User:Skam1279/Portal hypertension

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Portal hypertension is defined as increased portal venous pressure, with a hepatic venous pressure gradient greater than 5 mmHg. Normal portal pressure is 1-4mmHg; clinically insignificant portal hypertension is present at portal pressures 5-9mmHg; clinically significant portal hypertension is present at portal pressures greater than 10mmHg. The portal vein and its branches, supply most of the blood and nutrients from the intestine to the liver.

Cirrhosis (a form of chronic liver failure) is the most common cause of portal hypertension; other, less frequent causes are grouped as non-cirrhotic portal hypertension. The signs and symptoms of both cirrhotic and non-cirrhotic portal hypertension are often similar depending on cause, with patients presenting with abdominal swelling due to ascites, vomiting of blood, and lab abnormalities such as elevated liver enzymes or low platelet counts.

Treatment is directed towards decreasing portal hypertension itself or in the management of its acute and chronic complications.[citation needed] Complications include ascites, spontaneous bacterial peritonitis, variceal hemorrhage, hepatic encephalopathy, hepatorenal syndrome, and cardiomyopathy.

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SIGNS & SYMPTOMS SECTION

Signs and symptoms of portal hypertension include:


 * Ascites (free fluid in the peritoneal cavity) -- abdominal swelling and tightness
 * Vomiting blood (hematemesis) from gastric or esophageal varices
 * Anorectal varices
 * Increased spleen size (splenomegaly), which may lead to lower platelet counts (thrombocytopenia)
 * Swollen veins on the anterior abdominal wall (referred to as caput medusae)

In addition, a widened (dilated) portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff value of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well.

PATHOPHYSIOLOGY SECTION


 * cirrhotic portal hypertension
 * The pathophysiology of cirrhotic portal hypertension is indicated by increased resistance to blood flow in vessels via multiple mechanisms.
 * There is sinusoidal endothelial cell dysfunction (SEC), hepatic stellate cell (HSC) activation, Kupffer cell activation, and myofibroblast activation. Normally, SECs generate nitric oxide, which has several functions, including the maintenance of vascular tone and prevention of HSC activation. Nitric oxide is an endogenous vasodilator and it regulates intrahepatic vascular tone (it is produced from L-arginine). Nitric oxide inhibition has been shown in some studies to increase portal hypertension and hepatic response to norepinephrine.
 * HSC activation results in liver fibrosis, which also predisposes to portal hypertension.
 * Rising portal pressures leads to increased production of vasodilators, defective response to vasoconstrictors, and the formation of new blood vessels all within the splanchnic circulation. All of this is done in order to recruit more blood to sinusoids, thereby promoting more blood flow within the portal vein, further contributing to portal hypertension.
 * splanchnic vasodilation results in decreased effective arterial blood volume (causing low blood pressure). To compensate for this low blood pressure, neurohumoral factors (RAAS, SNS, ADH) are activated, leading to sodium and water retention. This leads to a high volume state.
 * The pathophysiology of non-cirrhotic portal hypertension is most commonly disrupted blood flow to or from the liver.
 * COMPLICATIONS SECTION
 * Ascites
 * pathogenesis
 * hypervolemia as a result of sodium & water retention (discussed above). increased hydrostatic pressure, decreased albumin production --> decreased oncotic pressure --> both combined leads to leakage of transudative fluid into the peritoneal cavity.
 * The management of ascites needs to be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, kidney failure and death. The management includes salt restriction in diet, diuretics to urinate excess salt and water (furosemide, spironolactone), paracentesis to manually remove the ascitic fluid, and transjugular intrahepatic portosystemic shunt (TIPS).
 * Spontaneous bacterial peritonitis
 * infection of ascitic fluid commonly caused by e. coli & klebsiella.
 * pathogenesis: bacterial overgrowth in the intestinal tract due to cirrhosis --> increased permeability*** of the intestinal wall --> movement of gut bacteria from the gastrointestinal tract into the ascitic fluid --> inflammatory markers increase vasodilation
 * diagnosis is made with paracentesis, gram stain & culture.
 * treatment empirically with a third generation cephalosporin (ceftriaxone or cefotaxime) after paracentesis. (narrow after gram stain/culture?), albumin
 * prevention: primary prevention for high-risk groups; secondary prophylaxis for anyone who has had sbp. Medications for prevention are usually fluoroquinolones or sulfonamides.
 * Variceal hemorrhage
 * pathogenesis: increased portal venous pressure leads to dilation of existing vessels and the formation of new vascular connections. These newly formed vascular connections are weak and prone to rupture, leading to bleeding. Esophageal varices are due to a connection between the left gastric vein and the azygos-hemiazygos veins; gastroesophageal varices are due to connections between either the anterior branch of the left gastric vein and esophageal veins or the short gastric & posterior gastric vein and esophageal veins.
 * management on other doc
 * Hepatic encephalopathy
 * pathogenesis: elevated ammonia levels crossing the blood brain barrier. as brain cells attempt to clear the ammonia, glutamine is formed excessively, which results in swelling of brain cells and neurologic dysfunction.
 * management already on page
 * Hepatorenal syndrome -- vora
 * pathogenesis: activated neurohumoral factors (discussed above) leads to renal vasoconstriction. this leads to a decreased blood supply to the kidneys --> decreased glomerular filtration rate.
 * can be an acute kidney injury (type 1) or a slowly progressive renal failure (type 2)
 * management: albumin and splanchnic vasoconstrictors such as terlipressin. This use of splanchnic vasoconstrictors increased mean arterial pressure, which increases the amount of blood supplied to the kidneys. This decreases the compensatory neurohumoral response that leads to renal vasoconstriction and improves kidney function. -- hrs management on doc
 * Cardiomyopathy
 * pathogenesis: initially, the heart compensates for the decreased effective arterial blood volume that is the result of splanchnic vasodilation by increasing cardiac output, which results in high-output heart failure (vora). Eventually, the heart will no longer be able to maintain this increased cardiac output in the setting of prolonged splanchnic vasodilation. As a result, the heart will not fill with or pump blood out appropriately.
 * management: diuretics, non-selective beta blockers have been successful in some clinical studies, liver transplant.
 * management: diuretics, non-selective beta blockers have been successful in some clinical studies, liver transplant.