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i have viva examination of ms ophthalmology of university, give me questions which can be asked on topic glaucoma

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AAO glaucoma preferred practice pattern primary open angle angle closure 2025

For an MS Ophthalmology glaucoma viva, examiners commonly move from basic concepts to case-based decisions. The core areas are:
  1. Fundamentals and aqueous dynamics
  2. Tonometry, gonioscopy, optic-disc and visual-field examination
  3. Primary open-angle glaucoma and normal-tension glaucoma
  4. Primary angle-closure disease and acute angle closure
  5. Secondary glaucomas
  6. Congenital and juvenile glaucoma
  7. Medical, laser, and surgical management
  8. Interpretation of OCT, perimetry, and clinical photographs
  9. Viva cases and surgical complications
A high-yield preparation should emphasize mechanism, differential diagnosis, test interpretation, indications/contraindications, and stepwise management. Current AAO POAG guidance emphasizes open angles on gonioscopy plus characteristic optic neuropathy/RNFL loss and corresponding field defects. For acute angle closure, prompt IOP lowering followed by definitive iridotomy or lens-based treatment is central in AAO angle-closure guidance.
Which section would you like first?

Give me 100 glaucoma viva questions with answers

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A set of 100 viva questions is best organized as follows:
  1. Basic science and aqueous humour: 1-12
  2. Clinical evaluation, tonometry and gonioscopy: 13-25
  3. Optic nerve, OCT and visual fields: 26-38
  4. Primary open-angle and normal-tension glaucoma: 39-52
  5. Primary angle-closure disease and acute angle closure: 53-65
  6. Secondary glaucomas: 66-78
  7. Congenital and juvenile glaucomas: 79-85
  8. Drugs, lasers, surgery and complications: 86-100
For MS viva preparation, answers should be short but structured: definition, mechanism, key signs/investigations, and management or indication. Examiners commonly ask follow-up questions on gonioscopy grading, target IOP, disc-field correlation, mechanisms of angle closure, steroid response, neovascular glaucoma, trabeculectomy complications, and laser indications.
Which section should I give first in full question-and-answer format?

Clinical evaluation, tonometry and gonioscopy: 13-25 Optic nerve, OCT and visual fields: 26-38 Primary open-angle and normal-tension glaucoma: 39-52

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glaucoma OCT perimetry

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AAO 2025 primary open angle glaucoma PPP tonometry gonioscopy OCT visual field

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Clinical evaluation, tonometry and gonioscopy

13. What are the essential components of a glaucoma evaluation?
Answer: History; visual acuity and refraction; slit-lamp examination; IOP measurement with pachymetry; gonioscopy; optic nerve head and retinal nerve fibre layer assessment; visual fields; OCT; and documentation with disc photographs where possible. Also assess risk factors, drug history, family history, and adherence.
14. What points in history are important in a patient with suspected glaucoma?
Answer:
  • Family history of glaucoma or blindness
  • Previous raised IOP, eye trauma, uveitis, surgery, laser treatment
  • Steroid exposure, topical, inhaled, oral, periocular, or intravitreal
  • Symptoms of angle closure: pain, halos, headache, nausea, blurred vision
  • Myopia, diabetes, hypertension, migraine, Raynaud phenomenon, sleep apnea
  • Current systemic medications, especially steroids, beta-blockers, anticholinergics, adrenergics, and sulfonamides
  • Previous visual-field and OCT reports, and medication adherence.
15. Define ocular hypertension.
Answer: Ocular hypertension is consistently elevated IOP, conventionally above 21 mmHg, with an open anterior chamber angle and no definite glaucomatous optic neuropathy or reproducible glaucomatous visual-field loss.
16. What is pre-perimetric glaucoma?
Answer: It is glaucomatous structural damage, such as suspicious optic-disc change or RNFL defect, without a detectable standard automated perimetry defect.
Kanski's Clinical Ophthalmology, 10th ed., p. 363.
17. What is the normal range of IOP?
Answer: Conventionally, 10-21 mmHg. However, glaucoma can occur at IOP of 21 mmHg or less, and many people with IOP above 21 mmHg do not develop glaucoma.
18. What is diurnal variation of IOP?
Answer: IOP fluctuates through the day, often with a higher level in the early morning. Diurnal phasing is useful when glaucoma is progressing despite apparently normal clinic IOP, particularly in suspected normal-tension glaucoma or when an IOP peak is suspected.
19. What is the gold-standard method of IOP measurement?
Answer: Goldmann applanation tonometry, provided the cornea is suitable and the technique is correct.
20. State the principle of Goldmann applanation tonometry.
Answer: It is based on the Imbert-Fick principle: pressure equals force divided by area of applanation. In Goldmann tonometry, flattening a 3.06 mm diameter corneal area balances corneal rigidity against tear-film surface tension, allowing IOP estimation.
Kanski's Clinical Ophthalmology, 10th ed., p. 43.
21. Describe the technique of Goldmann applanation tonometry.
Answer:
  1. Instil topical anesthetic and fluorescein.
  2. Seat the patient at the slit lamp, forehead firmly against the headrest.
  3. Use cobalt-blue illumination and align the prism on the corneal apex.
  4. Bring the prism gently into contact with the cornea.
  5. Adjust the dial until the inner borders of the two fluorescein semicircular mires just touch.
  6. Multiply the dial reading by 10 to obtain IOP in mmHg.
    Kanski's Clinical Ophthalmology, 10th ed., p. 43.
22. What are the common errors in Goldmann applanation tonometry?
Answer:
  • Excess fluorescein: falsely high IOP
  • Too little fluorescein: falsely low IOP
  • Thick cornea: overestimation
  • Thin cornea or post-refractive surgery cornea: underestimation
  • Eyelid squeezing, Valsalva, examiner pressure on globe: falsely high
  • Corneal edema: often falsely low
  • Significant astigmatism, irregular cornea, scar, contact lens, or poor patient positioning.
23. Why is central corneal thickness important in glaucoma?
Answer: It influences Goldmann readings and is an independent risk marker. A thin cornea can cause IOP underestimation and is associated with higher risk of conversion from ocular hypertension to glaucoma. A thick cornea can lead to falsely high Goldmann readings. Do not use simplistic correction tables as a substitute for clinical judgment.
Kanski's Clinical Ophthalmology, 10th ed., p. 44.
24. What is gonioscopy and why is it necessary?
Answer: Gonioscopy is examination of the anterior chamber angle using a contact lens. It determines whether the angle is open, narrow, closed, or has secondary pathology such as peripheral anterior synechiae, pigmentation, pseudoexfoliative material, neovascularization, recession, or angle tumors. It is indispensable in evaluating ocular hypertension and glaucoma.
Kanski's Clinical Ophthalmology, 10th ed., p. 46.
25. Why can the angle not be viewed directly through the cornea?
Answer: Light from angle structures undergoes total internal reflection at the cornea-air or tear-film-air interface. A gonioscopy lens eliminates this interface and permits visualization of the angle.
26. Name the angle structures seen on gonioscopy from anterior to posterior.
Answer:
  1. Schwalbe line
  2. Trabecular meshwork, anterior non-pigmented and posterior pigmented
  3. Scleral spur
  4. Ciliary body band
  5. Iris root
27. Differentiate appositional angle closure from synechial closure.
Answer:
  • Appositional closure: Iridotrabecular contact without permanent adhesion. The angle may open with indentation gonioscopy.
  • Synechial closure: Permanent adhesion of peripheral iris to the trabecular meshwork, termed peripheral anterior synechiae or PAS. It does not open on indentation.
28. What is indentation gonioscopy? State its uses.
Answer: A small-contact-area lens is used to apply gentle central corneal pressure, which pushes aqueous peripherally and can open an appositionally closed angle. It helps differentiate appositional closure from PAS, identify plateau iris configuration, and assess angle recession or trabecular pigmentation.
29. What are the major gonioscopic grading systems?
Answer: Shaffer grading, Scheie grading, and Spaeth grading. In routine viva practice, Shaffer grading is most frequently used.
30. Describe Shaffer grading.
Answer: It estimates the angle width:
  • Grade 4: 35-45°, wide open, closure impossible
  • Grade 3: 25-35°, open, closure unlikely
  • Grade 2: about 20°, narrow, closure possible
  • Grade 1: about 10°, extremely narrow, closure likely
  • Slit: very narrow, closure probable
  • Grade 0: closed angle
31. What is the Van Herick technique?
Answer: It is a slit-lamp screening method for peripheral anterior chamber depth. A narrow bright beam is placed at the temporal limbus and the peripheral chamber depth is compared with corneal thickness. It does not replace gonioscopy.
32. What are the limitations of Van Herick grading?
Answer: It assesses only peripheral chamber depth, commonly temporally, and may miss focal angle closure, plateau iris, PAS, or secondary angle pathology. Gonioscopy remains necessary.
33. What gonioscopic signs suggest secondary open-angle glaucoma?
Answer:
  • Heavy trabecular pigmentation: pigmentary glaucoma
  • Pseudoexfoliative material and Sampaolesi line: pseudoexfoliation syndrome
  • Angle recession: traumatic glaucoma
  • Neovascularization: neovascular glaucoma
  • Blood in Schlemm canal: raised episcleral venous pressure
  • Inflammatory cells, pigment, or PAS: uveitic glaucoma
  • Foreign body or tumor infiltration.
34. When should gonioscopy be performed?
Answer: At baseline in all glaucoma suspects and glaucoma patients, when IOP rises unexpectedly, before laser trabeculoplasty, in asymmetric disease, when angle closure is suspected, after trauma, and periodically during follow-up. The AAO glaucoma-suspect guidance includes gonioscopy among core tests.
35. What is the role of anterior-segment OCT and UBM in glaucoma?
Answer: They complement but do not replace gonioscopy. AS-OCT is useful for documenting angle configuration and iridotrabecular contact. UBM visualizes structures behind the iris, including ciliary body position, and is especially useful in plateau iris, ciliary-body lesions, and mechanisms of angle closure.
Kanski's Clinical Ophthalmology, 10th ed., p. 372.

Optic nerve, OCT and visual fields

36. Describe a normal optic disc.
Answer: A normal optic disc has a pink neuroretinal rim, central cup, clear margins, and vessels that bend at the cup margin. The cup-disc ratio varies with disc size, so rim appearance and inter-eye asymmetry are more informative than cup-disc ratio alone.
37. What are the important signs of glaucomatous optic neuropathy?
Answer:
  • Progressive cup enlargement
  • Vertical cup elongation
  • Focal neuroretinal rim thinning or notching, commonly inferotemporal or superotemporal
  • Violation of the ISNT rule
  • Inter-eye cup-disc asymmetry
  • Bayoneting of vessels and baring of circumlinear vessels
  • Laminar-dot sign
  • Peripapillary RNFL defect
  • Disc hemorrhage.
38. What is the ISNT rule?
Answer: In a normal disc, rim thickness is usually greatest inferiorly, then superiorly, nasally, and temporally: I > S > N > T. Focal violation, especially inferior or superior rim thinning, suggests glaucoma. It is less reliable in tilted discs, very large discs, and myopic discs.
39. What is a glaucomatous disc hemorrhage?
Answer: It is usually a splinter or flame-shaped hemorrhage at the disc margin, often inferotemporally or superotemporally, extending from the neuroretinal rim into the adjacent retina. It is a risk marker for glaucoma development and progression, and is more frequent in normal-tension glaucoma.
Kanski's Clinical Ophthalmology, 10th ed., p. 366.
40. What is the significance of cup-disc ratio asymmetry?
Answer: Asymmetry greater than about 0.2 is suspicious, but interpretation depends on disc size and asymmetry of disc size. Documented progressive cupping is always significant.
41. What is a retinal nerve fibre layer defect in glaucoma?
Answer: It is a localized wedge-shaped or diffuse area of RNFL thinning, usually extending toward the optic disc. It may precede detectable disc and standard automated visual-field change.
42. What is OCT and what does it measure in glaucoma?
Answer: Optical coherence tomography is a non-contact imaging modality. In glaucoma, it quantifies peripapillary RNFL thickness, optic-nerve-head parameters, and macular ganglion-cell complex or ganglion cell-inner plexiform layer thickness.
43. What are the roles of OCT in glaucoma?
Answer:
  • Detect structural damage in glaucoma suspects
  • Establish a baseline
  • Identify RNFL and macular ganglion-cell thinning
  • Monitor structural progression
  • Correlate structural changes with optic-disc examination and visual fields.
    OCT should supplement, not replace, clinical examination and perimetry. It is most informative in suspects and early-to-moderate glaucoma, and less useful in advanced disease because of a measurement “floor.”
    Kanski's Clinical Ophthalmology, 10th ed., p. 372.
44. What are common OCT artifacts or pitfalls?
Answer:
  • Poor signal strength due to dry eye, cataract, small pupil, or media opacity
  • Segmentation error
  • Motion artifact
  • High myopia, tilted disc, and peripapillary atrophy
  • Incorrect scan centering
  • Non-glaucomatous optic neuropathy
  • “Red disease” from false-positive classification and “green disease” from apparently normal values despite true disease.
    Always inspect the raw B-scans and correlate clinically.
45. What is standard automated perimetry?
Answer: It is computerized static perimetry that tests retinal sensitivity at predetermined points using light stimuli on a uniformly illuminated background. It is the standard functional test for detecting and monitoring glaucomatous visual-field loss.
46. What visual-field programs are commonly used in glaucoma?
Answer:
  • 24-2: Standard test for most glaucoma patients
  • 30-2: Wider central field assessment
  • 10-2: Detects or monitors central/paracentral defects, especially in advanced glaucoma or normal-tension glaucoma
  • 24-2C: Adds selected central test locations and may better detect central loss.
47. What are the reliability indices on Humphrey visual-field testing?
Answer:
  • Fixation losses
  • False-positive responses
  • False-negative responses
    Also assess gaze tracking, test duration, pattern of defects, and whether the result is reproducible. High false positives can produce an abnormally “white” field and misleadingly good sensitivity.
48. What are the earliest glaucomatous visual-field defects?
Answer:
  • Paracentral scotoma
  • Nasal step of Roenne
  • Seidel scotoma, an extension of the blind spot
  • Early arcuate defect
  • Temporal wedge, less commonly.
49. Describe the typical progression of glaucomatous field loss.
Answer: Localized paracentral or nasal defects enlarge to arcuate scotomas, which may join to form a double arcuate or ring scotoma. With progression, only central and temporal islands may remain, followed by tubular vision and eventual loss of all useful field.
50. Explain disc-field correlation.
Answer: Retinal image inversion means superior optic-disc/RNFL damage produces inferior field defects, and inferior disc damage produces superior field defects. Damage at the inferotemporal disc commonly correlates with a superior arcuate defect or superior nasal step.
51. What is mean deviation and pattern standard deviation?
Answer:
  • Mean deviation, MD: Average depression of the visual field compared with age-matched normals. It reflects overall functional loss but is affected by cataract and diffuse media opacity.
  • Pattern standard deviation, PSD: Measures localized irregularity in the field. It is often elevated in early localized glaucomatous damage but may decrease in end-stage diffuse loss.
52. How do you confirm glaucomatous progression?
Answer: Confirm with serial, good-quality, reproducible evidence, not a single test. Look for:
  • Progressive optic-disc rim loss or new disc hemorrhage
  • OCT RNFL or macular ganglion-cell thinning on trend/event analysis
  • Reproducible worsening in the same visual-field area
  • Increasing MD loss or progression analysis changes
  • IOP pattern, adherence, and risk factors.
The AAO POAG guideline defines POAG through an open angle plus compatible optic-nerve, RNFL/macular ganglion-cell, and visual-field findings, after excluding secondary causes.

