INI CET 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. Classify diabetic retinopathy into its main stages.

   Non-proliferative (NPDR: microaneurysms, dot/blot hemorrhages, hard exudates, cotton-wool spots) and proliferative (PDR: neovascularization of disc/elsewhere, vitreous hemorrhage, tractional detachment). Diabetic macular edema can occur at any stage.

2. What is the gold-standard treatment for proliferative diabetic retinopathy and for diabetic macular edema?

   Pan-retinal photocoagulation (PRP) laser for PDR; intravitreal anti-VEGF (and/or focal laser) for centre-involving diabetic macular edema.

3. Differentiate dry (non-exudative) from wet (exudative) age-related macular degeneration (AMD).

   Dry AMD has drusen and geographic atrophy with gradual central vision loss; wet AMD has choroidal neovascularization causing sudden distortion (metamorphopsia), hemorrhage, and rapid central vision loss.

4. What is the treatment for wet AMD and a simple home monitoring tool for AMD?

   Intravitreal anti-VEGF injections (ranibizumab, aflibercept, bevacizumab) for wet AMD; the Amsler grid is used at home to detect metamorphopsia/scotoma indicating progression.

5. What are the three main types of retinal detachment?

   Rhegmatogenous (a retinal break/tear lets fluid under the retina; most common), tractional (fibrovascular traction, e.g., PDR), and exudative/serous (fluid leak from tumor or inflammation, no break).

6. What are the classic symptoms of a rhegmatogenous retinal detachment?

   Sudden onset of floaters and flashes of light (photopsia) followed by a progressive curtain/shadow over the visual field and painless visual loss.

7. What are the features of anterior ischemic optic neuropathy (AION) and its most dangerous cause?

   Sudden painless monocular vision loss with a swollen optic disc, altitudinal field defect, and RAPD; the dangerous cause is arteritic AION from giant cell (temporal) arteritis, requiring urgent high-dose steroids to protect the other eye.

8. How does optic neuritis typically present and what disease is it associated with?

   Subacute monocular vision loss with pain on eye movement, dyschromatopsia (red desaturation), central scotoma, and RAPD; strongly associated with multiple sclerosis.

9. Describe the eye position in a complete third (oculomotor) nerve palsy.

   The eye is 'down and out' (due to unopposed lateral rectus and superior oblique), with ptosis and a dilated, unreactive pupil if the palsy is compressive (e.g., posterior communicating artery aneurysm).

10. What is the deficit in a sixth (abducens) nerve palsy and in a fourth (trochlear) nerve palsy?

    Sixth nerve palsy: inability to abduct the eye, causing horizontal diplopia worse on gaze to the affected side. Fourth nerve palsy: weak superior oblique, causing vertical/torsional diplopia worse on looking down (e.g., reading, stairs) with a compensatory head tilt away.

11. What is the pupillary finding and lesion site in Horner's syndrome?

    Miosis, partial ptosis, and anhidrosis from disruption of the sympathetic pathway; the pupil dilates poorly in the dark (dilation lag).

12. What is internuclear ophthalmoplegia (INO) and where is the lesion?

    Failure of adduction in the affected eye with nystagmus of the abducting eye on lateral gaze, due to a lesion of the medial longitudinal fasciculus (MLF); bilateral INO in a young patient suggests multiple sclerosis.

13. What is amblyopia and name its main causes.

    Amblyopia ('lazy eye') is reduced best-corrected vision in a structurally normal eye from abnormal visual development in childhood; causes are strabismic, refractive (anisometropic/ametropic), and stimulus deprivation (e.g., congenital cataract, ptosis).

14. What is the main treatment of amblyopia and the critical factor for success?

    Treat the underlying cause (correct refraction/remove deprivation) then occlusion (patching) or atropine penalization of the better eye; success depends on treating early within the sensitive period (best before ~7-8 years).

15. Differentiate esotropia from exotropia.

    Esotropia is inward (convergent) deviation of the eye; exotropia is outward (divergent) deviation. Hypertropia/hypotropia are vertical deviations.

16. What is the cover test used to detect in strabismus?

    It detects manifest (tropia) and latent (phoria) ocular deviations; in the cover-uncover test, movement of the uncovered eye to fixate reveals a tropia, while movement of the covered eye on uncovering reveals a phoria.

17. Define microphthalmos, anophthalmos, and buphthalmos.

    Microphthalmos: abnormally small but formed eye; anophthalmos: complete absence of ocular tissue; buphthalmos: enlarged eye from congenital glaucoma in infancy due to a distensible immature sclera.

18. Differentiate viral, bacterial, and allergic conjunctivitis by discharge.

    Viral: watery discharge with follicles and preauricular node (often adenovirus); bacterial: purulent/mucopurulent discharge with papillae; allergic: stringy/mucoid discharge with itching and bilateral involvement.

19. What causes ophthalmia neonatorum within the first 48 hours of life and how is it managed?

    Neisseria gonorrhoeae (hyperacute, profuse purulent discharge, can perforate the cornea); managed urgently with systemic plus topical antibiotics (e.g., ceftriaxone) - a medical emergency.

20. What is dry eye syndrome and how is tear film stability/production assessed?

    Dry eye is tear deficiency or excessive evaporation causing ocular surface damage; assessed by Schirmer's test (aqueous production), tear break-up time (TBUT, film stability), and ocular surface staining (fluorescein/rose bengal).

21. Differentiate anterior from posterior blepharitis.

    Anterior blepharitis affects the eyelash base (staphylococcal or seborrheic, with crusting/collarettes); posterior blepharitis involves meibomian gland dysfunction causing frothy tears and evaporative dry eye.

22. What is the most common primary intraocular malignancy in children and its classic signs?

    Retinoblastoma; presents with leukocoria (white pupillary reflex) and strabismus, caused by mutation of the RB1 tumor suppressor gene (the 'two-hit' hypothesis).

23. What is the most common primary orbital malignancy of childhood and the most common primary intraocular malignancy in adults?

    Rhabdomyosarcoma is the most common primary orbital malignancy of childhood (rapidly progressive proptosis); choroidal/uveal melanoma is the most common primary intraocular malignancy in adults.

24. What are the ophthalmic features of thyroid eye disease (Graves' orbitopathy) and the mnemonic for signs?

    Exophthalmos/proptosis, lid retraction and lid lag, restrictive myopathy with diplopia, conjunctival injection/chemosis, and risk of compressive optic neuropathy; signs are summarized by NO SPECS (No signs, Only lid signs, Soft tissue, Proptosis, Extraocular muscle, Corneal, Sight loss). Inferior and medial rectus are most commonly enlarged.

What this deck covers

Ophthalmology flashcards FAQ