Central Serous Chorioretinopathy MCQ — NEET PG Practice Question | NEETPGAI
Central Serous Chorioretinopathy
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eye Ophthalmology
A 38-year-old man presents with acute-onset, painless blurred central vision and metamorphopsia for 2 weeks. He reports objects appearing smaller than usual and a central scotoma. He is a high-stress investment banker on inhaled corticosteroids for asthma. Fundoscopy reveals a well-circumscribed dome-shaped lesion at the posterior pole with loss of the foveal reflex. OCT confirms a dome-shaped serous detachment of the neurosensory retina with elongated photoreceptor outer segments, as marked **A** in the diagram. Which of the following best describes the pathophysiological basis of the structure marked **A**?
A. Choroidal hyperpermeability with focal RPE dysfunction allowing fluid accumulation in the subretinal space
B. Photoreceptor apoptosis secondary to chronic light exposure and oxidative stress
C. Vitreous traction on the internal limiting membrane leading to tractional separation of the neurosensory retina
D. Retinal pigment epithelium necrosis from viral infection causing breakdown of the outer blood-retinal barrier
Explanation
Why "Choroidal hyperpermeability with focal RPE dysfunction allowing fluid accumulation in the subretinal space" is right
Central serous chorioretinopathy (CSCR) is fundamentally a disease of choroidal hyperpermeability combined with focal RPE dysfunction. The serous neurosensory retinal detachment marked A arises when fluid leaks from the choroid through a defective RPE into the subretinal space. This is the core pathophysiological mechanism documented in the AAO BCSC Section 12 and is the reason the condition is called "chorioretinopathy"—the primary defect is choroidal, not retinal. The patient's corticosteroid use (a major modifiable risk factor) and stress further support this diagnosis and its mechanism.
Why each distractor is wrong
Photoreceptor apoptosis secondary to chronic light exposure and oxidative stress: This describes photoreceptor degeneration seen in age-related macular degeneration or phototoxic retinopathy, not the acute serous detachment of CSCR. CSCR is not a degenerative process but a fluid accumulation disorder.
Retinal pigment epithelium necrosis from viral infection causing breakdown of the outer blood-retinal barrier: While RPE dysfunction is involved in CSCR, the mechanism is not necrosis from viral infection. CSCR is idiopathic or triggered by steroids/stress, not infectious. The outer blood-retinal barrier is the RPE itself; the defect is functional hyperpermeability, not necrotic breakdown.
Vitreous traction on the internal limiting membrane leading to tractional separation of the neurosensory retina: This describes tractional retinal detachment seen in proliferative diabetic retinopathy or advanced proliferative vitreoretinopathy, not the serous detachment of CSCR. CSCR is exudative, not tractional.
High-YieldNEET PG
CSCR = choroidal hyperpermeability + RPE dysfunction → serous (fluid) detachment; steroids and stress are key modifiable risk factors; most acute cases resolve spontaneously within 3 months.
AAO BCSC Section 12: Retina (2024)
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