Crack Cocaine

Author: Elisa Bergaggio
Date: 31/05/2014


Elisa Bergaggio
Sara Pautasso

Crack Cocaine

Crack cocaine is a derived form of cocaine.
It can be prepared directly from cocaine paste or cocaine hydrochloride by dissolving either form in a water base or by using an organic solvent and adding a base such as sodium hydroxide or sodium bicarbonate. Crack comes in a rock crystal form that can be heated and inhaled or smoked. It is called 'crack' in reference to the cracking sound it makes when it is heated. Crack cocaine is a highly addictive stimulant. Chemistry

Crack cocaine is frequently purchased already in rock form, although it is not uncommon for some users to "wash up" or "cook" powder cocaine into crack themselves.
This process is frequently done with baking soda (sodium bicarbonate), water and a spoon. Crack is very different in its chemical propreties than cocaine hydrochloride. It vaporizes near temperature 90°C, much lower than the cocaine hydrochloride melting point of 190°C and thus whereas cocaine hydrochloride cannot be smoked (burns with no effect). Crack cocaine when smoked allows for quick absorption into the blood stream, and reaches the brain in 8 seconds. Crack cocaine is generally smoked through a glass handpipe or waterpipe. It can also be injected intravenously with the same effect as powder cocaine or even snorted, but these methods are less common. However, whereas powder cocaine dissolves in water, crack must be dissolved in an acidic solution such as lemon juice or white vinegar. It is the most addicting form of cocaine and one of the most addicting forms of any drug.
Manual of Adolescent Substance Abuse Treatment, Todd Wilk Estroff, M.D.,2001
Crack cocaine and cocaine hydrochloride. Are the differences myth or reality?, Hatsukami 1996
CESAR Center for Substance Abuse Research, University of Maryland
Crack cocaine must be distinguished from freebase cocaine: the latter is cocaine freed from impurities by treatment (usually with ether) by heating it to produce vapors for inhalation. This neutralize the HCI, leaving pure cocaine (purity between 90 and 100%). This is commonly confused with crack, which is typically 2 parts cocaine, 1 part baking soda and a little water heated gently to form crystals, which the user then smokes/inhale, with a purity between 50 et 95%. Both are derived from cocaine and the effects are similar but freebase and crack are not created equal.
Comment réduire les risques avec le crack ou la freebase?, J. Turmel (L’Injecteur, 2008)
Urban dictionary


Sodium bicarbonate (NaHCO 3 , common baking soda) is a base used in preparation of crack, although other weak bases may substitute for it.
The reaction when using sodium bicarbonate is:

Coc - H + Cl - + NaHCO 3 → Coc + H 2 O + CO 2 + NaCl

With ammonium bicarbonate:

Coc - H + Cl - + NH 4 HCO 3 → Coc + NH 4 Cl + CO 2 + H 2 O

With ammonium carbonate:

2(Coc - H + Cl -) + (NH 4)2CO 3 → 2 Coc + 2 NH 4 Cl + CO 2 + H 2 O



Crack cocaine was first developed during the cocaine boom of the 1970's, and its use became enormously popular in the mid 1980s, particularly in urban areas. Part of its popularity is due to the fact that almost anyone can make it, with the right tools, and it is less expensive than equivalent drugs. Producers make the drug by mixing cocaine with a base and water. As the water dissolves, dried crystals, known as crack cocaine form.
Coalition against drug abuse: The Effects of Crack Use

