Professional Documents
Culture Documents
cirrhosis
Esophageal varices
discussion
PORTAL SYSTEM
Superior mesenteric + Splenic vein+ gastric + part from inferior mesentric = Portal vein Portal Vein carries outflow from: 1.) Spleen 2.) Oesophagus 3.) Stomach 4.) Pancreas 5.) Small and large intestine
Very low pressure in the hepatic portal vein approx. 5-8 mmHg with only a small gradient across the liver to the hepatic vein which returns the blood to the inferior vena cava
Cirrhosis Hepatis
Definition
o Cirrhosis is a complication of many liver disease that is characterized by abnormal structure and function of the liver o It is characterized by widespread fibrosis with nodular regeneration. Its presence implies previous or continuing hepatic cell damage
A normal liver (left) shows no signs of scarring. In cirrhosis (right), scar tissue replaces normal liver tissue.
etiology
1. Alcohol (>70%) 2. Chronic infections hepatitis C, B, B+D brucellosis, syphilis 3. Chr. biliary obstruction PBC, PSC, stricture, stones, cystic fibrosis, billiary atresia 4. Autoimmune 5. Drugs and chemical
pathogenesis
Clinical manifestation
Many people with cirrhosis have no symptoms during the early phases of the disease. Symptoms are caused by either of 2 problems: Gradual failure of the liver to carry out its natural functions Distortion of the liver's usual shape and size because of scarring
Clinical manifestation
Early cirrhosis : Tiredness ( fatigue) or even exhaustion Weakness Nausea Loss of appetite leading to weight loss Loss of sex drive
Clinical manifestation
Advance cirrhosis: Jaundice Spider naevi, caput Medusae Bloody, black stools or unusually light-colored stools Vomiting of blood In women, abnormal menstrual periods In men, enlargement of the breasts (gynecomastia) scrotal swelling
ascites
Caput medusae
Esophageal Varices
definition
Esophageal varices are abnormal, enlarged veins in the lower part of the esophagus. varices occur most often in people with serious liver diseases. Esophageal varices can rupture, causing lifethreatening bleeding.
etiology
Severe liver scarring (cirrhosis). Blood clot (thrombosis). A parasitic infection
Discussion
CIRRHOSIS
PORTAL HYPERTENSION
ESOPHAGEAL VARICES
Portal hypertension results from both: 1.Increased resistance to portal flow (R) 2.Increased portal venous inflow (Q)
Portal Hypertension
Portal vein - Hepatic vein pressure gradient greater than 5 mm Hg
Cirrhosis
Increased splanchnic + peripheral NO
Decreased intrahepatic NO
Collaterals
Increase portal blood flow
Maintains portal hypertension
Sodium retention
Collateral
The portal venous system has several anastomosis with the systemic venous system. Four collateral pathways Esophageal and gastric venous plexus umbilical vein from the left portal vein to the epigastric venous system retroperitoneal collateral vessels the hemorrhoidal venous plexus In cases of portal hypertension these anastamoses may become engorged, dilated, or varicosed and subsequently rupture
No varices
Small varices
Large varices
treatments
prevent bleeding
Non selective beta blocker endoscopic variceal band ligation
ocreotide Somatostatin endoscopic sclerotherapy and banding
Stop bleeding
betablockers, endoscopic variceal ligation or the combination of beta-blockers and endoscopic variceal ligation TIPS (surgical)
conclusion
Cirrhosis is a condition that is defined histopathologically and has a variety of clinical manifestations and complications, some of which can be life-threatening, portal hypertension is directly responsible for the major complications of cirrhosis, variceal hemorrhage. Variceal hemorrhage is an immediate life-threatening problem with a 2030% mortality associated with each episode of bleeding. There are treatments to stop bleeding in such as vasoactivedrugs, vasopressin, somatostatin, octreotide, endoscopic sclerotherapy and banding, and endoscopic variceal ligation. -Blockers and endoscopic variceal band ligation are the treatments to prevent bleeding.
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