Glaucoma — MCQs

Glaucoma Indian Medical PG Practice Questions and MCQs

Question 191: Which of the following is NOT a cause of a shallow anterior chamber?

A. Hypermetropia with a small axial length
B. Pupil block due to vitreous bulge after intracapsular cataract extraction
C. Iris bombe
D. Pathological myopia (Correct Answer)

Explanation: **Explanation:** The depth of the anterior chamber (AC) is determined by the anatomical dimensions of the eyeball and the pressure relationship between the posterior and anterior chambers. **Why Pathological Myopia is the Correct Answer:** In **Pathological Myopia**, the eyeball is abnormally long (increased axial length). This elongation typically results in a **deep anterior chamber**, a wide iridocorneal angle, and a large crystalline lens. Because the question asks for which condition does *NOT* cause a shallow AC, pathological myopia is the correct choice. **Analysis of Incorrect Options:** * **Hypermetropia with small axial length:** Hypermetropic eyes are anatomically smaller. A short axial length combined with a relatively large lens crowds the anterior segment, leading to a shallow AC and predisposing the patient to primary angle-closure glaucoma. * **Pupil block due to vitreous bulge (Aphakic Glaucoma):** After intracapsular cataract extraction (ICCE), the vitreous face can move forward and block the pupil. This prevents aqueous humor from reaching the AC, causing a pressure buildup in the posterior chamber that pushes the iris forward, shallowing the AC. * **Iris bombe:** This occurs due to 360-degree posterior synechiae (seclusio pupillae). The trapped aqueous in the posterior chamber causes the peripheral iris to bulge forward (bombe), significantly shallowing the AC. **NEET-PG High-Yield Pearls:** * **Normal AC Depth:** Approximately 2.5 to 3.0 mm. * **Shallow AC Causes:** Hypermetropia, Intumescent cataract (phacomorphic), Malignant glaucoma (ciliary block), and Plateau iris syndrome. * **Deep AC Causes:** Myopia, Aphakia, Keratoglobus, and Buphthalmos (Congenital Glaucoma). * **Clinical Sign:** A shallow AC is a hallmark of **Angle-Closure Glaucoma**, while a deep AC is typically seen in **Open-Angle Glaucoma**.

Question 192: Peripheral anterior synechiae after an attack of acute congestive glaucoma occur earliest in which location?

A. Inferior part
B. Superior part (Correct Answer)
C. Inferior and nasal part
D. Inferior and temporal part

Explanation: In **Acute Congestive Glaucoma** (Angle-Closure Glaucoma), Peripheral Anterior Synechiae (PAS) are permanent adhesions between the iris root and the trabecular meshwork. These form due to prolonged contact and subsequent inflammation during an acute attack. **Why the Superior Part is Correct:** The **superior part** of the iridocorneal angle is anatomically the **narrowest** part of the angle in the normal eye. Because the superior angle is already more shallow than other quadrants, it is the first area where the iris makes contact with the cornea/trabecular meshwork during an attack. Consequently, inflammatory exudates organize here first, leading to the earliest formation of PAS. **Analysis of Incorrect Options:** * **A, C, and D (Inferior, Nasal, and Temporal parts):** These quadrants are anatomically **wider** than the superior quadrant. Gravitational factors and the natural shape of the anterior chamber ensure that the inferior angle is typically the deepest. Therefore, these areas are involved later in the disease process as the angle closure progresses circumferentially. **High-Yield Clinical Pearls for NEET-PG:** * **Gonioscopy:** This is the gold standard for identifying PAS. PAS are distinguished from "iris processes" by their broad base and ability to obscure the trabecular meshwork. * **Sequence of Angle Width:** Inferior > Temporal > Nasal > Superior (The superior angle is the narrowest). * **Management:** Laser Peripheral Iridotomy (LPI) is the definitive treatment to bypass pupillary block, but it cannot reverse established PAS. * **Van Herick Technique:** A slit-lamp method to grade the angle; it is most commonly performed at the temporal limbus for ease, but the superior angle remains the most vulnerable.

Question 193: What is the first visual field defect observed in open-angle glaucoma?

