Portal Hypertension

Question 1

HVPG typically present in ascites

Answer 1

at least 8 mm HG

Question 2

HVPG typically seen in Variceal bleeding

Answer 2

> 10-12 mm Hg

Question 3

Classifications of Portal Hypertension

Answer 3

1. Pre-hepatic - tumors, thrombosis, atresia, etc
2. hepatic - cirrhosis, fibrosis (Wilson, hemochromatosis)
3. Post-hepatic (Budd-Chiari, CHF, Constrictive pericarditis)

Question 4

Characteristics of refractory ascites

Answer 4

1. does not respond to diuretics
2. oliguria
3. reduction in Na excretion

Question 5

1 year mortality rate of refractory ascites

Answer 5

50% die in 1 year

Question 6

MELD Score a/w good prognosis in TIPS
MELD Score a/w poor prognosis in TIPS
MELD score that would contraindicate TIPS

Answer 6

<18
>18 but <24
>24

Question 7

amount of protein lost in 10 liters of ascites

Answer 7

200 g (20 g/L)

Question 8

Purpose of Child-Pugh Score

Answer 8

1. assess the prognosis of chronic liver disease and cirrhosis.
2. Originally developed in 1973 to predict surgical outcomes in patients presenting with bleeding esophageal varices
3. The score is used with the Model for End-Stage Liver Disease (MELD) to determine priority for liver transplantation.

Question 9

normal Portal Vein Pressure

Answer 9

5-10 mm Hg

Question 10

1. two main types of cirrhosis
2. two main complications of decompensated cirrhosis

Answer 10

1. compensated and decompensated
2. portal hypertension and liver insufficiency

Question 11

1. HVPG for portal htn
2. clinically significant HVPG
3. HVPG for risk of variceal bleeding and ascites
4. HVPG for variceal bleeding unlikely to respond to conventional medical therapy

Answer 11

1. HPVG >6
2. HVPG> 10
3. HVPG> 12
4. HVPG> 20

Question 12

2 components causing the pathophysiology of portal htn

Answer 12

1. Fixed component: sinusoidal fibrosis and compression by regenerative nodules
2. reversible component: vasoconstriction (deficiency in intrahepatic NO and enhanced activity of vasoconstriction)

Question 13

how are liver sinusoidal endothelial cells affected in portal htn

Answer 13

• 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

Question 14

in portal htn, how does deficient NO activity in the liver affected the mesenteric vasculature

Answer 14

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)

Question 15

contraindications to beta blockers

Answer 15

1. symptomatic bradycardia
2. av block
3. decompensated heart failure
4. asthma

Question 16

what are target hemoglobin levels for variceal hemorrhage

Answer 16

7-8 g/dL; 9-11 g/dL have been shown to hvae increase mortality

Question 17

treatment summary of esophageal variceal bleeding

Answer 17

1. antibiotics
2. octreotide
3. Transfuse Hb 7-8
4. EGD
5. blakemore/TIPS when non-responsive