Regarding the pharmacological properties of corticosteroids, all of the following statements are correct EXCEPT:

## Analysis of Corticosteroid Pharmacology ### Correct Statements (Options 0, 1, 2) **Option 0: Gluconeogenesis and glucose utilization** - Glucocorticoids are hyperglycemic agents - They promote hepatic gluconeogenesis by inducing gluconeogenic enzymes (PEPCK, G6Pase) - They decrease glucose uptake and utilization in peripheral tissues - This is a well-established metabolic effect [cite:KD Tripathi Ch 57] **Option 1: Mineralocorticoid mechanism** - Aldosterone and other mineralocorticoids act on principal cells of the collecting duct (not DCT as commonly taught, but DCT is the site of early sodium reabsorption) - They increase ENaC (epithelial sodium channel) expression - Result: sodium reabsorption and potassium excretion - This is the classic mechanism of action [cite:Harrison Ch 377] **Option 2: Phospholipase A2 inhibition** - Glucocorticoids induce lipocortin-1 (annexin-1), which inhibits phospholipase A2 - This blocks the release of arachidonic acid from cell membranes - Reduces synthesis of prostaglandins, leukotrienes, and other eicosanoids - This is the basis of their anti-inflammatory action [cite:Robbins Ch 3] ### Incorrect Statement (Option 3: Beta-2 receptor affinity) **Key Point:** Glucocorticoids do NOT increase the affinity of beta-2 adrenergic receptors for catecholamines. Instead, glucocorticoids: - **Increase the number (upregulate) beta-2 adrenergic receptors** on cell surfaces - Enhance the responsiveness of tissues to catecholamines (permissive effect) - This is why they are used as adjuncts in severe asthma and anaphylaxis - The mechanism is increased receptor expression, not increased affinity of individual receptors **High-Yield:** This is a common exam trap — confusing "receptor upregulation" with "increased receptor affinity." Affinity is the intrinsic property of a receptor to bind a ligand; corticosteroids do not alter this. They increase the NUMBER of receptors available. **Clinical Pearl:** This permissive effect on catecholamine action is why corticosteroids are contraindicated in some patients with hypertension or coronary artery disease — they amplify sympathomimetic effects. ## Summary Table | Property | Glucocorticoids | Mineralocorticoids | | --- | --- | --- | | **Glucose metabolism** | ↑ Gluconeogenesis, ↓ utilization | Minimal effect | | **Electrolytes** | ↑ Na⁺ reabsorption (weak) | ↑ Na⁺ reabsorption (strong) | | **Anti-inflammatory** | Via PLA2 inhibition | Minimal | | **Beta-2 effect** | ↑ Receptor NUMBER (upregulation) | No significant effect | | **Stress response** | Primary mediator | Permissive role |