Glaucoma Practice Questions

Q: A 68-year-old female presents with severe right eye pain, blurred vision, nausea, and vomiting. Earlier in the day, she underwent a difficult colonoscopy for Crohn's disease. What is the likely cause of her painful red eye?

Acute angle closure glaucoma. **Explanation:** The patient is presenting with a classic case of **Acute Angle Closure Glaucoma (AACG)**. The underlying mechanism is a sudden rise in intraocular pressure (IOP) due to the blockage of aqueous humor outflow at the iridocorneal angle. **Why it is the correct answer:** The clinical triad of severe ocular pain, blurred vision (often with halos), and systemic symptoms like nausea/vomiting is pathognomonic for AACG. The crucial "NEET-PG trigger" here is the **colonoscopy**. During difficult endoscopies, antispasmodic drugs like **Hyoscine (Buscopan)** or other anticholinergics are frequently administered. These drugs cause **mydriasis** (pupillary dilation), which can crowd the angle and precipitate an acute attack in predisposed individuals (e.g., elderly females with hypermetropia). **Why other options are incorrect:** * **Anterior Uveitis:** Presents with pain and photophobia, but the pupil is typically **constricted (miotic)** and irregular, not mid-dilated. It does not cause sudden nausea/vomiting. * **Acute Conjunctivitis:** Characterized by discharge and grittiness rather than severe deep-seated pain. Vision remains normal. * **Episcleritis:** Usually a localized, sectoral redness; it is typically painless or associated with mild discomfort and does not affect vision. **Clinical Pearls for NEET-PG:** * **Classic Sign:** A "mid-dilated, vertically oval, non-reactive pupil" with a "steamy/hazy cornea." * **Risk Factors:** Hypermetropia (short axial length), shallow anterior chamber, and increasing age. * **Immediate Management:** IV Acetazolamide, topical beta-blockers, and **Pilocarpine** (once IOP drops) to induce miosis. * **Definitive Treatment:** Peripheral Iridotomy (usually YAG laser) for both the affected and the fellow (prophylactic) eye.

Q: Which of the following characterizes chronic simple glaucoma?

Elevated intraocular pressure with optic nerve damage.. **Explanation:** Chronic Simple Glaucoma, also known as **Primary Open-Angle Glaucoma (POAG)**, is a chronic, progressive optic neuropathy. The diagnosis is fundamentally based on a triad: **elevated intraocular pressure (IOP)**, characteristic **optic nerve head changes** (cupping), and corresponding **visual field defects**. 1. **Why Option B is correct:** In POAG, the resistance to aqueous outflow occurs at the level of the trabecular meshwork. The resulting elevation in IOP leads to mechanical and ischemic damage to the retinal ganglion cells, manifesting as pathological cupping of the optic disc and progressive vision loss. 2. **Why other options are incorrect:** * **Option A:** Elevated IOP without optic nerve damage or field loss is termed **Ocular Hypertension**, not glaucoma. * **Option C:** Visual field defects in glaucoma are a direct consequence of optic nerve fiber loss. You cannot have glaucomatous field defects without corresponding structural changes in the optic nerve. * **Option D:** A pink optic disc indicates a healthy, well-perfused nerve. In glaucoma, the disc appears **pale** (due to atrophy) and shows increased **cupping**. **Clinical Pearls for NEET-PG:** * **Risk Factors:** Age >40, high myopia, family history, and Diabetes Mellitus. * **Early Sign:** The earliest visual field defect is often a **Siedel’s scotoma** (extension of the blind spot), progressing to a **Bjerrum’s (arcuate) scotoma**. * **Gold Standard Diagnosis:** Applanation tonometry for IOP, Automated Perimetry (HFA) for fields, and slit-lamp biomicroscopy for disc evaluation. * **Treatment:** Prostaglandin analogues (e.g., Latanoprost) are the first-line medical management.

Q: Increased episcleral venous pressure can affect intraocular pressure (IOP) in which way?

