Hepatic disease cirrhosis

Hypoglycemia can also be induced by concomitant diseases, for example renal disease, hepatic disease (cirrhosis), hypopituitarism, hypoadrenocorticalism, hypoglucagonism, hypothyroidism, malnutrition, anorexia nervosa, pregnancy, termination of pregnancy, recovery from infections, operations, or stress. 

Progression of alcoholic liver disease moves through several distinct phases from development of fatty liver to the development of alcoholic hepatitis and cirrhosis. Fatty liver and alcoholic hepatitis may be reversible with cessation of alcohol intake, but cirrhosis itself is irreversible. Although the scarring of cirrhosis is permanent, maintaining abstinence from alcohol can still decrease complications and slow development to end-stage liver disease.22 Continuing to imbibe speeds the advancement of liver dysfunction and its complications. 

Hereditary hemochromatosis is an autosomal recessive disease of increased intestinal iron absorption and deposition in hepatic, cardiac, and pancreatic tissue. Hepatic iron overload results in the development of fibrosis, hepatic scarring, cirrhosis, and hepatocellular carcinoma. Hemochromatosis can also be caused by repeated blood transfusions, but this mechanism rarely leads to cirrhosis. 

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. 

Hepatic function impairment The average plasma concentration in patients with advanced cirrhosis was slightly higher than that seen in older subjects. Because of limited experience in patients with severe hepatic disease, who may have bleeding diatheses, the use of ticlopidine is not recommended. 

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. 

Oral Active hepatic disease, such as hepatitis and cirrhosis where spasticity is used to sustain upright posture and balance in locomotion or to obtain or maintain increased function treatment of skeletal muscle spasm resulting from rheumatic disorders. 

Liver Methotrexate causes hepatotoxicity, fibrosis, and cirrhosis, but generally only after prolonged use. Acutely, liver enzyme elevations are frequent, usually transient and asymptomatic, and also do not appear predictive of subsequent hepatic disease. Liver biopsy after sustained use often shows histologic changes, and fibrosis and cirrhosis have occurred these latter lesions often are not preceded by symptoms or abnormal liver function tests (see Precautions). For this reason, periodic liver biopsies are usually recommended for psoriatic patients who are under long-term treatment. Persistent abnormalities in liver function tests may precede appearance of fibrosis or cirrhosis in the RA population. 

Milk thistle has been used to treat acute and chronic viral hepatitis, alcoholic liver disease, and toxin-induced liver injury in human patients. Milk thistle has most often been studied in the treatment of alcoholic hepatitis and cirrhosis. In both of these disorders, outcomes have been mixed and reports include significant reductions in markers of liver dysfunction and in mortality, as well as no effect. In acute viral hepatitis, studies have generally involved small sample sizes and have shown mixed outcomes of improved liver function (eg, aminotransferase values, bilirubin, prothrombin time) or no effect. Studies in chronic viral hepatitis and toxin-induced injury have also been of small size but have reported mostly favorable results. Parenteral silybin is marketed and used in Europe as an antidote in Amanitaphalloides mushroom poisoning, based on favorable outcomes reported in case-control studies. 

UGT activity is modulated by various hormones. Excess thyroid hormone and ethinyl oestradiol (but not other oral contraceptives) inhibit bilirubin glucuronidation. In contrast, the combination of progestational and oestrogenic steroids results in increased enzyme activity. Bihrubin glucuronidation can also be inhibited by certain antibiotics (e.g. novobiocin or gentamicin, at serum concentrations exceeding therapeutic levels) and by chronic hepatitis, advanced cirrhosis and Wilson s disease. 

Liver disease is now recognised as a major complication of type 2 diabetes. Diabetes mellitus can lead to metabolic changes that alter normal hepatic and biliary function and structure. Type 2 diabetes is associated with an increased risk of a range of hepatobiliary diseases, including non-alcoholic fatty liver disease, cirrhosis, acute liver failure, hepatocellular carcinoma and cholelithiasis [22]. 

Approximately 3-10% of patients with inflammatory bowel disease have some degree of liver abnormality. The spectrum of liver dysfnnction associated with inflammatory bowel disease ranges from fatty changes to pericholangitis, sclerosing cholangitis, chronic active hepatitis and cirrhosis. Ulcerative colitis is more commonly associated with liver abnormality than Crohn s disease. 

It is less likely in other forms of liver disease, such as acute hepatitis and cirrhosis. Cirrhosis may actually protect against atherosclerosis [5, 8, 9]. The reasons for this are not clear. Secondary hypercholesterolaemia frequently occurs in cholestatic conditions, but usually does not require treatment [10]. Other risk factors for hyperlipidaemia and cardiovascular disease should be assessed, as their presence may independently indicate a need for medical intervention [9]. In PBC, patients with severe, chronic disease do not appear to have an increased cardiovascular risk as a result of their hypercholesterolaemia this may be due to the presence of cirrhosis. In contrast, in less severe PBC... 

Hepatic Fibrosis/Cirrhosis Fibrosis usually results from chronic inflammation which can be the result of continuous exposure to a variety of hepatotoxic chemicals such as organic arscnicals, vinyl chloride, or high doses of vitamin A (Zimmerman, 1999), chronic ethanol ingestion and nonalcoholic fatty liver disease. Fibrosis usually occurs around the portal area, in the space of Disse, and around the central veins. This results in loss of liver architecture and function. The hepatocytes are replaced with fibrous material and thus there is hepatocyte loss. Periportal fibrosis may lead to portal hypertension. 

Hepatic cirrhosis is typically the end stage of liver disease. Cirrhosis describes an irreversible change (Treinen-Moslen, 2001) characterized by accumulation of excessive collagen deposition in the form of bridging fibrosis which disrupts the hepatic architecture. Cirrhosis may be micronodular or macronodular depending on the amount of fibrosis and tissue regeneration. Liver transplantation is the only solution to restore adequate liver fimction in human medicine. 

Local anesthetics containing an amide linkage are metabolized principally by the liver.Thus, patients with hepatic disease may be more likely to exhibit toxic effects from the injectable anesthetics. Local tissue infiltration or nerve blocks should be avoided or performed using minimally effective anesthetic doses in patients with hepatitis, cirrhosis, extrahepatic obstruction (e.g., lithiasis), or other clinically significant hepatic dysfunction. 

In contrast to cancer and inflammatory diseases, the decrease of the filtrate wave under the normal value takes place with patients suffering from infectious hepatitis or cirrhosis of the liver [154, 155]. 

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