Alcohol poisoning with

Lobeline has also been advantageous for the treatment of victims who have been electrocuted or asphyxiated by toxic gasses. Moreover, it was useful in the case of the paralysis of respiratory centers after drug poisoning with alcohol, soporifics, or morphine or after narcosis. Lastly, it has also been used to treat asphyxia in newborn infants. 

Mononitrothiophene is an active poison. The accidental contact of an ethereal solution with the skin has produced painful blisters. In case of accident the compound should be removed from the exposed surface by washing with alcohol. 

Prominent co-catalysts for the Pt-on-carbon anode catalyst in the oxidation of polyhydric alcohols are Ru or Ce02 [54, 60]. Their increased resistance to poisoning with mainly CO during operation is associated with the existence of a bifunctional mechanism (Scheme 11.6). 

Finely chop the glands with a razor blade or pulverize in a blender. Extract the adrenalin into a small excess of hot H2O concentrate in a vacuum. Remove the salts and proteins (if proteins are not removed, they will give the same effect as blood poisoning from a rattle snake bite, but worse) by precipitating with alcohol and remove this precipitate by filtration. The filtrate is then distilled in vacuo to remove the adrenalin (1 would perform the filtration above, at room temp). Add a little ammonia to precipitate the active compound and filter from the water. The amount of ammonia depends on the amount of substance. To experiment, to get the proper amount, add a very little amount of ammonia to the distillate and filter off any precipitate if any forms. Add a little more ammonia and filter. Repeat until no more precipitate is formed, remember the amount of ammonia used and use this amount on the same amount of filtrate during the extraction of the next batch. 

Chromyl chloride reacts violently with alcohol, ammonia, and turpentine, igniting these liquids. Reactions with other oxidiazable substances can be violent. The liquid is corrosive and possibly a poison. Skin contact can cause bhs-ters. Exposure to its vapors causes severe irritation of the eyes, nose, and respiratory tract. Prolonged or excessive inhalation can cause death. 

In general, SSRI doses of 50 to 75 times the common daily doses result in minor symptoms. Higher doses cause serious symptoms of seizure, arrhythmias, and decreased consciousness only doses greater than 150 times the common daily therapeutic dose can result in death (Barbey and Roose, 1998). Overdose in combination with alcohol or other drugs increases toxicity and accounts for most fatalities involving the SSRIs. Nevertheless, compared to TCA medications, which annually results in 100 to 150 fatal overdoses reported to the American Association of Poison Control Centers (AAPCC), the SSRI agents accounted for only 16 fatal overdoses reported to that organization between 1987 and 1996 (Barbey and Roose, 1998). 

After 3 5 g of the hypnotic paraldehyde a qualitatively similar pattern of action was observed as with alcohol, although the stimulation phase was briefer and less pronounced and the paralysing action of the preparation was stronger. Following the intake of chloral hydrate and with the inhalation poisons the paralysing effect was still more pronounced. 

At this point, every patient with altered mental status should receive a challenge with concentrated dextrose, unless a rapid bedside blood glucose test demonstrates that the patient is not hypoglycemic. Adults are given 25 g (50 mL of 50% dextrose solution) intravenously, children 0.5 g/kg (2 mL/kg of 25% dextrose). Hypoglycemic patients may appear to be intoxicated, and there is no rapid and reliable way to distinguish them from poisoned patients. Alcoholic or malnourished patients should also receive 100 mg of thiamine intramuscularly or in the intravenous infusion solution at this time to prevent Wernicke s syndrome. 

Fig. 14. Taft correlation with polar substituent constants (a ) of the vapour phase esterification of acetic acid with alcohols ( ) and of the olefin formation from alcohols (O) over Na-poisoned silica—alumina at 250°C [126]. 1, Methanol 2, ethanol 3, 1-propanol 4, 1-butanol 5, 2-methyl-l-propanol 6, 2-propanol 7, 2-butanol 8, 2-methyl-2-propanol.

On the other hand, drugs may inhibit the metabolism of other drugs. For example, allopurinol (a xanthine oxidase inhibitor that inhibits the synthesis of uric acid) increases the effectiveness of anticoagulants by inhibiting their metabolism. Chloramphenicol (a potent inhibitor of microsomal protein synthesis) and cimetidine (an H2-receptor blocker used in acid-pepsin disease) have similar properties. In addition, drugs may compete with each other in metabolic reactions. In methyl alcohol (methanol) poisoning, ethyl alcohol may be given intravenously to avert methanol-induced blindness and minimize the severe acidosis. Ethyl alcohol competes with methyl alcohol for... 

