Methanol poisoning ethanol

Contraindications Intestinal obstruction, GI tract not anatomically intact patients at risk of hemorrhage or GI perforation, if use would increase risk and severity of aspiration not effective for cyanide, mineral acids, caustic alkalis, organic solvents, iron, ethanol, methanol poisoning, lithium do not use charcoal with sorbitol in patients with fructose intolerance, hypersensitivity to charcoal or any component of the formulation... 

Alkali AletalIodides. Potassium iodide [7681-11-0] KI, mol wt 166.02, mp 686°C, 76.45% I, forms colorless cubic crystals, which are soluble in water, ethanol, methanol, and acetone. KI is used in animal feeds, catalysts, photographic chemicals, for sanitation, and for radiation treatment of radiation poisoning resulting from nuclear accidents. Potassium iodide is prepared by reaction of potassium hydroxide and iodine, from HI and KHCO, or by electrolytic processes (107,108). The product is purified by crystallization from water (see also Feeds and feed additives Photography). 

Biological oxidation of methanol and ethanol in the body produces the corresponding aldehyde followed by the acid. At times the alcoholics, by mistake, drink ethanol, mixed with methanol also called denatured alcohol. In the body, methanol is oxidised first to methanal and then to methanoic acid, which may cause blindness and death. A methanol poisoned patient is treated by giving intravenous infusions of diluted ethanol. The enz5mie responsible for oxidation of aldehyde (HCHO) to acid is swamped allowing time for kidneys to excrete methanol. 

Ekins BR et al Standardized treatment of severe methanol poisoning with ethanol and hemodialysis. WestJ Med 142 337-340, 1985... 

It is critical that the blood methanol level be determined as soon as possible if the diagnosis is suspected. Methanol concentrations higher than 50 mg/dL are thought to be an absolute indication for hemodialysis and treatment with fomepizole or ethanol, although formate blood levels are a better indication of clinical pathology. Additional laboratory evidence includes metabolic acidosis with an elevated anion gap and osmolar gap (see Chapter 59). A decrease in serum bicarbonate is a uniform feature of severe methanol poisoning. 

As with methanol poisoning, early fomepizole or ethanol infusion and hemodialysis are standard treatments for ethylene glycol poisoning. Fomepizole, an inhibitor of alcohol dehydrogenase, has FDA approval for treatment of ethylene glycol poisoning in adults based on its ability to decrease concentrations of toxic metabolites in blood and urine and to prevent... 

Table 58-2 lists the concentration and expected contribution to the serum osmolality in ethanol, methanol, ethylene glycol, and isopropanol poisonings. 

We have already discussed a therapeutic application of inhibition in the example of ethanol being used as an antidote to ethylene glycol or methanol poisoning. There are many other such cases which could also be cited. Antabuse , disulfiram, prevents the metabolism of ethanol. As a result a person under treatment with Antabuse will become violently ill if s/he consumes ethanol. Barbiturates are rapidly metabolized especially if a person has been on a prescription for some time. Administering the antibacterial chloramphenicol will inhibit the breakdown of barbiturates and in so doing prolong their sedative action. 

Ethyl alcohol has a density of 0.79 g/mL. What volume of ethyl alcohol is needed to treat methanol poisoning, if the physician orders 200 g of ethanol ... 

A chronic alcoholic requires a much larger dose of ethanol as an antidote to methanol poisoning than does a nonalcoholic patient. Suggest a reason why a larger dose of the competitive inhibitor is required for an alcoholic. 

Because alcohol dehydrogenase has a higher affinity for ethanol than methanol, methanol poisoning is treated by giving ethanol to the afflicted individual. With both methanol and ethanol in the patient s system, alcohol dehydrogenase reacts more readily with ethanol, allowing the methanol to be excreted unchanged without the formation of methanol s toxic oxidation products. 

Treatment begins with supportive care, and enteric suction is useful only if recent ingestion or retained gastric methanol is suspected. To prevent formation of toxic metabolites, fomepizole (4-methyl pyrazole or 4-MP) or ethanol to inhibit ADH should be administered. Fomepizole is preferred over ethanol if available [93]. It is well tolerated and may improve initial visual defects [94]. Mild methanol poisoning with levels below 20 mg/ dL can likely be treated with fomepizole only and bicarbonate however a methanol elimination half-life of over 50 hours with fomepizole requires prolonged infusion and monitoring [95]. Folic or folinic acid should be administered to promote conversion of formate to water and carbon dioxide [96]. 

Large epidemics of methanol poisoning have resulted from it being substituted for ethanol in Moonshine (illegally produced drinking alcohol). Recently, a new antidote, fomepizole, has been approved for use in the United States. 

Typically, the effects noted in methanol poisoning can be divided into three stages (1) narcosis or CNS depression similar to that observed in ethanol intoxication (2) a latent period, generally 10-15 h but can be prolonged if ethanol is coingested and (3) visual disturbances, metabolic acidosis and possibly multiorgan failure leading to death. 

C. Ethanol will prevent formation of formaldehyde in methanol poisoning. 

Ethanol Methanol or ethylene glycol Fomepizole (ADH inhibitor) now approved for ethylene glycol and methanol poisoning... 

Any two compounds which are metabolized by the same enzyme may competitively inhibit the metabolism of the other. The extent of this will depend on the affinity each compound has for the enzyme. One example where this is important toxicologically is in the treatment of ethylene glycol and methanol poisoning. Both of these compounds are toxic as a result of metabolism by the enzyme alcohol dehydrogenase (see Chapter 7). Consequently one method of treatment is to reduce this by administration of ethanol, which has a greater affinity for the enzyme and so reduces metabolism and toxicity. 

The treatment of methanol poisoning involves firstly the administration of an antidote, ethanol, which blocks metabolism. Ethanol competes with methanol for alcohol dehydrogenase as the enzyme has a greater affinity for ethanol. Methanol metabolism can be reduced by as much as 90% by an equimolar dose of ethanol and the half-life becomes extended to 46 h. 4-Methylpyrazole, which also binds to alcohol dehydrogenase, has been used successfully in monkeys to treat methanol poisoning, as has folic acid. 

Side note Methanol Poisoning. An interesting and imponant example competitive substrate inhibition is the enzyme alcohol dehydrogenase (AC in the presence of ethanol and methanol. If a person ingests methanol, Al will convert it to formaldehyde and then formate, which causes blindne Consequently, the treatment involves intravenously injecting ethanol (wh is metabolized at a slower rate than methanol at a controlled rate to tie ADH to slow the metabolism of methanol-to-formaldehyde-to-formate so l the kidneys have time to filter out the methanol which is then excreted in urine. With this treatment, blindness is avoided. For more on the met nol/ethanol competitive inhibition, see Problem P7 2Sc. 

The emergency room treatment for methanol poisoning is to inject ethanol intravenously to tie up the alcohol dehydrogenase enzyme so that methanol will not be converted to formic acid and formate, which causes blindness. The goal of this open-ended problem is to build on the physiological-based model for ethanol metabolism to predict the ethanol injection rate for methanol poisoning. One can find a start on this problem by reading problem P7-25c. 

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