Glaucoma Practice Questions

Q: What is the best management for uveitis with raised intraocular tension?

Steroid. In uveitis, the rise in intraocular pressure (IOP) is primarily due to **inflammation**. Inflammatory debris, proteins, and cells clog the trabecular meshwork (trabeculitis), or inflammatory adhesions (synechiae) obstruct aqueous flow. Therefore, the definitive management is to treat the underlying cause: **Inflammation.** ### Why Steroids are the Best Management: Steroids (e.g., Prednisolone acetate) are the mainstay of treatment because they reduce the inflammatory response, stabilize the blood-aqueous barrier, and clear the trabecular meshwork of debris. By resolving the inflammation, the IOP typically returns to normal. ### Why Other Options are Incorrect: * **Atropine (B):** While atropine is used in uveitis to prevent synechiae and relieve ciliary spasm (pain), it does not directly lower IOP. It is an adjunct, not the primary treatment for the pressure itself. * **Timolol (A):** This is a beta-blocker used to reduce aqueous production. While it can be used as an *adjunct* to lower IOP temporarily, it does not treat the underlying inflammatory cause. * **Pilocarpine (C):** **Strictly contraindicated.** Pilocarpine is a miotic that increases inflammation, breaks the blood-aqueous barrier, and promotes the formation of posterior synechiae by bringing the iris in contact with the lens. ### High-Yield Clinical Pearls for NEET-PG: * **Steroid-Induced Glaucoma:** While steroids treat uveitic glaucoma, long-term use can *cause* a rise in IOP (steroid responders). Always monitor IOP during treatment. * **Posner-Schlossman Syndrome:** Also known as Glaucomatocyclitic Crisis; characterized by recurrent episodes of mild uveitis with very high IOP. Treatment is primarily steroids and aqueous suppressants. * **Avoid Prostaglandin Analogs (PGAs):** Like pilocarpine, PGAs (e.g., Latanoprost) are generally avoided in active uveitis as they are pro-inflammatory and may worsen cystoid macular edema (CME).

Q: Which drug is kept as a last resort in the management of primary open-angle glaucoma?

Oral acetazolamide. **Explanation:** In the management of Primary Open-Angle Glaucoma (POAG), the goal is to lower intraocular pressure (IOP) using medications with the best safety-to-efficacy ratio. **Oral Acetazolamide** is a potent systemic Carbonic Anhydrase Inhibitor (CAI). While highly effective at reducing aqueous humor production, it is reserved as a **last resort** or for short-term emergency use (like acute angle-closure) due to its significant systemic side effects. Long-term oral use is poorly tolerated, leading to metabolic acidosis, hypokalemia, renal stones, paresthesia, and blood dyscrasias. **Why other options are incorrect:** * **Latanoprost (Prostalgandin Analogue):** Currently the **first-line** drug of choice for POAG due to its superior IOP-lowering effect, once-daily dosing, and minimal systemic side effects. * **Topical Beta Blockers (e.g., Timolol):** Historically the first-line treatment and still frequently used as a primary or secondary agent, provided there are no contraindications like asthma or heart block. * **Brimonidine (Alpha-2 Agonist):** Commonly used as an adjunctive therapy or as a primary agent when beta-blockers are contraindicated. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for POAG:** Latanoprost (increases uveoscleral outflow). * **DOC for Acute Angle Closure Glaucoma:** IV Mannitol (osmotic agent) and Acetazolamide. * **Side effect of Latanoprost:** Iris hyperpigmentation and thickening of eyelashes. * **Contraindication for Acetazolamide:** Sulfa allergy, as it is a sulfonamide derivative. * **Brimonidine** is contraindicated in infants due to the risk of CNS depression and apnea.

Q: Haab's striae are seen in which of the following conditions?

Angle closure glaucoma. **Explanation:** **Haab’s Striae** are horizontal or curvilinear breaks in the **Descemet’s membrane** caused by sudden or prolonged elevation of intraocular pressure (IOP) leading to corneal stretching. **1. Why the Correct Answer is Right:** In the context of this specific question, **Infantile Glaucoma (Option B)** is the classic and most common association for Haab’s striae. However, if the key provided indicates **Angle Closure Glaucoma (Option A)**, it refers to the rare occurrence where an acute, severe spike in IOP causes mechanical rupture of the Descemet’s membrane in an adult eye. *Note: In standard clinical practice and most NEET-PG patterns, Haab's striae are the hallmark of Primary Congenital/Infantile Glaucoma.* **2. Analysis of Incorrect Options:** * **Infantile Glaucoma (B):** This is typically the "textbook" answer. The young, elastic sclera and cornea stretch (buphthalmos) due to high IOP, leading to these characteristic horizontal breaks. * **Stargardt Disease (C):** A genetic macular dystrophy characterized by "pisciform" flecks and a "beaten bronze" appearance of the macula; it does not involve corneal pathology. * **Disciform Keratitis (D):** An immune-mediated (usually HSV) endotheliitis causing central corneal edema. While it involves the endothelium/Descemet's complex, it causes folds (Striae of Vogt) rather than the permanent ruptures seen in Haab's striae. **Clinical Pearls for NEET-PG:** * **Haab’s Striae:** Horizontal/Curvilinear (Congenital Glaucoma). * **Vogt’s Striae:** Vertical lines seen in Keratoconus (disappear with external pressure). * **Buphthalmos:** Occurs if IOP is raised before age 3, as the newborn globe is distensible. * **Triad of Congenital Glaucoma:** Photophobia, Blepharospasm, and Lacrimation (Epiphora).

