(TROPLD)

Ahmed Abdelnabi Fathi

Mohamed

7233395
 portal hypertension
Portal hypertension is elevated blood pressure in
portal vein and the smaller veins that branch off
from it — portal venous system. The portal venous
system drains blood from your stomach, intestines,
pancreas and spleen into liver through the portal
vein. liver filters the blood and then sends it back to
heart and into general circulation in body.

When something blocks or slows the blood flow

through portal vein, it causes increased pressure
throughout portal venous system body attempts to
compensate for this pressure by diverting the blood
flow into other veins. The extra blood flow makes
these veins expand and makes their walls stretch
and weaken. They may leak fluids into abdomen,
and they can also break and bleed.
 Symptoms

The 5 main symptoms of portal hypertension

Up to 90% of people with cirrhosis already have
portal hypertension before they have symptoms.
Up to 40% already have large varices (enlarged
veins). The first noticeable symptoms of portal
hypertension are usually related to new, enlarged,
leaky and bleeding veins, such as:
Blood in vomit.
Blood in poop.
Bloated stomach with rapid weight gain (from
fluid).
Swelling in your legs and feet (edema).
Mental confusion or disorientation.

 Causes of portal hypertension

Cirrhosis of the liver. This is generally the end

stage of chronic liver disease, most commonly
 viral hepatitis C, alcohol-induced hepatitis and
nonalcoholic fatty liver disease.
Granulomas of the liver. Granulomas are
collections of inflammatory cells that
accompany various infections and inflammatory
diseases (such as schistosomiasis). They can
obstruct the portal venous system as benign
tumors and they often precede fibrosis
(scarring) to come later.
Blood clots. Thrombosis in the portal venous
system can obstruct blood flow into the liver,
through the liver or out of the liver. Many
things can cause this, including inherited
diseases.
 Complications of portal hypertension
Ascites.
Gastrointestinal bleeding.
Hypersplenism
Low blood oxygen.
 Kidney failure.
 Diagnosis and Tests
Blood tests can
Imaging tests
Endoscopy

 clinical signs of portal hypertension

suspect portal hypertension if there:

Enlarged varices.
Enlarged spleen.
Gastrointestinal bleeding.
Ascites (fluid in your abdomen).
Signs of mild cognitive impairment.
Low blood cell counts.
Easy bleeding and bruising.
  Management and Treatment
Portal hypertension itself may or may not be
reversible, depending on its cause.
First-line treatments to stop gastrointestinal
bleeding
Medication Beta-blockers can reduce portal
pressure, while vasoconstrictors can help
reduce dilated blood vessels.
Other first-line treatments for complicated
portal hypertension may include:

i. Oxygen therapy for hepatopulmonary

syndrome.
ii. Dialysis for hepatorenal syndrome.
iii. Medication to treat hepatic encephalopathy.
iv. Paracentesis to remove excess fluid from ascites
and test it for peritonitis
 hepatic sinusoids function

A liver sinusoid is a type of capillary known as a

sinusoidal capillary, discontinuous capillary or
sinusoid, having discontinuous endothelium that
serves as a location for mixing of the oxygen-rich
blood from the hepatic artery and the nutrient-rich
blood from the portal vein.

The liver sinusoid has a larger caliber than other

types of capillaries and has a lining of specialized
endothelial cells known as the liver sinusoidal
endothelial cells (LSECs) , and Kupffer cells .The
cells are porous and have a scavenging function.
 The LSECs make up around half of the non-
parenchymal cells in the liver and are flattened and
fenestrated. LSECs have many fenestrae that gives
easy communication between the sinusoidal lumen
and the space of Disse. They play a part in filtration,
endocytosis, and in the regulation of blood flow in
the sinusoids.

The Kupffer cells can take up and destroy foreign

material such as bacteria.
Hepatocytes are separated from the sinusoids by
the space of Disse. Hepatic stellate cells are present
in the space of Disse and are involved in scar
formation in response to liver damage.

Defenestration happens when LSECs are lost

rendering the sinusoid as an ordinary capillary. This
process precedes fibrosis.