Primary open-angle glaucoma and normal-tension glaucoma

53. Define primary open-angle glaucoma.
Answer: POAG is a chronic progressive optic neuropathy characterized by an open anterior chamber angle, glaucomatous optic-disc and RNFL damage, and corresponding visual-field loss, without another ocular or systemic cause that better explains the optic neuropathy. IOP may be elevated or within the statistically normal range.
54. What are the risk factors for POAG?
Answer:
  • Raised IOP
  • Older age
  • Family history
  • African or Latino/Hispanic ancestry
  • Thin central cornea and low corneal hysteresis
  • Myopia
  • Diabetes
  • Large cup-disc ratio or disc hemorrhage
  • Lower ocular perfusion pressure
  • Vascular factors and possibly sleep apnea.
These are consistent with the AAO 2025 POAG guideline.
55. What are the clinical features of POAG?
Answer: Typically asymptomatic until advanced. The eye is quiet, the angle is open, IOP may be raised or normal, and there is characteristic glaucomatous cupping, RNFL loss, and corresponding visual-field defects.
56. What is the pathophysiology of POAG?
Answer: There is increased resistance to aqueous outflow through the trabecular meshwork and Schlemm canal, often with raised IOP. Retinal ganglion-cell axonal injury at the lamina cribrosa and other IOP-dependent and IOP-independent mechanisms lead to progressive optic neuropathy.
57. Differentiate POAG from ocular hypertension.
Answer:
  • Ocular hypertension: Raised IOP without glaucomatous structural or functional damage.
  • POAG: Glaucomatous optic neuropathy with compatible field loss and open angles, with or without raised IOP.
58. What is a glaucoma suspect?
Answer: A person is a glaucoma suspect if they have ocular hypertension, suspicious optic-disc appearance, suspicious RNFL or ganglion-cell thinning, suspicious visual-field defect, a narrow angle, or significant risk factors without definite established glaucoma.
59. When should ocular hypertension be treated?
Answer: Treat selectively after assessing lifetime risk, IOP level, age, CCT, disc appearance, visual-field/OCT findings, family history, fellow-eye status, patient preference, and capacity for follow-up. Patients at high risk of conversion merit treatment. A reasonable initial target for treated POAG suspects is often about a 20% IOP reduction, as described in the AAO suspect guideline.
60. What is target IOP?
Answer: Target IOP is an individualized upper IOP level at which further glaucomatous damage is unlikely to occur during the patient’s expected lifetime. It is not fixed and must be revised if progression occurs.
61. How do you set target IOP in POAG?
Answer: Consider baseline untreated IOP, stage and rate of progression, age and life expectancy, optic-disc and field status, fellow-eye damage, CCT, vascular risk, treatment burden, and surgical risk. Greater damage, faster progression, or fixation-threatening loss requires a lower target.
62. What is normal-tension glaucoma?
Answer: NTG is open-angle glaucoma with typical glaucomatous optic neuropathy and corresponding visual-field loss, but consistently measured IOP at or below 21 mmHg on diurnal assessment, after excluding secondary glaucoma and non-glaucomatous optic neuropathy.
Kanski's Clinical Ophthalmology, 10th ed., p. 386.
63. What are the characteristic features of NTG?
Answer:
  • Open angles
  • IOP consistently 21 mmHg or less on diurnal testing
  • Typical glaucomatous disc and RNFL damage
  • Corresponding field loss, often focal, deep, and closer to fixation
  • Disc hemorrhage may occur more often
  • Absence of secondary glaucoma or another optic neuropathy.
    Kanski's Clinical Ophthalmology, 10th ed., p. 386.
64. What risk factors are associated with NTG?
Answer:
  • Older age
  • Family history
  • Thin CCT
  • Nocturnal hypotension or excessive nocturnal blood-pressure dip
  • Migraine and Raynaud phenomenon
  • Obstructive sleep apnea
  • Vascular dysregulation and reduced ocular perfusion
  • Possible nocturnal IOP spikes.
    Kanski's Clinical Ophthalmology, 10th ed., pp. 386-387.
65. What must be excluded before diagnosing NTG?
Answer:
  • Undetected IOP peaks and inaccurate IOP due to thin CCT
  • Steroid response or other secondary open-angle glaucoma
  • Compressive optic neuropathy
  • Previous optic neuritis or ischemic optic neuropathy
  • Congenital disc anomalies
  • Retinal disease causing field defects
  • Neurological visual-field defects.
66. When should neuroimaging be considered in presumed NTG?
Answer: Consider MRI of brain and orbits if there is marked acuity loss, dyschromatopsia, pallor greater than cupping, young age, vertically respecting field defect, disproportionate central loss, rapidly progressive or unilateral disease, or a field defect not matching the disc.
67. How is NTG managed?
Answer:
  1. Establish whether there is true progression with reliable serial disc, OCT, and field data.
  2. Reduce IOP, usually with a target reduction of about 30% from baseline in progressing disease.
  3. Identify and address contributing factors such as nocturnal hypotension, sleep apnea, smoking, and vascular disease in coordination with the physician.
  4. Use topical treatment, SLT where appropriate, and surgery if target IOP is not achieved or progression continues.
68. What is the role of IOP lowering in NTG?
Answer: IOP lowering remains the only established modifiable ocular treatment. Even when baseline IOP is within the statistical normal range, further reduction slows progression in many patients.
69. How does POAG differ from NTG?
Answer: Both have open angles and characteristic glaucomatous optic neuropathy. In POAG, IOP is often above 21 mmHg at some point. In NTG, IOP remains within the conventional normal range on diurnal assessment, and vascular or non-IOP factors may have greater relative importance.
70. What are the indications to escalate therapy in POAG or NTG?
Answer:
  • IOP above target
  • Documented progression in disc, OCT, or visual field
  • New disc hemorrhage with other evidence of risk
  • Advanced damage or defect threatening fixation
  • Poor adherence or intolerance requiring a different approach
  • Large IOP fluctuations despite apparently acceptable clinic IOP.

Primary angle-closure disease and acute angle closure: 53-65 Secondary glaucomas: 66-78 Congenital and juvenile glaucomas: 79-85 Drugs, lasers, surgery and complications: 86-100

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AAO 2025 primary angle closure glaucoma preferred practice pattern acute angle closure laser iridotomy

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Primary angle-closure disease and acute angle closure

53. Define primary angle-closure suspect (PACS).
Answer: PACS is an anatomically narrow or occludable angle with iridotrabecular contact, but without raised IOP, peripheral anterior synechiae (PAS), or glaucomatous optic neuropathy.
54. Define primary angle closure (PAC).
Answer: PAC is an occludable angle with evidence of trabecular obstruction, such as raised IOP, PAS, iris whorling, or excessive trabecular pigmentation, but without glaucomatous optic neuropathy.
55. Define primary angle-closure glaucoma (PACG).
Answer: PACG is PAC associated with glaucomatous optic neuropathy and corresponding visual-field loss.
56. What are the risk factors for primary angle closure?
Answer:
  • Older age
  • Female sex
  • Asian or Inuit ancestry
  • Family history
  • Hypermetropia
  • Shallow anterior chamber and short axial length
  • Thick or anteriorly placed lens
  • Plateau iris configuration
  • Drugs causing pupillary dilation, for example anticholinergics, sympathomimetics, and some antidepressants.
57. What are the mechanisms of angle closure?
Answer:
  1. Pupillary block: resistance to aqueous passage from posterior to anterior chamber causes iris bombe.
  2. Plateau iris: anteriorly positioned ciliary processes push the peripheral iris forward.
  3. Lens-related crowding: thick or anterior lens causes relative pupillary block and angle narrowing.
  4. Posterior pushing mechanisms: ciliary body effusion, choroidal effusion, tumor, or aqueous misdirection push the iris-lens diaphragm forward.
58. What are the symptoms and signs of acute primary angle closure?
Answer:
Symptoms: severe ocular pain, headache, halos around lights, blurred vision, nausea, and vomiting.
Signs: reduced visual acuity, ciliary congestion, corneal epithelial edema, shallow anterior chamber, mid-dilated poorly reactive pupil, very high IOP, and a closed angle. IOP is often 50-80 mmHg.
Kanski's Clinical Ophthalmology, 10th ed., p. 395.
59. Describe the immediate management of acute angle closure.
Answer:
  • Confirm diagnosis and assess both eyes.
  • Rapidly lower IOP with topical aqueous suppressants such as beta-blocker, alpha-2 agonist, and topical carbonic anhydrase inhibitor.
  • Give systemic acetazolamide unless contraindicated.
  • Consider hyperosmotic therapy if IOP remains very high.
  • Give topical steroid and analgesic/antiemetic treatment.
  • Use pilocarpine once the iris becomes responsive and IOP has fallen.
  • Once corneal edema permits, perform definitive laser peripheral iridotomy.
The AAO angle-closure guideline recommends prompt IOP lowering followed by laser peripheral iridotomy, surgical iridectomy, or lens extraction as appropriate.
60. Why is pilocarpine not useful initially in severe acute angle closure?
Answer: At very high IOP, the ischemic iris sphincter is unresponsive to miotics. Pilocarpine is more useful after initial IOP lowering. Very strong miotics may worsen pupillary block by increasing anterior lens-iris apposition.
61. What is the definitive treatment of pupillary-block angle closure?
Answer: Laser peripheral iridotomy (LPI), which creates an alternative route for aqueous from the posterior to anterior chamber and abolishes pupillary block. Lens extraction is increasingly important when lens-related crowding is substantial or IOP remains uncontrolled.
62. What is the management of the fellow eye after an acute attack?
Answer: Perform gonioscopy and usually offer prompt prophylactic LPI if the fellow eye is phakic with a narrow or occludable angle. The fellow eye carries substantial risk of angle closure without prophylaxis.
63. What is plateau iris syndrome?
Answer: Persistent appositional angle closure after a patent peripheral iridotomy due to anteriorly positioned ciliary processes supporting the peripheral iris. Gonioscopy may show the “double-hump” sign on indentation. Management may include argon laser peripheral iridoplasty and, in selected cases, lens extraction.
64. What is laser peripheral iridoplasty?
Answer: Argon laser burns are applied to the extreme peripheral iris, causing stromal contraction and pulling the iris away from the trabecular meshwork. It is useful for persistent appositional closure, particularly plateau iris, or when LPI cannot be performed immediately.
65. What are the complications of laser peripheral iridotomy?
