Glaucoma Practice Questions

Q: All except one of the following predispose to angle closure glaucoma?

Flat cornea. **Explanation:** Primary Angle Closure Glaucoma (PACG) typically occurs in eyes with specific anatomical predispositions that lead to "crowding" of the anterior segment. **Why "Flat Cornea" is the correct answer:** A **steep cornea** (increased curvature), not a flat one, is a predisposing factor for angle closure. A flat cornea (large radius of curvature) is actually associated with a deeper anterior chamber and is more common in myopic eyes, which are predisposed to Open Angle Glaucoma, not Angle Closure. **Analysis of Incorrect Options:** * **Small Cornea:** A smaller corneal diameter (microcornea) results in a smaller anterior segment volume, leading to a narrower iridocorneal angle. * **Shallow Anterior Chamber:** This is the hallmark anatomical risk factor. A decreased distance between the cornea and the lens iris diaphragm facilitates pupillary block and angle crowding. * **Short Axial Length:** This is characteristic of **hypermetropic (farsighted) eyes**. In these eyes, the intraocular contents are "crowded" into a smaller space, and the lens is often relatively large and positioned anteriorly, significantly increasing the risk of PACG. **High-Yield Clinical Pearls for NEET-PG:** * **The "Typical" PACG Patient:** Elderly, female (3:1 ratio), hypermetropic, with a family history. * **Lens Factor:** As age increases, the lens grows in thickness (phakomorphic component) and moves forward, further shallowing the anterior chamber. * **Precipitating Factor:** Mydriasis (pupil dilation) due to darkness, stress, or drugs (e.g., Atropine) can trigger an acute attack by causing the peripheral iris to bunch up in the angle. * **Gold Standard Treatment:** Laser Peripheral Iridotomy (LPI).

Q: A patient presented with an acute attack of asthma after starting treatment for glaucoma. What is the most likely causative drug?

Timolol. **Explanation:** The correct answer is **Timolol**. **1. Why Timolol is correct:** Timolol is a **non-selective beta-blocker** (blocking both $\beta_1$ and $\beta_2$ receptors). While it effectively reduces intraocular pressure by decreasing aqueous humor production, its systemic absorption through the nasolacrimal duct can lead to significant side effects. Blocking **$\beta_2$ receptors** in the bronchial smooth muscles causes bronchoconstriction, which can precipitate a life-threatening acute asthma attack in susceptible individuals. **2. Analysis of Incorrect Options:** * **Betaxolol:** This is a **cardioselective ($\beta_1$) blocker**. Because it has minimal effect on $\beta_2$ receptors, it is the safest topical beta-blocker for patients with respiratory issues, though it should still be used with caution. * **Clonidine:** This is an $\alpha_2$-adrenergic agonist. While its derivative, Apraclonidine, is used in glaucoma, it does not typically cause bronchospasm. * **Acetazolamide:** This is a carbonic anhydrase inhibitor. Its primary systemic side effects include metabolic acidosis, hypokalemia, and paresthesia, but not acute asthma. **Clinical Pearls for NEET-PG:** * **Gold Standard:** Timolol is often the first-line beta-blocker for glaucoma but is strictly contraindicated in Asthma and COPD. * **Systemic Absorption:** To minimize systemic side effects of eye drops, advise patients to perform **punctal occlusion** (pressing the inner corner of the eye) for 2 minutes after instillation. * **Drug of Choice:** For a glaucoma patient with asthma, **Betaxolol** is the preferred beta-blocker, but Prostaglandin analogues (e.g., Latanoprost) are generally the overall first-line choice.

Q: In acute congestive glaucoma, what is the best prophylaxis for the other eye?

