Glaucoma Practice Questions

Q: Which procedure is being done in the patient?

Indentation tonometry. ***Indentation tonometry*** - Uses the **Schiotz tonometer** which applies a weighted plunger to the cornea, measuring **intraocular pressure** by the degree of corneal indentation. - The instrument consists of a **footplate** that rests on the cornea and a **weighted plunger** that indents the eye, with pressure readings from a scale. *Applanation tonometry* - Uses the **Goldmann applanation tonometer** which flattens a small area of the cornea rather than indenting it. - Considered the **gold standard** for IOP measurement, requiring **fluorescein dye** and a **cobalt blue light** for visualization. *A scan ultrasonography* - An **ultrasonic technique** used to measure **axial length** of the eye and assess intraocular structures. - Primarily used for **biometry** in cataract surgery planning and detecting **posterior segment pathology**, not for pressure measurement. *Keratometry* - Measures the **curvature of the anterior corneal surface** to determine **corneal astigmatism** and **refractive power**. - Used for **contact lens fitting** and **pre-operative assessment** for refractive surgery, not related to intraocular pressure.

Q: What is the main mechanism of action of brimonidine in glaucoma?

Decreased aqueous humor secretion. **Explanation:** **Brimonidine** is a highly selective **alpha-2 (α2) adrenergic agonist**. Its primary mechanism of action in lowering intraocular pressure (IOP) is twofold, but its **initial and main effect** is the **reduction of aqueous humor production** (secretion) from the ciliary body. 1. **Why Option A is correct:** Alpha-2 receptors are located on the ciliary epithelium. Stimulation of these receptors inhibits the enzyme adenylate cyclase, leading to a decrease in cAMP levels. This biochemical pathway results in a significant reduction in the active secretion of aqueous humor. 2. **Why Option C is partially correct but not the "main" mechanism:** Brimonidine is unique because it has a **dual mechanism**. While it primarily decreases production, it also increases **uveoscleral outflow** (via prostaglandin release). However, in the context of standard examinations like NEET-PG, "decreased secretion" is recognized as the primary/initial action. 3. **Why Options B and D are incorrect:** Brimonidine has no significant effect on the trabecular (conventional) outflow pathway (unlike miotics or Rho-kinase inhibitors). It also does not affect vitreous volume (a mechanism associated with hyperosmotic agents like Mannitol). **High-Yield Clinical Pearls for NEET-PG:** * **Neuroprotection:** Brimonidine is the only antiglaucoma medication currently credited with potential neuroprotective properties for the optic nerve. * **Side Effects:** It is notorious for causing **Lid Retraction** and **Allergic Conjunctivitis** (follicular conjunctivitis). * **Contraindication:** It is strictly **contraindicated in infants and children** (under 2 years) as it can cross the blood-brain barrier, causing CNS depression, apnea, and bradycardia.

Q: What is not true about the ciliary body?

Located at 10 mm from the corneo-scleral junction.. **Explanation:** The ciliary body is a vital part of the uveal tract, extending from the root of the iris to the ora serrata. **Why Option A is the correct answer (False statement):** The ciliary body extends from the limbus (corneo-scleral junction) to approximately **6–7 mm** posteriorly, not 10 mm. Specifically, the pars plicata occupies the first 2 mm, and the pars plana extends for the next 4–4.5 mm. Understanding these dimensions is crucial for surgical procedures like pars plana vitrectomy, where ports are typically placed 3.5–4 mm from the limbus to avoid damaging the lens or retina. **Analysis of incorrect options (True statements):** * **Option B:** Anatomically, it is divided into the **pars plicata** (anterior 2 mm with ciliary processes) and the **pars plana** (posterior 4 mm, relatively avascular). * **Option C:** Contraction of the ciliary muscle (innervated by parasympathetic fibers of the CN III) reduces tension on the zonules. This allows the lens to become more spherical, increasing its refractive power for **accommodation**. * **Option D:** The non-pigmented epithelium of the ciliary processes in the pars plicata actively secretes **aqueous humor** into the posterior chamber. **High-Yield Clinical Pearls for NEET-PG:** * **Blood Supply:** Derived from the long posterior ciliary arteries and anterior ciliary arteries (forming the Major Arterial Circle of the Iris). * **Nerve Supply:** Parasympathetic fibers via the **short ciliary nerves** (from the ciliary ganglion) mediate accommodation. * **Surgical Landmark:** The pars plana is the safest site for intraocular entries (intravitreal injections/vitrectomy) because it is less vascular and lacks retinal tissue.

