Portal Hypertension Flashcards
HVPG typically present in ascites
at least 8 mm HG
HVPG typically seen in Variceal bleeding
> 10-12 mm Hg
Classifications of Portal Hypertension
- Pre-hepatic - tumors, thrombosis, atresia, etc
- hepatic - cirrhosis, fibrosis (Wilson, hemochromatosis)
- Post-hepatic (Budd-Chiari, CHF, Constrictive pericarditis)
Characteristics of refractory ascites
- does not respond to diuretics
- oliguria
- reduction in Na excretion
1 year mortality rate of refractory ascites
50% die in 1 year
MELD Score a/w good prognosis in TIPS
MELD Score a/w poor prognosis in TIPS
MELD score that would contraindicate TIPS
<18
>18 but <24
>24
amount of protein lost in 10 liters of ascites
200 g (20 g/L)
Purpose of Child-Pugh Score
- assess the prognosis of chronic liver disease and cirrhosis.
- Originally developed in 1973 to predict surgical outcomes in patients presenting with bleeding esophageal varices
- The score is used with the Model for End-Stage Liver Disease (MELD) to determine priority for liver transplantation.
normal Portal Vein Pressure
5-10 mm Hg
- two main types of cirrhosis
- two main complications of decompensated cirrhosis
- compensated and decompensated
- portal hypertension and liver insufficiency
- HVPG for portal htn
- clinically significant HVPG
- HVPG for risk of variceal bleeding and ascites
- HVPG for variceal bleeding unlikely to respond to conventional medical therapy
- HPVG >6
- HVPG> 10
- HVPG> 12
- HVPG> 20
2 components causing the pathophysiology of portal htn
- Fixed component: sinusoidal fibrosis and compression by regenerative nodules
- reversible component: vasoconstriction (deficiency in intrahepatic NO and enhanced activity of vasoconstriction)
how are liver sinusoidal endothelial cells affected in portal htn
- liver sinusoidal endothelial cells lose their fenestrae in cirrhosis and a fibrous basement membrane develops “capillarization”
- VEGF is necessary for maintaining fenestrae
- VEGF function is dependent on NO production
in portal htn, how does deficient NO activity in the liver affected the mesenteric vasculature
it causes mesenteric arteriolar vasodilation and therefore increased portal venous inflow
- you’ll have splanchnic and systemic vasodilation (your body wants to counteract the intrahepatic vasoconstriction and creates vasodilators outside the liver)
contraindications to beta blockers
- symptomatic bradycardia
- av block
- decompensated heart failure
- asthma