A. Arcuate scotoma
B. Extension above the blind spot (Correct Answer)
C. Roene's nasal step
D. Siedel's scotoma

Explanation: In Primary Open-Angle Glaucoma (POAG), visual field defects follow a specific chronological sequence based on the damage to the retinal nerve fiber layer (RNFL). ### **Explanation of the Correct Answer** The earliest clinically detectable visual field change in glaucoma is **generalized depression** of the field, followed by localized changes. Among the localized defects, the **extension above or below the blind spot** (also known as a **Baring of the blind spot**) is traditionally considered the earliest sign. This occurs due to subtle damage to the arcuate nerve fibers as they enter the superior or inferior poles of the optic disc. ### **Analysis of Incorrect Options** * **A. Arcuate scotoma (Bjerrum’s scotoma):** This is a late-stage defect. It forms when Seidel’s scotomas coalesce to create a complete arch-shaped defect extending from the blind spot to the horizontal meridian. * **C. Roenne’s nasal step:** This occurs when arcuate fibers meet at the horizontal raphe. Because the fibers from the superior and inferior halves do not cross the raphe, a "step" like discrepancy is created. This is a characteristic sign but usually appears after the initial paracentral defects. * **D. Seidel’s scotoma:** This is the next stage after the initial extension. It is a sickle-shaped extension of the blind spot that reaches toward the nasal field but has not yet formed a full arc. ### **High-Yield Clinical Pearls for NEET-PG** * **Sequence of Defects:** Generalized depression → Baring of blind spot → Paracentral scotoma (most common early localized defect) → Seidel’s scotoma → Arcuate/Bjerrum scotoma → Roenne’s nasal step → Ring scotoma → Tubular vision → Temporal island. * **Gold Standard for Diagnosis:** Automated Perimetry (Humphrey Visual Field Analyzer) using the SITA-Standard 24-2 or 30-2 program. * **Key Anatomy:** Glaucomatous damage typically starts at the **inferotemporal and superotemporal** poles of the optic nerve head (ISNT rule violation).

Question 194: What is the primary mechanism by which carbonic anhydrase inhibitors reduce intraocular pressure (IOP)?

A. Increase uveoscleral outflow
B. Increase trabecular meshwork outflow
C. Decrease aqueous humor production (Correct Answer)
D. All of the above

Explanation: ### Explanation **Primary Mechanism: Decrease Aqueous Humor Production** Carbonic anhydrase inhibitors (CAIs), such as Acetazolamide (oral) and Dorzolamide (topical), work by inhibiting the enzyme **carbonic anhydrase II** located in the non-pigmented ciliary epithelium. Under normal conditions, this enzyme facilitates the reaction: $CO_2 + H_2O \rightleftharpoons H_2CO_3 \rightleftharpoons H^+ + HCO_3^-$ The bicarbonate ($HCO_3^-$) ions are essential for the active transport of sodium and water into the posterior chamber. By inhibiting this enzyme, CAIs reduce the availability of bicarbonate ions, leading to a significant decrease (up to 40-60%) in the active secretion of aqueous humor, thereby lowering IOP. **Analysis of Incorrect Options:** * **Option A (Uveoscleral Outflow):** This is the primary mechanism for **Prostaglandin analogues** (e.g., Latanoprost). * **Option B (Trabecular Outflow):** This is the primary mechanism for **Miotics** (e.g., Pilocarpine) and Rho-kinase inhibitors. * **Option D:** Incorrect, as CAIs have no significant effect on the outflow pathways. **High-Yield Clinical Pearls for NEET-PG:** * **Systemic Side Effects (Acetazolamide):** Paresthesia (most common), metabolic acidosis, hypokalemia, and renal stones. * **Contraindications:** Avoid in patients with **Sulfa allergy**, severe renal/hepatic impairment, and COPD (due to acidosis). * **Topical CAIs:** Dorzolamide and Brinzolamide are preferred for chronic management to avoid systemic side effects, though they may cause a bitter taste (dysgeusia). * **Drug of Choice:** Acetazolamide is the drug of choice for rapid IOP reduction in **Acute Angle Closure Glaucoma**.

Question 195: What is the first-line treatment for open-angle glaucoma?

