Glaucoma Practice Questions

Q: In normal diurnal variation, what is the pattern of intraocular pressure?

Highest on awakening and lowest during the evening. **Explanation:** The intraocular pressure (IOP) is not static; it follows a **circadian rhythm** known as diurnal variation. In a healthy individual, the IOP typically peaks in the **early morning hours (on awakening)** and reaches its trough (lowest point) in the **late evening or night**. **Why the correct answer is right:** The morning peak is primarily attributed to the **supine position** during sleep, which increases episcleral venous pressure. Additionally, there is a surge in endogenous cortisol and catecholamines in the early morning, which may influence aqueous humor production. As the day progresses and the individual remains upright, the IOP gradually declines, reaching its minimum in the evening. **Analysis of incorrect options:** * **Option B:** This describes a "reverse" pattern. While some glaucoma patients may show atypical peaks, it is not the "normal" physiological pattern. * **Options C & D:** IOP follows a sinusoidal curve with one major peak and one major trough; it does not typically stay consistently high or low at both ends of the day. **NEET-PG High-Yield Pearls:** 1. **Normal Range:** The average diurnal variation in a healthy eye is **3–6 mmHg**. 2. **Glaucoma Indicator:** A diurnal fluctuation of **>8 mmHg** is highly suggestive of glaucoma. 3. **Phakic vs. Aphakic:** The diurnal rhythm is independent of the lens status but is heavily influenced by posture. 4. **Clinical Significance:** Since IOP peaks in the morning, a single "normal" reading in the afternoon does not rule out glaucoma. This is why **Diurnal Variation Recording (DVR)**—measuring IOP every 3–4 hours—is a gold standard for diagnosis.

Q: Which antiglaucoma drug acts by increasing uveoscleral outflow?

Latanoprost. **Explanation:** The correct answer is **Latanoprost**. To understand why, we must look at how aqueous humor exits the eye. There are two main pathways: the **Trabecular (conventional) pathway** (80-90%) and the **Uveoscleral (unconventional) pathway** (10-20%). **1. Why Latanoprost is correct:** Latanoprost is a **Prostaglandin F2α analogue**. It works by remodeling the extracellular matrix in the ciliary muscle, reducing resistance and significantly increasing **uveoscleral outflow**. Due to their high efficacy and once-daily dosing, PG analogues are the first-line treatment for Primary Open Angle Glaucoma (POAG). **2. Why the other options are incorrect:** * **Apraclonidine:** An alpha-2 agonist. It primarily acts by **decreasing aqueous production** and, to a lesser extent, increasing trabecular outflow. * **Timolol:** A non-selective beta-blocker. It acts solely by **decreasing aqueous production** from the ciliary epithelium. It has no effect on outflow. * **Brinzolamide:** A topical Carbonic Anhydrase Inhibitor (CAI). It reduces the secretion of aqueous humor by inhibiting the enzyme required for bicarbonate production in the ciliary body. **High-Yield Clinical Pearls for NEET-PG:** * **Uveoscleral Outflow:** Increased by Prostaglandins (Latanoprost, Bimatoprost) and Alpha-agonists (Brimonidine). * **Trabecular Outflow:** Increased by Miotics (Pilocarpine) and Rho-kinase inhibitors (Netarsudil). * **Side Effects of Latanoprost:** Increased iris pigmentation (heterochromia), hypertrichosis (thickening of eyelashes), and cystoid macular edema (CME) in aphakic patients. * **Contraindication:** Avoid PG analogues in inflammatory glaucoma (uveitic glaucoma) as they may exacerbate inflammation.

Q: Secondary glaucoma in the early stage of herpes zoster ophthalmicus occurs due to:

Trabeculitis. **Explanation:** The correct answer is **A. Trabeculitis.** In the **early stage** of Herpes Zoster Ophthalmicus (HZO), secondary glaucoma is primarily caused by an inflammatory process involving the trabecular meshwork, known as **trabeculitis**. The Varicella-Zoster Virus (VZV) causes direct viral infiltration and inflammation of the trabecular cells, leading to edema and reduced outflow facility of the aqueous humor. This results in a sudden, often significant, rise in intraocular pressure (IOP). **Analysis of Options:** * **B. Iridocyclitis:** While HZO frequently causes iridocyclitis (uveitis), the glaucoma associated with it is specifically due to the inflammation of the drainage channels (trabeculitis) rather than the inflammation of the iris/ciliary body itself. In late stages, uveitis can cause glaucoma via synechiae, but trabeculitis is the hallmark of the early phase. * **C. Hemorrhagic hypopyon:** This is a rare finding and not a standard mechanism for glaucoma in HZO. * **D. Hypersecretion of aqueous humor:** Glaucoma is almost always a result of decreased outflow, not increased production (hypersecretion) of aqueous humor. **High-Yield Clinical Pearls for NEET-PG:** * **Hutchinson’s Sign:** Vesicles on the tip or side of the nose (involving the nasociliary nerve) indicate a high risk of ocular involvement in HZO. * **Sectoral Iris Atrophy:** A classic late-stage complication of HZO-related uveitis due to ischemic vasculitis. * **Treatment:** Management involves topical steroids to control inflammation and aqueous suppressants (like Beta-blockers or Carbonic anhydrase inhibitors) to lower IOP. **Prostaglandin analogues** are generally avoided in active viral uveitis as they may exacerbate inflammation.

