Glaucoma — MCQs

Glaucoma Indian Medical PG Practice Questions and MCQs

Question 261: Which of the following drugs is not used in the management of acute angle-closure glaucoma?

A. Pilocarpine
B. Clozapine (Correct Answer)
C. Fluphenazine
D. Duloxetine

Explanation: **Explanation:** The management of **Acute Angle-Closure Glaucoma (AACG)** focuses on rapidly lowering intraocular pressure (IOP) and reopening the drainage angle. **Why Clozapine is the correct answer:** The question asks for a drug **not used** in management. However, there is a clinical nuance here: **Clozapine**, along with **Fluphenazine** (Antipsychotics) and **Duloxetine** (SNRI), are actually drugs that can **precipitate or worsen** angle-closure glaucoma due to their anticholinergic or sympathomimetic effects. In the context of this specific question (often seen in recent NEET-PG patterns), the focus is on identifying which drug is *contraindicated* or a *causative agent* rather than a treatment. *Note: There appears to be a technical error in the provided key/options as B, C, and D are all potential triggers for glaucoma, while only A is a treatment. However, focusing on the pharmacology:* 1. **Pilocarpine (Option A):** This is a **miotic (parasympathomimetic)** and a mainstay of treatment. It constricts the pupil, pulling the peripheral iris away from the trabecular meshwork to open the angle. 2. **Clozapine (Option B):** An atypical antipsychotic with significant **anticholinergic** activity. It causes mydriasis (pupillary dilation), which can crowd the angle and trigger an acute attack. It is never used for treatment. 3. **Fluphenazine (Option C):** A typical antipsychotic that also possesses anticholinergic properties, potentially inducing angle closure. 4. **Duloxetine (Option D):** An SNRI that can lead to weak mydriasis via increased noradrenergic tone, making it a risk factor for AACG. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (Immediate IOP lowering):** IV Acetazolamide or IV Mannitol. * **Definitive Treatment:** Peripheral Iridotomy (usually YAG laser). * **Pilocarpine Caution:** Do not use pilocarpine if IOP is >40-50 mmHg, as the iris sphincter becomes ischemic and unresponsive to the drug. Lower the IOP first with osmotic agents. * **Mnemonic for Triggers:** "SANS" (Sympathomimetics, Anticholinergics, Nasal decongestants, Selective Serotonin Reuptake Inhibitors).

Question 262: Neovascular glaucoma can occur in all of the following conditions, except?

A. Central Retinal Vein Occlusion (CRVO)
B. Eale's disease
C. Retinopathy of prematurity (Correct Answer)
D. Hypertension

Explanation: **Explanation:** Neovascular Glaucoma (NVG) is a secondary glaucoma caused by the formation of a fibrovascular membrane over the trabecular meshwork, triggered by **retinal ischemia** and the subsequent release of **VEGF** (Vascular Endothelial Growth Factor). **Why Retinopathy of Prematurity (ROP) is the correct answer:** While ROP involves retinal ischemia and neovascularization, it typically results in **tractional retinal detachment** or **cicatricial changes**. While secondary angle-closure glaucoma can occur in ROP due to forward displacement of the lens-iris diaphragm (Stage 5), it is **not** a classic cause of neovascular glaucoma. **Analysis of other options:** * **CRVO (Central Retinal Vein Occlusion):** Specifically the ischemic type, it is the most common cause of NVG. It is famously known as **"100-day glaucoma"** because NVG typically develops about 3 months after the occlusion. * **Eale’s Disease:** This is an idiopathic peripheral perivasculitis characterized by severe retinal ischemia and peripheral neovascularization, which can lead to rubeosis iridis and NVG. * **Hypertension:** While not a direct cause, systemic hypertension is a major risk factor for **Central Retinal Artery Occlusion (CRAO)** and **Diabetic Retinopathy**, both of which are potent triggers for NVG. **High-Yield Clinical Pearls for NEET-PG:** 1. **Top 3 Causes of NVG:** 1. Diabetic Retinopathy (most common overall), 2. Ischemic CRVO (most common acute cause), 3. Carotid Artery Occlusive Disease. 2. **Rubeosis Iridis:** The first sign of NVG is the appearance of new vessels at the **pupillary margin**, which then migrate toward the angle. 3. **Treatment:** The definitive management for the underlying cause is **Pan-retinal Photocoagulation (PRP)** to reduce the ischemic drive. Anti-VEGF injections are used as an adjunct.