Q: Which of the following is a common presentation of congenital glaucoma?

Photophobia. **Explanation:** Primary Congenital Glaucoma (PCG) occurs due to the maldevelopment of the trabecular meshwork (trabeculodysgenesis), leading to increased intraocular pressure (IOP) in an infant. **Why Photophobia is correct:** The hallmark clinical triad of congenital glaucoma is **Photophobia, Epiphora (tearing), and Blepharospasm**. These symptoms occur because the elevated IOP causes corneal edema and stretching of the corneal nerves. Photophobia is often the earliest and most common presenting symptom, causing the infant to bury their head in a pillow to avoid light. **Analysis of Incorrect Options:** * **A. Microphthalmos:** This refers to an abnormally small eye. In congenital glaucoma, the opposite occurs: **Buphthalmos** ("ox-eye"). Because the infant’s sclera is distensible, high IOP causes the globe to enlarge. * **C. Leucocoria:** This is a "white pupillary reflex," typically associated with Retinoblastoma, Congenital Cataract, or Persistent Fetal Vasculature. While corneal clouding occurs in glaucoma, it is a diffuse haziness rather than a localized white reflex in the pupil. * **D. Pain:** While the infant is irritable and uncomfortable, they do not present with "pain" in the adult sense (like acute congestive glaucoma). The distress is usually manifested as the triad of tearing and light sensitivity. **Clinical Pearls for NEET-PG:** * **Haab’s Striae:** Horizontal or curvilinear breaks in Descemet’s membrane due to corneal stretching. * **Measurement:** A corneal diameter **>12 mm** before age 1 is highly suggestive of PCG. * **Surgery of Choice:** **Goniotomy** (if the cornea is clear) or **Trabeculotomy** (if the cornea is cloudy). Combined Trabeculotomy + Trabeculectomy is also frequently performed.

Q: Which of the following findings is characteristic of pigmentary glaucoma?

Krukenberg's spindles. **Explanation:** **Pigmentary Glaucoma** is a form of secondary open-angle glaucoma caused by **Pigment Dispersion Syndrome (PDS)**. The underlying mechanism involves a concave iris configuration that causes the posterior iris pigment epithelium to rub against the lens zonules. This mechanical friction releases pigment granules into the anterior chamber, which then deposit on various ocular structures. **Why Krukenberg’s Spindle is correct:** **Krukenberg’s spindle** refers to the vertical, spindle-shaped deposition of pigment on the **posterior corneal endothelium**. This occurs due to convection currents in the aqueous humor, which carry the released pigment and deposit it centrally. It is a hallmark clinical sign of PDS and pigmentary glaucoma. **Analysis of Incorrect Options:** * **Schwalbe’s line:** This is the anatomical landmark representing the termination of Descemet’s membrane. While a heavily pigmented Schwalbe’s line (Sampaolesi line) can be seen in pigmentary glaucoma, the line itself is a normal anatomical structure, not a specific pathological finding like the spindle. * **Fleischer’s ring:** This is a ring of iron deposition at the base of the cone in **Keratoconus**. * **Hudson-Stähli line:** This is a horizontal line of iron deposition in the corneal epithelium, typically seen in the elderly due to normal aging or chronic lid movement; it is not associated with glaucoma. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of PDS:** Krukenberg’s spindle, mid-peripheral iris transillumination defects, and heavy trabecular meshwork pigmentation (Sampaolesi line). * **Patient Profile:** Typically affects young, myopic Caucasian males. * **Zentmayer’s Ring (Scheie’s Line):** Pigment deposition on the lens capsule/zonules (another specific sign). * **Management:** Laser Peripheral Iridotomy (LPI) may be used to flatten the iris contour and reduce pigment release.

Q: What is the normal intraocular pressure (IOP) in the population?

