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I have sufficient information from the library and my knowledge. Here are the answers to all 6 questions:
Answers
Q1. Treatment of choice for the other (fellow) eye in angle closure glaucoma
Answer: B - YAG laser iridotomy
When one eye has an acute angle closure attack, the fellow eye has a very high risk (~50% within 5 years) of a similar attack due to the same anatomical predisposition (narrow angles). The standard prophylactic treatment for the fellow eye is Nd:YAG laser peripheral iridotomy (LPI). It creates a small hole in the iris, equalizing pressure between the anterior and posterior chambers and opening the angle - preventing future attacks.
- Surgical peripheral iridectomy (A) is the older, open surgical equivalent - still valid but laser is preferred today.
- Trabeculotomy (C) and trabeculectomy (D) are for open-angle or congenital glaucoma management.
Q2. 1-month-old baby with photophobia, watering, normal tear passages, large cornea
Answer: D - Buphthalmos
This is a classic presentation of congenital glaucoma (buphthalmos):
- Photophobia + lacrimation (epiphora) + large cornea (corneal diameter >12 mm before age 1) are the hallmark triad
- Normal tear passages rules out congenital dacryocystitis (A)
- Interstitial keratitis (B) presents with corneal clouding/vascularization, usually not a large cornea
- Keratoconus (C) is a degenerative condition, not seen in 1-month-olds
The elevated IOP in congenital glaucoma causes the soft infant eye to enlarge, giving the characteristic ox eye (buphthalmos) appearance with a large, clear but hazy cornea and Haab's striae. - Wills Eye Manual
Q3. Elevated IOP can damage:
Answer: A - Ganglion cells
Elevated IOP in glaucoma primarily damages the retinal ganglion cells (RGCs) and their axons (which form the optic nerve/retinal nerve fiber layer). This is the core mechanism of glaucomatous optic neuropathy. The ganglion cell layer is the innermost retinal layer most vulnerable to pressure-induced ischemia and mechanical compression at the optic nerve head.
- Rods and cones (B) - photoreceptors in the outer retina - are affected in retinal degeneration, not primarily in glaucoma
- Outer/inner nuclear layers (C) - affected in retinal dystrophies
- Pigmented epithelium (D) - affected in AMD and toxic retinopathies
Q4. Route of drainage of aqueous humour includes ALL EXCEPT:
Answer: C - Central retinal vein
Aqueous humour drains via:
- A. Trabecular meshwork (conventional/pressure-dependent route) - ~85% of outflow → Schlemm's canal → episcleral veins
- B. Uveoscleral outflow (unconventional/pressure-independent route) - ~15% flows through the ciliary muscle into the suprachoroidal space
The central retinal vein (C) carries venous blood from the retina - it has absolutely no role in aqueous humour drainage.
Q5. All associated with open-angle glaucoma EXCEPT:
Answer: E - Soft drusen
Features of open-angle glaucoma:
- A. Roenne's nasal step - a characteristic visual field defect (step at horizontal meridian in nasal field) ✓
- B. Enlarged blind spot - early visual field defect ✓
- C. Optic disc cupping - increased cup-to-disc ratio, hallmark finding ✓
- D. Thinning of nerve fiber layers - RNFL thinning detectable on OCT ✓
- E. Soft drusen - these are sub-retinal pigment epithelium deposits associated with Age-related Macular Degeneration (AMD), NOT glaucoma
Q6. Neovascular glaucoma follows:
Answer: A - Thrombosis of central retinal vein (CRVO)
Neovascular glaucoma (NVG) is caused by conditions leading to retinal ischemia, which triggers VEGF release, causing neovascularization of the iris (rubeosis iridis) and angle, ultimately blocking outflow.
Most common causes:
-
Central retinal vein occlusion (CRVO) - ~36% of cases (ischemic type)
-
Proliferative diabetic retinopathy - ~32%
-
Central retinal artery occlusion
-
Acute congestive glaucoma (B) is angle-closure glaucoma - a different mechanism
-
Staphylococcal infection (C) has no direct link to NVG
-
Hypertension (D) alone does not cause NVG (though it is a risk factor for CRVO)
The Kanski's Clinical Ophthalmology textbook confirms CRVO as a major cause of neovascular glaucoma.
