Question 24

College Answer

This question was very broad, requiring the discussion of corticosteroid pharmacology. This embraces the pharmacokinetics, pharmacodynamics and pharmaceutics of the drug class. Synthesis from cholesterol and hepatic metabolism was included in better answers. Comparison of mineralocorticoids versus glucocorticoids was expected. The mechanism of action through  binding to intracellular receptors to affect protein synthesis should have been described. 
Additional marks were awarded for description of indications, preparations and routes of administration. In any pharmacology question, a list of common adverse effects is important. Of particular relevance is the suppression of the adrenal axis with prolonged administration.

Discussion

Nobody would have thought of writing anything about biosynthesis from cholesterol here, because the question asked about "corticosteroid drugs" specifically, rather than corticosteroid hormones.

The best you can do with a question like this is list some of the common features, and note any of the outliers

Pharmacokinetics

• Absorption:
  • Some have good bioavailability (hydrocortisone, prednisolone, dexamethasone)
  • Some have poor bioavailability and are only suitable for inhaled or topical use (fluticasone, budesonide, mometasone)
  • All are highly lipid soluble with pKa ~12.0
• Distribution
  • Most are highly protein-bound, mainly to albumin
  • VOD is generally modest, 0.5 -1.5 L/kg  
  • Hydrocortisone binds to the corticosteroid-binding globulin intended as the chaperone for cortisol
  • Dexamethasone is the least protein bound, hence better CNS penetration
• Metabolism
  • Extensive hepatic metabolism into progressively less active and more water soluble metabolites
• Elimination
  • Water soluble metabolites are renally eliminated

Pharmacodynamics

• Act by binding to glucocorticoid and mineralocorticoid receptors, which are cytoplasmic and nuclear receptors, that regulates gene transcription and protein synthesis (but some actions are also attributed to membrane-bound receptors and nongenomic pathways)
• Effects include:     
  - Immunosuppression (decreased granulocyte and lymphocyte activity)
  - Reduced airway oedema, bronchodilation
  - Sensitisation to catecholamines, increased cardiac output
  - Neuropsychiatric effects (euphoria, mania, insomnia, psychosis)
  - Metabolic effects (hyperglycaemia, hyperlipidemia, decreased insulin sensitivity)
  - Fatty tissue redistribution, osteoporosis, proximal myopathy
  - Hypernaremia, hypokalemia, water retention (mineralocorticoid effect)
  - Adrenal suppression
  - Increased risk of opportunistic infections (Aspergillus, Pneumocystis, Strongyloides) 

Williams, Dennis M. "Clinical pharmacology of corticosteroids." Respiratory care 63.6 (2018): 655-670.

Scherholz, Megerle L., Naomi Schlesinger, and Ioannis P. Androulakis. "Chronopharmacology of glucocorticoids." Advanced drug delivery reviews 151 (2019): 245-261.

Timmermans, Steven, Jolien Souffriau, and Claude Libert. "A general introduction to glucocorticoid biology." Frontiers in immunology 10 (2019): 1545.