Glaucoma Practice Questions

Q: Glaucoma flecken is defined as:

Lens opacity. **Explanation:** **Glaukomflecken** (also known as Vogt’s spots) refers to multiple, small, grey-white subcapsular opacities found in the anterior lens. These represent focal areas of lens epithelial necrosis caused by a sudden, severe rise in intraocular pressure (IOP). **Why the correct answer is right:** In the setting of **Acute Angle Closure Glaucoma (AACG)**, the rapid and extreme elevation of IOP causes stagnation of the aqueous humor. This leads to localized ischemia and metabolic distress of the anterior lens epithelium, resulting in permanent necrotic spots. These opacities are pathognomonic of a **previous** attack of acute congestive glaucoma. **Why the incorrect options are wrong:** * **A. Acute uveitis:** While uveitis can cause lens changes (like posterior synechiae or complicated cataracts), Glaukomflecken is specifically a post-glaucomatous sequela. * **C. Retinal detachment:** This involves the separation of the neurosensory retina from the RPE and does not manifest as focal lens opacities. * **D. Corneal opacity:** Acute glaucoma causes corneal *edema* (due to endothelial pump failure), but Glaukomflecken is strictly a lenticular finding. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Anterior subcapsular region of the lens. * **Significance:** It serves as a "diagnostic footprint" of a past acute primary angle-closure attack. * **Triad of post-acute glaucoma:** Glaukomflecken, iris atrophy (sectoral), and a mid-dilated non-reactive pupil. * **Differential:** Do not confuse with *Vossius ring*, which is a ring of iris pigment on the anterior lens capsule following blunt trauma.

Q: Aqueous humor drains through all of the following routes except:

Sclera. **Explanation:** Aqueous humor is produced by the ciliary body and must be drained to maintain intraocular pressure (IOP). There are two primary pathways for drainage, along with minor accessory routes. **Why Sclera is the Correct Answer:** The **Sclera** itself is a dense, fibrous protective layer and does not serve as a direct drainage route for aqueous humor. While the uveoscleral pathway involves fluid passing *through* the interstitial spaces of the ciliary muscle toward the suprachoroidal space, the fluid eventually enters the venous circulation of the choroid and sclera. However, the sclera as a tissue does not possess a drainage mechanism; it acts as a container. **Analysis of Other Options:** * **Trabecular Meshwork (Option A):** This is the **conventional (pressure-dependent) pathway**, accounting for approximately **90%** of aqueous drainage. Fluid passes through the meshwork into the Canal of Schlemm and then into episcleral veins. * **Uveoscleral Outflow (Option B):** This is the **unconventional (pressure-independent) pathway**, accounting for about **10%** of drainage. Fluid exits through the ciliary muscle into the suprachoroidal space. * **Iris (Option C):** A very small amount of aqueous humor (minor route) can be absorbed through the **iris crypts** and its anterior surface into the iris vessels. **High-Yield Clinical Pearls for NEET-PG:** * **Prostaglandin Analogs (e.g., Latanoprost):** The first-line drug in Glaucoma; they work by increasing **uveoscleral outflow**. * **Miotics (e.g., Pilocarpine):** Increase drainage through the **trabecular meshwork** by contracting the ciliary muscle. * **Goldmann Equation:** Used to determine IOP ($IOP = (F/C) + Pv$), where $F$ is aqueous formation, $C$ is facility of outflow, and $Pv$ is episcleral venous pressure.

Q: A vertically oval dilated pupil is seen in which condition?

