Glaucoma Practice Questions

Q: Which of the following findings is most helpful in the diagnosis of open-angle glaucoma?

Cupping of the optic disc. **Explanation:** The diagnosis of **Primary Open-Angle Glaucoma (POAG)** relies on a triad of findings: raised intraocular pressure (IOP), characteristic optic disc changes, and corresponding visual field defects. Among the options provided, **cupping of the optic disc** is the most definitive clinical sign of glaucomatous structural damage. 1. **Why Option A is correct:** Glaucoma is essentially an optic neuropathy. Increased IOP or vascular insufficiency leads to the death of retinal ganglion cells, resulting in the enlargement of the "cup" relative to the "disc" (increased Cup-Disc Ratio). Findings like vertical expansion of the cup, thinning of the neuroretinal rim, and **Bayoneting sign** are hallmark diagnostic features that confirm structural damage. 2. **Why other options are incorrect:** * **Option B & D:** The depth and angle of the anterior chamber are used to **classify** the type of glaucoma (Open vs. Angle-closure) via gonioscopy, but they do not diagnose the presence of the disease itself. In POAG, the angle is characteristically normal and open. * **Option C:** Visual acuity often remains 6/6 (normal) until the very advanced stages of POAG, as peripheral vision is lost first. Refractive error (like high myopia) is a risk factor but not a diagnostic finding. **High-Yield Clinical Pearls for NEET-PG:** * **ISNT Rule:** In a normal disc, the thickness of the neuroretinal rim follows the order Inferior > Superior > Nasal > Temporal. Glaucoma often breaks this rule (Inferior/Superior thinning occurs first). * **Goldmann Applanation Tonometry:** The gold standard for measuring IOP. * **Humphrey Visual Field (HVF) Analysis:** The standard for detecting functional damage (e.g., Arcuate/Bjerrum scotoma). * **Early Sign:** The earliest clinical sign of POAG is often an increase in IOP, but the earliest structural sign is often **RNFL (Retinal Nerve Fiber Layer) thinning** on OCT.

Q: Campimetry (Scotometry) is performed in the visual field area of:

30 degrees. **Explanation:** **Campimetry**, also known as **Scotometry**, is a method used to evaluate the central portion of the visual field. The correct answer is **30 degrees** because this technique specifically focuses on mapping the central field and identifying scotomas (blind spots) within this range. * **Why 30 degrees is correct:** Campimetry is traditionally performed using a **Bjerrum’s screen** (a black tangential screen). Since most glaucomatous field defects (like Bjerrum’s scotoma, Seidel’s sign, and Paracentral scotomas) manifest within the central 30 degrees, this area is the clinical focus of the test. * **Why other options are incorrect:** * **50, 60, and 90 degrees** refer to the **peripheral visual field**. While the human visual field extends to approximately 90-100 degrees temporally, Campimetry is not designed to measure these peripheral limits. Peripheral fields are instead assessed using **Perimetry** (e.g., Goldmann Perimeter or Automated Humprey Field Analyzer). **Clinical Pearls for NEET-PG:** * **Bjerrum’s Area:** This is the arcuate area located between **10 to 20 degrees** from the fixation point, where early glaucomatous damage is most frequently detected. * **Distance:** Campimetry is typically performed at a distance of **1 meter** or **2 meters** from the screen. * **Isopter:** A line connecting points with the same visual sensitivity. * **Key Difference:** Remember, **Campimetry** = Central 30° (Flat screen); **Perimetry** = Full field (Arc or Bowl-shaped).

Q: Which of the following drugs is not used topically for the treatment of open-angle glaucoma?

Acetazolamide. **Explanation:** The correct answer is **Acetazolamide** because of its **route of administration**. While it is a potent Carbonic Anhydrase Inhibitor (CAI) used to reduce intraocular pressure (IOP), it is administered **systemically** (oral or intravenous), not topically. **Analysis of Options:** * **Acetazolamide (Option C):** It is a systemic CAI. Due to its significant systemic side effects (paresthesia, metabolic acidosis, hypokalemia, and renal stones), it is generally reserved for short-term management of acute angle-closure glaucoma or as a temporary measure before surgery, rather than long-term topical therapy for open-angle glaucoma. * **Latanoprost (Option A):** A Prostaglandin F2α analogue. It is used **topically** once daily and is currently the first-line treatment for open-angle glaucoma due to its superior efficacy in increasing uveoscleral outflow. * **Brimonidine (Option B):** A selective Alpha-2 agonist used **topically**. It works by decreasing aqueous production and increasing uveoscleral outflow. It also has potential neuroprotective properties. * **Dorzolamide (Option D):** A **topical** Carbonic Anhydrase Inhibitor. It was developed specifically to provide the IOP-lowering benefits of CAIs while avoiding the systemic side effects associated with acetazolamide. **High-Yield Clinical Pearls for NEET-PG:** * **First-line drug for POAG:** Prostaglandin analogues (e.g., Latanoprost). * **Side effect of Latanoprost:** Iris hyperpigmentation, thickening of eyelashes, and cystoid macular edema. * **Side effect of Brimonidine:** Follicular conjunctivitis; it is contraindicated in infants due to the risk of CNS depression/apnea. * **Drug of choice for Acute Angle Closure Glaucoma:** IV Mannitol (osmotic agent) and Acetazolamide.

Q: On mutation, which of the following may give rise to hereditary glaucoma?

Optineurin. ### Explanation **Correct Answer: A. Optineurin** **Mechanism and Clinical Context:** Glaucoma is a group of optic neuropathies characterized by progressive degeneration of retinal ganglion cells (RGCs). While many cases are sporadic, several genes are linked to hereditary forms. **Optineurin (OPTN)**, located on chromosome 10p13, is a high-yield gene associated primarily with **Normal Tension Glaucoma (NTG)** and some forms of Primary Open Angle Glaucoma (POAG). Optineurin is involved in neuroprotection and vesicular trafficking; mutations lead to increased susceptibility of RGCs to apoptosis, even in the absence of elevated intraocular pressure. **Analysis of Incorrect Options:** * **B. Ephrins:** These are proteins involved in cell signaling, particularly in axon guidance and angiogenesis during embryonic development. They are not linked to the pathogenesis of hereditary glaucoma. * **C. RBA8:** This is not a recognized gene or protein associated with ophthalmic pathology or glaucoma genetics. * **D. Huntingtin:** This protein is encoded by the HTT gene. Mutations (CAG repeats) in this gene cause **Huntington’s Disease**, a neurodegenerative disorder characterized by chorea and cognitive decline, but it is not a cause of glaucoma. **High-Yield Clinical Pearls for NEET-PG:** * **MYOC (Myocilin):** The most common gene mutated in Juvenile Open Angle Glaucoma (JOAG) and adult-onset POAG (Chromosome 1q). * **CYP1B1:** The primary gene associated with **Primary Congenital Glaucoma** (Autosomal Recessive). * **PITX2 and FOXC1:** Associated with Axenfeld-Rieger Syndrome (Anterior segment dysgenesis with secondary glaucoma). * **WDR36:** Another gene linked to adult-onset POAG.

Q: A 55-year-old woman presents with acute pain and redness in her right eye, accompanied by nausea, vomiting, and seeing halos around lights. Examination reveals lacrimation, lid edema, conjunctival injection, a steamy cornea, and a fixed mid-dilated pupil. Her intraocular pressure (IOP) is markedly elevated, and visual acuity in the right eye is 20/200. She has no family history of eye diseases. What is the most likely diagnosis?

Acute closed-angle glaucoma. ### Explanation **1. Why Acute Closed-Angle Glaucoma (ACG) is Correct:** This clinical presentation is a classic medical emergency. ACG occurs when the iris-corneal angle closes abruptly, blocking aqueous humor outflow and causing a rapid rise in intraocular pressure (IOP). * **Key Symptoms:** Sudden severe pain, nausea/vomiting (due to vagal stimulation), and **halos around lights** (caused by corneal edema diffracting light). * **Key Signs:** The **fixed, mid-dilated pupil** is pathognomonic (due to iris sphincter ischemia), accompanied by a **"steamy" or "ground-glass" cornea** (epithelial edema) and ciliary injection. **2. Why the Other Options are Incorrect:** * **Corneal Laceration:** While it causes pain and redness, it typically follows trauma and presents with a shallow anterior chamber or a peaked pupil, not a fixed mid-dilated one. * **Ocular Hypertension:** This refers to elevated IOP (>21 mmHg) *without* optic nerve damage or symptoms. It is an asymptomatic, incidental finding. * **Open-Angle Glaucoma:** This is the "silent thief of sight." It is chronic, painless, and bilateral, characterized by progressive peripheral vision loss rather than an acute symptomatic crisis. **3. NEET-PG High-Yield Pearls:** * **Immediate Management:** Systemic Acetazolamide (to decrease production) and topical Pilocarpine (to induce miosis and open the angle). Note: Pilocarpine is ineffective if IOP >40-50 mmHg due to sphincter ischemia. * **Definitive Treatment:** Peripheral Iridotomy (usually YAG laser) in **both eyes** (the fellow eye is at high risk). * **Risk Factors:** Hypermetropia (small eyes), elderly females, and triggers like darkness (mydriasis) or certain medications (anticholinergics). * **Differential Diagnosis:** Must be distinguished from Acute Ureitis (constricted pupil, normal/low IOP).

