Glaucoma Practice Questions

Q: Trabeculectomy for glaucoma leads to the formation of a channel between which two spaces?

Subconjunctival space and anterior chamber. **Explanation:** Trabeculectomy is the "gold standard" filtering surgery for glaucoma. The primary goal of the procedure is to create a new drainage pathway for aqueous humor to bypass the obstructed trabecular meshwork, thereby lowering intraocular pressure (IOP). **Why Option A is Correct:** During a trabeculectomy, a partial-thickness scleral flap is created, and a small piece of the limbal tissue (including the trabecular meshwork) is removed to create an opening into the **anterior chamber**. The aqueous humor flows through this opening, under the scleral flap, and into the **subconjunctival space**. This results in the formation of a **filtering bleb**, where the fluid is eventually absorbed by the conjunctival capillaries and lymphatics. **Why Other Options are Incorrect:** * **Option B:** A channel between the anterior and posterior chambers is created during a **Peripheral Iridectomy (PI)** or YAG laser iridotomy, used to treat angle-closure glaucoma by equalizing pressure between the two chambers. * **Option C:** This is anatomically incorrect for glaucoma filtration. The posterior chamber is located behind the iris; draining fluid directly from here to the subconjunctival space is not the standard surgical approach for trabeculectomy. **High-Yield Clinical Pearls for NEET-PG:** * **Antimetabolites:** Mitomycin-C (MMC) or 5-Fluorouracil (5-FU) are often applied during surgery to inhibit fibroblast proliferation and prevent bleb scarring (the most common cause of failure). * **Iridectomy:** A "peripheral iridectomy" is always performed during trabeculectomy to prevent the iris from plugging the internal ostium. * **Success Indicator:** The presence of a diffuse, shallow, and minimally vascularized **filtering bleb** indicates a functioning shunt.

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: 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 most common cause of rubeosis iridis?

Diabetic retinopathy. **Explanation:** **Rubeosis iridis** (neovascularization of the iris) is a serious condition where new, fragile blood vessels form on the iris surface in response to chronic retinal ischemia. **Why Diabetic Retinopathy is Correct:** The underlying mechanism is **retinal hypoxia**, which triggers the release of **Vascular Endothelial Growth Factor (VEGF)**. VEGF diffuses into the anterior segment, stimulating angiogenesis. **Diabetic Retinopathy (DR)**, specifically Proliferative Diabetic Retinopathy (PDR), is the **most common cause** of rubeosis iridis worldwide due to the high prevalence of the disease and the extensive retinal ischemia it induces. **Analysis of Incorrect Options:** * **Central Retinal Artery Occlusion (CRAO):** While CRAO causes ischemia, it is a less common cause of rubeosis (occurring in ~2% of cases) compared to Central Retinal Vein Occlusion (CRVO) or DR. * **Radiation Retinopathy:** This can cause rubeosis due to capillary non-perfusion, but it is a rare clinical entity compared to the systemic burden of diabetes. * **Tumors:** Intraocular tumors like retinoblastoma or melanoma can cause rubeosis via angiogenic factors, but they are statistically infrequent causes. **High-Yield Clinical Pearls for NEET-PG:** 1. **Top 3 Causes:** 1. Diabetic Retinopathy (Most common), 2. Central Retinal Vein Occlusion (CRVO - specifically the ischemic type, often called "100-day glaucoma"), 3. Carotid Artery Occlusive Disease. 2. **Complication:** Rubeosis iridis leads to **Neovascular Glaucoma (NVG)** as the new vessels and associated fibrous membranes pull the iris forward, causing synechial angle closure. 3. **Management:** The mainstay of treatment is **Pan-retinal Photocoagulation (PRP)** to reduce the ischemic drive, often supplemented by anti-VEGF injections.

Q: Vogt's triad of primary angle closure glaucoma does not include which of the following?

Fixed pupils. **Explanation:** **Vogt’s Triad** consists of clinical signs that indicate a **previous episode** of acute congestive angle-closure glaucoma. These signs are essentially "scars" or permanent markers left behind after the intraocular pressure (IOP) has normalized. 1. **Why "Fixed Pupils" is the correct answer:** While a **vertically oval, mid-dilated, and fixed pupil** is a classic sign of an *active* acute attack (due to sphincter ischemia), it is not part of Vogt’s Triad. The triad specifically refers to post-congestive sequelae, whereas a fixed pupil is a feature of the acute stage itself. 2. **Analysis of the Triad components (Incorrect Options):** * **Glaukomflecken (Option B):** These are small, grey-white subcapsular lenticular opacities caused by focal necrosis of the lens epithelium due to high IOP. They are pathognomonic of a prior acute attack. * **Pigment deposition on corneal endothelium (Option C):** During an attack, the iris rubs against the lens and cornea, releasing pigment. This pigment settles on the endothelium (often as a Krukenberg-like distribution) once the attack subsides. * **Patches of iris atrophy (Option D):** Ischemia during the pressure spike leads to sectorial atrophy of the iris stroma, often resulting in permanent structural changes and pigment loss. **High-Yield Clinical Pearls for NEET-PG:** * **Vogt’s Triad:** Glaukomflecken + Iris Atrophy + Endothelial Pigment. * **Acute Attack Presentation:** Sudden painful loss of vision, "halos" around lights (due to corneal edema), and a stony-hard eye. * **Management:** The definitive treatment for the fellow eye in angle closure is **Prophylactic Laser Peripheral Iridotomy (LPI)**, as the condition is usually bilateral. * **Glaukomflecken** is often described as "milk-white spots" and is one of the most reliable signs that a patient has suffered a significant hypertensive crisis in the eye.

Q: Kusumlata presents with acute painful red eye and a mildly dilated, vertically oval pupil. What is the most likely diagnosis?

Acute angle closure glaucoma. ### Explanation **Correct Answer: B. Acute angle closure glaucoma** The clinical presentation of an **acute painful red eye** associated with a **mildly dilated, vertically oval, and non-reactive pupil** is a classic "textbook" description of **Acute Angle Closure Glaucoma (AACG)**. In AACG, a sudden rise in intraocular pressure (IOP) causes ischemia and paralysis of the iris sphincter muscle. This results in the characteristic mid-dilated, vertically oval pupil. Other associated features include a "steamy" or hazy cornea (due to epithelial edema), a shallow anterior chamber, and severe ocular pain often accompanied by nausea and vomiting. **Why the other options are incorrect:** * **A. Acute retrobulbar neuritis:** Characterized by sudden vision loss and pain on eye movement, but the eye appears **"white and quiet"** externally. The pupil typically shows an Afferent Pupillary Defect (RAPD/Marcus Gunn pupil), not a mid-dilated oval shape. * **C. Acute anterior uveitis:** While it presents with a painful red eye, the pupil is typically **small (miotic)** and irregular due to the formation of posterior synechiae. * **D. Severe kerato-conjunctivitis:** Presents with redness and discharge; however, the pupil size and reaction remain **normal**, and there is no significant rise in IOP. **High-Yield Clinical Pearls for NEET-PG:** * **Immediate Management:** Systemic Acetazolamide (IV/Oral) and hyperosmotic agents (Mannitol/Glycerol) to lower IOP, followed by topical Pilocarpine (once IOP <40 mmHg) and definitive **Peripheral Iridotomy (Laser or Surgical)**. * **The "Vertical Oval" Pupil:** This occurs because the vertical fibers of the iris sphincter are more susceptible to ischemic paralysis than the horizontal ones. * **Differential Diagnosis Tip:** Always check the pupil! * *Miosis (Constricted):* Uveitis. * *Mid-dilated/Oval:* Glaucoma. * *Normal:* Conjunctivitis.

Question 1

Trabeculectomy for glaucoma leads to the formation of a channel between which two spaces?

Accepted Answer

Subconjunctival space and anterior chamber

Answer

Anterior chamber and posterior chamber

Answer

Subconjunctival space and posterior chamber

Answer

None of the above

Question 2

Which procedure is being done in the patient?

Accepted Answer

Indentation tonometry

Answer

Applanation tonometry

Answer

A scan ultrasonography

Answer

Keratometry

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

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 5

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

Accepted Answer

Corneal oedema

Answer

Increase IOP

Answer

Lenticular changes

Answer

Lacrimation

Question 6

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 7

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 8

What is the most common cause of rubeosis iridis?

Accepted Answer

Diabetic retinopathy

Answer

Tumor

Answer

Central retinal artery occlusion (CRAO)

Answer

Radiation retinopathy

Question 9

Vogt's triad of primary angle closure glaucoma does not include which of the following?

Accepted Answer

Fixed pupils

Answer

Glaucoma flecks

Answer

Pigment deposition on corneal endothelium

Answer

Patches of iris atrophy

Question 10

Kusumlata presents with acute painful red eye and a mildly dilated, vertically oval pupil. What is the most likely diagnosis?

Accepted Answer

Acute angle closure glaucoma

Answer

Acute retrobulbar neuritis

Answer

Acute anterior uveitis

Answer

Severe kerato-conjunctivitis

Glaucoma — MCQs

Glaucoma — MCQs

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