Mechanism of action

The pharmacodynamics of crack cocaine involve the relationships of neurotransmitters, including dopamine, serotonin, and glutamate, among others.
The most effect of crack cocaine on the central nervous system is the blockade of the dopamine transporter (DAT) protein. Dopamine transmitter released during neural signaling is normally recycled via the transporter; the transporter binds the transmitter and pumps it out of the synaptic cleft back into the presynaptic neuron, where it is taken up into storage vesicles. Crack cocaine binds tightly at the dopamine transporter forming a complex that blocks the transporter’s function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. This results in an enhanced and prolonged postsynaptic effect of dopaminergic signaling at dopamine receptors on the receiving neuron. Prolonged exposure to the drug, as occurs with habitual use, leads to homeostatic dysregulation of normal dopaminergic signaling via down-regulation of dopamine receptors and enhanced signal transduction. The decreased dopaminergic signaling after chronic cocaine use may contribute to depressive mood disorders and sensitize this important brain reward circuit to the reinforcing effects of cocaine (e.g. enhanced dopaminergic signaling only when cocaine is self-administered). This sensitization contributes to the intractable nature of addiction and relapse.
Crack cocaine’s effects on serotonin (5-hydroxytryptamine, 5-HT) show across multiple serotonin receptors, and is shown to inhibit the re-uptake of 5-HT3 specifically as an important contributor to the effects of crack cocaine. The 5-HT2 receptor (particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) show influence in the evocation of hyperactivity.
Sigma receptors are effected by crack cocaine, as cocaine functions as a sigma ligand agonist.
Further specific receptors it has been demonstrated to function on are NMDA, the D1 dopamine receptor, and the 5th subtype of the Metamorphic Glutamate Receptor (MGluR5). MGluR5 was considered an essential factor in cocaine self-administration and locomotor effects. Some authors prove that the reinforcing properties of cocaine are absent in mice that lack MGluR5 and an MgluR5 antagonist dose dependently decreased cocaine self-administration, but several subsequent studies have failed to completely replicate these results.
While previous studies have shown that mGluR5 - / - mice, or mice treated with mGlu5 receptor antagonist MTEP, have no ambulatory locomotor response to cocaine compared to mGluR5 + / + mice, the latest results indicate that mGluR5 - / - mice exhibit normal locomotor responses at low to moderate doses of cocaine.
Regarding the reward effect, have been found normal conditioned place-preference (a test to evaluate the conditioned rewarding effects) in mGluR5 - / - mice, compared to mGluR5 + / + mice.
So it’s possible that mGluR5 receptors are not involved in the drug-paired conditioned rewarding effects of cocaine while the direct rewarding property of cocaine relies on mGluR5.
Instead several studies have confirmed the role of mGluR5 neurotransmission in reinstated cocaine-seeking.
Cocaine also blocks sodium channels, thereby interfering with the propagation of action potentials; thus it acts as a local anesthetic.
In addition to this, cocaine has some target binding to the site of the Kappa-opioid receptor and it inhibits monoamine uptake in rats.
Pharmacology for Anesthetists, John D. Curren
Nature precedings
Dissociable roles of mGlu5 and dopamine receptors in the rewarding and sensitizing properties of morphine and cocaine (Veeneman, et al.; 2010)

Short-Term Effects

The effect from crack cocaine begins almost immediately after the vapors are inhaled and lasts about 5 to 15 minutes. Crack cocaine affecting the brain chemistry of the user causes intense euphoria, supreme confidence, alertness, increased energy. Its initial effect is to release a large amount of dopamine, inducing feelings of euphoria.
The short-term effects include:
• Increased blood pressure and heart rate
• Constricted peripheral blood vessels
• Increased rate of breathing
• Dilated pupils
• Decreased appetite
• Insomnia
• Anxiety and paranoia
• Aggressive, paranoid behavior
• Depression
• Intense drug craving
• Sudden death: even one use can cause overdose or death
After 5-15 minutes dopamine levels in the brain plummet, leaving the user feeling depressed and low.
CESAR Center for Substance Abuse Research, University of Maryland

Long-Term Effects

Prolonged crack cocaine abuse causes a number of problems, including:
• Severe depression
• Irritability and mood disturbances
• Aggressive, paranoid behavior
• Delirium or psychosis
• Tolerance and addiction, even after just one use
• Auditory and tactile hallucinations
• Heart attack and heart disease
• Stroke
• Respiratory failure
• Brain seizures
• Sexual dysfunction (for both men and women)
• Reproductive damage and infertility (for both men and women)
• Increased frequency of risky behavior
• Death
CESAR Center for Substance Abuse Research, University of Maryland
Health consequences of cocaine use

Addiction and withdrawal

Cocaine is a highly addictive substance. Users quickly develop a tolerance to crack cocaine, needing more of the substance to achieve the desired effects. Because the high from crack cocaine is so short-lived, users commonly smoke it repeatedly in order to sustain the high. This can lead to an even faster onset of addiction. Also, because crack cocaine works on the brain's system of reward and punishment, withdrawal symptoms occur when the drug's effects wear off.
These symptoms can include depression, irritability, extreme fatigue, anxiety, an intense craving for the drug, and sometimes even psychosis. Users will often keep using crack cocaine simply to avoid the negative effects of withdrawal.
Epidemiological estimates of risk in the process of becoming dependent upon cocaine, Chen 2004: cocaine hydrochloride powder versus crack cocaine
Crack users show high rates of antisocial personality disorder, engagement in illegal activities and other psychosocial problems, Paim 2012

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