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Category: Stimulant

Named after the plant from which it is derived the cocaine hydrochloride (cocaine HCL, the hydrochloride salt of cocaine), is sold illegally in different degrees of purity and which may also appear on the streets as “crack” or “free base”.

Street Names

Cocaine has many street names,th most common being “coca” or “blow”. Other possible names could be “Flake”, “Nose Candy”, “White Lady”, “Bolivian Rock”, “Toot”, “snow”, “Mother of Pearl”, “columbian gold”, etc.

Principle additive

The principle additive is always cocaine base, which is liberated from the plant by a chemical .

“Powder”: cocaine hydrochloride is usually consumed by sniffing, liberating itself from additives once inside the body.

“Crack”:Appeared first in california in 1981 and then diffusing itself throughout America and Europe by the end of the 80’s It is produced by transforming cocaine hydrochloride and arriving at the pure crystals of cocaine base, which gets chopped and separated for sale or consumption. In this way a gram of cocaine can be transformed into 6-8 pieces of crack.

“Free base cocaine”:Is another way of producing cocaine base starting from cocaine-HCL the only difference from crack is the way it is manufactured.

Modes of use

Nasal consumption is the most populare among cocaine users. Consumption in this manner will generate a “high” lasting 15 to 60 minutes.

“Intravenous injection”
Usually this method comes combined with heroin (speedball). Intravenously the user will reach his or her “high” much faster.

“Smokine and Inhalation”
Crack and cocaine base are smoked using “pipe “, in a “joint” or inhaled from a piece of aluminum foil heated from underneath.

Lethal dose 1-1,2 grams

Effects and Collateral Effects

On the Central Nervous System
Traditionally the psychic effects of cocaine have been summerized in four stages of varying severity depending on dose and frequency of use:

Characterized by euphoria, emotional instability, increased cognitive and motor performance, hypervigilance, anorexia and insomnia;
Characterized by sadness, depression, apathy, poor attention and concentration, anorexia and insomnia;
Characterized by suspiciousness, paranoia, hallucinations and insomnia;
Characterized by hallucinations, stereotyped behaviour, paranoid ideation, insomnia, loss of impulse control, disorientation.

At a Peripheral Level
The increased release of biogenic amins such as dopamine, epinepherine and norepinepherine into the boby triggers an alarm response, with activation of the cardiovascular system and resultant tachycardia and hypertension. There are also tremors, muscle twitching, skin flushing and dilated pupils, accompanied by a delayed emptying of the bladder and bowels.

Mechanisms of action and Pharmacokinetics
The rewarding effect of cocaine is attained by the activation of dopamine neurons in the mesolimbic system.
Cocaine enhances dopaminergic transmission by increasing the concentration of dopamine.
The increase of dopamine occurs due to the blockage of the carriers that normally recapture (reuptake) it from the synaptic cleft.
Repeated use leads to an impairment of dopaminergic function, with a reductionin synaptic dopamine concentration and hypersensitivity of the post-synaptic receptors observed in the treatment chronic users.

Cocaine also exerts aninabilty to reuptake other neurotransmitters such as norepinephrine and seratonin.

The local anesthetic action of cocaine comes from the blocking of nerve conduction impulses at the channel level, voltage sensative Na+, which bines with moderate affinity.


Cocaine is detectable at the plasma level for 4-6 hours after the last dose nasally. In individuals who regularly use cocaine, the half-life is about 48 minutes after the last dose intravenously. Cocaine easily passes the blood brain barrier and is no-longer detectable in the brain tissue 6-8 hours after the last dose.

It’s rapidly and completely matabalized by the liver and plasma cholinesterase that hydrolyse it to an inactive metabalite: ecgonine methyl ester.

Small quatities of cocaine, less than 10%, are excreted unchanged in the urine. It can be found in the urine for 8 hours ofter a nasal dose of 1.5 mg/kg , up to a maximum limit of 12 hours.However the hydrated metabalite of the drug, benzoylecgonine, can be detectable for up to 144 hours after use.


Develops rapidly. The tolerance is reflected in the reduction of the pleasurable effects, which become less intence and are only partially overcome by increasing dosages and the redunction of the intervals between doses. At the same time develops an awareness for artificial and dysphoric states.


The desire to retry the initial pleasure and escape leads to anxiety and the compolsive use of the drug, reaching to true “binges” during which the subject dose not eat , sleep and becomes less and less euphoric , more and more dysphoric, agitated and aggressive.

Complications and Special Dangers

Vasoconstrictions and spasms can lead to the onset of heart attacks. Atherosclerosis is accentuated by cocaine and its use has been linked to thrombi. Hypertensive crisis , caused by cocaine, can lead to bleeding in the brain. Nasal inhalation of cocaine leads to vasoconstrictor effects , necrosis and perforation of the septum. At a pulminary level hypertesion and oedema has been observed, a syndrome also known as “crack lung”.

Chronic use of cocaine , diminishes stocks of dopamine, can also cause hyperprolactinemia with gynecomestia ( the development of breasts in males), galactorrhea and amenorrea. A decrease in libido and sexual performance, impotance in men and anorgasmia in women.

Finally, cocaine is also an epiliptogenic agent, generallized convulsions in-crease with repeated use.