THE HEPATIC PORTAL SYSTEM

The Hepatic Portal System

Introduction:
Portal System begins in the capillaries of the digestive organs and ends in the portal vein. Consequently, portal blood contains substances absorbed by the stomach and intestines. Portal blood is passed through the hepatic lobules where nutrients and toxins are absorbed, excreted or converted. Restriction of outflow through the hepatic portal system can lead to portal hypertension.

The liver is unusual in that it has a double blood supply:

1. The right and left hepatic arteries carry oxygenated blood to the liver
2. The portal vein carries venous blood from the GI tract to the liver.

The venous blood from the GI tract drains into the superior and inferior mesenteric veins; these two vessels are then joined by the splenic vein just posterior to the neck of the pancreas to form the portal vein. This then splits to form the right and left branches, each supplying about half of the liver.On entering the liver, the blood drains into the hepatic sinusoids, where it is screened by specialised macrophages (Kupffer cells) to remove any pathogens that manage to get past the GI defences. The plasma is filtered through the endothelial lining of the sinusoids and bathes the hepatocytes; these cells contain vast numbers of enzymes capable of braking down and metabolising most of what has been absorbed.

The portal venous blood contains all of the products of digestion absorbed from the GI tract, so all useful and non-useful products are processed in the liver before being either released back into the hepatic veins which join the inferior vena cava just inferior to the diaphragm, or stored in the liver for later use.


The venous blood from the GI tract drains into the superior and inferior mesenteric veins; these two vessels are then joined by the splenic vein just posterior to the neck of the pancreas to form the portal vein.

This then splits to form the right and left branches, each supplying about half of the liver.On entering the liver, the blood drains into the hepatic sinusoids, where it is screened by specialised macrophages (Kupffer cells) to remove any pathogens that manage to get past the GI defences. The plasma is filtered through the endothelial lining of the sinusoids and bathes the hepatocytes; these cells contain vast numbers of enzymes capable of breaking down and metabolising most of what has been absorbed.

The portal venous blood contains all of the products of digestion absorbed from the GI tract, so all useful and non-useful products are processed in the liver before being either released back into the hepatic veins which join the inferior vena cava just inferior to the diaphragm, or stored in the liver for later use.

Chronic liver injury results in activation of stellate cells within the space of Disse. This leads to the deposition of collagen and in time histologic changes of cirrhosis.
Cirrhosis also results in endothelial dysfunction and increased in resistance to flow within the hepatic sinusoids.

Sinusoidal hypertension and endothelial dysfunction produce Portal hypertension.

Three cardinal features:

1. Increased resistance to mesenteric vascular flow
2. Activation of the renal-angiotensin-aldosterone system resulting in Na and water retention and increased intravascular volume.
3. Increased mesenteric blood flow as a consequence of a hyperdynamic circulation.


Portal hypertension is responsible for the 5 complications of chronic liver disease:

1. Gastrointestinal bleeding

2. Ascites

3. Portosystemic encephalopathy

4. Hepato renal syndrome

5. Pulmonary disease:
a. Hepatopulmonary syndrome
b. Portopulmonary hypertension

The consequences of portal hypertension are due to portal systemic anastomosis formed by the body as an attempt to bypass the obstructed liver circulation. These collateral vessels form along the falciform ligament, diaphragm, spleen, stomach and peritoneum. The collaterals find their way to the renal vein where blood drained from the digestive organs is let into the systemic circulation.