java barcode reader library open source NONCIRRHOTIC PORTAL HYPERTENSION in Objective-C

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NONCIRRHOTIC PORTAL HYPERTENSION
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Noncirrhotic portal hypertension must be considered in the differential diagnosis of splenomegaly or upper gastrointestinal bleeding due to esophageal or gastric varices in patients with little if any liver dysfunction This syndrome may be due to extrahepatic portal vein obstruction
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MRI may reveal the presence of intrahepatic defects On MRI, characteristic findings include high signal intensity on T2weighted images and rim enhancement The characteristic CT appearance of hepatic candidiasis, usually seen in the setting of systemic candidiasis, is that of multiple bulls-eyes, but imaging studies may be negative in neutropenic patients
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PYOGENIC HEPATIC ABSCESS
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ESSENTIALS OF DIAGNOSIS
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Fever, right upper quadrant pain, jaundice Often in setting of biliary disease but up to 40% are cryptogenic in origin Detected by imaging studies
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Treatment
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Treatment should consist of antimicrobial agents (a thirdgeneration cephalosporin such as cefoperazone 1 2 g intravenously every 12 hours and metronidazole 500 mg intravenously every 6 hours) that are effective against coliform organisms and anaerobes Antibiotics are administered for 2 3 weeks, and sometimes up to 6 weeks If the abscess is at least 5 cm in diameter or the response to antibiotic therapy is not rapid, intermittent needle aspiration or catheter or surgical (eg, laparoscopic) drainage should be done The mortality rate is still substantial ( 8% in most studies) and is highest in patients with underlying biliary malignancy or severe multiorgan dysfunction Hepatic candidiasis often responds to intravenous amphotericin B (total dose of 2 9 g) Fungal abscesses are associated with mortality rates of up to 50% and are treated with intravenous amphotericin B and drainage
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Giorgio A et al Percutaneous needle aspiration of multiple pyogenic abscesses of the liver: 13-year single-center experience AJR Am J Roentgenol 2006 Dec;187(6):1585 90 [PMID: 17114554]
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General Considerations
The liver can be invaded by bacteria via (1) the portal vein (pylephlebitis); (2) the common duct (ascending cholangitis); (3) the hepatic artery, secondary to bacteremia; (4) direct extension from an infectious process; and (5) traumatic implantation of bacteria through the abdominal wall Risk factors for liver abscess include older age and male gender Predisposing conditions include malignancy, diabetes, inflammatory bowel disease, cirrhosis, and liver transplantation Ascending cholangitis resulting from biliary obstruction due to a stone, stricture, or neoplasm is the most common identifiable cause of hepatic abscess in the United States In 10% of cases, liver abscess is secondary to appendicitis or diverticulitis At least 40% of abscesses have no demonstrable cause and are classified as cryptogenic A dental source is identified in some cases The most frequently encountered organisms are E coli, Klebsiella pneumoniae, Proteus vulgaris, Enterobacter aerogenes, and multiple microaerophilic and anaerobic species (eg, Streptococcus milleri) Staphylococcus aureus is usually the causative organism in patients with chronic granulomatous disease Unusual causative organisms include Salmonella, Haemophilus, and Yersinia Hepatic candidiasis, tuberculosis, and actinomycosis are seen in immunocompromised patients and those with hematologic malignancies Rarely, hepatocellular carcinoma can present as a pyogenic abscess because of tumor necrosis, biliary obstruction, and superimposed bacterial infection The possibility of an amebic liver abscess must always be considered (see 35)
BENIGN LIVER NEOPLASMS
The most common benign neoplasm of the liver is the cavernous hemangioma, often an incidental finding on ultrasound or CT scan This lesion may enlarge in women who take hormonal therapy and must be differentiated from other space-occupying intrahepatic lesions, usually by MRI Rarely, fine-needle biopsy is necessary to differentiate these lesions and does not appear to carry an increased risk of bleeding Surgical resection of cavernous hemangiomas is rarely necessary but may be required for abdominal pain or to exclude malignancy In addition to rare instances of sinusoidal dilatation and peliosis hepatis, two distinct benign lesions with characteristic clinical, radiologic, and histopathologic features have been described in women taking oral contraceptives focal nodular hyperplasia and hepatic adenoma Focal nodular hyperplasia occurs at all ages and is probably not caused by oral contraceptives It is often asymptomatic and appears as a hypervascular mass, often with a central hypodense stellate scar on CT scan or MRI Microscopically, focal nodular hyperplasia consists of hyperplastic units of hepatocytes with a central stellate scar containing proliferating bile ducts It is not a true neoplasm but a nonspecific reaction to altered blood flow and may also occur in patients with cirrhosis, with exposure to certain drugs such as azathioprine, and in antiphospholipid syndrome The prevalence of hepatic hemangiomas is increased in patients with focal nodular hyperplasia Hepatic adenoma occurs most commonly in the third and fourth decades of life and is usually caused by oral contraceptives; acute abdominal pain may occur if the tumor undergoes necrosis or hemorrhage The tumor may be associated with mutations in (1) the gene coding for hepatocyte nuclear factor
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