Diseases of the Retina — MCQs

A 56-year-old woman presents to the emergency room 3 hours after experiencing visual loss in her right eye. Her visual acuity is limited to light perception in the right eye. Examination reveals a pupillary defect, while the anterior surfaces of both eyes are normal. Fundus examination shows a cherry-red spot with a pale retina. What is the probable diagnosis?

Q68Medium

Recurrent toxoplasmic retinochoroiditis, all are true except:

Q69Medium

What are the causes of exudative retinal detachment?

Q70Easy

Amaurosis fugax refers to occlusion of:

Diseases of the Retina Indian Medical PG Practice Questions and MCQs

Question 61: What is the most common type of retinal detachment seen in proliferative diabetic retinopathy?

A. Rhegmatogenous
B. Tractional (Correct Answer)
C. Exudative
D. Retinoschisis

Explanation: **Explanation:** The correct answer is **Tractional Retinal Detachment (TRD)**. **1. Why Tractional is Correct:** In Proliferative Diabetic Retinopathy (PDR), chronic ischemia triggers the release of Vascular Endothelial Growth Factor (VEGF), leading to **neovascularization**. These fragile new vessels grow along with a fibrous scaffold (fibrovascular proliferation) into the vitreous. Over time, this fibrous tissue contracts, creating mechanical "traction" that pulls the sensory retina away from the underlying Retinal Pigment Epithelium (RPE). Unlike other types, TRD occurs without a retinal break and typically presents with a concave, immobile surface. **2. Why Other Options are Incorrect:** * **Rhegmatogenous (A):** This is the most common type of RD overall, caused by a **retinal break/hole** allowing fluid to enter the subretinal space. While a "combined" tractional-rhegmatogenous RD can occur in late-stage PDR, pure TRD is the hallmark. * **Exudative (C):** Also known as serous RD, this occurs due to fluid leakage (e.g., inflammation or tumors) without traction or breaks. While PDR involves leakage (macular edema), it does not typically cause extensive exudative RD. * **Retinoschisis (D):** This is a splitting of the retinal layers (usually at the outer plexiform layer), not a true detachment of the retina from the RPE. **Clinical Pearls for NEET-PG:** * **Management:** The gold standard treatment for Tractional RD involving the macula is **Pars Plana Vitrectomy (PPV)** to relieve the traction. * **Configuration:** TRD is typically **concave** and limited in mobility, whereas Rhegmatogenous RD is **convex** and ripples with eye movement. * **High-Yield Fact:** The most common cause of vitreous hemorrhage in adults is PDR; if the fundus is obscured by blood, **B-Scan Ultrasonography** is mandatory to rule out an underlying TRD.

Question 62: Tabular vision is caused by which of the following conditions?

A. Retinitis pigmentosa (Correct Answer)
B. Narrow angle glaucoma
C. Nuclear cataract
D. Papilledema

Explanation: **Explanation:** **Tubular vision** (also known as tunnel vision) refers to the loss of peripheral vision with the retention of only a small central field. **Why Retinitis Pigmentosa (RP) is the correct answer:** Retinitis Pigmentosa is a hereditary dystrophy primarily affecting the **rod photoreceptors**. Since rods are concentrated in the mid-periphery of the retina, their degeneration leads to **ring scotomas**. As the disease progresses, these scotomas expand peripherally and centrally, leaving only a small island of central vision (macular sparing). This clinical phenomenon is termed "tubular vision." **Analysis of Incorrect Options:** * **Narrow-angle glaucoma:** While advanced chronic glaucoma causes tunnel vision, acute narrow-angle glaucoma typically presents with sudden vision loss, halos, and ocular pain rather than progressive tubular field loss. * **Nuclear cataract:** This causes a gradual decrease in visual acuity and a "second sight" phenomenon (myopic shift), but it does not cause peripheral field constriction. * **Papilledema:** Early papilledema typically presents with an **enlarged blind spot** (negative scotoma). Tubular vision only occurs in the terminal stages of secondary optic atrophy following chronic papilledema, making RP the more definitive primary cause. **NEET-PG High-Yield Pearls:** * **Classic Triad of RP:** Bony spicule pigmentation, Arteriolar attenuation (narrowing), and Waxy pallor of the optic disc. * **Earliest Symptom:** Nyctalopia (night blindness) due to rod dysfunction. * **ERG Findings:** The Electroretinogram (ERG) is subnormal or extinguished even before fundus changes appear. * **Associated Syndrome:** Usher’s Syndrome (RP + Sensorineural hearing loss) is a common exam favorite.