Q: Iridocorneal endothelial syndrome is associated with which of the following?

Progressive atrophy of iris stroma. **Explanation:** **Iridocorneal Endothelial (ICE) Syndrome** is a rare group of conditions characterized by an abnormal corneal endothelial cell layer that migrates across the anterior chamber angle and onto the iris surface. **Why Option A is Correct:** The hallmark of ICE syndrome is the proliferation of "beaten bronze" appearance endothelial cells. As this abnormal membrane contracts, it leads to **progressive atrophy of the iris stroma**, corectopia (displaced pupil), and pseudopolycoria (multiple holes in the iris). This is most classically seen in the **Essential Iris Atrophy** variant of the syndrome. **Analysis of Incorrect Options:** * **Option B:** ICE syndrome is characteristically **unilateral**. While corneal edema occurs due to endothelial pump failure, the iris involvement is atrophic rather than edematous. * **Options C & D:** The pathology involves the migration of an abnormal endothelial basement membrane over the angle and iris. It does not involve the primary deposition of collagen or glycosaminoglycans within Descemet’s membrane itself. **High-Yield Clinical Pearls for NEET-PG:** * **The Triad of ICE Syndrome:** Includes (1) Progressive Iris Atrophy, (2) Chandler Syndrome (predominant corneal edema), and (3) Cogan-Reese Syndrome (iris nodules/pedunculated lesions). * **Demographics:** Typically affects young to middle-aged females. * **Mechanism of Glaucoma:** Contraction of the abnormal membrane leads to secondary **angle-closure glaucoma** due to the formation of high peripheral anterior synechiae (PAS). * **Specular Microscopy:** Shows characteristic "dark holes" or "ice-pick" appearance of endothelial cells.

Q: Laser trabeculoplasty is indicated in which of the following types of glaucoma?

Pseudoexfoliative glaucoma. **Explanation:** **Laser Trabeculoplasty (ALT/SLT)** works by applying laser energy to the trabecular meshwork (TM) to increase aqueous outflow. For this procedure to be effective and safe, the **angle must be open** and the TM must be visible. 1. **Why Pseudoexfoliative Glaucoma (PXG) is correct:** PXG is a type of secondary open-angle glaucoma. In PXG, there is heavy deposition of pigment and fibrillar material within the trabecular meshwork (Sampaolesi line). This increased pigmentation makes the TM an excellent target for laser absorption, often resulting in a **more profound pressure-lowering response** compared to primary open-angle glaucoma. 2. **Why the other options are incorrect:** * **Neovascular Glaucoma (NVG):** This is a secondary closed-angle glaucoma where a fibrovascular membrane pulls the iris over the TM. Laser trabeculoplasty is ineffective because the TM is physically obstructed. * **Chronic Angle Closure Glaucoma (CACG):** In CACG, the angle is narrowed or closed by peripheral anterior synechiae (PAS). If the TM cannot be visualized, trabeculoplasty cannot be performed. * **Uveitic Glaucoma:** This is a relative contraindication. Laser energy can exacerbate intraocular inflammation, potentially leading to a "spike" in IOP or the formation of further synechiae. **High-Yield Clinical Pearls for NEET-PG:** * **Prerequisite:** A clear, open iridocorneal angle (Gonioscopy is mandatory). * **Mechanism:** Argon Laser Trabeculoplasty (ALT) causes mechanical tightening of the TM; Selective Laser Trabeculoplasty (SLT) uses a "cold laser" to stimulate biological remodeling without thermal damage. * **Best Candidates:** Pigmentary glaucoma and Pseudoexfoliative glaucoma (due to high TM pigmentation). * **Common Complication:** Transient post-operative rise in IOP (IOP spike).

