Glaucoma Practice Questions

Q: Which test is used to measure intraocular pressure?

Tonometry. ***Tonometry*** - **Tonometry** is the specific test designed to measure the **intraocular pressure (IOP)** within the eye. - This measurement is crucial for diagnosing and monitoring conditions like **glaucoma**, where elevated IOP can damage the **optic nerve**. *Gonioscopy* - **Gonioscopy** is a technique used to visualize the **anterior chamber angle** of the eye. - It helps in assessing the drainage angle and identifying types of **glaucoma**, but it does not directly measure pressure. *Perimetry* - **Perimetry**, also known as a visual field test, assesses a patient's **peripheral and central vision**. - It is used to detect and monitor **visual field defects** which can be caused by conditions like glaucoma, but it does not measure IOP. *Ophthalmoscopy* - **Ophthalmoscopy** is a procedure used to examine the posterior structures of the eye, including the **retina**, **optic disc**, and **blood vessels**. - It helps assess for signs of disease, such as **optic nerve damage** in glaucoma, but it does not directly measure intraocular pressure.

Q: A patient with chronic glaucoma is found to have optic nerve head cupping and visual field loss. What is the most well-established mechanism of optic nerve damage in glaucoma?

Increased intraocular pressure. ***Increased intraocular pressure*** - **Elevated intraocular pressure** is the most significant and well-established risk factor for **optic nerve damage** in glaucoma, leading to mechanical stress and axonal injury. - This increased pressure causes **optic nerve head cupping** and **visual field loss** by damaging the retinal ganglion cell axons at the lamina cribrosa. *Vascular insufficiency* - While vascular factors may contribute to **optic nerve damage** in some glaucoma patients, particularly in normal-tension glaucoma, they are not considered the primary or **most well-established mechanism** across all forms of the disease. - Reduced blood flow can exacerbate damage, but **intraocular pressure** remains the leading cause. *Genetic predisposition* - **Genetic factors** play a role in susceptibility to glaucoma and can influence the severity and age of onset, but they are not a direct mechanism of **optic nerve damage**. - Genes predispose individuals to develop glaucoma, but the actual damage is mediated by **downstream mechanisms** like elevated IOP. *Inflammation* - **Inflammation** is not a primary or well-established mechanism of **optic nerve damage** in chronic glaucoma. - While some research explores inflammatory components, it is not considered the main pathophysiological pathway, unlike in conditions such as **optic neuritis**.

Q: Which type of visual field defect is typically observed in glaucoma?

Arcuate scotoma. ***Arcuate scotoma*** - An **arcuate scotoma** is a characteristic visual field defect in glaucoma, following the path of the **retinal nerve fibers** as they arc over the macula to the optic nerve head. - It typically starts as a **paracentral scotoma** and then expands, eventually connecting to the blind spot and forming an arc-shaped defect. *Central scotoma* - A **central scotoma** involves the fovea and is common in **macular diseases** such as **age-related macular degeneration** or optic neuropathies other than glaucoma. - This defect directly affects central vision and is not typically the primary visual field defect in glaucoma. *Homonymous hemianopia* - **Homonymous hemianopia** is a loss of visual field on the same side in both eyes, indicating a lesion in the **visual pathway posterior to the optic chiasm** (e.g., stroke, tumor). - This type of defect is not associated with glaucoma, which is an optic nerve disease affecting individual eyes. *Bitemporal hemianopia* - **Bitemporal hemianopia** is a loss of vision in the outer half of both visual fields, typically caused by compression of the **optic chiasm**, most commonly by a **pituitary adenoma**. - This specific pattern of visual field loss is distinct from the damage caused by elevated intraocular pressure in glaucoma.

Q: Which of the following is NOT a sign of angle closure glaucoma?