Q: Very high intraocular pressure, vertically oval mid-dilated pupil, and shallow anterior chamber are seen in which condition?

Acute primary angle closure glaucoma. ### Explanation **Correct Answer: B. Acute primary angle closure glaucoma (APACG)** The clinical triad described—**very high intraocular pressure (IOP)**, a **vertically oval mid-dilated pupil**, and a **shallow anterior chamber**—is the classic presentation of an acute attack of angle-closure glaucoma. * **Pathophysiology:** A sudden total blockage of the drainage angle leads to a rapid rise in IOP (often 40–70 mmHg). This high pressure causes **ischemia of the iris sphincter muscle**, resulting in a pupil that is non-reactive and fixed in a mid-dilated, vertically oval position. The shallow anterior chamber is the predisposing anatomical factor. **Why other options are incorrect:** * **A. Primary Open Angle Glaucoma (POAG):** This is a "silent" chronic condition. The IOP rises gradually, the anterior chamber depth is normal, and the pupil remains normal. * **C. Malignant Glaucoma (Ciliary Block):** While it presents with a shallow chamber and high IOP, it typically occurs **post-operatively** (e.g., after glaucoma surgery). The hallmark is the flattening of both the central and peripheral anterior chamber. * **D. Pupillary Block Glaucoma:** This is the *mechanism* behind most cases of angle closure, but "Acute Primary Angle Closure Glaucoma" is the specific clinical diagnosis that encompasses the full constellation of symptoms (pain, vomiting, and pupillary changes). **High-Yield Clinical Pearls for NEET-PG:** * **Symptoms:** Sudden ocular pain, headache, nausea, vomiting, and seeing **colored halos** around lights (due to corneal edema). * **Cornea:** Appears "steamy" or "cloudy" (ground-glass appearance). * **Immediate Management:** IV Mannitol, Acetazolamide, and topical Beta-blockers to lower IOP. * **Definitive Treatment:** **Laser Peripheral Iridotomy (LPI)** is the treatment of choice for both the affected eye and the fellow (prophylactic) eye.

Q: Primary open-angle glaucoma is associated with all of the following EXCEPT?

Pars planitis. **Explanation:** Primary Open-Angle Glaucoma (POAG) is a chronic, progressive optic neuropathy characterized by an open anterior chamber angle and typical optic disc changes. The question asks for the condition **not** associated with POAG. **Why Pars Planitis is the correct answer:** Pars planitis is a form of intermediate uveitis. While it can lead to increased intraocular pressure, it causes **Secondary Glaucoma** (due to inflammatory debris or steroid use), not Primary Open-Angle Glaucoma. POAG, by definition, occurs in the absence of an underlying ocular or systemic disease that physically obstructs the trabecular meshwork. **Analysis of incorrect options (Risk factors for POAG):** * **Diabetes Mellitus:** There is a strong clinical association between DM and POAG. Proposed mechanisms include microangiopathy of the optic nerve head and metabolic dysfunction of the trabecular meshwork. * **Myopia:** High myopia is a well-established risk factor. Myopic eyes often have structural changes in the lamina cribrosa that make the optic nerve more susceptible to pressure-induced damage. * **Hyperthyroidism:** Thyroid eye disease (Graves' ophthalmopathy) is associated with increased episcleral venous pressure and orbital congestion, which correlates with a higher prevalence of open-angle glaucoma. **High-Yield Clinical Pearls for NEET-PG:** * **Major Risk Factors for POAG:** Age (>40 years), Family history (Heredity), Race (African-Americans), Raised IOP, and Cardiovascular disease (Hypertension). * **Steroid-Induced Glaucoma:** This is a type of secondary open-angle glaucoma that must be differentiated from POAG. * **Genetic Link:** Mutations in the **MYOC** (Myocilin) gene are most commonly associated with POAG. * **Diagnosis:** Requires the triad of raised IOP (usually), characteristic optic disc cupping, and specific visual field defects (e.g., Bjerrum’s scotoma).

Q: What is the earliest symptom of congenital glaucoma?

Photophobia. **Explanation:** Congenital glaucoma (Buphthalmos) results from developmental anomalies of the angle of the anterior chamber, leading to increased intraocular pressure (IOP). **Why Photophobia is the correct answer:** Photophobia is considered the **earliest** and most common symptom. It occurs due to corneal edema caused by elevated IOP. When the cornea swells, it causes light to scatter, irritating the rich nerve endings of the corneal epithelium. This leads to the classic triad of symptoms: **Photophobia, Lacrimation, and Blepharospasm.** While all three often appear together, photophobia is clinically recognized as the initial sign that parents notice. **Analysis of Incorrect Options:** * **Lacrimation (A) and Blepharospasm (B):** These are part of the classic triad but are usually secondary responses to the irritation caused by corneal edema and photophobia. They occur almost simultaneously but are preceded by light sensitivity. * **Diminution of vision (D):** This is a late feature. In infants, vision loss occurs much later due to optic nerve damage (cupping), corneal scarring, or secondary amblyopia. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Photophobia + Lacrimation + Blepharospasm. * **Earliest Sign:** Corneal edema (hazy cornea). * **Haab’s Striae:** Horizontal or curvilinear breaks in Descemet’s membrane due to corneal stretching. * **Buphthalmos:** "Ox-eye" appearance; occurs because the infant's sclera is distensible and stretches when IOP is >21 mmHg (usually seen if glaucoma occurs before age 3). * **Treatment of Choice:** Surgery is the primary treatment. **Goniotomy** (if the cornea is clear) or **Trabeculotomy/Trabeculectomy** (if the cornea is hazy). Medical therapy is only a temporary measure.

Q: Which type of glaucoma is associated with cataract?

Phacomorphic glaucoma. **Explanation:** **Phacomorphic glaucoma** is a type of secondary angle-closure glaucoma caused directly by an advanced cataract. As the lens becomes **intumescent** (swollen and enlarged) during the cataractous process, it pushes the iris-lens diaphragm forward. This leads to pupillary block and subsequent narrowing or closure of the anterior chamber angle, resulting in a rapid rise in intraocular pressure (IOP). **Analysis of Incorrect Options:** * **Neovascular glaucoma:** This is a secondary glaucoma caused by the growth of new vessels (neovascularization) on the iris and angle, typically triggered by retinal ischemia (e.g., Diabetic Retinopathy or CRVO), not the lens itself. * **Phacoanaphylactic glaucoma:** This is an inflammatory (uveitic) glaucoma caused by a hypersensitivity reaction to lens proteins following trauma or surgery. While lens-related, it is primarily an **immunological** response rather than a direct mechanical effect of the cataractous mass. * **Buphthalmos:** This refers to the "ox-eye" appearance (enlarged eyeball) seen in **Congenital Glaucoma** due to the distensibility of the infant sclera under high IOP. It is not associated with adult cataract formation. **High-Yield Clinical Pearls for NEET-PG:** * **Phacolytic Glaucoma:** Occurs when a **hypermature** cataract leaks soluble lens proteins through an intact capsule, which then clog the trabecular meshwork (a form of open-angle glaucoma). * **Treatment of Phacomorphic Glaucoma:** Immediate medical management to lower IOP, followed by **cataract extraction** (definitive treatment). * **Key Distinction:** Phacomorphic = Swollen lens (Angle-closure); Phacolytic = Leaking proteins (Open-angle).

Q: Painless loss of vision is seen in all of the following conditions EXCEPT:

Acute angle-closure glaucoma. **Explanation:** The correct answer is **D. Acute angle-closure glaucoma.** In clinical ophthalmology, vision loss is broadly categorized into "painless" and "painful." **Acute angle-closure glaucoma (AACG)** is a classic cause of **sudden, painful loss of vision.** The underlying mechanism involves a rapid rise in intraocular pressure (IOP) due to the mechanical blockage of the trabecular meshwork by the iris. This sudden pressure spike causes corneal edema and stretches the sensory nerves of the eye, leading to severe ocular pain, headache, nausea, and vomiting. **Why the other options are incorrect:** * **Vitreous hemorrhage:** Causes sudden, **painless** loss of vision or floaters. There are no sensory nerves in the vitreous to transmit pain. * **Optic atrophy:** Represents the end-stage of various optic nerve pathologies. It results in a gradual or sudden **painless** decline in vision and field defects. * **Developmental cataract:** Causes a gradual, **painless** blurring of vision as the lens opacity interferes with the light path to the retina. **Clinical Pearls for NEET-PG:** * **Painful Vision Loss (The "Big 3"):** Acute Angle-Closure Glaucoma, Uveitis, and Optic Neuritis (pain exacerbated by eye movements). * **Painless Sudden Vision Loss:** Central Retinal Artery Occlusion (CRAO), Central Retinal Vein Occlusion (CRVO), Vitreous Hemorrhage, and Retinal Detachment. * **AACG Presentation:** Look for "halos around lights" (due to corneal edema), a "mid-dilated non-reactive pupil," and a "stony hard eye" on palpation.

