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endocrine:drugs:fluticasone

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Corticosteroids

Corticosteroids are synthetic analogs of adrenal cortex hormones used for their potent anti-inflammatory and immunosuppressive effects.

They mimic:

  • Cortisol (glucocorticoid activity)
  • Aldosterone (mineralocorticoid activity – some agents)

Used across systems:


Classification

Systemic Glucocorticoids

Inhaled / Intranasal

Topical

  • Various potency classes

Mechanism of Action

Corticosteroids act via intracellular glucocorticoid receptors.

Stepwise:

1) Drug diffuses across cell membrane
2) Binds cytoplasmic glucocorticoid receptor
3) Complex translocates to nucleus
4) Alters gene transcription

Results:

  • ↓ Pro-inflammatory cytokines (IL-1, IL-2, IL-4, IL-5, IL-6, TNF-α)
  • ↓ Eosinophil survival
  • ↓ T-cell activation
  • ↓ Mast cell mediator release
  • ↓ Prostaglandin synthesis (via ↓ phospholipase A2)
  • ↓ Leukotriene production

Effect:

Broad suppression of inflammation.

Onset:

  • Hours to days (genomic mechanism)

Glucocorticoid vs Mineralocorticoid Activity

Drug Glucocorticoid Potency Mineralocorticoid Activity
Hydrocortisone Low Moderate
Prednisone Moderate Low
Methylprednisolone Moderate Minimal
Dexamethasone High None

Clinical relevance:

  • Mineralocorticoid activity → fluid retention, hypertension
  • Dexamethasone preferred when fluid retention undesirable

Indications (Allergy Context)

Type I hypersensitivity late-phase control:

Allergic rhinitis:

  • Intranasal first-line

Asthma:

  • Inhaled maintenance therapy

Severe allergic reactions:

  • Adjunct in anaphylaxis (not first-line)

Autoimmune and inflammatory disease:

  • Broad use

Adverse Effects

Short-term:

  • Mood changes
  • Hyperglycemia
  • Fluid retention
  • Insomnia

Long-term:

  • Adrenal suppression
  • Osteoporosis
  • Cushingoid appearance
  • Muscle wasting
  • Increased infection risk
  • Peptic ulcer disease

Mechanism:

Systemic immunosuppression and metabolic alteration.

Hypothalamic–Pituitary–Adrenal (HPA) Axis Suppression

Chronic steroid use suppresses endogenous cortisol production.

Abrupt withdrawal may cause:

  • Adrenal insufficiency
  • Hypotension
  • Fatigue
  • Crisis in severe cases

Taper when:

  • High dose
  • Prolonged use (>2–3 weeks)

Clinical Pearls

  • Intranasal corticosteroids are superior to oral antihistamines for nasal congestion.
  • Steroids suppress late-phase allergic inflammation.
  • Dexamethasone has no mineralocorticoid activity.
  • Always consider HPA suppression with prolonged systemic therapy.
  • In anaphylaxis, epinephrine is first-line — steroids are adjunctive.

endocrine/drugs/fluticasone.1770925111.txt.gz · Last modified: by andrew2393cns