Glaucoma Practice Questions

Q: An elderly man presents with a painful red eye. On examination, the pupil is noted to be dilated and fixed. What is the next line of investigation?

Tonometry. **Explanation:** The clinical presentation of a **painful red eye** associated with a **dilated, fixed, vertically oval pupil** is a classic hallmark of **Acute Angle-Closure Glaucoma (AACG)**. In this emergency, the sudden rise in intraocular pressure (IOP) causes iris ischemia, leading to pupillary paralysis. 1. **Why Tonometry is the correct answer:** The immediate priority in a suspected case of AACG is to confirm the diagnosis by measuring the intraocular pressure. **Tonometry** (specifically Applanation Tonometry) is the definitive investigation to document the elevated IOP, which often exceeds 40–70 mmHg in these patients. Prompt diagnosis is vital to initiate pressure-lowering treatment and prevent permanent optic nerve damage. 2. **Why other options are incorrect:** * **Visual Evoked Potential (VEP):** This is used to assess the functional integrity of the visual pathway (e.g., optic neuritis) and has no role in the acute management of a red eye. * **Retinal Angiogram (FFA):** This is used to evaluate vascular pathologies like diabetic retinopathy or macular degeneration; it is not indicated in acute glaucoma. * **Slit Lamp Examination:** While useful for seeing a shallow anterior chamber or corneal edema, it is a diagnostic tool rather than the specific investigation to confirm the *pressure* elevation. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of AACG:** Sudden ocular pain, "halos" around lights, and a stony-hard eye on palpation. * **Gold Standard for Diagnosis:** Gonioscopy (to visualize the closed angle), but **Tonometry** is the immediate next step for pressure assessment. * **Drug of Choice (Immediate):** IV Acetazolamide and topical pilocarpine (once IOP drops below 40 mmHg). * **Definitive Treatment:** Peripheral Iridotomy (Laser or Surgical).

Q: What is the normal diurnal variation of intraocular pressure?

3-6 mm of Hg. ### Explanation **1. Understanding the Correct Answer (C: 3-6 mm Hg)** Intraocular pressure (IOP) is not static; it fluctuates throughout a 24-hour period due to changes in aqueous humor production and drainage, as well as variations in circulating cortisol and melatonin levels. In a healthy, non-glaucomatous eye, this **diurnal variation** typically ranges between **3 to 6 mm Hg**. IOP is generally highest in the early morning hours (phasic variation) and lowest in the evening. **2. Analysis of Incorrect Options** * **Options A & B (0-3 mm Hg):** These values are too narrow. While some individuals may show very stable IOP, the physiological norm accounts for a wider range of fluctuation due to postural changes and circadian rhythms. * **Option D (6-8 mm Hg):** This range is considered suspicious. A diurnal variation exceeding **8 mm Hg** is highly suggestive of **Glaucoma**, even if the absolute IOP readings fall within the "normal" range (10-21 mm Hg) during office hours. **3. Clinical Pearls for NEET-PG** * **Gold Standard for Measurement:** The **Goldmann Applanation Tonometer (GAT)** is the gold standard for measuring IOP. * **Glaucoma Diagnosis:** In glaucomatous eyes, the diurnal fluctuation is exaggerated (often >10 mm Hg). This is why a single "normal" IOP reading in the afternoon does not rule out glaucoma. * **Diurnal Variation Recording:** To accurately capture these peaks, a **Diurnal Variation Chart (DVC)** is maintained, measuring IOP every 3-4 hours over a 24-hour period. * **Postural Influence:** IOP is typically higher in the **supine position** compared to the sitting position due to increased episcleral venous pressure.

