Portal Hypertension Questions

Q1 Which is not true regarding physiology of portal hypertension?
a) Both the portal blood flow as well as portal resistance increases
b) There is extensive hyperdynamic circulation
c) Blood flow towards the portal vein increases because the systemic venous pressure increases.

d) Splanchnic vasodilatation is caused by relaxation of splanchnic arterioles and  splanchnic hyperemia

Q2.False about site of porto systemic collaterals in portal hypertension is
a)  Rectal Varices- Where Inferior mesenteric vein meets  vein
b)   veins- Comunication between the iliac and renal veins
c) Umbilicus- Obliterated umbilical vein and Left portal vein

d)  Varices in  lower esophagus and stomach

Q3 Treatment of Choice for gastric varices is
a) Sclerotherapy
b) Band Ligation
c) Transjugular Intrahepatic Portosystemic Shunt
d) Application of cyanoacrylate glue

e) Shunt Surgery

Q4. Most Accurate and clinically useful Measurement of Portal vein pressure is
a)  Hepatic venous pressure gradient (HVPG)
b) Direct measurement of portal pressure
c) Splenic pulp pressure

d) Wedged hepatic vein pressure

Q5. False statement regarding endoscopic management of varices
a) All patients with cirrhosis should undergo screening endoscopy.
b) If  no varices are found endocscopy should be done every 2-3 years

c) Endoscopy screening may be more cost effective than endoscopic screening

1. c
Both the portal flow and resistance increases in portal hypertension, one exception is AV fistulas in which only the portal flow increases. The portal resistance increases because of cirrhosis.
The increase in hepatic resistance results from mechanical factors in combination with dynamic vasoconstriction mediated by increased nitric oxide (NO) production and increased endothelin-1 (ET-1) production from the hepatocyte endothelium.
There is hyperdynamic circulation which means peripheral and splanchnic vasodilatation, reduced mean arterial pressure, and increased cardiac output.
The flow toward the portal circulation is reversed in portal hypertension because the increased portal pressure exceeds systemic venous pressure. Therefore, flow is reversed in these collateral vessels, and blood flows out of the portal circulation toward the systemic venous circulation.

Ref:Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 9th ed.

 2) b

The sites of collateral formation are the rectum, where the inferior mesenteric vein connects with the pudendal vein and rectal varices develop; the umbilicus, where the vestigial umbilical vein communicates with the left portal vein and gives rise to prominent collaterals around the umbilicus (caput medusae); the retroperitoneum, where collaterals, especially in women, communicate between the ovarian vessels and iliac veins; and the distal esophagus and proximal stomach, where gastroesophageal varices are the major collaterals formed between the portal venous system and systemic venous system.

 3. d
Controlled studies evaluating pharmacologic therapy for gastric variceal bleeding are lacking, the agents used are based on extension of the data relating to esophageal varices. Medical management with vasoactive agents should be started as early as possible, preferably at least 30 minutes before endoscopic therapy is carried out. The preferred endoscopic therapy for fundal gastric variceal bleeding is injection of polymers of cyanoacrylate, usually N-butyl-2-cyanoacrylate,. Obliteration of the varices occurs when the injected cyanoacrylate adhesive hardens on contact with blood. The mucosa overlying the varix eventually sloughs, and the hardened polymer is extruded. Fortunately, the resulting ulcers occur late, and the risk of bleeding is lower than that associated with sclerotherapy-related ulcers. Cyanoacrylate injection has been found to be superior to both variceal band ligation and sclerotherapy using alcohol.Complications of cyanoacrylate injection include bacteremia and variceal ulceration. Pulmonary and cerebral emboli have been reported on occasion, usually in patients with spontaneous large portosystemic or intrapulmonary shunts. The endoscope may be damaged by the glue, but the risk is minimized if silicone gel is used and suction is avoided for 15 to 20 seconds following injection
Ref:Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 9th ed.
Read about esophageal varices here
4) a
The HVPG has been used to assess portal hypertension since its first description in 195. It is the difference between the wedged hepatic vein pressure and free hepatic vein pressure. Wedged hepatic vein pressure- requires passage of a catheter into the hepatic vein under radiologic guidance until the catheter can be passed no further, that is, until the catheter has been “wedged” in the hepatic vein. It measures the sinusoidal pressure.
The most important thing to note is that HVPG is 0 in cases of extrahepatic (presinusoidal) portal hypertension.
The current consensus is that all patients with cirrhosis of the liver should be screened for esophageal varices by endoscopy. In patients in whom no varices are detected on initial endoscopy, endoscopy to look for varices should be repeated in 2 to 3 years. If small varices are detected on the initial endoscopy, endoscopy should be repeated in 1 to 2 years.
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