| Class | Barrier |
|---|---|
| Chemistry |
Complex salt of aluminium hydroxide and sulfated sucrose |
| Routes of administration |
Oral, rectal, topical |
| Absorption |
Minimally absorbed (mainly the aluminium) |
| Solubility |
pKa 0.43; completely insoluble in water |
| Distribution |
Does not distribute anywhere (not absorbed) |
| Metabolism |
Not metabolised to any meanigful degree |
| Elimination |
Eliminated via the faeces over 24-48 hrs |
| Time course of action |
Duration of action is unpredictable, usually up to 6 hours |
| Target receptor |
Any positively charged molecules are theoretically a molecular target |
| Mechanism of action |
By dissociating from aluminium, sucralfate becomes negatively charged sucrose sulfate molecules, whcih bind to anything positively charged (eg. mucus molecules, cell surface proteins) and crosslinks with these molecules, creating a protective barrier |
| Clinical effects |
Constipation, ileus, bowel obstruction, and interactions with other drugs (by binding them to the gel layer, they are rendered inactive) |
| Literature reference |
McCarthy (1991) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |