Alcohol acute ingestion

Drug-induced AF is relatively uncommon, and the list of drugs that may induce AF is relatively small.13 However, acute ingestion of large amounts of alcohol may cause AF this phenomenon has been referred to as the holiday heart syndrome.19... 

Chronic ethanol use increases the risk of hepatotoxicity when acetaminophen is used in high doses however, acute ingestion of alcohol along with an acetaminophen overdose decreases the toxicity of acetaminophen. 

In addition to the acute ingestion of these hallucinogenic drugs, the chronic use of alcohol, amphetamines, or cocaine can lead to paranoia that in many respects resembles the psychosis of schizophrenia. In these cases, the psychotic symptoms may persist long after the substance use has been stopped. 

Ethanol. Alcohol (ethanol) ingestion has repeatedly been associated with potentiation of carbon tetrachloride-induced hepatic and renal injury in humans. In two cases in which men cleaned furniture and draperies with carbon tetrachloride, one man, a heavy drinker, became ill and died (Smetana 1939). His coworker, a nondrinker, suffered a headache and nausea but recovered quickly after breathing fresh air. Both men were subjected to the same carbon tetrachloride exposure, as they had been working in the same room for the same amount of time. In 19 cases of acute renal failure due to carbon tetrachloride inhalation or ingestion, 17 of 19 patients had been drinking alcoholic beverages at about the time of their carbon tetrachloride exposure (New et al. 

BETA-BLOCKERS ALCOHOL Acute alcohol ingestion may t hypotensive effect. Chronic moderate/heavy drinking 1 hypotensive effect Additive hypotensive effect. Mechanism of opposite effect with chronic intake is uncertain Monitor BP closely as unpredictable responses can occur. Advise patients to drink only in moderation and to avoid large variations in the amount of alcohol drunk... 

POTASSIUM CHANNEL ACTIVATORS ALCOHOL Acute alcohol ingestion may t hypotensive effects. Chronic moderate/heavy drinking 1 hypotensive effect... 

SSRIs ALCOHOL t risk of sedation Additive CNS depressant effects. Acute ingestion of alcohol inhibits CYP2D6 and CYP2C19, whereas chronic use induces CYP2E1 and CYP3A4 Be aware and caution against excessive alcohol intake... 

Alcohol. Alcohol induces hyperzincuria (8,9). The mechanism is unknown. A direct eflFect of alcohol on renal tubular epithelium may be responsible for hyperzincuria. Acute ingestion of alcohol did not induce zincuria (30) in some experiments, however, Gudbjamason and Prasad (31) reported increased urinary zinc excretion following alcohol intake. This eflFect was evident when complete urine collection was analyzed for zinc during first three-hour and second three-hour periods, following ingestion of six ounces of chilled vodka. 

Intoxicating amounts of alcohol stimulate the release of cortisol, although the effect is more related to the intoxication than to the alcohol per se. SympatheticomeduUary activity is increased by acute alcohol ingestion but without detectable effect on the plasma epinephrine concentration and only a mild effect on norepinephrine. With intoxication, plasma concentrations of catecholamines are substantially increased. Acute ingestion of alcohol leads to a sharp reduction in the plasma testosterone in men, with an increase in the plasma luteinizing hormone concentration. 

Chronic liver disease reduces cortisol clearance and the production of urinary metabolites. Cortisol concentrations are elevated by acute ingestion of alcohol. Individuals with alcoholic cirrhosis have normal to elevated basal cortisol concentrations, blunted circadian rhythms, and prolonged clearance rates. 

In a study designed to test the effeets of acute alcohol intoxication in epileptics, 25 patients were given a 12 oz (about 340 mL) drink of alcohol 25%. Blood-alcohol levels ranged from 39 to 284 mg%. All patients had signs of alcohol intoxication without any effect on seizure frequency. The metabolism of a single dose of phenytoin was not affected in one study in healthy subjects by the acute ingestion of alcohol. However, the manufacturers say that acute alcoholic intake may increase phenytoin serum levels. ... 

Acute ingestion of alcohol markedly increases the levels of circulating estradiol in women using oral HRT a smaller increase is seen with transdermal HRT. In addition, alcohol intake appears to increase the risk of breast cancer in women receiving HRT. Small amounts of alcohol may possibly improve some aspects of cognitive function in patients using HRT. Estradiol does not affect blood-alcohol levels. 

Empirical C16H32 Formula CH3(CH2)i3CH=CH2 Properties Colorless liq., mild hydrocarbon odor sol. in alcohol, ether, petrol, and coal-tar soivs. si. sol. in water dens. 0.785 b.p. 518-554 F m.p. 37 F ref. index 1.4420 flash pt. (Seta) 272 F Toxicology Irritating to skin and eyes low acute inhalation toxicity low acute ingestion toxicity but ingestion may cause vomiting, aspiration of vomitus... 

Toxicity. Sugar alcohols are classified as relatively harmless. Acute oral toxicity values in mice for mannitol and sorbitol (5) are given in Table 4. The acute oral LD q value for xyUtol in mice is 25.7 g/kg (205). Ingestion of 10 g/d of either mannitol or sorbitol by a normal human subject for one month resulted in no untoward effects (206). XyUtol given to healthy humans for 21 d in increasing doses up to 75 g/d produced no adverse effects (207). The limiting dose of xyUtol for production of diarrhea in humans is 20—30 g (4), but tolerance usually develops on continued adrninistration (207). 

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 ... 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to carbon monoxide diabetic ketoacidosis, hypothyroidism and myxedema coma, labyrinthitis, and lactic acidosis toxic exposures resulting in methemoglobinemia ingestion of alcohols or narcotics and diseases that cause gastroenteritis, encephalitis, meningitis, and acute respiratory distress syndrome. 

On the basis of acute animal studies, n-propyl alcohol appears to be slightly more toxic than isopropyl alcohol. No chronic effects have been reported in humans, although a human fatality has been ascribed to ingestion. Exposure to 400 ppm for 3-5 minutes will reportedly... 

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. 

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. 

Fatalities due to acute BZD overdose alone are extremely rare. Nevertheless, fatal overdoses with triazolam in the elderly have been reported ( 192, 193). Even with ingestion of massive doses, recovery appears to be rapid and without serious complications or aftereffects ( 194, 195, 196 and 197). Combined ingestion of BZDs with other CNS depressants (alcohol, barbiturates, narcotics, orTCAs), however, may result in severe CNS and respiratory depression or hypotension. Severity of symptoms appears to depend more on the type and quantity of the other drugs than on the BZD plasma level (194, 195, 196 and 197). 

Clinical signs and symptoms include sudden onset of irrational, combative, or destructive behavior after ingesting relatively small amounts of alcohol. The behavior is atypical of the individual when not drinking, and usually begins within minutes to hours. After the acute outburst, the patient usually lapses into deep sleep and upon awakening has only fragmentary memory or total amnesia for the episode. Treatment should attempt to diminish stimulation as much as possible, and antipsychotics, such as haloperidol (2 to 5 mg orally, i.m., or i.v.) may reduce combative or destructive behavior. 

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