Question 63: Which of the following is NOT a treatment modality for wet age-related macular degeneration (ARMD)?

A. Anti-VEGF therapy
B. Photodynamic therapy
C. Macular grid photocoagulation
D. Panretinal photocoagulation (Correct Answer)

Explanation: **Explanation:** The core pathology in **Wet (Neovascular) Age-Related Macular Degeneration (ARMD)** is the development of **Choroidal Neovascularization (CNV)**. These abnormal vessels leak fluid and blood under the macula, leading to rapid vision loss. **Why Panretinal Photocoagulation (PRP) is the correct answer:** PRP involves applying laser burns to the peripheral retina to reduce the overall oxygen demand, thereby regressing neovascularization. It is the gold standard treatment for **Proliferative Diabetic Retinopathy (PDR)** and **Ischemic Central Retinal Vein Occlusion (CRVO)**. It is **not** used for ARMD because the pathology in ARMD is localized to the macula, and applying PRP would not address the subfoveal CNV. **Analysis of other options:** * **Anti-VEGF therapy (e.g., Ranibizumab, Bevacizumab, Aflibercept):** This is the **first-line treatment** for wet ARMD. It inhibits Vascular Endothelial Growth Factor, reducing vascular permeability and clinical edema. * **Photodynamic Therapy (PDT):** Uses a photosensitizer (Verteporfin) and a cold laser to selectively destroy CNV membranes while sparing the overlying retina. It is used in specific cases like Polypoidal Choroidal Vasculopathy (PCV). * **Macular Grid Photocoagulation:** While largely replaced by Anti-VEGF, focal or grid laser was historically used for well-defined extrafoveal CNV in ARMD. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest symptom of ARMD:** Metamorphopsia (distortion of vision), tested using the **Amsler Grid**. * **Hallmark of Dry ARMD:** Drusen (sub-retinal yellow deposits) and geographic atrophy. * **Investigation of choice:** **Optical Coherence Tomography (OCT)** is used for monitoring; **Fundus Fluorescein Angiography (FFA)** is used to confirm and type the CNV. * **Dietary Supplement:** AREDS-2 formulation (Antioxidants, Zinc, Lutein, Zeaxanthin) is used to slow progression in *Dry* ARMD.

Question 64: The mother of a one and a half year old child gives a history of a white reflex from one eye for the past 1 month. On computed tomography scan of the orbit, calcification is seen within the globe. What is the most likely diagnosis?

A. Congenital cataract
B. Retinoblastoma (Correct Answer)
C. Endophthalmitis
D. Coats disease

Explanation: ### **Explanation** The clinical presentation of a **white pupillary reflex (leukocoria)** in a child under the age of two, combined with **intraocular calcification** on imaging, is pathognomonic for **Retinoblastoma** until proven otherwise. **1. Why Retinoblastoma is Correct:** Retinoblastoma is the most common primary intraocular malignancy of childhood. It typically presents before age 3. The "chalky white" calcification seen on CT scans (present in >90% of cases) represents DNA-calcium complexes (the **Fujiwara effect**) resulting from tumor necrosis. This is a hallmark diagnostic feature that distinguishes it from other causes of leukocoria. **2. Why Other Options are Incorrect:** * **Congenital Cataract:** While it is the most common cause of leukocoria, it presents as an opacification of the lens. It does not show intraocular mass-like calcification on CT. * **Endophthalmitis:** This is an intraocular inflammation (often post-traumatic or metastatic). While it can cause a yellow-white reflex (pseudoglioma), it is usually associated with pain, redness, and a history of infection, lacking the specific calcification pattern of a tumor. * **Coats Disease:** An idiopathic exudative retinopathy typically seen in slightly older boys (6–8 years). While it causes leukocoria due to retinal detachment, calcification is extremely rare, and imaging usually shows subretinal exudates. **3. NEET-PG High-Yield Pearls:** * **Most common presentation:** Leukocoria (60%), followed by Strabismus (20%). * **Genetics:** Mutation in the **RB1 gene** on chromosome **13q14**. It follows Knudson’s "Two-hit hypothesis." * **Histopathology:** Look for **Flexner-Wintersteiner rosettes** (highly specific) and Homer-Wright rosettes. * **Investigation of Choice:** **MRI** is preferred over CT to evaluate optic nerve involvement and to avoid radiation, though CT is superior for detecting calcification. * **Trilateral Retinoblastoma:** Bilateral retinoblastoma associated with a Pinealoblastoma.

