Diseases of the Cornea — MCQs

Diseases of the Cornea Indian Medical PG Practice Questions and MCQs

Question 41: Which of the following can cause corneal vascularization?

A. Chemical burn, contact lens, viral infection, and graft rejection
B. Graft rejection, chemical burn, contact lens, and viral infection (Correct Answer)
C. Graft rejection, contact lens, vitreous hemorrhage, and viral infection
D. Graft rejection, chemical burn, vitreous hemorrhage, and viral infection

Explanation: **Explanation:** Corneal vascularization (neovascularization) is a pathological condition where new blood vessels grow into the normally avascular cornea. This occurs when the **angiogenic-antiangiogenic balance** is disrupted, typically due to chronic hypoxia, inflammation, or limbal stem cell deficiency. **Why Option B is Correct:** Each component in this option is a classic cause of corneal neovascularization: * **Chemical Burns:** Alkali burns, in particular, cause extensive limbal ischemia and destruction of the limbal stem cell barrier, leading to conjunctivalization and deep vascularization. * **Contact Lens Wear:** Chronic hypoxia (low oxygen) induced by tight-fitting or low-Dk lenses triggers the release of VEGF (Vascular Endothelial Growth Factor). * **Viral Infection:** Chronic or recurrent Herpetic Keratitis (HSV/VZV) leads to stromal inflammation and subsequent scarring with vascularization. * **Graft Rejection:** Neovascularization is both a risk factor for and a sign of corneal graft rejection, as vessels provide a pathway for immune cells to reach the donor tissue. **Analysis of Incorrect Options:** * **Options C and D:** These include **Vitreous Hemorrhage**. The vitreous is located in the posterior segment of the eye. Hemorrhage there has no anatomical or physiological mechanism to cause corneal vascularization, which is an anterior segment pathology. **High-Yield Clinical Pearls for NEET-PG:** * **Superficial Vascularization:** Vessels are continuous with conjunctival vessels and cross the limbus (seen in Trachoma, Phlyctenular Keratoconjunctivitis). * **Deep Vascularization:** Vessels arise from anterior ciliary arteries and disappear at the limbus (seen in Interstitial Keratitis, Disciform Keratitis). * **Pannus:** A specific type of superficial vascularization with infiltration of granulation tissue (e.g., superior pannus in Trachoma). * **Treatment:** Topical steroids (to reduce inflammation) and anti-VEGF agents (like Bevacizumab) are used to manage active neovascularization.

Question 42: Which corneal ulcer is characterized by satellite lesions?

A. Trachoma
B. Fungal keratitis (Correct Answer)
C. Angular conjunctivitis
D. Herpes simplex keratitis

Explanation: **Explanation:** **Fungal Keratitis (Correct Answer):** Fungal corneal ulcers (keratomycosis) are typically caused by filamentous fungi like *Aspergillus* or *Fusarium* (often following trauma with vegetative matter) or *Candida*. **Satellite lesions** are a hallmark clinical feature; they are small, isolated infiltrates located away from the main ulcer margin, caused by the fungal hyphae penetrating deep into the stroma and spreading laterally. Other characteristic features include a dry, "feathery" finger-like margin, a sterile hypopyon, and an immune ring (Wessely ring). **Incorrect Options:** * **Trachoma:** Caused by *Chlamydia trachomatis* (Serotypes A, B, Ba, C). It primarily affects the conjunctiva, leading to follicles, Herbert’s pits, and cicatricial entropion, rather than acute ulcerative satellite lesions. * **Angular Conjunctivitis:** Characterized by inflammation at the outer or inner canthi, typically caused by *Moraxella lacunata*. It presents with excoriation of the skin and redness, not corneal satellite lesions. * **Herpes Simplex Keratitis:** Classically presents as a **dendritic ulcer** (linear, branching with terminal bulbs) or a geographic ulcer. It is characterized by diminished corneal sensations. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Natamycin (5%) is the topical treatment of choice for filamentous fungi; Fluconazole is preferred for *Candida*. * **Staining:** Use **Gomori Methenamine Silver (GMS)** or Periodic Acid-Schiff (PAS) to visualize hyphae. Calcofluor white is the most sensitive fluorescent stain. * **Contraindication:** Never use topical steroids in suspected fungal keratitis, as they lead to rapid fungal proliferation and potential perforation.

