| Class | Proton pump inhibitor |
|---|---|
| Chemistry |
Benzimidazole derivative |
| Routes of administration |
Oral and IV |
| Absorption |
Well absorbed in the small intestine; needs enteric coating. Bioavailability 80% |
| Solubility |
pKa 3.83; practically insoluble in water |
| Distribution |
VOD = 0.22L/kg; 97% protein-bound |
| Metabolism |
Inactive prodrug; metabolised by CYP450 in the liver. Biotransformed into the active form (a sulfenamide derivative) by the acidic environment of parietal cells |
| Elimination |
Minimal renal clearance as unchaged drug - mostly inactive metabolites are excreted in this way. |
| Time course of action |
Half-life is 1.5 hours; duration of proton pump inhibition is up to 24 hours |
| Target receptor |
H+/K+ ATPase pumps, or "proton pumps" on the apical surface of gastric parietal cells |
| Mechanism of action |
By binding covalently to active proton pumps on the luminal surface of the gastric parietal cells, the action of the pump is disrupted, which results in the cessation of gastric acid secretion. This leads to a neutralisation of gastric pH. |
| Clinical effects |
Neutralisation of gastric pH (up to 6.0 with IV infusion). Side effects include |
| Literature reference |
Fock et al (2008) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |