Primary Open-Angle Glaucoma Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Primary Open-Angle Glaucoma. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Primary Open-Angle Glaucoma Indian Medical PG Question 1: What is the best drug for open-angle glaucoma?
- A. Latanoprost (Correct Answer)
- B. Pilocarpine
- C. Physostigmine
- D. Apraclonidine
Primary Open-Angle Glaucoma Explanation: Latanoprost
- Latanoprost is a prostaglandin analog and is often considered a first-line treatment for open-angle glaucoma due to its efficacy in reducing intraocular pressure (IOP) and its once-daily dosing.
- It works by increasing the outflow of aqueous humor through the uveoscleral pathway, thereby lowering IOP.
Pilocarpine
- Pilocarpine is a cholinergic agonist that causes miosis and ciliary muscle contraction [3], increasing the outflow of aqueous humor through the trabecular meshwork [4].
- While effective, its side effects (e.g., accommodative spasm, miosis) [1] and more frequent dosing make it generally a second-line or third-line agent for long-term management compared to prostaglandins.
Physostigmine
- Physostigmine is an acetylcholinesterase inhibitor that indirectly increases acetylcholine, mimicking cholinergic stimulation.
- Although it can lower IOP, it is generally not used for open-angle glaucoma due to significant side effects and the availability of safer, more effective alternatives [1].
Apraclonidine
- Apraclonidine is an alpha-2 adrenergic agonist [2] used primarily for short-term control of IOP, especially before or after ocular surgery, or as an adjunct therapy.
- Its efficacy as a long-term monotherapy for open-angle glaucoma is limited by tachyphylaxis and potential for significant systemic side effects with chronic use.
Primary Open-Angle Glaucoma Indian Medical PG Question 2: What are the characteristic features of Posner-Schlossman syndrome?
- A. Ipsilateral optic atrophy with contralateral papilloedema
- B. Unilateral glaucomatous changes with mild anterior uveitis (Correct Answer)
- C. Granulomatous uveitis with iris heterochromia
- D. None of the options
Primary Open-Angle Glaucoma Explanation: ***Unilateral glaucomatous changes with mild anterior uveitis***
- Posner-Schlossman syndrome, also known as **glaucomatocyclitic crisis**, is characterized by recurrent, acute attacks of **unilateral elevated intraocular pressure** (glaucomatous changes).
- These attacks are accompanied by **mild anterior uveitis**, which typically presents with few or no precipitates and minimal redness.
*Ipsilateral optic atrophy with contralateral papilloedema*
- This constellation of symptoms, known as **Foster Kennedy syndrome**, is associated with intracranial masses, not Posner-Schlossman syndrome.
- It involves **optic atrophy** in one eye due to direct pressure on the optic nerve and **papilledema** in the other eye due to increased intracranial pressure.
*Granulomatous uveitis with iris heterochromia*
- **Granulomatous uveitis** is characterized by large mutton-fat keratic precipitates and often seen in diseases like sarcoidosis or tuberculosis, which is not typical for Posner-Schlossman.
- **Iris heterochromia** (different colored irises) is a characteristic feature of **Fuchs' heterochromic cyclitis**, another form of chronic anterior uveitis, but not Posner-Schlossman syndrome.
*None of the options*
- This option is incorrect as one of the provided choices accurately describes the characteristic features of Posner-Schlossman syndrome.
- The other options describe different ophthalmological conditions.
Primary Open-Angle Glaucoma Indian Medical PG Question 3: Recurrent anterior uveitis with increased intraocular tension is seen in which of the following conditions?
- A. Posner-Schlossman syndrome (Correct Answer)
- B. Foster-Kennedy syndrome
- C. Vogt-Koyanagi-Harada syndrome
- D. Fuchs heterochromic iridocyclitis
Primary Open-Angle Glaucoma Explanation: ***Posner-Schlossman syndrome***
- Characterized by **recurrent, unilateral, non-granulomatous anterior uveitis** associated with markedly **elevated intraocular pressure (IOP)**.
- The condition is also known as **glaucomatocyclitic crisis**, highlighting the episodic inflammation and glaucoma.
- Key features include **acute attacks** lasting hours to weeks with **dramatic IOP elevation** (often >40 mmHg).
*Foster-Kennedy syndrome*
- This syndrome is defined by ipsilateral **optic atrophy**, contralateral **papilledema**, and often **anosmia**, typically due to a frontal lobe tumor.