Q: In closed-angle glaucoma, all of the following are true EXCEPT:

Nonsystemic manifestations occur.. In **Acute Angle-Closure Glaucoma (AACG)**, the sudden rise in intraocular pressure (IOP) is a medical emergency characterized by both ocular and significant **systemic manifestations**. ### Why Option C is the Correct Answer (The "Except") The statement "Nonsystemic manifestations occur" is false because AACG is notorious for causing **severe systemic symptoms**. Due to the oculo-visceral reflex (mediated by the Vagus nerve), patients often present with: * Nausea and vomiting. * Severe headache and prostration. * Bradycardia and sweating. These symptoms are so prominent that cases are sometimes misdiagnosed as acute abdominal or neurological emergencies. ### Explanation of Incorrect Options * **A. Iridectomy is performed:** This is true. Laser Peripheral Iridotomy (LPI) or surgical iridectomy is the definitive treatment. It creates a bypass for aqueous humor, relieving the pupillary block. * **B. Pilocarpine is used:** This is true. Pilocarpine (a miotic) is used to pull the iris away from the angle, opening the drainage pathway. Note: It is usually started once IOP has dropped below 40 mmHg, as the iris sphincter is ischemic at very high pressures. * **D. Atropine is not used:** This is true. Atropine is a **mydriatic** (dilates the pupil), which causes further crowding of the angle and can worsen or precipitate an attack of closed-angle glaucoma. It is strictly contraindicated. ### NEET-PG High-Yield Pearls * **Drug of Choice for immediate IOP reduction:** Intravenous Mannitol (osmotic diuretic) or Acetazolamide. * **Clinical Sign:** "Steamy" or "Cloudy" cornea with a vertically oval, semi-dilated, non-reacting pupil. * **Prophylaxis:** Always treat the fellow eye ("Direct Fellow Eye") with prophylactic Laser Peripheral Iridotomy, as the anatomical predisposition is bilateral.

Q: Inverse glaucoma is seen with which condition?

Instillation of miotics. **Explanation:** **Inverse Glaucoma** refers to a paradoxical rise in intraocular pressure (IOP) following the administration of **miotics** (like Pilocarpine). This phenomenon is classically associated with **Spherophakia** (seen in conditions like Weill-Marchesani syndrome) and **Subluxated lens**. 1. **Why Miotics are the cause:** In Spherophakia, the lens is small and spherical. When a miotic is instilled, it causes contraction of the ciliary muscle, which relaxes the zonules. This allows the already globular lens to move forward and increase its anteroposterior diameter, leading to a **pupillary block**. This pushes the iris forward, closing the angle and causing a sudden rise in IOP—the opposite of the expected effect of miotics in typical angle-closure glaucoma. 2. **Why other options are incorrect:** * **Steroids:** Steroid-induced glaucoma is a secondary open-angle glaucoma caused by increased resistance to aqueous outflow due to structural changes in the trabecular meshwork (accumulation of glycosaminoglycans). It is not "inverse." * **Mydriatics:** These typically cause pupillary block or angle crowding in predisposed eyes (primary angle-closure), which is the standard mechanism, not a paradoxical "inverse" reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of Inverse Glaucoma:** The definitive management is the instillation of **Mydriatics/Cycloplegics** (e.g., Atropine). These tighten the zonules, pulling the lens backward and relieving the pupillary block. * **Associated Syndrome:** Always look for **Weill-Marchesani Syndrome** (short stature, brachydactyly, and spherophakia) in questions involving inverse glaucoma. * **Contrast:** In standard Primary Angle Closure Glaucoma (PACG), miotics are used to pull the iris away from the angle; in Inverse Glaucoma, they worsen the block.

Q: What is the first-line drug of choice for primary open-angle glaucoma?

Prostaglandin analogues. **Explanation:** **Prostaglandin Analogues (PGAs)**, such as Latanoprost, Bimatoprost, and Travoprost, are currently the **first-line drug of choice** for Primary Open-Angle Glaucoma (POAG). **Why Prostaglandin Analogues?** The primary mechanism of PGAs is increasing the **uveoscleral outflow** of aqueous humor. They are preferred because they provide the most potent reduction in intraocular pressure (IOP), have a long duration of action allowing for **once-daily dosing** (improving patient compliance), and lack systemic side effects compared to other classes. **Analysis of Incorrect Options:** * **Beta-blockers (e.g., Timolol):** Formerly the first-line treatment, they work by decreasing aqueous humor production [3]. They are now considered second-line due to systemic contraindications, such as bradycardia, heart block, and bronchospasm (asthma/COPD). * **Carbonic Anhydrase Inhibitors (e.g., Dorzolamide, Acetazolamide):** These reduce aqueous secretion by inhibiting carbonic anhydrase in the ciliary body epithelium but are generally less efficacious than PGAs [3]. * **Miotics (e.g., Pilocarpine):** These increase trabecular outflow but are rarely used for POAG due to side effects like miosis, brow ache, and risk of retinal detachment [1]. They remain the drug of choice for Acute Angle-Closure Glaucoma. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects of PGAs:** Increased iris pigmentation (permanent), thickening/darkening of eyelashes, and deepening of the sulcus. * **Latanoprostene bunod:** A newer agent that works via both uveoscleral outflow (prostaglandin) and trabecular meshwork (nitric oxide). * **Apraclonidine:** Used specifically to prevent post-laser (iridotomy/trabeculoplasty) IOP spikes [2].

Q: Neovascularization of the iris is not seen in which of the following conditions?

Pigment Dispersion Syndrome. **Explanation:** **Neovascularization of the Iris (Rubeosis Iridis)** is a pathological process where new, fragile blood vessels form on the surface of the iris. This occurs primarily due to **retinal ischemia**, which triggers the release of Vascular Endothelial Growth Factor (VEGF). VEGF diffuses anteriorly, stimulating angiogenesis in the iris and the iridocorneal angle. * **Why Pigment Dispersion Syndrome (PDS) is the correct answer:** PDS is a mechanical condition where pigment is rubbed off the posterior iris surface due to contact with lens zonules. While it can lead to Pigmentary Glaucoma, it is **not an ischemic condition**. Therefore, there is no stimulus for VEGF production or neovascularization. **Analysis of Incorrect Options:** * **CRVO (Central Retinal Vein Occlusion):** Specifically the "Ischemic" type, it is a classic cause of rubeosis iridis, often leading to "100-day glaucoma" (Neovascular Glaucoma). * **Ocular Ischemic Syndrome:** Caused by chronic hypoperfusion (usually due to carotid artery stenosis), it leads to global ocular ischemia and is a potent trigger for iris neovascularization. * **Diabetic Retinopathy:** Proliferative Diabetic Retinopathy (PDR) is the most common cause of rubeosis iridis worldwide due to widespread retinal capillary non-perfusion. **Clinical Pearls for NEET-PG:** * **The "Rule of 90":** In ischemic CRVO, neovascular glaucoma typically develops within 90 days (3 months). * **Commonest cause of Rubeosis Iridis:** Diabetic Retinopathy. * **Commonest cause of unilateral Rubeosis Iridis:** Ischemic CRVO. * **Clinical Sign:** New vessels usually appear first at the **pupillary margin** before spreading to the angle.

Q: A 36-year-old female develops eye pain during a prone dark room test. Which of the following drugs should be avoided?

Atropine. ### Explanation **Core Concept: Angle-Closure Glaucoma (ACG)** The **Prone Dark Room Test** is a provocative test used to diagnose **Primary Angle-Closure Susceptibility**. Placing a patient in a prone position in the dark causes the lens to move forward and the pupil to dilate (mydriasis), which crowds the angle of the anterior chamber. If the patient develops eye pain and increased intraocular pressure (IOP) during this test, it indicates a narrow/occludable angle. **Why Atropine is the Correct Answer:** Atropine is a potent **parasympatholytic (mydriatic)** agent. It causes pupillary dilation, which leads to further crowding of the angle and can precipitate a full-blown attack of **Acute Congestive Glaucoma** in a patient with a positive provocative test. Therefore, mydriatics are strictly contraindicated in patients with narrow angles. **Analysis of Incorrect Options:** * **Acetazolamide:** A carbonic anhydrase inhibitor that decreases aqueous humor production. It is used to *lower* IOP in acute glaucoma. * **Pilocarpine:** A miotic (parasympathomimetic) that constricts the pupil, pulling the iris away from the angle. It is a treatment of choice for ACG (after initial IOP reduction). * **Timolol:** A topical beta-blocker that reduces aqueous production. It is a standard treatment to lower IOP and is safe in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of choice for Acute Glaucoma:** IV Mannitol (to rapidly lower IOP) or Acetazolamide. * **Definitive treatment for ACG:** Peripheral Iridotomy (usually via YAG laser). * **Mydriatic of choice for fundus exam in narrow angles:** Phenylephrine (it is easily reversible), but only after assessing the risk. * **Classic Presentation:** "Halos around lights," "steamy cornea," and a "mid-dilated non-reactive pupil."

