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Emma GI > Cirrhosis and Portal HTN > Flashcards

Cirrhosis and Portal HTN Flashcards

1
Q

increased resistance in cirrhosis is due to

A

reduction in sinusoidal radius

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2
Q

initial MOA leading to portal HTN in cirrhosis

A

increased intrahepatic resistance

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3
Q

in portal HTN, splanchnic vasodilation results from an inc in

A

nitric oxide

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4
Q

backward theory of portal HTN (R)

A

intrahepatic vascular tree distorted by fibrosis, etc

portal HTN foley a consequence of inc vascular resistance

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5
Q

forward theory of portal HTN (Q)

A

portal HTN maintained by inc splanchnic flow despite collaterals

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6
Q

portal HTN is the result of increases in both

A
  1. resistance to portal flow

2. portal venous inflow

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7
Q

safest and most reproducible method of portal pressure

A

hepatic venous pressure gradient (HVPG)

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8
Q

HVPG=

A

HVPG=WHVP-FHVP

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9
Q

normal HVPG value

A

3-5mmHg

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10
Q

HPVG is inc or dec in sinusoidal portal HTN

A

increased

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11
Q

post-sinusoidal portal HTN

A

centrilobular fibrosis (VOD)

comm w/ BM transplantation, radiation to whole bod

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12
Q

acute variceal bleed

pharm tx

A

goal: reduce portal P
agents: somatostatin/ocreotide, non-specific beta blockers

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13
Q

acute variceal bleed

Non-pharm tx?

A

sengstaken-blakemore tube
(apply pressure to open wound) temporizing measure

endoscope (obstruct BF) sclerotherapy, band ligation, TIPS

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14
Q

peripheral vasodilation occurs as the result of

A

dec hepatic Cl of vasodialtors such as glucagon and NO

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15
Q

best for classifying ascites into portal/non-portal hypertensive causes

A

Serum Ascites Albumin Gradient

SAAG

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16
Q

contraindications to dx paracentesis for ascites

A

none

17
Q

TIPS (transjugular intrahepatic portosystemic shunt)

A

creation of a direct connection between the portal vein and hepatic vein through the parenchyma of the liver

used in managing ascites

18
Q

hepatorenal syndrome

A

renal failure in pt w/ cirrhosis, advanced liver failure and severe sinusoidal portal hypertension

absence of significant histo changes in kidney

marked arteriolar vasodilation in extra-renal circulation

marked renal vasoconstriction leading to reduced glomerular filtration rate

19
Q

hepatorenal syndrome 2 types

A
  1. progressive rapid renal failure

2. more slowly progressive

20
Q

major criteria to dx hepatorenal syndrome

A
  • advanced hepatic failure and portal HTN
  • creatinine >1.5 or Cr Cl <40 ml/min
  • absence of shock, bacteria infection, nephrotoxic drugs
  • absence of xs GI or renal fluid loss
  • no improvement in renal function after plasma volume expansion of IV albumin x2d
  • urinary protein <500 mg/dL, normal renal US
21
Q

which two conditions are always present in hepatorenal syndrome?

A

ascites and hyponatremia

22
Q

dec arteriolar resistance (vasodilatation) caused by cirrhosis leads to the activation of which systems

A

RAAS, epinephrine, ADH

23
Q

hepatic encephalopathy dx is made by the presence of which neurological features

A

asterisks (flapping)

constructional apraxia

abnormal EEG (slowing)

24
Q

hepatic encephalopathy MOA

A
  • inc ammonia
  • inc GABA
  • inc endogenous benzo –> enhanced GABA inhib neurotramsmission
25
Q

stages of hepatic encephalopathy

A
  1. mild confusion/incoordination, inverted sleep
  2. personality changes, asterixis
  3. somnolent, gross disorientation, hyperreflexia, Babinski
  4. coma, no pain response
26
Q

T/F

Ammonia levels are used to dx hepatic encephalopathy

A

F. they are unreliable

27
Q

hepatic encephalopathy precipitants

A 
xs protein
Gi bleeding 
sedatives/hyponotics 
TIPS
Temp, infections
Diuretics
28
Q

hepatic encephalopathy tx

A

ID/treat precipitating factor
lactulose
rifaximin (*not absorbed)
protein restriction (short term)

29
Q

lactulose

A

dec pH –> alters metabolism of intestinal microflora –> decreased ammonia prod in gut

inc cathartic effect

30
Q

MELD score (assesses severity of advanced liver disease) takes into account which fx?

A

Sodium, PT/INR, Total bilirubin, and Creatinine

Emma GI (18 decks)

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