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GI > Cirrhosis and Chronic Liver disease > Flashcards

Cirrhosis and Chronic Liver disease Flashcards

1
Q

Natural history of chronic liver disease

A

chronic liver disease –> compensated cirrhosis –> decompensated cirrhosis (variceal hemorrhage, ascites, encephalopathy, jaundice) –> death or liver transplant

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2
Q

Causes of complications from cirrhosis

A

portal hypertension –> variceal hemorrhage, ascites, encephalopathy

liver insufficiency –> encephalopathy, jaundice

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3
Q

in whom should we suspect cirrhosis?

A

any patient with chronic abnormal ALT and/or alk phos

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4
Q

lab signs of liver insufficiency

A

low albumin, prolonged PT/INR, high bilirubin

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5
Q

lab signs of portal hypertension

A

low platelets (less than 150,000)

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6
Q

cirrhosis findings on imaging

A

nodular liver, caudate hypertrophy, ascites, splenomegaly, venous collaterals, HCC

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7
Q

liver biopsy is NOT necessary in the presence of

A

decompensated cirrhosis, CT scan diagnostic of cirrhosis (nodular liver surface)

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8
Q

When should you do a liver biopsy?

A

chronic liver disease without:

variceal hemorrhage/ascites/hepatic encephalopathy + no physical findings of enlarged L hepatic lobe, splenomegaly, or stigmata of CLD + no labs showing thrombocytopenia or impaired hepatic synthetic dysfunction (albumin, PT) + no radiological findings

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9
Q

Purpose of the MELD score

A

estimates risk of 3-month mortality

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10
Q

Components of MELD score

A

serum total bilirubin, serum creatinine, INR

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11
Q

Computing the MELD score

A

6.4 + 9.8 x log (INR) + 11.2 x log (Cr) + 3.8 x log (bilirubin)

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12
Q

Who has the highest priority in organ allocation for liver transplant

A

person with the highest MELD score among those with identical blood types

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13
Q

Two mechanisms of portal hypertension

A

increased resistance to portal flow

increase in portal venous inflow

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14
Q

initial mechanism of portal hypertension in cirrhosis

A

increased intrahepatic resistance in the sinusoids (sinusoidal fibrosis + active vasoconstriction)

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15
Q

mechanism of vasoconstriction in cirrhosis

A

cirrhosis –> reduced endothelial NO –> vasoconstriction and increased resistance

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16
Q

mechanism of increased portal venous inflow

A

cirrhosis –> increased resistance to portal flow –> increased portal pressure –> decreased splanchnic arteriolar resistance (NO release) –> increased portal blood inflow

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17
Q

safest and most reproducible method to measure portal pressure

A

measure the hepatic venous pressure gradient

HVPG = WHVP (wedged hepatic venous pressure) - FHVP (free hepatic venous pressure)

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18
Q

normal values in HVPG equation

A

HVPG = WHVP (5) - FHVP (2) = 3 mm Hg

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19
Q

HVPG in presinusoidal portal hypertension

A

normal (3 mmHg)

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20
Q

HVPG in sinusoidal portal hypertension

A

elevated (~18 mmHg)

WHVP ~20 mmHg

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21
Q

HVPG in post-sinusoidal portal hypertension

A

elevated (~18 mmHg)

WHVP = ~20 mmHg

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22
Q

HVPG in post-hepatic (heart failure) portal hypertension

A

normal

WHVP = 20
FHVP = 18
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23
Q

portal hypertension with normal HVPG

A

pre-hepatic, pre-sinusoidal, post-hepatic

24
Q

major determinent of variceal rupture

A

variceal wall tension

= transmural pressure x (radius/wall thickness)

25
Q

management of increased resistance to portal flow

A

TIPS (transjugular intrahepatic portosystemic shunt)

26
Q

management of increased portal blood inflow

A

vasoconstrictors (octreotide) –> increased splanschnic arteriolar resistance

27
Q

management of varices/variceal hemorrhage

A

beta blockers

variceal ligation, if contraindicated for beta blockers

28
Q

most common cause of ascites

A

cirrhosis (80%)

29
Q

mechanism of ascites development

A

portal hypertension –> shear stress –> NO increase –> vasodilation –> activation of RAAS –> Na and water retention –> ascites

