Glaucoma Practice Questions

Q: Which of the following is NOT a feature of congenital glaucoma?

Shallow anterior chamber. In congenital glaucoma (Buphthalmos), the primary pathology is a developmental defect in the trabecular meshwork (trabeculodysgenesis) that leads to increased intraocular pressure (IOP) in an infant's eye. **Why "Shallow Anterior Chamber" is the correct answer:** In congenital glaucoma, the eye is highly distensible. The increased IOP causes the entire globe to enlarge (Buphthalmos). As the cornea and sclera stretch, the **anterior chamber becomes characteristically deep**, not shallow. A shallow anterior chamber is typically a feature of primary angle-closure glaucoma in adults, where the eye is anatomically small (hypermetropic). **Explanation of other options:** * **Haab’s Striae:** These are horizontal or curvilinear breaks in the Descemet’s membrane caused by the stretching of the cornea. They are a hallmark clinical sign. * **Blue Sclera:** The sclera in infants is thin. When it stretches due to high IOP, the underlying uveal tissue (choroid) shows through, giving the sclera a bluish appearance. * **Corneal Edema:** This is often the first sign noticed by parents. High IOP causes fluid to enter the corneal stroma and epithelium, leading to cloudiness, photophobia, and lacrimation. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Symptoms:** Photophobia, Blepharospasm, and Lacrimation (Epiphora). * **Corneal Diameter:** Diagnosis is suspected if the diameter is >12 mm before age 1. * **Management:** The treatment is primarily **surgical**. The procedures of choice are **Goniotomy** (if the cornea is clear) or **Trabeculotomy** (if the cornea is hazy). * **Barkan’s Membrane:** A controversial persistent embryonic tissue layer that may cover the trabecular meshwork.

Q: Hypersecretory glaucoma is seen in which of the following conditions?

Epidemic dropsy. **Explanation:** **Epidemic dropsy** is the correct answer because it is one of the few clinical conditions characterized by **hypersecretory glaucoma**. This condition occurs due to the consumption of mustard oil adulterated with **Argemone mexicana** oil. The toxic alkaloid **Sanguinarine** increases the permeability of the ciliary body capillaries and stimulates the secretion of aqueous humor. This leads to a significant rise in intraocular pressure (IOP) despite an open drainage angle. **Analysis of Incorrect Options:** * **Marfan’s Syndrome:** This is associated with **ectopia lentis** (typically superotemporal subluxation). Glaucoma in Marfan’s is usually secondary to pupillary block or angle anomalies, not hypersecretion. * **Hypertension:** While systemic hypertension can slightly increase IOP by increasing ultrafiltration, it does not cause a specific clinical entity known as hypersecretory glaucoma. * **Diabetes:** Diabetes is a risk factor for Primary Open Angle Glaucoma (POAG) and can lead to **Neovascular Glaucoma** (due to rubeosis iridis), which is a type of secondary closed-angle glaucoma. **Clinical Pearls for NEET-PG:** * **Triad of Epidemic Dropsy:** Bilateral pitting edema of legs, gastrointestinal symptoms, and cardiac failure. * **Ocular Findings:** The glaucoma is typically **bilateral, painless, and associated with a wide-open angle**. * **Key Pathophysiology:** Sanguinarine inhibits Na+/K+ ATPase and increases prostaglandin levels, leading to increased aqueous production and dilated uveal vessels. * **Treatment:** The primary treatment is the removal of the adulterated oil; medical management of IOP is secondary. Miotics (like Pilocarpine) are generally avoided as they may worsen inflammation.

Q: A patient presents with a miotic pupil of size 2 mm in diameter. The intraocular pressure (IOP) is 25 mm Hg. The cornea is hazy. The anterior chamber is shallow in the fellow eye. What is the most probable diagnosis?

