Diseases of the Cornea — MCQs
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In Herpes zoster Keratitis, which of the following does NOT occur?
Schwalbe's line represents the peripheral limit of which corneal layer?
Which of the following is true of a dendritic ulcer?
What happens to the corneal endothelium after injury?
K F Ring is seen in which condition?
Cogan's syndrome is associated with which of the following?
Schwalbe's line represents:
Bowman's membrane is seen in which structure?
What is the initial treatment for a perforated corneal ulcer?
Corneal dystrophy associated with acid mucopolysaccharidosis is:
Diseases of the Cornea Indian Medical PG Practice Questions and MCQs
Question 141: In Herpes zoster Keratitis, which of the following does NOT occur?
- A. Pseudodendritic keratitis
- B. Anterior stromal keratitis
- C. Sclerokeratitis (Correct Answer)
- D. Endothelitis
Explanation: In **Herpes Zoster Ophthalmicus (HZO)**, the varicella-zoster virus affects the ophthalmic division of the trigeminal nerve. While HZO can involve almost any ocular structure, the question asks which of the listed options does **NOT** typically occur as a primary corneal manifestation of the disease. ### **Explanation of the Correct Answer** **C. Sclerokeratitis:** This is the correct answer because, while HZO can cause **scleritis** and **keratitis** independently, "Sclerokeratitis" (an inflammatory process involving both the limbus and peripheral cornea, often seen in systemic autoimmune diseases like Rheumatoid Arthritis) is not a classic or defining feature of Herpes Zoster Keratitis. ### **Why the Other Options are Incorrect** * **A. Pseudodendritic keratitis:** This is a hallmark of HZO. Unlike the true dendrites of Herpes Simplex (HSV), these are elevated, "stuck-on" epithelial plaques without terminal bulbs and they stain poorly with fluorescein. * **B. Anterior stromal keratitis:** This occurs in about 5% of cases, appearing as multiple fine granular infiltrates (nummular keratitis) in the subepithelial/anterior stroma, usually beneath the site of previous epithelial lesions. * **D. Endothelitis:** HZO frequently causes inflammation of the corneal endothelium, leading to corneal edema, keratic precipitates (KPs), and often an associated secondary glaucoma (hypertensive uveitis). ### **NEET-PG High-Yield Pearls** * **Hutchinson’s Sign:** Involvement of the tip of the nose (nasociliary nerve) strongly predicts ocular involvement. * **HSV vs. HZO Dendrites:** * **HSV:** True dendrite, central ulceration (excavated), terminal bulbs present, stains well with fluorescein. * **HZO:** Pseudodendrite, elevated (stuck-on), no terminal bulbs, stains poorly with fluorescein (but well with Rose Bengal). * **Neurotrophic Keratopathy:** A common late complication due to loss of corneal sensation, leading to non-healing ulcers.
Question 142: Schwalbe's line represents the peripheral limit of which corneal layer?
- A. Bowman's layer
- B. Stroma
- C. Descemet's layer (Correct Answer)
- D. Endothelium
Explanation: **Explanation:** **Schwalbe’s line** is a critical anatomical landmark in the anterior chamber angle. It represents the **peripheral termination of Descemet’s membrane** (the basement membrane of the corneal endothelium). As the cornea transitions into the sclera at the limbus, Descemet’s membrane thickens and ends, forming this visible ridge. * **Why Option C is Correct:** Descemet’s membrane is a resilient, elastic layer. Its peripheral limit marks the anterior boundary of the trabecular meshwork. During gonioscopy, Schwalbe’s line is the most anterior structure identified in the angle. * **Why Options A & B are Incorrect:** **Bowman’s layer** (Option A) ends abruptly at the limbus and does not extend into the angle structures. The **Stroma** (Option B) is continuous with the sclera (corneoscleral junction) rather than ending at a specific "line." * **Why Option D is Incorrect:** The **Endothelium** (Option D) is a monolayer of cells that continues over the trabecular meshwork as the mesenchymal lining; it does not form the anatomical ridge known as Schwalbe’s line. **High-Yield Clinical Pearls for NEET-PG:** * **Gonioscopy:** Schwalbe’s line is the first structure seen from the "top" (anteriorly) when performing gonioscopy. * **Sampaolesi Line:** In Pigmentary Glaucoma or Pseudoexfoliation syndrome, dark pigment often deposits on or anterior to Schwalbe’s line, creating a "Sampaolesi line." * **Posterior Embryotoxon:** An abnormally thickened and anteriorly displaced Schwalbe’s line is termed "Posterior Embryotoxon," which can be an isolated finding or associated with **Alagille syndrome** or **Axenfeld-Rieger syndrome**.
Question 143: Which of the following is true of a dendritic ulcer?
- A. Caused by Herpes simplex virus (Correct Answer)
- B. Topical corticosteroid given suppresses the symptoms
- C. Oral acyclovir is effective in treatment
- D. All of the above
Explanation: **Explanation:** **Dendritic ulcer** is the classic clinical presentation of **Herpes Simplex Keratitis (HSK)**, specifically caused by the Herpes Simplex Virus Type 1 (HSV-1). 1. **Why Option A is correct:** The virus infects the corneal epithelium, leading to the formation of linear, branching (dendritic) lesions. These ulcers are characterized by **terminal bulbs** and stain vividly with **Fluorescein** (the bed) and **Rose Bengal** (the swollen margins containing live virus). 2. **Why Option B is incorrect:** Topical corticosteroids are **strictly contraindicated** in the presence of an active epithelial dendritic ulcer. Steroids promote viral replication, leading to the enlargement of the ulcer into a "geographic" or "amoeboid" ulcer and increasing the risk of corneal perforation. 3. **Why Option C is incorrect:** While oral acyclovir is used for recurrent HSK or stromal involvement, the **primary treatment** for a simple dendritic epithelial ulcer is **topical antiviral therapy** (e.g., Ganciclovir 0.15% gel or Acyclovir 3% ointment). Oral acyclovir is generally reserved for prophylaxis or complicated cases, making "A" the most definitive "true" statement regarding the etiology. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Sign:** Reduced or absent corneal sensations (tested with a wisp of cotton). * **Staining:** Fluorescein stains the ulcer base; Rose Bengal/Lissamine Green stains the devitalized cells at the margin. * **Morphology:** True dendrites have **terminal bulbs**, which distinguish them from "pseudodendrites" seen in Acanthamoeba or Herpes Zoster Ophthalmicus. * **Treatment:** Debridement + Topical Antivirals. **Never use steroids in epithelial disease.**
Question 144: What happens to the corneal endothelium after injury?
