What is the most common etiopathogenetic cause of glaucoma?
Which of the following is NOT a feature of Primary Infantile (Congenital) glaucoma?
Which of the following statements about congenital glaucoma is incorrect?
Descemet membrane breach is seen in ?
What condition are miotics the treatment of choice for?
What is the cause of glaucoma in retinoblastoma?
What is the primary function of glaucoma drainage devices?
A 44-year-old woman presents with sudden painless loss of vision with a history of previous similar episodes. Fundoscopy shows no glow. What could be the possible diagnosis?
All of the following are true for retinopathy of prematurity except which of the following?
What is the primary predisposing factor for retinopathy of prematurity?
NEET-PG 2015 - Ophthalmology NEET-PG Practice Questions and MCQs
Question 31: What is the most common etiopathogenetic cause of glaucoma?
- A. Raised pressure in episcleral veins
- B. Decreased outflow (Correct Answer)
- C. Increased formation of aqueous humour
- D. Increased scleral outflow
Explanation: ***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 32: Which of the following is NOT a feature of Primary Infantile (Congenital) glaucoma?
- A. Aniridia may be associated (Correct Answer)
- B. Treatment includes trabeculotomy
- C. Buphthalmos can occur
- D. Cornea is typically enlarged and cloudy.
Explanation: ***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.
Question 33: Which of the following statements about congenital glaucoma is incorrect?
- A. Thin and blue sclera seen
- B. Anterior chamber is shallow (Correct Answer)
- C. Photophobia is most common symptom
- D. Haab's Striae may be seen
Explanation: ***Anterior chamber is shallow*** - In congenital glaucoma, the **anterior chamber depth is typically normal or deep**, not shallow. - A shallow anterior chamber is more characteristic of **angle-closure glaucoma**, which is mechanistically different. - This makes the statement incorrect, as congenital glaucoma is associated with a **deep anterior chamber** due to globe enlargement. *Photophobia is most common symptom* - **Photophobia** (sensitivity to light) is indeed one of the classic presenting symptoms in congenital glaucoma. - It forms part of the classic triad: **photophobia, epiphora (tearing), and blepharospasm**. - This occurs due to **increased intraocular pressure** causing corneal edema and irritation. *Thin and blue sclera seen* - The **sclera** can appear thin and blue due to **buphthalmos** (enlargement of the eye) and stretching of the globe. - The stretching allows the underlying **uveal tissue** to show through, giving the characteristic blue appearance. - This is a direct consequence of elevated intraocular pressure in a developing eye. *Haab's Striae may be seen* - **Haab's striae** are **Descemet's membrane tears** that are pathognomonic of congenital glaucoma. - These horizontal or curvilinear breaks occur due to stretching of the cornea from **elevated intraocular pressure**. - They appear as visible linear opacities on corneal examination.
Question 34: Descemet membrane breach is seen in ?
- A. Angle closure glaucoma
- B. Acute Iridocyclitis
- C. Subconjunctival hemorrhage
- D. Congenital glaucoma (Buphthalmos) (Correct Answer)
Explanation: ***Congenital glaucoma (Buphthalmos)*** - In **congenital glaucoma**, increased intraocular pressure (IOP) in infancy stretches the developing eye, leading to enlargement (buphthalmos) and **Descemet membrane breaches** or ruptures. - These ruptures appear as fine, parallel, or branching lines on the posterior corneal surface, known as **Haab's striae**, which are characteristic signs of this condition. *Angle closure glaucoma* - This condition involves a sudden rise in IOP due to physical obstruction of the **aqueous humor outflow** and does not typically cause Descemet membrane breaks. - Clinical signs include **corneal edema** due to endothelial dysfunction, but not membrane breaches. *Acute Iridocyclitis* - **Acute iridocyclitis** is an inflammatory condition of the iris and ciliary body, primarily causing cells and flare in the anterior chamber. - It does not directly lead to **Descemet membrane breaches** or structural damage like stretching of the cornea. *Subconjunctival hemorrhage* - This condition is characterized by **bleeding under the conjunctiva** and is typically due to ruptured conjunctival blood vessels. - It is a superficial condition that does not involve the cornea or the Descemet membrane.
Question 35: What condition are miotics the treatment of choice for?
- A. Angle closure glaucoma
- B. Open-angle glaucoma (Correct Answer)
- C. Buphthalmos
- D. Sympathetic ophthalmia
Explanation: ***Open-angle glaucoma*** - Miotics, such as **pilocarpine**, are a classical treatment option for **primary open-angle glaucoma (POAG)**. - They work by **contracting the ciliary muscle**, which opens up the **trabecular meshwork** and increases aqueous humor outflow. - This results in **reduction of intraocular pressure (IOP)**, the primary goal in glaucoma management. - Though less commonly used today due to side effects (brow ache, miosis affecting vision), they remain effective and are particularly useful in patients who cannot tolerate other medications. *Angle closure glaucoma* - Miotics are **contraindicated in acute angle-closure glaucoma** as they can worsen pupillary block during the acute attack. - The initial treatment involves **IOP-lowering agents, systemic medications, and laser iridotomy**, not miotics. - Miotics may have a limited role in chronic angle closure after definitive treatment, but they are NOT the treatment of choice. *Buphthalmos* - This refers to **enlargement of the eyeball** in infants due to congenital glaucoma. - Management primarily involves **surgical intervention** (goniotomy, trabeculotomy) to address the developmental anomalies of the drainage angle. - Medical management alone, including miotics, is insufficient. *Sympathetic ophthalmia* - A rare **bilateral granulomatous panuveitis** following penetrating trauma or surgery to one eye. - Treated with **corticosteroids and immunosuppressive agents**. - Miotics have no role in managing this inflammatory condition.
Question 36: What is the cause of glaucoma in retinoblastoma?
- A. Neovascularisation (Correct Answer)
- B. Mass effect of the tumour
- C. Blockage of trabecular network
- D. Lysis of the lens
Explanation: ***Neovascularisation*** - Retinoblastoma leads to **neovascularization of the iris (NVI)** and **angle structures** due to tumor necrosis, ischemia, and release of **angiogenic factors (VEGF)**. - The **neovascular membrane** grows over and obstructs the **trabecular meshwork** and anterior chamber angle, causing **secondary neovascular glaucoma**. - This is the **most characteristic and common mechanism** of glaucoma in advanced retinoblastoma. - Neovascular glaucoma in retinoblastoma is typically **refractory to medical treatment** and indicates poor prognosis. *Blockage of trabecular network* - While tumor cells can directly seed into the anterior chamber and block the trabecular meshwork, this mechanism is **less common** than neovascularization. - This option is also **less specific** as it doesn't identify the underlying pathophysiological process (neovascularization) that is characteristic of retinoblastoma-associated glaucoma. - Direct trabecular blockage by tumor cells typically occurs in advanced disease and often coexists with neovascularization. *Mass effect of the tumour* - The tumor mass itself rarely causes glaucoma through direct mechanical compression of outflow pathways. - Retinoblastoma causes glaucoma primarily through **secondary mechanisms** such as inflammation, neovascularization, or cellular seeding, not simple bulk effect. - Massive tumors may cause angle closure, but this is uncommon compared to neovascular mechanisms. *Lysis of the lens* - **Phacolytic glaucoma** from lens protein leakage is rare in retinoblastoma. - While lens damage can occur with advanced tumors, it is **not a typical or characteristic cause** of glaucoma in retinoblastoma. - The primary mechanisms involve the **tumor-angle-trabecular meshwork axis**, not lens pathology.
Question 37: What is the primary function of glaucoma drainage devices?
- A. Drain aqueous humour to the posterior segment
- B. Drain aqueous humour to an external device (Correct Answer)
- C. Open the trabeculae mechanically
- D. Reduce the aqueous secretion by compressing the ciliary epithelium
Explanation: **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.
Question 38: A 44-year-old woman presents with sudden painless loss of vision with a history of previous similar episodes. Fundoscopy shows no glow. What could be the possible diagnosis?
- A. Vitreous Hemorrhage (Correct Answer)
- B. Rhegmatogenous Retinal Detachment
- C. Acute Angle-Closure Glaucoma
- D. Fungal Keratitis
Explanation: ***Vitreous Hemorrhage*** - **Painless vision loss** is a hallmark symptom, and **previous similar episodes** suggest a recurrent condition, characteristic of vitreous hemorrhage from fragile vessels. - The **"no glow"** on fundoscopy indicates that light from the ophthalmoscope is unable to reflect off the retina due to something obstructing the clear media, such as blood in the vitreous cavity. *Rhegmatogenous Retinal Detachment* - While it causes **painless vision loss**, patients often report **floaters** or **flashes of light** preceding the detachment, which are not mentioned here. - Fundoscopy in rhegmatogenous retinal detachment would typically show a **grayish, elevated retina**, often with folds, not a complete loss of red reflex or ''no glow.'' *Acute Angle-Closure Glaucoma* - Characterized by **sudden, severe eye pain**, blurred vision, and often a **red eye** with a fixed, mid-dilated pupil. - Fundoscopy would typically reveal a **cupped optic disc** in advanced stages, but the primary finding is elevated intraocular pressure, with a clear vitreous, thus allowing an initial glow. *Fungal Keratitis* - This is an **infection of the cornea** that typically presents with pain, redness, photophobia, and a visible corneal ulcer or infiltrate. - Vision loss is gradual, and fundoscopy would still show a **normal red reflex** unless the corneal opacity is extremely dense, which is not implied by "no glow."
Question 39: All of the following are true for retinopathy of prematurity except which of the following?
- A. Due to hypoxia there occurs neovascularization followed by fibroproliferation
- B. Occurs in premature infants due to abnormal retinal blood vessel development.
- C. End result is bilateral blindness (Correct Answer)
- D. Blindness can be prevented by early diagnosis and ablation of avascular peripheral retina with cryotherapy or photocoagulation
Explanation: ***End result is bilateral blindness*** - While retinopathy of prematurity (ROP) can lead to severe vision loss or blindness, it is not always a bilateral end result, especially with early diagnosis and treatment. The severity can vary between eyes, and some cases resolve spontaneously. - Modern screening and intervention strategies, such as laser photocoagulation or anti-VEGF injections, are often successful in preventing complete blindness in one or both eyes. *Due to hypoxia there occurs neovascularization followed by fibroproliferation* - This statement accurately describes the pathogenesis of ROP. The initial phase involves delayed normal retinal vascularization, followed by a proliferative phase characterized by **neovascularization** in response to hypoxia in the avascular retina. - These new, abnormal vessels are fragile and prone to bleeding, and their associated **fibrovascular proliferation** can lead to retinal detachment. *Blindness can be prevented by early diagnosis and ablation of vascular premature retina with cryotherapy or photocoagulation* - This is a true statement. **Early diagnosis** through ophthalmologic screening of premature infants is crucial, and treatments like **laser photocoagulation** or **cryotherapy** are effective in ablating the avascular peripheral retina to halt the progression of abnormal vessel growth. - These interventions reduce the hypoxic drive that fuels neovascularization, thereby preventing severe retinal detachment and subsequent blindness. *Occurs in premature infants due to abnormal retinal blood vessel development.* - This statement is correct. ROP is a disease primarily affecting **premature infants** because their retinal blood vessels have not completed development by the time of birth. - Postnatal factors, including oxygen fluctuations and low birth weight, further disrupt this critical development, leading to **abnormal vascularization**.
Question 40: What is the primary predisposing factor for retinopathy of prematurity?
- A. Oxygen toxicity
- B. Carbohydrate excess
- C. Low birth weight
- D. Low gestational age (Correct Answer)
Explanation: ***Low gestational age*** - **Prematurity** is the most significant risk factor, as the **retinal vasculature** is still immature and susceptible to abnormal development. - The earlier the gestational age, the **higher the risk** of ROP developing and progressing to severe stages. *Low birth weight* - While strongly correlated with ROP, **low birth weight** is often a consequence of prematurity rather than the primary predisposing factor itself. - Many term infants can have low birth weight due to **intrauterine growth restriction** but do not typically develop ROP. *Oxygen toxicity* - **Supplemental oxygen** can exacerbate ROP by causing initial **vasoconstriction** and subsequent abnormal vessel proliferation. - However, it acts as a secondary trigger in an already vulnerable, premature retina, not the primary predisposing factor. *Carbohydrate excess* - **Carbohydrate excess** is not a recognized predisposing factor for retinopathy of prematurity. - This condition is primarily related to the **vascular development of the retina** in premature infants.