Acute anterior uveitis. ### Explanation The key to solving this clinical scenario lies in the **pupillary findings**. **1. Why Acute Anterior Uveitis is correct:** In **Acute Anterior Uveitis**, the hallmark pupillary finding is a **miotic (constricted) pupil**, caused by iris sphincter spasm and the presence of inflammatory mediators. While uveitis typically presents with low IOP (due to ciliary body exhaustion), it can present with **elevated IOP** (Hypertensive Uveitis) if inflammatory debris or cells clog the trabecular meshwork. The "hazy cornea" is due to inflammatory keratic precipitates or mild edema. **2. Why the other options are incorrect:** * **Acute Congestive Glaucoma (ACG):** This is the most common distractor. While ACG presents with high IOP, a hazy cornea, and a shallow AC, the pupil is characteristically **vertically oval and semi-dilated (4–6 mm)**, not miotic. * **Chronic Simple Glaucoma (POAG):** This is a painless, chronic condition. It typically presents with a clear cornea, normal AC depth, and no acute pupillary changes. * **Endophthalmitis:** While this presents with a hazy cornea and high/low IOP, it is usually a post-surgical or traumatic complication characterized by severe pain, loss of vision, and a **hypopyon**; it does not specifically present with a 2 mm miotic pupil as a defining feature. **Clinical Pearls for NEET-PG:** * **The "Golden Rule" for Pupils:** * Miotic pupil + High IOP = Hypertensive Uveitis. * Mid-dilated/Oval pupil + High IOP = Acute Angle Closure Glaucoma. * **Shallow AC in the fellow eye:** This indicates a "predisposing eye" for angle closure, but the pupillary size (2 mm) remains the pathognomonic sign that points away from ACG in this specific question. * **Management Tip:** In uveitis, we use **Mydriatics** (Atropine) to break synechiae and relieve pain; in ACG, we use **Miotics** (Pilocarpine) to open the angle. Using the wrong one can worsen the condition.

Q: Which of the following is NOT used in the treatment of glaucoma?

Atropine. **Explanation:** The goal of glaucoma treatment is to lower intraocular pressure (IOP) by either decreasing aqueous humor production or increasing its outflow. **Why Atropine is the correct answer:** Atropine is a **potent cycloplegic and mydriatic** (anti-muscarinic). It causes pupillary dilation (mydriasis), which leads to the bunching up of the iris tissue toward the peripheral angle. In patients with narrow angles, this can precipitate **Acute Angle Closure Glaucoma**. Furthermore, by paralyzing the ciliary muscle (cycloplegia), it reduces the tension on the trabecular meshwork, potentially decreasing aqueous outflow. Therefore, Atropine is generally **contraindicated** in glaucoma. **Analysis of incorrect options:** * **Latanoprost (Option A):** A Prostaglandin F2α analogue. It is the first-line treatment for Open Angle Glaucoma, acting by increasing **uveoscleral outflow**. * **Brinzolamide (Option C):** A topical **Carbonic Anhydrase Inhibitor**. It reduces IOP by decreasing the production of aqueous humor from the ciliary body epithelia. * **Mannitol (Option D):** An **osmotic diuretic**. It is used as an emergency systemic agent to rapidly lower IOP in acute congestive glaucoma by drawing fluid out of the vitreous humor into the bloodstream. **Clinical Pearls for NEET-PG:** * **Drug of choice (DOC)** for Primary Open Angle Glaucoma: **Latanoprost**. * **DOC** for Acute Angle Closure Glaucoma: **IV Mannitol** (to lower IOP) and **Acetazolamide**; definitive treatment is **Laser Peripheral Iridotomy**. * **Miotics (Pilocarpine)** were historically used to open the angle, whereas **Mydriatics (Atropine)** can trigger a crisis. * **Side effect of Latanoprost:** Increased iris pigmentation, thickening/lengthening of eyelashes, and cystoid macular edema.

Q: Malignant glaucoma is seen in which of the following conditions?

After surgery for cataract or glaucoma. **Explanation:** **Malignant Glaucoma**, also known as **Ciliary Block Glaucoma** or **Aqueous Misdirection Syndrome**, is a rare but vision-threatening complication. **Why Option B is Correct:** The underlying mechanism is the **misdirection of aqueous humor** into the vitreous cavity rather than the posterior chamber. This causes an increase in vitreous volume, which pushes the lens-iris diaphragm forward, resulting in a shallowing of the anterior chamber and a secondary rise in intraocular pressure (IOP). It most commonly occurs as a postoperative complication following **cataract surgery** or **filtering surgery (trabeculectomy)**, especially in patients with a history of primary angle-closure glaucoma. **Why Other Options are Incorrect:** * **Option A (Malignancy):** Despite the name, "malignant" glaucoma is not a neoplastic condition. The term was historically used because it was "malignant" to treatment (resistant to conventional therapy). * **Option C & D (Trauma/Thrombosis):** While trauma can cause secondary glaucoma (e.g., angle recession or ghost cell glaucoma) and thrombosis (Central Retinal Vein Occlusion) can lead to Neovascular Glaucoma, they are not the primary triggers for the aqueous misdirection seen in malignant glaucoma. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Presentation:** Shallowing of both the central and peripheral anterior chamber in the presence of high IOP, typically following surgery. * **Key Risk Factor:** Small eyes (Hypermetropia/Microphthalmos) and previous angle-closure. * **Medical Management:** Mydriatic-cycloplegics (e.g., **Atropine**) are the drug of choice to pull the ciliary body back and tighten the zonules. **Avoid miotics (Pilocarpine)** as they worsen the condition. * **Definitive Treatment:** Nd:YAG laser capsulotomy/hyaloidotomy or Pars Plana Vitrectomy (to remove the misdirected fluid).

Q: A patient presents with diabetic macular edema and glaucoma. Which of the following drugs should be used last for this patient?

Prostaglandin analogues. **Explanation:** The correct answer is **Prostaglandin analogues (PGAs)**. **Why PGAs are the last choice:** Prostaglandin analogues (e.g., Latanoprost, Bimatoprost) work by increasing the uveoscleral outflow. However, they are known to increase the levels of endogenous prostaglandins, which can lead to a breakdown of the blood-aqueous and blood-retinal barriers. This mechanism significantly increases the risk of developing or worsening **Cystoid Macular Edema (CME)**. In a patient who already has **Diabetic Macular Edema (DME)**, PGAs are generally avoided or used as a last resort to prevent further retinal thickening and vision loss. **Analysis of Incorrect Options:** * **Alpha agonists (e.g., Brimonidine):** These are generally safe in diabetic patients. Brimonidine may even have potential neuroprotective properties, making it a viable option. * **Acetazolamide (Carbonic Anhydrase Inhibitor):** This is actually beneficial in some cases of macular edema. Systemic or topical CAIs are often used to help "pump" fluid out of the subretinal space and reduce edema. * **Beta blockers (e.g., Timolol):** These are standard first-line treatments for glaucoma and do not have a direct adverse effect on the macula or retinal edema. **NEET-PG High-Yield Pearls:** * **PGA Side Effects:** Iris heterochromia (permanent), hypertrichosis (increased eyelash growth), and deepening of the upper eyelid sulcus. * **Contraindications for PGAs:** Active uveitis (pro-inflammatory), history of Herpetic Keratitis, and patients with/at risk of CME (Aphakia, Pseudophakia with torn posterior capsule, or DME). * **Drug of choice for DME:** Intravitreal Anti-VEGF (e.g., Ranibizumab, Bevacizumab).

Q: In Fincham's test, what is observed?

Glaucomatous halo remains intact. **Explanation:** **Fincham’s Test** (also known as the Stenopeic Slit Test) is a clinical bedside test used to differentiate between halos caused by **Glaucoma** (corneal edema) and those caused by **Immature Cataract** (lenticular changes). 1. **Why Option A is Correct:** In **Glaucoma**, halos are produced by corneal edema (specifically fluid in the corneal epithelium). When a stenopeic slit is passed across the pupil, the light rays are refracted uniformly by the diffuse edema. Therefore, the **glaucomatous halo remains intact** and does not break into segments. 2. **Why the Other Options are Incorrect:** * **Option B:** In an **Immature Cataract**, halos are caused by the radial arrangement of lens fibers acting as a diffraction grating. When a stenopeic slit is moved across, the halo **breaks into segments** (it disappears in some areas and remains in others). * **Option C:** Halos in **Mucopurulent Conjunctivitis** are caused by mucus flakes on the corneal surface. These halos are transient and typically **disappear after washing the eyes** or blinking; they are not characterized by "breaking into segments" via the Fincham test. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Glaucomatous halos are due to the accumulation of fluid in the corneal epithelium (diffraction of light). * **Differential Diagnosis of Halos:** * **Glaucoma:** Halo is circular, intact on Fincham's test, and associated with high IOP. * **Cataract:** Halo breaks into segments on Fincham's test. * **Conjunctivitis:** Halo disappears after blinking/washing. * **Color Sequence:** In both glaucoma and cataract, the halo is colored (blue is innermost and red is outermost).

