| Class | Anticholinergic |
|---|---|
| Chemistry |
Tropane alkaloid |
| Routes of administration |
Oral, IV, subcutaneous, inhaled, intraocular, and topical on the mucosa |
| Absorption |
Well absorbed - 90% bioavailability |
| Solubility |
pKa 9.7; the sulfate salt is reasonably water-soluble, 1g in 455ml of water |
| Distribution |
VOD=1-6L/kg; 50% protein bound |
| Metabolism |
50% metabolised, maiNly by hepatic enzymatic hydrolysis, into a variety of metabolities, including tropane, tropic acid, and noratropine |
| Elimination |
50% is eliminated unchanged |
| Time course of action |
Half life is 2-5 hours, but the duration of tissue-specific efects could be longer, eg. mydriasis could last as long as 96 hours |
| Target receptor |
Muscarinic receptors (M1-M5), which are mainly Gq-coupled receptors |
| Mechanism of action |
By competitively blocking the effects of acetylcholine on Gq-coupled muscarinic receptors, atropine decreases the intracellular concentration of ionised calcium and cAMP. This results in numerous downstream clinical effects |
| Clinical effects |
- Decreased airway secretions |
| Literature reference |
Shutt, 1979 |
| CICM details of understanding | Level 1 |
| Mentioned around Deranged Physiology |
Anticholinergic drugs, as it somehow hasn't scored a chapter of its own |
| Related SAQs |
Question 19 from the second paper of 2019 (atropine alone) Question 3 from the first paper of 2011 (atropine vs. glycopyrrolate) |