Anti-inflammatory Drugs

Ocular Steroids - Powerhouse Potions

• Potent anti-inflammatory & immunosuppressive agents, crucial in ophthalmology.
• Mechanism:
  • Inhibit phospholipase A2 (PLA2) via lipocortin → ↓ arachidonic acid synthesis → ↓ prostaglandins & leukotrienes.
  • Stabilize mast cells, reduce capillary permeability & cellular exudation.
• Types (Potency & Penetration):
  • Strong (High Potency): Prednisolone acetate (1% susp.), Dexamethasone (0.1%), Difluprednate (0.05% emulsion - very potent).
    • Excellent penetration: Prednisolone acetate, Difluprednate.
  • Moderate Potency: Fluorometholone (FML) (0.1%), Loteprednol etabonate (0.2%, 0.5%).
    • 📌 "Soft steroids" (Loteprednol, FML): Ester-based, rapidly metabolized locally; lower risk of ↑ IOP.
  • Weak Potency: Medrysone, Hydrocortisone (rarely used topically for significant inflammation).
• Key Indications: Uveitis (all forms), severe allergic conjunctivitis/keratoconjunctivitis, post-operative inflammation, non-necrotizing scleritis, interstitial keratitis (non-infectious).
• Major Side Effects:
  • ↑ Intraocular Pressure (IOP) → Steroid-induced glaucoma (monitor closely!).
  • ⭐ > Most common type of cataract induced by steroids is Posterior Subcapsular Cataract (PSC).
  • Delayed corneal epithelial wound healing.
  • ↑ Susceptibility to secondary infections (e.g., fungal keratitis, HSV reactivation).
  • Corneal thinning/perforation (prolonged use).
• ⚠️ Cautions: Active infections (esp. dendritic HSV keratitis, fungal). Always taper dose gradually to prevent rebound inflammation.

Ocular NSAIDs - Soothing Cyclo-Stoppers

• Mechanism: Inhibit cyclooxygenase (COX-1 & COX-2) enzymes $ ightarrow$ ↓ prostaglandin synthesis.
• Key Drugs & Properties:
  • Ketorolac 0.4% / 0.5%: Potent analgesic; widely used post-op.
  • Diclofenac 0.1%: Good anti-inflammatory; stings on instillation.
  • Flurbiprofen 0.03%: Intraoperative miosis inhibition.
  • Nepafenac 0.1% / 0.3%: Prodrug, better penetration; used for CME prevention post-cataract surgery.
  • Bromfenac 0.09%: Long half-life, once/twice daily dosing.
• Primary Uses:
  • Post-operative inflammation & pain (cataract, refractive surgery).
  • Cystoid Macular Edema (CME) prophylaxis & treatment.
  • Allergic conjunctivitis (mild cases).
  • Episcleritis/Scleritis (adjunct or alternative to steroids).
  • Corneal abrasion pain relief.
• Side Effects:
  • Stinging/burning on instillation (common).
  • Delayed corneal epithelial healing.
  • Rare: Corneal thinning/melt (especially with prolonged use or in compromised corneas).

⭐ Topical NSAIDs, especially ketorolac and diclofenac, can be associated with corneal melt in predisposed eyes (e.g., dry eye, rheumatoid arthritis).

• Advantages over Steroids:
  • No risk of ↑ Intraocular Pressure (IOP).
  • No risk of cataract formation.
  • Less immunosuppression. 📌 No Sight-threatening Adverse Incidents Daily (usually safe, but watch cornea!)

Other Immunomodulators - Specialized Shields

• For chronic/severe immune ocular conditions; steroid-sparing.
• Cyclosporine A (CsA): Calcineurin inhibitor; ↓ T-cell activation.
  • Topical (0.05%, 0.09%): ↑ tear production in KCS; VKC, AKC.

  ⭐ Topical Cyclosporine A (e.g., 0.05%) works by inhibiting T-cell activation and cytokine production, approved for increasing tear production in keratoconjunctivitis sicca (KCS).

  • Systemic: Severe uveitis (e.g., Behçet's). Key SE: Nephrotoxicity.
• Tacrolimus (FK506): Calcineurin inhibitor (potent).
  • Topical (0.03%): VKC, AKC.
  • Systemic: Severe uveitis.
• Sirolimus (Rapamycin): mTOR inhibitor. Uveitis.
• Other Systemic Agents: For refractory uveitis.
  • Antimetabolites: Methotrexate, Azathioprine, Mycophenolate Mofetil (MMF).
  • Biologics: TNF-α inhibitors (e.g., Adalimumab for JIA-uveitis).

High‑Yield Points - ⚡ Biggest Takeaways

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