Glaucoma — MCQs
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Campimetry (Scotometry) is performed in the visual field area of:
Which of the following is NOT a side effect of apraclonidine?
What is the treatment of choice in acute congestive glaucoma?
On mutation, which of the following may give rise to hereditary glaucoma?
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?
What is the initial drug of choice for open-angle glaucoma?
Argon laser trabeculoplasty is indicated in which of the following conditions?
Which instrument is used to visualize the angle of the anterior chamber?
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?
Increased intraocular pressure along with an enlarged and thick cornea with a large eye may suggest which of the following conditions?
Glaucoma Indian Medical PG Practice Questions and MCQs
Question 41: Campimetry (Scotometry) is performed in the visual field area of:
- A. 50 degrees
- B. 30 degrees (Correct Answer)
- C. 60 degrees
- D. 90 degrees
Explanation: **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).
Question 42: Which of the following is NOT a side effect of apraclonidine?
- A. Lid dermatitis
- B. Follicular conjunctivitis
- C. Eyelid retraction
- D. Watering of mouth (Correct Answer)
Explanation: **Explanation:** **Apraclonidine** is a selective alpha-2 adrenergic agonist used primarily to prevent or treat post-laser intraocular pressure (IOP) spikes. **Why "Watering of mouth" is the correct answer:** Apraclonidine, like its relative Brimonidine, is a sympathomimetic. A common systemic side effect of alpha-2 agonists is **Xerostomia (dryness of mouth)**, not watering. This occurs due to the activation of alpha-2 receptors in the salivary glands and the central nervous system, which inhibits salivary secretion. **Analysis of incorrect options:** * **Lid dermatitis & Follicular conjunctivitis:** These are common **local allergic reactions** associated with long-term use of topical alpha-agonists. Apraclonidine has a high rate of delayed hypersensitivity (up to 30-40%), which often manifests as blepharoconjunctivitis. * **Eyelid retraction:** This is a unique side effect of Apraclonidine. It occurs because the drug stimulates the alpha-adrenergic receptors of **Müller’s muscle** (a smooth muscle in the upper eyelid), leading to its contraction and subsequent lid elevation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Reduces IOP by decreasing aqueous humor production and increasing uveoscleral outflow. * **Tachyphylaxis:** Apraclonidine is notorious for losing its efficacy over time (tachyphylaxis), making it unsuitable for long-term chronic glaucoma management. * **Clinical Use:** It is the drug of choice for preventing IOP spikes after **Nd:YAG laser capsulotomy** or **Laser Peripheral Iridotomy (LPI)**. * **Diagnostic Use:** It is used in the diagnosis of **Horner’s Syndrome**; it causes pupillary dilation in the affected eye (due to denervation supersensitivity) while having no effect on a normal pupil.
Question 43: What is the treatment of choice in acute congestive glaucoma?
- A. Pilocarpine
- B. Laser iridotomy (Correct Answer)
- C. Timolol
- D. Trabeculoplasty
Explanation: **Explanation:** Acute congestive glaucoma (Acute Angle-Closure Glaucoma) is a medical emergency caused by a sudden rise in intraocular pressure (IOP) due to a pupillary block, which prevents aqueous humor from reaching the anterior chamber angle. **Why Laser Peripheral Iridotomy (LPI) is the Treatment of Choice:** The definitive treatment for angle closure is **Laser Iridotomy**. It creates a small hole in the peripheral iris, establishing a bypass for aqueous humor to flow from the posterior to the anterior chamber. This eliminates the pressure gradient (pupillary block), allows the iris to fall back, and opens the drainage angle. It is also performed prophylactically in the fellow (contralateral) eye, as there is a high risk of a similar attack. **Analysis of Incorrect Options:** * **Pilocarpine (A):** While used to constrict the pupil and pull the iris away from the angle, it is **not** the definitive treatment. In very high IOP (>40-50 mmHg), the iris sphincter is ischemic and unresponsive to pilocarpine. It is typically administered only after the IOP has been lowered by systemic agents. * **Timolol (C):** This is a beta-blocker used to decrease aqueous production. It is an adjunctive therapy to lower IOP but does not address the underlying anatomical cause (pupillary block). * **Trabeculoplasty (D):** This (e.g., ALT/SLT) is used in **Open-Angle Glaucoma** to increase outflow through the trabecular meshwork. It is contraindicated in acute angle closure because the angle is physically obstructed by the iris. **NEET-PG High-Yield Pearls:** * **Immediate Management:** The first-line medical management to rapidly lower IOP is **IV Acetazolamide** or IV Mannitol. * **Drug of Choice for definitive treatment:** Laser Peripheral Iridotomy (LPI). * **Surgical Iridectomy:** Indicated if LPI cannot be performed (e.g., due to a hazy cornea or flat anterior chamber). * **Classic Presentation:** Sudden painful red eye, "halos" around lights, mid-dilated non-reactive pupil, and a "stony hard" eye on palpation.
