Cocaine is rapidly absorbed once deposited in the nasal mucosa. It is detected in blood at 15 minutes, where the peak concentration reached at most one hour after being inhaled, although the maximum euphoric effect is achieved before arriving at the peak concentration, between 20-30 minutes after inhaled. The substance is absorbed almost entirely.
Oral administration produces a peak concentration higher than the intranasal route, although the euphoric effect is delayed 30 minutes with respect to the latter.
Drug bioavailability is 60%, being metabolized by plasma cholinesterase and liver to inactive metabolites, which reach its peak concentration 4-5 hours after inhalation. Since degradation by cholinesterase is the only metabolic pathway of the drug, interactions are usually from pharmacodynamic nature, although some chemicals and drugs produce pharmacokinetic interactions by inhibiting plasma cholinesterase or liver, a phenomenon known for some addicts to increase or prolong the effects of the drug.
When the drug is smoked, absorption via the lung is rapid, reaching peak concentration at 30-40 minutes.
At autopsy are detected the highest concentrations, both urine as kidney, followed by the brain, blood and liver. This substance easily crosses the blood brain barrier to reach into the brain concentration four times the peak plasma concentration. After one to two hours from this time, the blood concentration falls more rapidly than in the brain. In cases of overdose with exitus, is common to find brain concentrations 10 times higher than in the plasma.
The drug is excreted by 95% in the urine.
A common combination of drugs of abuse is called speedball, with cocaine and heroin. Those who use this combination refer to experience an strong state of euphoria. Apparently, cocaine reduces opioid withdrawal symptoms and heroin can reduce the irritability that can be observed in long-standing cocaine consumers.
Simultaneous use of cocaine and sympathomimetic substances increases CNS stimulation. In addition, joint with dobutamine, dopamine or epinephrine topical may increase the cardiovascular effects of the two substances and the risk of significant adverse effects.
it is particularly dangerous mixing cocaine powder with adrenaline solution for nasal interventions, that is potentially fatal, due to the frequency of occurrence of hypertensive crises and arrhythmias.
Adding adrenaline to the drug does not prolong the action of the substance of abuse or delays its absorption, so that the mixture, in addition to dangerous, is useless.
Concurrent use of levothyroxine and cocaine may increase the effects of both substances. Thyroid hormone increases the risk of presenting signs of coronary insufficiency when sympathomimetic agents are administered to patients with severe coronary artery insufficiency prior
The combination of both substances raised to approximately 50 beats/min additional heart rate with respect to the use of either drug alone.
Simultaneous use of both abused drugs gives rise to a significant interaction. In the presence of ethyl alcohol. A part of cocaine is transesterified to cocaethylene, with the same power as cocaine to block the action of dopamine uptake, which increases the effects of cocaine.
Cocaine reduces antianginal effect of these substances.
Taking cocaine immediately or shortly before surgery with anesthesia by using chloroform, cyclopropane or halothane trichlorethylene increases the risk of ventricular fibrillation or other arrtimias, particularly in patients with cardiac disease prior. The cause is that these anesthetics sensitize the myocardium to sympathomimetic effects.
If it have prior knowledge of drug use prior to the operation, action must be very careful and monitor the patient closely. Isoflurane, enflurane and methoxyflurane may sensitize the myocardium also against sympathomimetics.
Cocaine may inhibit the therapeutic effect of beta blockers. However, these drugs are indicated to reduce tachycardia, myocardial ischemia and arrhythmias induced by cocaine.
The simultaneous use of beta blockers with cocaine may increase the risk of hypertension, excessive bradycardia and perhaps block. These risks are lower when labetalol is used instead of other drugs, because this drug has some alpha-adrenergic blocking activity.
It should be highlighted this interaction to patients receiving beta-blockers locally to combat ocular hypertension.
Cocaine may diminish the antihypertensive effect of postganglionic blockers guanethidine and guanadrel. So, patients using cocaine should be monitored if received any of these antihypertensive medicines. Furthermore, these drugs can enhance sympathetic stimulation induced by cocaine, thus increasing the risk of hypertension and arrhythmias.
CENTRAL NERVOUS SYSTEM STIMULANTS ▲
Concomitant use of CNS stimulants with cocaine can cause excessive stimulation, so it may appear or increase symptoms such as insomnia, irritability, nervousness and perhaps arrhythmias or seizures
TRICYCLIC ANTIDEPRESSANTS, DIGITAL, LEVODOPA AND METHYLDOPA ▲
The simultaneous use of any of these drugs with cocaine may increase the risk of arrhythmias.
CHOLINESTERASE INHIBITORS ▲
Inhibition of cholinesterase activity by substances such as drugs for the treatment of myasthenia gravis, cyclophosphamide, demecarium, echothiophate, neurotoxic insecticides including malathion, isoflurophate, and thiotepa reduce or block the degradation of cocaine, substrate, as indicated above, of plasma cholinesterase and liver. This inhibition, which can last months, causes an increased and prolonged effects of cocaine.
ORGANOPHOSPHATE INSECTICIDES ▲
Some patients may ingest organophosphate insecticides while smoking crack to prolong the effect of the drug, since those chemical agents inhibit cholinesterase. A case report includes the case of a pregnant patient who developed weakness after an hour of taking the drug, followed by vomiting, twitching and generalized tonoclonal seizures.
MAOIs can enhance and prolong vasopressors and cardiostimulatory effects of cocaine, due to the release of catecholamines produced during the inhibition of MAO intraneuronally accumulated, which may result in severe hypertension, severe headache, vomiting, potentially lethal arrhythmias or crises of hyperpyrexia. As with other interacting drugs, consumers should refrain from consuming cocaine during the two weeks following the administration of MAO inhibitors.
Phenelzine also inhibits serum cholinesterase so that it can increase and prolong the effects of cocaine.
Reserpine and dopamine potentiate the adverse effects of cocaine.
Cocaine during pregnancy
Date of update of this page: November 10, 2008.
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