Glaucoma Practice Questions

Q: Uveoscleral outflow is increased by which of the following medications?

Bimatoprost. **Explanation:** The intraocular pressure (IOP) is regulated by the balance between aqueous humor production and its drainage. Aqueous drainage occurs via two pathways: the **Trabecular (conventional) pathway** (~90%) and the **Uveoscleral (unconventional) pathway** (~10%). **Why Bimatoprost is correct:** Bimatoprost is a **Prostaglandin Analogue (PGA)**. PGAs are the most potent topical drugs for lowering IOP. They work primarily by remodeling the extracellular matrix in the ciliary muscle, thereby reducing resistance and **increasing uveoscleral outflow**. This makes them the first-line treatment for Primary Open Angle Glaucoma (POAG). **Analysis of Incorrect Options:** * **A. Timolol:** A non-selective Beta-blocker. It lowers IOP by **decreasing the production** of aqueous humor from the ciliary body epithelium, rather than affecting outflow. * **C. Mannitol:** An osmotic diuretic. It works by creating an osmotic gradient that **draws water out of the vitreous humor** into the bloodstream. It is used for emergency reduction of IOP in acute congestive glaucoma. * **D. Dorzolamide:** A topical Carbonic Anhydrase Inhibitor (CAI). Like beta-blockers, it reduces IOP by **inhibiting aqueous humor secretion**. **High-Yield Clinical Pearls for NEET-PG:** * **PGA Side Effects:** Increased iris pigmentation (heterochromia), lengthening of eyelashes (trichomegaly), and deepening of the upper eyelid sulcus. * **Drug of Choice:** PGAs are the DOC for POAG; Pilocarpine (a miotic) increases **trabecular** outflow and is the DOC for Angle Closure Glaucoma (pre-iridotomy). * **Contraindication:** Avoid PGAs in inflammatory glaucoma (uveitic glaucoma) as they are pro-inflammatory.

Q: A middle-aged man presents with unilateral headache, right eye congestion and pain, accompanied by sudden vision loss. What is the most likely diagnosis?

Angle Closure Glaucoma. ### Explanation The clinical presentation of a middle-aged patient with **unilateral headache, eye pain, congestion (ciliary flush), and sudden vision loss** is a classic description of an **Acute Attack of Angle Closure Glaucoma (AACG)**. **1. Why Option A is Correct:** In AACG, there is a sudden mechanical obstruction of the aqueous outflow at the iridocorneal angle, leading to a rapid and severe rise in Intraocular Pressure (IOP). This high IOP causes: * **Pain & Headache:** Due to trigeminal nerve stimulation. * **Congestion:** Ciliary injection resulting from vascular engorgement. * **Vision Loss:** Caused by corneal edema (due to endothelial pump failure at high IOP) and potential optic nerve ischemia. **2. Why Other Options are Incorrect:** * **Option B (Corneal Edema):** This is a *sign* of glaucoma, not a primary diagnosis. While it causes blurred vision and halos, it doesn't explain the systemic symptoms like severe headache. * **Option C (CRVO):** Presents as sudden, painless loss of vision. Fundus examination typically shows a "blood and thunder" appearance (disc edema and flame-shaped hemorrhages). * **Option D (CRAO):** Presents as sudden, painless, profound loss of vision. Key findings include a "cherry-red spot" at the macula and a milky-white retina. **3. NEET-PG High-Yield Pearls:** * **Classic Triad:** Fixed mid-dilated pupil, hazy cornea (steamy), and a "stony hard" eye on palpation. * **Precipitating Factors:** Mydriatics, dark rooms (cinema halls), or emotional stress. * **Immediate Management:** IV Mannitol (osmotic diuretic) and Acetazolamide to lower IOP, followed by topical Pilocarpine (miotic) once IOP drops. * **Definitive Treatment:** Peripheral Iridotomy (usually YAG laser) for both the affected and the fellow (prophylactic) eye.

Q: What is a common symptom of open-angle glaucoma?