A. Timolol (Correct Answer)
B. Pilocarpine
C. Epinephrine
D. Carbonic anhydrase inhibitor

Explanation: **Explanation:** **Primary Open-Angle Glaucoma (POAG)** is characterized by a progressive optic neuropathy associated with increased intraocular pressure (IOP). The primary goal of treatment is to lower IOP to prevent further damage to the optic nerve. **Why Timolol is the Correct Answer:** Historically and traditionally for exams like NEET-PG, **Beta-blockers (e.g., Timolol)** are considered the first-line medical therapy. Timolol works by decreasing the production of aqueous humor from the ciliary body. It is preferred due to its efficacy, relatively low cost, and twice-daily dosing schedule. *Note: In modern clinical practice, Prostaglandin analogues (like Latanoprost) are often the first choice due to superior efficacy, but among the provided options, Timolol is the standard answer.* **Analysis of Incorrect Options:** * **B. Pilocarpine:** A miotic (cholinergic agonist) that increases aqueous outflow. It is now rarely used as first-line therapy for POAG due to side effects like miosis, brow ache, and the risk of retinal detachment. It remains a drug of choice for Angle-Closure Glaucoma. * **C. Epinephrine:** It reduces IOP by increasing outflow but is rarely used today because of significant ocular side effects (e.g., adrenochrome deposits, cystoid macular edema) and systemic sympathomimetic effects. * **D. Carbonic Anhydrase Inhibitors (e.g., Acetazolamide):** These decrease aqueous production. While effective, systemic forms have significant side effects (paresthesia, metabolic acidosis), making them second or third-line adjuncts rather than initial monotherapy. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindications for Timolol:** Always screen for bronchial asthma, COPD, or heart block, as systemic absorption can trigger bronchospasm or bradycardia. * **Drug of Choice (DOC) for POAG:** If Prostaglandin Analogues (PGAs) are in the options, they are currently the DOC. If not, Beta-blockers are the answer. * **Mechanism of PGAs:** They increase **uveoscleral outflow**, whereas Beta-blockers decrease **aqueous production**.

Question 196: What is the initial treatment of malignant glaucoma?

A. Atropine (Correct Answer)
B. Topical pilocarpine
C. Intravenous mannitol
D. Vitreous aspiration

Explanation: **Malignant Glaucoma (Ciliary Block Glaucoma)** is a rare but serious condition characterized by a shallow anterior chamber and elevated intraocular pressure (IOP), typically occurring after intraocular surgery in patients with narrow angles. ### **Why Atropine is the Correct Answer** The primary pathophysiology involves a **posterior diversion of aqueous humor** into the vitreous cavity, which pushes the lens-iris diaphragm forward. **Atropine (1% drops or ointment)** is the drug of choice because: 1. **Cycloplegia:** It relaxes the ciliary muscle, which tightens the suspensory ligaments (zonules). This pulls the lens backward into its normal anatomical position. 2. **Stabilization:** It helps reform the anterior chamber and breaks the "ciliary block" cycle. ### **Why Other Options are Incorrect** * **B. Topical Pilocarpine:** This is **contraindicated**. Pilocarpine causes miosis and ciliary muscle contraction, which moves the lens-iris diaphragm further forward, worsening the pupillary block and the condition. * **C. Intravenous Mannitol:** While hyperosmotics are used to dehydrate the vitreous and lower IOP, they are **adjunctive** treatments. Atropine remains the definitive initial medical step to reverse the underlying mechanism. * **D. Vitreous Aspiration:** This is a surgical intervention (Pars Plana Vitrectomy) reserved for cases that are refractory to medical management. ### **NEET-PG High-Yield Pearls** * **Classic Presentation:** Shallow anterior chamber (both central and peripheral) + High IOP + History of recent surgery (e.g., iridectomy or cataract surgery). * **Medical Management Triad:** Mydriatic-cycloplegics (Atropine), Carbonic anhydrase inhibitors (Acetazolamide), and Hyperosmotics (Mannitol). * **Definitive Surgical Treatment:** Nd:YAG laser hyaloidotomy or Pars Plana Vitrectomy (PPV) to create a communication between the vitreous and the anterior chamber.

Question 197: Peripheral iridectomy is indicated in which of the following conditions?

A. Primary open-angle glaucoma
B. Absolute glaucoma
C. Closed-angle glaucoma (Correct Answer)
D. Cataract

Explanation: **Explanation:** **Peripheral Iridectomy (PI)** is a surgical procedure where a small piece of the peripheral iris is removed to create a communication between the posterior and anterior chambers. **Why Closed-angle Glaucoma is Correct:** The primary mechanism in Primary Angle-Closure Glaucoma (PACG) is **pupillary block**. This occurs when the iris remains in close contact with the lens, obstructing the flow of aqueous humor from the posterior to the anterior chamber. This leads to increased pressure in the posterior chamber, causing the iris to bulge forward (**iris bombe**) and mechanically block the drainage angle. A PI (or Laser Peripheral Iridotomy) bypasses this block, equalizing pressure between the chambers and allowing the iris to fall back, thereby opening the angle. **Why Other Options are Incorrect:** * **Primary Open-Angle Glaucoma (POAG):** The pathology lies in the microscopic resistance within the trabecular meshwork, not a pupillary block. Treatment involves medical therapy or filtration surgeries like trabeculectomy. * **Absolute Glaucoma:** This is the final, blind, and painful stage of any glaucoma. Treatment focuses on pain relief (e.g., cyclodestruction or enucleation) rather than restoring drainage. * **Cataract:** This is an opacification of the lens. The definitive treatment is lens extraction (Phacoemulsification), not an iridectomy. **High-Yield Clinical Pearls for NEET-PG:** * **Laser Peripheral Iridotomy (LPI)** using Nd:YAG laser is now the **preferred first-line treatment** over surgical PI. * **Prophylaxis:** PI/LPI is also indicated in the **fellow eye** of a patient with an acute attack of angle closure, as there is a high risk of a similar attack. * **Indication:** PI is only effective if at least **180° of the angle is not permanently closed** by synechiae (PAS). If the angle is permanently closed, a filtering surgery (Trabeculectomy) is required.

Question 198: Which of the following statements regarding pigmentary glaucoma is false?

A. It is a type of secondary open-angle glaucoma.
B. Slit-lamp microscopy shows Krukenberg spindles of pigment on the corneal endothelium.
C. Gonioscopy may show a Sampaolesi line.
D. It is an angle closure glaucoma caused by the accumulation of pigments. (Correct Answer)

Explanation: ### Explanation **Pigmentary Glaucoma (PG)** is a form of **secondary open-angle glaucoma** caused by the liberation of pigment from the iris pigment epithelium. This occurs due to "pigment dispersion syndrome," where the posterior surface of the iris rubs against the lens zonules (mechanical friction), leading to pigment release and subsequent blockage of the trabecular meshwork. #### Why Option D is the Correct Answer (The False Statement) Option D is incorrect because Pigmentary Glaucoma is fundamentally an **open-angle glaucoma**, not an angle-closure glaucoma. The intraocular pressure (IOP) rises because the pigment granules physically clog the trabecular meshwork, increasing resistance to aqueous outflow, even though the anatomical angle remains wide open. #### Analysis of Other Options * **Option A:** Correct. It is classified as a secondary open-angle glaucoma because the underlying cause is external to the drainage system (pigment) but the angle remains open. * **Option B:** Correct. **Krukenberg spindles** are vertical, spindle-shaped deposits of pigment on the corneal endothelium, formed by convection currents in the aqueous humor. * **Option C:** Correct. **Sampaolesi line** refers to increased pigment deposition on or anterior to Schwalbe’s line. While classically associated with Pseudoexfoliation syndrome, it is frequently seen in pigmentary glaucoma due to heavy pigment load. #### High-Yield Clinical Pearls for NEET-PG * **Patient Profile:** Typically affects **young, myopic Caucasian males** (20–40 years). * **Triad of Pigment Dispersion:** Krukenberg spindle, slit-like mid-peripheral iris transillumination defects, and heavy trabecular pigmentation. * **Mechanism:** **Reverse pupillary block** (posterior bowing of the iris). * **Management:** Laser Peripheral Iridotomy (LPI) can flatten the iris and reduce friction; however, standard glaucoma medications and trabeculectomy are used if IOP remains uncontrolled. * **Exercise-Induced IOP Spikes:** Physical exertion can trigger a sudden release of pigment, leading to acute IOP elevation and "halos" around lights.

