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The presence of urobilinogen and its increased levels indicate that there are more than normal amounts of bilirubin in the intestine, showing that jaundice observed is not due to the blockage of bile flow, and is of pre-hepatic or hepatic causes. [32] Normal colour of the patient's urine indicates the absence of unconjugated bilirubin. [27]
Jaundice, also known as icterus, is a yellowish or greenish pigmentation of the skin and sclera due to high bilirubin levels. [3] [6] Jaundice in adults is typically a sign indicating the presence of underlying diseases involving abnormal heme metabolism, liver dysfunction, or biliary-tract obstruction. [7]
Hepatitis, commonly virus- or alcohol-induced, causes internal liver inflammation and disrupts conjugated bilirubin transport. [6] Among primary hepatotropic viruses, Hepatitis A presents acute onset of jaundice, usually after the first 2–3 days upon entering the icteric phase while chronic Hepatitis B and C manifest jaundice gradually. [21]
Jaundice may be noticeable in the sclera of the eyes at levels of about 2 to 3 mg/dl (34 to 51 μmol/L), [22] and in the skin at higher levels. [note 1] Jaundice is classified, depending upon whether the bilirubin is free or conjugated to glucuronic acid, into conjugated jaundice or unconjugated jaundice. [citation needed]
Rotor syndrome (also known as Rotor type hyperbilirubinemia) [2] is a rare cause of mixed direct (conjugated) and indirect (unconjugated) hyperbilirubinemia, relatively benign, autosomal recessive [3] bilirubin disorder characterized by non-hemolytic jaundice due to the chronic elevation of predominantly conjugated bilirubin.
Pathological jaundice in newborns should be suspected when the serum bilirubin level rises by more than 5 mg/dL per day, serum bilirubin more than the physiological range, clinical jaundice more than 2 weeks, and conjugated bilirubin (dark urine staining clothes). Haemolytic jaundice is the commonest
Gilbert syndrome has been reported to contribute to an accelerated onset of neonatal jaundice. The syndrome cannot cause severe indirect hyperbilirubinemia in neonates by itself, but it may have a summative effect on rising bilirubin when combined with other factors, [10] for example in the presence of increased red blood cell destruction due ...
The causes for portal hypertension are classified as originating in the portal venous system before it reaches the liver (prehepatic causes), within the liver (intrahepatic) or between the liver and the heart (post-hepatic). The most common cause is cirrhosis (chronic liver failure). Other causes include: [1] [10] [11] Prehepatic causes