Difficulty in dark adaptation. **Explanation:** **Primary Open-Angle Glaucoma (POAG)** is often called the "silent thief of sight" because it is typically asymptomatic in the early stages. However, as the disease progresses, patients frequently experience **difficulty in dark adaptation**. This occurs due to the progressive loss of peripheral rod photoreceptors and retinal ganglion cells, which are essential for vision in low-light conditions. As the visual field constricts (tunnel vision), the patient’s ability to navigate dimly lit environments significantly diminishes. **Analysis of Incorrect Options:** * **A. Sudden loss of vision:** This is characteristic of Acute Angle-Closure Glaucoma or vascular events like Central Retinal Artery Occlusion. POAG causes a slow, painless, and progressive loss of vision. * **C. Amaurosis fugax:** This refers to transient monocular blindness, usually caused by retinal emboli or carotid artery disease, not elevated intraocular pressure. * **D. Uniocular diplopia:** This is typically caused by refractive errors, cataracts (incipient stage), or iris abnormalities (polycoria), rather than glaucomatous nerve damage. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Visual Field Defect:** Paracentral scotoma (specifically in Bjerrum’s area). * **Earliest Sign:** Increase in cup-disc ratio or disc pallor. * **Gold Standard for Diagnosis:** Goldmann Applanation Tonometry (IOP) and Automated Perimetry (Visual Fields). * **Treatment of Choice:** Prostaglandin analogues (e.g., Latanoprost) are the first-line medical therapy.

Q: A 66-year-old patient presents to the emergency department with sudden onset of severe pain and blurred vision in the right eye. Examination reveals decreased visual acuity with a shallow and hazy cornea in the affected eye. The eye has a stony hard consistency. What is the likely diagnosis?

Glaucoma. The clinical presentation described is a classic case of **Acute Angle-Closure Glaucoma (AACG)**, a medical emergency characterized by a sudden, critical rise in intraocular pressure (IOP). ### Why Glaucoma is Correct The diagnosis is confirmed by the triad of **sudden severe pain**, **blurred vision** (due to corneal edema), and a **"stony hard" eye** on palpation. The "stony hard" consistency is a pathognomonic sign of severely elevated IOP. The **shallow anterior chamber** and **hazy cornea** (corneal edema) occur because the high pressure forces fluid into the corneal stroma and compromises the drainage angle. ### Why Other Options are Incorrect * **Keratitis:** While it causes pain and blurred vision, it typically presents with a corneal ulcer or infiltrate and a normal-depth anterior chamber. It does not cause a "stony hard" eye. * **Uveitis:** Acute anterior uveitis presents with pain and photophobia, but the pupil is usually **constricted (miotic)** and the IOP is often low or normal. In AACG, the pupil is typically **mid-dilated and vertically oval**. * **Conjunctivitis:** This presents with discharge, grittiness, and redness, but **never** with severe pain, loss of vision, or increased eye hardness. ### NEET-PG High-Yield Pearls * **Classic Triad:** Severe ocular pain, colored halos (due to corneal edema), and vomiting (often misdiagnosed as a GI issue). * **Pupil Sign:** Mid-dilated, vertically oval, and non-reactive to light. * **Immediate Management:** IV Acetazolamide and topical pilocarpine (once IOP drops below 40 mmHg). * **Definitive Treatment:** Peripheral Iridotomy (Laser or Surgical) for both the affected and the fellow (prophylactic) eye.

Q: Which retinal nerve fibres are most sensitive to glaucomatous damage?

