Alcohol: V Sem Kmc Ic

Alcohol V Sem KMC IC

ACUTE ETHANOL INTOXICATION

• An increased reaction time, • diminished fine motor control, • impulsivity, • and impaired judgment become evident when the concentration of ethanol in the blood is 20 to 30 mg/dl. • More than 50% of persons are grossly intoxicated by a concentration of 150 mg/dl. • In fatal cases, the average concentration is about 400 mg/dl. • In the United States, most states set the ethanol level defined as intoxication at 80 mg/dl. • There is increasing evidence that lowering the limit to 50 to 80 mg/dl can reduce motor vehicle injuries and fatalities significantly. • While alcohol can be measured in saliva, urine, sweat, and blood, measurement of levels in

Treatment of acute alcohol intoxication

• The treatment of acute alcohol intoxication is based on the severity of respiratory and CNS depression. • Acute alcohol intoxication can be a medical emergency, • Patients who are comatose and who exhibit evidence of respiratory depression • Should be intubated to protect the airway and to provide ventilatory assistance. • The stomach may be lavaged, but care must be taken to prevent pulmonary aspiration of the return flow. • Since ethanol is freely miscible with water,

• Acute alcohol intoxication is not always associated with coma, and careful observation is the primary treatment. • Usual care involves observing the patient in the emergency room for 4 to 6 hours while the patient metabolizes the ingested ethanol. • Blood alcohol levels will be reduced at a rate of about 15 mg/dl per hour. • During this period, some individuals may display extremely violent behavior. • Sedatives and antipsychotic agents have been employed to quiet such patients. • Great care must be taken, however, when using sedatives to treat patients who have ingested an excessive amount of another CNS depressant, i.e., ethanol, because of synergistic effects.

• The use of alcohol to treat patients in alcohol withdrawal or obstetrical patients with premature contractions is no longer recommended. • Some medical centers continue to use alcohol to prevent or reduce the risk of alcohol withdrawal in postoperative patients, • but administering a combination of a benzodiazepine with haloperidol or clonidine may be more appropriate.

Methanol Poisoning • Added to rectified spirit to render it unfit for drinking • No pharmacological relevence • Highly toxic

Treatment consists of

• Keep patient in quiet,dark room:protect eyes from light---even 15ml of methanol has caused blindness • Gastric Lavage with sodium bicarbonate to combat acidosis, • hemodialysis, and the • Pot Chloride is needed only when hypokalemia occurs • administration of ethanol, • Slows formate production by competing with methanol • For metabolism by alcohol dehydrogenase. • Fomipezole – inhibits Alcohol Dh • Folate therapy-Ca leucovorin reduces blood formate levels

CLINICAL USES OF ETHANOL • Dehydrated alcohol may be injected in close proximity to nerves or sympathetic ganglia -to relieve the long-lasting pain related to trigeminal neuralgia, inoperable carcinoma, and other conditions. • Epidural, subarachnoid, and lumbar paravertebral injections of ethanol also have been employed for inoperable pain. • For example, lumbar paravertebral injections of ethanol may destroy sympathetic ganglia • and thereby produce vasodilation, relieve pain, and • promote healing of lesions in patients with

• Systemically administered ethanol is confined to the treatment of poisoning by methyl alcohol and ethylene glycol. • The ingestion results in • formation of methanol's metabolites, formaldehyde and formic acid . • Formic acid causes nerve damage; its effects on the retina and optic nerve can cause blindness.

PHARMACOTHERAPY OF ALCOHOLISM • Currently, three drugs are approved in the United States for treatment of alcoholism: disulfiram (ANTABUSE), naltrexone (REVIA), and acamprosate.

• The goal of these medications is to assist the patient in maintaining abstinence. Naltrexone approved by the FDA for treatment of alcoholism in 1994. • opioid-receptor antagonist • has higher oral bioavailability and a longer duration of action. • Animal research and clinical experience suggested that

• blocks activation by alcohol of dopaminergic pathways in the brain that are thought to be critical to reward. Reduces the urge to drink and increasing control when a "slip" occurs. • not a "cure”. • It typically is administered after detoxification and given at a dose of 50 mg/day for several months. Adherence to the regimen is

Side effect of naltrexone • Nausea, which is more common in women than in men subsides if the patients abstain from alcohol When given in excessive doses, naltrexone can cause liver damage. It is contraindicated in patients with liver failure or acute hepatitis

Disulfiram (tetraethylthiuram disulfide; ANTABUSE)

• Similar responses to alcohol ingestion are produced by various congeners of disulfiram, namely, • cyanamide, • the fungus Coprinus atramentarius, • the hypoglycemic sulfonylureas, metronidazole, • certain cephalosporins, • and animal charcoal.

• It inhibits ALDH activity • causes the blood acetaldehyde concentration to rise to 5 to 10 times • when ethanol is given to an individual not pretreated with disulfiram. • oxidation of ethanol by ADH produces Acetaldehyde, • does not accumulate in the body because it is further oxidized almost as soon as it is formed primarily by ALDH

• Following the administration of disulfiram, • both cytosolic and mitochondrial forms of ALDH are irreversibly inactivated to varying degrees, • Concentration of acetaldehyde rises. • It is unlikely that disulfiram itself & • several active metabolites of the drug, especially diethylthiomethylcarbamate, • behave as suicide-substrate inhibitors of ALDH

• The ingestion of alcohol by individuals previously treated with disulfiram • Gives rise to marked signs and symptoms of acetaldehyde poisoning. • Within 5 to 10 minutes, • the face feels hot and soon afterward becomes flushed and scarlet in appearance. • As the vasodilation spreads over the whole body,

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Respiratory difficulties, nausea, copious vomiting, sweating, thirst, chest pain, considerable hypotension, orthostatic syncope, marked uneasiness, weakness, vertigo, blurred vision, and confusion are

• The drug never should be administered until the patient has abstained from alcohol for at least 12 hours. • In the initial phase of treatment, a maximal daily dose of 500 mg is given for 1 to 2 weeks. • Maintenance dosage then ranges from 125 to 500 mg daily depending on tolerance to side effects. • Sensitization to alcohol may last as long as 14 days after the last ingestion of disulfiram because of the

• Patients must learn to avoid disguised forms of alcohol, • as in sauces, • fermented vinegar, • cough syrups, • and even after-shave lotions and back rubs.

Side Effects • Rashes ,Metallic taste • Nervousness,malaise,abdominal pain • It inhibits a number of enzymes including Alcohol Dehydrogenase and Dopamine Beta Hydroxylase • Thus shall prolong the t half of many drugs • Disulfiram like reaction--Metronidazole

Acamprosate • Weak NMDA receptor antagonist with modest GABAA receptor antagonistic activity • Used in conjugation with Motivational therapy • Reduces relapse of drinking behaviour • Efficacy comparable to naltrexone