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Illicit Drug (Ecstasy MDMA) Ecstasy, scientifically known as 3, 4 -methylenedioxy-methamphetamine (MDMA), represents a known street illicit drug and simultaneously entirely synthetic substances, which does not exist in nature. From the chemical perspective, MDMA is a derivative of a derivative of methamphetamine and its parent compound amphetamine. Practically, it differs from the mentioned chemicals in a single but important aspect: due to the specific location of its methylenedioxy (-O-CH^sub 2 ^-O-) group it resembles the structure of the hallucinogenic material mescaline. The drug was patented in 1914 as an appetite suppressant, and has been investigated as a mood-modifying drug. Its clinical use was banned in the USA in 1985 because of its neurotoxicity and its potential for misuse. In the UK, MDMA has been listed since 1977 as a class A drug under the Misuse of Drugs Act, 1971.
Although misuse of MDMA in the USA has caused deaths, mainly from cardiac arrhythmias (Dowling & McDonough, 1987), there have been several cases of severe toxicity in the UK with a different clinical pattern. There were few enquiries to the hospitals until the second half of 1995 when a striking increase in calls was noted. Laboratory detection of MDMA and 3, 4 -methylenedioxyamphetamine (MDA) increased similarly, but MDMA was more commonly found. Although what was being sold as "ecstasy" usually contained MDMA, other substances, such as MDA or amphetamine, were also identified; mixtures were uncommon. Since MDA is a metabolite of MDMA, co ingestion of MDA with MDMA could not be excluded by analysis of biological samples.
Although the doses involved were difficult to establish with certainty, it seems that in most cases only a few tablets or capsules were consumed; the pattern of toxicity did not seem to be a result of overdose. One analytically documented overdose of a large amount of MDMA (allegedly 42 tablets taken at home; plasma MDMA 7 - 72 mg/ 1) was accompanied by no symptoms other than a "hangover", with tachycardia and hypertension (Suarez & Reimersma, 1995). Ecstasy practically attains its peak concentration in the plasma in 2 hours after oral ingestion (21). Concentrations of 50 mg, 75 mg, and 125 mg resulted in blood concentration of 106 ng / m L, 131 ng / m L and 236 ng / m L respectively, were administered to research volunteers and subsequently were considered to be low, however helpful in comparison with the levels indicated in patients, experienced significant and fatal effects from MDMA overdose.
In organism, MDMA is broken down in the liver metabolically with the help of enzyme CYP 2 D 6 (Maurer et al, 2000). Drug elimination is characterized with slow pace 20 % drug elimination exceeds 8 hour period. Practically, it takes up to 45 - 50 hours for over 95 % of MDMA to be cleared from organism; however, some troublesome effects can last 2 days of primary ingestion. Contemporary medicine possesses a considerable amount of evidence, both research and clinical, that MDMA acts by increasing the net release of the monoamine neurotransmitters, namely serotonin, noradrenaline and dopamine (Green et al, 1995). MDMA does not work by directly releasing serotonin. Practically, it binds and therefore blocks, the transporter used in its reuptake.
During experiments using rats, animals, specifically trained to differentiate between the effects of saline and those of serotonin, respond to MDMA as if it were serotonin (Glennon et al, 2000). A similar action was also noted on the reuptake of dopamine. The physiological effects of MDMA in mice were characterized as similar to those of amphetamine, acting like a releaser of dopamine and noradrenaline. Simultaneously, researchers possess a small amount of experimental evidence that the total release of acetylcholine is increased by MDMA, however, the importance of the trend in humans is unknown. But it is evident that the increase in the total release of serotonin along with dopamine explains the distinctive mental effects of ecstasy. The ability of MDMA to intensify the concentration of serotonin in the synapse underlies its functioning in improving mood and effect on sensory alterations.
Being examined with high doses, researchers indicated that the massive release of serotonin not only produce increase of acute psychotic symptoms but causes significant chemical damage to the cells that released it. During studies of long-term MDMA users, it has been revealed that being free of drug, patients have abnormally low levels of serotonin and its metabolites in the cerebrospinal fluid, reduced numbers of serotonin transporter molecules, increased numbers of glial cells, and altered patterns of glucose metabolism and blood flow in certain parts of the brain (Ricaurte et al, 2000). Reports on MDMA from the USA suggest that the drug is only mildly toxic despite widespread recreational misuse. The main cause of severe toxicity and death is cardiac arrhythmias; rhabdomyolysis and disseminated intravascular coagulation (DIC) may also take place, with 2 such fatalities reported in the UK.
Most cases about which scientists were consulted had mild symptoms, and the general pattern on presentation was that of agitation, tachycardia, hypertension, widely dilated pupils, trismus, and sweating. There was a clear pattern of toxicity in the most severe cases, which were characterized by hypothermia, DIC, rhabdomyolysis, and acute renal failure. Death was probably due to heatstroke, in which severe hypothermia was accompanied by DIC. This pattern of toxicity may occasionally result from amphetamine sulphate overdose, but a similar pattern with MDMA has only recently been seen in the UK; the reason for its emergence is not clear.
There is no evidence that an impurity or variation in manufacture is responsible, and medical specialists suggest that the mechanism may involve a combination of direct effects of the drug and the circumstances associated with ingestion. MDMA can cause hypothermia in laboratory animals, which is more pronounced at high ambient temperatures. Most of the serious cases and all of the fatal cases that researchers have encountered were among people at crowded parties or clubs where "ecstasy" is taken as a mood enhancer and as a "dance drug." At such venues, sustained physical activity (which may itself be an effect of the drug), a high ambient temperature, and inadequate fluid replacement could all reduce heat loss and potentiate a direct effect of the drug on thermo regulatory mechanisms, thereby leading to fulminant hypothermia. Because of this pattern, they suggest early management with intravenous fluids and intravenous dantrolene. Those users who develop severe toxicity might also have a metabolic myopathy, as do some of those with exceptional heatstroke. There have been no previous reports of hepatotoxicity as a complication of MDMA misuse.
Some cases that have been reported were associated with ingestion of "ecstasy." None had a history of heavy alcohol or intravenous drug misuse, and none had evidence of infectious hepatitis. Hyperthermic liver toxicity can be excluded. Moreover, analytical confirmation of MDMA was not possible as misuse had ceased. An idiosyncratic toxic hepatitis might be responsible; whether these cases are due to MDMA or a metabolite, a contaminant in MDMA manufacture, or to an additive in tablet or capsule formulation, is not yet clear. However, hepatotoxicity seems to be increasing in frequency, and may be related to repeated exposure to MDMA as the number of long-term users increases. Experts suggest that a history of "ecstasy" misuse should be obtained in young people presenting with unexplained jaundice or hepatomegaly.
The recent increase in cases of toxicity due to MDMA and drugs sold as "ecstasy" deserves to be publicized widely for several reasons. First, in a culture in which multi-drug misuse is increasingly accepted, there is a general impression that "recreational" drug use is unlikely to have serious adverse effects. "Ecstasy" is widely misrepresented as being safe. Second, clinicians should be aware of the pattern of toxicity so as to permit correct diagnosis and management. The differential diagnosis of severe hyperthermia should include misuse of MDMA as well as severe infections, stroke, heatstroke, narcoleptic malignant syndrome, malignant hyperthermia, and monoamine oxidase inhibitor overdose, together with the adverse affects of amphetamine, methamphetamine, and cocaine. Third, young people with behavioral disturbances and victims of motor vehicle or other accidents may be under the influence of MDMA.
Misuse should be suspected, and analytical confirmation may be needed, when the circumstances suggest that MDMA is involved. Finally, hepatotoxicity should be included as a complication of MDMA misuse, and this may account for unexplained jaundice or hepatomegaly. Scientists insist that MDMA is capable of causing severe toxicity, and that its pattern of acute toxicity as seen in the series of research may be due mainly to the circumstances in which it is misused. Apart from those effects described, experimental data indicate that MDMA is a neurotoxin, and cases have been reported of psychosis, panic and depression. The frequency and degree of long-term adverse effects on the human brain and mental function remain unknown, but in view of widespread and continuing illegal distribution, both acute and chronic effects of this drug deserve further study. Bibliography Dowling GP, McDonough ET, Bost RO. (1987). "Eve" and "Ecstasy." A report on five deaths associated with the use of MDEA and MDMA.
JAMA; 257: 1615 Suarez RV, Reimersma R. (1985). "Ecstasy" and sudden cardiac death. American Journal of Forensic Medical Pathology; 9: 339 - 41 Maurer HH, Bickeboeller-Friedrich J, Kraemer T, Peters FT. (2000). Toxicokinetics and analytical toxicology of amphetamine-derived designer drugs ('ecstasy'). Toxicology Letter; 112 - 3: 133 - 42 Green AR, Cross AJ, Goodwin GM. (1995). Review of the pharmacology and clinical pharmacology of 3, 4 -methylenedioxymethamphetamine (MDMA or "ecstasy"). Psychopharmacology (Berl); 119 (3): 247 - 60 Glennon RA, Young R. (2000).
MDMA stimulus generalization to the 5 -HT (lA) serotonin agonist 8 -hydroxy- 2 - (di-n-propyl amino) terrain. Pharmacology and Biochemistry Behavior; 66: 483 - 8. Ricaurte GA, McCann UD, Szabo Z, Scheffel U. (2000). Toxicodynamics and longterm toxicity of the recreational drug, 3, 4 -methylenedioxymethamphetamine (MDMA, 'ecstasy). Toxicol Lett; 112 - 3: 143 - 6
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