| Class | Glucocorticoid |
|---|---|
| Chemistry |
Steroid |
| Routes of administration |
Oral |
| Absorption |
80% oral bioavailability |
| Solubility |
pKa=12.59; poor water solubility; highly lipid soluble |
| Distribution |
VOD=1.0 L/kg; <50% protein-bound |
| Metabolism |
Metabolised in the liver into prednislone, which is the active form of the drug. |
| Elimination |
Eliminated rapidly by being converted into prednisolone, which is then eliminated by hepatic metabolism. Also is a substrate for P-glycoprotein, which is an efflux pump into the lumen of the gut. |
| Time course of action |
Converted rapidly (over minutes) into prednisolone; half life of prednisolone is closer to 2-3 hrs |
| 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 glucocorticoid receptors |
| Clinical effects |
- Immunosuppression (decreased granulocyte and lymphocyte activity) |
| Literature reference |
Czock et al (2019) |
| CICM details of understanding | Level 2 |
| Mentioned around Deranged Physiology | |
| Related SAQs |