Chapter 38 - Disorders of Hepatobiliary & Exocrine Pancreas

• a stool sample can be used to confirm the fecal shedding of hepatitis A virus
• fecal shedding in HAV occurs up to 2 weeks before the development of symptoms and end as IgM levels rise
• serum level of IgM antibodies can be used to confirm the diagnosis of acute HAV and usually appear during the first week of symptomatic disease and begin to decline in a few months
• serum levels of IgG antibodies can be used to confirm the diagnosis of HAV and occur after 1 month of illness and may persist for years
• IgG antibodies provide long-term protective immunity against re-infection of HAV
• the presence of IgG antibodies documents past exposure of HAV, not acute hepatitis
• hepatitis A is the most commonly transmitted by the fecal-oral route
• the best method to protect anyone from getting hepatitis A is vaccination
• immunization is recommended for persons at high risk for HAV exposure and include travelers to regions where sanitation is poor and endemic HAV infections are high, children living in communities with high rates of HAV infection, homosexually active men, and users of illicit drugs
• persons with preexisting chronic liver disease may benefit from hepatitis A vaccination
• with the gradual obstruction of venous blood flow in the liver, the pressure in the portal veins increases and large collateral channels develop between the portal and systemic veins that supply the esophagus and other areas
• clinically, the most important collateral channels are those connecting the portal and coronary veins that lead to the reversal of flow and formation of thin-walled varicosities in the submucosa of the esophagus
• the thin-walled esophageal varicosities are subject to rupture, producing massive and sometimes fatal hemorrhage
• liver failure causes disorders of synthesis and storage functions
• liver failure can cause anemia, thrombocytopenia, coagulation defects, and leukopenia
• because factors V, VII, IX, and X, prothrombin, and fibrinogen are synthesized by the liver, their decline in liver disease contributed to bleeding disorders
• a person with liver failure is then subject to purpura, easy bruising, hematuria, and abnormal menstrual bleeding and is vulnerable to bleeding from the esophagus and other segments of the GI tract
• treatment of esophageal varices is directed at prevention of initial hemorrhage, management of acute hemorrhage, and prevention of recurrent hemorrhage
• pharmacologic therapy of esophageal varices is used to lower portal venous pressure and prevent initial hemorrhage
• beta adrenergic blocking drugs (e.g., propranolol) are commonly used as pharmacological therapy for esophageal varices
• beta adrenergic agents reduce portal venous pressure by decreasing splanchnic blood flow, thereby decreasing blood flow in collateral channels
• several methods are used to control acute hemorrhage, including administration of octreotide or vasopressin, balloon tamponade, endoscopic injection sclerotherapy, vessel ligation, or esophageal transection
• octreotide reducing splanchnic and hepatic blood flow and portal pressures
• vasopressin is used to vasoconstrict the vessels
• balloon tamponade provides compression of the varices via an esophageal balloon
• with endoscopic sclerotherapy, the esophageal varices are injected with a sclerosing solution to obliterate the vessel lumen
• prevention of recurrent esophageal hemorrhage focuses on lowering portal venous pressure and diverting blood flow away from the easily ruptured collateral channels into a systemic vein
• the surgical creation of a postosystemic shunt or transjugular intrahepatic portosystemic shunt helps to divert blood flow away from the easily ruptured collateral channels into a systemic vein
• many people with gallstones are asymptomatic
• after eating, food entering the intestine causes the gallbladder to contract and the sphincter of the bile duct to relax, so that bile stored in the gallbladder moves into the duodenum
• cholecystokinin from the mucosa of the duodenum provides a strong stimulus for gallbladder contraction
• gallstones cause symptoms when they obstruct bile flow
• small gallstones pass into the common duct, producing symptoms of indigestion and biliary colic
• larger gallstones are more likely to obstruct bile flow and cause jaundice
• the pain of biliary colic usually is abrupt in onset, increases in intensity, persists for 2 to 8 hours, and is followed by soreness in the URQ
• the URQ is the usual location of biliary colic pain, often radiating to other areas such as the upper back, right shoulder, or midscapular region
• jaundice results from abnormally high accumulation of bilirubin in the blood, as a result of which there is a yellowish discolouration to the skin and deep tissues
• because normal skin has a yellow cast, the early signs of jaundice are often difficult to detect, especially in persons with dark skin
• bilirubin has a special affinity for elastic tissue
• the sclera of the eye, which contains considerable elastic fibers, usually is one of the first structures in which jaundice can be detected