Question 65: Vitreous hemorrhage is seen in all the following conditions except:

A. Central retinal artery occlusion (CRAO) (Correct Answer)
B. Central retinal vein occlusion (CRVO)
C. Coat's disease
D. Eales' disease

Explanation: **Explanation:** Vitreous hemorrhage (VH) typically occurs due to the rupture of newly formed, fragile blood vessels (**neovascularization**) or the mechanical tearing of normal retinal vessels. **Why CRAO is the correct answer:** In **Central Retinal Artery Occlusion (CRAO)**, there is an acute blockage of blood flow to the inner retina, leading to immediate ischemic necrosis. Because the retina is infarcted and "dead," it generally does not produce the chronic angiogenic stimulus (like VEGF) required for neovascularization of the disc or retina. Therefore, VH is **not** a feature of CRAO. (Note: Neovascular glaucoma can rarely occur, but VH remains clinically atypical for CRAO). **Why the other options are incorrect:** * **Central Retinal Vein Occlusion (CRVO):** Ischemic CRVO leads to significant retinal hypoxia and high VEGF levels, resulting in neovascularization of the disc (NVD) or elsewhere (NVE), which can bleed into the vitreous. * **Coat’s Disease:** This is characterized by telangiectatic retinal vessels and aneurysms. While exudation is more common, these abnormal vessels can leak or rupture, leading to VH. * **Eales’ Disease:** An idiopathic peripheral perivasculitis (common in young males) that causes extensive peripheral ischemia, leading to neovascularization and recurrent vitreous hemorrhages (one of its hallmark presentations). **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause of VH:** Proliferative Diabetic Retinopathy (PDR). 2. **Most common cause of VH in young adults:** Trauma or Eales' disease. 3. **Terson Syndrome:** Vitreous hemorrhage associated with subarachnoid hemorrhage (SAH). 4. **B-Scan Ultrasound:** The investigation of choice to rule out retinal detachment when the fundus is obscured by VH.

Question 66: The "salt and pepper fundus" is a characteristic clinical finding in which of the following conditions?

A. Multiple sclerosis
B. Cystinosis
C. Weill-Marchesani syndrome
D. Congenital syphilis (Correct Answer)

Explanation: **Explanation:** The **"Salt and Pepper Fundus"** refers to a characteristic pigmentary retinopathy consisting of diffuse, fine, mottled areas of retinal pigment epithelium (RPE) atrophy (the "salt") interspersed with clumps of pigment hypertrophy (the "pepper"). **1. Why Congenital Syphilis is Correct:** In **Congenital Syphilis**, this finding is a classic late manifestation. It results from a chronic, low-grade inflammatory process (chorioretinitis) caused by *Treponema pallidum*. Unlike Retinitis Pigmentosa, it is usually non-progressive, and the retinal vessels and optic disc typically remain normal. It is often asymptomatic but can be associated with interstitial keratitis and Hutchinson’s teeth (Hutchinson’s Triad). **2. Analysis of Incorrect Options:** * **Multiple Sclerosis:** Primarily associated with **Optic Neuritis** (sudden vision loss, RAPD) and Internuclear Ophthalmoplegia (INO), not pigmentary retinal changes. * **Cystinosis:** Characterized by the deposition of shimmering, needle-shaped **cystine crystals** in the cornea and conjunctiva, leading to photophobia. * **Weill-Marchesani Syndrome:** A connective tissue disorder characterized by **microspherophakia** (small, spherical lens), high myopia, and ectopia lentis, but not a salt and pepper fundus. **3. NEET-PG High-Yield Clinical Pearls:** * **Differential Diagnosis of Salt and Pepper Fundus:** 1. **Congenital Syphilis** (Most common association). 2. **Congenital Rubella** (Most common ocular finding in Rubella). 3. **Leber’s Congenital Amaurosis** (Early stage). 4. **Cystinosis** (Can occasionally show peripheral mottling, but crystals are the hallmark). 5. **Cockayne Syndrome.** * **Key Distinction:** In syphilis, the "salt and pepper" appearance is usually peripheral and does not significantly affect the Electroretinogram (ERG), whereas in hereditary dystrophies, the ERG is typically extinguished.