Acute primary angle closure glaucoma. **Explanation:** In **Acute Primary Angle Closure Glaucoma (APACG)**, the sudden and severe rise in intraocular pressure (IOP) leads to ischemia and subsequent paralysis of the iris sphincter muscle. This results in a pupil that is **semi-dilated, vertically oval, and non-reactive to light**. The vertical elongation occurs because the ischemia is often most pronounced in the superior and inferior segments of the iris. **Analysis of Incorrect Options:** * **Wernicke-Korsakoff Psychosis:** This condition, caused by Thiamine (B1) deficiency, typically presents with the triad of ophthalmoplegia (most commonly lateral rectus palsy), ataxia, and confusion. It does not cause a vertically oval pupil. * **Neurosyphilis:** Classically associated with the **Argyll Robertson Pupil**, which is characterized by small, irregular pupils that demonstrate "accommodation-reflex present, but light-reflex absent" (ARP). * **Paralysis of Oculomotor Nerve (3rd Nerve Palsy):** This results in a **completely dilated (mydriatic)** and fixed pupil due to loss of parasympathetic supply, accompanied by ptosis and a "down and out" deviation of the eye. **High-Yield Clinical Pearls for NEET-PG:** * **APACG Presentation:** Sudden onset of severe pain, "halos" around lights, stony hard eye, and a shallow anterior chamber. * **Immediate Management:** Systemic Acetazolamide and topical Pilocarpine (once IOP drops below 40 mmHg to restore iris vascularity). * **Definitive Treatment:** Laser Peripheral Iridotomy (LPI) for both the affected and the fellow (prophylactic) eye. * **Festooned Pupil:** Seen in chronic iridocyclitis due to posterior synechiae.

Q: Which prostaglandin is used in the management of glaucoma?

All of the above. **Explanation:** Prostaglandin analogues (PGAs) are currently the **first-line medical therapy** for Primary Open Angle Glaucoma (POAG) and Ocular Hypertension. They work primarily by increasing the **uveoscleral outflow** of aqueous humor (and to a lesser extent, trabecular outflow) by remodeling the extracellular matrix in the ciliary muscle. **Analysis of Options:** * **Latanoprost (0.005%):** A selective FP receptor agonist. It was the first PGA introduced and remains a gold standard for efficacy and safety. * **Travoprost (0.004%):** A full agonist at the FP receptor, showing similar efficacy to Latanoprost. * **Bimatoprost (0.03%):** Technically a synthetic prostamide. It is often considered the most potent in this class for lowering Intraocular Pressure (IOP) but may have a higher incidence of conjunctival hyperemia. Since all three agents are FDA-approved and standard clinical choices for glaucoma management, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Increase uveoscleral outflow (High-yield: "U" for Prostaglandins, "T" for Beta-blockers/Trabecular). * **Dosage:** Once-daily (HS - at bedtime) dosing improves patient compliance. * **Side Effects:** * **Iris heterochromia** (permanent darkening of the iris due to increased melanin). * **Hypertrichosis** (increased eyelash growth; Bimatoprost is also used for eyelash hypotrichosis). * **Prostaglandin-associated periorbitopathy** (fat loss around eyes). * **Cystoid Macular Edema (CME):** Use with caution in aphakic or pseudophakic patients. * **Contraindication:** Active uveitis (pro-inflammatory nature).

Q: Which drug should be avoided in a patient with angle closure glaucoma?

Atropine. **Explanation:** **Why Atropine is the Correct Answer:** Atropine is a potent **parasympatholytic (anticholinergic)** agent that causes **mydriasis** (dilation of the pupil). In patients with narrow angles, mydriasis leads to the bunching up of the peripheral iris tissue towards the drainage angle. This further obstructs the trabecular meshwork, severely impeding the outflow of aqueous humor. Consequently, it can precipitate or worsen an attack of **Acute Angle Closure Glaucoma (AACG)**. Therefore, mydriatics are strictly contraindicated in eyes with narrow angles. **Analysis of Incorrect Options:** * **Acetazolamide (Option A):** A Carbonic Anhydrase Inhibitor that reduces aqueous production. It is a first-line systemic drug used to rapidly lower Intraocular Pressure (IOP) during an acute attack. * **Timolol (Option C):** A topical Beta-blocker that decreases aqueous humor secretion by the ciliary body. It is a standard treatment for managing various types of glaucoma, including angle closure. * **Mannitol (Option D):** An intravenous hyperosmotic agent. It creates an osmotic gradient that draws fluid out of the vitreous into the bloodstream, rapidly reducing IOP in emergency AACG scenarios. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for AACG:** IV Mannitol or Acetazolamide (to lower IOP) followed by **Pilocarpine** (miotic) once IOP is <30 mmHg. * **Definitive Treatment:** Peripheral Iridotomy (usually via YAG Laser). * **Mydriatic Danger:** Always perform a torch light or slit-lamp examination (Van Herick technique) to assess angle depth before instilling mydriatics like Atropine or Tropicamide. * **Paradoxical Effect:** While Pilocarpine (miotic) is used in AACG, very high concentrations can occasionally worsen the condition by increasing pupillary block.