Increase IOP. **Explanation:** The relationship between episcleral venous pressure (EVP) and intraocular pressure (IOP) is governed by **Goldmann’s Equation**: **IOP = (F / C) + Pe** *(Where F = rate of aqueous formation, C = facility of outflow, and Pe = episcleral venous pressure).* In a healthy eye, aqueous humor flows from the anterior chamber through the trabecular meshwork and Schlemm’s canal into the episcleral veins. Because this is a pressure-dependent drainage system, any rise in the downstream pressure (EVP) creates resistance to the outflow of aqueous. According to the equation, for every **1 mmHg rise in EVP, there is a corresponding 1 mmHg rise in IOP**. **Analysis of Options:** * **Option A (Correct):** Increased EVP directly resists aqueous drainage, leading to a linear increase in IOP. * **Option B & C:** These are incorrect because the outflow system is passive; if the "exit" pressure increases, the "internal" pressure must rise to maintain flow. * **Option D:** There is no physiological compensatory mechanism that eventually decreases IOP if the EVP remains chronically elevated. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Signs:** Patients often present with **dilated, tortuous (corkscrew) episcleral vessels**. * **Blood in Schlemm’s Canal:** On gonioscopy, blood may be seen in Schlemm’s canal due to backflow from high venous pressure. * **Common Causes:** 1. **Carotid-Cavernous Fistula (CCF):** Most common cause of sudden, pulsatile proptosis with high EVP. 2. **Sturge-Weber Syndrome:** Associated with episcleral hemangiomas. 3. **Thyroid Eye Disease:** Due to venous compression by enlarged extraocular muscles. 4. **Superior Vena Cava Syndrome.**

Q: Iridectomy is a treatment option in which of the following conditions?

Angle closure glaucoma. **Explanation:** **1. Why Angle Closure Glaucoma (ACG) is correct:** The primary mechanism in primary angle-closure glaucoma is **pupillary block**. In this condition, the contact between the iris and the lens prevents aqueous humor from flowing from the posterior chamber to the anterior chamber. This creates a pressure gradient that pushes the peripheral iris forward (**iris bombé**), physically blocking the trabecular meshwork. * **Iridectomy** (surgical or laser peripheral iridotomy) creates a bypass channel in the iris. This equalizes the pressure between the chambers, allows the iris to fall back into its normal position, and opens the drainage angle. It is the definitive treatment for ACG. **2. Why the other options are incorrect:** * **A & C (Pigmentary and Pseudoexfoliative Glaucoma):** These are types of **Secondary Open Angle Glaucomas**. In these conditions, the drainage angle is physically open, but the trabecular meshwork is clogged by pigment granules or fibrillary material, respectively. Since there is no pupillary block, an iridectomy will not lower the intraocular pressure. * **D (Open Angle Glaucoma):** In Primary Open Angle Glaucoma (POAG), the pathology lies within the microscopic resistance of the trabecular meshwork itself. The anatomical relationship between the iris and lens is normal; therefore, an iridectomy serves no therapeutic purpose. **Clinical Pearls for NEET-PG:** * **Laser Peripheral Iridotomy (LPI)** is the preferred modern procedure over surgical iridectomy. * **Prophylaxis:** In a patient with acute congestive glaucoma, the **fellow eye** must always undergo a prophylactic iridectomy because there is a high risk of a similar attack. * **Nd:YAG Laser** is the most common tool used for performing a peripheral iridotomy.

Q: A patient presents with acute pain and redness of the eye, diminished vision, and vomiting. What is the most likely finding?

Mid-dilated pupil. ### Explanation The clinical presentation of acute ocular pain, redness, diminished vision, and systemic symptoms like vomiting is a classic triad for **Acute Angle Closure Glaucoma (AACG)**. **1. Why "Mid-dilated pupil" is correct:** In AACG, a sudden rise in intraocular pressure (IOP) causes ischemia and paralysis of the iris sphincter muscle. This results in a pupil that is **vertically oval, mid-dilated, and non-reactive to light**. The vomiting is a result of the oculo-emetic reflex triggered by the extremely high IOP (often >50–60 mmHg). **2. Why the other options are incorrect:** * **Hypopyon:** This refers to a collection of inflammatory cells in the anterior chamber, typically seen in **Endophthalmitis** or severe **Uveitis**. While these cause pain and redness, the pupil is usually constricted (miotic) due to ciliary spasm, not mid-dilated. * **Dislocated eye lens:** While a dislocated lens (Ectopia lentis) can cause secondary glaucoma (e.g., phacomorphic glaucoma), it is not a primary finding of the acute attack itself. It is usually associated with trauma or systemic syndromes like Marfan’s. * **Dendritic ulcer:** This is the hallmark of **Herpes Simplex Keratitis**. It presents with pain and redness, but vision loss is usually less sudden, and the pupil is typically normal or miotic. **Clinical Pearls for NEET-PG:** * **Corneal appearance:** In AACG, the cornea appears "steamy" or "cloudy" due to epithelial edema. * **Shallow Anterior Chamber:** This is a predisposing anatomical factor. * **Immediate Management:** IV Acetazolamide and topical pilocarpine (once IOP drops below 40 mmHg). * **Definitive Treatment:** Peripheral Iridotomy (Laser or Surgical) for both the affected and the fellow (prophylactic) eye.

Q: Facility of aqueous outflow is ______ I/min/mm Hg.

0.2. ### Explanation The **facility of aqueous outflow (C)** is a measure of the ease with which aqueous humor leaves the eye through the trabecular meshwork and uveoscleral pathways. It is defined as the volume of aqueous humor (in microliters) that leaves the eye per minute for every millimeter of mercury (mm Hg) of intraocular pressure (IOP). **1. Why Option D (0.2) is Correct:** The normal average value for the facility of outflow in a healthy adult eye is approximately **0.22 µl/min/mm Hg** (commonly rounded to **0.2** in exams). This value is calculated using the Tonography equation: $F = C \times (IOP - P_e)$, where $F$ is the rate of aqueous formation and $P_e$ is the episcleral venous pressure. A value below **0.18** is often considered suspicious, and below **0.11** is diagnostic of glaucoma. **2. Why Other Options are Incorrect:** * **Options A (0.8) and B (0.6):** These values are significantly higher than physiological norms. Such high facility would result in hypotony (abnormally low IOP), as the fluid would exit the eye too rapidly. * **Option C (0.4):** While closer to the range, this is still double the normal physiological average. **3. High-Yield Clinical Pearls for NEET-PG:** * **Aqueous Production Rate:** Normal rate is **2.0 to 2.5 µl/min**. * **Outflow Pathways:** * **Trabecular (Conventional):** 90% of outflow; pressure-dependent. * **Uveoscleral (Unconventional):** 10% of outflow; pressure-independent (targeted by Prostaglandin analogues). * **Goldmann Equation:** $P = (F/C) + P_e$. * **Ageing Effect:** The facility of outflow **decreases** with age and is significantly reduced in Primary Open Angle Glaucoma (POAG) due to increased resistance in the trabecular meshwork.

Q: Which of the following prostaglandin analogues is used for the treatment of primary open-angle glaucoma?

PG F2alpha. **Explanation:** Prostaglandin analogues (PGAs) are currently the first-line medical therapy for Primary Open-Angle Glaucoma (POAG) due to their superior efficacy in lowering intraocular pressure (IOP) and their once-daily dosing schedule. **Why PGF2α is Correct:** The prostaglandin analogues used in ophthalmology (such as **Latanoprost, Bimatoprost, and Travoprost**) are synthetic derivatives of **Prostaglandin F2alpha (PGF2α)**. These drugs act as selective agonists at the **FP receptors** located in the ciliary muscle. Their primary mechanism of action is increasing the **uveoscleral outflow** (the non-conventional pathway) of aqueous humor by remodeling the extracellular matrix in the ciliary body. **Why Other Options are Incorrect:** * **PGI2 (Prostacyclin):** Primarily functions as a potent vasodilator and inhibitor of platelet aggregation; it does not play a clinical role in lowering IOP. * **PGD2:** Involved in allergic responses and sleep regulation; it is not used in glaucoma management. * **PGE2 (Dinoprostone):** Primarily used in obstetrics for cervical ripening and induction of labor. While it can affect IOP, it is not used therapeutically for glaucoma due to its inflammatory potential. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Increases uveoscleral outflow (NOT trabecular outflow). * **Side Effects:** Increased brown pigmentation of the iris, hypertrichosis (increased eyelash growth), darkening of periocular skin, and cystoid macular edema (CME). * **Contraindication:** Relative contraindication in patients with active uveitis or a history of herpetic keratitis. * **Latanoprostene bunod:** A newer agent that combines a PGF2α analogue with a nitric oxide (NO) donor to target both uveoscleral and trabecular pathways.

Q: What is the earliest drug used in the management of acute angle closure glaucoma?