Question 67: A 56-year-old woman presents to the emergency room 3 hours after experiencing visual loss in her right eye. Her visual acuity is limited to light perception in the right eye. Examination reveals a pupillary defect, while the anterior surfaces of both eyes are normal. Fundus examination shows a cherry-red spot with a pale retina. What is the probable diagnosis?

A. Central retinal vein occlusion
B. Proliferative diabetic retinopathy
C. Background diabetic retinopathy
D. Central retinal artery occlusion (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Central Retinal Artery Occlusion (CRAO)** The clinical presentation is a classic textbook case of **Central Retinal Artery Occlusion**. The underlying pathophysiology involves a sudden blockage of the central retinal artery (usually by an embolus), leading to ischemia of the inner retinal layers. * **Sudden, painless loss of vision:** CRAO presents as a dramatic drop in visual acuity (often to Light Perception or Hand Movements) within seconds or minutes. * **Relative Afferent Pupillary Defect (RAPD):** This indicates significant optic nerve or extensive retinal ischemia. * **Cherry-red spot:** The hallmark sign. The fovea remains red because it is the thinnest part of the retina, allowing the underlying vascular choroid to show through. In contrast, the surrounding infarcted retina becomes opaque and milky-white (pale) due to intracellular edema. **Why the other options are incorrect:** * **A. Central Retinal Vein Occlusion (CRVO):** Characterized by a "blood and thunder" fundus with extensive flame-shaped hemorrhages, dilated tortuous veins, and disc edema, rather than a pale retina. * **B & C. Diabetic Retinopathy (Proliferative/Background):** These are chronic, progressive conditions. While they can cause vision loss (via vitreous hemorrhage or macular edema), they do not present with a sudden cherry-red spot and acute retinal pallor. **NEET-PG High-Yield Pearls:** * **"Time is Tissue":** CRAO is an ocular emergency. Irreversible retinal damage occurs within **90–100 minutes**. * **Management:** Immediate ocular massage, anterior chamber paracentesis, and IV acetazolamide to lower IOP and dislodge the embolus. * **Differential for Cherry-Red Spot:** CRAO, Tay-Sachs disease, Niemann-Pick disease, and Gaucher’s disease. * **Cilioretinal Artery:** In 15–20% of the population, this artery (spared in CRAO) may preserve a small island of central vision.

Question 68: Recurrent toxoplasmic retinochoroiditis, all are true except:

A. Manifests at an average age of 25 years
B. The infestation is acquired by eating the undercooked meat of intermediate host containing cyst of the parasite (Correct Answer)
C. Typical lesion is a patch of focal necrotizing retinochoroiditis adjacent to a pigmented scar
D. There may be associated iritis

Explanation: **Explanation:** The question asks for the "Except" statement regarding **Recurrent Toxoplasmic Retinochoroiditis**. **1. Why Option B is the Correct Answer (The False Statement):** While *Toxoplasma gondii* can indeed be acquired by eating undercooked meat (containing bradyzoites) or through oocyst ingestion from cat feces, **recurrent** ocular toxoplasmosis is almost always a reactivation of a **congenital infection**. In these cases, the parasite was acquired transplacentally during pregnancy and remained dormant in the retina as tissue cysts. Therefore, the recurrence itself is not due to a new "infestation" via meat, but the breakdown of old cysts from a pre-existing congenital infection. **2. Analysis of Other Options:** * **Option A:** Recurrent episodes typically manifest in the second or third decade of life, with a mean age of approximately 25 years, as the dormant cysts reactivate. * **Option C:** This describes the classic **"Satellite Lesion."** The hallmark of recurrence is a new area of fluffy, white focal necrotizing retinitis located immediately adjacent to an old, pigmented chorioretinal scar. * **Option D:** Recurrent posterior segment inflammation often triggers a "spill-over" anterior uveitis, manifesting as iritis with granulomatous or non-granulomatous keratic precipitates. **Clinical Pearls for NEET-PG:** * **Classic Appearance:** "Headlight in the fog" (active white retinitis seen through vitritis). * **Most Common Cause:** Toxoplasmosis is the most common cause of posterior uveitis worldwide. * **Treatment:** The "Triple Therapy" includes Pyrimethamine, Sulfadiazine, and Folinic acid (to prevent bone marrow toxicity). Steroids are added only *after* starting anti-parasitics. * **Macula:** It has a predilection for the macula, often leading to permanent central vision loss.

Question 69: What are the causes of exudative retinal detachment?

A. Central retinal artery occlusion
B. Hypertensive retinopathy
C. Harada's syndrome (Correct Answer)
D. All of the above

Explanation: **Explanation:** **Exudative Retinal Detachment (ERD)** occurs when fluid accumulates in the subretinal space due to damage to the Blood-Retinal Barrier (BRB) or the Retinal Pigment Epithelium (RPE), without any retinal breaks or traction. **Why Harada’s Syndrome is Correct:** Harada’s syndrome (part of Vogt-Koyanagi-Harada or VKH disease) is a multisystem autoimmune disorder characterized by granulomatous uveitis. The primary pathology involves intense inflammation of the choroid, leading to increased vascular permeability. This fluid leaks through the RPE into the subretinal space, causing a classic **multifocal exudative retinal detachment**. **Analysis of Incorrect Options:** * **Central Retinal Artery Occlusion (CRAO):** This is a vascular emergency causing inner retinal ischemia and edema (cloudy swelling). It typically presents with a "cherry-red spot" but does not cause fluid accumulation in the subretinal space or detachment. * **Hypertensive Retinopathy:** While severe (Grade IV) hypertension can cause exudates and disc edema, it is not a primary cause of ERD in the same way inflammatory or neoplastic conditions are. (Note: While *Toxemia of Pregnancy* can cause ERD, standard hypertensive retinopathy does not). **High-Yield Clinical Pearls for NEET-PG:** * **Shifting Fluid Sign:** This is the pathognomonic clinical feature of Exudative RD; the subretinal fluid moves to the most dependent part of the retina with changes in head position. * **Common Causes of ERD:** * **Inflammatory:** VKH syndrome, Posterior Scleritis. * **Neoplastic:** Choroidal Melanoma (most common intraocular tumor causing ERD), Metastasis. * **Vascular/Systemic:** Eclampsia, Chronic Renal Failure. * **Management:** Unlike Rhegmatogenous RD (which requires surgery), ERD is primarily managed by treating the **underlying systemic cause** (e.g., systemic steroids for VKH).

Question 70: Amaurosis fugax refers to occlusion of:

A. Middle cerebral artery
B. Branch retinal vein
C. Branch retinal artery (Correct Answer)
D. Choroidal artery

Explanation: **Explanation:** **Amaurosis Fugax** is defined as sudden, painless, transient monocular vision loss (often described as a "curtain falling" over the eye) that typically lasts seconds to minutes, followed by complete recovery. **Why the correct answer is right:** The most common cause of amaurosis fugax is an **embolus** (Hollenhorst plaque) originating from an atherosclerotic carotid artery. This embolus travels through the internal carotid and ophthalmic arteries to lodge temporarily in the **retinal arterial system**. While it can affect the Central Retinal Artery (CRA), it frequently involves a **Branch Retinal Artery (BRA)**. The transient occlusion leads to ischemia of the inner retinal layers, causing temporary vision loss until the embolus dissolves or moves distally. **Why the incorrect options are wrong:** * **Middle Cerebral Artery (MCA):** Occlusion of the MCA typically results in contralateral hemiparesis and hemianesthesia. While it can cause visual field defects (homonymous hemianopia), it does not cause monocular transient vision loss. * **Branch Retinal Vein (BRV):** Venous occlusions present with sudden, *persistent* (not transient) blurring of vision and characteristic "blood and thunder" fundus findings (hemorrhages). * **Choroidal Artery:** Occlusion here would affect the outer retina and RPE, but it is not the classic pathological mechanism associated with the clinical syndrome of amaurosis fugax. **High-Yield Clinical Pearls for NEET-PG:** * **Hollenhorst Plaques:** Cholesterol emboli seen at retinal artery bifurcations; a hallmark sign of carotid artery disease. * **Investigation of Choice:** Carotid Doppler (to rule out carotid stenosis). * **Differential Diagnosis:** Must be distinguished from Giant Cell Arteritis (GCA) in elderly patients. * **Significance:** Amaurosis fugax is considered a "TIA of the eye" and is a strong predictor of a future stroke.

Practice by Chapter

Retinal Anatomy and Physiology

Practice Questions

Age-Related Macular Degeneration

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Diabetic Retinopathy

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Retinal Vascular Diseases

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Retinal Detachment

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Hereditary Retinal Dystrophies

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Inflammatory Retinal Diseases

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Retinal Tumors

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Retinopathy of Prematurity

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Retinal Imaging Techniques

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Intravitreal Pharmacotherapy

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Vitreoretinal Surgery

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