Q: Argon laser trabeculoplasty is indicated in which of the following conditions?

Open angle glaucoma. **Explanation:** **Argon Laser Trabeculoplasty (ALT)** is a laser procedure designed to increase aqueous outflow by applying thermal energy to the trabecular meshwork. **Why Option D is Correct:** In **Open Angle Glaucoma (OAG)**, the drainage angle is anatomically open, but there is resistance to aqueous outflow within the trabecular meshwork. ALT works by applying laser burns to the junction of the pigmented and non-pigmented trabecular meshwork. This causes localized tissue contraction, which mechanically "stretches" the adjacent untreated meshwork and opens the Schlemm’s canal, thereby reducing intraocular pressure (IOP). It is typically indicated when medical therapy is insufficient or poorly tolerated. **Why Other Options are Incorrect:** * **A. Aphakic Glaucoma:** This is often complex, involving vitreous incarceration or peripheral anterior synechiae (PAS). The trabecular meshwork is frequently distorted, making ALT ineffective. * **B. Neovascular Glaucoma:** This is caused by a fibrovascular membrane pulling the iris over the angle. Laser treatment to the meshwork cannot overcome this mechanical obstruction; treatment focuses on Panretinal Photocoagulation (PRP) or valves. * **C. Closed Angle Glaucoma:** ALT requires a clear view of the trabecular meshwork. In closed-angle glaucoma, the angle is physically obstructed by the iris, making it impossible to visualize or treat the meshwork with ALT. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Laser:** Junction of the anterior (non-pigmented) and posterior (pigmented) trabecular meshwork. * **Selective Laser Trabeculoplasty (SLT):** A newer alternative to ALT that uses a Q-switched Nd:YAG laser. It is "selective" because it targets only pigmented cells without causing thermal damage, making it repeatable (unlike ALT). * **Contraindication:** ALT is ineffective in **Uveitic Glaucoma** due to the risk of increasing inflammation and further scarring of the angle.

Q: Which instrument is used to visualize the angle of the anterior chamber?

Gonioscopy. **Explanation:** **1. Why Gonioscopy is the Correct Answer:** The angle of the anterior chamber cannot be visualized directly through a slit lamp because of **total internal reflection** at the cornea-air interface. Light rays from the angle strike the cornea at an angle greater than the critical angle (approx. 46°), reflecting back into the eye. A **Goniolens** (e.g., Goldmann 3-mirror or Zeiss 4-mirror) eliminates this air-interface, allowing the clinician to visualize structures like the Schwalbe’s line, Trabecular meshwork, Scleral spur, and Ciliary body band. This is essential for differentiating between Open-Angle and Angle-Closure Glaucoma. **2. Why Other Options are Incorrect:** * **Slit lamp examination:** While used to assess the *depth* of the peripheral anterior chamber (Van Herick’s technique), it cannot visualize the internal structures of the angle itself without a specialized lens. * **Keratometry:** This measures the curvature of the anterior corneal surface, primarily used for IOL power calculation and astigmatism assessment. * **Indirect ophthalmoscopy:** This is used for a wide-field examination of the posterior segment (retina and vitreous), not the anterior chamber angle. **3. Clinical Pearls for NEET-PG:** * **Gold Standard:** Gonioscopy remains the clinical gold standard for angle evaluation. * **Van Herick Technique:** A screening method using a slit lamp to estimate angle width before performing gonioscopy. * **Shaffer’s Grading:** The most common system used to grade the angle (Grade 0: Closed; Grade 4: Wide open). * **Direct vs. Indirect Gonioscopy:** Koeppe lens (Direct) provides an upright image (used in surgery); Goldmann/Zeiss (Indirect) provides an inverted image via mirrors.

