Cirrhosis, alcoholic

Case study level 1 - Alcoholic cirrhosis alcohol withdrawal... 

Case study level 1 - Alcoholic cirrhosis alcohol withdrawal 338 Case study level 2 - Alcoholic cirrhosis management of bleeding risk and treatment for the maintenance of alcohol abstinence 339 Case study level 3 - Hepatic encephalopathy and ascites 341 Case study level Ma - Pulmonary tuberculosis 342 Case study level Mb - Liver failure 344... 

Alcohol dehydrogenase (ADH) is involved in the metabolism of ethanol to acetaldehyde, which in turn is converted to acetate by aldehyde dehydrogenase (ALDH). Because the hepatic expressions of these enzymes are influenced by both ethanol consumption and liver cirrhosis, which may be the consequence of ethanol consumption, it is sometimes difficult to know which of these factors is resulting in modulation of the enzyme. There is generally a reduction in ADH in alcoholic cirrhosis [77, 78], whereas in non-alcoholic cirrhotic patients some studies have detected a reduction in ADH [77] but others have detected no change [78]. Total ALDH is reduced in primary biliary cirrhosis, alcoholic and non-alcoholic cirrhosis compared to controls [77, 78]. 

Predisposition The additional liver damage caused by the accumulation of urocarboxyporphyrins (UCP) and heptacarboxyporphyrins (HCP) in hepatic tissue is a prerequisite for clinically manifest PCT. Several forms of liver disease increase susceptibility to PCT, e. g. viral hepatitis B, and more particularly type C (286, 287, 302, 309), fibrosis, siderosis, cirrhosis, alcohol-induced liver... 

Alcohol abuse Alcohol abuse is the most common cause of cirrhosis. Nevertheless, no more than 40-60% of alcoholics contract the disease. Thus genetic factors must also be involved in the development of alcoholic cirrhosis. Alcohol itself can be a facilitative factor or cofactor. Moreover, so-called additives contained in various alcoholic beverages in widely different quantities may also be of greater importance than has hitherto been assmned. (100, 171, 186) (s. pp 528, 532) (s. fig. 28.13, 28.14)... 

Both central and peripheral defects in thyroid secretion are noted in patients with cirrhosis. Alcohol plays a major role with direct toxic effects on the thyroid gland. Management includes thyroid hormone... 

The results of treatment with plant-derived liver therapeutics are improvement or normalisation of the biochemical data (seen after a blood analysis) and disappearence of various secondary symptoms. In patients with liver cirrhosis (alcoholics) the survival rate is improved. 

Vertemati M, Minola E, Goffredi M, et al. Computerized morphometry of the cirrhotic liver comparative analysis in primary biliary cirrhosis, alcoholic cirrhosis, and posthepatitic cirrhosis. Microsc Res Tech. 2004 65 113-121. 

Cirrhosis, alcoholic hepatitis, pancreatitis, gastric or duodenal ulcer, esophageal varices, middle-age onset of diabetes, gastrointestinal cancer, hypertension, peripheral neuropathies, myopathies, cardiomyopathy, cerebral vascular accidents, erectile dysfunction, vitamin deficiencies, pernicious anemia, and brain disorders including Wemicke-Korsakoff syndrome (mortality rate of untreated Wernicke is 50% treatment is with thiamine)... 

Tallaksen, C.M., Bell, H., and Bohmer, T., 1992a. The concentration of thiamin and thiamin phosphate esters in patients with alcoholic liver cirrhosis. Alcohol and Alcoholism. 27 523-530. 

Some authorities question whether dmnkeimess can result from the inhalation of ethyl alcohol vapors. Experience has demonstrated that in any event such intoxication is indeed rare (281). There is no concrete evidence that the inhalation of ethyl alcohol vapor will cause cirrhosis. Liver function is definitely impaired during alcohol intoxication (282), making the subject more susceptible to the toxic effects of chlorinated hydrocarbons. 

