Vogt-Koyanagi-Harada Syndrome MCQ — NEET PG Practice Question | NEETPGAI
Vogt-Koyanagi-Harada Syndrome
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eye Ophthalmology
A 32-year-old woman of Hispanic descent presents with a 2-week history of severe bilateral eye pain, photophobia, and blurred vision. She reports preceding headache, tinnitus, and neck stiffness 1 week prior. Fundoscopy reveals bilateral optic disc hyperemia and multifocal serous retinal detachments. EDI-OCT confirms diffuse choroidal thickening. Over the following weeks, she develops the characteristic appearance marked **B** in the diagram—diffuse retinal pigment epithelium depigmentation with exposure of the underlying orange choroidal vasculature. She also notices whitening of her eyelashes and eyebrows, and patchy hair loss on her scalp.
Which of the following BEST describes the underlying pathophysiology of the condition marked **B**?
A. T-cell-mediated autoimmune response against melanocyte tyrosinase-family proteins, with strong HLA-DRB1*0405 association in susceptible populations
B. Immune complex deposition at the choriocapillaris with secondary RPE atrophy and loss of melanin
C. Viral reactivation of herpes simplex virus with direct cytolytic destruction of melanocytes
D. Bacterial lipopolysaccharide-triggered innate immune response causing acute granulomatous choroiditis
Explanation
Why option 1 is correct
The condition marked B (Vogt-Koyanagi-Harada syndrome) is fundamentally a T-cell-mediated autoimmune panuveitis directed against melanocytes expressing tyrosinase-family proteins. This explains both the ocular manifestations (granulomatous uveitis, serous retinal detachments, and the pathognomonic sunset glow fundus from RPE depigmentation) and the systemic integumentary findings (vitiligo, poliosis, alopecia). The strong association with HLA-DRB1*0405 in Asian, Hispanic, Native American, and Middle Eastern populations confirms the autoimmune genetic predisposition. The four-stage evolution—prodromal (meningismus, tinnitus), acute uveitic (bilateral granulomatous panuveitis with serous detachments), chronic/convalescent (sunset glow, Sugiura sign), and recurrent phases—is pathognomonic for VKH and reflects progressive T-cell-mediated melanocyte destruction.
Why each distractor is wrong
Option 2 (Immune complex deposition): While immune complexes may play a secondary role, VKH is primarily a T-cell-mediated (cellular) response, not an immune complex (humoral) disease. Immune complex vasculitis does not explain the selective melanocyte targeting or the HLA-DRB1*0405 association.
Option 3 (Viral reactivation/HSV): VKH is not a viral disease. While the prodromal phase may mimic viral meningitis, CSF pleocytosis is lymphocytic and sterile. HSV does not cause bilateral granulomatous panuveitis or the integumentary manifestations characteristic of VKH.
Option 4 (Bacterial LPS/innate immunity): VKH is not triggered by bacterial antigens and does not involve acute innate immune activation. The disease requires HLA-DRB1*0405 (adaptive immunity), and there is no evidence of bacterial infection. This mechanism does not explain the melanocyte-specific targeting.
High-YieldNEET PG
VKH = T-cell autoimmunity against melanocyte tyrosinase in genetically predisposed (HLA-DRB1*0405) populations; sunset glow fundus is the chronic hallmark from RPE depigmentation; treat early and aggressively with high-dose systemic corticosteroids + steroid-sparing immunosuppressants to prevent recurrent disease.
