Cocaine cns stimulent

cocaine [KOE Kane] is an inexpensive, widely available, and highly addictive drug that is currently abused daily by more than three million
people in the United States. Because of its abuse potential; ccaine is classified as a Schedule II drug by the United States.
1 Mechanism of action: The primary mechanism of action 'underly­ing the central and peripheral effects of cocaine is blockade of re-uptake of the monoamines (norepinephrine. serotonin, and dopamine) into the presynaptic terminals from which these neuro­transmitters are released. This blockade is effected by binding to the monoaminergic re-uptake transporters and, thus, potentiates and prolongs the CNS and peripheral actions of these monoamines. in particular, the prolongation of dopaminer pleasure system (limbic system) pro duces the intense euphoria that cocaine initiariy causes. Chronic intake of cocaine depletes dopamine. This depletion triggers the vicious cycle of craving for cocaine that temporarily relieves from depression.
Actions:
a. CNS: The behavioral effects of cocaine result from powerful stimulation of the cortex and brainstem. Cocaine acutely increases mental awareness and produces a feeling of well-being and euphoria similar to that caused by amphetamine. Like amphetamine, cocaine can produce hallucinations, delu­sions, and paranoia. Cocaine increases motor activity, and at high doses, it causes tremors and convulsions, followed by respiratory and vasomotor depression.

b. Sympathetic nervous system: Peripherally,, cocaine potenti­ates the action of norepinephririe, and produces the tight or flight" syndrome characteristic of adrenergic stimulation This is associated with tachycardia, hypertension,pupillary dilation. and peripheral vasoconstriction. Recent evidence suggests that the ability of baroreceptor reflexes to buffer the hyperten­sive effect may be impaired.

c. Hyperthermia: 'Cocaine is unique among illicit drugs in that death can result not only as a function of dose, but also from the drug's propensity to cause hyperthermia. [Note: Mortality rates for cocaine overdose rise in hot weather.] Even a small dose of intranasal cocaine impairs sweating and cutaneous vasodilatation. Perception of,thermal discomfort is also decreased.‑

_3. Therapeutic uses: Cocaine has a local anesthetic action that rep-resents the only current rationale for the therapeutic use of cocaine. For example, cocaine is applied topically as a local anes­thetic during eye, ear, nose, and throat surgery. Whereas the local anesthetic action of cocaine is due to a block of voltage-activated sodium channels, an interaction' with potassium channels may contribute to the ability of cocaine to cause cardiac arrhythmias.[Note: Cocaine is the only local anesthetic' that causes vasocon­striction. This effect is responsible for the necrosis and perforation of the nasal septum seen in association with chronic inhalation of cocaine powder.]

4. Pharmacokfnetics: Cocaine is often self-administered by chewing, intranasal snorting, smoking, or intravenous (IV) injection. The peak effect occurs at fifteen to twenty minutes after intranasal intake of cocaine powder, and the "high" disappears in 1 to 1.5 hours. Rapid but short-lived effects are achieved following IV injection of cocaine or by smoking the freebase form of the drug ("crack"). Because the onset of action is most rapid, the potential for overdosage and dependence is greatest with IV injection and crack smoking. Cocaine is rapidly de-psterified and demethylated to benzoylecgonine, which is excreted in the urine. Detection of this substance in the urine identifies a user.
5. Adverse effects:
a. Anxiety: The toxic response to acute cocaine ingestion can pre­cipitate an anxiety reaction that includes hypertension, tachy­cardia, sweating. and paranoia. Because of the irritability, many users take cocaine with alcohol. A product of-cocaine metabo­lites and ethanol is cocaethylene, which-is also psychoactive.
b. Depression: Like all stimulant drugs, cocaine stimulation of the CPI is followed by a period of mental depression. Addicts withdrawing from cocaine exhibit physical and emo­tional depression as. well as agitation. These symptoms can he treated with benzodiazepines or phenothiazines. '
c. Heart disease: Cocaine can induce seizures as well as fatal cardiac arrhythmias (Figure 10.8). IV diazepam and propra­nolol may be required to control cocaine-induced seizures and cardiac arrhythmias, respectively. The incidence of myocardial infarction is cocaine users is unrelated to dose, to duration of use, or to route of administration. There is no marker to identify those individuals whi,-may have life-threat­ening cardiac effects after taking cocaine.