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Pain associated with alcoholic hepatitis, especially when accompanied by fever, jaundice, and leukocytosis, may be sufficiently severe to simulate an acute surgical abdomen (Mendenhall, f982). Although hepatocellular jaundice is usually painless, a dull ache or "heavy sensation" in the right upper quadrant may attend acute hepatitis of any cause. Abdominal pain frequently accompanies jaundice, and its character may point to a specific diagnosis. Symptoms associated with jaundice often provide a diagnosis. A past history of jaundice, although potentially unrelated to the immediate problem, may implicate chronic hepatitis, cirrhosis, benign recurrent intrahepatic cholestasis, or a genetic nonhemolytic hyperbilirubinemeia (i.e., Gilbert's or Dubin–Johnson syndrome) as the cause. Jaundice of fluctuating intensity implicates gallstones, ampullary carcinoma, or possible drug hepatitis. Jaundice appearing over the course of weeks implies a subacute hepatitis or extrahepatic obstruction due to malignancy, gallstone, chronic pancreatitis, or stricture in the common bile duct. Jaundice appearing over a few days to a week implies hepatitis, whether drug or toxin induced, viral or bacterial (i.e., leptospirosis).
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The mode of onset of jaundice often provides the pathophysiologic basis, if not the specific diagnosis at its root. Recurrent brief episodes of anorexia, nausea, or emesis extending over months to years, especially when accompanied by right upper quadrant abdominal pain, implicate gallstones. The same symptoms occurring continuously for more than 2 weeks prior to the appearance of jaundice suggest a malignant biliary obstruction, chronic hepatitis, or toxin exposure (especially alcohol). Anorexia, nausea, emesis, or weight loss appearing within 2 weeks prior to onset of jaundice suggests hepatitis or biliary obstruction secondary to gallstones.
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Serum bilirubin levels are normal in patients with yellow skin caused by carotenemia or quinacrine.Īssessment of constitutional symptoms often provides the first clue to the mechanism of jaundice. Quinacrine, commonly used for treatment of giardiasis, may produce a yellow skin color, but the urine remains normal. The resultant yellow skin color is differentiated from jaundice by the absence of yellow color in mucous membranes and sclerae, the normal urine color, and the accentuation of yellow-brown carotenoid pigment in the palms, soles, and nasolabial folds. Eating large quantities of green and yellow vegetables, tomatoes, or yellow corn may result in excess carotene intake.
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Jaundice must be distinguished from yellow or green skin color resulting from carotenemia or quinacrine ingestion. Although many sources confidently say that jaundice can be recognized when the serum bilirubin rises to 2 to 2.5 mg/dl, experienced clinicians often cannot see a yellow skin coloration until the serum bilirubin is at least 7 to 8 mg/dl. Depending on the clinical situation, jaundice and cholestasis may coexist or each may exist without the other. Jaundice should be distinguished from cholestasis, which refers to a decreased rate of bile flow. Jaundice is the yellow color of skin and mucous membranes due to accumulation of bile pigments in blood and their deposition in body tissues.