100+ Free FC Ophth(SA) Final Practice Questions

Explanation: The clinical presentation of severe pain out of proportion to signs, radial keratoneuritis, ring infiltrate, and double-walled cysts is diagnostic of Acanthamoeba keratitis. Polyhexamethylene biguanide (PHMB) 0.02% or chlorhexidine 0.02% are biguanides that effectively eradicate both active trophozoites and dormant cysts. Combination anti-amoebic therapy with a diamidine (such as propamidine isethionate/Brolene) is often added to maximize cysticidal activity.

Explanation: Corneal collagen cross-linking (CXL) utilizing riboflavin (vitamin B2) photo-sensitizer and ultraviolet A (UVA 365 nm) irradiation is the only proven disease-modifying treatment that halts the biomechanical progression of keratoconus. Riboflavin acts as a photosensitizer creating covalent chemical bonds between stromal collagen fibrils. Pachymetry above 400 µm after epithelial debridement ensures endothelial safety during the standard Dresden CXL protocol.

Explanation: Herpes simplex virus (HSV) epithelial keratitis manifests classically as a true dendritic ulcer with terminal bulbs. The primary therapy is topical antiviral medication (ganciclovir 0.15% gel or aciclovir 3% ointment) or oral antiviral therapy (valaciclovir / aciclovir). Topical corticosteroids are strictly contraindicated during active viral epithelial replication because they enhance viral proliferation, transform dendrites into geographic ulcers, and increase corneal perforation risk.

Explanation: Topical natamycin 5% suspension is the FDA-approved first-line drug of choice for filamentous fungal keratitis (such as Fusarium and Aspergillus species), particularly following vegetative ocular trauma. The Mycotic Keratitis Treatment Trial I (MKTT I) demonstrated that natamycin achieved significantly superior visual outcomes and lower perforation rates compared to topical voriconazole 1% for filamentous fungal keratitis.

Explanation: Fuchs endothelial corneal dystrophy (FECD) results from progressive loss of corneal endothelial cells. Descemet Membrane Endothelial Keratoplasty (DMEK) involves selective transplantation of isolated donor Descemet membrane and endothelium (~10–15 µm thick) without donor stroma. DMEK provides the fastest visual recovery, superior anatomical restoration, and significantly lower immunologic graft rejection rates (<1%) compared to DSAEK or penetrating keratoplasty.

Explanation: Peripheral Ulcerative Keratitis (PUK) associated with systemic autoimmune disease (especially Rheumatoid Arthritis) represents a sight- and life-threatening necrotizing vasculitis. Systemic immune suppression with high-dose intravenous pulse methylprednisolone followed by oral steroids and steroid-sparing immunosuppressants (e.g., Rituximab, Cyclophosphamide) is essential. Systemic therapy halts systemic necrotizing vasculitis and corneal destruction; mortality in untreated PUK patients reaches 30% at 10 years due to systemic vasculitic complications.

Explanation: Pseudomonas aeruginosa is the classic causative organism of rapidly progressive, liquefactive bacterial keratitis in contact lens wearers, driven by bacterial proteases and exotoxin A. Gram-negative rods on Gram stain confirm Pseudomonas. Intensive broad-spectrum topical therapy using fortified aminoglycoside (tobramycin 1.5%) plus fortified cephalosporin (cefuroxime 5%) or intensive high-potency fluoroquinolones (e.g., moxifloxacin/levofloxacin) is required immediately.

Explanation: Mooren ulcer is an idiopathic, painful, progressive outer-lamellar ulcerative keratitis that originates at the corneal margin and spreads circumferentially and centrally with a characteristic steep, overhanging undermined central border. By definition, Mooren ulcer is a diagnosis of exclusion in which all systemic autoimmune and vasculitic diseases (such as RA, GPA, polyarteritis nodosa) have been thoroughly ruled out.

Explanation: Ocular Cicatricial Pemphigoid (OCP) / Mucous Membrane Pemphigoid (MMP) is a systemic autoimmune blistering disease characterized by autoantibodies against basement membrane zone antigens (such as BP180, BP230, or integrin beta-4). Management requires systemic immunosuppression: dapsone is first-line for mild-to-moderate disease, while rapidly progressive or severe disease requires systemic cyclophosphamide, mycophenolate mofetil, or rituximab to arrest cicatrization.

Explanation: Terrien marginal degeneration is a rare, non-inflammatory, typically bilateral ectatic corneal condition characterized by painless superonasal marginal thinning with intact epithelium, fine superficial pannus, and a characteristic yellow line of lipid deposition at the central advancing edge. Ectasia in the peripheral zone leads to high against-the-rule or oblique astigmatism.