| Class | Recreational sympathomimetic |
|---|---|
| Chemistry |
Tropane alkaloid, related to hyoscine |
| Routes of administration |
oral, nasal, IM, s.c, IV |
| Absorption |
Oral bioavailability 30-40% |
| Solubility |
pKa = 8.6, slightly soluble in water (but often available as a highly soluble hydrochloride salt) |
| Distribution |
VOD= 1-3L/kg, 92% protein-bound |
| Metabolism |
Rapidly metabolised by plasma pseudocholinesterase and hepatic carboxylesterases |
| Elimination |
Minimal free drug is eliminated in the urine |
| Time course of action |
Half-life around 1 hour |
| Target receptor |
Blocks the action of DAT, NET and SERT (but mainly DAT), thereby preventing the reuptake of monoamines from the synaptic cleft |
| Mechanism of action |
By increasing the synaptic concentration of noradrenaline and dopamine (mostly dopamine), cocaine acts as an indirect sympathomimetic. Because they act centrally, this effect translates into increased alertness and arousal, as well as broadly adrenaline-like peripheral effects. The potent dopaminergic effect of cocaine underlies its desireable effects on mood. |
| Clinical effects |
Increased alertness, psychomotor stimulation, tachycardia and tachypnoea due to systemic adrenaline release, coronary artery vasconstriction, hyperthermia, mydriasis, seizures, arrhythmias, stroke and large vesel dissection |
| Literature reference |
Benowitz (1993) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |