Glaucoma Practice Questions

Q: What is the earliest sign in the visual field suggestive of glaucoma?

Isopter contraction. **Explanation:** In the context of glaucoma, visual field defects follow a specific chronological sequence. Understanding this progression is vital for NEET-PG. **1. Why Isopter Contraction is Correct:** The earliest clinical sign of glaucoma in the visual field is **Isopter Contraction**. This refers to a generalized constriction of the visual field, particularly to small or dim targets. It occurs due to the diffuse loss of retinal nerve fibers before localized scotomas become apparent. Specifically, "generalized depression" of the field is the very first change, followed by peripheral isopter contraction. **2. Analysis of Incorrect Options:** * **Baring of the Blind Spot:** This was historically considered an early sign, where the physiological blind spot appears to "open" into the peripheral field. However, it is now considered **non-specific**, as it can occur in normal individuals due to pupil size or refractive errors. * **Seidel’s Scotoma:** This is a sickle-shaped extension of the blind spot (either upwards or downwards). While it is an early sign, it occurs **after** isopter contraction and generalized depression. * **Arcuate (Bjerrum) Scotoma:** This is a late-stage defect where Seidel’s scotoma extends to meet the horizontal raphe, forming a complete arch. It indicates significant nerve fiber layer damage. **Clinical Pearls for NEET-PG:** * **Earliest Change overall:** Generalized depression/Isopter contraction. * **Earliest *Specific* Change:** Small, isolated paracentral scotomas (usually in Bjerrum’s area, 10°–20° from fixation). * **Roenne’s Nasal Step:** A defect that respects the horizontal midline on the nasal side; it is a characteristic feature of glaucomatous damage. * **Gold Standard for Diagnosis:** Automated Perimetry (e.g., Humphrey Field Analyzer) is the current standard for detecting these defects.

Q: Which anti-glaucoma drug is known to cause black deposits in the conjunctiva?

Adrenaline. **Explanation:** The correct answer is **Adrenaline (Option C)**. **Mechanism of Action & Side Effects:** Adrenaline (Epinephrine) was historically used as a topical anti-glaucoma agent to increase aqueous outflow. However, its use is now limited due to significant local side effects. The "black deposits" mentioned are known as **Adrenochrome deposits**. These occur because adrenaline undergoes oxidation into a pigment called adrenochrome, which gets trapped in the conjunctival stroma or within the follicles of the palpebral conjunctiva. These deposits are typically asymptomatic but can be mistaken for a foreign body or a pigmented lesion. **Analysis of Other Options:** * **Alpha blockers (e.g., Brimonidine):** These are commonly associated with **follicular conjunctivitis** and allergic blepharoconjunctivitis, but they do not cause black pigmentation. * **Prostaglandin analogues (e.g., Latanoprost):** These are notorious for causing **iris hyperpigmentation** (turning light eyes brown), eyelash lengthening (trichomegaly), and periorbital skin darkening, but they do not cause discrete black deposits in the conjunctiva. * **Carbonic anhydrase inhibitors (e.g., Dorzolamide):** These primarily cause local stinging, a bitter taste (dysgeusia), and rarely, punctate keratitis, but no pigmentary changes. **High-Yield Clinical Pearls for NEET-PG:** * **Adrenochrome deposits:** Look for the keyword "black/brown spots" in the conjunctiva or fornix. * **Adrenaline Contraindication:** It is strictly contraindicated in **Angle-Closure Glaucoma** because it can cause pupillary dilation (mydriasis), potentially precipitating an acute attack. * **Cystoid Macular Edema (CME):** Adrenaline can cause CME in **aphakic** patients (those without a lens). * **Dipivefrin:** A prodrug of adrenaline designed to have better penetration and fewer systemic side effects.

Q: Which of the following is NOT a characteristic of neovascularization of the iris?

Do not cross the scleral spur. **Explanation:** Neovascularization of the Iris (NVI), also known as **Rubeosis Iridis**, is a pathological process driven by retinal ischemia. It is a hallmark of Neovascular Glaucoma (NVG). **Why Option C is the correct answer:** Unlike normal iris vessels, which are radial and do not cross the scleral spur, **neovascular vessels are abnormal and characteristically cross the scleral spur** to reach the trabecular meshwork. Once they cross the spur, they form a fibrovascular membrane that contracts, leading to peripheral anterior synechiae (PAS) and secondary angle-closure glaucoma. Therefore, saying they "do not cross" is incorrect. **Analysis of Incorrect Options:** * **Option A:** Neovascular vessels are thin, fragile, and lack a muscularis layer, making them appear **fine and irregular** compared to the thicker, radial normal iris vessels. * **Option B:** NVI typically begins at the **pupillary margin** (often seen as tiny red tufts) and progresses toward the **ciliary border and the iridocorneal angle**. * **Option C:** Ischemia leads to the release of **Vascular Endothelial Growth Factor (VEGF)**. This is the primary chemical mediator that stimulates the proliferation of these new, leaky vessels. **High-Yield Clinical Pearls for NEET-PG:** * **Commonest causes:** Central Retinal Vein Occlusion (CRVO)—specifically the ischemic type—and Proliferative Diabetic Retinopathy (PDR). * **The "100-Day Glaucoma":** A classic term for NVG following ischemic CRVO, typically occurring around 3 months post-event. * **Treatment:** Pan-retinal photocoagulation (PRP) to reduce the VEGF load and Anti-VEGF injections (e.g., Ranibizumab, Bevacizumab).

Q: A male patient with insulin-dependent diabetes and macular edema develops glaucoma. Which medication should be used as a last resort for treatment?

Prostaglandin analogue. ### Explanation The correct answer is **Prostaglandin analogue (PGA)**. **Why Prostaglandin Analogues are the Last Resort:** In this clinical scenario, the patient has **Diabetes Mellitus** and existing **Macular Edema**. Prostaglandin analogues (e.g., Latanoprost) 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 barrier. This can exacerbate or induce **Cystoid Macular Edema (CME)**. In a patient who already has diabetic macular edema, PGAs are generally avoided or used as a last resort to prevent worsening of the central vision. **Analysis of Other Options:** * **Alpha Agonists (e.g., Brimonidine):** These are generally safe in diabetics but should be used with caution in patients with cardiovascular disease. They do not have a direct contraindication related to macular edema. * **Pilocarpine:** This is a miotic (cholinergic). While it can cause side effects like brow ache or retinal detachment in predisposed individuals, it does not specifically worsen macular edema. * **Beta Blockers (e.g., Timolol):** These are often first-line agents. While they must be avoided in patients with asthma or heart block, they do not adversely affect macular edema. **High-Yield Clinical Pearls for NEET-PG:** * **PGA Side Effects:** Iris heterochromia (permanent), lengthening of eyelashes (hypertrichosis), and activation of Herpes Simplex Keratitis. * **Drug of Choice (DOC):** PGAs are the DOC for Primary Open Angle Glaucoma (POAG) due to high efficacy and once-daily dosing, *except* when inflammatory conditions or macular edema are present. * **Brimonidine:** Can cause "Granulomatous Anterior Uveitis" and is contraindicated in infants due to CNS depression (apnea).

Q: Which of the following symptoms is characteristic of acute angle closure glaucoma?

Colored haloes are present. **Explanation:** **Acute Angle Closure Glaucoma (AACG)** is a sight-threatening emergency characterized by a sudden rise in intraocular pressure (IOP) due to the mechanical obstruction of the trabecular meshwork by the peripheral iris. **Why "Colored Haloes" is Correct:** In AACG, the sudden and severe elevation of IOP causes the corneal endothelium to fail, leading to **corneal edema**. The excess fluid in the corneal stroma and epithelium acts as a diffraction grating, splitting white light into its constituent spectral colors. This phenomenon is known as **Fincham’s Test** positive. Patients typically report seeing "rainbow-colored haloes" around bright lights. **Why Other Options are Incorrect:** * **B. Flashes of light (Photopsia):** This is a classic symptom of **vitreoretinal traction** or retinal detachment, not glaucoma. In AACG, patients experience severe pain and blurred vision, but not flashes. * **C. The anterior chamber is deep:** This is anatomically incorrect for AACG. A **shallow anterior chamber** is a primary predisposing factor for angle closure. A deep anterior chamber is more characteristic of conditions like high myopia or aphakia. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of AACG:** Mid-dilated non-reactive pupil, hazy/steamy cornea, and a stony-hard globe on palpation. * **Systemic Symptoms:** AACG often presents with nausea, vomiting, and severe headache, which can be misdiagnosed as an acute abdominal or neurological emergency. * **Immediate Management:** IV Mannitol (to lower IOP), Acetazolamide, and topical Pilocarpine (once IOP drops below 40 mmHg). * **Definitive Treatment:** **Laser Peripheral Iridotomy (LPI)** is the gold standard for both the affected and the fellow (prophylactic) eye.

Q: In the investigation of open-angle glaucoma, which of the following is LEAST commonly performed?

Indirect ophthalmoscopy. In the management of Primary Open-Angle Glaucoma (POAG), the diagnostic focus is on intraocular pressure (IOP), optic nerve head (ONH) morphology, and visual field analysis. **Why Indirect Ophthalmoscopy is the Correct Answer:** Indirect ophthalmoscopy (IDO) is primarily used for peripheral retinal examination. While it provides a wide field of view, it offers **low magnification (3x–5x)**, which is insufficient for the detailed evaluation of the optic disc cup, neuroretinal rim, and peripapillary atrophy required in glaucoma. Therefore, it is the least common tool for routine glaucoma assessment compared to methods that offer higher magnification. **Analysis of Incorrect Options:** * **Tonometry (B):** This is a fundamental screening and monitoring tool used to measure IOP. Goldmann Applanation Tonometry (GAT) remains the gold standard. * **Direct Ophthalmoscopy (C):** Although being replaced by slit-lamp biomicroscopy (using 78D/90D lenses), direct ophthalmoscopy provides **high magnification (15x)**, allowing for the visualization of subtle disc changes like Drance hemorrhages or cup-to-disc ratio (CDR) changes. It is a standard bedside/clinic tool for ONH evaluation. * **Perimetry (D):** Automated Perimetry (e.g., Humphrey Visual Field) is the gold standard for detecting and monitoring functional visual field defects (e.g., Bjerrum’s scotoma) in glaucoma. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for ONH Evaluation:** Slit-lamp biomicroscopy with a 78D or 90D lens (provides stereoscopic view). * **Early Sign of Glaucoma:** Ischaemic changes at the poles (Notching) and Nerve Fiber Layer (NFL) defects (Hoyt’s changes). * **Key Triad of POAG:** 1. Raised IOP (>21 mmHg), 2. Optic disc cupping, 3. Characteristic visual field defects. * **Pachymetry:** Essential to measure Central Corneal Thickness (CCT), as thin corneas can underestimate true IOP.

Q: What is the drug of choice for acute congestive glaucoma?

1-2% pilocarpine. **Explanation:** **Acute Congestive Glaucoma** (Acute Angle-Closure Glaucoma) is a medical emergency characterized by a sudden rise in intraocular pressure (IOP) due to mechanical closure of the anterior chamber angle by the peripheral iris. **Why Pilocarpine is the Drug of Choice:** Pilocarpine is a direct-acting parasympathomimetic (miotic). In angle-closure glaucoma, the primary goal is to pull the iris away from the trabecular meshwork to open the drainage angle. Pilocarpine causes **miosis** (contraction of the sphincter pupillae), which stretches the iris tissue, thinning it and pulling it out of the angle, thereby restoring aqueous outflow. *Note:* In clinical practice, systemic hyperosmotics (like Mannitol) or Acetazolamide are often given first to lower IOP before pilocarpine can work effectively, as the sphincter muscle is often ischemic when IOP is >40-50 mmHg. **Analysis of Incorrect Options:** * **B & C (Timolol/Levobunanol):** These are topical Beta-blockers. While they help reduce aqueous production and are used as adjunctive therapy, they do not address the underlying mechanical obstruction (the closed angle). * **D (Atropine):** This is a potent **mydriatic** (dilator). It is strictly **contraindicated** in narrow-angle glaucoma as it causes iris crowding in the angle, potentially worsening or precipitating an acute attack. **High-Yield Clinical Pearls for NEET-PG:** * **Definitive Treatment:** The definitive treatment for acute angle-closure glaucoma is **Peripheral Iridotomy (Laser or Surgical)**. * **The "Mid-Dilated" Pupil:** A vertically oval, semi-dilated, non-reactive pupil is a classic sign of an acute attack. * **Prophylaxis:** Always perform a prophylactic laser iridotomy in the fellow (contralateral) eye, as it is anatomically predisposed to a similar attack.

Q: What is the term for trabeculae blocked by lens proteins?

Lens protein glaucoma. ### Explanation The correct answer is **Lens protein glaucoma**, also traditionally known as **Phacolytic glaucoma**. #### 1. Underlying Medical Concept In a hypermature or morgagnian cataract, high-molecular-weight lens proteins leak through the intact but microscopic pores of the lens capsule into the aqueous humor. These proteins, along with macrophages that have ingested them, physically obstruct the trabecular meshwork. This leads to a sudden rise in intraocular pressure (IOP), characterized by a deep anterior chamber and white "fluffs" or floating particles in the aqueous. #### 2. Analysis of Incorrect Options * **A. Lens particle glaucoma:** This occurs when the lens capsule is **ruptured** (due to trauma or surgery), allowing actual fragments of lens cortex to physically block the trabecular meshwork. * **C. Phacotopic glaucoma:** This refers to glaucoma secondary to **lens displacement** (ectopia lentis), such as subluxation or dislocation, which can cause pupillary block. * **D. Phacomorphic glaucoma:** This is a secondary **angle-closure** glaucoma caused by an intumescent (swollen) lens that pushes the iris forward, narrowing the iridocorneal angle. #### 3. NEET-PG High-Yield Pearls * **Phacolytic vs. Phacomorphic:** Phacolytic presents with a **deep** anterior chamber; Phacomorphic presents with a **shallow** anterior chamber. * **Key Histology:** The presence of **eosinophilic material** and **macrophages** in the aqueous is pathognomonic for phacolytic (lens protein) glaucoma. * **Management:** Immediate medical reduction of IOP followed by urgent cataract extraction (SICS/Phacoemulsification). * **Triad of Phacolytic Glaucoma:** Hypermature cataract + High IOP + Deep anterior chamber with cells/flare.

Q: A patient presents with a reddish eye and excessive watering of the left eye, accompanied by a shallow anterior chamber. What is the next best investigation?

Tonometry. ### Explanation The clinical presentation of a **red eye, excessive watering (epiphora), and a shallow anterior chamber** is highly suggestive of **Acute Angle-Closure Glaucoma (AACG)**. In any suspected case of glaucoma, the immediate priority is to confirm the diagnosis by measuring the **Intraocular Pressure (IOP)**. **1. Why Tonometry is the Correct Answer:** Tonometry is the gold standard for measuring IOP. In AACG, the IOP is typically severely elevated (often >40-60 mmHg). Establishing this elevation is the most critical "next step" to initiate emergency management (e.g., IV Mannitol, Acetazolamide) to prevent permanent optic nerve damage. **2. Why Other Options are Incorrect:** * **Gonioscopy:** While essential to visualize the angle and confirm "closure," it is technically difficult to perform during an acute attack due to corneal edema (haze). It is usually performed after the IOP is lowered and the cornea clears. * **Cup-to-disc (C:D) ratio & Ophthalmoscopy:** These assess the optic nerve head for chronic glaucomatous damage. In an acute attack, the priority is the pressure, not the morphology. Furthermore, corneal edema often obscures the view of the fundus during the initial presentation. **Clinical Pearls for NEET-PG:** * **Gold Standard Tonometry:** Goldmann Applanation Tonometry (GAT). * **Classic Triad of AACG:** Sudden ocular pain, "halos" around lights, and a mid-dilated non-reactive pupil. * **Definitive Treatment:** Peripheral Iridotomy (usually YAG laser) once the acute attack is controlled. * **Shallow Anterior Chamber:** Always predisposes a patient to angle closure; avoid mydriatics in such patients.

