| Class | Acetylcholinesterase inhibitor |
|---|---|
| Chemistry |
Organophosphate
|
| Routes of administration |
Oral, inhaled, or transdermal |
| Absorption |
100% oral bioavailability, and generally absorbed rapidly via any route, including dermal and inhaled
|
| Solubility |
pKa values between 6 and 8; most are only soluble in organic solvents, which give them the characteristic smell.
|
| Distribution |
VOD= 1-5L/kg, but very variable. Moderate to high protein binding (30–90%),
|
| Metabolism |
Mostly metabolism by the liver; and a fair few have active metabolites.
|
| Elimination |
minimal renal elimination
|
| Time course of action |
There is a wide range of half-lives, but most a reasonably long-lived (eg. chlorpyrifos, 27 hrs).
|
| Target receptor |
Acetylcholinesterase |
| Mechanism of action |
By binding to acetylcholinesterase, organophosphates acts as competing substrates, replacing acetylcholine and decreasing acetylcholinesterase activity. The drug is metabolised much more slowly than acetylcholine, which means the enzyme is blocked for a sustained period. The bond between the drug and the enzyme also increases with age. |
| Clinical effects | |
| Literature reference |
Testai et al, 2010 |
| CICM details of understanding | Level 3 |
| Mentioned around Deranged Physiology |
Cholinergic drugs and acetylcholinesterase inhibitors, of which Organophosphate poisoning is a sub-trope. Follows into Effects of acetylcholine receptor activation. |
| Related SAQs |