Summary Table
| Q | Answer | Key Point |
|---|---|---|
| 1 | B - YAG laser iridotomy | Prophylactic LPI for fellow eye in angle closure |
| 2 | D - Buphthalmos | Congenital glaucoma: photophobia + watering + large cornea |
| 3 | A - Ganglion cells | IOP damages RGCs - core of glaucomatous optic neuropathy |
| 4 | C - Central retinal vein | Not a route of aqueous drainage |
| 5 | E - Soft drusen | Drusen = AMD, not glaucoma |
| 6 | A - Thrombosis of CRV | CRVO causes ischemia → VEGF → neovascular glaucoma |
+16 more
give answers
I can see all the questions across the images. I also notice one image shows the answer key with red letters marked. Let me provide complete answers with explanations for all questions visible.
Complete Answers
From the answer sheet (red markings confirmed) + my explanations:
Q1. Meibomian glands are:
Answer: A - Modified sebaceous glands found in the tarsal plates
Meibomian glands are modified sebaceous glands embedded in the tarsal plates of both upper and lower eyelids. They secrete the lipid layer of the tear film, preventing evaporation.
Q2. Automated static perimetry is a method for:
Answer: C - Examination of visual fields
Automated static perimetry (e.g., Humphrey Visual Field Analyzer) tests visual field sensitivity at fixed points - the gold standard for detecting and monitoring glaucomatous field loss.
Q3. Decrease in number or complete loss of lashes is:
Answer: B - Madorosis
- Madorosis = loss/decrease of eyelashes (and/or eyebrows)
- Distichiasis = extra row of lashes from meibomian gland orifices
- Poliosis = whitening of lashes
- Trichiasis = misdirected lashes
Q4. Lipogranulomatous inflammation centred on a dysfunctional meibomian gland:
Answer: C - Chalazion
A chalazion is a chronic, sterile lipogranuloma resulting from retained meibomian gland secretions. It differs from a hordeolum (stye), which is infectious.
Q5. Dacryoadenitis - clinical features include all EXCEPT:
Answer: C - Inflammation of the uveal tract
Dacryoadenitis (inflammation of the lacrimal gland) presents with:
- Hyperemia/oedema/pain in upper-outer orbit (A) ✓
- Eyeball displaced down and nasally (B) ✓
- S-shaped deformity of rima ophthalmica (D) ✓
- Inflammation of the uveal tract (C) is NOT a feature - that is uveitis, a completely separate condition.
Q7. Important diagnostic point in open angle glaucoma:
Answer: B - Optic disc cupping
Open angle glaucoma is defined by an OPEN angle (so A and C are features of angle-CLOSURE glaucoma). The hallmark diagnostic finding is increased cup-to-disc ratio (optic disc cupping) with RNFL loss. Visual acuity is preserved until late stages.
Q8. Risk factors for primary open angle glaucoma include:
Answer: E - All of them
All four listed are established risk factors per major guidelines:
- Higher IOP - the main modifiable risk factor
- Older age - prevalence rises with age
- Family history - first-degree relatives have 3-9x increased risk
- Thinner central corneal thickness (CCT) - independent risk factor (confirmed by the Ocular Hypertension Treatment Study)
Q9. Optic nerve head examination in POAG shows all EXCEPT:
Answer: D - Optic disc temporal pallor
In POAG, the optic nerve head shows:
- Vertical elongation of the cup (A) ✓
- Excavation/cupping of the cup (B) ✓
- Thinning of RNFL (C) ✓
- Focal notching, especially inferotemporal/superotemporal (E) ✓
Temporal pallor (D) is the exception - pallor of the entire disc suggests optic atrophy from other causes (e.g., optic neuritis, compressive lesions, ischemic optic neuropathy), NOT typical glaucoma. In glaucoma, the neuroretinal rim tissue is lost, creating a larger cup, but the remaining rim stays pink.
Q10. Medications reducing production of aqueous humor:
Answer: E - A and B only (Beta-blockers and Carbonic anhydrase inhibitors)
- Beta-blockers (timolol, betaxolol) - reduce aqueous production by the ciliary body
- Carbonic anhydrase inhibitors (dorzolamide, brinzolamide, acetazolamide) - reduce aqueous production by inhibiting CA-II in ciliary epithelium
- Prostaglandins (C) - work by increasing uveoscleral outflow, NOT reducing production
So the answer is E (A and B).