Q: Laser iridotomy is indicated for which type of glaucoma?

Primary angle-closure glaucoma (PACG). **Explanation:** **1. Why Primary Angle-Closure Glaucoma (PACG) is correct:** The fundamental mechanism in PACG is **pupillary block**, where the iris is in close contact with the lens, obstructing the flow of aqueous humor from the posterior to the anterior chamber. This leads to increased pressure in the posterior chamber, causing the iris to bulge forward (**iris bombe**) and mechanically block the trabecular meshwork. **Laser Peripheral Iridotomy (LPI)** creates a small hole in the peripheral iris, providing an alternative pathway for aqueous flow. This equalizes the pressure between the chambers, flattens the iris, and opens the drainage angle. It is the definitive treatment for PACG. **2. Why other options are incorrect:** * **Primary Open-Angle Glaucoma (POAG):** The angle is already open; the resistance to outflow is within the trabecular meshwork itself. LPI has no role here. Treatment involves medical therapy or Laser Trabeculoplasty. * **Congenital Glaucoma:** This is caused by a structural abnormality (dysgenesis) of the angle (Barkan’s membrane). The primary treatment is surgical, specifically **Goniotomy** or **Trabeculotomy**. * **Secondary Angle-Closure Glaucoma:** While LPI may be used in specific subtypes (like seclusio pupillae), it is not the standard indication for all secondary closures (e.g., neovascular glaucoma), where the underlying cause must be addressed. **3. Clinical Pearls for NEET-PG:** * **Prophylaxis:** LPI is also indicated in the fellow eye of a patient with an acute attack of PACG, as there is a 50-75% risk of a similar attack in the other eye. * **YAG Laser:** The Nd:YAG laser is the most common instrument used for performing iridotomy. * **Complication:** A common transient complication of LPI is a spike in intraocular pressure (IOP) and hyphema.

Q: What is the sickle-shaped extension of the blind spot known as?

Seidel's sign. ### Explanation In glaucoma, visual field defects follow a specific progression based on the anatomy of the retinal nerve fiber layer (RNFL). **Why Seidel’s Sign is Correct:** **Seidel’s sign** represents an early glaucomatous field defect. It is a **sickle-shaped extension** of the physiological blind spot, caused by the involvement of the arcuate nerve fibers (specifically the small-diameter fibers). It typically starts at the upper or lower pole of the blind spot and curves around the fixation point, following the path of the arcuate fibers. **Analysis of Incorrect Options:** * **Down’s Sign:** This is not a recognized term in glaucomatous perimetry. * **Bjerrum’s Sign (Arcuate Scotoma):** This is a more advanced stage where the Seidel’s scotoma extends further to meet the horizontal raphe. It forms a complete arc-shaped defect (usually between 10° and 20° from fixation). * **Baring of Blind Spot:** This occurs when an island of vision is lost, making the blind spot appear "open" to the outside of the visual field. While common in glaucoma, it is considered **non-specific** and can occur in normal individuals. **High-Yield Clinical Pearls for NEET-PG:** 1. **Sequence of Defects:** Ischaemic (Paracentral) scotoma → Seidel’s sign → Bjerrum’s scotoma → Double arcuate (Ring) scotoma → Roenne’s nasal step → Tubular vision → Temporal island. 2. **Bjerrum’s Area:** The area of the retina between 10° and 20° from the fixation point where early glaucomatous damage is most frequently detected. 3. **Gold Standard:** Automated Perimetry (specifically the Humphrey Field Analyzer) is the gold standard for monitoring these defects.

Q: A 78-year-old male presents with a chief complaint of diminution of vision in both eyes. Intraocular pressure (IOP) in both eyes is 24 mm Hg, and an inferior notch is seen in the optic nerve head. Visual fields reveal a paracentral scotoma. What is the drug of choice?

