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Dilation of the lumen of the appendix insomnia in older adults best modafinil 200 mg, called a mucocele sleep aid commercial with cats best modafinil 200mg, may be caused by Gastrointestinal System Answers 373 mucosal hyperplasia, a benign cystadenoma, or a malignant mucinous cystadenocarcinoma. If the latter tumor ruptures, it may seed the entire peritoneal cavity, causing the condition called pseudomyxoma peritonei. Grossly it is yellow in color and is typically located at the tip of the appendix. Focal scattered necrosis is characteristic of viral hepatitis, but may also be seen with bacterial infections or other toxic insults. In focal necrosis, there is necrosis of single hepatocytes, or small clusters of hepatocytes, that is randomly located in some, but not all, of the liver lobules. In contrast, zonal necrosis refers to the finding of hepatocellular necrosis in identical areas in all of the liver lobules. Centrilobular (acinar zone 3) necrosis is characteristic of ischemic injury (heart failure or shock), toxic effects (acetaminophen toxicity), carbon tetrachloride exposure, or chloroform ingestion. Drugs such as acetaminophen may be metabolized in zone 1 to toxic compounds that cause necrosis of zone 3 hepatocytes because they receive the blood from zone 1. Midzonal (zone 2) necrosis is quite rare, but may be seen in yellow fever, while periportal (zone 1) necrosis is seen in phosphorus poisoning or eclampsia. Submassive necrosis refers to liver cell necrosis that crosses the normal lobular boundaries. Classically the necrosis goes from portal areas to central veins (or vice versa) and is called bridging necrosis. This type of extensive necrosis is described as acute yellow atrophy, because grossly the liver appears soft, yellow, flabby, and decreased in size with a wrinkled capsule. Unconjugated bilirubin is not soluble in an aqueous solution, is complexed to albumin, and cannot 374 Pathology be excreted in the urine. Unconjugated hyperbilirubinemia may result from excessive production of bilirubin, which occurs with hemolytic anemias (acute intravascular hemolysis also produces hemoglobinemia, hemoglobinuria and decreased levels of haptoglobin. Unconjugated hyperbilirubinemia may result from impaired conjugation of bilirubin. In contrast, a defective urea cycle, which results in hyperammonemia, and a foul-smelling breath (fetor hepaticus) are both signs of liver failure. Fetor hepaticus is thought to occur due to volatile, sulfur-containing mercaptans being produced in the gut. Despite various underlying causes, the clinical features of all types of liver failure are similar. Additionally, deranged bilirubin metabolism results in jaundice (mainly conjugated hyperbilirubinemia), while a decreased synthesis of albumin (hypoalbuminemia) results in ascites. Symptoms of hepatic encephalopathy, a metabolic disorder of the neuromuscular system, include stupor, hyperreflexia, and asterixis (a peculiar flapping tremor of the hands). Finally, impaired estrogen metabolism in males can result in gynecomastia, testicular atrophy, palmar erythema, and spider angiomas of the skin. In contrast, physiologic jaundice of the newborn refers to mild elevation of the serum bilirubin levels that begins on days 2 to 4 of life. It is important to clinically differentiate breast milk jaundice from Gastrointestinal System Answers 375 physiologic jaundice of the newborn in order to predict the length of the hyperbilirubinemia. The elevated indirect bilirubin with breast milk jaundice persists longer (up to 6 weeks) than physiologic jaundice (usually less than 2 weeks). Also note that breast milk jaundice is different from breastfeeding jaundice, which occurs before first 4 to 7 days of life and is caused by insufficient breast milk (decreased plasma volume). With these abnormalities the increased serum bilirubin is mainly unconjugated (indirect) bilirubin. In full-term infants, the maximum bilirubin levels are less than 6 mg/dL (normal is less than 2 mg/dL). It is important to realize that in newborns the blood-brain barrier is not fully developed and unconjugated bilirubin may be deposited in the brain, particularly in the lipid-rich basal ganglia, producing severe neurologic abnormalities. Note that kernicterus does not result unless serum bilirubin levels are greater than 20 mg/dL. Treatment, if needed, consists of exposing the skin to light (440 to 470 nm), which activates oxygen and converts bilirubin to photobilirubin. Finally, with hemolytic disease of the newborn serum hemoglobin levels are decreased, while inspissated bile syndrome, which can contribute to jaundice, is seen in neonates with sepsis in which thick bile can cause obstruction. This results in defective excretion of bilirubin glucuronide and other organic anions from hepatocytes.
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