Glaucoma — MCQs

Glaucoma Indian Medical PG Practice Questions and MCQs

Question 221: Which of the following is NOT a risk factor for primary open-angle glaucoma?

A. Heredity
B. Diabetes mellitus
C. Cigarette smoking
D. Hypermetropia (Correct Answer)

Explanation: **Explanation:** Primary Open-Angle Glaucoma (POAG) is a chronic, progressive optic neuropathy characterized by an open anterior chamber angle and specific visual field defects. Understanding its risk factors is crucial for NEET-PG. **Why Hypermetropia is the correct answer:** Hypermetropia (farsightedness) is associated with a **short axial length** and a shallow anterior chamber. These anatomical features predispose an individual to **Primary Angle-Closure Glaucoma (PACG)**, not POAG. Conversely, **Myopia** (nearsightedness) is a significant and well-established risk factor for POAG due to structural changes in the lamina cribrosa. **Analysis of Incorrect Options:** * **Heredity:** POAG has a strong genetic component. A positive family history (especially in first-degree relatives) increases the risk significantly. Specific genes like *MYOC* (Myocilin) and *OPTN* (Optineurin) are often implicated. * **Diabetes Mellitus:** Systemic vascular diseases, including Diabetes, are considered secondary risk factors. Diabetes can affect the microvasculature of the optic nerve head, making it more susceptible to glaucomatous damage. * **Cigarette Smoking:** Smoking is a known risk factor as it contributes to oxidative stress and vascular insufficiency, both of which play a role in the pathogenesis of optic nerve degeneration in POAG. **High-Yield Clinical Pearls for NEET-PG:** * **Most Important Risk Factor:** Elevated Intraocular Pressure (IOP) is the most significant modifiable risk factor. * **Age & Race:** Risk increases with age (>40 years) and is significantly higher in the African-American population. * **Steroid Responders:** Individuals who show a significant rise in IOP following topical steroid use are at a higher risk of developing POAG. * **Central Corneal Thickness (CCT):** A thin cornea is an independent risk factor for the progression of POAG.

Question 222: True about pilocarpine?

A. It acts by decreasing secretion from ciliary epithelium
B. Side effects include bitter taste and renal calculi
C. It is the drug of choice for treatment of angle-closure glaucoma (Correct Answer)
D. It is a hyperosmotic agent

Explanation: ### Explanation **Pilocarpine** is a direct-acting parasympathomimetic (cholinergic agonist) that plays a crucial role in the management of glaucoma. **Why Option C is Correct:** In **Acute Angle-Closure Glaucoma (AACG)**, the primary pathology is the mechanical obstruction of the trabecular meshwork by the peripheral iris. Pilocarpine causes contraction of the **sphincter pupillae** muscle, leading to **miosis** (pupillary constriction). This action pulls the peripheral iris away from the iridocorneal angle, physically opening the drainage pathway and allowing aqueous humor to reach the trabecular meshwork. It is considered the definitive medical treatment to break an acute attack. **Analysis of Incorrect Options:** * **Option A:** Pilocarpine does **not** decrease secretion. It increases aqueous outflow by opening the angle (in closed-angle) and by contracting the ciliary muscle to stretch the trabecular meshwork (in open-angle). Drugs that decrease secretion include Beta-blockers, Alpha-2 agonists, and Carbonic Anhydrase Inhibitors (CAIs). * **Option B:** Bitter taste and renal calculi are classic side effects of **Carbonic Anhydrase Inhibitors** (e.g., Acetazolamide), not pilocarpine. * **Option C:** Pilocarpine is a miotic, not a hyperosmotic agent. Examples of hyperosmotic agents used in glaucoma include **Mannitol** and **Glycerol**. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism in POAG:** In Primary Open-Angle Glaucoma, it acts by contracting the **ciliary muscle**, which pulls on the scleral spur and increases trabecular outflow. * **Side Effects:** Brow ache (due to ciliary spasm), induced myopia, and retinal detachment (rare). * **Contraindication:** It should be avoided in **Uveitic Glaucoma** as it can promote the formation of posterior synechiae and increase inflammation. * **Pre-requisite:** In AACG, pilocarpine is ineffective if Intraocular Pressure (IOP) is >40-50 mmHg because the iris sphincter becomes ischemic and unresponsive. IOP must first be lowered with systemic agents (like Mannitol) before pilocarpine can work.

Question 223: Which of the following is FALSE about Open Angle Glaucoma?

A. Mild to moderate increase in intraocular pressure
B. Shallow anterior chamber (Correct Answer)
C. Progressive peripheral visual field loss
D. Cupping of the optic disc

Explanation: **Explanation:** Primary Open Angle Glaucoma (POAG) is a chronic, progressive optic neuropathy characterized by an open anterior chamber angle and typical optic nerve head changes. **Why "Shallow anterior chamber" is FALSE:** In POAG, the anterior chamber depth and the iridocorneal angle are **normal/deep**. A shallow anterior chamber is the hallmark anatomical predisposition for **Angle Closure Glaucoma**, where the peripheral iris obstructs the trabecular meshwork. In POAG, the resistance to aqueous outflow is located within the trabecular meshwork itself, not due to the physical narrowing of the angle. **Analysis of other options:** * **Mild to moderate increase in IOP:** POAG typically presents with a slow, insidious rise in IOP (often 22–30 mmHg), unlike the acute, severe spikes seen in angle closure. * **Progressive peripheral visual field loss:** The disease is often asymptomatic until late stages because it starts with peripheral field defects (e.g., arcuate scotoma, nasal step) while central vision remains preserved until the end-stage ("tunnel vision"). * **Cupping of the optic disc:** This is a cardinal sign. Increased IOP leads to the death of retinal ganglion cells, resulting in an increased cup-to-disc ratio (CDR >0.7), neuroretinal rim thinning, and bayoneting sign. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Age >40, Myopia, Diabetes Mellitus, and Family History. * **Diagnosis:** Requires the triad of Raised IOP (usually), Optic Disc Cupping, and Visual Field Defects (on Humphrey Field Analysis). * **Drug of Choice:** Prostaglandin analogues (e.g., Latanoprost) are the first-line treatment as they increase uveoscleral outflow. * **Gold Standard Tonometry:** Goldmann Applanation Tonometry.

Question 224: In post trabeculectomy, shallow anterior chamber with increased IOP is due to all EXCEPT?

A. Choroidal detachment (Correct Answer)
B. Suprachoroidal hemorrhage
C. Pupillary block
D. Malignant glaucoma

Explanation: To approach this question, remember the **"Shallow Anterior Chamber (AC) Rule"** post-trabeculectomy. A shallow AC can occur with either **Low IOP** or **High IOP**. This distinction is the most high-yield concept for this topic. ### 1. Why Choroidal Detachment is the Correct Answer **Choroidal Detachment** is associated with **Low IOP (Hypotony)**. It occurs due to over-filtration or a wound leak, leading to fluid accumulation in the suprachoroidal space. This pushes the iris-lens diaphragm forward, shallowing the AC, but because the primary cause is fluid loss/leakage, the pressure remains low. ### 2. Explanation of Incorrect Options (Causes of Shallow AC with High IOP) The other three options are classic causes of a shallow AC accompanied by **Increased IOP**: * **Pupillary Block:** Resistance to aqueous flow from the posterior to the anterior chamber causes "iris bombe," pushing the iris forward and raising IOP. * **Malignant Glaucoma (Ciliary Block):** Aqueous is misdirected into the vitreous cavity, pushing the entire lens-iris diaphragm forward. This is a surgical emergency with very high IOP. * **Suprachoroidal Hemorrhage:** Sudden bursting of long/short posterior ciliary arteries fills the suprachoroidal space with blood, acutely pushing the intraocular contents forward and spiking IOP. ### 3. NEET-PG High-Yield Pearls * **Malignant Glaucoma Management:** Initial treatment is medical (Atropine to relax ciliary muscles + Carbonic Anhydrase Inhibitors). If it fails, Pars Plana Vitrectomy is required. * **Differential Diagnosis Tip:** If the question mentions a shallow AC with **Low IOP**, think of **Choroidal Detachment** or **Wound Leak (Seidel’s Test positive)**. If it mentions **High IOP**, think of **Malignant Glaucoma** or **Pupillary Block**. * **Atropine Use:** Atropine is *indicated* in Malignant Glaucoma but *contraindicated* in Primary Angle Closure Glaucoma.

Question 225: What is the ocular symptom of Von Recklinghausen disease?

A. Deformed anterior chamber with reduced angle of AC
B. Glaucoma (Correct Answer)
C. Choroidal hemangioma
D. Subretinal neovascularization

Explanation: **Explanation:** **Von Recklinghausen disease**, also known as **Neurofibromatosis Type 1 (NF1)**, is a multisystem neuroectodermal disorder. The most characteristic ocular association of NF1 is **Glaucoma**, which occurs in approximately 1/300 cases. It is typically unilateral and congenital or infantile in onset. The pathogenesis is multifactorial, involving: 1. Infiltration of the anterior chamber angle by neurofibromatomatous tissue. 2. Developmental anomalies of the angle (similar to primary congenital glaucoma). 3. Secondary angle closure due to neurofibromas of the ciliary body or iris. **Analysis of Incorrect Options:** * **Option A:** While the anterior chamber may be shallow in cases of ciliary body neurofibromas, "deformed anterior chamber" is not a specific clinical descriptor for NF1. * **Option C:** **Choroidal hemangioma** is a classic feature of **Sturge-Weber Syndrome** (Encephalotrigeminal Angiomatosis), not NF1. NF1 is instead associated with Lisch nodules and occasionally choroidal nevi or hamartomas. * **Option D:** Subretinal neovascularization is not a primary feature of NF1; it is more commonly associated with conditions like Age-Related Macular Degeneration (ARMD) or high myopia. **High-Yield Clinical Pearls for NEET-PG:** * **Lisch Nodules:** Melanocytic hamartomas of the iris; the most common ocular finding in NF1 (present in >95% of adults). * **Plexiform Neurofibroma:** Described as a "bag of worms" sensation on palpation of the eyelid; often associated with an S-shaped ptosis. * **Optic Nerve Glioma:** A common CNS tumor in NF1; usually presents as painless axial proptosis and vision loss in children. * **Sphenoid Wing Dysplasia:** A skeletal hallmark that can lead to pulsating exophthalmos.

Question 226: Sudden acute loss of vision with shallow anterior chamber is suggestive of?

A. Acute angle closure glaucoma (Correct Answer)
B. Acute iridocyclitis
C. Open angle glaucoma
D. Viral keratitis

Explanation: ### Explanation **Correct Answer: A. Acute angle closure glaucoma** The clinical presentation of **sudden, painful loss of vision** associated with a **shallow anterior chamber** is a classic hallmark of Acute Angle Closure Glaucoma (AACG). In this condition, the peripheral iris physically obstructs the trabecular meshwork, leading to a rapid rise in intraocular pressure (IOP). The shallow anterior chamber is a predisposing anatomical factor (often seen in hypermetropes) that facilitates pupillary block, causing the iris to bulge forward (iris bombé) and close the angle. **Why the other options are incorrect:** * **B. Acute iridocyclitis:** While it presents with sudden pain and redness, the anterior chamber is typically of **normal depth** (or occasionally deep). Key findings include aqueous cells/flare and a small, irregular pupil, rather than the mid-dilated pupil seen in AACG. * **C. Open angle glaucoma:** This is a "silent thief of sight." It is characterized by a **painless, progressive, and chronic** loss of peripheral vision. The anterior chamber depth remains **normal**. * **D. Viral keratitis:** This typically presents with foreign body sensation, photophobia, and redness. While vision may be blurred, the diagnostic feature is a corneal lesion (e.g., dendritic ulcer) rather than a shallow anterior chamber. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad of AACG:** Sudden ocular pain, colored halos around lights, and a hazy/steamy cornea. * **Physical Exam:** Look for a **fixed, mid-dilated, vertically oval pupil** and a stony-hard eyeball on palpation. * **Immediate Management:** Systemic Acetazolamide and topical pilocarpine (once IOP drops). * **Definitive Treatment:** Peripheral Iridotomy (Laser or Surgical) is the treatment of choice for both the affected and the fellow (prophylactic) eye.

