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METH

House M.D.

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BACKGROUND AND HISTORY.
Methamphetamine (N-methyl-alpha-methylphenylethylamine) is a "strong" representative of the amphetamine substances.​
Мethamphetamine, was first synthesized in 1887 in Germany by Romanian chemist Lazar Edeleanu. He named it phenylisopropylamine. Then, methamphetamine was synthesized from ephedrine in 1893 by Japanese chemist Nagai Nagayoshi. Three decades later, in 1919, methamphetamine hydrochloride was synthesized by pharmacologist Akira Ogata via reduction of ephedrine using red phosphorus and iodine.
Dark market and street names: Batu, Bikers Coffee, Black Beauties, Chalk, ChickenFeed, Crank, Crystal, Glass, Go-Fast, Hiropon, Ice, Meth, Methlies Quick, Poor Man’s Cocaine, Shabu, Shards, Speed, Stove Top, Tina, Trash, Tweak, Uppers, Ventana, Vidrio, Yaba, and Yellow Bam.

Stimulant that speeds up body’s system that comes as pill or powder. Available in prescription as Desoxyn to treat obesity and ADHD. Crystal meth resembles glass fragments and is an illegally altered version of the prescription drug that is cooked with over-the-counter drugs in meth labs.

Pharmacy prescriptions: Desoxyn, Methedrine.

Methamphetamine is a Schedule II stimulant under the Controlled Substances Act, which means that it has a high potential for abuse and a currently accepted medical use (in FDA-approved products). It is available only through a prescription that cannot be refilled. Today, there is only one legal meth product, Desoxyn. It is currently marketed in 5, 10, and 15-milligram tablets (immediate release and extended release formulations) and has very limited use in the treatment of obesity and attention deficit hyperactivity disorder (ADHD).


PHARMACOLOGY AND NEUROCHEMISTRY.
Methamphetamine alters the action of the dopamine transporter (DAT) by activating TAAR1. Activation of TAAR1 also causes some dopamine transporters to move into presynaptic neurons and restricts transport. On VMAT2, methamphetamine causes an outflow of dopamine (release).

✓ Methamphetamine has been identified as a potent full agonist of trace amine-associated receptor 1 (TAAR1), a G protein-coupled receptor (GPCR) that regulates brain catecholamine systems. Activation of TAAR1 increases cyclic adenosine monophosphate (cAMP) production and either completely inhibits or reverses the transport direction of the dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT). When methamphetamine binds to TAAR1, it triggers transporter phosphorylation via protein kinase A (PKA) and protein kinase C (PKC) signaling, ultimately resulting in the internalization or reverse function of monoamine transporters.

✓ Methamphetamine is also known to increase intracellular calcium, an effect which is associated with DAT phosphorylation through a Ca2+/calmodulin-dependent protein kinase (CAMK)-dependent signaling pathway, in turn producing dopamine efflux. TAAR1 has been shown to reduce the firing rate of neurons through direct activation of G protein-coupled inwardly-rectifying potassium channels. TAAR1 activation by methamphetamine in astrocytes appears to negatively modulate the membrane expression and function of EAAT2, a type of glutamate transporter.

✓ In addition to its effect on the plasma membrane monoamine transporters, methamphetamine inhibits synaptic vesicle function by inhibiting VMAT2, which prevents monoamine uptake into the vesicles and promotes their release. This results in the outflow of monoamines from synaptic vesicles into the cytosol (intracellular fluid) of the presynaptic neuron, and their subsequent release into the synaptic cleft by the phosphorylated transporters. Other transporters that methamphetamine is known to inhibit are SLC22A3 and SLC22A5. SLC22A3 is an extraneuronal monoamine transporter that is present in astrocytes, and SLC22A5 is a high-affinity carnitine transporter.

✓ Methamphetamine is also an agonist of the alpha-2 adrenergic receptors and sigma receptors with a greater affinity for σ1 than σ2, and inhibits monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). Sigma receptor activation by methamphetamine may facilitate its central nervous system stimulant effects and promote neurotoxicity within the brain. Dextromethamphetamine is a stronger psychostimulant, but levomethamphetamine has stronger peripheral effects, a longer half-life, and longer perceived effects among addicts. At high doses, both enantiomers of methamphetamine can induce similar stereotype and methamphetamine psychosis, but levomethamphetamine has shorter psychodynamic effects.
Science suggested, based on animal research, that calcitriol, the active metabolite of vitamin D, can provide significant protection against the DA- and 5-HT-depleting effects of neurotoxic doses of methamphetamine.