30
Q

most sensitive method for detection of ascites

A

abd US

31
Q

routine ascites fluid analysis

A

albumin, protein, PMN cell count, cultures

32
Q

indications for diagnostic paracentesis

A

new-onset ascites, admission to hospital, s/sx of SBP, renal dysfunction, unexplained encephalopathy

33
Q

mechanism of refractory ascites caused by cirrhosis

A

cirrhosis –> increased intrahepatic resistance –> increased sinusoidal pressure –> refractory ascites

cirrhosis –> decreased systemic arteriolar resistance –> decreased effective arterial blood volume –> increased activation of RAAS –> Na and water retention –> refractory ascites

34
Q

treatment of uncomplicated ascites

A

salt restriction + diuretics

large volume paracentesis with tense ascites

35
Q

treatment of refractory ascites

A

LVP + albumin

TIPS (decrease sinusoidal pressure, increase effective arterial blood volume)

36
Q

characteristics of hepatorenal syndrome

A

functional renal failure in patients with cirrhosis

marked arteriolar vasodilation in extra-renal circulation

renal vasoconstriction –> reduced GFR

37
Q

Type 1 hepatorenal syndrome

A

rapidly progressive renal failure, creatinine > 2.5 or CrCl less than 20 ml/min

38
Q

Type 2 hepatorenal syndrome

A

more slowly progressive, creatinine > 1.5 or CrCl lower than 40 ml/min

39
Q

which type of hepatorenal syndrome is associated with refractory ascites?

A

Type 2

40
Q

pathogenesis of hepatorenal syndrome

A

cirrhosis –> decreased arteriolar resistance –> decreased effective arterial blood volume –> increased activation of RAAS –> increased renal vasoconstriction –> hepatorenal syndrome

41
Q

natural history of hepatorenal syndrome

A

type 2 –> spontaneous bacterial peritonitis –> type 1

42
Q

Major criteria for dx of hepatorenal syndrome

A

advanced hepatic failure and portal HTN
Creatinine > 1.5 or CrCl lower than 40
Absence of shock, bacterial infection or nephrotoxic drugs
Absence of excessive GI or renal fluid loss
No improvement in renal function after 1.5L of isotonic saline
Urinary protein less than 500 and normal renal US

43
Q

Always present in HRS

A

ascites and hyponatremia

44
Q

Management of HRS

A

liver transplant

45
Q

Most common infection in cirrhotic patients

A

spontaneous bacterial peritonitis

46
Q

Mechanism of SBP

A

bacterial translocation: intestinal dysmotility –> bacterial overgrowth –> increased intestinal permeability –> impaired immunity –> transient bacteremia –> prolonged bacteremia –> ascites colonization –> SBP

47
Q

paracentesis –> PMN count > 250

A

SBP

48
Q

Which organisms are most often isolated in SBP

A

G- bacilli (E coli, Klebsiella), G+ cocci (Strep)

49
Q

Initial empiric therapy of SBP

A 
IV cefotaxime, augmentin
oral ofloxacin (uncomplicated SBP)
50
Q

When is SBP more likely to occur?

A

in patients with low-protein ascites

51
Q

Characteristics of hepatic encephalopathy

A

failure to metabolize neurotoxic substances (increased ammonia –> glutamine accumulation) + altered astrocyte morphology and function (astrocytes are the only brain cells that can metabolize ammonia) (Alzheimer’s Type 2 astrocytosis)

52
Q

Pathophys of hepatic encephalopathy

A

increased ammonia –> cross BBB –> upregulation of astrocytic peripheral benzodiazepine receptors (PBR) –> neurosteroid production –> modulation of GABA-a receptor –> cortical depression –> hepatic encephalopathy

53
Q

Diagnosis of hepatic encephalopathy

A

Clinical findings and history

ammonia levels are unreliable and poorly correlate with diagnosis

54
Q

Hepatic encephalopathy precipitants

A

excess protein, GI bleeding, sedatives/hypnotics, diuretics, TIPS, sepsis, azotemia caused by hypokalemia

55
Q

treatment of hepatic encephalopathy

A

identify and treat precipitating factor, lactulose, short-term protein restriction

56
Q

mechanism of lactulose

A

lowers colon pH –> converts ammonia to ammonium –> ammonium excreted in feces, increased cathartic effect

GI (19 decks)

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