Q: Which field of vision is the last to be affected in chronic simple glaucoma?

Temporal. In Chronic Simple Glaucoma (Primary Open Angle Glaucoma), the pattern of visual field loss follows a specific sequence due to the arrangement of nerve fibers in the retina. **Explanation of the Correct Answer:** The **Temporal field** is the last to be lost. This occurs because the nerve fibers corresponding to the temporal field are located on the **nasal side of the optic disc**. These nasal fibers are the most resistant to glaucomatous damage compared to the arcuate fibers (which form Bjerrum’s area). Consequently, even in advanced stages, a small "temporal island" of vision often persists alongside a small central pocket. **Analysis of Incorrect Options:** * **Nasal Field:** This is typically the **first** area to show significant loss (e.g., Roenne’s nasal step). Glaucoma preferentially affects the superior and inferior poles of the optic nerve, leading to early defects in the nasal field. * **Peripheral Field:** Peripheral vision is lost progressively throughout the disease. While the extreme temporal periphery is the last to go, the general "peripheral field" is compromised long before the final stages. * **Central Field:** Central vision is remarkably preserved until the very late stages (forming "tubular vision"), but it is usually lost **just before** the temporal island disappears. **Clinical Pearls for NEET-PG:** * **Sequence of Loss:** Nasal field → Peripheral field → Central field → Temporal field. * **Tubular Vision:** A late-stage finding where only a small central island (5–10 degrees) remains. * **10-2 Perimetry:** Used specifically to monitor patients with advanced glaucoma who have only central/temporal islands remaining. * **ISNT Rule:** In glaucoma, the Inferior and Superior neuroretinal rims are thinned first; the Nasal rim is the last to be affected (correlating to the temporal field).

Q: Which of the following is NOT a mechanism in hemolytic glaucoma?

Inflammation. **Explanation:** Hemolytic glaucoma is a type of **secondary open-angle glaucoma** caused by the breakdown of red blood cells (RBCs) following a long-standing vitreous hemorrhage. **Why "Inflammation" is the correct answer:** Hemolytic glaucoma is a **non-inflammatory** condition. The rise in intraocular pressure (IOP) is purely mechanical, caused by the physical obstruction of the trabecular meshwork by cellular debris and hemoglobin products. If inflammation were present (e.g., macrophages ingesting RBCs and blocking the angle), the condition would be termed **Phacolytic-like** or specifically **Ghost Cell Glaucoma** (though these are distinct entities, the absence of active uveitis is a hallmark of hemolytic glaucoma). **Analysis of incorrect options:** * **RBC clogging the trabeculae:** This is the primary mechanism. Intact RBCs, cell membranes, and debris migrate from the vitreous into the anterior chamber, physically obstructing aqueous outflow. * **Deposition of haemosiderin:** As RBCs lyse, they release hemoglobin. This is broken down into hemosiderin, which is then phagocytosed by macrophages or deposited directly into the trabecular tissues. * **Siderosis of trabeculae:** Iron released from the hemoglobin (hemosiderin) can have a direct toxic effect on the trabecular meshwork cells (siderosis), leading to further sclerosis and reduced outflow facility. **High-Yield Clinical Pearls for NEET-PG:** * **Ghost Cell Glaucoma:** Occurs when rigid, less pliable "ghost cells" (empty RBC membranes) block the trabeculae. * **Hemosiderotic Glaucoma:** A subset where iron toxicity causes permanent damage to the trabecular meshwork. * **Clinical Sign:** Look for "red-tinted" cells in the anterior chamber and a history of vitreous hemorrhage (e.g., from trauma or diabetic retinopathy). * **Treatment:** Primarily involves washing out the anterior chamber and managing IOP; the underlying vitreous hemorrhage may require vitrectomy.

Q: Which of the following statements regarding the optic nerve head is NOT true?