Laser Iridotomy. **Explanation:** Acute congestive glaucoma (Acute Angle-Closure Glaucoma) is a medical emergency often caused by **pupillary block** in anatomically predisposed eyes. Because the anatomical predisposition (shallow anterior chamber, narrow angles) is almost always **bilateral**, the fellow eye (the "other eye") is at an extremely high risk (approx. 50-80%) of developing a similar acute attack within 5-10 years. **Why Laser Iridotomy is the Correct Answer:** **Laser Peripheral Iridotomy (LPI)** is the gold standard for prophylaxis. It creates a small hole in the peripheral iris, providing an alternative pathway for aqueous humor to flow from the posterior to the anterior chamber. This bypasses the pupillary block, equalizes pressure between the two chambers, and causes the iris to fall away from the trabecular meshwork, effectively "opening" the angle. It is preferred over surgery because it is non-invasive, outpatient-based, and has fewer complications. **Analysis of Incorrect Options:** * **Topical Steroids:** These are used to reduce inflammation during an acute attack but do not address the underlying anatomical blockage. * **Trabeculectomy:** This is a filtering surgery used for chronic glaucoma when medical/laser therapy fails. It is too invasive for prophylaxis in an eye with normal intraocular pressure. * **Surgical Peripheral Iridectomy:** While physiologically similar to LPI, it is an incisional intraocular surgery. It is now reserved only for cases where LPI cannot be performed (e.g., hazy cornea or very thick iris). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (Medical):** IV Mannitol (to rapidly lower IOP) and Acetazolamide. * **Definitive Treatment:** Laser Peripheral Iridotomy (LPI). * **Fellow Eye Management:** Always perform prophylactic LPI, as it is considered a "ticking time bomb." * **Classic Presentation:** Mid-dilated non-reactive pupil, hazy cornea, and "halos" around lights.

Q: What is the most common cause of rubeosis iridis?

Diabetic retinopathy. **Explanation:** **Rubeosis iridis** (neovascularization of the iris) is a serious condition where new, fragile blood vessels form on the iris surface in response to chronic retinal ischemia. **Why Diabetic Retinopathy is Correct:** The underlying mechanism is **retinal hypoxia**, which triggers the release of **Vascular Endothelial Growth Factor (VEGF)**. VEGF diffuses into the anterior segment, stimulating angiogenesis. **Diabetic Retinopathy (DR)**, specifically Proliferative Diabetic Retinopathy (PDR), is the **most common cause** of rubeosis iridis worldwide due to the high prevalence of the disease and the extensive retinal ischemia it induces. **Analysis of Incorrect Options:** * **Central Retinal Artery Occlusion (CRAO):** While CRAO causes ischemia, it is a less common cause of rubeosis (occurring in ~2% of cases) compared to Central Retinal Vein Occlusion (CRVO) or DR. * **Radiation Retinopathy:** This can cause rubeosis due to capillary non-perfusion, but it is a rare clinical entity compared to the systemic burden of diabetes. * **Tumors:** Intraocular tumors like retinoblastoma or melanoma can cause rubeosis via angiogenic factors, but they are statistically infrequent causes. **High-Yield Clinical Pearls for NEET-PG:** 1. **Top 3 Causes:** 1. Diabetic Retinopathy (Most common), 2. Central Retinal Vein Occlusion (CRVO - specifically the ischemic type, often called "100-day glaucoma"), 3. Carotid Artery Occlusive Disease. 2. **Complication:** Rubeosis iridis leads to **Neovascular Glaucoma (NVG)** as the new vessels and associated fibrous membranes pull the iris forward, causing synechial angle closure. 3. **Management:** The mainstay of treatment is **Pan-retinal Photocoagulation (PRP)** to reduce the ischemic drive, often supplemented by anti-VEGF injections.

Q: Angle closure glaucoma may be associated with which refractive error?

