| Class | Acetylcholinesterase inhibitor |
|---|---|
| Chemistry |
Organophosphate
|
| Routes of administration |
Inhaled or transdermal |
| Absorption |
100% oral bioavailability, and generally absorbed rapidly via any route, including dermal and inhaled
|
| Solubility |
pKa = 7.9; excellent water and lipid solubility
|
| Distribution |
VOD probably about 1L/kg, probably minimally protein bound
|
| Metabolism |
Rapidly and completely metabolised by plasma esterase
|
| Elimination |
minimal renal elimination
|
| Time course of action |
Half-life of several hours
|
| Target receptor |
Acetylcholinesterase |
| Mechanism of action |
By binding to acetylcholinesterase, VX acts as a competing substrate, 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. |
| Clinical effects |
The effects are mostly neuromuscular: tby producing an excess of acetylcholine, this agent acts as a depolarising neuromuscular junction blocker. Other cholinergic side effects (salivation, bronchorrhoea, bradycardia, lacrimation, urinary incontinence and diarrhoea) take time to develop and are therefore only seen clinically if the patient is rescued with mechanical ventilation shortly after exposure.
|
| Literature reference |
Gupta (2006) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| 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 |