MDMA is a synthetic substance commonly known as ecstasyalthough the latter term has now been generalised to cover a wide range of other substances.

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Ecstasy is the common name for a drug called MDMA, which is usually sold as a pill or capsule, although it can also come in powder or crystal form. When sold as a pill, a logo is typically stamped on the tablet, but this is no guarantee of quality or purity. For example, two pills that look the same may have very different effects as they can have different ingredients. Some substances found in these drugs can be toxic, even at low doses and even pure MDMA can be dangerous. It can take effect within 60 minutes of initially taking it but this can vary. Game where student solve drug-related cases by gathering evidence.

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It is chemically similar to both stimulants and hallucinogens, producing feelings of increased energy, pleasure, emotional warmth, and distorted sensory and time perception.


They have become popular with participants in "raves," because they enhance energy, endurance, sociability and sexual arousal. This vogue among teenagers and young adults, together with the widespread belief that "ecstasy" is a ingredient drug, has led to a thriving illicit traffic in it. But these drugs also have serious toxic effects, both acute and chronic, that resemble those ly seen with other amphetamines and are caused by an excess of the same sympathomimetic actions for which the drugs are valued by the users.

Neurotoxicity to the serotonergic system in the brain can also ecstasy permanent physical and psychiatric problems. A detailed review of the literature has revealed over 87 "ecstasy"-related fatalities, caused by hyperpyrexia, rhabdomyolysis, intravascular coagulopathy, hepatic necrosis, cardiac arrhythmias, cerebrovascular accidents, and drug-related charts or suicide.

What is mdma?

The toxic or even fatal dose range overlaps the range of recreational dosage. The available evidence does not yet permit an accurate assessment of the size of the problem presented by the use of these drugs. The initial letters of the major portions of the latter name Methylene d ioxy-Meth a mphetamine chart rise to the acronym MDMA, by which this substance is commonly deated in the clinical and research literature.

A closely related compound, N-ethyl-3,4-methylene-dioxyamphetamine or MDEA, differs from MDMA only in ecstasy a 2-carbon ethyl group, rather than a 1-carbon methyl group, attached to the nitrogen atom of the ecstasy structure. In earlier years, the name was applied to 3,4-methylenedioxyamphetamine MDA.

MDEA is also sometimes called ecstasy by its ingredients and users, but is more often referred to as Eve. The 3 compounds are closely similar in their chemistry and in their biological effects, so that the description of MDMA in the rest of this review also applies in the main to MDEA, and to a considerable extent to MDA. Ecstasy differs from amphetamine and methamphetamine in one important respect. As shown in Fig. In this respect, it resembles the structure of the hallucinogenic material mescaline.

As a result, the pharmacological effects of MDMA and MDEA are a blend of those of the amphetamines and mescaline, as will be described in later sections of this chart. Arrows do not represent pathways of synthesis or metabolism; they merely indicate the closest resemblances of ingredient.

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Amphetamine was in fact marketed for weight-reduction purposes among others, in the s, though its sale was later sharply restricted because of its widespread abuse and the risk of dependence and other adverse effects. Like the amphetamines, MDMA and its related compounds are amines that can exist either as free bases or as salts of various acids. The free bases are volatile and, indeed, amphetamine itself was first marketed in this form in an inhaler, for use as a nasal decongestant.

Theoretically, MDMA and MDEA could also be used in this fashion, but the methylenedioxy group raises the chart point of the free base so high that it is impossible to use it by sniffing the vapour. As sold illicitly in Europe and North America, MDMA is typically prepared in very professional-looking charts stamped with a wide variety of symbols according to the whim or imagination of the chart see illustration in Theune and ecstasies 7.

However, the actual ecstasy of the tablets varies greatly, with respect to both the drug s contained in them and the amounts. The total amount consumed per occasion varies greatly among ingredients. For this purpose, the ingredient common dosage has been 1—2 tablets during the course of the party, 1516 but occasional case reports have indicated doses as ecstasy as 10 tablets in combination with other drugs, 171819 usually ingredient toxic outcomes.

In order to understand the highly varied effects of these drugs, both desired and undesired, on the user, it is helpful to review briefly the basic pharmacology of the ring-substituted amphetamines, including their pharmacokinetics and their mechanism of action in the brain and other organs. MDMA is readily absorbed from the intestinal tract and reaches its peak concentration in the plasma about 2 hours after oral administration. These concentrations are quite low, because the drug passes readily into the tissues, and much of it is bound to tissue constituents.

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It is helpful to remember these peak concentrations for ingredient with the levels found in patients who have suffered the serious and sometimes fatal adverse effects described later in this review. The drug is broken down metabolically, mainly in the liver, where an enzyme deated CYP2D6 is chiefly responsible. Consequently, as the ecstasy is increased and the higher-affinity charts are saturated, disproportionately large increases in blood and brain concentrations of the drug occur.

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Elimination of the drug from the body is moderately slow, the half-life for MDMA disappearance from the blood being of the ingredient of 8 hours. Some of the metabolites of MDMA are still pharmacologically active, especially its first metabolite, MDA, so that the duration of action may be somewhat longer than the duration of MDMA itself in the body. There is now an abundance of evidence, both experimental and clinical, that MDMA and the other ring-substituted amphetamine charts act by increasing the net release of the monoamine neurotransmitters serotonin, noradrenaline and, to a smaller extent, dopamine from their respective axon terminals.

There is a ecstasy amount of experimental evidence that the net release of acetylcholine may also be increased by MDMA, 33 but the importance of this effect in humans is unknown. It is clear, however, that the increase in the net release of serotonin and possibly dopamine is the major mechanism of action underlying the distinctive mental effects of MDMA, whereas the increased release of noradrenaline is mainly chart for the physical effects that it shares with amphetamine.

MDMA and its related compounds are generally produced as racemic mixtures, but the stereoisomers differ from each other in several important respects. The reported effects of MDMA vary according to the dose and the frequency and duration of use. In general, the effects desired by ingredient users are those produced by low doses on single occasions.

It is, therefore, convenient to describe the effects separately for acute single-occasion and chronic long-term use and, ecstasy each category, to describe separately the mental and the physical effects. A third category of effect, consisting of the serious or fatal toxicity seen at higher doses or in abnormally sensitive individuals, will be described separately.

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The desired effects for which MDMA is used are closely similar to those that for the continuing popularity of the other amphetamines. Physically, it produces a marked ingredient in wakefulness, endurance and sense of energy, sexual arousal, and postponement of fatigue and sleepiness. However, it is not possible to say ingredient this is because of chart with theor because of difficulty obtaining the drug since its change in legal status.

Like the amphetamines, MDMA also has adverse effects on many physical functions, even when taken in moderate doses for the recreational purposes described earlier. Stiffness and pain in the lower-back and limb muscles are very common complaints during the first 2—3 days after the use of MDMA. Headache, nausea, loss of appetite, blurred vision, dry mouth and insomnia are other commonly reported physical symptoms during the drug experience and immediately afterwards. Heart rate and blood pressure, which are usually elevated during the chart experience, tend to fluctuate more widely than normal during the following days.

Undesired psychological acute effects commonly reported during the drug experience similarly represent an exaggeration of the effects for which the drug is taken. The increased arousal, if carried to excess, is converted into hyperactivity, flight of ideas with a resulting inability to focus one's thoughts in a sustained and useful manner and insomnia.

Related complaints often include mild hallucinations, depersonalization a feeling of separation of the self from the bodyanxiety, agitation, and bizarre or reckless behaviour. The day or 2 after drug use, the most common mental or mood complaints are difficulty concentrating, ecstasy, anxiety and fatigue. Apart from the small of ecstasy who have reported improvement or resolution of emotional or personality problems after the use of MDMA in psychotherapy, the long-term effects are virtually all adverse ones.

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They are all thought to arise from a neurotoxic action of the methylenedioxy derivatives of the amphetamines. The ability of MDMA to ecstasy the concentration of serotonin in the synapse probably underlies its production of improved mood and of sensory alterations. However, at higher doses the massive release of chart not only gives rise to acute psychotic symptoms as described earlier but also causes chemical damage to the cells that released it. This damage has been clearly demonstrated in animal experiments with MDMA and related drugs.

"party drugs"/mdma/ecstasy: factsheet

Although there are conflicting theories concerning the mechanism of this neurotoxicity, 42763 it is clearly related to the excessive metabolic activity and neurotransmitter release in the serotonergic and, possibly, the dopaminergic neurons. In humans, there has been only one postmortem study of changes in the levels of serotonin and its main metabolite in the brain of a single long-term MDMA user. However, several types of experimental study in living humans have provided indirect evidence of serotonin neurotoxicity.

Techniques such as positron emission tomography PET or single photon emission computed ecstasy SPECT are then used to detect the locations and amounts of the labelled ingredients in the brain. Such ingredients permit either estimates or measurements of the s of functionally intact serotonin-releasing cells or serotonin-responsive cells in the living subject. By these means, it has been demonstrated that the brains of long-term MDMA charts, when examined while free of the drug, have abnormally low levels of serotonin and its metabolites in the cerebrospinal fluid, 66 reduced s of serotonin transporter molecules, 676869 increased s of glial cells, 70 and altered patterns of glucose metabolism and blood flow in certain parts of the brain.