Q: A patient presents with a history of evening halos and occasional headaches for several months. Examination reveals normal intraocular pressure but a shallow anterior chamber. In which stage of glaucoma is this patient?

Prodrome. ### Explanation This clinical scenario describes **Primary Angle-Closure Glaucoma (PACG)** in the **Prodromal Stage**. **Why "Prodrome" is correct:** The prodromal stage is characterized by transient, self-limiting episodes of increased intraocular pressure (IOP). These episodes typically occur in the evening or in low light (mydriasis causes the iris to block the angle). * **Evening Halos:** Caused by transient corneal edema due to a sudden rise in IOP. * **Headaches/Ocular Pain:** Result from the pressure spike. * **Normal IOP on Examination:** Between episodes, the IOP returns to normal, and the eye appears quiet, though the **shallow anterior chamber** remains a constant anatomical risk factor. **Why the other options are incorrect:** * **Acute Stage:** This is a medical emergency. The patient presents with sudden, severe pain, nausea, vomiting, a stony-hard eye (very high IOP), a vertically oval semi-dilated pupil, and "steamy" cornea. It does not resolve spontaneously. * **Absolute Stage:** This is the terminal stage where the eye is completely blind (No Perception of Light). The eye may be painful or painless, and the optic disc shows total glaucomatous cupping. * **Constant Instability (Chronic Stage):** Here, the angle is permanently closed by synechiae (PAS). The IOP is persistently high, and there is progressive optic nerve damage and field defects, unlike the intermittent nature of the prodromal stage. **High-Yield Clinical Pearls for NEET-PG:** * **Anatomical Predisposition:** Hypermetropic eyes, small eyeballs, and advancing age (enlarging lens) are risk factors for shallow chambers. * **Provocative Tests:** The Dark Room Test or Prone Position Test can be used to induce an attack in suspected prodromal cases. * **Definitive Treatment:** **Peripheral Iridotomy (Laser or Surgical)** is the treatment of choice to bypass the pupillary block and prevent future acute attacks.

Question 1

Which of the following drugs is not used in the management of acute angle-closure glaucoma?

Accepted Answer

Clozapine

Answer

Pilocarpine

Answer

Fluphenazine

Answer

Duloxetine

Question 2

Glaucoma flecken is defined as:

Accepted Answer

Lens opacity

Answer

Acute uveitis

Answer

Retinal detachment

Answer

Corneal opacity

Question 3

Aqueous humor drains through all of the following routes except:

Accepted Answer

Sclera

Answer

Trabecular meshwork

Answer

Uveoscleral outflow

Answer

Iris

Question 4

A vertically oval dilated pupil is seen in which condition?

Accepted Answer

Acute primary angle closure glaucoma

Answer

Wernicke's Korsakoff psychosis

Answer

Neurosyphilis

Answer

Paralysis of oculomotor nerve

Question 5

Which prostaglandin is used in the management of glaucoma?

Accepted Answer

All of the above

Answer

Bimatoprost 0.03%

Answer

Travoprost 0.004%

Answer

Latanoprost 0.005%

Question 6

Which of the following is considered primary glaucoma?

Accepted Answer

Juvenile glaucoma

Answer

Steroid-induced glaucoma

Answer

Pigmentary glaucoma

Answer

All of the above

Question 7

Field defects in chronic simple glaucoma includes all EXCEPT:

Accepted Answer

Paracentral scotoma

Answer

Arcuate scotoma

Answer

Seidel scotoma

Question 8

Which drug should be avoided in a patient with angle closure glaucoma?

Accepted Answer

Atropine

Answer

Acetazolamide

Answer

Timolol

Answer

Mannitol

Question 9

A patient presents with a history of evening halos and occasional headaches for several months. Examination reveals normal intraocular pressure but a shallow anterior chamber. In which stage of glaucoma is this patient?

Accepted Answer

Prodrome

Answer

Acute

Answer

Absolute

Answer

Constant instability

Question 10

A patient complains of seeing colored halos around lights in the evening and blurring of vision for the past few days, with normal intraocular pressure. What is the most likely diagnosis?

Accepted Answer

Prodromal phase of acute angle closure glaucoma

Answer

Acute angle closure glaucoma

Answer

Chronic glaucoma

Answer

Epidemic dropsy

Glaucoma — MCQs

Glaucoma — MCQs

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