Q: All of the following findings can be seen in Axenfeld's anomaly, except:

Ectopia of the lens. **Explanation:** Axenfeld-Rieger Syndrome (ARS) is a spectrum of autosomal dominant disorders involving the maldevelopment of the anterior segment (neural crest cell dysgenesis). The correct answer is **Ectopia of the lens**, as it is not a feature of this spectrum; it is instead characteristically associated with conditions like Marfan syndrome, Homocystinuria, or Weill-Marchesani syndrome. **Analysis of Options:** * **Posterior Embryotoxon (Option A):** This is the hallmark of the Axenfeld-Rieger spectrum. It represents an anteriorly displaced and prominent Schwalbe’s line (the junction of Descemet’s membrane and trabecular meshwork). * **Iris Synechiae (Option B):** In Axenfeld’s anomaly, peripheral iris strands (synechiae) extend across the angle to attach to the prominent Schwalbe’s line. * **Glaucoma (Option D):** Approximately 50% of patients with Axenfeld-Rieger spectrum develop glaucoma due to associated angle dysgenesis or secondary obstruction of aqueous outflow by iris strands. **Clinical Pearls for NEET-PG:** * **Axenfeld Anomaly:** Posterior embryotoxon + Iris strands. * **Axenfeld Syndrome:** Axenfeld anomaly + Glaucoma. * **Rieger Anomaly:** Axenfeld anomaly + Iris thinning, corectopia (displaced pupil), and polycoria (multiple pupils). * **Rieger Syndrome:** Rieger anomaly + Systemic findings (dental hypoplasia/microdontia, redundant periumbilical skin, and maxillary hypoplasia). * **Genetics:** Most cases are associated with mutations in **PITX2** and **FOXC1** genes.

Question 1

Which of the following findings is most helpful in the diagnosis of open-angle glaucoma?

Accepted Answer

Cupping of the optic disc

Answer

Depth of the anterior chamber

Answer

Visual acuity and refractive error

Answer

Angle of the anterior chamber

Question 2

Campimetry (Scotometry) is performed in the visual field area of:

Accepted Answer

30 degrees

Answer

50 degrees

Answer

60 degrees

Answer

90 degrees

Question 3

Which of the following drugs is not used topically for the treatment of open-angle glaucoma?

Accepted Answer

Acetazolamide

Answer

Latanoprost

Answer

Brimonidine

Answer

Dorzolamide

Question 4

What is the treatment of choice in acute congestive glaucoma?

Accepted Answer

Laser iridotomy

Answer

Pilocarpine

Answer

Timolol

Answer

Trabeculoplasty

Question 5

On mutation, which of the following may give rise to hereditary glaucoma?

Accepted Answer

Optineurin

Answer

Ephrins

Answer

RBA8

Answer

Huntingtin

Question 6

A 55-year-old woman presents with acute pain and redness in her right eye, accompanied by nausea, vomiting, and seeing halos around lights. Examination reveals lacrimation, lid edema, conjunctival injection, a steamy cornea, and a fixed mid-dilated pupil. Her intraocular pressure (IOP) is markedly elevated, and visual acuity in the right eye is 20/200. She has no family history of eye diseases. What is the most likely diagnosis?

Accepted Answer

Acute closed-angle glaucoma

Answer

Corneal laceration

Answer

Ocular hypertension without glaucoma

Answer

Open angle glaucoma

Question 7

Argon laser trabeculoplasty is indicated in which of the following conditions?

Accepted Answer

Open angle glaucoma

Answer

Aphakic glaucoma

Answer

Neovascular glaucoma

Answer

Closed angle glaucoma

Question 8

Which instrument is used to visualize the angle of the anterior chamber?

Accepted Answer

Gonioscopy

Answer

Slit lamp examination

Answer

Keratometry

Answer

Indirect ophthalmoscopy

Question 9

A 30-year-old patient presented with a miotic pupil with raised intraocular pressure and normal anterior chamber in one eye, and a hazy cornea with shallow anterior chamber in the fellow eye. What is the most likely diagnosis?

Accepted Answer

Acute anterior uveitis

Answer

Acute congestive glaucoma

Answer

Chronic simple glaucoma

Answer

Endophthalmitis

Question 10

All of the following findings can be seen in Axenfeld's anomaly, except:

Accepted Answer

Ectopia of the lens

Answer

Posterior embryotoxon

Answer

Iris synechiae to Schwalbe's line

Answer

Glaucoma

Glaucoma — MCQs

Glaucoma — MCQs

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