Question 44: On mutation, which of the following may give rise to hereditary glaucoma?
- A. Optineurin (Correct Answer)
- B. Ephrins
- C. RBA8
- D. Huntingtin
Explanation: ### 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.
Question 45: 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?
- A. Acute closed-angle glaucoma (Correct Answer)
- B. Corneal laceration
- C. Ocular hypertension without glaucoma
- D. Open angle glaucoma
Explanation: ### 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).
Question 46: What is the initial drug of choice for open-angle glaucoma?
- A. Beta-blocker (Correct Answer)
- B. Pilocarpine
- C. Anticholinergics
- D. Physostigmine
Explanation: **Explanation:** In the management of **Primary Open-Angle Glaucoma (POAG)**, the goal is to lower intraocular pressure (IOP) to prevent optic nerve damage. **Why Beta-blockers are the correct choice:** Historically and for the purpose of standard examinations like NEET-PG, **Topical Beta-blockers (e.g., Timolol)** are considered the first-line medical therapy. They work by **decreasing the production of aqueous humor** from the ciliary epithelium. Timolol is preferred due to its potent IOP-lowering effect, twice-daily dosing, and relatively low cost. (Note: While Prostaglandin analogues are increasingly used as first-line in modern clinical practice, Beta-blockers remain the classic textbook answer for this question). **Analysis of Incorrect Options:** * **B. Pilocarpine:** This is a miotic (parasympathomimetic). While it increases aqueous outflow through the trabecular meshwork, it is no longer first-line due to side effects like miosis, brow ache, and increased risk of retinal detachment. It is, however, the drug of choice in **Acute Angle Closure Glaucoma**. * **C. Anticholinergics:** These drugs (like Atropine) cause mydriasis and can precipitate acute angle-closure glaucoma in predisposed eyes. They are **contraindicated** in glaucoma. * **D. Physostigmine:** This is an indirect-acting cholinergic (anticholinesterase). Like pilocarpine, it is rarely used today due to significant local side effects and the availability of superior drugs. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Timolol:** Non-selective $\beta_1$ and $\beta_2$ blockade; reduces aqueous secretion. * **Contraindications:** Always screen for **Bronchial Asthma** or **COPD** (due to $\beta_2$ blockade causing bronchospasm) and **Bradycardia/Heart block** (due to $\beta_1$ blockade). * **Drug of choice for Acute Congestive Glaucoma:** IV Mannitol (to rapidly lower IOP) and Pilocarpine (once IOP drops below 40 mmHg). * **Drug of choice for Pregnancy:** Brimonidine (but avoid near term/delivery).
Question 47: Argon laser trabeculoplasty is indicated in which of the following conditions?
- A. Aphakic glaucoma
- B. Neovascular glaucoma
- C. Closed angle glaucoma
- D. Open angle glaucoma (Correct Answer)
Explanation: **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.
Question 48: Which instrument is used to visualize the angle of the anterior chamber?
- A. Slit lamp examination
- B. Keratometry
- C. Gonioscopy (Correct Answer)
- D. Indirect ophthalmoscopy
Explanation: **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.
Question 49: 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?