- It does not involve anterior uveitis or primary elevated intraocular tension.
- This is a neuro-ophthalmologic syndrome, not an inflammatory ocular condition.
*Vogt-Koyanagi-Harada syndrome*
- An autoimmune disorder affecting pigmented tissues, leading to **bilateral granulomatous panuveitis**, often with hearing loss, vitiligo, poliosis, and neurological symptoms.
- While it involves uveitis, it is typically **bilateral and panuveitis**, not recurrent unilateral anterior uveitis.
- IOP may be elevated but not the defining feature with dramatic episodic rises.
*Fuchs heterochromic iridocyclitis*
- A chronic, **unilateral, low-grade anterior uveitis** with characteristic iris heterochromia.
- May have mild IOP elevation but **not recurrent episodic attacks** with marked pressure spikes.
- Inflammation is typically **quiet and chronic** rather than acute and recurrent.
Primary Open-Angle Glaucoma Indian Medical PG Question 4: Intumescent cataract is associated with which type of glaucoma?
- A. Phacolytic glaucoma
- B. Phacotopic glaucoma
- C. Pseudophakic glaucoma
- D. Phacomorphic glaucoma (Correct Answer)
Primary Open-Angle Glaucoma Explanation: ***Phacomorphic glaucoma***
- **Intumescent cataract** refers to a mature or hypermature cataract that has absorbed water, leading to a swollen lens.
- This swelling can cause the lens to push the iris forward, leading to secondary **angle closure glaucoma** due to pupillary block, which is characteristic of phacomorphic glaucoma.
*Phacolytic glaucoma*
- This type of glaucoma is caused by leakage of **high-molecular-weight lens proteins** from a mature or hypermature cataract into the aqueous humor, triggering a macrophagic response and obstruction of the trabecular meshwork.
- It results in an **open-angle glaucoma** and anterior chamber inflammation, unlike the angle closure seen with intumescent cataracts.
*Phacotopic glaucoma*
- This is a rare term and not a recognized distinct category of glaucoma related to lens swelling. It may refer loosely to glaucoma associated with **lens dislocation** or subluxation.
- It does not specifically describe glaucoma caused by an **intumescent cataract**.
*Pseudophakic glaucoma*
- This refers to glaucoma that develops in patients who have undergone **cataract surgery** and have an **intraocular lens (IOL)** implant (pseudophakia).
- It can be caused by various mechanisms post-surgery, such as inflammation, steroid response, or IOL-related issues, but it is not directly associated with the presence of an intumescent natural lens.
Primary Open-Angle Glaucoma Indian Medical PG Question 5: Which of the following is not a feature of open-angle glaucoma?
- A. Elevated intraocular pressure
- B. Increased cup-to-disc ratio
- C. Gradual peripheral vision loss
- D. Pain and redness (Correct Answer)
Primary Open-Angle Glaucoma Explanation: ***Pain and redness***
- **Open-angle glaucoma** is typically a **painless** condition, often referred to as the "silent thief of sight", because central vision is preserved until late stages.
- **Pain** and **redness** are more characteristic of **acute angle-closure glaucoma** or other inflammatory eye conditions, not the chronic, progressive nature of open-angle glaucoma.
*Elevated intraocular pressure*
- **Elevated intraocular pressure** (IOP) is a primary risk factor and a hallmark feature of **open-angle glaucoma**, although normal-tension glaucoma exists.
- Sustained high IOP can lead to **optic nerve damage** over time.
*Increased cup-to-disc ratio*
- An **increased cup-to-disc ratio** on examination of the optic disc is a key diagnostic feature of **open-angle glaucoma**, indicating **optic nerve damage** and atrophy.
- This enlargement of the optic cup is due to the loss of nerve fibers.
*Gradual peripheral vision loss*
- **Gradual peripheral vision loss** is the characteristic pattern of vision loss in **open-angle glaucoma**, often unnoticed by the patient until advanced stages.
- The central vision remains relatively intact until late in the disease, making early detection challenging.
Primary Open-Angle Glaucoma Indian Medical PG Question 6: A 58-year-old male presents with gradual loss of peripheral vision in both eyes. On fundus examination, significant cupping of the optic disc and arcuate scotomas were noted. IOP was 28 mmHg. Based on these findings, which pathway is most likely affected in this patient’s disease?
