Alcohol ingestion

Ethanol distributes rapidly, with concentrations in body water 10 times higher than in body fat. The tissues with the greatest blood supply equdibrate most rapidly with arterial blood circulation. Shortly after alcohol ingestion, the ethanol concentration in the brain is higher than the venous concentration. 

Dietary factors such as coffee, tea, cola, beer, and a highly-spiced diet may cause dyspepsia, but they have not been shown to independently increase PUD risk. Although caffeine increases gastric acid secretion and alcohol ingestion causes acute gastritis, there is inconclusive evidence to confirm that either of these substances are independent risk factors for peptic ulcers. 

A 50- year-old male chronic alcoholic ingests methanol. Which of the following findings is associated with acute methanol ingestion ... 

Because total cholesterol is composed of cholesterol derived from LDL, VLDL, and HDL, determination of HDL is useful when total plasma cholesterol is elevated. HDL may be elevated by moderate alcohol ingestion (fewer than two drinks per day), physical exercise, smoking cessation, weight loss, oral contraceptives, phenytoin, and terbutaline. HDL may be lowered by smoking, obesity, a sedentary lifestyle, and drugs such as /1-blockers. 

Patients taking metronidazole should be instructed to avoid alcohol ingestion during therapy and for 1 to 2 days after completion of therapy because of a possible disulfiram-like effect. 

Calculate the amounts of the major components of the food (carbohydrate, fat, protein, including alcohol) ingested, from knowledge of the composition of the meal (obtained from information provided on the package of the food item or from food composition tables). 

Intoxication results in a characteristic intense, throbbing headache, presumably due to cerebral vasodilation, often associated with dizziness and nausea and occasionally with vomiting and abdominal pain. More severe exposure also causes hypotension, flushing, palpitation, low levels of methemoglobinemia, delirium, and depression of the central nervous system. Aggravation of these symptoms after alcohol ingestion has been observed. On repeated exposure, a tolerance to headache develops but is usually lost after a few days without exposure. At times, persistent tachycardia, diastolic hypertension, and reduced pulse pressure have been observed. On rare occasions, a worker may have an attack of angina pectoris a few days after cessation of repeated exposures, a manifestation of cardiac ischemia. Sudden death due to unheralded cardiac arrest has also been reported under these circumstances. ... 

Intolerance to alcohol, presenting as a transient redness affecting mainly the face and neck (trichloroethylene flush) has frequently been observed after repeated exposure to TCE and alcohol ingestion. It has been suggested that ingestion of alcohol may potentiate the effect of TCE intoxication. ... 

Disuifiram-aicohoi reaction Disulfiram plus alcohol, even small amounts, produces flushing, throbbing in head and neck, throbbing headaches, respiratory difficulty, nausea, copious vomiting, sweating, thirst, chest pain, palpitations, dyspnea, hyperventilation, tachycardia, hypotension, syncope, marked uneasiness, weakness, vertigo, blurred vision, and confusion. In severe reactions there may be respiratory depression, cardiovascular collapse, arrhythmias. Ml, acute CHF, unconsciousness, convulsions, and death. The intensity of the reaction is proportional to the amounts of disulfiram and alcohol ingested. The duration of the reaction varies from 30 to 60 minutes to several hours. 

Avoid alcohol ingestion, CNS depressants, OTC medications (cold, weight loss, hay... 

Alcohol has a triphasic effect on the elimination rates of drugs that require extensive biotransformation (21). For example, acute alcohol ingestion in combination with a TCA in a teetotaler who attempts suicide will significantly block the first-pass metabolism of the TCA. This chemical inhibition can triple the peak concentration of a TCA by increasing its bioavailability. This is why the consumption of alcohol in association with a TCA overdose increases lethality. 

Chronic alcohol ingestion can cause cirrhosis, reducing hepatic CYP enzyme concentration and liver mass, and causing portacaval shunting. These effects will result in increased plasma drug levels due to both greater bioavailability (due to reduced first pass metabolism) and due to decreased clearance. Thus, dose adjustment is necessary and should be guided by TDM when possible. 

Other portions of the gastrointestinal tract can also be injured. Chronic alcohol ingestion is by far the most common cause of chronic pancreatitis in the Western world. In addition to its direct toxic effect on pancreatic acinar cells, alcohol alters pancreatic epithelial permeability and promotes the formation of protein plugs and calcium carbonate-containing stones. 

In the body, Antabuse inhibits acetaldehyde oxidase, presumably via tbe soft-soft molybdenum-sulfur interaction.84 Any alcohol ingested will be converted to acetaldehyde which, in the absence of a pathwny to destroy it, will build up with severely unpleasant effects, discouraging further consumption. 

Yesavage, J. and Leirer, V., Hangover effects on aircraft pilots 14 hours after alcohol ingestion a preliminary report, Am. J. Psychiatry, 143, 1546, 1986. 

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