Question 263: Glaucoma flecken is defined as:

A. Acute uveitis
B. Lens opacity (Correct Answer)
C. Retinal detachment
D. Corneal opacity

Explanation: **Explanation:** **Glaukomflecken** (also known as Vogt’s spots) refers to multiple, small, grey-white subcapsular opacities found in the anterior lens. These represent focal areas of lens epithelial necrosis caused by a sudden, severe rise in intraocular pressure (IOP). **Why the correct answer is right:** In the setting of **Acute Angle Closure Glaucoma (AACG)**, the rapid and extreme elevation of IOP causes stagnation of the aqueous humor. This leads to localized ischemia and metabolic distress of the anterior lens epithelium, resulting in permanent necrotic spots. These opacities are pathognomonic of a **previous** attack of acute congestive glaucoma. **Why the incorrect options are wrong:** * **A. Acute uveitis:** While uveitis can cause lens changes (like posterior synechiae or complicated cataracts), Glaukomflecken is specifically a post-glaucomatous sequela. * **C. Retinal detachment:** This involves the separation of the neurosensory retina from the RPE and does not manifest as focal lens opacities. * **D. Corneal opacity:** Acute glaucoma causes corneal *edema* (due to endothelial pump failure), but Glaukomflecken is strictly a lenticular finding. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Anterior subcapsular region of the lens. * **Significance:** It serves as a "diagnostic footprint" of a past acute primary angle-closure attack. * **Triad of post-acute glaucoma:** Glaukomflecken, iris atrophy (sectoral), and a mid-dilated non-reactive pupil. * **Differential:** Do not confuse with *Vossius ring*, which is a ring of iris pigment on the anterior lens capsule following blunt trauma.

Question 264: Aqueous humor drains through all of the following routes except:

A. Trabecular meshwork
B. Uveoscleral outflow
C. Iris
D. Sclera (Correct Answer)

Explanation: **Explanation:** Aqueous humor is produced by the ciliary body and must be drained to maintain intraocular pressure (IOP). There are two primary pathways for drainage, along with minor accessory routes. **Why Sclera is the Correct Answer:** The **Sclera** itself is a dense, fibrous protective layer and does not serve as a direct drainage route for aqueous humor. While the uveoscleral pathway involves fluid passing *through* the interstitial spaces of the ciliary muscle toward the suprachoroidal space, the fluid eventually enters the venous circulation of the choroid and sclera. However, the sclera as a tissue does not possess a drainage mechanism; it acts as a container. **Analysis of Other Options:** * **Trabecular Meshwork (Option A):** This is the **conventional (pressure-dependent) pathway**, accounting for approximately **90%** of aqueous drainage. Fluid passes through the meshwork into the Canal of Schlemm and then into episcleral veins. * **Uveoscleral Outflow (Option B):** This is the **unconventional (pressure-independent) pathway**, accounting for about **10%** of drainage. Fluid exits through the ciliary muscle into the suprachoroidal space. * **Iris (Option C):** A very small amount of aqueous humor (minor route) can be absorbed through the **iris crypts** and its anterior surface into the iris vessels. **High-Yield Clinical Pearls for NEET-PG:** * **Prostaglandin Analogs (e.g., Latanoprost):** The first-line drug in Glaucoma; they work by increasing **uveoscleral outflow**. * **Miotics (e.g., Pilocarpine):** Increase drainage through the **trabecular meshwork** by contracting the ciliary muscle. * **Goldmann Equation:** Used to determine IOP ($IOP = (F/C) + Pv$), where $F$ is aqueous formation, $C$ is facility of outflow, and $Pv$ is episcleral venous pressure.

Question 265: A vertically oval dilated pupil is seen in which condition?

A. Acute primary angle closure glaucoma (Correct Answer)
B. Wernicke's Korsakoff psychosis
C. Neurosyphilis
D. Paralysis of oculomotor nerve

Explanation: **Explanation:** In **Acute Primary Angle Closure Glaucoma (APACG)**, the sudden and severe rise in intraocular pressure (IOP) leads to ischemia and subsequent paralysis of the iris sphincter muscle. This results in a pupil that is **semi-dilated, vertically oval, and non-reactive to light**. The vertical elongation occurs because the ischemia is often most pronounced in the superior and inferior segments of the iris. **Analysis of Incorrect Options:** * **Wernicke-Korsakoff Psychosis:** This condition, caused by Thiamine (B1) deficiency, typically presents with the triad of ophthalmoplegia (most commonly lateral rectus palsy), ataxia, and confusion. It does not cause a vertically oval pupil. * **Neurosyphilis:** Classically associated with the **Argyll Robertson Pupil**, which is characterized by small, irregular pupils that demonstrate "accommodation-reflex present, but light-reflex absent" (ARP). * **Paralysis of Oculomotor Nerve (3rd Nerve Palsy):** This results in a **completely dilated (mydriatic)** and fixed pupil due to loss of parasympathetic supply, accompanied by ptosis and a "down and out" deviation of the eye. **High-Yield Clinical Pearls for NEET-PG:** * **APACG Presentation:** Sudden onset of severe pain, "halos" around lights, stony hard eye, and a shallow anterior chamber. * **Immediate Management:** Systemic Acetazolamide and topical Pilocarpine (once IOP drops below 40 mmHg to restore iris vascularity). * **Definitive Treatment:** Laser Peripheral Iridotomy (LPI) for both the affected and the fellow (prophylactic) eye. * **Festooned Pupil:** Seen in chronic iridocyclitis due to posterior synechiae.

Question 266: Which of the following is considered primary glaucoma?

A. Juvenile glaucoma (Correct Answer)
B. Steroid-induced glaucoma
C. Pigmentary glaucoma
D. All of the above

Explanation: ### Explanation **Concept Overview:** Glaucoma is classified into **Primary** and **Secondary** types. Primary glaucoma occurs due to idiopathic factors or developmental anomalies without an identifiable systemic or ocular disease causing the rise in intraocular pressure (IOP). Secondary glaucoma occurs as a complication of a pre-existing ocular condition, systemic disease, or external factors (like drugs or trauma). **Why Juvenile Glaucoma is Correct:** **Juvenile Glaucoma** (specifically Juvenile Open-Angle Glaucoma or JOAG) is a subset of **Primary Open-Angle Glaucoma (POAG)**. It typically manifests between the ages of 3 and 35 years. It is considered "primary" because the elevation in IOP is due to an idiopathic functional abnormality of the trabecular meshwork, often associated with mutations in the **MYOC (Myocilin)** gene, rather than an acquired ocular pathology. **Analysis of Incorrect Options:** * **Steroid-induced glaucoma:** This is a **Secondary** glaucoma. It occurs due to the exogenous administration of corticosteroids (topical, systemic, or intravitreal), which increases resistance to aqueous outflow by altering the extracellular matrix of the trabecular meshwork. * **Pigmentary glaucoma:** This is a **Secondary** glaucoma. It is caused by "Pigment Dispersion Syndrome," where pigment granules are mechanically rubbed off the posterior iris surface and physically clog the trabecular meshwork. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Glaucomas include:** Congenital glaucoma (Buphthalmos), JOAG, POAG, and Primary Angle-Closure Glaucoma (PACG). * **JOAG Inheritance:** Often follows an **Autosomal Dominant** pattern. * **Steroid Responders:** Approximately 5–10% of the population are "high responders" who develop significant IOP spikes with steroid use; this risk is much higher in patients with pre-existing POAG. * **Pigmentary Glaucoma Triad:** Look for Krukenberg’s spindle (cornea), Zentmayer ring (lens), and heavy trabecular pigmentation (Sampaolesi’s line).

Question 267: Field defects in chronic simple glaucoma includes all EXCEPT:

A. Paracentral scotoma
B. Paracentral scotoma (Correct Answer)
C. Arcuate scotoma
D. Seidel scotoma

Explanation: In Chronic Simple Glaucoma (Primary Open Angle Glaucoma), visual field defects follow a characteristic progression due to the damage of retinal nerve fibers at the optic nerve head. **Explanation of the Correct Answer:** The question contains a typographical error in the options provided (Option A and B are identical). However, based on standard ophthalmology textbooks (like Khurana), **Paracentral scotoma** is actually a classic early field defect in glaucoma. *Note for NEET-PG:* If this question appeared in an exam where "Paracentral scotoma" is marked as the "Except" answer, it is likely due to a technical error in the question paper or a specific distinction where the scotoma is considered a *component* of the progression rather than a separate entity. In a standard clinical context, all three listed (Paracentral, Seidel, and Arcuate) **are** characteristic defects of glaucoma. **Analysis of Options:** * **Paracentral Scotoma:** One of the earliest defects. These are small, isolated islands of vision loss typically located between 10° and 20° from fixation (Bjerrum’s area). * **Seidel’s Scotoma:** Occurs when a paracentral scotoma reaches the blind spot, creating a sickle-shaped extension. * **Arcuate (Bjerrum) Scotoma:** Formed by the coalescence of paracentral scotomas. It follows the arcuate path of nerve fibers, extending from the blind spot around the fixation point to the nasal horizontal meridian. **High-Yield Clinical Pearls for NEET-PG:** 1. **Sequence of Defects:** Isildur’s/Baring of blind spot (earliest/non-specific) → Paracentral scotoma → Seidel’s scotoma → Arcuate/Bjerrum scotoma → Double Arcuate (Ring) scotoma → Roenne’s Nasal Step → Tubular vision → Total blindness. 2. **Bjerrum’s Area:** The area between 10° and 25° from fixation where glaucomatous damage is most prominent. 3. **Tubular Vision:** Peripheral vision is lost first; central vision is often preserved until the end-stage. 4. **10-2 Perimetry:** Used to monitor advanced glaucoma when only central vision remains.

Question 268: A patient presents with a history of evening halos and occasional headaches for several months. Examination reveals normal intraocular pressure but a shallow anterior chamber. In which stage of glaucoma is this patient?

A. Acute
B. Absolute
C. Prodrome (Correct Answer)
D. Constant instability

Explanation: ### Explanation This clinical scenario describes **Primary Angle-Closure Glaucoma (PACG)** in the **Prodromal Stage**. **Why "Prodrome" is correct:** The prodromal stage is characterized by transient, self-limiting episodes of increased intraocular pressure (IOP). These episodes typically occur in the evening or in low light (mydriasis causes the iris to block the angle). * **Evening Halos:** Caused by transient corneal edema due to a sudden rise in IOP. * **Headaches/Ocular Pain:** Result from the pressure spike. * **Normal IOP on Examination:** Between episodes, the IOP returns to normal, and the eye appears quiet, though the **shallow anterior chamber** remains a constant anatomical risk factor. **Why the other options are incorrect:** * **Acute Stage:** This is a medical emergency. The patient presents with sudden, severe pain, nausea, vomiting, a stony-hard eye (very high IOP), a vertically oval semi-dilated pupil, and "steamy" cornea. It does not resolve spontaneously. * **Absolute Stage:** This is the terminal stage where the eye is completely blind (No Perception of Light). The eye may be painful or painless, and the optic disc shows total glaucomatous cupping. * **Constant Instability (Chronic Stage):** Here, the angle is permanently closed by synechiae (PAS). The IOP is persistently high, and there is progressive optic nerve damage and field defects, unlike the intermittent nature of the prodromal stage. **High-Yield Clinical Pearls for NEET-PG:** * **Anatomical Predisposition:** Hypermetropic eyes, small eyeballs, and advancing age (enlarging lens) are risk factors for shallow chambers. * **Provocative Tests:** The Dark Room Test or Prone Position Test can be used to induce an attack in suspected prodromal cases. * **Definitive Treatment:** **Peripheral Iridotomy (Laser or Surgical)** is the treatment of choice to bypass the pupillary block and prevent future acute attacks.

Question 269: A patient complains of seeing colored halos around lights in the evening and blurring of vision for the past few days, with normal intraocular pressure. What is the most likely diagnosis?