- A. Increased aqueous humor production
- B. Retinal ganglion cell apoptosis (Correct Answer)
- C. Retinal detachment
- D. Phototransduction in rods and cones
Primary Open-Angle Glaucoma Explanation: ***Retinal ganglion cell apoptosis***
- This is the **fundamental pathway** affected in glaucoma and directly explains all the clinical findings in this patient.
- The patient's **peripheral vision loss**, **optic disc cupping**, and **arcuate scotomas** all result from progressive **death of retinal ganglion cells (RGCs)** and their axons.
- In **primary open-angle glaucoma**, sustained elevated IOP (28 mmHg in this case) causes **mechanical compression** and **ischemic injury** at the optic nerve head, triggering RGC apoptosis.
- Loss of RGC axons creates the characteristic **optic disc cupping** and **nerve fiber bundle defects** (arcuate scotomas), leading to irreversible vision loss.
*Increased aqueous humor production*
- While aqueous humor dynamics are involved in glaucoma pathophysiology, the primary issue is **impaired trabecular outflow**, not increased production.
- Increased production alone would elevate IOP but does not explain the specific **RGC damage pattern**, optic disc cupping, or arcuate scotomas seen in this patient.
- This addresses the mechanism of elevated IOP, not the pathway of vision loss.
*Retinal detachment*
- Retinal detachment presents with **sudden onset** symptoms like **photopsia (flashes)**, **floaters**, and a **curtain-like visual field defect**, not gradual peripheral vision loss.
- Fundoscopy would show a **detached, elevated retina**, not the optic disc cupping and arcuate scotomas characteristic of glaucoma.
- This condition involves separation of the neurosensory retina from the retinal pigment epithelium, not RGC damage.
*Phototransduction in rods and cones*
- Phototransduction abnormalities affect **photoreceptor cells** (rods and cones), seen in conditions like **retinitis pigmentosa** or **cone-rod dystrophies**.
- These conditions present with **night blindness**, **tunnel vision** (from peripheral rod loss), or **central vision loss** (from cone dysfunction), and do not cause elevated IOP or optic disc cupping.
- The patient's elevated IOP and specific glaucomatous findings indicate damage to **ganglion cells**, not photoreceptors.
Primary Open-Angle Glaucoma Indian Medical PG Question 7: Which of the following conditions is least likely to be associated with neovascular glaucoma?
- A. Diabetes
- B. Open angle glaucoma (Correct Answer)
- C. CRVO
- D. Eale's disease
Primary Open-Angle Glaucoma Explanation: ***Open angle glaucoma*** ✓
- **Open-angle glaucoma** is a primary **neurodegenerative disease** of the optic nerve, characterized by progressive loss of **retinal ganglion cells** and their axons, leading to characteristic **optic neuropathy** and visual field defects.
- It does **NOT** directly cause **neovascularization** or increased VEGF production, which are the underlying mechanisms for **neovascular glaucoma**.
- This is the **least likely** association among the given options.
*Diabetes*
- **Diabetic retinopathy** is a **major cause** of **neovascularization** due to retinal ischemia and increased production of **vascular endothelial growth factor (VEGF)**, which can lead to **neovascular glaucoma**.
- **Neovascularization** on the iris (rubeosis iridis) and angle can block aqueous outflow, causing a severe, rapidly progressing form of secondary glaucoma.
*CRVO (Central Retinal Vein Occlusion)*
- **CRVO** leads to significant retinal ischemia and subsequent release of **VEGF**, which prompts the growth of new, fragile blood vessels.
- These new vessels (neovascularization) can grow in the iris and angle, obstructing aqueous humor outflow and causing **neovascular glaucoma**.
- **Ischemic CRVO** is one of the **most common causes** of neovascular glaucoma.
*Eale's disease*
- **Eale's disease** is an **idiopathic occlusive vasculitis** primarily affecting the **peripheral retinal veins**, leading to **retinal ischemia**.
- This ischemia stimulates **neovascularization** and the production of **VEGF**, increasing the risk of **neovascular glaucoma** due to the formation of new blood vessels in the anterior chamber.
Primary Open-Angle Glaucoma Indian Medical PG Question 8: Which of the following is most likely to cause bilateral angle closure glaucoma?
- A. Sulfonamide medications
- B. Adrenergic agonists
- C. Topiramate (Correct Answer)
- D. Anticholinergic drugs
Primary Open-Angle Glaucoma Explanation: ***Topiramate can cause bilateral angle closure glaucoma***
- **Topiramate** is known to cause a unique form of **bilateral angle closure glaucoma** due to ciliary body edema and anterior displacement of the iris-lens diaphragm, leading to acute myopia and angle closure.
