Stimulants:Cocaine-Crack, Amphetamines
Basic Olicognograph: * * * * * *
Cocaine Crack
Cocaine is derived from leaves of the erythroxylum coca plant, grown in the Andes mountains. When treated with hydrochloric acid it becomes cocaine hydrochloride salt which is water soluble and decomposes on heating. Such properties make this form amenable to intravenous injection or snorting through the nasal mucosa. Cocaine alkaloid (freebase or crack cocaine) is an insoluble crystalline substance that when heated converts to a vapour that can be inhaled
Cocaine produces its effects by acting on the brain’s limbic system, a set of interconnected regions that regulate pleasure and motivation. An initial, short-term effect (buildup of dopamine) gives rise to euphoria and a desire to take the drug again. Dopamine acts as a pacesetter for many nerve cells throughout the brain. At every moment dopamine is responsible for keeping cells operating at the appropriate levels of activity to accomplish our needs and aims. Whenever we need to mobilize our muscles or mind to work harder or faster, dopamine drives some of the involved brain cells to step up to the challenge.
Cocaine interferes with control mechanism: It ties up the dopamine transporter, a protein that dopaminergic cells use to retrieve dopamine reuptake from surroundings. One particular part of the limbic system, the nucleus accumbens (NAc), seems to be the most important site of the cocaine high. Amount of dopamine connecting to receptors in the NAc after a dose of cocaine can exceed the amounts associated with natural activities, producing pleasure greater than that which follows thirst-quenching or sex. Limbic system also includes important memory centers as hippocampus and amygdala. These help us remember. They integrate information and weighs different courses of action. Also frontal cortex acts as a brake on the other regions of the limbic system, when we decide to forgo a pleasure in order to avoid its negative. Person heed the disastrous prognosis of continued cocaine abuse and suppress drug-taking urges emanating from the NAc, hippocampus, and amygdala.
Cocaine intoxication is a common problem in emergency departments. Morbidity and mortality in cocaine abusers are accentuated by co-ingestion of illicit drugs (heroin), alcohol and nicotine. Potentially fatal complications of cocaine abuse include delirium, hyperthermia, myocardial infarction, stroke, intracerebral bleeding or acute renal failure due to rhabdomyolysis (destruction of striated muscle). Non-selective beta-adrenergic receptor antagonists are contraindicated in the treatment of cardiovascular complications associated with cocaine abuse. Selective beta-blocking agents are not recommended. Benzodiazepines are effective as first line treatment for cocaine-related clinical symptoms such as delirium, hyperthermia, hypertension and tachycardia.
With some individuals, the recreational use of cocaine evolves into entrenched patterns of addiction that progressively dominate all aspects of their lives. Why some but not all cocaine users cross the line into addiction is not known. Profound loss of control is the hallmark of cocaine addiction and a quintessential issue in its treatment. Denial, another essential element of cocaine addiction, prevents cocaine-addicted individuals from realizing their loss of control and shields them from their progressive impairment even when it is obvious to everyone else in their life. As a result of denial, these patients overestimate their ability to quit cocaine and erroneously believe they can reduce or otherwise control the amount consumed. Cocaine euphoria and craving alternate over time to form a cycle of addiction that becomes increasingly entrenched and uncontrollable. The severity of cocaine addiction also progresses very rapidly in vulnerable individuals. While it may take years or decades for alcoholics to develop end stage alcoholism, progression to severe cocaine dependence typically occurs more rapidly. Cocaine produces rebound craving and uncontrollable binges.
General treatment directives: - Maintain total abstinence from cocaine (cardinal), alcohol, opiods, marijuana, and addictive pills (avoid stimuli that induce cocaine craving). - Avoid people, places and things associated with cocaine use (Cognitive behavioral therapy may be very effective in this regard). - Overcome denial and admit to the consequences of the addiction (Most are able to remain abstinent for one day, but worrying about staying abstinent for years or decades can be demoralizing, often leading the person to rationalize the immediate use of cocaine). - Attend treatment sessions on a regular basis (psychotherapy research has demonstrated efficacy for several specialized treatments in cocaine-addicted patients). Maintain openness and honesty in treatment. - Discuss emotionally important issues. - Learn drug-free coping skills. - Utilize craving reduction techniques.
Contingency management approaches that provide payment vouchers to abstinent cocaine patients have been reported to improve both retention rates and outcome. Cognitive behavioral therapy has also been shown to improve outcome in cocaine-addicted individuals and provide benefit for comorbid psychosocial problems. Individual drug counseling utilizing a disease model is particularly effective in cocaine addiction, underscoring the value of 12-step principles. Patients enrolled in treatment programs should be regularly monitored for relapse. When denial, urine benzoylecgonine levels (a cocaine metabolite with urinary persistence for several days) are monitored to identify relapse and provide deterrence. Deterioration in attitude, such as the emergence of negativity, resistance, or cynicism, usually precedes relapse and should be openly discussed with the patient.
Amphetamines is a group of addictive drugs that has potent effects by stimulating the release of monoamines, primarilly of dopamine from nerve terminals via the dopamine transporter, inhibiting monoamine oxidase, and blocking neuronal reuptake of monoamines from the synapse . It is noted for its marked CNS stimulant actions. Amphetamines are used for the subjective “high” that they produce, to extend periods of wakefulness, as by lorry drivers and students studying for exams. In addition, they are used as appetite suppressants. Medically, amphetamines are still used only in the treatment of narcolepsy and symptoms of attention deficit hyperactivity disorder in children. Amphetamines are stimulants of the central nervous system that produce increased alertness, arousal, energy, motor and speech activity, increased selfconfidence and ability to concentrate, an overall feeling of well-being and reduced hunger.
Amphetamines
Amphetamine is a potent psychotomimetic, and can intensify symptoms or precipitate a psychotic episode in vulnerable individuals. People who use amphetamine chronically often develop a psychosis very similar to schizophrenia. Increase in the hyperactivity or stereotypy induced by chronic use of amphetamine also occurs, even if the doses are spread out over days or weeks. Cross-sensitization with cocaine occurs.
Amphetamine users sometimes ingest increasing quantities of amphetamine in “runs” that last 3–6 days.This pattern of use is neurotoxic and produces brain damage. Some antidepressant drugs may decrease craving for amphetamines. Ecstasy or MDMA (3,4-methylenedioxy- methamphetamine) will be also introduced in club drugs.
