Central nervous system stimulants cocaine

Cocaine is the oldest of the local anaesthetics. It is a central nervous system stimulant and is habit-forming. See ecgonine. 

Many alkaloids have pronounced biological properties, and a substantial number of the pharmaceutical agents used today are derived from naturally occurring amines. As a few examples, morphine, an analgesic agent, is obtained from the opium poppy Papaver somnifemm. Cocaine, both an anesthetic and a central nervous system stimulant, is obtained front the coca bush Erythroxylon coca, endemic to upland rain forest areas of Colombia, Ecuador, Peru, Bolivia, and western Brazil. Reserpine, a tranquilizer and antihypertensive, comes from powdered roots of the semitropical plant Rauwolfia serpentina. Ephedrine, a bronchodilator and decongestant, is obtained front the Chinese plant Ephedra sinica. 

Angrist, B. M. Cocaine in the context of prior central nervous system stimulant epidemics. In Cocaine in the Brain (Mind in Medicine Series), Volkow, N. and Swann, A.C., Eds. Rutgers University Press, New Brunswick, NJ, 1990, 7. 

Substance-Induced Anxiety Disorder. Numerous medicines and drugs of abuse can produce panic attacks. Panic attacks can be triggered by central nervous system stimulants such as cocaine, methamphetamine, caffeine, over-the-counter herbal stimulants such as ephedra, or any of the medications commonly used to treat narcolepsy and ADHD, including psychostimulants and modafinil. Thyroid supplementation with thyroxine (Synthroid) or triiodothyronine (Cytomel) can rarely produce panic attacks. Abrupt withdrawal from central nervous system depressants such as alcohol, barbiturates, and benzodiazepines can cause panic attacks as well. This can be especially problematic with short-acting benzodiazepines such as alprazolam (Xanax), which is an effective treatment for panic disorder but which has been associated with between dose withdrawal symptoms. 

Castells X, Casas M, Vildal X, Bosch R, Roncero C, Ramos-Quiroga JA Capella D (2007) Efficacy of central nervous system stimulant treatment for cocaine dependence a systematic review and meta-analysis of randomized controlled clinical trials. Addiction, 102, 1871-87 Chaisson RE, Bacchetti P, Osmond D, Brodie B, Sande MA Moss AR (1989). Cocaine use and HIV infection in intravenous drug users in San Francisco. Journal of the American Medical Association, 261, 561-5 Chapleo CB Walter DS (1997). The bupre-norphine-naloxone combination product. Research and Clinical Forums, 19, 55-8 Cheskin LJ, Fudala PJ Johnson RE (1994). A controlled comparison of buprenorphine and clonidine for acute detoxification from opioids. Drug and Alcohol Dependence, 36, 115-21... 

Other drugs may increase the effects of dextroamphetamine. For example, bicarbonate and other alkalin-izing agents increase the amount of amphetamines absorbed in the digestive system. Thiazides (potassium-depleting diuretics) decrease the amount of amphetamines that leave the body in urine. Also, other central nervous system stimulants, such as cocaine and nicotine, can amplify the stimulating effects of dextroamphetamines. 

Central nervous system stimulants, e.g., amphetamine, methylphenidate (Ritalin) and cocaine... 

Cocaine exhibits several pharmacologic effects. After local application it acts as an anesthetic by blocking the initiation and conduction of nerve impulses. In addition, it has been shown to block neuronal reuptake of norepinephrine, thus potentiating adrenergic activity. Moderate doses increase heart rate and cause vasoconstriction. The most striking systemic effect of cocaine is central nervous system stimulation. 

The most striking effect of systemic absorption of cocaine is central nervous system stimulation. Signs and symptoms can include excitement, restlessness, rapid and irregular pulse, dilated pupils, headache, gastrointestinal upset, delirium, and convulsions. Death usually results from respiratory feilure. Moderate doses of cocaine can also raise body temperature. Systemic absorption through mucous membranes is rapid and has been compared in speed with that of intravenous administration. 

Central Nervous System Stimulants Central nervous system stimulants include agents such as the amphetamines (Dexedrine) and methylphenidate hydrochloride (Ritalin), used to elevate mood, suppress appetite, and control hyperkinetic disorders in children. Other examples include the illegal drugs methamphet-amine and cocaine. The mechanism of action of these drugs is to augment actions of the adrenergic nervous system. 

Cocaine is a central nervous system stimulant that inhibits the peripheral reuptake of catecholamines, leading to increased sympathomimetic activity [129]. Its abuse is associated with a variety of medical problems. These include acute myocardial infarction, cardiac arrhythmias, cerebrovascular accidents, hyperpyrexia and stimulated sympathetic activity, seizures and coma, obstetrical comphcations, intestinal ischemia and a variety of psychiatric complications [128-131]. A number of reports in the mid to late 1980 s described patients who developed rhabdomyolysis while using cocaine [132-134]. Some of these patients experienced acute kidney injury [135-139]. While the exact incidence of acute kidney injury secondary to cocaine rhabdomyolysis is unknown, in one reported series it occurred... 

Alkaloids are classified according to their heterocyclic rings. For example, cocaine, a central nervous system stimulant, and atropine, a muscle relaxant, are examples of the tropane alkaloids in which a nitrogen appears in a bridge of a seven-membered ring structure. Nicotine, the addictive and toxic component of tobacco, is an example of the pyridine alkaloids in which a nitrogen appears as a member of a six atom aromatic ring. (Nicotine is an effective insecticide.) The addictive... 