Question 199: Which one of the following is NOT used in the management of glaucoma?

A. Timolol
B. Physostigmine
C. Donepezil (Correct Answer)
D. Dipivefrine

Explanation: **Explanation:** The management of glaucoma focuses on lowering intraocular pressure (IOP) by either decreasing aqueous humor production or increasing its outflow. **Why Donepezil is the Correct Answer:** **Donepezil** is a centrally acting reversible acetylcholinesterase inhibitor used primarily in the treatment of **Alzheimer’s disease**. While it increases acetylcholine levels in the brain to improve cognitive function, it has no clinical role in the management of glaucoma. In fact, because of its cholinergic effects, it can theoretically cause miosis or worsen certain types of glaucoma, though it is not used therapeutically for eye conditions. **Analysis of Incorrect Options:** * **Timolol (Option A):** A non-selective **beta-blocker** and traditionally the first-line treatment for glaucoma. It works by decreasing aqueous humor production from the ciliary body. * **Physostigmine (Option B):** A **parasympathomimetic (miotic)** agent. It is an acetylcholinesterase inhibitor that increases acetylcholine at the iris sphincter, causing miosis and opening the trabecular meshwork to increase aqueous outflow. * **Dipivefrine (Option C):** A **prodrug of epinephrine**. It is more lipophilic and penetrates the cornea better than epinephrine. It lowers IOP by increasing uveoscleral outflow and decreasing aqueous production. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC):** Prostaglandin analogues (e.g., Latanoprost) are currently the first-line treatment for Primary Open Angle Glaucoma (POAG) due to superior efficacy and once-daily dosing. * **Mechanism of Action (MOA) Tip:** Beta-blockers and Carbonic Anhydrase Inhibitors (Acetazolamide) **decrease production**, while Miotics and Prostaglandins **increase outflow**. * **Contraindication:** Avoid Beta-blockers (Timolol) in patients with asthma or heart block.

Question 200: Which of the following is not a disc sign in glaucoma?

A. Bayonetting
B. Nasalization of vessels
C. Disc edema (Correct Answer)
D. Large cup

Explanation: In glaucoma, the primary pathological process is **progressive optic neuropathy** characterized by the death of retinal ganglion cells and loss of the neuroretinal rim. This leads to **pathological cupping**, not swelling. **Why Disc Edema is the Correct Answer:** Disc edema (swelling) is a sign of axonal stasis and increased volume of the optic nerve head. It is typically seen in conditions like papilledema (raised intracranial pressure), optic neuritis, or ischemic optic neuropathy. In contrast, glaucoma is a "hollowing out" process. While rare "splinter hemorrhages" (Drance hemorrhages) occur in glaucoma, the disc itself remains pale and excavated, never edematous. **Explanation of Incorrect Options (Glaucomatous Signs):** * **Bayonetting Sign:** This occurs when a vessel climbing out of the deep cup makes a sharp, 90-degree turn at the disc margin, appearing broken or shifted. * **Nasalization of Vessels:** As the cup expands temporally, the central retinal vessels are pushed toward the nasal side of the optic disc. * **Large Cup:** An increased Cup-Disc Ratio (CDR) >0.5 or asymmetry between eyes >0.2 is a hallmark of glaucomatous damage. **High-Yield Clinical Pearls for NEET-PG:** * **ISNT Rule:** In a normal disc, the neuroretinal rim thickness follows the order Inferior > Superior > Nasal > Temporal. Glaucoma often causes **notching**, usually starting at the inferior or superior poles, violating this rule. * **Laminar Dot Sign:** Exposure of the fenestrations of the lamina cribrosa due to deep cupping. * **Baring of Circumlinear Vessels:** A space develops between the vessel and the disc rim as the rim recedes. * **Alpha and Beta Zones:** Peripapillary atrophy; the **Beta zone** (adjacent to the disc) is more specific for glaucoma.

Practice by Chapter

Aqueous Humor Dynamics

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Primary Open-Angle Glaucoma

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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

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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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