Superior and inferior arcuate fibres. **Explanation:** In glaucoma, the primary site of damage is the optic nerve head. The **superior and inferior arcuate fibres** (also known as the Bjerrum area fibres) are the most sensitive to increased intraocular pressure (IOP). This susceptibility is due to the structural anatomy of the **Lamina Cribrosa**. The pores in the superior and inferior poles of the lamina cribrosa are larger and provide less structural support to the nerve fiber bundles compared to the nasal and temporal sectors. Consequently, these fibers are the first to undergo mechanical compression and ischemic damage, leading to characteristic early glaucomatous field defects like Seidel’s scotoma and Arcuate (Bjerrum) scotoma. **Analysis of Incorrect Options:** * **B. Macular fibres:** These form the papillomacular bundle. They are highly resistant to early glaucomatous damage and are typically the last to be affected, which is why "central vision" is preserved until the end-stage of the disease. * **C & D. Radiating fibres:** These fibers are located in the nasal retina. While they can be affected as the disease progresses (forming a nasal step), they are not as vulnerable as the arcuate bundles in the early stages. **High-Yield Clinical Pearls for NEET-PG:** * **ISNT Rule:** In a healthy eye, the Neuroretinal Rim thickness follows the order Inferior > Superior > Nasal > Temporal. In glaucoma, this rule is broken (Inferior and Superior thinning occurs first). * **Early Field Defect:** The earliest clinically significant field defect is often the **Nasal (Roenne’s) Step**, but the most characteristic early defect is the **Siedel’s scotoma**. * **10-2 Perimetry:** Used specifically when only macular fibers remain (advanced glaucoma) to monitor the remaining central visual field.

Q: In acute congestive glaucoma, what is the typical pupil appearance?

Oval and vertical. In **Acute Congestive Glaucoma** (Acute Angle Closure Glaucoma), the sudden and severe rise in intraocular pressure (IOP) leads to ischemia and paralysis of the iris sphincter muscle. ### Why the pupil is Oval and Vertical: The correct answer is **B**. The extreme elevation of IOP (often >60 mmHg) causes pressure-induced ischemia of the iris stroma. The iris sphincter muscle becomes paretic (paralyzed), particularly in the superior and inferior segments. This segmental paralysis, combined with the radial pull of the dilator muscle, results in a **vertically oval, mid-dilated, and non-reactive pupil**. ### Why the other options are incorrect: * **A. Oval and horizontal:** This is not a standard clinical finding in glaucoma. Vertical elongation is the hallmark due to the specific distribution of iris ischemia. * **C. Circular:** A circular pupil is seen in normal eyes or in cases of pharmacological miosis/mydriasis. In acute glaucoma, the pupil loses its circularity due to segmental muscle failure. * **D. Slit-like:** Slit-like pupils are characteristic of certain animals (like cats) or may occur in specific iris traumas/congenital anomalies (e.g., persistent pupillary membrane), but not in acute glaucoma. ### High-Yield Clinical Pearls for NEET-PG: * **The Triad of Acute Glaucoma:** Mid-dilated vertical oval pupil + Steamy/Cloudy cornea + Stony hard eyeball on palpation. * **Symptoms:** Sudden onset excruciating pain, halos around lights (due to corneal edema), and vomiting (often misdiagnosed as an abdominal emergency). * **Immediate Management:** IV Mannitol (osmotic diuretic) and Acetazolamide to lower IOP, followed by topical Pilocarpine (once IOP drops below 40 mmHg) and definitive **Laser Peripheral Iridotomy (LPI)**. * **Glaukomflecken:** Small, grey-white anterior subcapsular lens opacities—a pathognomonic sign of a previous attack of acute angle closure.

Q: An elderly male with a history of glaucoma presents with a bulging cornea on examination. What is the most likely diagnosis?