A. Prodromal phase of acute angle closure glaucoma (Correct Answer)
B. Acute angle closure glaucoma
C. Chronic glaucoma
D. Epidemic dropsy

Explanation: ### Explanation The correct answer is **A. Prodromal phase of acute angle closure glaucoma.** **1. Why Option A is Correct:** The prodromal phase of Primary Angle Closure Glaucoma (PACG) is characterized by **transient, self-limiting attacks** of increased intraocular pressure (IOP). During these episodes, the IOP rises enough to cause **corneal edema**, which acts as a prism, splitting light into its component colors and creating **colored halos** (typically with the red ring outside and blue/violet inside). Between these episodes, the IOP returns to **normal**, which explains why the patient’s pressure was normal at the time of examination. These attacks are often triggered in the **evening** due to physiological mydriasis (pupillary dilation) in low light, which crowds the angle. **2. Why Other Options are Incorrect:** * **B. Acute angle closure glaucoma:** This is a full-blown attack. The patient would present with severe pain, nausea, vomiting, a stony-hard eye, and a significantly **elevated IOP** (often 40–70 mmHg) that does not normalize without treatment. * **C. Chronic glaucoma:** Primary Open Angle Glaucoma (POAG) is typically asymptomatic ("the silent thief of sight") and does not cause colored halos or transient blurring until very advanced stages. * **D. Epidemic dropsy:** While this can cause glaucoma (due to Sanguinarine toxin), it typically presents with bilateral, markedly elevated IOP and systemic features like pedal edema and cardiac failure. **3. NEET-PG High-Yield Pearls:** * **Fincham’s Test:** Used to differentiate halos of glaucoma from cataract. In glaucoma, halos are intact; in cataract, they are broken. * **Trigger factors for Prodromal stage:** Emotional stress, reading in dim light, or pharmacological mydriasis. * **Management:** The definitive treatment for the prodromal stage to prevent a full-blown attack is **Peripheral Iridotomy (Laser PI)** in both eyes (prophylactic for the fellow eye).

Question 270: Which of the following is a new drug approved for the treatment of glaucoma?

A. Netarsudil (Correct Answer)
B. Semaglutide
C. Etelcalcetide
D. Plecanatide

Explanation: **Explanation:** **Netarsudil (Option A)** is the correct answer. It represents a novel class of glaucoma medications known as **Rho-kinase (ROCK) inhibitors**. Unlike traditional drugs that primarily reduce aqueous production or increase uveoscleral outflow, Netarsudil works by increasing aqueous outflow through the **trabecular meshwork** (the primary physiological pathway). It achieves this by inhibiting the Rho-kinase enzyme, which reduces cellular stiffness and relaxes the trabecular meshwork fibers. Additionally, it lowers episcleral venous pressure and reduces aqueous production. **Analysis of Incorrect Options:** * **Semaglutide (Option B):** A GLP-1 receptor agonist used in the management of Type 2 Diabetes Mellitus and obesity. * **Etelcalcetide (Option C):** A calcimimetic agent used to treat secondary hyperparathyroidism in patients with chronic kidney disease on dialysis. * **Plecanatide (Option D):** A guanylate cyclase-C agonist used for the treatment of chronic idiopathic constipation (CIC) and irritable bowel syndrome with constipation (IBS-C). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Netarsudil is unique because it targets the "diseased" trabecular meshwork directly. * **Fixed-Dose Combination:** *Rocklatan* is a recently approved combination of Netarsudil and Latanoprost. * **Common Side Effect:** The most characteristic side effect of Netarsudil is **conjunctival hyperemia** (redness) and **conjunctival hemorrhages** (petechiae). * **Corneal Verticillata:** Netarsudil can cause vortex keratopathy (whorl-like deposits), similar to Amiodarone or Fabry disease.

Practice by Chapter

Aqueous Humor Dynamics

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Primary Open-Angle Glaucoma

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Primary Angle-Closure Glaucoma

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Secondary Open-Angle Glaucomas

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Secondary Angle-Closure Glaucomas

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Developmental and Congenital Glaucomas

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Medical Management of Glaucoma

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Laser Therapy in Glaucoma

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Glaucoma Filtration Surgery

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Glaucoma Drainage Devices

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Angle Assessment Techniques

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Visual Field Testing in Glaucoma

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Glaucoma — MCQs

Glaucoma — MCQs

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