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Historical records of indigenous cultures in South America describe early stimulant use by chewing leaves of the Erythroxylum coca plant, a practice that continues today. Cocaine was first used therapeutically in 1884 for ophthalmologic procedures, accompanied closely by reports of severe toxicity. Amphetamines were synthesized in 1887, and in 1932, they were marketed medicinally in an inhaler form as a bronchodilator. Use of methamphetamine to enhance physical and intellectual performance began in the 1930s. Amphetamines were widely used as an alertness aid for troops by both Allied and Axis powers during World War II. Today, cocaine and amphetamines have limited therapeutic roles but are widely used as drugs of abuse. Clinical effects and toxicity are due to sympathetic nervous system stimulation.



Cocaine is the naturally occurring alkaloid found in E. coca, a plant indigenous to South America. The water-soluble hydrochloride salt is absorbed across all mucosal surfaces, including oral, nasal, GI, and vaginal epithelium; cocaine can thus be topically applied, swallowed, or injected IV. The hydrochloride salt (powder) form is most often insufflated (snorted) or dissolved in water and injected IV; it degrades rapidly when pyrolyzed. Freebase cocaine can be smoked because it melts at a much lower temperature and can be prepared in many ways. A common method uses an alkali, such as sodium bicarbonate, to produce “crack cocaine,” which, when smoked, produces the popping sound that characterizes its name. The onset and duration of action vary with the route of administration (Table 187-1).

TABLE 187-1Pharmacokinetics of Cocaine

When cocaine is insufflated nasally, the delayed and prolonged effect is a result of vasoconstrictive properties that limit mucosal absorption followed by swallowing a portion of the insufflated cocaine, which is then absorbed from the stomach. GI absorption is also prolonged by vasoconstriction, producing delayed peak effect.

Cocaine is primarily metabolized to ecgonine methyl ester by plasma cholinesterase. Relative deficiency of this enzyme may predispose affected patients to life-threatening toxicity.1 Benzoylecgonine is the other major metabolite excreted in the urine and is the target compound detected in routine urine toxicology screens. Cocaethylene is a long-acting metabolite formed when cocaine is used in combination with ethanol. Cocaethylene has vasoconstrictive properties similar to those of cocaine.

Cocaine is both a CNS stimulant and a local anesthetic.2,3 Central ...

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