Hypermetropia. **Explanation:** **Primary Angle Closure Glaucoma (PACG)** occurs due to anatomical predisposition. The correct answer is **Hypermetropia** because hypermetropic eyes are characteristically smaller than emmetropic eyes. **Why Hypermetropia is correct:** Hypermetropic eyes have a **short axial length**, a **shallow anterior chamber**, and a relatively **large crystalline lens** compared to the overall size of the eye. This "crowding" of the anterior segment narrows the iridocorneal angle. As the lens continues to grow with age, it pushes the iris forward, increasing iridolenticular contact. This leads to physiological pupillary block, causing the peripheral iris to bulge forward (iris bombé) and obstruct the trabecular meshwork, triggering an angle-closure attack. **Why other options are incorrect:** * **Myopia:** Myopic eyes are typically larger with a **long axial length** and a deep anterior chamber. Myopia is strongly associated with **Primary Open Angle Glaucoma (POAG)** and pigmentary glaucoma, not angle closure. * **Pseudomyopia:** This is a temporary shift in refractive error caused by ciliary muscle spasm (accommodative spasm). It is a functional condition rather than an anatomical one and does not predispose to angle closure. * **Pseudohypermetropia:** This is a rare clinical mimic (e.g., due to macular edema or orbital tumors pushing the globe) and is not a primary anatomical risk factor for PACG. **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** PACG is more common in females (3:1 ratio), elderly patients, and individuals of South East Asian descent. * **Precipitating Factors:** Mydriasis (e.g., sitting in a dark cinema hall or use of atropine) can trigger an acute attack. * **Drug of Choice:** The definitive treatment for PACG is **Laser Peripheral Iridotomy (LPI)**. * **Immediate Management:** IV Mannitol and topical Acetazolamide are used to rapidly lower Intraocular Pressure (IOP).

Q: A 60-year-old male presents with coloured halos. On Fincham's test, the halos split and then reunite. The most probable diagnosis is?

Senile immature cataract. **Explanation:** The presence of colored halos is a classic symptom in ophthalmology, typically caused by the diffraction of light. The **Fincham’s Test** is the definitive clinical maneuver used to differentiate the cause of these halos. **1. Why Senile Immature Cataract is correct:** In an immature cataract, the halos are produced by the **radial arrangement of lens fibers**, which act as a diffraction grating. When a stenopeic slit is moved across the pupil (Fincham’s Test), the halos **split and then reunite**. This "splitting" is pathognomonic for lenticular halos (cataract). **2. Why the other options are incorrect:** * **Acute Congestive Glaucoma:** Halos are caused by **corneal edema** (fluid droplets in the epithelium). Since the edema is uniform and lacks a radial structure, the halos **do not split** during Fincham’s test; they simply disappear or diminish in intensity. * **Open Angle Glaucoma:** This condition is usually asymptomatic in early stages and does not typically present with colored halos unless the intraocular pressure is acutely very high. * **Mucopurulent Conjunctivitis:** Halos here are caused by **mucus flakes** on the corneal surface. These halos are transient and **disappear after blinking** or washing the eyes. **Clinical Pearls for NEET-PG:** * **Glaucomatous Halos:** The blue-violet ring is innermost, and the red ring is outermost. * **Fincham’s Test Result:** * *Splitting:* Lenticular (Cataract) * *No Splitting:* Corneal (Glaucoma) * **Differential Diagnosis of Halos:** Remember the "3 C's": **C**ataract, **C**orneal Edema (Glaucoma), and **C**onjunctivitis (Mucus). * **Stenopeic Slit:** This is the tool used to perform Fincham's test.

Q: Vogt's triad of primary angle closure glaucoma does not include which of the following?

