| Class | Mineralocorticoid |
|---|---|
| Chemistry |
Steroid |
| Routes of administration |
Oral |
| Absorption |
70-100% oral bioavailability, but very variable |
| Solubility |
pKa=12.55; poor water solubility; highly lipid soluble |
| Distribution |
VOD=1.2L/kg; 70-80% protein-bound |
| Metabolism |
Metabolised extensively in the liver |
| Elimination |
Inactive metabolites are eliminated in the urine |
| Time course of action |
Half-life is 18- 36 hours. |
| Target receptor |
Glucocorticoid receptor, which is a cytoplasmic and nuclear receptor, that regulates gene transcription and protein synthesis (but some actions are also attributed to membrane-bound receptors and nongenomic pathways) |
| Mechanism of action |
A combination of genomic effects and nongenomic effects, where some (medium and long term) activity is mediated by the regulation of protein synthesis, and some more immediate effects are mediated by the interference in cell membrane function, intracellular second messenger systems and membrane-bound mineralocorticoid receptors. Most of the major effects are due to the increased expression of aldosterone-sensitive ENaC channels on the surface of distal nephron tubular cells, resulting in sodium reabsorption and potassium loss. |
| Clinical effects |
- Hypernaremia, hypokalemia, water retention |
| Literature reference |
Rahman et al, 2022 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |