Glaucoma — MCQs

Glaucoma Indian Medical PG Practice Questions and MCQs

Question 81: What is the value of diurnal variation of intraocular pressure (IOP) above which a diagnosis of glaucoma can be made?

A. 5 mm of Hg
B. 6 mm of Hg
C. 8 mm of Hg (Correct Answer)
D. 10 mm of Hg

Explanation: **Explanation:** Intraocular pressure (IOP) is not static; it fluctuates throughout the day following a circadian rhythm, a phenomenon known as **diurnal variation**. In a healthy individual, this variation typically ranges between **2 to 5 mm Hg**, usually peaking in the early morning hours. **Why 8 mm Hg is the correct answer:** In patients with glaucoma, the homeostatic mechanisms regulating aqueous humor dynamics are impaired, leading to wider fluctuations in IOP. A diurnal variation of **more than 8 mm Hg** is considered pathological and is a strong diagnostic indicator of glaucoma, even if individual "spot" readings fall within the statistically normal range (10–21 mm Hg). **Analysis of Incorrect Options:** * **A & B (5 mm Hg and 6 mm Hg):** These values fall within the physiological or borderline range. While a variation of 5–6 mm Hg might be suspicious if other clinical signs are present, it is not diagnostic of glaucoma on its own. * **D (10 mm Hg):** While a 10 mm Hg variation is certainly pathological, the diagnostic threshold established in standard ophthalmology textbooks (like Parsons and Khurana) is 8 mm Hg. Choosing 10 mm Hg would miss earlier diagnostic cases. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Measurement:** Diurnal variation is best measured using **Goldmann Applanation Tonometry (GAT)** every 3–4 hours over a 24-hour period (Phasing). * **Peak Timing:** In most individuals, IOP is highest in the **early morning (8 AM)** and lowest at night; however, some patients may show an "inverse" pattern. * **Clinical Significance:** Large fluctuations in IOP are an independent risk factor for the progression of visual field defects, even in patients with well-controlled mean IOP.

Question 82: Cupping of optic disc is seen in:

A. Trachoma
B. Open angle glaucoma (Correct Answer)
C. Retinitis pigmentosa
D. Retinoblastoma

Explanation: **Explanation:** **Cupping of the optic disc** is the hallmark clinical feature of glaucoma. In **Open-angle glaucoma (OAG)**, chronically elevated intraocular pressure (IOP) leads to mechanical compression and ischemic damage to the retinal nerve fiber layer (RNFL). As these nerve fibers atrophy, the neural rim of the optic disc thins, and the central depression (the cup) enlarges. This results in an increased **cup-to-disc ratio (CDR)**, typically >0.5 or an asymmetry of >0.2 between eyes. **Why other options are incorrect:** * **Trachoma:** This is a chronic keratoconjunctivitis caused by *Chlamydia trachomatis*. It primarily affects the conjunctiva and cornea (leading to scarring and blindness), not the optic nerve. * **Retinitis Pigmentosa:** This is a hereditary dystrophy of the photoreceptors (primarily rods). Classic fundus findings include bony spicule pigmentation, arteriolar attenuation, and **waxy pallor** of the disc, but not cupping. * **Retinoblastoma:** This is a primary intraocular malignancy of childhood. It presents with leukocoria (white reflex) and an intraocular mass, often with calcification, rather than glaucomatous disc changes. **High-Yield Clinical Pearls for NEET-PG:** * **ISNT Rule:** In a normal disc, the thickness of the neuroretinal rim follows the order Inferior > Superior > Nasal > Temporal. Glaucoma often causes "notching" by breaking this rule (usually affecting inferior/superior rims first). * **Bayoneting Sign:** This occurs when retinal vessels make a sharp 90-degree turn as they pass over the steep edge of the excavated cup. * **Laminar Dot Sign:** Exposure of the pores of the lamina cribrosa at the base of a deep cup. * **Other causes of cupping:** While synonymous with glaucoma, "physiologic cupping" can be seen in large healthy discs, and "pseudocupping" may occur in compressive optic neuropathies.

Question 83: Which of the following statements is true regarding the given investigation?

A. It is a type of manual perimetry
B. A kinetic stimulus is used
C. Stimulus brightness is constant (Correct Answer)
D. All of the above

Explanation: ***Stimulus brightness is constant*** - In **automated static perimetry** (Humphrey Field Analyzer), the **stimulus brightness is kept constant** while the **threshold sensitivity** is measured at fixed locations. - This method uses **static stimuli** presented at predetermined points to detect **visual field defects** characteristic of glaucoma. *It is a type of manual perimetry* - **Automated static perimetry** is performed using computerized equipment like the **Humphrey Field Analyzer**, not manually. - **Manual perimetry** refers to **Goldmann perimetry**, where the examiner manually controls the stimulus presentation. *A kinetic stimulus is used* - **Static perimetry** uses **stationary stimuli** presented at fixed locations, not moving stimuli. - **Kinetic perimetry** (like **Goldmann perimetry**) uses **moving stimuli** of constant size and brightness to map visual field boundaries. *All of the above* - This option is incorrect since only **"stimulus brightness is constant"** accurately describes automated static perimetry. - The other statements incorrectly describe features of **manual kinetic perimetry** rather than automated static perimetry.

Question 84: All of the following conditions are contraindicated or likely to cause issues in a patient treated with Timolol maleate 0.5% eye drops for Primary Open Angle glaucoma, EXCEPT:

A. Hypertension (Correct Answer)
B. Hypercholesterolemia
C. Depression
D. Bronchial asthma

Explanation: **Explanation:** Timolol maleate is a **non-selective beta-blocker** (blocking both $\beta_1$ and $\beta_2$ receptors). When administered topically as eye drops, it undergoes significant systemic absorption via the nasolacrimal duct, bypassing first-pass metabolism and potentially causing systemic side effects similar to oral beta-blockers. **Why Hypertension is the Correct Answer:** Beta-blockers are actually a standard class of drugs used to **treat** hypertension. Therefore, Timolol is not contraindicated in hypertensive patients; if anything, it may have a synergistic (though usually negligible) effect on lowering blood pressure. **Analysis of Incorrect Options:** * **Bronchial Asthma:** This is a **strict contraindication**. Blocking $\beta_2$ receptors in the lungs causes bronchoconstriction, which can precipitate a life-threatening asthma attack. * **Depression:** Beta-blockers are known to cross the blood-brain barrier and are associated with central nervous system side effects, including fatigue, lethargy, and worsening of clinical depression. * **Hypercholesterolemia:** Non-selective beta-blockers can adversely affect the lipid profile by decreasing HDL ("good" cholesterol) and increasing triglycerides. While not a total contraindication, it is a metabolic "issue" to monitor. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC):** Prostaglandin analogues (e.g., Latanoprost) are the first-line treatment for POAG, but Timolol remains a frequently tested classic. * **Betaxolol:** If a patient has respiratory issues but requires a beta-blocker, **Betaxolol** (a cardioselective $\beta_1$ blocker) is the preferred alternative as it has less effect on pulmonary $\beta_2$ receptors. * **Cardiac Contraindications:** Avoid Timolol in patients with Bradycardia, 2nd or 3rd-degree Heart Block, or Overt Cardiac Failure.

Question 85: Schwalbe's line is:

A. The anterior limit of Bowman's membrane
B. The posterior limit of Bowman's membrane
C. The anterior limit of Descemet's membrane (Correct Answer)
D. The posterior limit of Descemet's membrane

Explanation: **Explanation:** **Schwalbe’s line** represents the anatomical junction where the corneal endothelium and Descemet’s membrane terminate and the trabecular meshwork begins. It is the most anterior structure visible during **gonioscopy**, appearing as a thin, pearly-white line. 1. **Why Option C is Correct:** Schwalbe’s line is histologically defined as the **anterior limit (peripheral termination) of Descemet’s membrane**. As the cornea transitions into the sclera at the limbus, Descemet’s membrane ends abruptly, forming this landmark. 2. **Why Other Options are Incorrect:** * **Options A & B:** Bowman’s membrane is a superficial layer of the cornea (between the epithelium and stroma). It ends at the limbus but does not form Schwalbe’s line, which is a deep posterior structure. * **Option D:** Descemet’s membrane begins at the corneal periphery (Schwalbe’s line) and covers the posterior surface of the cornea. There is no "posterior limit" in the context of the angle; its termination point is always anterior relative to the drainage structures. **Clinical Pearls for NEET-PG:** * **Gonioscopy Sequence (Anterior to Posterior):** Use the mnemonic **"I Can't See This Stuff"** → **I** (Internal border of Schwalbe’s line), **C** (non-pigmented Trabecular Meshwork), **S** (Scleral spur), **T** (Trabecular meshwork - pigmented), **S** (Ciliary Body Band). * **Sampaolesi Line:** In conditions like Pigment Dispersion Syndrome or Pseudoexfoliation Syndrome, pigment is deposited on or anterior to Schwalbe’s line, creating a "Sampaolesi line." * **Posterior Embryotoxon:** An abnormally thickened and anteriorly displaced Schwalbe’s line, visible on slit-lamp examination without a goniolens. It is a hallmark of Alagille syndrome and Axenfeld-Rieger syndrome.

Question 86: A young male presents with painless loss of vision and an intraocular pressure of 60mm Hg. Which of the following is the most likely diagnosis?

A. Angle closure glaucoma
B. Acute anterior uveitis
C. Chronic papilledema
D. Glaucomatocyclitic crisis (Correct Answer)

Explanation: **Explanation:** The correct answer is **Glaucomatocyclitic crisis (Posner-Schlossman Syndrome)**. This condition is characterized by recurrent episodes of markedly elevated intraocular pressure (IOP), often ranging from 40–60 mmHg, associated with mild anterior chamber inflammation. **Why D is correct:** The hallmark of Posner-Schlossman Syndrome is the **disproportion** between the very high IOP and the lack of symptoms. Unlike acute angle-closure glaucoma, the eye remains "white," and the patient experiences minimal pain or only mild blurring/halos. It typically affects young to middle-aged adults and presents with an open angle on gonioscopy and a few fine, stellate keratic precipitates (KPs). **Why other options are incorrect:** * **A. Angle closure glaucoma:** While IOP can reach 60 mmHg, it is an ocular emergency presenting with severe pain, nausea, vomiting, a "stony hard" eye, and a shallow anterior chamber. It is rarely "painless." * **B. Acute anterior uveitis:** This typically presents with **low** IOP (due to ciliary body exhaustion) or only mildly elevated IOP. It is characterized by significant pain, photophobia, and ciliary congestion. * **C. Chronic papilledema:** This involves optic disc swelling due to increased intracranial pressure. While it causes vision loss, it does not typically cause an elevation in intraocular pressure. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Posner-Schlossman:** Unilateral high IOP + Open angles + Fine KPs. * **Treatment:** Medical management with topical steroids (to control inflammation) and aqueous suppressants (to lower IOP). Miotics (Pilocarpine) are generally avoided. * **Key differentiator:** If the question mentions "high IOP in a white, quiet eye" in a young patient, always think of Glaucomatocyclitic crisis.

Question 87: All of the following can be seen in Axenfeld-Rieger syndrome, except?

A. Ectopia of the lens (Correct Answer)
B. Glaucoma
C. Iris synechiae to Schwalbe's line
D. Posterior embryotoxon

Explanation: **Explanation:** Axenfeld-Rieger Syndrome (ARS) is an autosomal dominant spectrum of anterior segment dysgenesis resulting from the abnormal migration and differentiation of **neural crest cells**. **Why "Ectopia of the lens" is the correct answer:** Ectopia lentis (dislocation of the lens) is **not** a feature of Axenfeld-Rieger syndrome. It is typically associated with conditions like Marfan syndrome, Homocystinuria, or Weill-Marchesani syndrome. In ARS, the primary defects are limited to the cornea, iris, and angle, along with systemic non-ocular findings. **Analysis of incorrect options:** * **Posterior Embryotoxon:** This is the hallmark of the syndrome. It represents an anteriorly displaced and prominent Schwalbe’s line. * **Iris synechiae to Schwalbe's line:** Also known as peripheral anterior synechiae (PAS), these are tissue strands that bridge the iridocorneal angle to the prominent Schwalbe’s line. * **Glaucoma:** Approximately 50% of patients develop glaucoma due to the underlying angle dysgenesis (arrested development of the trabecular meshwork). **NEET-PG High-Yield Pearls:** 1. **The Spectrum:** It includes Axenfeld anomaly (isolated ocular findings), Rieger anomaly (ocular + iris changes like polycoria/corectopia), and Rieger syndrome (ocular + systemic findings). 2. **Systemic Features:** Look for **dental anomalies** (hypodontia, microdontia), **facial dysmorphism** (maxillary hypoplasia, telecanthus), and redundant periumbilical skin. 3. **Genetics:** Associated with mutations in **PITX2** and **FOXC1** genes. 4. **Management:** Glaucoma in ARS is often refractory to medical therapy and may require surgical intervention (Goniotomy or Trabeculectomy).

Question 88: Which of the following tonometers can be used in a diseased cornea?

A. Schiotz
B. Malkalov
C. Perkins
D. Tonopen (Correct Answer)

Explanation: **Explanation:** The correct answer is **Tonopen**. The underlying medical concept is the principle of **electronic Mackay-Marg tonometry**. Unlike traditional applanation tonometers that require a large, perfectly smooth, and regular corneal surface to satisfy the Imbert-Fick law, the Tonopen uses a micro-strain gauge and a small sensing plunger. Because it has a very small surface area of contact, it can accurately measure Intraocular Pressure (IOP) even on **irregular, scarred, edematous, or diseased corneas**, and it can even be used over bandage contact lenses. **Analysis of Incorrect Options:** * **Schiotz Tonometer:** This is an indentation tonometer. It is highly dependent on **scleral rigidity** and requires a smooth corneal surface for the footplate to rest upon; it is inaccurate in diseased or distorted corneas. * **Maklakov Tonometer:** An early form of applanation tonometry that uses a weighted cylinder and dye. It requires a large area of contact, making it unsuitable for irregular corneal surfaces. * **Perkins Tonometer:** This is essentially a portable version of the **Goldmann Applanation Tonometer (GAT)**. Since it relies on the same biprism principle as GAT, it requires a clear, regular cornea and a stable tear film to visualize the fluorescein mires accurately. **Clinical Pearls for NEET-PG:** * **Gold Standard:** Goldmann Applanation Tonometry (GAT) remains the gold standard for IOP measurement. * **Pneumotonometry:** Another excellent option for irregular corneas (similar to Tonopen). * **Rebound Tonometry (iCare):** Useful in pediatrics as it requires no topical anesthesia. * **Sterilization:** Tonopen uses disposable "Ocu-film" tips, making it ideal for preventing cross-infection (e.g., Epidemic Keratoconjunctivitis).

Question 89: What is the mechanism of steroid-induced glaucoma?

A. Narrowing of the angle of the anterior chamber
B. Neovascularization of the iris
C. Inhibition of prostaglandin E (PGE) synthesis (Correct Answer)
D. Deposition of hemosiderin

Explanation: **Explanation:** Steroid-induced glaucoma is a form of secondary open-angle glaucoma caused by the administration of corticosteroids (topical, systemic, or periocular). **Mechanism of the Correct Answer:** The primary mechanism involves an **increase in resistance to aqueous outflow** at the level of the trabecular meshwork (TM). Steroids inhibit the synthesis of **Prostaglandin E (PGE)** and other prostaglandins that normally facilitate aqueous drainage. Additionally, steroids lead to: 1. **Accumulation of Glycosaminoglycans (GAGs):** Steroids inhibit the release of lysosomal enzymes that degrade GAGs, leading to their buildup and subsequent "hydration" (swelling) of the TM. 2. **Structural Changes:** They increase the expression of **myocilin (MYOC) protein** and promote the formation of "Cross-linked Actin Networks" (CLANs) in TM cells, making the meshwork less permeable. **Analysis of Incorrect Options:** * **Option A:** Steroid-induced glaucoma occurs in the presence of an **open angle**. Narrowing of the angle is characteristic of Primary Angle Closure Glaucoma. * **Option B:** Neovascularization of the iris (Rubeosis iridis) leads to **Neovascular Glaucoma**, typically seen in ischemic conditions like Diabetic Retinopathy or Central Retinal Vein Occlusion. * **Option C:** Deposition of hemosiderin is seen in **Siderotic Glaucoma** following intraocular iron foreign bodies. **High-Yield NEET-PG Pearls:** * **Steroid Responders:** Approximately 5-10% of the population are "high responders" who develop significant IOP elevation. This is highly prevalent in patients with **Primary Open Angle Glaucoma (POAG)** and their first-degree relatives. * **Potency:** Dexamethasone and Betamethasone have the highest potential to raise IOP; **Fluorometholone** and **Loteprednol** are safer "soft steroids" with lower risk. * **Management:** The first step is to **withdraw the steroid**. If IOP remains high, topical aqueous suppressants (Beta-blockers/Alpha-agonists) are used. Prostaglandin analogues are generally avoided if the steroid has induced inflammation.

Question 90: Haab's striae is seen in which of the following conditions?

A. Trachoma
B. Congenital glaucoma (Correct Answer)
C. Scleritis
D. Cataract

Explanation: **Explanation:** **Haab’s striae** are a hallmark clinical sign of **Primary Congenital Glaucoma (PCG)**. They represent horizontal or curvilinear breaks in the **Descemet’s membrane** of the cornea. These breaks occur because the infant’s eye is elastic; when intraocular pressure (IOP) rises significantly, the globe stretches (buphthalmos). While the corneal stroma can stretch, the brittle Descemet’s membrane cannot, leading to ruptures that result in permanent linear scars. **Analysis of Options:** * **Congenital Glaucoma (Correct):** The classic triad includes epiphora, photophobia, and blepharospasm. Haab's striae are typically horizontal or concentric to the limbus, distinguishing them from birth trauma (forceps injury), which causes vertical or oblique tears. * **Trachoma:** Characterized by Arlt’s lines (conjunctival scarring) and Herbert’s pits (limbal depressions), not corneal membrane ruptures. * **Scleritis:** An inflammation of the sclera presenting with severe pain and localized or diffuse redness; it does not involve Descemet’s membrane breaks. * **Cataract:** An opacification of the crystalline lens. While congenital cataracts exist, they do not cause the corneal stretching associated with Haab’s striae. **High-Yield Clinical Pearls for NEET-PG:** * **Buphthalmos:** Term for "ox-eye" seen in congenital glaucoma due to increased globe diameter (>12 mm before age 3). * **Haab’s Striae vs. Forceps Injury:** Haab’s = Horizontal/Curvilinear; Forceps = Vertical/Oblique. * **Management:** Unlike adult glaucoma, the primary treatment for congenital glaucoma is **surgical** (Goniotomy or Trabeculotomy). * **Barkan’s Membrane:** A persistent embryonic tissue covering the trabecular meshwork, often implicated in the pathogenesis of PCG.

Practice by Chapter

Aqueous Humor Dynamics

Practice Questions

Primary Open-Angle Glaucoma

Practice Questions

Primary Angle-Closure Glaucoma

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Secondary Open-Angle Glaucomas

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Secondary Angle-Closure Glaucomas

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Developmental and Congenital Glaucomas

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Medical Management of Glaucoma

Practice Questions

Laser Therapy in Glaucoma

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Glaucoma Filtration Surgery

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Glaucoma Drainage Devices

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Angle Assessment Techniques

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Visual Field Testing in Glaucoma

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Glaucoma — MCQs

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