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Ethanol abuse

O The most common causes of acute and chronic pancreatitis in adults are ethanol abuse and biliary stones. [Pg.337]

Treatment of chronic pancreatitis is aimed at removing the cause (ethanol abuse or biliary stones), providing analgesia, supplementing with pancreatic enzyme preparations, and implementing dietary restrictions. [Pg.337]

Ethanol abuse may cause precipitation of pancreatic enzymes in the ducts of the pancreas leading to chronic inflammation and damage. Ethanol itself may be directly toxic to the pancreatic cells. Gallstones may obstruct the ampulla of Vater causing pancreatic enzymes or bile to move in a retrograde fashion into the pancreas.1... [Pg.338]

The incidence of chronic pancreatitis is approximately 1 in 10,000 people. O The most common cause of chronic pancreatitis in adults in Western countries is ethanol abuse. The most common cause in children is cystic fibrosis, due to preexisting pancreatic insufficiency inherent in the disease. Gallstones can occur at the same time as chronic pancreatitis but are not often implicated as the cause. Unlike acute pancreatitis, chronic pancreatitis has an unknown etiology in a significant number of cases (30%).29,3°... [Pg.341]

Wilson, L.D., Jeromin, J., Garvey, L., and Dorbandt, A., Cocaine, ethanol, and cocaethylene cardiotox-icity in an animal model of cocaine and ethanol abuse, Acad. Emerg. Med., 8, 211, 2001. [Pg.19]

Monitoring Perform periodic complete blood counts and clinical chemistry tests. Monitor serum amylase levels in those individuals who have a history of elevated amylase, pancreatitis, ethanol abuse, who are on parenteral nutrition, or who are otherwise at high risk of pancreatitis. [Pg.1865]

EtG and EtS are minor phase II metabolites of alcohol and their presence in a biological sample unequivocally attests exposure to this substance. They can be measured in serum [7] and urine [9,11-13] even after ethanol has been eliminated. Recently, the determination of EtG in hair has been proposed as a sensitive and specific marker of chronic ethanol abuse [8,10], The determination of EtG in postmortem blood enables the discrimination between ethanol postmortem formation and alcohol intake before death [17],... [Pg.663]

Serum amylase and triglyceride concentrations in patients with history of elevated amylase, pancreatitis, ethanol abuse, or receiving parenteral nutrition... [Pg.1313]

Manno M, Rezzadore M, Grossi M, Sbrana C. 1996. Potentiation of occupational carbon tetrachloride toxicity by ethanol abuse. Hum Exp Toxicol 15 294—300. [Pg.251]

Alcohol abuse can predispose to paracetamol hepatotoxicity (84-91), even in moderate social drinkers who take therapeutic or modestly excessive doses (92), and there have been anecdotal reports of severe hepatotoxicity in chronic ethanol abusers after ingestion of 4 g/day (93). Alcoholics are more likely to exceed the recommended dosage of paracetamol and consequently may be at higher risk of hepatotoxicity than non-alcoholics (91,94). [Pg.2686]

A 37-year-old man with a history of ethanol abuse presented with hepatic failure and non-cardiogenic pulmonary edema after an overdose of paracetamol, codeine, ibuprofen, and diazepam. He received two... [Pg.3681]

Chemical/Pharmaceutical/Other Class Thiuram derivative Ethanol abuse deterrent... [Pg.895]

The mainstay of medical treatment of patients with ethanol toxicity is supportive care. In general, a conservative approach is recommended for ethanol intoxication. Supportive therapy for overdose may include treatment for respiratory depression, hypotension, and altered glucose or thiamine levels. If the ingestion occurred within one hour of presentation, placing a nasogastric tube and evacuating the stomach contents can prove helpful. In patients with chronic ethanol abuse, therapy may include administration of thiamine to prevent neurologic injury. The administration of medications to cause emesis is not recommended because of the rapid onset of CNS depression as well as aspiration risks. [Pg.1076]

The complications of ethanol abuse are many. Ethanol-containing mouthwash products may be used by a chronic abuser as an alcohol substitute. [Pg.1747]

Obsessive compulsive disorder, panic disorder, generalized anxiety disorder, bulimia nervosa, social anxiety disorders, post-traumatic stress disorder, dementia, dysthymia, premature ejaculation. Citalo-pram (investigational) is used for dementia, smoking cessation, ethanol abuse, OCD in children with diabetic neuropathy. Sertraline and Sarafem (contains fluoxetine) are also used to treat premenstrual dysphoric disorder. [Pg.2471]