Fixed pupils. **Explanation:** **Vogt’s Triad** consists of clinical signs that indicate a **previous episode** of acute congestive angle-closure glaucoma. These signs are essentially "scars" or permanent markers left behind after the intraocular pressure (IOP) has normalized. 1. **Why "Fixed Pupils" is the correct answer:** While a **vertically oval, mid-dilated, and fixed pupil** is a classic sign of an *active* acute attack (due to sphincter ischemia), it is not part of Vogt’s Triad. The triad specifically refers to post-congestive sequelae, whereas a fixed pupil is a feature of the acute stage itself. 2. **Analysis of the Triad components (Incorrect Options):** * **Glaukomflecken (Option B):** These are small, grey-white subcapsular lenticular opacities caused by focal necrosis of the lens epithelium due to high IOP. They are pathognomonic of a prior acute attack. * **Pigment deposition on corneal endothelium (Option C):** During an attack, the iris rubs against the lens and cornea, releasing pigment. This pigment settles on the endothelium (often as a Krukenberg-like distribution) once the attack subsides. * **Patches of iris atrophy (Option D):** Ischemia during the pressure spike leads to sectorial atrophy of the iris stroma, often resulting in permanent structural changes and pigment loss. **High-Yield Clinical Pearls for NEET-PG:** * **Vogt’s Triad:** Glaukomflecken + Iris Atrophy + Endothelial Pigment. * **Acute Attack Presentation:** Sudden painful loss of vision, "halos" around lights (due to corneal edema), and a stony-hard eye. * **Management:** The definitive treatment for the fellow eye in angle closure is **Prophylactic Laser Peripheral Iridotomy (LPI)**, as the condition is usually bilateral. * **Glaukomflecken** is often described as "milk-white spots" and is one of the most reliable signs that a patient has suffered a significant hypertensive crisis in the eye.

Q: Kusumlata presents with acute painful red eye and a mildly dilated, vertically oval pupil. What is the most likely diagnosis?

Acute angle closure glaucoma. ### Explanation **Correct Answer: B. Acute angle closure glaucoma** The clinical presentation of an **acute painful red eye** associated with a **mildly dilated, vertically oval, and non-reactive pupil** is a classic "textbook" description of **Acute Angle Closure Glaucoma (AACG)**. In AACG, a sudden rise in intraocular pressure (IOP) causes ischemia and paralysis of the iris sphincter muscle. This results in the characteristic mid-dilated, vertically oval pupil. Other associated features include a "steamy" or hazy cornea (due to epithelial edema), a shallow anterior chamber, and severe ocular pain often accompanied by nausea and vomiting. **Why the other options are incorrect:** * **A. Acute retrobulbar neuritis:** Characterized by sudden vision loss and pain on eye movement, but the eye appears **"white and quiet"** externally. The pupil typically shows an Afferent Pupillary Defect (RAPD/Marcus Gunn pupil), not a mid-dilated oval shape. * **C. Acute anterior uveitis:** While it presents with a painful red eye, the pupil is typically **small (miotic)** and irregular due to the formation of posterior synechiae. * **D. Severe kerato-conjunctivitis:** Presents with redness and discharge; however, the pupil size and reaction remain **normal**, and there is no significant rise in IOP. **High-Yield Clinical Pearls for NEET-PG:** * **Immediate Management:** Systemic Acetazolamide (IV/Oral) and hyperosmotic agents (Mannitol/Glycerol) to lower IOP, followed by topical Pilocarpine (once IOP <40 mmHg) and definitive **Peripheral Iridotomy (Laser or Surgical)**. * **The "Vertical Oval" Pupil:** This occurs because the vertical fibers of the iris sphincter are more susceptible to ischemic paralysis than the horizontal ones. * **Differential Diagnosis Tip:** Always check the pupil! * *Miosis (Constricted):* Uveitis. * *Mid-dilated/Oval:* Glaucoma. * *Normal:* Conjunctivitis.