- This reaction typically occurs within the first few weeks of starting the drug, is **bilateral**, and is not related to angle anatomy.
*Sulfonamide medications*
- While some **sulfonamides** can cause acute myopia and secondary angle closure, similar to topiramate, this is a less consistently reported and less recognized association compared to topiramate.
- The mechanism involves **ciliary body edema** leading to anterior displacement of the iris-lens diaphragm, but topiramate is a more classic example.
*Adrenergic agonists*
- **Adrenergic agonists** typically cause **mydriasis** (pupil dilation), which can precipitate acute angle closure in eyes with an already **narrow angle**.
- However, they usually trigger **unilateral** angle closure and do not cause the same ciliary body edema mechanism seen with topiramate that results in bilateral involvement.
*Anticholinergic drugs*
- **Anticholinergic drugs** also cause **mydriasis** and can lead to **acute angle closure glaucoma** by widening the pupil and potentially blocking aqueous outflow in susceptible individuals.
- Similar to adrenergic agonists, this is usually a **unilateral** event and does not involve the characteristic ciliary body edema and resultant bilateral acute myopia associated with topiramate.
Primary Open-Angle Glaucoma Indian Medical PG Question 9: Secondary glaucoma associated with angle recession is seen in:
- A. Penetrating injury
- B. Concussion injury (Correct Answer)
- C. Chemical injury
- D. Radiation injury
Primary Open-Angle Glaucoma Explanation: ***Concussion injury***
- **Concussion injuries** (blunt trauma) to the eye lead to shearing forces between the ciliary body and sclera, causing a tear in the ciliary body and trabecular meshwork.
- This anatomical alteration, known as **angle recession**, impairs aqueous humor outflow over time, leading to secondary open-angle glaucoma.
*Penetrating injury*
- **Penetrating injuries** breach the globe and can cause direct damage to ocular structures, but angle recession leading to glaucoma is more characteristic of blunt trauma.
- Such injuries often lead to other forms of glaucoma, like **pupillary block** or **phacolytic glaucoma**, depending on the extent of damage and inflammation.
*Chemical injury*
- **Chemical injuries** (e.g., acid or alkali burns) cause severe inflammation, tissue necrosis, and scarring within the anterior segment.
- Glaucoma following chemical injury is typically due to **trabecular meshwork damage** from inflammation and scarring, or **peripheral anterior synechiae formation**, rather than angle recession.
*Radiation injury*
- **Radiation injury** to the eye is rare but can occur with radiation therapy for tumors, causing damage to vascular structures and contributing to neovascularization.
- Glaucoma associated with radiation injury is usually secondary to **neovascularization** of the angle or **inflammatory processes**, not angle recession.
Primary Open-Angle Glaucoma Indian Medical PG Question 10: A patient presents with eye ache and difficulty in vision after watching a movie. What will be the first line of management?
- A. Mannitol with Moxifloxacin
- B. Mannitol with Atropine
- C. Mannitol with lubricating eye drops
- D. Mannitol with Pilocarpine (Correct Answer)
Primary Open-Angle Glaucoma Explanation: ***Mannitol with Pilocarpine***
- This combination is appropriate for **acute angle-closure glaucoma (AACG)**, which can be triggered by pupillary dilation (e.g., in a dark movie theater). **Mannitol** is an osmotic diuretic that rapidly reduces intraocular pressure.
- **Pilocarpine** is a miotic agent that constricts the pupil, pulling the iris away from the trabecular meshwork and opening the drainage angle to facilitate aqueous humor outflow.
*Mannitol with Moxifloxacin*
- While mannitol helps with intraocular pressure, **Moxifloxacin is an antibiotic** used to treat bacterial infections.
- There is no indication of an ocular infection in this scenario, so an antibiotic would not be the first-line treatment for sudden eye pain and vision difficulty after watching a movie.
*Mannitol with Atropine*
- Adding **Atropine, a cycloplegic agent**, would cause further pupillary dilation, which would worsen acute angle-closure glaucoma and increase intraocular pressure.
- Atropine is contraindicated in AACG and would exacerbate the patient's condition.
*Mannitol with lubricating eye drops*
- While mannitol helps with intraocular pressure, **lubricating eye drops** are used for dry eyes or surface irritation, not for acute angle-closure glaucoma.
- Lubricating drops do not address the underlying pathology of increased intraocular pressure due to angle closure.
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