevated aminotransferase
elevated alkaline phosphatase with GGT rise 
decreased serum albumin 
elevated INR
hyperbilitubinemia
increased serum creatinine
hyponatremia 
thrombocytopenia, leukopenia
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17
Q

abnormal radiographic tests

A

ultrasonography - detects hepatic nodules, ascites

CT, MRI - detect hepatic nodules, ascites, varices

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18
Q

child pugh classification used for

A

recommending drug dosage adjustments

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19
Q

model for end stage liver disease score used for

A

allocation of liver transplants

predicts 3 month mortality

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20
Q

grade A child pugh

A

<7points

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21
Q

grade B child pugh

A

7-9 points

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22
Q

grade C child pugh

A

> 9 points

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23
Q

treat patients with no varices or small varices with no risk factors ?

A

no

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24
Q

what are risk factors for variceal hemorrhage

A

red wales

child pugh score C

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25
Q

treat small varices with risk factors for variceal hemorrhage?

A

yes with non selective beta blocker

26
Q

treat medium to large varices with no bleeding?

A

yes with non selective beta blocker

27
Q

what to treat varices with if have asthma or diabetes (beta blocker intolerant)

A

endoscopic variceal ligation - banding

28
Q

non selective beta blocker options

A

propranolol 20mg BID
nadolol 20mg daily
carvediol 6.25 BID

29
Q

monitoring of non selective beta blockers

A

titrate every 3 days to HR 55-6o bbp

30
Q

when do you stop beta blocker therapy for varices

A

when in end stage liver disease

31
Q

beta blocker MOA

A

decrease portal venous inflow by decreasing cardiac output - beta1
decreasing splanchnic blood flow - beta2

32
Q

treatment of acute variceal bleeding

A

maintain BP with fluids, control bleeding
octreotide asap
endoscopic variceal ligation
prophylaxis for SBP

33
Q

what to do if still bleeding after octreotide and EVL

A

transjugular intrahepatic portosystemic shunt

34
Q

octreotide dosing

A

50mcg IV then 50mcg/hr IV continuous x 3-5days

35
Q

octreotide mechanism

A

inhibits vasodilatory glucagon and has local splanchnic vasoconstrictive effect

36
Q

prophylaxis treatment for SBP durign acute variceal bleeding

A

cipro or ceftriaxone for 7 days

37
Q

what is a transjugular intrahepatic portosystemic shunt

A

shunt that bypasses the liver

38
Q

secondary prophylaxis of varices to prevent rebleed

A

non selective beta blocker + chronic EVL

if had TIPS possible liver transplant candidate

39
Q

things to do for diagnosing of ascites

A

measure cell count, ascitic fluid total protein, ascitic fluid cultures
calculate serum asciteis albumin gradient (serum albumin - ascitic fluid albumin)

40
Q

diagnosis of ascites

A

SAAG >11g/L

41
Q

treatment of ascites

A

furosemide 40 + spironolactone 100

42
Q

non pharm for ascites

A

restrict salt <2g/day
fluid too if hyponatremia
avoid nsaids, acei

43
Q

monitoring of ascites treament

A

titrate diuretics up every 3-5 days for 0.5kg weight loss daily
monitor potassium and serum creatinine

44
Q

treatment for ascites resistent to diuretics

A

therapeutic paracentesis

45
Q

presentation of SBP

A

fever, ab pain, encephalopathy, confusion, renal failure

46
Q

diagnoses of SBP

A

PMN >250cells/mm3 and positive ascitic fluid bacterial cultures

47
Q

when to treat SBP

A

treat empirically (before culture back) if PMN >250 or signs/sx of infection

48
Q

treatment of SBP

A

3rd generation cephalosporins perferred

quinolone second line

49
Q

why cefotaxime is preferred over ceftriaxone

A

less bound to proteins in the blood and more easily passed into acidic fluid

50
Q

cefotaxime treatment SBP dosing

A

2g IV q8h

5 day treatment course

51
Q

long term prophylaxis after SBP episode

A

septra lower dosing than standard treatment

ex septra DS 5x a week

52
Q

precipitating factors for hepatic encephalopathy

A

electrolyte abnormalities - dehydration, diuretic overuse
infection
GI bleeding
constipation

53
Q

mainstay of hepatic encephalopathy treatment

A

reduce ammonia levels

54
Q

first line for hepatic encephalopathy

A

lactulose - non absorbable disaccharide

55
Q

how often to give lactulose and preferred route

A

q1hr

oral

56
Q

mechanism of lactulose lowering ammonia

A

laxative effect - less time for systemic ammonia absorption from gut
decreased pH so charged NH4+ cations trapped in acidic colon

57
Q

titration for lactulose

A

3 soft stools daily

58
Q

monitoring for lactulose

A

3 soft stools dialy

improved mental status

59
Q

rifaximin MOA

A

porrly absorbed antibiotic

reduces ammonia producing bacteria in the gut

60
Q

when to use rifaximin

A

with lactulose in recurrent HR not responding to max tolerated lactulose

61
Q

why arent neomycin and metro use anymore

A

higher risk of side effects

Clinical 2.0 winter (28 decks)

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