MAIN PHYSICAL EFFECTS.
The physical effects of methamphetamine can include:
loss of appetitediarrhea
hyperactivityconstipation
flushed skinblurred vision
excessive sweatingdizziness
increased movementtwitching
dry mouth and teeth grinding (leading to "meth mouth")numbness
headachetremors
irregular heartbeatdry skin
rapid breathingacne
high blood pressure, and low blood pressuredilated pupils
high body temperature
pale appearance

Chronic meth users may have sores on their skin; these may be caused by scratching due to itchiness or the belief that insects are crawling under their skin, and the damage is compounded by poor diet and hygiene. Numerous deaths related to methamphetamine overdoses have also been reported as well.

PSYCHO-CLINICAL MANIFESTATIONS.
Meth is a highly addictive drug with potent central nervous system (CNS) stimulant properties. Those who smoke or inject it report a brief, intense sensation, or rush. Oral ingestion or snorting produces a long-lasting high instead of a rush, which reportedly can continue for as long as half a day. Both the rush and the high are believed to result from the release of very high levels of the neurotransmitter dopamine into areas of the brain that regulate feelings of pleasure. Long-term meth use results in many damaging effects, including addiction.

Better preferred to avoid using methamphetamine because its primarily toxic for nervous system, has an adverse effect on the body, causes brain damage, "kills" receptors, causes rapid and strong dependence and high tolerance of neurotransmitter receptors. Abuse of this substance has the standard consequences inherent in stimulants - problems with the heart and blood vessels.

Meth-addiction manifests itself in the form of various mental disorders, which leads to depletion of the nervous system. Most often, there are depressive disorders and psychotic abnormalities that lead to the debut of psychosis. Long experience of admission leads to the formation of schizophrenic disorders. Taking methamphetamine in young or adolescence provokes the formation of mental retardation. Affect disorders can occur at any age, the formation of which mainly depends on the type of personality.

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Chronic meth users feel:
✓ Violent behavior,
✓ Anxiety,
✓ Confusion,
✓ Insomnia,
✓ Psychotic features including paranoia,
✓ Aggression,
✓ Visual and auditory hallucinations,
✓ Mood disturbances,
✓ Delusions such as the sensation of insects creeping on or under the skin.

Such paranoia can result in homicidal or suicidal thoughts. Researchers have reported that as much as 50 percent of the dopamine-producing cells in the brain can be damaged after prolonged exposure to relatively low levels of meth. Some studies suggested that the use of methamphetamine may also result in serotonergic neurotoxicity.

Addiction syndrome is characterized by the following behavior signs:
  • Constant thoughts about the drug,​
  • Depressed state,​
  • Dissatisfaction with what is happening,​
  • Sharp rise in mood while waiting for methamphetamine (pathological revival syndrome).​
There is a certain difficulty in identifying mental dependence, since the patient has an internal "desire" to deny it as such. But the identification and treatment of mental dependence is the main factor preventing relapses, since physical dependence on taking methamphetamine is not pronounced.

The introduction of a new dose of the drug into the body leads only to the formation of a state of comfort and does not guarantee the achievement of euphoria. But, being on inpatient treatment and receiving drug therapy, the addict may feel psychological discomfort, since he has an attitude to achieve psychological comfort only when taking methamphetamine.

METHODS OF USE:
  • ORALLY - The most recommended way to use is to keep your nose healthy, veins intact, lungs untouched. Popular methods are the dissolution in warm water, mixing with juice or other favorite drink and drinking, but also you can do "bombs" (wrap in a small piece of paper napkin or place in a capsule) and swallow.​
  • INTRANASAL - The most common way to use. Use in this way can cause problems with the mucosa or less often - inflammation of the nasal passages, paranasal sinuses, the back wall of the oropharynx. It is better to use plastic straws for drinks and abandon the use of money banknotes.​
  • SMOKING - No less popular way of using this substance, but having classic disadvantages - the risks of problems with the respiratory system. The popularity of this method is due to the receipt of strong euphoria. The action is sharp and enveloping with a wave of joy, lightness and pleasure. People who prefer this method instantly form a persistent desire to use, an obsessive desire to use more and more. The result is chronic use, overdose, tolerance, difficulties in the fight against addiction.​
  • INTRAVENOUS - Used by injection lovers. The effect is close to smoking. The substance enters the body directly and begins to act instantly.​
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RECOMMENDED DOSE:
Very Low: Up to 10 mg.
Low: 10 - 20 mg.
Medium: 20 - 40 mg.
High: 40 - 70 mg.
Very high: from 70 mg and above.

TRIP DURATION TIME:
Total - up to 12 hours.
Entrance - up to 40 minutes (depending on the method of use).
Plateau - 3-5 hours.
Output - up to 4 hours.
Post effects - up to 24 hours.