Latanoprost. **Explanation:** The clinical presentation of elevated intraocular pressure (24 mm Hg), characteristic optic disc changes (inferior notch), and corresponding visual field defects (paracentral scotoma) confirms a diagnosis of **Primary Open-Angle Glaucoma (POAG)**. **1. Why Latanoprost is the Correct Answer:** **Prostalgandin Analogues (PGAs)** like Latanoprost are the **first-line drug of choice** for POAG. They work by increasing the **uveoscleral outflow** of aqueous humor. They are preferred because of their superior efficacy in lowering IOP (25-35%), once-daily dosing (improving compliance), and lack of systemic side effects compared to beta-blockers. **2. Analysis of Incorrect Options:** * **Timolol (Beta-blocker):** Previously the first-line treatment, it is now considered second-line. It works by decreasing aqueous production. It is often contraindicated in elderly patients with potential systemic comorbidities like asthma, COPD, or heart block. * **Carbonic Anhydrase Inhibitors (e.g., Dorzolamide):** These are less potent than PGAs and are typically used as adjunctive therapy rather than monotherapy. * **Brimonidine (Alpha-2 Agonist):** Primarily used as an add-on therapy. While it has potential neuroprotective properties, it has a high incidence of local allergic reactions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of PGAs:** Increase uveoscleral outflow (the "alternative" pathway). * **Side Effects of PGAs:** Increased iris pigmentation (heterochromia), hypertrichosis (thickening of eyelashes), and deepening of the sulcus. * **Early Field Defect:** Small islands of vision loss like the **paracentral scotoma** or **Siedel’s scotoma** are early signs; the **Arcuate (Bjerrum) scotoma** is the most classic. * **ISNT Rule:** In a healthy disc, the Neuroretinal Rim width follows Inferior > Superior > Nasal > Temporal. Notching (as seen in this patient) indicates a violation of this rule.

Question 1

An elderly man presents with a painful red eye. On examination, the pupil is noted to be dilated and fixed. What is the next line of investigation?

Accepted Answer

Tonometry

Answer

Visual evoked potential

Answer

Retinal angiogram

Answer

Slit lamp examination

Question 2

What is the normal diurnal variation of intraocular pressure?

Accepted Answer

3-6 mm of Hg

Answer

0-2 mm of Hg

Answer

2-3 mm of Hg

Answer

6-8 mm of Hg

Question 3

In closed-angle glaucoma, all of the following are true EXCEPT:

Accepted Answer

Nonsystemic manifestations occur.

Answer

Iridectomy is performed.

Answer

Pilocarpine is used.

Answer

Atropine is not used.

Question 4

Inverse glaucoma is seen with which condition?

Accepted Answer

Instillation of miotics

Answer

Instillation of steroids

Answer

Instillation of mydriatics

Answer

All of the above

Question 5

What is the first-line drug of choice for primary open-angle glaucoma?

Accepted Answer

Prostaglandin analogues

Answer

Beta-blockers

Answer

Carbonic anhydrase inhibitors

Answer

Miotics

Question 6

Neovascularization of the iris is not seen in which of the following conditions?

Accepted Answer

Pigment Dispersion Syndrome

Answer

Central Retinal Vein Occlusion (CRVO)

Answer

Ocular Ischemic Syndrome

Answer

Diabetic Retinopathy

Question 7

A 36-year-old female develops eye pain during a prone dark room test. Which of the following drugs should be avoided?

Accepted Answer

Atropine

Answer

Acetazolamide

Answer

Pilocarpine

Answer

Timolol

Question 8

Laser iridotomy is indicated for which type of glaucoma?

Accepted Answer

Primary angle-closure glaucoma (PACG)

Answer

Primary open-angle glaucoma (POAG)

Answer

Congenital glaucoma

Answer

Secondary angle-closure glaucoma

Question 9

What is the sickle-shaped extension of the blind spot known as?

Accepted Answer

Seidel's sign

Answer

Down's sign

Answer

Bjerrum's sign

Answer

Baring of blind spot

Question 10

A 78-year-old male presents with a chief complaint of diminution of vision in both eyes. Intraocular pressure (IOP) in both eyes is 24 mm Hg, and an inferior notch is seen in the optic nerve head. Visual fields reveal a paracentral scotoma. What is the drug of choice?

Accepted Answer

Latanoprost

Answer

Timolol

Answer

Carbonic anhydrase inhibitor

Answer

Brimonidine

Glaucoma — MCQs

Glaucoma — MCQs

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