Glaucoma Practice Questions

Q: What is the earliest drug used in the management of acute angle closure glaucoma?

Diamox. In the management of **Acute Angle Closure Glaucoma (AACG)**, the primary goal is to rapidly lower the intraocular pressure (IOP) to prevent optic nerve damage and clear corneal edema. **Why Diamox (Acetazolamide) is the correct answer:** Diamox is a potent **Carbonic Anhydrase Inhibitor** that acts systemically to decrease the production of aqueous humor by the ciliary body. In an acute attack, the IOP is often so high (frequently >50-60 mmHg) that the iris sphincter becomes ischemic and unresponsive to topical miotics. Therefore, systemic medication like intravenous or oral Acetazolamide is the **earliest and most effective** first-line treatment to break the attack and lower the pressure enough for other treatments to work. **Analysis of Incorrect Options:** * **Pilocarpine:** While it is the definitive medical treatment to open the angle (miotic), it **cannot work initially** when IOP is very high because the iris sphincter is paralyzed by ischemia. It is usually administered only after the IOP has been lowered by systemic agents. * **Atropine:** This is a mydriatic (dilates the pupil). It is **strictly contraindicated** in AACG as it would further crowd the angle and worsen the condition. * **DFP (Diisopropyl Fluorophosphate):** This is a potent, irreversible cholinesterase inhibitor. It is not used in acute glaucoma because it can cause intense congestion and potentially worsen the pupillary block. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Management:** 1. Systemic Hyperosmotics (Mannitol) or CAIs (Diamox) → 2. Topical Beta-blockers → 3. Topical Pilocarpine (once IOP <30 mmHg). * **Definitive Treatment:** The definitive treatment for AACG is **Laser Peripheral Iridotomy (LPI)**, performed on both the affected and the fellow (prophylactic) eye. * **Side Effects of Diamox:** Watch for paresthesia, hypokalemia, and metabolic acidosis. It is contraindicated in patients with sulfonamide allergies.

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.

Question 1

What is the earliest drug used in the management of acute angle closure glaucoma?

Accepted Answer

Diamox

Answer

Pilocarpine

Answer

Atropine

Answer

DFP

Question 2

What is the earliest functional change in glaucoma?

Accepted Answer

Baring of the blind spot

Answer

Papilloedema

Answer

Hazy cornea

Answer

Sickle scotoma

Question 3

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 4

Uveoscleral outflow is increased by which of the following medications?

Accepted Answer

Bimatoprost

Answer

Timolol

Answer

Mannitol

Answer

Dorzolamide

Question 5

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 6

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 7

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 8

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 9

Which of the following procedures does not require pupillary dilation?

Accepted Answer

Gonioscopy

Answer

Fundus examination

Answer

Laser inferometry

Answer

Retinoscopy

Question 10

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

Glaucoma — MCQs

Glaucoma — MCQs

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