Portal hypertension

Portal hypertension

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Portal hypertension is increased blood pressure over 12 mmHg in the portal system and is frequently associated with esophageal varices and ascites formation. Cirrhosis of the liver is the predominant cause.
Portal vein drains blood from the pancreas, intestines, gallbladder, spleen and stomach. Superior mesenteric vein and splenic vein unite behind the pancreatic neck and form the portal vein. Venous port trunk divides into two lobar veins. The cystic vein drains right and the left umbilical vein and receives paraombilicale that cause hypertension and increase in umbilical veins. Coronary veins which run along the small curvature of the stomach receives the distal esophagus that enlarge the veins also form esophageal varices.
Esophageal varices are the most common complication associated with the development of portal hypertension. Approximately 90% of patients with cirrhosis develop varices and 30% of them singereaza. The first bleeding episode is estimated to have a mortality of 30-50%. Predominant cause of portal hypertension is cirrhosis or liver scarring. Cirrhosis results in healing injuries caused by hepatitis, alcohol abuse, hepatotoxic drugs or other causes. Fibrous tissue that forms blocks blood flow through the liver and slows its functions.
Common symptoms include: gastrointestinal hemorrhage, melena stools, haematemesis, ascites, encephalopathy, confusion, memory loss.
Portal hypertension is diagnosed by endoscopic examination, radiology and laboratory tests to confirm variceal hemorrhage. Most cases of hypertension can be treated. Therapy is directed toward prevention or control of complications. Diet, medications, endoscopic therapy, surgery and radiological procedures all have a role in the management of complications of portal hypertension.
Pathogenesis
There are two important factors in the pathology of portal hypertension: leaking blood flow and vascular resistance. In most types of portal hypertension factoir both are affected.
Increased vascular resistance is initially trigger factor. This is caused by increased blood viscosity, hematocrit and decrease that is diametrically radius of the lumen of blood vessels. In cirrhosis, portal hypertension, portal hypertension is the sine and impaired hepatic microcirculation. Increased vascular resistance in liver cirrhosis is not only a mechanical consequence of changing the architecture of the liver, but also a dynamic component due to active contraction miofibroblastilor, activated stellate cells and vascular smooth muscle cells of hepatic veins. Endogenous factors and pharmaceutical agents that modify the dynamic component include those which increase vascular resistance: endothelin, alpha-adrenergic stimuli and angiotensin II, and those who fall: nitric oxide, prostacyclin and vasodilator drugs.
Increased portal blood flow The second factor contributing to the pathogenesis of portal hypertension. It is caused by dilation of blood vessels by releasing excessive splanhice endogenous vasodilators. Increased portal blood flow in portal hypertension worsens despite portosistemice collateral formation may deviate more than 80% of portal blood. Manifestations include greater vasodilation splanhice venous cardiac output, hypotension and hypervolaemia.
Pathophysiological Consequences Developing or enhancing portocave anastomoses: -Cardio-esophageal varices, resulting in the occurrence of esophageal and cardiotuberozitare can ever bleeding in the evolution of portal hypertension -Responsible for hemorrhoids hemorrhoid- -Abdominal skin-based supraombilical frequently at the anterior chest and periombiliacal "Medusa head."
Splenomegaly is the result of mechanical distension by blood stasis. It is always present, or may be associated with hypersplenism and may decrease the volume after upper digestive hemorrhage.
The decrease of portal blood flow to the liver and consequently decreased oxygen and nutrients eventually may lead to a hepatocellular failure.
Better appearance by overproduction lymphatic ascites, transsudarea determine the liver capsule.