Multiple iris nodules. ***Multiple iris nodules*** - **Iris nodules**, such as **Lisch nodules** in neurofibromatosis or **Brushfield spots** in Down syndrome, are developmental anomalies or manifestations of systemic diseases, not signs of acute angle-closure glaucoma. - Their presence does not relate to the rapid increase in **intraocular pressure** characteristic of acute angle closure. *Mid-dilated fixed pupil* - A **mid-dilated, fixed pupil** (typically 4-6 mm) that is poorly reactive or non-reactive to light is a classic sign of **acute angle-closure glaucoma**. - The pupil becomes fixed due to **iris sphincter ischemia** from the sudden elevation of intraocular pressure, and may appear **vertically oval** or irregular. *Edematous cornea* - **Corneal edema** (swelling) results from very high **intraocular pressure** exceeding the osmotic gradient that ordinarily keeps the cornea clear and deturgescent. - This leads to a hazy or cloudy cornea, causing **blurred vision** and often **halos around lights**. *Edematous and hyperemic optic disc* - While less common in acute angle closure compared to chronic forms, severe and prolonged elevations in **intraocular pressure** can lead to **optic disc edema** (swelling and congestion of the optic nerve head). - This is an indicator of optic nerve compromise due to pressure and impaired axoplasmic flow.

Q: Recurrent non-granulomatous uveitis is seen in:

Posner-Schlossman syndrome. ***Posner-Schlossman syndrome*** - Also known as **glaucomatocyclitic crisis**, this syndrome is characterized by recurrent attacks of **unilateral acute non-granulomatous anterior uveitis** with significantly **elevated intraocular pressure**. - The inflammation is typically mild and transient, without posterior synechiae or significant vision loss, but the recurrent nature and association with high IOP are key features. *Vogt-Koyanagi-Harada syndrome* - This is a **granulomatous panuveitis** associated with neurological, auditory, and dermatological manifestations, which is distinct from the non-granulomatous and recurrent nature described. - It is an autoimmune disorder that affects melanin-containing tissues, leading to symptoms like **vitiligo**, **poliosis**, and **hearing loss** in addition to the uveitis. *Tuberculosis* - Ocular tuberculosis can cause various forms of uveitis, but it typically presents as a **granulomatous uveitis**, which contradicts the "non-granulomatous" description in the question. - It is often associated with systemic tuberculosis, and diagnosis requires evidence of mycobacterial infection. *Sarcoidosis* - Ocular sarcoidosis commonly manifests as a **granulomatous uveitis**, often with characteristic "mutton-fat" keratic precipitates and possibly **posterior uveitis** or **vasculitis**. - Like tuberculosis, its granulomatous nature distinguishes it from the non-granulomatous presentation in the question.

Q: Which drug is primarily used in the treatment of acute angle-closure glaucoma?

Pilocarpine. ***Pilocarpine*** - **Pilocarpine** is a **direct-acting miotic agent** that causes pupillary constriction, which pulls the iris away from the trabecular meshwork, thereby opening the angle and facilitating aqueous humor outflow. - This action effectively **reduces intraocular pressure (IOP)** in **acute angle-closure glaucoma** by directly addressing the anatomical cause of angle closure. - It is the **primary topical agent** used to mechanically open the closed angle in acute attacks. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production and is highly effective in rapidly lowering IOP. - Given **systemically (IV or oral)**, it is often used **alongside pilocarpine** in the acute management of angle-closure glaucoma. - While both drugs are essential in treatment, pilocarpine is considered primary because it directly addresses the **mechanical angle closure**, whereas acetazolamide provides rapid IOP reduction through decreased aqueous production. *Atropine* - **Atropine** is a **mydriatic agent** (dilates the pupil) and would worsen acute angle-closure glaucoma by further closing the angle and increasing IOP. - It works by **blocking muscarinic acetylcholine receptors**, leading to paralysis of the iris sphincter muscle. - Contraindicated in acute angle-closure glaucoma. *None of the options* - This option is incorrect as **Pilocarpine** is the primary drug that mechanically addresses the pathophysiology of acute angle-closure glaucoma.

Q: Which of the following conditions is NOT treated with Pilocarpine?