Q: What is the Amsler sign associated with?

Fuchs heterochromatic iridocyclitis. **Explanation:** **Fuchs Heterochromatic Iridocyclitis (FHI)** is a chronic, typically unilateral, low-grade uveitis. The **Amsler sign** (also known as the Amsler-Verrey sign) refers to the occurrence of **hyphema** (bleeding into the anterior chamber) following a minor trauma, such as a paracentesis or during intraocular surgery (like cataract extraction). The underlying mechanism is the presence of **fragile, fine neovascular vessels** in the angle of the anterior chamber. These filiform vessels bridge the chamber angle and rupture easily when the intraocular pressure (IOP) drops suddenly, leading to characteristic filiform hemorrhages. **Why other options are incorrect:** * **Posner-Schlossman Syndrome (Glaucomatocyclitic Crisis):** Characterized by recurrent episodes of very high IOP with minimal inflammation. It is not associated with angle neovascularization or the Amsler sign. * **Uveal Effusion Syndrome:** Involves idiopathic exudative detachment of the choroid, ciliary body, and retina. It presents with "leopard spot" pigmentary changes, not hyphema upon surgical entry. **High-Yield Clinical Pearls for FHI:** 1. **Triad:** Heterochromia (affected eye is usually lighter), cataract, and small, stellate keratic precipitates (KPs) distributed over the entire corneal endothelium. 2. **No Synechiae:** Unlike most forms of iridocyclitis, FHI typically does **not** form posterior synechiae. 3. **Treatment:** It generally does not respond well to topical steroids; management focuses on complications like glaucoma and cataract.

Question 1

What is the earliest sign in the visual field suggestive of glaucoma?

Accepted Answer

Isopter contraction

Answer

Baring of the blind spot

Answer

Seidel's scotoma

Answer

Arcuate scotoma

Question 2

Which anti-glaucoma drug is known to cause black deposits in the conjunctiva?

Accepted Answer

Adrenaline

Answer

Alpha blocker

Answer

Prostaglandin analogue

Answer

Carbonic anhydrase inhibitor

Question 3

Which of the following is NOT a characteristic of neovascularization of the iris?

Accepted Answer

Do not cross the scleral spur

Answer

Fine and irregular vessels

Answer

Can be seen on the pupillary border or angle

Answer

Indicate VEGF secretion

Question 4

A male patient with insulin-dependent diabetes and macular edema develops glaucoma. Which medication should be used as a last resort for treatment?

Accepted Answer

Prostaglandin analogue

Answer

Alpha agonist

Answer

Pilocarpine

Answer

Beta blocker

Question 5

Which of the following symptoms is characteristic of acute angle closure glaucoma?

Accepted Answer

Colored haloes are present

Answer

Flashes of light are seen

Answer

The anterior chamber is deep

Answer

All of the above

Question 6

In the investigation of open-angle glaucoma, which of the following is LEAST commonly performed?

Accepted Answer

Indirect ophthalmoscopy

Answer

Tonometry

Answer

Direct ophthalmoscopy

Answer

Perimetry

Question 7

What is the drug of choice for acute congestive glaucoma?

Accepted Answer

1-2% pilocarpine

Answer

Timolol

Answer

Levobunanol

Answer

Atropine

Question 8

What is the term for trabeculae blocked by lens proteins?

Accepted Answer

Lens protein glaucoma

Answer

Lens particle glaucoma

Answer

Phacotopic glaucoma

Answer

Phacomorphic glaucoma

Question 9

A patient presents with a reddish eye and excessive watering of the left eye, accompanied by a shallow anterior chamber. What is the next best investigation?

Accepted Answer

Tonometry

Answer

Cup-to-disc ratio

Answer

Gonioscopy

Answer

Ophthalmoscopy

Question 10

What is the Amsler sign associated with?

Accepted Answer

Fuchs heterochromatic iridocyclitis

Answer

Posner-Schlossman syndrome

Answer

Uveal effusion syndrome

Answer

None of the above

Glaucoma — MCQs

Glaucoma — MCQs

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