Q: The cause of a coloured halo in narrow angle glaucoma is?

Corneal oedema. **Explanation:** In **Narrow-Angle Glaucoma** (specifically Acute Angle Closure), a sudden and severe rise in Intraocular Pressure (IOP) exceeds the pumping capacity of the corneal endothelium. This leads to the accumulation of fluid within the corneal stroma and epithelium, a condition known as **Corneal Oedema**. The oedematous corneal epithelium acts as a **diffraction grating**, breaking up white light into its constituent spectral colors. This optical phenomenon results in the patient seeing "rainbow-colored halos" around lights. **Analysis of Options:** * **Corneal Oedema (Correct):** This is the direct anatomical cause of the diffraction. Specifically, the fluid droplets between epithelial cells act like tiny prisms. * **Increased IOP (Incorrect):** While high IOP is the *triggering event*, it is not the direct optical cause of the halo. The halo is a secondary effect of the resulting oedema. * **Lenticular changes (Incorrect):** While cataracts (lenticular changes) can cause halos, they are typically "dull" and do not resolve with treatment, unlike the vivid halos of glaucoma which disappear once IOP is lowered. * **Lacrimation (Incorrect):** Excessive tearing may cause blurred vision or light scattering, but it does not produce the classic structured colored halos seen in glaucoma. **High-Yield Clinical Pearls for NEET-PG:** 1. **Finchan’s Test:** Used to differentiate glaucomatous halos from cataractous halos. When a stenopaeic slit is passed across the pupil, glaucomatous halos remain intact, whereas cataractous halos break into segments. 2. **Differential Diagnosis:** Colored halos are also seen in **Mucopurulent Conjunctivitis** (due to mucus flakes; these disappear after washing the eyes/blinking). 3. **Management:** The definitive treatment for Narrow-Angle Glaucoma is **Laser Peripheral Iridotomy (LPI)**.

Q: What is the most common cause of neovascular glaucoma?

Diabetes mellitus. **Explanation:** Neovascular Glaucoma (NVG) is a secondary glaucoma caused by retinal ischemia, which triggers the release of **Vascular Endothelial Growth Factor (VEGF)**. This leads to the formation of new vessels (neovascularization) on the iris (rubeosis iridis) and the anterior chamber angle, eventually causing mechanical obstruction of aqueous outflow. **1. Why Diabetes Mellitus is correct:** **Diabetic Retinopathy (specifically PDR)** is the most common cause of NVG worldwide, accounting for approximately **33-50%** of cases. The chronic, widespread retinal ischemia in diabetic patients provides a persistent stimulus for VEGF production. **2. Analysis of Incorrect Options:** * **Central Retinal Vein Occlusion (CRVO):** This is the **second** most common cause. Ischemic CRVO is famously associated with "100-day glaucoma" because NVG typically develops within 3 months of the event. While it is a classic association, statistically, Diabetes is more frequent. * **Central Retinal Artery Occlusion (CRAO):** This is a rare cause of NVG (approx. 1-5% of cases). Since the inner retina is infarcted, there is often insufficient viable tissue to produce sustained VEGF compared to venous stasis or diabetes. * **Eale’s Disease:** While this idiopathic peripheral perivasculitis causes ischemia and neovascularization, it is a much less common cause of NVG compared to systemic metabolic diseases like Diabetes. **Clinical Pearls for NEET-PG:** * **The "100-Day Glaucoma":** Specifically refers to NVG following **Ischemic CRVO**. * **Sequence of NVG:** Rubeosis iridis (at pupillary margin) → Neovascularization of the angle (NVA) → Open-angle stage → **Synechial Angle-closure stage** (contracture of fibrovascular membrane). * **Management Gold Standard:** **Pan-retinal Photocoagulation (PRP)** to reduce the ischemic drive, often combined with Anti-VEGF injections.

Q: What is the classical sign of neovascular glaucoma?