Question 43: Kayser-Fleischer rings affect which ocular structure?

A. Conjunctiva
B. Epithelial layer
C. Bowman's layer
D. Descemet's membrane (Correct Answer)

Explanation: **Explanation:** The **Kayser-Fleischer (KF) ring** is a pathognomonic sign of **Wilson’s disease** (hepatolenticular degeneration), a genetic disorder of copper metabolism. The ring is formed by the deposition of **copper** in the peripheral part of the **Descemet’s membrane** of the cornea. 1. **Why Descemet’s membrane is correct:** Copper is deposited as fine granules in the posterior layers of the cornea, specifically the Descemet’s membrane. It typically appears as a golden-brown or greenish-brown ring starting at the Schwalbe’s line and extending centrally. It usually appears first in the superior quadrant, followed by the inferior quadrant. 2. **Why other options are incorrect:** * **Conjunctiva:** While some systemic conditions cause conjunctival discoloration (e.g., jaundice), copper in Wilson’s disease specifically targets the corneal basement membrane. * **Epithelial layer:** This is the site for iron deposition in conditions like *Hudson-Stahli lines*. * **Bowman’s layer:** This layer is involved in calcific band keratopathy (calcium deposition), not copper deposition. **High-Yield Clinical Pearls for NEET-PG:** * **Composition:** The ring consists of **copper** (specifically in the form of sulfur-rich chelates). * **Clinical Significance:** KF rings are present in 95% of patients with neurological Wilson’s disease but may be absent in those with only hepatic involvement. * **Reversibility:** The ring **disappears** with effective chelation therapy (e.g., D-penicillamine). * **Sunflower Cataract:** Another ocular feature of Wilson’s disease where copper deposits in the anterior lens capsule. * **Examination:** While visible to the naked eye in advanced cases, a **Slit-lamp examination** is the gold standard for early detection.

Question 44: Ophthalmic examination of a patient shows 'Herbe pits' on the cornea. Which of the following infections is characteristic of this finding?

A. Trachoma (Correct Answer)
B. Psoriasis
C. Spring catarrh
D. Fungal keratitis

Explanation: **Explanation:** **Herbert’s Pits** are a pathognomonic clinical feature of **Trachoma**, a chronic keratoconjunctivitis caused by *Chlamydia trachomatis* (serotypes A, B, Ba, and C). 1. **Why Trachoma is correct:** During the active stage of Trachoma (Stage IIb), lymphoid follicles develop at the superior limbus. As these follicles heal by cicatrization, they leave behind small, circular, shallow depressions in the limbal area known as Herbert’s pits. These are essentially the scarred remnants of limbal follicles and are diagnostic of past or chronic trachomatous infection. 2. **Why other options are incorrect:** * **Psoriasis:** While it can have ocular manifestations like blepharitis or nonspecific conjunctivitis, it does not produce limbal follicles or Herbert’s pits. * **Spring Catarrh (VKC):** Characterized by **Horner-Trantas dots** (white dots consisting of eosinophils and epithelial debris at the limbus) and "cobblestone" papillae. It does not result in the permanent pitted scarring seen in Trachoma. * **Fungal Keratitis:** Typically presents with a dry-looking corneal ulcer, feathery margins, satellite lesions, and an immune ring (Wessely ring). It is an acute infectious process, not a chronic follicular scarring disease. **High-Yield Clinical Pearls for NEET-PG:** * **Arlt’s Line:** A horizontal band of scarring in the palpebral conjunctiva (junction of anterior 1/3rd and posterior 2/3rd) seen in Trachoma. * **S.A.F.E. Strategy:** WHO-recommended management (Surgery, Antibiotics—Azithromycin, Facial cleanliness, Environmental improvement). * **Pannus:** Trachomatous pannus is typically **superior** and progressive. * **Vector:** The common housefly (*Musca sorbens*) is the primary carrier.

Question 45: What is true about fungal corneal ulcer?

A. Satellite lesion (Correct Answer)
B. Symptoms are disproportionately severe compared to signs
C. Purulent ulcer
D. All of the above

Explanation: **Explanation:** Fungal keratitis (keratomycosis) is a serious ocular infection often following trauma with vegetative matter (e.g., a branch or leaf). **1. Why "Satellite Lesions" is correct:** Satellite lesions are a hallmark clinical feature of fungal ulcers. They represent small, isolated infiltrates located away from the main ulcer margin. These occur because fungal hyphae can penetrate deep into the corneal stroma and spread laterally, creating secondary foci of infection. Other characteristic signs include a "feathery" or "dry" appearance of the ulcer and a fixed, sterile hypopyon. **2. Why other options are incorrect:** * **Option B:** In fungal ulcers, **signs are disproportionately severe compared to symptoms**. Patients often present with a large, advanced-looking ulcer but report relatively minimal pain or irritation initially. The opposite (symptoms > signs) is characteristic of *Acanthamoeba* keratitis. * **Option C:** Fungal ulcers are typically **non-purulent**. They are characterized by dry, greyish-white infiltrates. A "purulent" ulcer with a yellow-green shaggy discharge is more typical of bacterial keratitis (specifically *Pseudomonas*). **Clinical Pearls for NEET-PG:** * **Commonest cause:** *Aspergillus* (overall), *Fusarium* (common in southern India/warm climates), and *Candida* (often in pre-existing ocular surface disease). * **Diagnosis:** Gold standard is **Sabouraud’s Dextrose Agar (SDA)**. Direct microscopy uses **KOH mount** (to see hyphae) or **Grocott-Gomori Methenamine Silver (GMS)** stain. * **Treatment:** Topical **Natamycin (5%)** is the drug of choice for filamentous fungi. Topical Amphotericin B is preferred for *Candida*. Avoid topical steroids as they worsen the infection.

Question 46: Cornea verticillata is caused by

A. Erythromycin
B. Amiodarone (Correct Answer)
C. Timolol
D. Tetracycline

Explanation: **Explanation:** **Cornea verticillata** (also known as vortex keratopathy) is a condition characterized by bilateral, symmetrical, golden-brown or greyish-brown epithelial deposits in the cornea, typically arranged in a whorl-like pattern. **Why Amiodarone is correct:** Amiodarone is a Class III anti-arrhythmic drug known for causing lipidosis-like changes. It is the most common pharmacological cause of cornea verticillata. The drug (and its metabolites) binds to polar lipids within the lysosomes of the corneal epithelium, leading to these characteristic deposits. They are usually asymptomatic, do not significantly affect vision, and are reversible upon discontinuation of the drug. **Why the other options are incorrect:** * **Erythromycin & Tetracycline:** These are antibiotics. While Tetracyclines can cause skin and tooth discoloration, they are not associated with whorl-like corneal deposits. * **Timolol:** This is a topical beta-blocker used for glaucoma. Common side effects include stinging, dry eyes, or systemic bradycardia, but it does not cause vortex keratopathy. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cornea Verticillata (CHAI-T):** * **C**hloroquine / Hydroxychloroquine * **H**eavy metals (e.g., Gold, Iron) * **A**miodarone (Most common) * **I**ndomethacin * **T**amoxifen * **Genetic Association:** If a patient presents with cornea verticillata without a drug history, suspect **Fabry’s Disease** (an X-linked lysosomal storage disorder due to alpha-galactosidase A deficiency). * **Amiodarone Monitoring:** Besides the cornea, amiodarone can cause **anterior subcapsular lens opacities** and, more seriously, **optic neuropathy**.

Question 47: Corneal dystrophies are:

A. Primary and unilateral
B. Primary and bilateral (Correct Answer)
C. Primary, bilateral, with systemic disease
D. Primary unilateral without systemic disease

Explanation: ### Explanation **Corneal dystrophies** are a group of progressive, usually genetic disorders that result in the accumulation of abnormal material within the layers of the cornea. **1. Why Option B is Correct:** The hallmark of corneal dystrophies is that they are **primary** (not caused by inflammation, trauma, or systemic disease) and **bilateral**. Because they are inherited (mostly autosomal dominant), they typically present with symmetrical, non-inflammatory opacities in both eyes. They usually manifest in the first or second decade of life and progress slowly. **2. Why the Other Options are Incorrect:** * **Options A & D (Unilateral):** Dystrophies are genetic/germline mutations; therefore, they affect both eyes. Unilateral corneal opacities are more characteristic of **corneal degenerations** (like Terrien’s marginal degeneration) or localized insults (trauma/infection). * **Option C (Systemic disease):** By definition, dystrophies are limited to the cornea. If a corneal deposit is associated with a systemic metabolic disorder (e.g., Wilson’s disease or Mucopolysaccharidosis), it is classified as a **corneal manifestation of a systemic disease**, not a primary dystrophy. **Clinical Pearls for NEET-PG:** * **Inheritance:** Most are **Autosomal Dominant** (AD). *Exception:* **Macular Dystrophy**, which is Autosomal Recessive (AR) and is the most severe. * **Layer-wise Classification:** * *Epithelial:* Meesmann dystrophy. * *Stromal:* Granular (Hyaline), Lattice (Amyloid), Macular (Acid Mucopolysaccharide) — Remember: **"MAM"** (Macular-Amyloid-Mucopolysaccharide is wrong; it's **M**acular-**A**cid **M**ucopolysaccharide). * *Endothelial:* **Fuchs’ Endothelial Dystrophy** (presents with *beaten metal* appearance/corneal guttata). * **Symptom:** Most cause a gradual decrease in vision or recurrent corneal erosions, but they are notably **painless** and **non-inflammatory**.

Question 48: Which of the following statements is NOT true regarding herpes zoster ophthalmicus?

A. Frontal nerve is the most commonly involved nerve.
B. Dendritic ulcers are a characteristic finding. (Correct Answer)
C. Punctate epithelial keratitis may be present.
D. Other cranial nerves can be involved.

Explanation: **Explanation:** The correct answer is **B**, as dendritic ulcers are the hallmark of **Herpes Simplex Keratitis (HSV)**, not Herpes Zoster Ophthalmicus (HZO). In HZO, the corneal lesions are typically **pseudodendrites**. Unlike true HSV dendrites, pseudodendrites are peripheral, elevated, lack terminal bulbs (knobs), and do not stain well with fluorescein (as there is no true ulceration of the basement membrane). * **Option A (Frontal nerve):** This is a true statement. The ophthalmic division (V1) of the trigeminal nerve is affected, and its **frontal branch** is the most frequently involved, leading to rashes on the forehead and upper eyelid. * **Option C (Punctate epithelial keratitis):** This is true. PEK is often the earliest corneal sign of HZO, appearing as multiple small, swollen epithelial spots that may later coalesce into pseudodendrites. * **Option D (Other cranial nerves):** This is true. While V1 is the primary site, HZO can be associated with palsies of the **III, IV, and VI cranial nerves** (leading to ophthalmoplegia) due to contiguous inflammation. **Clinical Pearls for NEET-PG:** * **Hutchinson’s Sign:** Involvement of the tip of the nose (nasociliary nerve) strongly predicts ocular involvement. * **Treatment:** Oral Acyclovir (800 mg 5x/day) is the mainstay. Note that the dose is double that used for HSV (400 mg). * **Complication:** Post-herpetic neuralgia is the most common debilitating complication in the elderly.

Question 49: All are true about Mooren's ulcer except?

A. It is a superficial ulcer.
B. It spreads circumferentially.
C. It is caused by infection. (Correct Answer)
D. Whitish overhanging margins are seen.

Explanation: **Explanation:** Mooren’s ulcer is a rare, idiopathic, and progressive **autoimmune** peripheral ulcerative keratitis (PUK). The fundamental concept to remember for NEET-PG is that it is a **non-infectious** (sterile) ulcer characterized by an autoimmune destruction of the corneal stroma. * **Why Option C is the correct answer:** Mooren’s ulcer is not caused by bacteria, fungi, or viruses. It is an **idiopathic autoimmune disease** triggered by a Type II and Type IV hypersensitivity reaction against corneal antigens. * **Why Option A is wrong:** It is indeed a **superficial** ulcer initially, involving the anterior one-third of the corneal stroma, though it can lead to thinning and perforation if left untreated. * **Why Option B is wrong:** A hallmark of Mooren’s ulcer is its **circumferential spread** (limbal) and subsequent centripetal progression toward the center of the cornea. * **Why Option D is wrong:** The presence of **whitish, undermined, or overhanging edges** at the advancing border is a classic clinical sign of Mooren’s ulcer. **High-Yield Clinical Pearls:** 1. **Two Clinical Types:** * **Type 1 (Benign):** Unilateral, occurs in elderly patients, responds well to treatment. * **Type 2 (Malignant):** Bilateral, occurs in younger patients (often of African descent), rapidly progressive, and resistant to therapy. 2. **Key Distinction:** Unlike other PUKs, Mooren’s ulcer is **not associated with systemic collagen vascular diseases** (like Rheumatoid Arthritis or Wegener’s). 3. **Treatment:** Topical steroids, conjunctival resection (peritomy) to remove the source of antibodies, and systemic immunosuppressants for bilateral cases.

Question 50: What is the primary pathology observed in keratomalacia?

A. Accumulation of desquamated debris
B. Absence of mucus
C. Breakdown of collagen fibers in the corneal stroma (Correct Answer)
D. Infection with Corynebacterium xerosis

Explanation: **Explanation:** **Keratomalacia** represents the most severe stage of Vitamin A deficiency (Xerophthalmia - WHO grade X3). The primary pathology is **liquefactive necrosis** of the cornea, characterized by the rapid **breakdown of collagen fibers in the corneal stroma**. This occurs due to the release of proteases and collagenases, leading to a "melting" of the cornea. If left untreated, it results in perforation, endophthalmitis, or phthisis bulbi. **Analysis of Options:** * **Option A (Incorrect):** Accumulation of desquamated debris mixed with *Corynebacterium xerosis* describes **Bitot’s spots** (Grade X1B), not the stromal destruction seen in keratomalacia. * **Option B (Incorrect):** While the **absence of mucus** (due to loss of goblet cells) is the hallmark of **conjunctival xerosis** (Grade X1A), it is an early feature. Keratomalacia involves deeper structural destruction beyond simple dryness. * **Option D (Incorrect):** *Corynebacterium xerosis* is a commensal that proliferates in the xerotic environment of Bitot’s spots; it is not the primary cause of the stromal melting in keratomalacia. **High-Yield Clinical Pearls for NEET-PG:** * **WHO Classification (Xerophthalmia):** X1A (Conjunctival xerosis), X1B (Bitot’s spots), X2 (Corneal xerosis), **X3A** (Keratomalacia <1/3rd cornea), **X3B** (Keratomalacia >1/3rd cornea). * **Night Blindness (XN):** The earliest clinical symptom. * **Conjunctival Xerosis:** The earliest clinical sign. * **Treatment:** Immediate Vitamin A supplementation (200,000 IU orally on days 0, 1, and 14) is a medical emergency to save the fellow eye and the child's life, as keratomalacia is often associated with high systemic mortality.

Practice by Chapter

Corneal Anatomy and Physiology

Practice Questions

Bacterial Keratitis

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Viral Keratitis

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Fungal Keratitis

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Protozoan Keratitis

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Corneal Degenerations

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Corneal Dystrophies

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Keratoconus and Ectatic Disorders

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Corneal Transplantation

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Corneal Topography and Imaging

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Dry Eye Disease

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Corneal Trauma

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