Malignant Glaucoma. ***Malignant Glaucoma*** - **Malignant glaucoma** (also known as aqueous misdirection syndrome) is characterized by posterior misdirection of aqueous humor into the vitreous, causing anterior displacement of the lens-iris diaphragm and marked intraocular pressure elevation. - Pilocarpine is **contraindicated** in malignant glaucoma because it causes **miosis** and increases ciliary muscle contraction, which can **exacerbate aqueous misdirection** and worsen the condition. - Treatment requires **cycloplegics** (atropine), not miotics like pilocarpine. *Primary Open-Angle Glaucoma* - **Pilocarpine** is a **miotic agent** that increases **aqueous humor outflow** through the trabecular meshwork, thereby lowering intraocular pressure (IOP). - It is used as medical therapy for controlling IOP in **primary open-angle glaucoma**, although it has largely been replaced by prostaglandin analogs, beta-blockers, and other agents with fewer side effects. *Acute Angle-Closure Glaucoma* - **Pilocarpine** is used in acute angle-closure glaucoma (after initial IOP reduction) to induce **miosis**, which pulls the iris away from the **trabecular meshwork** and opens the angle. - It works by constricting the pupil and causing ciliary muscle contraction, which helps relieve pupillary block and facilitate aqueous outflow. *Chronic Synechial Angle-Closure Glaucoma* - In chronic synechial angle-closure glaucoma with **extensive peripheral anterior synechiae (PAS)**, pilocarpine has **very limited effectiveness** because the angle is mechanically closed by permanent adhesions. - While pilocarpine may be attempted in **early cases** where some functional angle remains open, once extensive synechiae have formed, miosis cannot reopen the closed angle, and **surgical intervention** is typically required. - However, pilocarpine is not absolutely **contraindicated** in this condition, unlike malignant glaucoma.

Q: Which of the following is NOT a feature of Primary Infantile (Congenital) glaucoma?

Aniridia may be associated. ***Aniridia may be associated*** - **Aniridia** is a congenital absence of the iris that causes **secondary glaucoma**, not primary infantile glaucoma. - Aniridia-associated glaucoma is a distinct entity from primary congenital glaucoma (PCG), which occurs due to isolated developmental abnormalities of the anterior chamber angle. - This is **NOT a feature** of primary infantile glaucoma, making it the correct answer to this negation question. *Treatment includes trabeculotomy* - **Trabeculotomy** or **goniotomy** are the primary surgical treatments for primary infantile glaucoma. - These procedures aim to improve aqueous outflow by incising or opening the trabecular meshwork. - This is a **true feature** of the management of primary infantile glaucoma. *Buphthalmos can occur* - **Buphthalmos** (\"ox eye\") refers to the enlargement of the globe due to elevated intraocular pressure in infants when the sclera is still distensible. - It is a **classic clinical sign** of primary infantile glaucoma, typically occurring before age 3 years. - This is a **characteristic feature** of the condition. *Cornea is typically enlarged and cloudy* - The **cornea becomes enlarged** (increased horizontal corneal diameter >12 mm in newborns) due to stretching from elevated IOP. - **Corneal cloudiness** results from corneal edema and Haab's striae (breaks in Descemet's membrane). - These are **pathognomonic findings** in primary infantile glaucoma.

Q: What is the primary function of glaucoma drainage devices?

Drain aqueous humour to an external device. **Drain aqueous humour to an external device** - Glaucoma drainage devices create an artificial outflow pathway, channeling excess **aqueous humour** from the anterior chamber to an external reservoir (usually under the conjunctiva) to lower intraocular pressure. - This bypasses the compromised natural drainage system, preventing further damage to the **optic nerve**. *Drain aqueous humour to the posterior segment* - Glaucoma drainage devices are designed to drain aqueous humour from the **anterior segment** (specifically the anterior chamber) of the eye, not the posterior segment. - The posterior segment primarily contains the **vitreous humour**, and drainage to this area is not the intended mechanism for IOP reduction. *Open the trabeculae mechanically* - Glaucoma drainage devices do not mechanically open the **trabecular meshwork**; this is the mechanism of action for procedures like goniotomy or trabeculoplasty. - These devices create an entirely new drainage pathway, bypassing the dysfunctional trabecular meshwork. *Reduce the aqueous secretion by compressing the ciliary epithelium* - Reducing aqueous humour secretion is the mechanism of action for medications like **beta-blockers** or **carbonic anhydrase inhibitors**, which act on the **ciliary epithelium**. - Glaucoma drainage devices focus on increasing outflow, not on reducing the production of aqueous humour.