INTERACTION.
Methamphetamine is metabolized by the liver enzyme CYP2D6, so CYP2D6 inhibitors will prolong the elimination half-life of methamphetamine. Methamphetamine also interacts with monoamine oxidase inhibitors (MAOIs), since both MAOIs and methamphetamine increase plasma catecholamines; therefore, concurrent use of both is dangerous. Methamphetamine may decrease the effects of sedatives and depressants and increase the effects of antidepressants and other stimulants as well. Methamphetamine may counteract the effects of antihypertensives and antipsychotics due to its effects on the cardiovascular system and cognition, respectively. The pH of gastrointestinal content and urine affects the absorption and excretion of methamphetamine. Specifically, acidic substances will reduce the absorption of methamphetamine and increase urinary excretion, while alkaline substances do the opposite. Due to the effect pH has on absorption, proton pump inhibitors, which reduce gastric acid, are known to interact with methamphetamine.
YOU SHOULDN'T MIX METHAMPHETAMINE WITH FOLLOWING DRUGS:
  • Other substances from this group: caffeine, Ritalin, amphetamine, cocaine and others.
  • Psychedelics and dissociatives, ranging from mushrooms and LSD, ending with DMT and others.
  • Stimulating psychedelics: DO*, 25-Nbome, 2 C*.
  • Pharmacy, especially with tramadol.
  • Antidepressants, especially with NOAS It is not recommended combining with euphoretics: MDMA and others, including mephedrone.
  • "Slow" drugs (depressants) - heroin, methadone, butyrates, alcohol.

HARM REDUCTION & ADDICTION.
Methamphetamine is not recommended being combined with anything but marijuana, but even smoking marijuana under its influence can lead to panic attacks and other negative manifestations. Strictly observe the dosage and remember that this is a serious substance, and it cannot be used for a long time. Take breaks between doses of the drug, give the body time to recover and eat at least light food, fruits.

Additional pharmacological support of the body:
  • L-carnitine (levocarnitine) - 1000 mg an hour before taking methamphetamine and 1000 mg after. This will protect your brains during the neurotoxic effects of meth.
  • Alphalipoic acid - 250 mg an hour before consumption and 250 mg after. Enhances effect of levocarnitine and increases antioxidant activity (cleaning out free radicals from the body)
  • Magnesium citrate 250 mg - 3 times a day for 2 weeks for prevention of magnesium deficiency if you often use stimulants
  • Vitamin C - 500 mg once a day and Aspirin(acetylsalicilius acid) 50 mg once a day when methamphetamine is used - help the liver work more efficiently.
Treatment of methamphetamine addiction is similar to working with cocaine addiction. Drug therapy is designed to restore the strength of a patient with experience and calm the overexcited nervous system. Antidepressants and neuroleptics are not used for this purpose, which can cause side reactions and do not give a serious effect. Drug therapy, psychiatric and psychological support is provided to the patient in this case up to three months.

Addiction treatment of meth should include ways to eliminate the destructive effect that this type of drug has on the brain. Psychosis, schizophrenic disorders, hallucinations and motor disorders should be eliminated with the help of individual selection of drugs and combined with psychotherapy sessions and classes with a psychologist. Unfortunately, self-elimination of addiction at home is impossible. The main task of the psychologist in individual and group classes with such patients is the formation of a stable desire to lead a healthy life, free from compulsive taking psychoactive substances.

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RISKS OF CHRONIC ABUSE:
  • Cardiovascular disorders,
  • Stroke,
  • Heart attack,
  • Impotence,
  • Convulsions,
  • Coma,
  • Death.
OVERDOSE TREATMENT.
Acute methamphetamine intoxication is largely managed by treating the symptoms, and treatments may initially include administration of activated charcoal and sedation. There is not enough evidence on hemodialysis or peritoneal dialysis in cases of methamphetamine intoxication to determine their usefulness. Forced acid diuresis (e.g., with vitamin C) will increase methamphetamine excretion but is not recommended as it may increase the risk of aggravating acidosis, or cause seizures or rhabdomyolysis. Hypertension presents a risk for intracranial hemorrhage (i.e., bleeding in the brain) and, if severe, is typically treated with intravenous phentolamine or nitroprusside. Blood pressure often drops gradually following sufficient sedation with a benzodiazepine and providing a calming environment.
Antipsychotics such as haloperidol are useful in treating agitation and psychosis from methamphetamine overdose. Beta blockers with lipophilic properties and CNS penetration such as metoprolol and labetalol may be useful for treating CNS and cardiovascular toxicity. The mixed alpha- and beta-blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine. The phenomenon of "unopposed alpha stimulation" has not been reported with the use of beta-blockers for treatment of methamphetamine toxicity.​
 
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