Q: Fincham's test is used to:

Differentiate acute congestive glaucoma from cataract. **Explanation:** **Fincham’s Test (Stenopeic Slit Test)** is a clinical maneuver used to differentiate the cause of colored halos around lights. Halos are a common symptom in both **Acute Congestive Glaucoma** and **Immature Senile Cataract**, but the underlying mechanism differs. 1. **Why the correct answer is right:** * In **Acute Congestive Glaucoma**, halos are caused by **corneal edema**. When a stenopeic slit is passed across the pupil, the halos remain intact and do not break up. * In **Cataract**, halos are caused by the **diffraction of light** by water clefts in the lens. When the stenopeic slit is passed across the pupil, the circular halo breaks into segments (it disappears and reappears). * Therefore, Fincham’s test is the definitive clinical method to distinguish between these two conditions based on the behavior of the halos. 2. **Why the incorrect options are wrong:** * **Option A & D:** Congenital glaucoma and congenital cataract are diagnosed primarily through clinical examination (buphthalmos, corneal diameter, and red reflex testing). Fincham’s test requires subjective feedback from the patient regarding halos, which is not feasible in infants. * **Option B:** While the test is used *during* an episode of acute congestive glaucoma, its specific purpose is differential diagnosis, not the primary diagnosis of the pressure elevation itself (which is done via tonometry). **High-Yield Clinical Pearls for NEET-PG:** * **Emsley’s Rule:** Glaucomatous halos have a specific color arrangement—**Blue is innermost** and **Red is outermost**. * **Other causes of halos:** Corneal dystrophy, conjunctivitis (due to mucus), and wearing ill-fitting contact lenses. * **Differential Diagnosis:** Always remember that a "mid-dilated non-reactive pupil" points toward Acute Glaucoma, while a "normal pupil with lens opacities" points toward Cataract.

Question 1

All except one of the following predispose to angle closure glaucoma?

Accepted Answer

Flat cornea

Answer

Small cornea

Answer

Shallow anterior chamber

Answer

Short axial length of eyeball

Question 2

A patient presented with an acute attack of asthma after starting treatment for glaucoma. What is the most likely causative drug?

Accepted Answer

Timolol

Answer

Betaxolol

Answer

Clonidine

Answer

Acetazolamide

Question 3

In acute congestive glaucoma, what is the best prophylaxis for the other eye?

Accepted Answer

Laser Iridotomy

Answer

Topical steroids

Answer

Trabeculectomy

Answer

Surgical peripheral Iridectomy

Question 4

Intraocular pressure is most accurately measured by which instrument?

Accepted Answer

Applanation tonometer

Answer

Schiotz tonometer

Answer

Non-contact tonometer

Answer

Digital tonometer

Question 5

What is the most common cause of rubeosis iridis?

Accepted Answer

Diabetic retinopathy

Answer

Tumor

Answer

Central retinal artery occlusion (CRAO)

Answer

Radiation retinopathy

Question 6

Angle closure glaucoma may be associated with which refractive error?

Accepted Answer

Hypermetropia

Answer

Myopia

Answer

Pseudomyopia

Answer

Pseudohypermetropia

Question 7

A 60-year-old male presents with coloured halos. On Fincham's test, the halos split and then reunite. The most probable diagnosis is?

Accepted Answer

Senile immature cataract

Answer

Acute congestive glaucoma

Answer

Open angle glaucoma

Answer

Mucopurulent conjunctivitis

Question 8

Vogt's triad of primary angle closure glaucoma does not include which of the following?

Accepted Answer

Fixed pupils

Answer

Glaucoma flecks

Answer

Pigment deposition on corneal endothelium

Answer

Patches of iris atrophy

Question 9

Kusumlata presents with acute painful red eye and a mildly dilated, vertically oval pupil. What is the most likely diagnosis?

Accepted Answer

Acute angle closure glaucoma

Answer

Acute retrobulbar neuritis

Answer

Acute anterior uveitis

Answer

Severe kerato-conjunctivitis

Question 10

Fincham's test is used to:

Accepted Answer

Differentiate acute congestive glaucoma from cataract

Answer

Diagnose congenital glaucoma

Answer

Diagnose acute congestive glaucoma

Answer

Diagnose congenital cataract

Glaucoma — MCQs

Glaucoma — MCQs

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