Answer: Transient IOP spike, anterior uveitis, hyphema, corneal endothelial damage, lens injury, dysphotopsia, closure of the iridotomy, and rarely retinal complications. Check patency and perform repeat gonioscopy after LPI.

Secondary glaucomas

66. Classify secondary glaucomas.
Answer:
  • Secondary open-angle glaucoma: pigmentary, pseudoexfoliative, steroid-induced, traumatic angle recession, uveitic, phacolytic, red-cell/ghost-cell, and glaucoma due to raised episcleral venous pressure.
  • Secondary angle-closure glaucoma with pupillary block: phacomorphic glaucoma, lens subluxation, seclusio pupillae, aphakic/pseudophakic pupillary block.
  • Secondary angle closure without pupillary block: neovascular glaucoma, ICE syndrome, uveitic PAS, malignant glaucoma, ciliary body/choroidal effusion, tumors, and drug-induced ciliochoroidal effusion.
    Kanski's Clinical Ophthalmology, 10th ed., p. 396.
67. What is pseudoexfoliation syndrome and pseudoexfoliative glaucoma?
Answer: Pseudoexfoliation syndrome is deposition of fibrillary extracellular material on anterior-segment structures. It may cause secondary open-angle glaucoma due to blockage and dysfunction of the trabecular meshwork. The glaucoma is often asymmetric, associated with high IOP fluctuations, marked trabecular pigmentation, and more rapid progression than POAG.
68. What are the clinical signs of pseudoexfoliation?
Answer:
  • White flaky material on the anterior lens capsule with a central disc, clear intermediate zone, and peripheral granular zone
  • Material at pupillary margin
  • Poor dilation
  • Sampaolesi line, a pigmented line anterior to Schwalbe line
  • Heavy trabecular pigmentation
  • Zonular weakness and increased risk during cataract surgery.
69. What is pigment dispersion syndrome?
Answer: It is liberation of pigment from posterior iris pigment epithelium due to iridozonular contact, often in young myopic males. Pigment deposits in the trabecular meshwork and may lead to pigmentary glaucoma.
70. What are the classical signs of pigment dispersion syndrome?
Answer:
  • Krukenberg spindle on corneal endothelium
  • Mid-peripheral radial iris transillumination defects
  • Dense trabecular pigmentation
  • Posterior bowing of iris
  • Pigment on anterior lens surface, sometimes Zentmayer or Scheie stripe.
71. What is steroid-induced glaucoma?
Answer: It is secondary open-angle glaucoma caused by corticosteroid-induced increase in trabecular outflow resistance. It can occur after topical, periocular, intravitreal, inhaled, oral, dermatological, or nasal steroids.
72. How do you manage steroid-induced glaucoma?
Answer:
  • Stop, reduce, or substitute the steroid if clinically safe.
  • Consider a less potent steroid where needed.
  • Start IOP-lowering treatment.
  • Monitor optic nerve and fields.
  • If steroid treatment is unavoidable and pressure remains uncontrolled, laser or surgery may be required.
73. What is angle-recession glaucoma?
Answer: It is glaucoma following blunt trauma that causes tearing between circular and longitudinal fibers of the ciliary body. Gonioscopy shows a widened ciliary body band, often with irregular angle recession. Glaucoma can appear months or years after trauma.
74. What is neovascular glaucoma?
Answer: It is secondary glaucoma caused by retinal ischemia leading to VEGF-mediated neovascularization of iris and angle. A fibrovascular membrane progressively closes the angle and causes severe, refractory elevation of IOP.
75. What are common causes of neovascular glaucoma?
Answer:
  • Proliferative diabetic retinopathy
  • Ischemic central retinal vein occlusion
  • Ocular ischemic syndrome from carotid disease
  • Long-standing retinal detachment
  • Intraocular tumors and severe retinal ischemic disease.
76. How is neovascular glaucoma managed?
Answer:
  • Urgently treat retinal ischemia with panretinal photocoagulation when possible.
  • Use intravitreal anti-VEGF for rapid regression of neovascularization.
  • Control inflammation and IOP medically.
  • Treat pain.
  • Consider glaucoma drainage device or cyclodestructive procedure if IOP remains uncontrolled.
    Treat the ischemic retinal cause, not only the IOP.
77. What is phacomorphic glaucoma?
Answer: It is secondary angle closure from an intumescent mature cataractous lens causing lens-related crowding and pupillary block. Definitive treatment is cataract extraction after controlling inflammation and IOP.
78. Differentiate phacolytic from lens-particle glaucoma.
Answer:
  • Phacolytic glaucoma: A hypermature cataract leaks high-molecular-weight lens proteins through an intact capsule. Macrophages engorged with lens material obstruct the trabecular meshwork. The angle is open.
  • Lens-particle glaucoma: Lens material enters the anterior chamber through a disrupted lens capsule, usually after trauma or surgery, and blocks the trabecular meshwork.