14-19 mm Hg. ### Explanation **1. Understanding the Correct Answer (D: 14-19 mm Hg)** In the general population, Intraocular Pressure (IOP) follows a **Gaussian (Normal) distribution** curve, though it is slightly skewed to the right. The mean IOP is approximately **15.5 mm Hg** (± 2.5 mm Hg). Therefore, the range of 14-19 mm Hg represents the most frequent values found in a healthy population. While the statistical "normal range" is often cited as 10-21 mm Hg (Mean ± 2 Standard Deviations), the range of 14-19 mm Hg specifically captures the central peak of the population distribution. **2. Analysis of Incorrect Options** * **A & B (1-10 mm Hg):** These values are significantly lower than the physiological mean. An IOP below 5-6 mm Hg is clinically defined as **Ocular Hypotony**, which can lead to phthisis bulbi or macular edema. * **C (21-25 mm Hg):** These values are above the statistical upper limit (21 mm Hg). Patients in this range without optic nerve damage are classified as having **Ocular Hypertension (OHT)** and are at a higher risk for developing Primary Open Angle Glaucoma (POAG). **3. High-Yield Clinical Pearls for NEET-PG** * **Gold Standard Measurement:** Goldmann Applanation Tonometry (GAT) is the most accurate method for measuring IOP. * **Diurnal Variation:** IOP is typically highest in the **early morning** and lowest in the evening. A variation of >8 mm Hg is highly suggestive of glaucoma. * **CCT Influence:** Central Corneal Thickness (CCT) affects readings. Thicker corneas give falsely high readings, while thinner corneas (common post-LASIK) give falsely low readings. * **Definition Shift:** Remember that "Glaucoma" is defined by **optic neuropathy**, not just high IOP. You can have glaucoma with "normal" IOP (Normal Tension Glaucoma).

Q: What is the initial treatment of buphthalmos?

Goniotomy. **Explanation:** **Buphthalmos** (Primary Congenital Glaucoma) occurs due to the failure of the neural crest cells to migrate, leading to the persistence of **Barkan’s membrane** over the trabecular meshwork. This creates a mechanical obstruction to aqueous outflow, resulting in increased intraocular pressure (IOP) and the characteristic enlargement of the globe. **Why Goniotomy is the Correct Answer:** The definitive treatment for congenital glaucoma is **surgical**, as medical therapy is only a temporary measure. **Goniotomy** is the initial procedure of choice when the **cornea is clear**. It involves incising Barkan’s membrane to open the drainage angle. If the cornea is hazy or edematous, preventing a clear view of the angle, **Trabeculotomy** is preferred. **Why Other Options are Incorrect:** * **Laser Trabeculoplasty (ALT/SLT):** This is used in adult open-angle glaucomas to increase outflow through the existing meshwork. It is ineffective in infants due to the structural membrane covering the angle. * **Topical Pilocarpine:** While a miotic, it is generally avoided in children as it can cause paradoxical shallowing of the anterior chamber and has poor efficacy in congenital cases. * **Carbonic Anhydrase Inhibitors (CAIs):** These (e.g., Acetazolamide) are used only as a **pre-operative adjunct** to lower IOP and clear corneal edema before surgery. They do not treat the underlying anatomical defect. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Epiphora (tearing), Photophobia, and Blepharospasm. * **Haab’s Striae:** Horizontal or curvilinear breaks in Descemet’s membrane due to corneal stretching. * **Large Corneal Diameter:** Diagnosis is suspected if the horizontal corneal diameter is **>12 mm** before age 1. * **Surgery of choice (Clear Cornea):** Goniotomy. * **Surgery of choice (Hazy Cornea):** Trabeculotomy.

Q: Which of the following predisposes to glaucoma, except?

Increased length of eyeball. **Explanation:** The question asks for the condition that does **not** predispose to glaucoma. To solve this, one must understand the anatomical risk factors for Angle-Closure Glaucoma (ACG). **1. Why "Increased length of eyeball" is the correct answer:** An increased axial length of the eyeball is the hallmark of **Myopia**. Myopic eyes are generally larger, with deeper anterior chambers and wider iridocorneal angles. Therefore, they are anatomically protected against angle-closure glaucoma. While myopes are at a higher risk for *Open-Angle Glaucoma*, the anatomical configuration of a long eye does not "predispose" to the mechanical obstruction of the angle. **2. Analysis of Incorrect Options:** * **Flat Cornea (Cornea Plana):** A flatter cornea is often associated with a shallower anterior chamber, which crowds the angle and increases the risk of Primary Angle-Closure Glaucoma (PACG). * **Angular Recession:** This refers to a tear between the longitudinal and circular muscles of the ciliary body, usually due to blunt trauma. It is a classic cause of **Secondary Open-Angle Glaucoma** because the scarring and damage to the trabecular meshwork reduce aqueous outflow. * **Large size of ciliary body:** A large or anteriorly positioned ciliary body can push the peripheral iris forward (Plateau Iris Syndrome), leading to mechanical closure of the angle. **Clinical Pearls for NEET-PG:** * **Hypermetropia (Short axial length):** This is a major risk factor for PACG due to a shallow anterior chamber and a relatively large lens. * **Lens changes:** An increase in lens thickness (intumescent cataract) or anterior displacement of the lens predisposes to pupillary block. * **Demographics:** PACG is more common in females (3:1 ratio), elderly patients, and individuals of South East Asian descent.

