| Class | Anticholinergic |
|---|---|
| Chemistry |
Tropane alkaloid |
| Routes of administration |
Oral, IV, or as patches |
| Absorption |
Oral bioavailability is about 29%, mostly because of poor and slow absorption |
| Solubility |
pKa 9.54, highly water-soluble. |
| Distribution |
VOD=12-30L/kg, highly protein bound (95%) |
| Metabolism |
Undergoes minimal hepatic metabolism |
| Elimination |
Excreted primarily through the urine and bile unchanged |
| Time course of action |
Half life is 7 hours |
| Target receptor |
Muscarinic receptors (M1-M5), which are mainly Gq-coupled receptors, but also targets antihistamine receptors. By a completely unrelated mechanism, it also acts as a potent inhibitor of presynaptic carrier-mediated dopamine transport. |
| Mechanism of action |
By compettively blocking the effets of acetylcholine on Gq-coupled muscrinic receptors, benzatropine decreases the intracellular concentration of ioniased calcium and cAMP. This results in numerous downstream clinical effects. It also causes sedation by its antagonist effects on CNS histamine receptors, and it reverses the extrapyramidal effects of dopamine antagonists (eg. maxolon-induced dystonia) by increasing synaptic dopamine concentrations through inhibitoon of presynaptic dopamine transport. |
| Clinical effects |
#NAME? |
| Literature reference |
This Canadian monograph from Pendopharm |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |