MBBS Ophthalmology Flashcards

24 sample cards from the Ophthalmology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the optical principle of a cataract and the most common type?

   A cataract is opacification of the crystalline lens that scatters/blocks light, causing painless progressive blurring and glare. Age-related (senile) cataract is most common, including nuclear sclerotic, cortical, and posterior subcapsular subtypes.

2. Compare nuclear sclerotic, cortical, and posterior subcapsular cataracts.

   Nuclear: central lens hardening, causes myopic shift ('second sight'), worse distance vision. Cortical: spoke-like (cuneiform) wedge opacities, glare. Posterior subcapsular (PSC): granular opacity at the back, causes early near-vision/glare problems, associated with steroids and diabetes; common in younger patients.

3. What is the definitive treatment of cataract, and the most common technique?

   Surgical removal with intraocular lens (IOL) implantation. Phacoemulsification (ultrasonic lens fragmentation through a small incision with foldable IOL) is the most common modern technique; extracapsular cataract extraction (ECCE) for very dense lenses.

4. List important causes of congenital cataract.

   Idiopathic; hereditary (often autosomal dominant); intrauterine TORCH infections (especially rubella); metabolic (galactosemia, Lowe syndrome, hypocalcemia); chromosomal (Down syndrome); and part of ocular malformations. Bilateral often metabolic/genetic; unilateral often idiopathic/local.

5. Why is congenital cataract an emergency, and how is it managed?

   A dense congenital cataract during the critical period of visual development causes deprivation (stimulus-deprivation) amblyopia, which can be irreversible. Visually significant cataracts need early surgery (ideally within the first weeks-months) plus optical correction and amblyopia therapy.

6. What is the leukocoria differential a clinician must exclude in a child?

   Leukocoria (white pupillary reflex) must prompt exclusion of retinoblastoma (malignant, life-threatening), as well as congenital cataract, retinopathy of prematurity, Coats disease, persistent fetal vasculature, and toxocariasis.

7. What are the phakomatoses?

   Neurocutaneous syndromes (neuro-oculo-cutaneous) with hamartomas in multiple organs. Classic ones: neurofibromatosis (1 and 2), tuberous sclerosis, von Hippel-Lindau, and Sturge-Weber syndrome (often grouped); ataxia-telangiectasia is sometimes included.

8. What are the characteristic ocular features of neurofibromatosis type 1?

   Lisch nodules (iris hamartomas), optic nerve glioma, plexiform neurofibroma of the eyelid (S-shaped ptosis), and congenital glaucoma. Systemic: café-au-lait spots, cutaneous neurofibromas, axillary freckling.

9. What are the ocular features of von Hippel-Lindau and Sturge-Weber syndromes?

   Von Hippel-Lindau: retinal capillary hemangioblastomas (with CNS hemangioblastomas, renal/pancreatic lesions, pheochromocytoma). Sturge-Weber: facial port-wine stain (trigeminal V1), ipsilateral congenital/secondary glaucoma, and diffuse choroidal hemangioma; leptomeningeal angioma.

10. Define glaucoma in modern terms.

    A progressive optic neuropathy with characteristic optic disc cupping and corresponding visual field loss, in which raised IOP is the principal modifiable risk factor (though it can occur at normal IOP — normal-tension glaucoma).

11. What are the characteristic features and management of primary open-angle glaucoma (POAG)?

    Chronic, bilateral, usually asymptomatic until late; open angle on gonioscopy; raised IOP from increased trabecular outflow resistance; progressive cupping (increased cup:disc ratio) and arcuate field defects sparing central vision until late. Treatment: lower IOP with topical drugs (prostaglandin analogs first-line), laser trabeculoplasty, or trabeculectomy.

12. What is a normal optic disc cup-to-disc ratio, and what suggests glaucoma?

    Normal cup:disc ratio is $\leq 0.3$. Glaucomatous suggestive signs: cup:disc $\geq 0.6$, asymmetry $> 0.2$ between eyes, notching/thinning of the neuroretinal rim, disc hemorrhage, and violation of the ISNT rule (rim normally thickest Inferior > Superior > Nasal > Temporal).

13. What is the classic presentation of acute angle-closure glaucoma?

    Sudden severe ocular pain, headache, nausea/vomiting, blurred vision with colored halos around lights; signs: red eye with ciliary injection, hazy (edematous) cornea, mid-dilated fixed oval pupil, shallow anterior chamber, and markedly raised IOP (often $> 40$–$50\,\text{mmHg}$). It is an emergency.

14. Outline the emergency management of acute angle-closure glaucoma.

    Lower IOP urgently: topical pilocarpine (miosis to open angle), topical beta-blocker, alpha-agonist, and topical/systemic carbonic anhydrase inhibitor (acetazolamide), plus IV mannitol if needed; analgesia/antiemetics. Definitive: laser peripheral iridotomy (and prophylactic iridotomy to the fellow eye).

15. What are common causes of secondary glaucoma?

    Neovascular (diabetes, CRVO), uveitic/inflammatory, lens-induced (phacomorphic, phacolytic), steroid-induced, pigmentary, pseudoexfoliation, traumatic (angle recession), and post-surgical. Mechanism may be open-angle or angle-closure depending on cause.

16. What is neovascular glaucoma and its mechanism?

    A secondary glaucoma where retinal ischemia (e.g., proliferative diabetic retinopathy, ischemic CRVO) drives VEGF release, causing new vessels and a fibrovascular membrane (rubeosis iridis) over the iris and angle, blocking trabecular outflow and leading to angle closure and very high IOP.

17. Describe the classification (stages) of diabetic retinopathy.

    Non-proliferative (NPDR): microaneurysms, dot/blot hemorrhages, hard exudates, cotton-wool spots, venous beading, IRMA (graded mild/moderate/severe by the 4-2-1 rule). Proliferative (PDR): neovascularization of disc/elsewhere, vitreous/preretinal hemorrhage, tractional retinal detachment. Diabetic maculopathy (macular edema) can occur at any stage.

18. What is the 4-2-1 rule for severe NPDR?

    Severe NPDR is diagnosed if ANY of: intraretinal hemorrhages/microaneurysms in all 4 quadrants, OR venous beading in $\geq 2$ quadrants, OR IRMA (intraretinal microvascular abnormalities) in $\geq 1$ quadrant — with no signs of proliferation.

19. How is diabetic retinopathy managed?

    Optimize systemic control (glycemia, BP, lipids). Pan-retinal photocoagulation (PRP) for proliferative DR; anti-VEGF intravitreal injections for diabetic macular edema (and PDR); focal/grid laser for some macular edema; vitrectomy for non-clearing vitreous hemorrhage or tractional detachment.

20. Compare dry (non-exudative) and wet (exudative) age-related macular degeneration.

    Dry AMD ($\approx 90\%$): drusen and RPE atrophy (geographic atrophy), gradual central vision loss, no specific drug treatment (AREDS vitamins may slow progression). Wet AMD ($\approx 10\%$ but causes most severe loss): choroidal neovascularization with leakage/hemorrhage, rapid distortion (metamorphopsia)/central scotoma; treated with intravitreal anti-VEGF injections.

21. What is the Amsler grid used for in macular disease?

    It is a grid of straight lines with a central fixation dot used to detect and monitor macular pathology; patients with AMD report metamorphopsia (wavy/distorted lines) or a central scotoma (missing area).

22. List the three main types of retinal detachment.

    1) Rhegmatogenous (most common) — a retinal break/tear lets fluid under the retina; 2) Tractional — fibrovascular membranes pull the retina off (e.g., PDR); 3) Exudative (serous) — subretinal fluid from inflammation/tumor/hypertension without a break.

23. What are the classic symptoms of rhegmatogenous retinal detachment?

    Sudden flashes of light (photopsia), a shower of new floaters, and a progressing curtain/shadow over the visual field, with painless visual loss when the macula is involved. It is an ophthalmic emergency requiring urgent surgical repair (e.g., scleral buckle, vitrectomy, pneumatic retinopexy).

24. What are key risk factors for rhegmatogenous retinal detachment?

    High myopia, posterior vitreous detachment, prior cataract surgery (aphakia/pseudophakia), ocular trauma, lattice degeneration, and a personal or family history of retinal detachment.

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