Q: What is the most common etiopathogenetic cause of glaucoma?

Decreased outflow. ***Decreased outflow*** - The most common cause of glaucoma is an **obstruction** or inefficiency in the drainage of **aqueous humor** from the eye, leading to its accumulation. - This reduced outflow results in an increase in **intraocular pressure (IOP)**, which damages the optic nerve. *Raised pressure in episcleral veins* - While elevated episcleral venous pressure can contribute to increased IOP and glaucoma, it is a **less common primary etiopathogenetic mechanism** compared to impaired outflow facility. - Conditions like **Sturge-Weber syndrome** or an **arteriovenous fistula** can cause this, but they are not the typical presentation of primary open-angle glaucoma. *Increased formation of aqueous humour* - An increase in the production of **aqueous humor** is rarely the primary cause of glaucoma. - The eye's regulatory mechanisms usually compensate, or if overproduction occurs, it is an **anatomical issue**, not an outflow issue. *Increased scleral outflow* - Increased **scleral outflow** (also known as uveoscleral outflow, which is a non-conventional drainage pathway) would actually lead to a **decrease** in intraocular pressure, not an increase. - This mechanism is often targeted by certain glaucoma medications (e.g., **prostaglandin analogues**) to lower IOP by facilitating drainage.

Question 1

Which test is used to measure intraocular pressure?

Accepted Answer

Tonometry

Answer

Gonioscopy

Answer

Perimetry

Answer

Ophthalmoscopy

Question 2

A patient with chronic glaucoma is found to have optic nerve head cupping and visual field loss. What is the most well-established mechanism of optic nerve damage in glaucoma?

Accepted Answer

Increased intraocular pressure

Answer

Vascular insufficiency

Answer

Genetic predisposition

Answer

Inflammation

Question 3

Which type of visual field defect is typically observed in glaucoma?

Accepted Answer

Arcuate scotoma

Answer

Central scotoma

Answer

Homonymous hemianopia

Answer

Bitemporal hemianopia

Question 4

Which of the following is NOT a sign of angle closure glaucoma?

Accepted Answer

Multiple iris nodules

Answer

Mid-dilated fixed pupil

Answer

Edematous cornea

Answer

Edematous and hyperemic optic disc

Question 5

Recurrent non-granulomatous uveitis is seen in:

Accepted Answer

Posner-Schlossman syndrome

Answer

Vogt-Koyanagi-Harada syndrome

Answer

Tuberculosis

Answer

Sarcoidosis

Question 6

Which drug is primarily used in the treatment of acute angle-closure glaucoma?

Accepted Answer

Pilocarpine

Answer

Acetazolamide

Answer

Atropine

Answer

None of the options

Question 7

Which of the following conditions is NOT treated with Pilocarpine?

Accepted Answer

Malignant Glaucoma

Answer

Primary, Open Angle Glaucoma

Answer

Acute Angle Closure Glaucoma

Answer

Chronic Synechial Angle Closure Glaucoma

Question 8

Which of the following is NOT a feature of Primary Infantile (Congenital) glaucoma?

Accepted Answer

Aniridia may be associated

Answer

Treatment includes trabeculotomy

Answer

Buphthalmos can occur

Answer

Cornea is typically enlarged and cloudy.

Question 9

What is the primary function of glaucoma drainage devices?

Accepted Answer

Drain aqueous humour to an external device

Answer

Drain aqueous humour to the posterior segment

Answer

Open the trabeculae mechanically

Answer

Reduce the aqueous secretion by compressing the ciliary epithelium

Question 10

What is the most common etiopathogenetic cause of glaucoma?

Accepted Answer

Decreased outflow

Answer

Raised pressure in episcleral veins

Answer

Increased formation of aqueous humour

Answer

Increased scleral outflow

Glaucoma — MCQs

Glaucoma — MCQs

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