The neuroretinal rim is thickest superiorly.. The correct answer is **D** because it violates the **ISNT rule**, a fundamental clinical concept in glaucoma assessment. ### 1. Why Option D is Incorrect (The Correct Answer) The neuroretinal rim (NRR) follows the **ISNT rule**, which dictates the order of rim thickness in a healthy optic nerve head. The rim is thickest **Inferiorly**, followed by **Superiorly**, then **Nasally**, and is thinnest **Temporally** (I > S > N > T). In glaucoma, the inferior and superior rims are typically the first to undergo thinning (notching), leading to a reversal or violation of this rule. ### 2. Analysis of Other Options * **Option A:** The optic nerve head is vertically oval. Its average dimensions are approximately **1.76 mm (horizontal) by 1.92 mm (vertical)**. Recognizing these dimensions helps clinicians identify "large discs" which may have physiological cupping. * **Option B:** Embryologically, the optic nerve (and its head) develops from the **optic stalk**, which connects the optic vesicle to the forebrain. * **Option C:** Aqueous humor drainage occurs via two pathways: the **Trabecular (conventional) pathway**, accounting for **90%** of outflow, and the **Uveoscleral (unconventional) pathway**, accounting for approximately **10%**. ### 3. High-Yield Clinical Pearls for NEET-PG * **ISNT Rule Violation:** The earliest sign of glaucomatous damage is often thinning of the inferior neuroretinal rim. * **Bayoneting Sign:** Characterized by the sharp angulation of vessels as they exit the cup and pass over the rim. * **Laminar Dot Sign:** Visibility of the pores of the lamina cribrosa due to the loss of nerve fibers in advanced glaucoma. * **Normal Cup-Disc Ratio (CDR):** Usually ≤ 0.3; an asymmetry of > 0.2 between the two eyes is highly suggestive of glaucoma.

Question 1

Which of the following is NOT a feature of congenital glaucoma?

Accepted Answer

Shallow anterior chamber

Answer

Haab's striae

Answer

Blue sclera

Answer

Corneal edema

Question 2

Hypersecretory glaucoma is seen in which of the following conditions?

Accepted Answer

Epidemic dropsy

Answer

Marfan's syndrome

Answer

Hypertension

Answer

Diabetes

Question 3

A patient presents with a miotic pupil of size 2 mm in diameter. The intraocular pressure (IOP) is 25 mm Hg. The cornea is hazy. The anterior chamber is shallow in the fellow eye. What is the most probable diagnosis?

Accepted Answer

Acute anterior uveitis

Answer

Acute congestive glaucoma

Answer

Chronic simple glaucoma

Answer

Endophthalmitis

Question 4

Which of the following is NOT used in the treatment of glaucoma?

Accepted Answer

Atropine

Answer

Latanoprost

Answer

Brinzolamide

Answer

Mannitol

Question 5

Malignant glaucoma is seen in which of the following conditions?

Accepted Answer

After surgery for cataract or glaucoma

Answer

Malignancy

Answer

Trauma

Answer

Thrombosis

Question 6

A patient presents with diabetic macular edema and glaucoma. Which of the following drugs should be used last for this patient?

Accepted Answer

Prostaglandin analogues

Answer

Alpha agonist

Answer

Acetazolamide

Answer

Beta blockers

Question 7

In Fincham's test, what is observed?

Accepted Answer

Glaucomatous halo remains intact

Answer

Halo due to immature cataract does not break into segments

Answer

Halo due to mucopurulent conjunctivitis is broken into segments

Answer

All of the above

Question 8

Which field of vision is the last to be affected in chronic simple glaucoma?

Accepted Answer

Temporal

Answer

Nasal

Answer

Peripheral

Answer

Central

Question 9

Which of the following is NOT a mechanism in hemolytic glaucoma?

Accepted Answer

Inflammation

Answer

Siderosis of trabeculae

Answer

Deposition of haemosiderin

Answer

RBC clogging the trabeculae

Question 10

Which of the following statements regarding the optic nerve head is NOT true?

Accepted Answer

The neuroretinal rim is thickest superiorly.

Answer

Its average dimensions are 1.76 mm horizontally by 1.92 mm vertically.

Answer

It develops from the optic stalk.

Answer

Anterior chamber outflow is 90-95% aqueous, and uveoscleral outflow is 10%.

Glaucoma — MCQs

Glaucoma — MCQs

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