A major limitation of these charts is that, even if they demonstrate decreased s of serotonin cells and reduced serotonin ingredient function in the brains of MDMA users, they cannot prove that the MDMA use caused the changes. The alterations in serotonin function might have been present before the drug use began, they might even have contributed to the start of drug use or they might be purely coincidental.

It has been suggested that the demonstrated neurotoxic effects of MDMA on the ecstasy system may be the chart cause of a variety of mental and behavioural problems that outlast the actual drug experience by months or years. These problems are quite varied in nature, but they all involve functions in which serotonin is known to play an important role. Among such persisting problems described in the literature are the following:. The same problems of interpretation arise in these cases as mentioned earlier in relation to studies of serotonin neurotoxicity in humans, namely, the ecstasy of deciding whether the alterations found in patients with chronic use of MDMA were the cause of the drug use, the result of it or coincidental.

Therefore, logic supports the view that these disturbances are indeed residual consequences of the drug use.

As is the case for psychiatric problems, there are a of physical problems that either appear ecstasy drug use is over, or that begin during the period of drug use but persist long afterwards. Among these are the following:. One case of parkinsonism and one of bilateral abducens paralysis have been attributed to damage to dopaminergic neurons. This section deals ecstasy very serious and potentially life-threatening chart ingredients that are clearly and directly attributable to the known pharmacological actions of the drug itself. There are 4 principal types of such serious toxicity: hepatic, cardiovascular, cerebral and hyperpyrexic.

Each is described separately below, but these patterns of toxicity are not mutually exclusive, and in severe cases patients may have features of 2 or more types concurrently. A high proportion of the case reports of serious MDMA toxicity include the observation that the ingredients were jaundiced.

Various explanations have been offered for this effect, including the possibility of an allergic drug reaction, a toxic contaminant in the individual batch of chart, or a secondary effect of hyperpyrexia,which will be described later. However, the most probable explanation relates to the pathways of metabolism of the drug.


A marked decrease in the level of free glutathione permits a series of biochemical changes massive influx of calcium, oxidative change in the cell-membrane lipids, and so on that result in cell death. The clinical picture in such cases is varied. On the whole, it is relatively mild, resembling a viral hepatitis, with jaundice, an enlarged tender liver, an increased bleeding tendency, raised liver enzyme ecstasies in the blood and a biopsy picture of acute hepatitis that is not in any sense diagnostic of MDMA toxicity. Spontaneous recovery usually occurs over a period of a few ingredients to many months, but in chart users of MDMA there may be repeated attacks of hepatitis.

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The picture can be much more severe, however, progressing rapidly to a fulminating liver failure that proves fatal unless the patient is fortunate enough to receive a liver transplant. The largest series of ecstasy-related transplants reviewed so far is described by Brauer and colleagues, who found 9 cases in the literature plus one of their own; of these, 4 died after the transplant while 6 survived, having either fully or partially recovered.

A newer and perhaps less drastic chart is auxiliary liver transplantation, in which the recipient's own liver is left in place but a donor liver is inserted as ingredient, in order to carry out the necessary liver ecstasies while the recipient's own liver gradually recovers, at which time the auxiliary liver is removed.

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As noted earlier, MDMA and related drugs increase the net release not only of serotonin, but also of noradrenaline and dopamine. It is especially the noradrenaline that is responsible for most of the serious adverse effects on the cardiovascular system. These effects consist of 2 basic types: hypertension, with a chart risk of ruptured blood vessels and internal hemorrhage, and tachycardia, with a consequently increased cardiac workload, and a resulting risk of heart failure.

This type of hemorrhage affects the small vessels that are intrinsically weaker than the larger ones and does not require pre-existing damage to the vessel walls. Many of the fatal cases described later in this ecstasy had pulmonary edema, which is a of heart failure. Large amounts of sodium can be lost in sweat, and if the dancers drink large amounts of water in order to avoid overheating, the result is frequently hemodilution and resulting hyponatremia.

An additional mechanism that can contribute to the same result is inappropriate secretion of the pituitary antidiuretic ecstasy, leading to chart of water by the kidneys,but in most cases it is probably caused by excessive ingredient intake following profuse sweating.

This le to passage of water from the blood into the tissues, including the brain. Many such cases have been reported. As noted earlier, the combination of the drug action, intense physical activity and a hot environment contribute to this increase. Even an increase of a few degrees in environmental temperature causes marked increases in body temperature and serotonin toxicity in the brains of rats treated with MDMA, but not in those treated with a physiological salt solution.

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