Cirrhosis and Portal HTN Flashcards
increased resistance in cirrhosis is due to
reduction in sinusoidal radius
initial MOA leading to portal HTN in cirrhosis
increased intrahepatic resistance
in portal HTN, splanchnic vasodilation results from an inc in
nitric oxide
backward theory of portal HTN (R)
intrahepatic vascular tree distorted by fibrosis, etc
portal HTN foley a consequence of inc vascular resistance
forward theory of portal HTN (Q)
portal HTN maintained by inc splanchnic flow despite collaterals
portal HTN is the result of increases in both
- resistance to portal flow
2. portal venous inflow
safest and most reproducible method of portal pressure
hepatic venous pressure gradient (HVPG)
HVPG=
HVPG=WHVP-FHVP
normal HVPG value
3-5mmHg
HPVG is inc or dec in sinusoidal portal HTN
increased
post-sinusoidal portal HTN
centrilobular fibrosis (VOD)
comm w/ BM transplantation, radiation to whole bod
acute variceal bleed
pharm tx
goal: reduce portal P
agents: somatostatin/ocreotide, non-specific beta blockers
acute variceal bleed
Non-pharm tx?
sengstaken-blakemore tube
(apply pressure to open wound) temporizing measure
endoscope (obstruct BF) sclerotherapy, band ligation, TIPS
peripheral vasodilation occurs as the result of
dec hepatic Cl of vasodialtors such as glucagon and NO
best for classifying ascites into portal/non-portal hypertensive causes
Serum Ascites Albumin Gradient
SAAG
contraindications to dx paracentesis for ascites
none
TIPS (transjugular intrahepatic portosystemic shunt)
creation of a direct connection between the portal vein and hepatic vein through the parenchyma of the liver
used in managing ascites
hepatorenal syndrome
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
hepatorenal syndrome 2 types
- progressive rapid renal failure
2. more slowly progressive
major criteria to dx hepatorenal syndrome
- 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
which two conditions are always present in hepatorenal syndrome?
ascites and hyponatremia
dec arteriolar resistance (vasodilatation) caused by cirrhosis leads to the activation of which systems
RAAS, epinephrine, ADH
hepatic encephalopathy dx is made by the presence of which neurological features
asterisks (flapping)
constructional apraxia
abnormal EEG (slowing)
hepatic encephalopathy MOA
- inc ammonia
- inc GABA
- inc endogenous benzo –> enhanced GABA inhib neurotramsmission
stages of hepatic encephalopathy
- mild confusion/incoordination, inverted sleep
- personality changes, asterixis
- somnolent, gross disorientation, hyperreflexia, Babinski
- coma, no pain response
T/F
Ammonia levels are used to dx hepatic encephalopathy
F. they are unreliable
hepatic encephalopathy precipitants
xs protein Gi bleeding sedatives/hyponotics TIPS Temp, infections Diuretics
hepatic encephalopathy tx
ID/treat precipitating factor
lactulose
rifaximin (*not absorbed)
protein restriction (short term)
lactulose
dec pH –> alters metabolism of intestinal microflora –> decreased ammonia prod in gut
inc cathartic effect
MELD score (assesses severity of advanced liver disease) takes into account which fx?
Sodium, PT/INR, Total bilirubin, and Creatinine