An unsavoury case study of TA poisoning was reported by Kintz et al. proving the systematic and continuous scopolamine intake of children who were forced by their own mother to take 4-10 Feminax tablets per day for months. Evidence of scopolamine was achieved by LC-ESI MS/MS analysis of hair samples (Table 3). The Children survived and their mother had to face a charge of their offence [56], Moreover, TA were also misused to commit suicide sometimes in combination with alcohol and other drugs [125-127],... 

Caution of Methyl Alcohol (Wood Alcohol) Methanol is commonly added to the rectified spirit, which makes it unfit to drink. Mixing methanol with alcoholic beverages results in methanol poisoning. Methanol is metabolized to formaldehyde and formic acid by aldehyde dehydrogenase. High blood levels (750 mg/dL) cause severe poisoning, which leads to blindness and even death. 

Biguanides This class of antidiabetics may cause acute poisoning with adverse effects such as acidosis and may be treated by supportive therapy. These drugs have therapeutic interactions with other antidiabetic drugs, alcohol, drugs that affect kidney function, and cimetidine. 

Figueras Roca and co-workers (346) have used preadsorbed TCNE to poison the basic sites specifically. The rate of ether formation from methanol and ethanol responded very sensitively to the poisoning with TCNE, so that the participation of basic sites in the bimolecular alcohol dehydration seems to be proved. 

A survey in Britain covering the decade of the 1980s demonstrated large numbers of successful suicides using BZs, either alone or in combination with alcohol (Serfaty et al., 1993 see also Buckley et al., 1995). Serfaty and Masterton (1993) found 891 fatalities with BZs alone and 591 in combination with alcohol. The total of all poisonings attributed to BZs was 1,576 during the 10-year period, putting them ahead of aspirin/ salicylates at 1,308 as well as amitriptyline (1,083) and dothiepin at 981. 

Prereduced rhenium heptoxide catalyst,65 especially the catalyst poisoned with pyridine, has been found to give high yields of unsaturated alcohols in the hydrogenation of unsaturated aldehydes (Table 5.2).66 A typical hydrogenation with the rhenium catalyst is shown in eq. 5.27. In the vapor phase hydrogenation of acrolein to allyl alcohol, the selectivity of rhenium catalysts has been found to be improved by poisoning with CO and CS2.67... 

Ruthenium tetroxide dissolves to a slight extent in water. It is also soluble in caustic alkali, from which solutions a black precipitate of finely divided ruthenium is obtained on addition of alcohol.2 Both the aqueous solution and the pure substance itself possess an odour resembling that of ozone. Its vapour, however, is not poisonous like that of the corresponding tetroxide of osmium. In contact with alcohol the solid tetroxide is reduced with explosive violence.3-4 When covered with water, to which a concentrated solution of caesium chloride is subsequently added and a little hydrochloric acid, ruthenium tetroxide is gradually converted into the oxy-salt, Cs2Ru02CI4. The corresponding rubidium salt has likewise been prepared.3... 

Several clinical studies have provided circumstantial evidence that a free-radical mechanism might be responsible for increased levels of 18 2(9-m,l -trans) in blood. Significantly raised levels of the isomer have been detected in the serum of chronic alcoholics (Fink et al., 1985 Szebeni et al., 1986). It is suggested that a free radical-dependent detoxifying mechanism is invoked by heavy alcohol loads in such persons and similar high levels have also been found in the plasma of persons poisoned with paraquat, the toxicity of which is known to involve free radicals (Crump et al., 1988), in chronic biliary cirrhosis... 

Carbon tetrachloride is colorless, heavy, non-flammable liquid with a characteristic odor. It has a boiling point of 78 Celsius, and a melting point of -23 Celsius. Carbon tetrachloride is insoluble in water, but miscible with alcohol, benzene, chloroform, ether, and carbon disulfide. Carbon tetrachloride is a potential poison, and inhalation, ingestion, and skin absorption should be avoided at all cost. Carbon tetrachloride may be a carcinogen. It is prepared on an industrial scale by the chlorination of methane, but can be conveniently prepared by reacting chlorine with carbon disulfide in the presence of iron fillings the carbon tetrachloride is recovered by distillation. 

NIOSH REL (Diisocyanates) TWA 0.005 ppm CL 0.02 ppm/lOM DOT CLASSIFICATION 6.1 Label Poison SAFETY PROFILE Poison by inhalation and intravenous routes. Moderately toxic by ingestion and skin contact. Potentially explosive reaction with alcohols + base. When heated to decomposition it emits toxic fumes of NO. See also CYANATES. 

---