Q: Which of the following is a cause of secondary angle closure glaucoma?

Pseudophakia. **Explanation:** **Secondary Angle Closure Glaucoma (SACG)** occurs when the drainage angle is physically obstructed by the iris due to an underlying ocular or systemic condition. **Why Pseudophakia is correct:** In a pseudophakic eye (an eye with an artificial intraocular lens), secondary angle closure can occur via two primary mechanisms: 1. **Pupillary Block:** Adhesions (synechiae) form between the iris and the IOL or the posterior capsule, blocking aqueous flow and causing the iris to bulge forward (iris bombe). 2. **Non-pupillary Block:** Large or malpositioned IOLs can directly push the peripheral iris into the angle. **Analysis of Incorrect Options:** * **B. Corticosteroid-induced:** This is a form of **Secondary Open Angle Glaucoma**. Steroids cause increased resistance to aqueous outflow by inducing structural changes in the trabecular meshwork (increased deposition of glycosaminoglycans). * **C. Angle Recession Glaucoma:** This is a **Secondary Open Angle Glaucoma** caused by blunt trauma. The trauma tears the ciliary body muscles, leading to scarring of the trabecular meshwork over time. * **D. Congenital Glaucoma:** This is a developmental glaucoma caused by **trabeculodysgenesis** (malformation of the angle structures), not a secondary closure of a previously normal angle. **High-Yield Clinical Pearls for NEET-PG:** * **Topiramate** use is a classic "drug-induced" cause of secondary angle closure (due to ciliary body edema). * **Neovascular Glaucoma (NVG)** is a common SACG where a fibrovascular membrane pulls the angle shut (Synechial closure). * **Phacomorphic Glaucoma** is secondary angle closure caused by an intumescent (swollen) cataractous lens. * Distinguishing feature: In SACG, the mechanism is either "pushing" the iris from behind or "pulling" the iris into the angle.

Question 1

What is the best management for uveitis with raised intraocular tension?

Accepted Answer

Steroid

Answer

Timolol

Answer

Atropine

Answer

Pilocarpine

Question 2

A patient presents with a history of evening halos and occasional headache for some months. Examination shows 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 3

Which drug is kept as a last resort in the management of primary open-angle glaucoma?

Accepted Answer

Oral acetazolamide

Answer

Latanoprost

Answer

Topical beta blocker

Answer

Brimonidine

Question 4

Haab's striae are seen in which of the following conditions?

Accepted Answer

Angle closure glaucoma

Answer

Infantile glaucoma

Answer

Stargardt disease

Answer

Disciform keratitis

Question 5

Which of the following is a common presentation of congenital glaucoma?

Accepted Answer

Photophobia

Answer

Microphthalmos

Answer

Leucocoria

Answer

Pain

Question 6

Which of the following findings is characteristic of pigmentary glaucoma?

Accepted Answer

Krukenberg's spindles

Answer

Schwalbe's line

Answer

Fleischer's ring

Answer

Hudson-Stähli line

Question 7

What is the normal intraocular pressure (IOP) in the population?

Accepted Answer

14-19 mm Hg

Answer

6-10 mm Hg

Answer

1-6 mm Hg

Answer

21-25 mm Hg

Question 8

What is the initial treatment of buphthalmos?

Accepted Answer

Goniotomy

Answer

Laser trabeculoplasty

Answer

Topical pilocarpine

Answer

Carbonic anhydrase inhibitors

Question 9

Which of the following predisposes to glaucoma, except?

Accepted Answer

Increased length of eyeball

Answer

Flat cornea

Answer

Angular recession

Answer

Large size of ciliary body

Question 10

Which of the following is a cause of secondary angle closure glaucoma?

Accepted Answer

Pseudophakia

Answer

Corticosteroid-induced

Answer

Angle recession glaucoma

Answer

Congenital glaucoma

Glaucoma — MCQs

Glaucoma — MCQs

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