The amounts of cocaine the Indians consiune in this way are extremely small. Without such a crutch of central-nervous-system stimulation, the natives of the Andes would probably find it more difficult to perform the nearly Herculean tasks of their daily lives, such as carrying heavy loads over the rugged mountainous terrain. Unfortunately, overindulgence can lead to mental and physical deterioration and eventually an unpleasant death. 

Hydrolysis of ester linkages has been found to occur in all animals and bacteria however, the relative rates of hydrolysis in various species can be significantly different. In the case of local anesthetics, their metabohc disposition is of great practical importance since their toxicity depends largely on the balance between their rate of absorption and their rate of destruction. In most animals the esterases which hydrolyze many local anesthetics occur both in the liver and in the plasma. In the case ot human plasma, esterase activity is high and is principally responsible for the inactivation of procaine [60]. Cocaine is principally destroyed by liver esterase in the human, whereas plasma esterase in the rabbit is responsible for the hydrolysis of cocaine. The horse has little effective esterase activity against procaine in either plasma or liver and manifests central nervous system stimulation because of the slow destruction of the drug [61]. 

Cocaine has lasting local anesthetic activity and also functions as a central nervous system stimulant. At the same time it causes narcosis, and the abuse of cocaine leads to addiction. 

The pharmacological activity and toxicity of coca is generally attributed to cocaine. In addition to its local anesthetic, central nervous system stimulant, and addictive (similar to amphetamines) properties, cocaine has many other activities (goodman and oilman list and hOrhammer martindale morton 3). Little is known of the effects of the other alkaloids present in coca leaf. ... 

Alternatively, other tropane alkaloids (here cocaine) are obtained if no decarboxylation occurs after the intramolecular Mannich reaction of 28b. Subsequent hydrolysis and methylation afford the methyl ester 34, which is reduced stereospecifically to methylecgonine (35). Esterification with benzoyl-CoA (derived from L-Phe [22]) yields cocaine (36), the well-known central nervous system stimulant present in leaves of the coca plant [9]. 

Cocaine. This lias a bitter taste, is mydriatic, produces local anaesthesia and is toxic. After absorption, or when taken internally, it acts chiefly by stimulation of the central nervous system, succeeded by depression. Since the two phases may be present in different areas simultaneously, a mixed result may ensue. With large doses the chief symptoms are those of medullary depression. Death is due to paralysis of the respiratory centre. The main use of cocaine in medicine is as a local anaesthetic. 

The various stimulants have no obvious chemical relationships and do not share primary neurochemical effects, despite their similar behavioral effects. Cocaines chemical strucmre does not resemble that of caffeine, nicotine, or amphetamine. Cocaine binds to the dopamine reuptake transporter in the central nervous system, effectively inhibiting dopamine reuptake. It has similar effects on the transporters that mediate norepinephrine and serotonin reuptake. As discussed later in this chapter in the section on neurochemical actions mediating stimulant reward, dopamine is very important in the reward system of the brain the increase of dopamine associated with use of cocaine probably accounts for the high dependence potential of the drug. 

Isolated seizures that are not epilepsy can be caused by stroke, central nervous system trauma, central nervous system infections, metabolic disturbances (e.g., hyponatremia and hypoglycemia), and hypoxia. If these underlying causes of seizures are not corrected, they may lead to the development of recurrent seizures I or epilepsy. Medications can also cause seizures. Some drugs that are commonly associated with seizures include tramadol, bupropion, theophylline, some antidepressants, some antipsy-chotics, amphetamines, cocaine, imipenem, lithium, excessive doses of penicillins or cephalosporins, and sympathomimetics or stimulants. 

BZ is usually disseminated as an aerosol with the primary route of entry into the body through the respiratory system the secondary route is through the digestive tract. BZ blocks the action of acetylcholine in both the peripheral and central nervous systems. As such, it lessens the degree and extent of the transmission of impulses from one nerve fiber to another through their connecting synaptic junctions. It stimulates the action of noradrenaline (norepinephrine) in the brain, much as do amphetamines and cocaine. Thus, it may induce vivid hallucinations as it sedates the victim. Toxic delirium is very common. 

Q75 Cocaine causes agitation, tachycardia and hypertension. Cocaine stimulates the central nervous system. 

Cocaine readily penetrates mucous membranes and is an effective topical local anaesthetic that demonstrates intensive vasoconstrictor action. It has stimulant effects on the central nervous system and is a drug of addiction. It causes agitation, dilated pupils, tachycardia, hypertension, hallucinations, hyperthermia, hypertonia, hyperreflexia and cardiac effects. 

Although this drug is categorized as a local anesthetic, I have chosen to put it in with the hallucinogens because of the psychotomimetic effects that it produces. Cocaine is not a phenylethyl-amine, but it produces central nervous system arousal or stimulant effects which closely resemble those of the amphetamines, the methylenedioxyamphetamines in particular. This is due to the inhibition by cocaine of re-uptake of the norepinephrine released by the adrenergic nerve terminals, leading to an enhanced adrenergic stimulation of norepinephrine receptors. The increased... 

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