Liver disorders hepatitis

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). 

Active hepatic disease, such as acute hepatitis or active cirrhosis if previous methyidopa therapy has been associated with liver disorders coadministration with MAOIs hypersensitivity to any component of these formulations, including sulfites. 

Hepatic effects Fatal and nonfatal liver disorders of an idiosyncratic or hypersensitivity type may occur. At the start of therapy, perform baseline liver function studies. If abnormalities exist, the potential for hepatotoxicity could be enhanced. 

Liver cirrhosis is among the top 10 causes of death in the Western world. The disease occurs after chronic damage to hepatic cells, mainly hepatocytes, which can be caused by viral hepatitis, chronic alcohol abuse or toxic injury, biliary disease, and metabolic liver disorders [64], Liver cirrhosis is characterized by an abnormal deposition of connective tissue in the liver, which hampers the normal functions of the liver. Other features of the disease are general tissue damage, chronic inflammation, and the conversion of normal liver architecture into structurally abnormal nodules. Secondary to these anatomical changes are disturbances in the liver function and in the hemodynamics leading to portal hypertension and intrahepatic shunting [39, 64, 103],... 

With respect to the correlation between liver disorders and the functions of the brain, discussion currently focuses on five hypotheses concerning the development of hepatic encephalopathy (7.) intoxication hypothesis, (2.) neurotransmitter hypothesis, (2.) deficiency hypothesis, (4.) synergistic neurotoxicity, and (J.) hypothesis of primary gliopathy. 

Most recorded cases of liver disorders occurred after either repeated exposure (38) or prolonged exposure (39) to halothane. In one case, hepatitis developed 3 weeks after a single halothane anesthetic in a 37-year-old renal transplant recipient who had previously been exposed to isoflurane (40) this report suggests that previous exposure to isoflurane may predispose to subsequent halothane toxicity. 

Three liver disorders that are attributable to drinking are fatty liver, alcohol hepatitis, and cirrhosis. The first two disorders are reversible with abstinence cirrhosis, a leading killer in the United States, is not. 

Inflammatory conditions of the liver, in particular inflammatory hepatocellular cholestasis, are one of the most frequent causes of jaundice in the clinic. The major underlying denominator of this disorder is the inhibition of transporter expression and function by proinflammatory cytokines, which are either induced systemically or within the liver. Alcoholic hepatitis accounts for up to two-thirds of patients and is the most frequent trigger, followed by idiosyncratic drug reactions, sepsis or other extrahepatic bacterial infections, some variants of viral hepatitis, and total parenteral nutrition [95, 96]. 

In the elderly, secondary to a decreased capacity for oxidation and alterations in the volume of distribution, drug accumulation can result. Patients with hepatic disease also are at risk for drug accumulation and subsequent complications. Therefore, intermediate- or short-acting benzodiazepines without active metabolites are preferred for chronic use in the elderly and those with liver disorders. Elderly patients are also sensitive to the CNS adverse effects of benzodiazepines (regardless of half-life) and their use is associated with a high frequency of falls and hip fractures. 

The rates and routes of metabolism can vary with age and the lower rates and reduced routes of metabolism usually seen in the yoimg and the old can make them more susceptible to drug action. Differences in hormonal levels, in particular, can lead to differences in metabolism between sexes. Dietary and environmental factors such as the presence of alcohol and cigarette smoke can affect metabolism, as can certain disease conditions, e.g., liver disorders, diabetes. Such conditions can lead to decreased enzyme activity, altered hepatic blood flow, and changes in plasma protein levels which, in turn, can affect circulating active drug levels. 

The situation with respect to the uncommon liver disorder of bihary cirrhosis is uncertain. Hypercholesterolemia, mainly as a rise in LDL cholesterol, is a common characteristic, although increased cardiovascular risk is not proportionate to the dyslipidemia. In 603 patients with primary biliary cirrhosis who took a statin for a mean duration of 41 months hepatic enzymes actually fell [30 ]. 

The two latter causes of jaundice are often found simultaneously in some liver disorders, e.g. hepatitis and cirrhosis. 

In Europe, clinical use is widespread for toxic liver damage in supportive treatment of chronic inflammatory liver disorders and cirrhosis, including chronic hepatitis and fatty infiltration of the liver by alcohol and other chemicals. In infusion therapy, silibinin preparations used for supportive treatment of Amanita mushroom poisoning. ... 

The dosage of flucytosine is 150—200 mg/kg orally in four portions every six hours. A 1% flucytosine solution has been developed for intravenous adrninistration. In some countries, a 10% ointment is also available. In patients with normal renal function, flucytosine is seldom toxic, but occasionally severe toxicity may be observed (leukopenia and thrombocytopenia). Plasma levels should be determined and the dose in patients with impaired renal function should be checked. Liver function tests (transaininases and alkaline phosphatase) should be performed regularly. In some patients with high flucytosine plasma levels, hepatic disorders have been observed (24). 

Kanamycin, neomycin, and paromomycin are used orally in the management of hepatic coma. In this disorder, liver failure results in an elevation of blood ammonia levels. By reducing tire number of ammoniaforming bacteria in the intestines, blood ammonia levels may be lowered, thereby temporarily reducing some of the symptoms associated with this disorder. 

When the hydantoins are used with odier CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. The hydantoins are used cautiously in patients widi liver or kidney disease and neurologic disorders. Phenytoin is used cautiously in patients widi hypotension, severe myocardial insufficiency, and hepatic impairment. 

The principal adverse reaction associated with warfarin is bleeding, which may range from very mild to severe. Bleeding may be seen in many areas of the body, such as the bladder, bowel, stomach, uterus, and mucous membranes. Other adverse reactions are rare but may include nausea, vomiting, alopecia (loss of hair), urticaria (severe skin rash), abdominal cramping, diarrhea, rash, hepatitis (inflammation of the liver), jaundice (yellowish discoloration of the skin and mucous membranes), and blood dyscrasias (disorders). 

While ammonia, derived mainly from the a-amino nitrogen of amino acids, is highly toxic, tissues convert ammonia to the amide nitrogen of nontoxic glutamine. Subsequent deamination of glutamine in the liver releases ammonia, which is then converted to nontoxic urea. If liver function is compromised, as in cirrhosis or hepatitis, elevated blood ammonia levels generate clinical signs and symptoms. Rare metabolic disorders involve each of the five urea cycle enzymes. 

Type I Crigler-Najjar syndrome is a rare autosomal recessive disorder. It is characterized by severe congenital jaundice (serum bilirubin usually exceeds 20 mg/dL) due to mutations in the gene encoding bilirubin-UGT activity in hepatic tissues. The disease is often fatal within the first 15 months of life. Children with this condition have been treated with phototherapy, resulting in some reduction in plasma bilirubin levels. Phenobarbital has no effect on the formation of bilirubin glucuronides in patients with type I Crigler-Najjar syndrome. A liver transplant may be curative. 

HBD is a biochemical rather than electrophoretic assessment of the LD isoenzyme which is associated with heart. All five isoenzymes of LD exhibit some activity toward cx-hydroxy-butyrate as substrate, but heart LD shows the greatest activity. Serum HBD measurement is not as valuable as the electrophoretic determination of heart LD isoenzyme. High HBD activity has also been found in diseases of the liver. Rises associated with the hepatic effects of congestive heart failure can be disconcerting in the differential diagnosis of myocardial infarction. Wilkinson has used the serum HBD/LD ratio for the differentiation of myocardial disease from other disorders in which HBD activity is elevated, whereas Rosalki has not found the ratio to be helpful (39). 

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