Adverse consequences of drinking include a variety of social, legal, medical, and psychiatric problems (Babor et al. 1987, 2003). Alcohol is among the top four causes of mortality in 1988, 107,800 deaths, or about 5% of all deaths in the United States, were attributed to alcohol-related causes (Stinson and DeBakey 1992). Approximately 17% of alcohol-related deaths were directly attributable to alcohol, 38% resulted from diseases indirecdy attributable to alcohol, and 45% were attributable to alcohol-related traumatic injury (U.S. Department of Health and Human Services 1994). Alcohol-related mortality declined during the latter part of the twentieth century. For example, the age-adjusted mortality rate from liver cirrhosis in 1993 (7.9 deaths per 100,000 persons) was just over half the rate in 1970 (14.6 deaths per 100,000) (Saadat-mand et al. 1997), and the proportion of automobile fatalities that was related to the use of alcohol fell to a two-decade low of 33.6% in 1993 (Lane et al. 1997). 

Saadatmand F, Stinson FS, Grant FB, et al Liver cirrhosis mortality in the United States, 1970-94 (Surveillance Report No 45). Rockville, MD, National Institute on Alcohol Abuse and Alcoholism, 1997... 

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. 

In Figure 40, one can see the effect on the ratio of total to free cholesterol in a patient with alcoholic cirrhosis. 

Decreased hepatic selenium content in alcoholic cirrhosis. Dig. Dis. Sci. 33, 1213-1217. 

Johansson, V., Johnsson, F., Joelsson, B., Beiglund, M. and Akesson, B. (1986). Selenium status in patients with liver cirrhosis and alcoholism. Br. J. Nutr. 55, 227-233. 

Alcohol abuse is a major clinical problem in many countries and has been the subject of investigation for many years by those interested in determining the molecular basis of ethanol-induced liver dam e (see Lieber, 1990). These intensive and extended efforts have revealed much about the metabolism of ethanol in the liver and about the toxicity of its primary oxidative product, acetaldehyde. They have not, however, folly elucidated the molecular mechanisms that lead to the typical features of alcoholic liver injury steatosis, necrosis and eventually cirrhosis. 

Cirrhosis is the result of long-term insult to the liver, so damage is typically not evident clinically until the fourth decade of life. Chronic liver disease and cirrhosis combined were the 12th leading cause of death in the United States in 2002. In patients between the ages of 25 and 64, damage from excessive alcohol use accounted for over one-half of the deaths.2 Alcoholic liver disease and viral hepatitis are the most common causes of cirrhosis in the United States and worldwide. 

Variations occur, but cirrhosis typically develops after 10 or more years of daily ingestion of 80 g of ethyl alcohol this is an average of 6 to 8 drinks per day (a drink is equivalent to 1 ounce... 

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. 

Non-alcoholic fatty liver disease begins with asymptomatic fatty liver but may progress to cirrhosis. This is a disease of exclusion elimination of any possible viral, genetic, or environmental causes must be made prior to making this diagnosis. Non-alcoholic fatty liver disease is related to numerous metabolic abnormalities. Risk factors include diabetes mellitus, dyslipidemia, obesity, and other conditions associated with increased hepatic fat.26... 

Lifestyle modifications can limit disease complications and slow further liver damage. Avoidance of additional hepatic insult is critical for successful cirrhosis treatment. The only proven treatment for alcoholic liver disease is the immediate cessation of alcohol consumption. Patients who have cirrhosis from etiologies other than alcoholic liver disease should also abstain from alcohol consumption to prevent further liver damage. 

Father was an alcoholic and died in his 50s of cirrhosis mother is alive and has an anxiety disorder and emphysema brother was incarcerated for attempted murder and drug trafficking sister has an anxiety disorder and self-medicates with marijuana SH... 

Non-cholestatic cirrhosis (e.g., alcoholic cirrhosis, postnecrotic cirrhosis, and drug-induced cirrhosis)... 

Immunosuppression—anatomic or functional asplenia, sickle cell disease, alcoholism, cirrhosis, immunoglobulin or complement deficiency cancer, HIV/AIDS, debilitated state of health... 

O Primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis.3 Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) average one episode of peritonitis every 2 years.4 Secondary peritonitis may be caused by perforation of a peptic ulcer traumatic perforation of the stomach, small or large bowel, uterus, or urinary bladder appendicitis pancreatitis diverticulitis bowel infarction inflammatory bowel disease cholecystitis operative contamination of the peritoneum or diseases of the female genital tract such as septic abortion, postoperative uterine infection, endometritis, or salpingitis. Appendicitis is one of the most common causes of intraabdominal infection. In 1998, 278,000 appendectomies were performed in the United States for suspected appendicitis.5... 

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