Iris neovascularization. **Explanation:** **Neovascular Glaucoma (NVG)** is a secondary glaucoma caused by retinal ischemia, most commonly due to Central Retinal Vein Occlusion (CRVO) or Proliferative Diabetic Retinopathy (PDR). **Why Option D is Correct:** The hallmark of NVG is **Iris neovascularization (Rubeosis Iridis)**. When the retina becomes ischemic, it releases Vascular Endothelial Growth Factor (VEGF). This factor diffuses forward into the anterior segment, stimulating the growth of new, fragile vessels on the iris surface and in the iridocorneal angle. These vessels are accompanied by a fibrovascular membrane that eventually contracts, pulling the peripheral iris toward the cornea (Peripheral Anterior Synechiae), leading to secondary angle-closure glaucoma. **Why Other Options are Incorrect:** * **A & B (Retinal/Disc Neovascularization):** While these often coexist with NVG (as they share the same ischemic trigger), they are signs of the underlying retinal disease (like PDR) rather than the defining clinical sign of the glaucoma itself. * **C (Ciliary Body Neovascularization):** This is not a standard clinical sign of NVG. The pathological process primarily involves the iris and the trabecular meshwork. **High-Yield Clinical Pearls for NEET-PG:** * **"100-Day Glaucoma":** A classic term for NVG occurring approximately 3 months after an Ischemic CRVO. * **Clinical Stages:** It begins as *Pre-glaucoma* (Rubeosis only), progresses to *Open-angle* (vessels blocking the meshwork), and ends in *Angle-closure* (membrane contraction). * **Management:** The mainstay of treatment is **Pan-retinal Photocoagulation (PRP)** to reduce the ischemic drive, often combined with Anti-VEGF injections. * **Early Sign:** Neovascularization usually first appears at the **pupillary margin** before spreading to the angle.

Question 1

Which procedure is being done in the patient?

Accepted Answer

Indentation tonometry

Answer

Applanation tonometry

Answer

A scan ultrasonography

Answer

Keratometry

Question 2

Pilocarpine is not used in young adults as it causes:

Accepted Answer

Myopia

Answer

Retinal detachment

Answer

Iris cysts

Answer

Shallow anterior chamber

Question 3

What is the main mechanism of action of brimonidine in glaucoma?

Accepted Answer

Decreased aqueous humor secretion

Answer

Increased trabecular outflow

Answer

Increased uveoscleral outflow

Answer

Reduced vitreous volume

Question 4

What is not true about the ciliary body?

Accepted Answer

Located at 10 mm from the corneo-scleral junction.

Answer

Consists of the pars plana and pars plicata.

Answer

Contraction of the ciliary body aids in accommodation.

Answer

Secretes aqueous humor.

Question 5

Iridocorneal endothelial syndrome is associated with which of the following?

Accepted Answer

Progressive atrophy of iris stroma

Answer

Bilateral stromal edema of iris and cornea

Answer

Deposition of collagen in Descemet's membrane

Answer

Deposition of glycosaminoglycan in Descemet's membrane

Question 6

Laser trabeculoplasty is indicated in which of the following types of glaucoma?

Accepted Answer

Pseudoexfoliative glaucoma

Answer

Neovascular glaucoma

Answer

Chronic angle closure glaucoma

Answer

Uveitic glaucoma

Question 7

The cause of a coloured halo in narrow angle glaucoma is?

Accepted Answer

Corneal oedema

Answer

Increase IOP

Answer

Lenticular changes

Answer

Lacrimation

Question 8

What is the most common cause of neovascular glaucoma?

Accepted Answer

Diabetes mellitus

Answer

Central retinal artery occlusion (CRAO)

Answer

Central retinal vein occlusion (CRVO)

Answer

Eale's disease

Question 9

A patient with open-angle glaucoma and 7 diopters of myopia complains of blurring of vision after administration of pilocarpine. What is the reason for this blurring?

Accepted Answer

Miosis (small pupil)

Answer

Increased myopic asymmetry

Answer

Increased hypermetropic asymmetry

Answer

Increased astigmatism

Question 10

What is the classical sign of neovascular glaucoma?

Accepted Answer

Iris neovascularization

Answer

Retinal neovascularization

Answer

Disc neovascularization

Answer

Ciliary body neovascularization

Glaucoma — MCQs

Glaucoma — MCQs

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