Question 227: What is the earliest sign in the visual field suggestive of glaucoma?

A. Isopter contraction (Correct Answer)
B. Baring of the blind spot
C. Seidel's scotoma
D. Arcuate scotoma

Explanation: **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.

Question 228: Which anti-glaucoma drug is known to cause black deposits in the conjunctiva?

A. Alpha blocker
B. Prostaglandin analogue
C. Adrenaline (Correct Answer)
D. Carbonic anhydrase inhibitor

Explanation: **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.

Question 229: Which of the following is NOT a characteristic of neovascularization of the iris?

A. Fine and irregular vessels
B. Can be seen on the pupillary border or angle
C. Do not cross the scleral spur (Correct Answer)
D. Indicate VEGF secretion

Explanation: **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).

Question 230: Rapid change of presbyopic glasses is a feature of which of the following conditions?

A. Senile cataract
B. Retinal detachment
C. Intumescent cataract
D. Open angle glaucoma (Correct Answer)

Explanation: **Explanation:** The correct answer is **Open Angle Glaucoma (OAG)**. The underlying mechanism for the rapid change of presbyopic glasses in OAG is the **weakness of the ciliary muscle**. In chronic glaucoma, the increased intraocular pressure (IOP) leads to pressure-induced atrophy or ischemia of the ciliary body. Since the ciliary muscle is responsible for accommodation, its insufficiency results in a premature or rapidly progressing need for higher-powered near-vision (presbyopic) glasses. **Analysis of Options:** * **Open Angle Glaucoma (Correct):** Frequent changes in presbyopic correction are a classic early warning sign of OAG due to accommodative failure. * **Senile Cataract:** While cataracts cause blurring of vision, they typically lead to a "second sight" phenomenon (myopic shift) where a patient may actually stop needing reading glasses temporarily, rather than needing frequent changes. * **Intumescent Cataract:** This is a stage of cataract where the lens becomes swollen. While it can cause a myopic shift or induce secondary angle-closure glaucoma, it does not specifically present with a rapid change in presbyopic power. * **Retinal Detachment:** This presents with sudden flashes (photopsia), floaters, or a "curtain-like" loss of vision, unrelated to refractive changes for near work. **Clinical Pearls for NEET-PG:** * **Early signs of POAG:** Frequent change of presbyopic glasses, delayed dark adaptation, and mild headaches. * **Second Sight:** Seen in nuclear cataracts due to lenticular myopia, allowing elderly patients to read without glasses. * **Rule of Thumb:** Any patient presenting with frequent changes in glasses should be screened for IOP and optic disc changes to rule out glaucoma.

Practice by Chapter

Aqueous Humor Dynamics

Practice Questions

Primary Open-Angle Glaucoma

Practice Questions

Primary Angle-Closure Glaucoma

Practice Questions

Secondary Open-Angle Glaucomas

Practice Questions

Secondary Angle-Closure Glaucomas

Practice Questions

Developmental and Congenital Glaucomas

Practice Questions

Medical Management of Glaucoma

Practice Questions

Laser Therapy in Glaucoma

Practice Questions

Glaucoma Filtration Surgery

Practice Questions

Glaucoma Drainage Devices

Practice Questions

Angle Assessment Techniques

Practice Questions

Visual Field Testing in Glaucoma

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Glaucoma — MCQs

Glaucoma — MCQs

On this page

Practice by Chapter

Want unlimited practice?