Fat malabsorption, particularly caused by celiac disease or chronic pancreatitis, and protein-energy malnutrition predispose to vitamin A deficiency. Liver disease diminishes RBP synthesis, and ethanol abuse leads both to hepatic injury and to a competition with retinol for alcohol dehydrogenase, which is necessary for the oxidation of retinol to retinal and retinoic acid. Vitamin A deficiency may lead to anemia, though the precise mechanism is not known. ... [Pg.1082]

Ketosis can occur in starvation, in ethanol abuse, and following exercise, the last because of a switch in blood... [Pg.376]

Alcoholism affects about 10% of the drinking population and alcohol (ethanol) abuse has been implicated in at least 20% of admissions to general hospitals. This chronic disease exhibits high mortality due to a wide variety of factors. Ethanol produces effects in virtually every organ system. The biochemical effects of ethanol are due to increased production of NADH that decreases the [NAD ]/[NADH] ratio in the cytoplasm of liver cells at least tenfold from the normal value of about 1000. Increased production of lactate and inhibition of gluconeo-genesis (Chapter 15) result. The hyperuricemia associated with ethanol consumption has been attributed to accelerated turnover of adenine nucleotides and their catabolism to uric acid (Chapter 27). Alcohol increases hepatic fatty acid and triacylglycerol synthesis and mobilization of fat from adipose tissue, which can lead to fatty liver, hepatitis, and cirrhosis. These effects are complicated by a deficiency of B vitamins and protein. [Pg.378]

Since hypercholesterolemia (in particular, LDL cholesterol) increases the risk of CHD, it seems reasonable to lower cholesterol levels in patients whose levels put them at risk. Before treatment, other risk factors such as hypertension, cigarette smoking, obesity, and glucose intolerance need to be evaluated and corrected. Disorders that exacerbate hyperlipoproteinemia (e.g., chronic ethanol abuse, hypothyroidism, diabetes mellitus) need to be treated before lipid-lowering measures are taken (discussed earlier. Table 20-7). [Pg.448]

We also demonstrated in this study that FAEE synthase activity could be induced nearly twofold in the WBC fraction of humans ingesting 2 oz of scotch whiskey for 6 d (Gorski. 1996). This supports the conclusion that FAEE synthase is regulated to some extent by the presence of ethanol. Ihe enzyme activity returned to baseline levels despite ingestion of 2 oz of scotch whiskey for an additional 3 d. In this report, it was also shown that alcoholic individuals have approximately half the WBC FAEE synthase activity detected in normal controls. The lower enzyme activity observed in the WBCs of alcoholics in a detoxification center may be the result of years of ethanol abuse, or it may be that alcoholics congenitally have low levels of FAEE synthase. If the latter is true, this finding may explain, in part, the genetic predisposition of many alcoholic individuals to ethanol abuse. [Pg.299]

Laposata EA, Lange LG. Presence of nonoxidative ethanol metabolism in human organs commonly damaged by ethanol abuse. Science 1986 231 497-499. [Pg.307]

I Chronic ethanol abusers are prone to a variety of serum electrolyte disorders including hypocalcemia, hypomagnesemia. [Pg.961]

The first step in clinical management of erectile dysfunction is to identify, and if possible to reverse, underlying causes. Risk factors for erectile dysfunction, including hypertension, diabetes mellitus, smoking, or chronic ethanol abuse, should be addressed and mini-... [Pg.1520]

Chronic alcohol abuse can be very difncull to detect, and is usually determined from the patient s history. In order to be more objective, there has been a continued search for markers of ethanol abuse. As yet there is no highly sensitive and specific marker. However, a number of blood components are altered and these can give an indication of chronic alcohol ingestion. The most commonly used are ... [Pg.33]

Serum 7GT is of limited value for diagnosis of ethanol abuse but good for monitoring abstinence. [Pg.33]


See other pages where Ethanol abuse is mentioned: [Pg.484]    [Pg.826]    [Pg.237]    [Pg.339]    [Pg.342]    [Pg.290]    [Pg.428]    [Pg.77]    [Pg.77]    [Pg.644]    [Pg.484]    [Pg.826]    [Pg.3072]    [Pg.895]    [Pg.260]    [Pg.179]    [Pg.345]    [Pg.440]    [Pg.291]    [Pg.293]    [Pg.294]    [Pg.295]    [Pg.33]   
See also in sourсe #XX -- [ Pg.179 ]

See also in sourсe #XX -- [ Pg.288 , Pg.292 ]

See also in sourсe #XX -- [ Pg.99 ]

See also in sourсe #XX -- [ Pg.457 ]




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