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Jaundice

This concept has now been largely abandoned in favor of more suitable methods for making this distinction, but it is of interest to re-examine it with more specific analytical methods than were available when the concept was popular. Table VII gives the results of comparing serum bile salt concentrations with total serum bilirubin concentrations and shows that jaundice with [Pg.73]

TABLE VII. Incidence of Dissociated Jaundice in Various Disease Groups [Pg.74]

Number of Percent of patients with jaundice but patients normal serum bile salt concentrations [Pg.74]

Portal cirrhosis Viral hepatitis Bile duct disease [Pg.74]

Thus when the concept of dissociated jaundice is examined by modern analytical techniques it is found to be true only to a very limited extent (i.e., more patients with cirrhosis or hepatitis will have dissociated jaundice than will those with bile duct disease), and the incidence of dissociated jaundice is so low in all groups as to be of little diagnostic usefulness—for the fact remains that more jaundiced patients (65 % or more) will have increased serum bile salt concentrations regardless of the type of disease. Dissociated jaundice is of limited diagnostic value only when it is present. [Pg.74]


Liver and Gallbladder. High dosages of oral estrogens have been reported to increase the risk for jaundice, cholestatic hepatitis, gallstones, and hepatic vein blood clots. Estrogens promote the development of hepatic neoplasms associated with increased hepatic cell regenerative activity (186,187). [Pg.245]

New impetus was given to photomedicine by development of lasers that are compatible with the clinical environment. These include HeNe, Ar ion, mby, and tunable dye lasers operating in the continuous wave (cw) mode. Prior to the advent of lasers in medicine, only the treatment of newborn jaundice, and the appHcation of long wavelength uv irradiation in conjunction with adininistration (or topical appHcation) of psoralen class sensitizers to treatment of skin diseases (86), principally psoriasis, were clinically important phototherapies. [Pg.394]

Bile Pigments. The oxidative degradation of heme yields open-chain tetrapyrrole as a waste product in humans and other higher animals. The yellow color of the skin in jaundice victims is caused by the presence of biluubin [635-65-4] (32, R = (CH2)2COOH). [Pg.359]

Clinical stresses which interfere with vitamin metabohsm, can result in calcium deficiency leading to osteomalacia and osteoporosis (secondary vitamin D deficiency). These stresses include intestinal malabsorption (lack of bile salts) stomach bypass surgery obstmctive jaundice alcoholism Hver or kidney failure decreasing hydroxylation of vitamin to active forms inborn error of metabohsm and use of anticonverdiants that may lead to increased requirement. [Pg.137]

Human incidents have been reported in workers involved in the production or uses of PCNs. In the United States as well as in Germany and Austraha, the severity of the PCN-induced toxicosis was higher after exposure to the higher chlorinated PCN mixtures. In humans the inhalation of hot vapors was the most important route of exposure and resulted in symptoms including rashes or chloracne, jaundice, weight loss, yellow atrophy of the hver, and in extreme cases, death (75,77—79). [Pg.67]

Bihmbin oxidase [80619-01 -8] derived from Mjrothecium verrucaria was modified with polyethyleneglycol when this conjugate was injected intravenously to jaundiced rats, the plasma bihmbin dropped to normal levels. This approach might have potential in the treatment of hyperbihmbinemia, fulminant hepatitis, and neonatal bihmbin encephalopathy (177). [Pg.312]

Hepatic Hepatic means "pertaining to the liver." For example, hepatitis is inflammation of the liver. Liver disorders are sometimes marked by jaundice, a yellowish coloration to the whites of the eyes and skin. Certain chemicals are hepatotoxins (toxic to the liver), usually as a result of chronic exposure. One example is carbon tetrachloride (CCI4). [Pg.531]

In 1916 Einstein completed his most widely known book on the special and the general theory of relativity, popularly explained, wrote the first paper on gravitational waves, and became president of the Deutsche Physikalische GeseJlschaft. In 1917 he became ill, suffering successively from a liver ailment, a stomach ulcer, jaundice, and general weakness, but nevertheless he managed to complete the first paper on relativistic cosmology. He did not fully recover until 1920. [Pg.384]

Heaviside s last years were spent as an embittered recluse at Torquay, Devon where he allowed only a few people to visit him. For much of his life he suffered from recurring jaundice that was to prove fatal. He died on February 3, 1925. Heaviside s work has been an inspiration to countless electrical engineers and mathematicians. Time has enhanced the esteem in which he is held succeeding generations have spent many hours studying his writings. As a lasting honor, craters on Mars and the Earth s moon were named after him. [Pg.617]

The most common adverse effects are myelosuppression, with leukopenia and thrombocytopenia appearing 7-10 days after treatment, as well as mild nausea. Liver toxicity with jaundice has been reported in rare cases. [Pg.149]

As the above mentioned studies with high supplementation dosages exemplarily show, there is no known toxicity for phylloquinone (vitamin Kl), although allergic reactions are possible. This is NOT true for menadione (vitamin K3) that can interfere with glutathione, a natural antioxidant, resulting in oxidative stress and cell membrane damage. Injections of menadione in infants led to jaundice and hemolytic anemia and therefore should not be used for the treatment of vitamin K deficiency. [Pg.1300]