Diamox. In the management of **Acute Angle Closure Glaucoma (AACG)**, the primary goal is to rapidly lower the intraocular pressure (IOP) to prevent optic nerve damage and clear corneal edema. **Why Diamox (Acetazolamide) is the correct answer:** Diamox is a potent **Carbonic Anhydrase Inhibitor** that acts systemically to decrease the production of aqueous humor by the ciliary body. In an acute attack, the IOP is often so high (frequently >50-60 mmHg) that the iris sphincter becomes ischemic and unresponsive to topical miotics. Therefore, systemic medication like intravenous or oral Acetazolamide is the **earliest and most effective** first-line treatment to break the attack and lower the pressure enough for other treatments to work. **Analysis of Incorrect Options:** * **Pilocarpine:** While it is the definitive medical treatment to open the angle (miotic), it **cannot work initially** when IOP is very high because the iris sphincter is paralyzed by ischemia. It is usually administered only after the IOP has been lowered by systemic agents. * **Atropine:** This is a mydriatic (dilates the pupil). It is **strictly contraindicated** in AACG as it would further crowd the angle and worsen the condition. * **DFP (Diisopropyl Fluorophosphate):** This is a potent, irreversible cholinesterase inhibitor. It is not used in acute glaucoma because it can cause intense congestion and potentially worsen the pupillary block. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Management:** 1. Systemic Hyperosmotics (Mannitol) or CAIs (Diamox) → 2. Topical Beta-blockers → 3. Topical Pilocarpine (once IOP <30 mmHg). * **Definitive Treatment:** The definitive treatment for AACG is **Laser Peripheral Iridotomy (LPI)**, performed on both the affected and the fellow (prophylactic) eye. * **Side Effects of Diamox:** Watch for paresthesia, hypokalemia, and metabolic acidosis. It is contraindicated in patients with sulfonamide allergies.

Question 1

A 68-year-old female presents with severe right eye pain, blurred vision, nausea, and vomiting. Earlier in the day, she underwent a difficult colonoscopy for Crohn's disease. What is the likely cause of her painful red eye?

Accepted Answer

Acute angle closure glaucoma

Answer

Anterior uveitis

Answer

Acute conjunctivitis

Answer

Episcleritis

Question 2

Which of the following characterizes chronic simple glaucoma?

Accepted Answer

Elevated intraocular pressure with optic nerve damage.

Answer

Elevated intraocular pressure without optic nerve damage.

Answer

Visual field defects without optic nerve changes.

Answer

A pink optic disc.

Question 3

Increased episcleral venous pressure can affect intraocular pressure (IOP) in which way?

Accepted Answer

Increase IOP

Answer

Decrease IOP

Answer

Have no effect on IOP

Answer

Initially increase then decrease IOP

Question 4

Iridectomy is a treatment option in which of the following conditions?

Accepted Answer

Angle closure glaucoma

Answer

Pigmentary glaucoma

Answer

Pseudoexfoliative glaucoma

Answer

Open angle glaucoma

Question 5

A patient presents with acute pain and redness of the eye, diminished vision, and vomiting. What is the most likely finding?

Accepted Answer

Mid-dilated pupil

Answer

Hypopyon

Answer

Dislocated eye lens

Answer

Dendritic ulcer

Question 6

Facility of aqueous outflow is ______ I/min/mm Hg.

Accepted Answer

0.2

Answer

0.8

Answer

0.6

Answer

0.4

Question 7

A 55-year-old female presents with severe eye pain, redness, and diminished vision. Examination reveals a visual acuity of 6/60, circumcorneal congestion, corneal edema, and a shallow anterior chamber. What is the best initial drug of choice?

Accepted Answer

Intravenous Mannitol

Answer

Atropine ointment

Answer

Ciprofloxacin eye drops

Answer

Betamethasone eye drops

Question 8

Which of the following prostaglandin analogues is used for the treatment of primary open-angle glaucoma?

Accepted Answer

PG F2alpha

Answer

PG12

Answer

PG D2

Answer

PGE2

Question 9

What is the earliest drug used in the management of acute angle closure glaucoma?

Accepted Answer

Diamox

Answer

Pilocarpine

Answer

Atropine

Answer

DFP

Question 10

What is the earliest functional change in glaucoma?

Accepted Answer

Baring of the blind spot

Answer

Papilloedema

Answer

Hazy cornea

Answer

Sickle scotoma

Glaucoma — MCQs

Glaucoma — MCQs

On this page

Practice by Chapter

Want unlimited practice?