Q: All are the features of an acute attack of primary narrow-angle glaucoma except?

Disc shows glaucomatous cupping. **Explanation:** Acute Angle Closure Glaucoma (AACG) is an ophthalmic emergency characterized by a sudden, precipitous rise in intraocular pressure (IOP) due to total mechanical obstruction of the trabecular meshwork by the peripheral iris. **Why Option C is the Correct Answer:** Glaucomatous cupping is a feature of **chronic** glaucoma. It occurs due to the progressive loss of retinal nerve fiber layer (RNFL) axons over time. In an **acute** attack, the optic disc is typically **congested, edematous, and hyperemic** due to the sudden mechanical pressure. Permanent cupping does not develop instantly; it requires prolonged exposure to high IOP. **Analysis of Incorrect Options:** * **Option A:** During an acute attack, IOP typically spikes to **60–70 mmHg**, far exceeding the normal range (10–21 mmHg). This causes corneal edema and severe pain. * **Option B:** The clinical presentation includes a "ciliary flush" (redness), excruciating pain (due to trigeminal nerve stimulation), and tenderness of the globe. * **Option C:** Primary Angle Closure is a **bilateral anatomical predisposition**. The "fellow eye" almost always has a shallow anterior chamber and a narrow angle, putting it at high risk for a future attack. **Clinical Pearls for NEET-PG:** * **Classic Sign:** Vertically oval, semi-dilated, non-reactive pupil. * **Symptoms:** Halos around lights (due to corneal edema), nausea, and vomiting (often misdiagnosed as an abdominal emergency). * **Immediate Management:** IV Mannitol, Acetazolamide, and topical beta-blockers to lower IOP. * **Definitive Treatment:** Laser Peripheral Iridotomy (LPI) for **both** the affected and the fellow eye (prophylactic).

Question 1

In normal diurnal variation, what is the pattern of intraocular pressure?

Accepted Answer

Highest on awakening and lowest during the evening

Answer

Lowest during the morning and highest during the evening

Answer

Highest in the morning and evening

Answer

Lowest in the morning and evening

Question 2

Which antiglaucoma drug acts by increasing uveoscleral outflow?

Accepted Answer

Latanoprost

Answer

Apraclonidine

Answer

Timolol

Answer

Brinzolamide

Question 3

Secondary glaucoma in the early stage of herpes zoster ophthalmicus occurs due to:

Accepted Answer

Trabeculitis

Answer

Iridocyclitis

Answer

Hemorrhagic hypopyon

Answer

Hypersecretion of aqueous humor

Question 4

Which tonometer is characterized by a variation in its application surface?

Accepted Answer

Maklakov tonometer

Answer

Mackey-Marg tonometer

Answer

Rebound tonometer

Answer

Dreger's tonometer

Question 5

Very high intraocular pressure, vertically oval mid-dilated pupil, and shallow anterior chamber are seen in which condition?

Accepted Answer

Acute primary angle closure glaucoma

Answer

Primary open angle glaucoma

Answer

Malignant glaucoma

Answer

Pupillary block glaucoma

Question 6

Primary open-angle glaucoma is associated with all of the following EXCEPT?

Accepted Answer

Pars planitis

Answer

Diabetes mellitus

Answer

Myopia

Answer

Hyperthyroidism

Question 7

What is the earliest symptom of congenital glaucoma?

Accepted Answer

Photophobia

Answer

Lacrimation

Answer

Blepharospasm

Answer

Diminution of vision

Question 8

Which type of glaucoma is associated with cataract?

Accepted Answer

Phacomorphic glaucoma

Answer

Neovascular glaucoma

Answer

Phacoanaphylactic glaucoma

Answer

Buphthalmos

Question 9

Painless loss of vision is seen in all of the following conditions EXCEPT:

Accepted Answer

Acute angle-closure glaucoma

Answer

Vitreous hemorrhage

Answer

Optic atrophy

Answer

Developmental cataract

Question 10

All are the features of an acute attack of primary narrow-angle glaucoma except?

Accepted Answer

Disc shows glaucomatous cupping

Answer

Intraocular pressure is raised up to 60-70 mm of Hg

Answer

Eye is red, painful and tender

Answer

Fellow eye also shows shallow anterior chamber

Glaucoma — MCQs

Glaucoma — MCQs

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