Congenital and juvenile glaucomas

79. Define primary congenital glaucoma (PCG).
Answer: PCG is developmental glaucoma due to isolated maldevelopment of the anterior chamber angle, causing impaired aqueous outflow. It is not associated with another major ocular anomaly.
Kanski's Clinical Ophthalmology, 10th ed., p. 415.
80. What are the clinical presentations of PCG by age?
Answer:
  • True congenital glaucoma: IOP raised in utero.
  • Infantile glaucoma: presents before 3 years of age.
  • Juvenile glaucoma: IOP elevation develops between 3 and 16 years.
    Kanski's Clinical Ophthalmology, 10th ed., p. 415.
81. What are the classic symptoms of primary congenital glaucoma?
Answer: The triad is:
  • Epiphora
  • Photophobia
  • Blepharospasm
These occur due to corneal edema and ocular discomfort.
82. What are the signs of primary congenital glaucoma?
Answer:
  • Enlarged corneal diameter
  • Corneal edema and Haab striae
  • Buphthalmos due to enlargement of the elastic infant globe
  • Deep anterior chamber
  • Raised IOP
  • Optic-disc cupping
  • Axial myopia and astigmatism.
83. What are Haab striae?
Answer: They are horizontal or curvilinear breaks in Descemet membrane caused by stretching of the enlarged cornea in congenital glaucoma. They must be differentiated from vertical Descemet tears in forceps injury.
84. How is primary congenital glaucoma treated?
Answer: It is primarily a surgical disease and should be treated promptly once diagnosed.
  • Goniotomy: preferred when cornea is sufficiently clear.
  • Trabeculotomy: useful when the cornea is cloudy.
  • Combined trabeculotomy-trabeculectomy, trabeculectomy, drainage devices, or cyclodestructive procedures are considered in refractory cases.
    Medical therapy is mainly temporary, before surgery or as adjunctive treatment.
    Kanski's Clinical Ophthalmology, 10th ed., p. 415.
85. What is juvenile open-angle glaucoma?
Answer: It is an early-onset form of open-angle glaucoma, often with markedly raised IOP, occurring in childhood or young adulthood. It may be familial, including autosomal dominant forms associated with MYOC mutations. It often needs early laser or surgical treatment because medical control may be insufficient.