Staphyloma. ### Explanation **Correct Answer: B. Staphyloma** The correct answer is **Staphyloma**. A staphyloma is a localized bulging of the outer coat of the eye (sclera or cornea) lined by uveal tissue. In the context of chronic, uncontrolled glaucoma, the persistent elevation of intraocular pressure (IOP) leads to thinning and stretching of the ocular coats. When the cornea thins and bulges forward due to high IOP, it is specifically termed an **Anterior Staphyloma**. This is a classic complication of secondary glaucoma following corneal perforation or severe thinning. **Why other options are incorrect:** * **Keratoconus (A):** While this involves a cone-shaped bulging of the cornea, it is a non-inflammatory, progressive thinning disorder usually bilateral and unrelated to high intraocular pressure or glaucoma. * **Glaucomatous iridocyclitis (C):** This refers to inflammation of the iris and ciliary body associated with glaucoma (e.g., Posner-Schlossman Syndrome). It presents with cells/flare in the anterior chamber, not a structural bulging of the cornea. * **Keratomalacia (D):** This is corneal melting and necrosis caused by severe Vitamin A deficiency. While it can lead to perforation and subsequent staphyloma, the term itself refers to the acute melting process, not the chronic bulging state. **Clinical Pearls for NEET-PG:** * **Definition:** Staphyloma = Ectasia (thinning) + Uveal tissue lining. * **Types of Staphyloma:** * **Anterior:** Involves the cornea (common after perforated corneal ulcers). * **Intercalary:** At the limbus (up to the ciliary body). * **Ciliary:** Over the ciliary body (2–8 mm behind the limbus). * **Equatorial:** At the exit of vortex veins. * **Posterior:** At the posterior pole (common in Pathological Myopia). * **Buphthalmos:** In **Congenital Glaucoma**, the *entire* eyeball enlarges (distensible sclera in infants), whereas Staphyloma is a *localized* bulge in adults.

Question 1

A 52-year-old female presented with a sudden attack of painful diminution of vision in the right eye, accompanied by colored halos and vomiting after watching a movie in a theater. On examination, the eye was stony hard. What is the first-line drug to be administered in this condition?

Accepted Answer

Acetazolamide

Answer

Mannitol

Answer

Latanoprost

Answer

Pilocarpine

Question 2

Uveoscleral outflow is increased by which of the following medications?

Accepted Answer

Bimatoprost

Answer

Timolol

Answer

Mannitol

Answer

Dorzolamide

Question 3

A middle-aged man presents with unilateral headache, right eye congestion and pain, accompanied by sudden vision loss. What is the most likely diagnosis?

Accepted Answer

Angle Closure Glaucoma

Answer

Corneal edema

Answer

Central Retinal Vein Occlusion (CRVO)

Answer

Central Retinal Artery Occlusion (CRAO)

Question 4

What is a common symptom of open-angle glaucoma?

Accepted Answer

Difficulty in dark adaptation

Answer

Sudden loss of vision

Answer

Amaurosis fugax

Answer

Uniocular diplopia

Question 5

A 75-year-old patient presents with deterioration of vision. On examination, the pupillary reflex is observed to be sluggish, and the intraocular pressure is normal. Optic disc evaluation shows a large and deep cup, and the visual field primarily shows paracentral scotomas. What is the most likely diagnosis?

Accepted Answer

Normal tension glaucoma

Answer

Primary narrow-angle glaucoma

Answer

Neovascular glaucoma

Answer

Absolute glaucoma

Question 6

A 66-year-old patient presents to the emergency department with sudden onset of severe pain and blurred vision in the right eye. Examination reveals decreased visual acuity with a shallow and hazy cornea in the affected eye. The eye has a stony hard consistency. What is the likely diagnosis?

Accepted Answer

Glaucoma

Answer

Keratitis

Answer

Uveitis

Answer

Conjunctivitis

Question 7

Which of the following procedures does not require pupillary dilation?

Accepted Answer

Gonioscopy

Answer

Fundus examination

Answer

Laser inferometry

Answer

Retinoscopy

Question 8

Which retinal nerve fibres are most sensitive to glaucomatous damage?

Accepted Answer

Superior and inferior arcuate fibres

Answer

Macular fibres

Answer

Superior radiating fibres

Answer

Inferior radiating fibres

Question 9

In acute congestive glaucoma, what is the typical pupil appearance?

Accepted Answer

Oval and vertical

Answer

Oval and horizontal

Answer

Circular

Answer

Slit-like

Question 10

An elderly male with a history of glaucoma presents with a bulging cornea on examination. What is the most likely diagnosis?

Accepted Answer

Staphyloma

Answer

Keratoconus

Answer

Glaucomatous iridocyclitis

Answer

Keratomalacia

Glaucoma — MCQs

Glaucoma — MCQs

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