- A. Acute congestive glaucoma
- B. Chronic simple glaucoma
- C. Acute anterior uveitis (Correct Answer)
- D. Endophthalmitis
Explanation: ### Explanation The correct answer is **Acute Anterior Uveitis**. **1. Why Acute Anterior Uveitis is correct:** The clinical presentation describes a classic case of **Glaucomatocyclitic Crisis (Posner-Schlossman Syndrome)** or, more broadly, **Hypertensive Uveitis**. * **Miotic Pupil:** In uveitis, the pupil is typically small (miotic) due to ciliary muscle spasm and iris congestion. This contrasts with the mid-dilated pupil seen in acute angle-closure glaucoma. * **Raised IOP:** While uveitis usually lowers IOP (due to ciliary body exhaustion), certain types (like Posner-Schlossman or Herpetic uveitis) cause a significant rise in IOP due to trabeculitis or inflammatory debris clogging the trabecular meshwork. * **Normal Anterior Chamber (AC):** This indicates an open-angle mechanism, distinguishing it from primary angle-closure. * **Fellow Eye:** The "hazy cornea and shallow AC" in the fellow eye is a distractor or may suggest a predisposition to secondary inflammatory changes, but the **miotic pupil** in the eye with high IOP is the pathognomonic "red flag" pointing toward uveitis rather than glaucoma. **2. Why other options are incorrect:** * **Acute Congestive Glaucoma:** Characterized by a **vertically oval, mid-dilated, non-reactive pupil** and a shallow AC. A miotic pupil excludes this diagnosis. * **Chronic Simple Glaucoma:** Typically asymptomatic, bilateral, and presents with a normal-looking eye and normal pupil until very late stages. It does not present with acute corneal haziness. * **Endophthalmitis:** An extreme emergency usually following surgery or trauma. While it features high/low IOP and inflammation, it presents with severe pain, loss of vision, and **hypopyon/vitritis**, which are not mentioned. **3. NEET-PG High-Yield Pearls:** * **Pupil in Glaucoma:** Mid-dilated and vertically oval. * **Pupil in Uveitis:** Miotic (small). * **Posner-Schlossman Syndrome:** Recurrent episodes of very high IOP, mild discomfort, open angles, and fine Keratic Precipitates (KPs). * **Treatment Tip:** In hypertensive uveitis, avoid pilocarpine (it worsens inflammation) and use topical steroids with aqueous suppressants.
Question 50: Increased intraocular pressure along with an enlarged and thick cornea with a large eye may suggest which of the following conditions?
- A. Congenital glaucoma (Correct Answer)
- B. Angle closure glaucoma
- C. Phacomorphic glaucoma
- D. Phacotopic glaucoma
Explanation: ### Explanation **1. Why Congenital Glaucoma is Correct:** The clinical triad of increased intraocular pressure (IOP), an enlarged eye (**Buphthalmos**), and a thick, cloudy cornea is pathognomonic for **Congenital Glaucoma** (specifically Primary Congenital Glaucoma). * **Pathophysiology:** In infants, the collagen fibers of the sclera and cornea are elastic. When IOP rises due to maldevelopment of the trabecular meshwork (trabeculodysgenesis), the globe stretches, leading to an increased corneal diameter (>12 mm) and axial length. * **Corneal Changes:** The stretching causes breaks in Descemet’s membrane (**Haab’s striae**), leading to corneal edema and subsequent thickening/opacification. **2. Why the Other Options are Incorrect:** * **Angle-closure Glaucoma:** Typically occurs in adults with **small eyes** (hypermetropia) and shallow anterior chambers. It does not cause enlargement of the globe because the adult sclera is rigid. * **Phacomorphic Glaucoma:** A secondary angle-closure glaucoma caused by an intumescent (swollen) cataractous lens. While it causes high IOP and corneal edema, it does not result in an enlarged eye. * **Phacotopic Glaucoma:** Glaucoma resulting from lens subluxation or dislocation (ectopia lentis). It is not associated with globe enlargement. **3. Clinical Pearls for NEET-PG:** * **Classic Triad:** Epiphora (tearing), Photophobia, and Blepharospasm. * **Buphthalmos:** Termed "Ox-eye" due to the massive enlargement. * **Measurement:** Normal newborn corneal diameter is ~10-10.5 mm. A diameter **>12 mm** is highly suggestive of glaucoma. * **Treatment of Choice:** Surgery is the primary treatment. **Goniotomy** (if the cornea is clear) or **Trabeculotomy/Trabeculectomy** (if the cornea is cloudy). Medical therapy is only a temporary measure.
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
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