Drugs, lasers, surgery and complications

86. Name the main classes of topical antiglaucoma drugs and their mechanisms.
Answer:
  • Prostaglandin analogues: increase uveoscleral outflow.
  • Beta-blockers: reduce aqueous production.
  • Alpha-2 agonists: reduce aqueous production and increase uveoscleral outflow.
  • Topical carbonic anhydrase inhibitors: reduce aqueous production.
  • Rho-kinase inhibitors: increase trabecular outflow and may reduce episcleral venous pressure.
  • Miotics: increase trabecular outflow by ciliary-muscle contraction and miosis.
87. What is usually the preferred first-line topical drug in POAG?
Answer: A prostaglandin analogue is commonly preferred because of effective once-daily IOP lowering, good systemic safety, and good adherence profile. Choice must be individualized according to contraindications, ocular surface disease, cost, pregnancy status, and patient preference.
88. What are adverse effects of prostaglandin analogues?
Answer: Conjunctival hyperemia, stinging, increased iris pigmentation, periocular skin pigmentation, eyelash growth, deepening of upper-lid sulcus, prostaglandin-associated periorbitopathy, and rarely uveitis or cystoid macular edema in predisposed eyes.
89. What are contraindications or cautions for topical beta-blockers?
Answer: Asthma, COPD with bronchospasm, bradycardia, heart block, heart failure, and concurrent systemic beta-blocker use. They can cause fatigue, hypotension, depression, erectile dysfunction, and masking of hypoglycemia.
90. What are common adverse effects of brimonidine?
Answer: Allergic follicular conjunctivitis, hyperemia, dry mouth, fatigue, drowsiness, and hypotension. It should generally be avoided in infants and very young children because of risk of central nervous system depression.
91. What are the indications for systemic acetazolamide?
Answer: It is used for short-term rapid IOP lowering, especially in acute angle closure, acute IOP spike, severe uncontrolled glaucoma, and perioperative control. It is not ideal as long-term routine treatment because of systemic adverse effects.
92. What are contraindications and adverse effects of acetazolamide?
Answer:
Adverse effects: paresthesia, fatigue, anorexia, metallic taste, nausea, metabolic acidosis, hypokalemia, renal stones, and rare blood dyscrasias.
Avoid or use extreme caution: sulfonamide hypersensitivity, severe renal or hepatic disease, adrenal insufficiency, and significant electrolyte or acid-base disturbance.
93. What is selective laser trabeculoplasty (SLT)?
Answer: SLT applies short-pulse frequency-doubled Nd:YAG laser energy selectively to pigmented trabecular meshwork cells, increasing aqueous outflow. It can be first-line treatment or an alternative/addition to topical medication in open-angle glaucoma.
94. What are indications and limitations of SLT?
Answer:
Indications: POAG, ocular hypertension, pigmentary glaucoma, and pseudoexfoliative glaucoma with open angles.
Limitations: it is not useful in a closed angle, has variable response, effect may decline with time, and may cause transient inflammation or IOP spike. Avoid excessive treatment in heavily pigmented angles.
Kanski's Clinical Ophthalmology, 10th ed., p. 409.
95. What is the mechanism and indication of laser peripheral iridotomy?
Answer: LPI creates a full-thickness iris opening, bypassing pupillary block and equalizing pressure between posterior and anterior chambers. It is indicated in acute or chronic primary angle closure, PACG, many occludable angles, and secondary pupillary-block glaucomas.
96. What is trabeculectomy?
Answer: Trabeculectomy is a guarded filtration procedure in which aqueous exits through a scleral fistula beneath a partial-thickness scleral flap into a subconjunctival bleb. Antimetabolites such as mitomycin-C may be used to reduce scarring.
97. What are the early complications of trabeculectomy?
Answer:
  • Shallow or flat anterior chamber
  • Hypotony
  • Wound leak
  • Choroidal effusion or hemorrhage
  • Hyphema
  • IOP spike due to blocked ostium, retained viscoelastic, or tight flap
  • Bleb encapsulation
  • Malignant glaucoma
  • Early blebitis or endophthalmitis, though less common.
98. What are late complications of trabeculectomy?
Answer:
  • Bleb failure from scarring
  • Late bleb leak
  • Thin avascular cystic bleb
  • Chronic hypotony and hypotony maculopathy
  • Bleb-related infection, blebitis, or endophthalmitis
  • Cataract formation or progression
  • Dysesthesia from a large bleb.
99. What is a glaucoma drainage device and when is it preferred?
Answer: A glaucoma drainage device consists of a tube directing aqueous to an episcleral plate where it forms a reservoir. It is especially useful in eyes at high risk of trabeculectomy failure, such as neovascular glaucoma, uveitic glaucoma, traumatic glaucoma, aphakia, extensive conjunctival scarring, failed filtering surgery, and some congenital glaucomas.
100. What is cyclodestructive treatment and when is it used?
Answer: Cyclodestructive treatment, most commonly transscleral diode cyclophotocoagulation, reduces aqueous production by ablating ciliary epithelium. It is usually reserved for refractory glaucoma, painful blind eyes, eyes with poor visual potential, or selected complex glaucomas when filtering surgery or drainage devices are unsuitable.
Recent evidence on MIGS and combined cataract surgery is expanding, but it does not replace the need to know trabeculectomy and drainage-device indications for MS viva. A 2025 systematic review found IOP and medication reduction with combined MIGS-phaco procedures in open-angle glaucoma, but procedure choice remains dependent on disease severity and target IOP (recent MIGS review).
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