Q11. Corneal transparency - all factors EXCEPT:
Answer: C - Myelinated nerve fibers
Corneal transparency is maintained by:
- Compact regular arrangement of stromal collagen fibers (A) ✓
- Avascularity - lack of blood vessels (B) ✓
- Relative dehydration maintained by endothelial pump
- Non-keratinized epithelium (D) ✓
Myelinated nerve fibers (C) would make the cornea opaque (as seen when myelination extends into the cornea - it appears white). Normal corneal nerves are unmyelinated for this reason.
Q12. Cornea is supplied by nerve fibers from:
Answer: C - Trigeminal nerve (CN V)
The cornea is the most densely innervated tissue in the body. Sensory supply comes from the nasociliary branch of the ophthalmic division (V1) of the trigeminal nerve via the long ciliary nerves.
Q13. In anterior uveitis the pupil is generally:
Answer: B - Constricted (miosis)
Anterior uveitis causes miosis (small pupil) due to:
- Ciliary muscle spasm
- Iris sphincter irritation from inflammation
- Posterior synechiae can also fix the pupil in irregular constriction (Note: mydriatics/cycloplegics are given therapeutically to dilate the pupil and prevent synechiae)
Q14. Inflammation of the entire uveal tract:
Answer: C - Panuveitis
- Adenitis = lymph node inflammation
- Choroiditis (chorioiditis) = posterior uveitis (choroid only)
- Panuveitis = inflammation of the entire uveal tract (iris + ciliary body + choroid)
- Neuroretinitis = optic nerve + retinal inflammation
Q15. Signs of anterior uveitis - all EXCEPT:
Answer: D - Hemophthalmus
Signs of anterior uveitis include:
- Synechiae - posterior (iris-lens) or anterior (iris-cornea) (A) ✓
- Keratic precipitates (KPs) on the endothelium (B) ✓
- Circumcorneal/ciliary congestion (C) ✓
- Hypopyon - layering of white cells in anterior chamber (E) ✓
Hemophthalmus (D) = blood in the vitreous - this is a feature of trauma or proliferative retinopathy, NOT anterior uveitis.
Q16. Gonioscopy is a method for:
Answer: B - Examination of the anterior chamber angle
Gonioscopy uses a mirrored contact lens to directly visualize the iridocorneal angle - identifying open vs. closed angles, angle structures (Schwalbe's line, trabecular meshwork, scleral spur, ciliary body band), and grading angle width (Shaffer/Van Herick grading).
Q17. A scotoma is:
Answer: D - An area of reduced or total loss of vision surrounded by a seeing area
- Isopter (A) = a line connecting points of equal sensitivity
- Apostilb (B) = unit of light stimulus intensity
- Decibel (C) = unit used in perimetry
- Scotoma = an island of visual loss within the visual field, surrounded by normal-seeing areas
Summary Table
| Q | Answer | Key Point |
|---|---|---|
| 1 | A | Meibomian = modified sebaceous in tarsal plates |
| 2 | C | Automated perimetry = visual field testing |
| 3 | B | Madorosis = loss of lashes |
| 4 | C | Chalazion = lipogranuloma of meibomian gland |
| 5 | C | Dacryoadenitis does NOT cause uveitis |
| 7 | B | Optic disc cupping = key OAG finding |
| 8 | E | All of them are POAG risk factors |
| 9 | D | Temporal pallor = optic atrophy, NOT glaucoma |
| 10 | E | Beta-blockers + CAIs reduce aqueous production; PGs increase outflow |
| 11 | C | Myelinated fibers would make cornea OPAQUE |
| 12 | C | Trigeminal nerve (V1) supplies cornea |
| 13 | B | Anterior uveitis = miosis (constricted pupil) |
| 14 | C | Panuveitis = entire uveal tract inflammation |
| 15 | D | Hemophthalmus is NOT a sign of anterior uveitis |
| 16 | B | Gonioscopy = anterior chamber angle exam |
| 17 | D | Scotoma = island of visual loss surrounded by seeing area |
+16 more
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