The incidence of adverse reactions appears to be higher when larger doses of isoniazid are prescribed. Adverse reactions include hypersensitivity reactions, hematologic changes, jaundice, fever, skin eruptions, nausea, vomiting, and epigastric distress. Severe, and sometimes fatal, hepatitis has been associated witii isoniazid tiierapy and may appear after many months of treatment. Peripheral neuropathy (numbness and tingling of the extremities) is the most common symptom of toxicity. [Pg.111]

Hepatotoxicily is the principal adverse reaction seen witii pyrazinamide use Symptoms of hepatotoxicily may range from none (except for slightly abnormal hepatic function tests) to a more severe reaction such as jaundice Nausea, vomiting, diarrhea, myalgia, and rashes also may be seen. [Pg.111]

Older adults are particularly susceptible to a potentially fatal hepatitis when taking isoniazd, especially if they consume alcohol on a regular basis. Two other antitubercular drugs rifampin and pyrazinamide, can cause liver dysfunction in the older adult. Careful observation and monitoring for signs of liver impairment are necessary (eg, increased serum aspartate transaminase, increased serum alanine transferase, increased serum bilirubin, and jaundice). [Pg.114]

DIDANOSINE Although rare, pancreatitis and peripheral neuropathy are possible adverse reactions seen with didanosine The nurse must be alert for symptoms of pancreatitis (nausea, vomiting, abdominal pain, jaundice, elevated enzymes) and for signs of peripheral neuropathy (numbness, tingling, or pain in the feet or hands). It is important to immediately report these signs to the primary health care provider. [Pg.126]

The nurse instructs patients to report any symptoms of infection such as an elevated temperature (even a slight elevation), sore throat, difficulty breathing, weakness, or lethargy. The patient must be aware of possible signs of pancreatitis (nausea, vomiting, abdominal pain, jaundice [yellow discoloration of the skin or eyes]) and peripheral neuritis (tingling, burning, numbness, or pain in the hands or feet). Any indication of pancreatitis or peripheral neuritis must be reported at once. [Pg.127]

ITRACONAZOLE Although rare, die patient may develop hepatitis during itraconazole administration. The nurse closely monitors die patient for signs of hepatitis, including anorexia, abdominal pain, unusual tiredness, jaundice, and dark urine. The primary healtii care provider may order periodic liver function tests. [Pg.136]

Acetaminophen causes few adverse reactions when used as directed on the label or recommended by the primary health care provider. Adverse reactions associated with the use of acetaminophen usually occur with chronic use or when the recommended dosage is exceeded. Adverse reactions to acetaminophen include skin eruptions, urticaria (hives), hemolytic anemia, pancytopenia (a reduction in all cellular components of the blood), hypoglycemia, jaundice (yellow discoloration of the skin), hepatotoxicily (damage to the liver), and hepatic failure (seen in chronic alcoholics taking the drug). [Pg.153]

The nurse immediately reportsany signs of acetaminophen toxicity, such as nausea, vomiting, anorexia, malaise, diaphoresis abdominal pain, confusion, liver tenderness hypotension, arrhythmias jaundice, and acute hepatic and renal failure. Early diagnoss is important because liver failure may be reversible. Toxicity is treated with gastric lavage, preferably within 4 hours of ingestion of the acetaminophen. Liver function studiesare perform ed frequently. Acetylcysteine (Mucomyst) is an antidote to acetaminophen toxicity and acts by protect-... [Pg.156]

Gastrointestinal tract—nausea, vomiting, diarrhea, constipation, epigastric pain, indigestion, abdominal distress or discomfort, intestinal ulceration, stomatitis, jaundice, bloating, anorexia, and dry mouth... [Pg.162]

The patient is observed for persistent nausea, fatigue, lethargy, anorexia, jaundice, dark urine, pruritus and right upper quadrant tenderness. [Pg.271]


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Acholuric jaundice

Bile Pigment Metabolism Causing Jaundice

Bile Pigments Metabolism and Jaundice

Bile Pigments in Jaundice

Bilirubin Hemolytic jaundice

Black liver jaundice

Breast milk jaundice

Carotene jaundice

Chlorpromazine jaundice

Cholestasis jaundice

Cholestatic jaundice

Cholestatic jaundice and hepatitis

Choluric jaundice

Congenital nonhemolytic jaundice

Crigler-Najjar syndrome jaundice)

Dissociated jaundice

Drug Jaundice

Haemolytic jaundice

Halothane jaundice

Hemolytic jaundice

Hepatic disease jaundice

Hepatitis Clinical manifestation, Jaundice

Hepatitis jaundice

Induced Jaundice

Infant jaundice

Jaundice Bilirubin

Jaundice Congenital familial

Jaundice Enzymes

Jaundice Glucuronyl transferase

Jaundice Hepatic

Jaundice Kernicterus

Jaundice Nonhemolytic

Jaundice Pathogenesis

Jaundice Subject

Jaundice acute liver failure

Jaundice alcoholic hepatitis

Jaundice alcoholic liver cirrhosis

Jaundice azathioprine

Jaundice cholestatic, drug-induced

Jaundice liver dysfunction sign

Jaundice methotrexate

Jaundice root

Jaundice salicylates

Jaundice systemic infections

Jaundice thioridazine

Jaundice, drug-induced

Jaundice, liver disease

Jaundice, remedies

Neonatal jaundice

Newborn jaundice

Obstructive jaundice

Phenothiazines jaundice

Phototherapy, neonatal jaundice

Physiologic jaundice

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