- A. Slowly regenerates
- B. Never regenerates
- C. Regenerates rapidly (Correct Answer)
- D. Forms a scar
Explanation: ### Explanation The corneal endothelium is a single layer of hexagonal cells that plays a critical role in maintaining corneal dehydration (deturgescence) via the Na+/K+ ATPase pump. **Why "Regenerates rapidly" is the correct answer:** In the context of clinical ophthalmology and standard textbook descriptions (like Khurana), the corneal endothelium is described as having **no regenerative capacity** in humans. However, when an injury occurs, the defect is "repaired" or "regenerated" in a functional sense not by cell division (mitosis), but by the **rapid migration and enlargement (pleomorphism and polymegethism)** of existing neighboring cells to cover the gap. This process happens very quickly to restore the endothelial pump function and prevent corneal edema. *Note: In many competitive exams, "Regenerates rapidly" refers to this rapid compensatory migration rather than true mitotic division.* **Analysis of Incorrect Options:** * **A & B:** While technically true that mitotic regeneration is near zero, these options are often considered incorrect in the context of the "rapid" functional recovery seen after minor trauma or surgery. * **D. Forms a scar:** Scarring is a feature of the corneal **stroma** (involving myofibroblasts). The endothelium does not form a traditional opaque scar; it either recovers its barrier function or fails, leading to bullous keratopathy. **High-Yield NEET-PG Pearls:** * **Cell Count:** Normal adult count is **2500–3000 cells/mm²**. * **Critical Limit:** If the count falls below **500 cells/mm²**, corneal decompensation and edema occur. * **Specular Microscopy:** The gold standard investigation to assess endothelial cell density and morphology. * **Schwalbe’s Line:** Represents the peripheral termination of the endothelial layer (Descemet’s membrane).
Question 145: K F Ring is seen in which condition?
- A. Chalcosis (Correct Answer)
- B. Sarcoidosis
- C. Tuberous Sclerosis
- D. VKH Syndrome
Explanation: **Explanation:** The **Kayser-Fleischer (KF) ring** is a classic clinical sign characterized by a golden-brown or greenish-brown pigment deposition in the **Descemet’s membrane** of the peripheral cornea. It is caused by the deposition of **copper**. 1. **Why Chalcosis is correct:** Chalcosis refers to the presence of intraocular copper (usually from a retained copper-containing foreign body). Since the KF ring is specifically a manifestation of copper deposition, it is seen in conditions of systemic copper overload (like **Wilson’s Disease**) or localized copper toxicity (**Chalcosis Bulbi**). In Wilson's disease, it starts superiorly, then inferiorly, and finally becomes circumferential. 2. **Why other options are incorrect:** * **Sarcoidosis:** Typically presents with granulomatous uveitis (Mutton-fat keratic precipitates) and "string of pearls" vitreous opacities, not copper deposition. * **Tuberous Sclerosis:** Associated with retinal astrocytic hamartomas (mulberry lesions), not corneal rings. * **VKH (Vogt-Koyanagi-Harada) Syndrome:** A multisystem autoimmune disease presenting with bilateral granulomatous panuveitis, exudative retinal detachment, and integumentary signs (poliosis, vitiligo), but no corneal copper rings. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** KF rings are always found in the **Descemet’s membrane**. * **Best Visualization:** Early KF rings are best detected using a **Gonioscope**. * **Sunflower Cataract:** Another high-yield copper-related finding seen in Wilson’s disease/Chalcosis (deposition in the anterior lens capsule). * **Fleischer Ring:** Do not confuse KF ring with Fleischer ring (iron deposition at the base of the cone in **Keratoconus**). * **Ferry’s Line:** Iron line at the edge of a filtering bleb. * **Stocker’s Line:** Iron line at the head of a Pterygium.
Question 146: Cogan's syndrome is associated with which of the following?
- A. Keratitis (Correct Answer)
- B. Conjunctivitis
- C. Iritis
- D. Myopia
Explanation: **Explanation:** **Cogan’s Syndrome** is a rare, non-syphilitic autoimmune vasculitis primarily affecting young adults. The classic clinical triad consists of **Interstitial Keratitis (IK)**, vestibulo-auditory dysfunction (Meniere-like symptoms), and systemic vasculitis (notably aortitis). 1. **Why Keratitis is correct:** The hallmark ocular manifestation is **nonsyphilitic interstitial keratitis**. Patients typically present with sudden onset of photophobia, lacrimation, and blurred vision. Examination reveals patchy subepithelial infiltrates in the peripheral cornea, which can progress to deep corneal neovascularization. 2. **Why other options are incorrect:** * **Conjunctivitis:** While mild redness may occur, it is not a defining or diagnostic feature of the syndrome. * **Iritis:** Though secondary anterior uveitis can occur as a complication of severe keratitis, it is not the primary diagnostic association. * **Myopia:** There is no pathological link between Cogan’s syndrome and refractive errors like myopia. **High-Yield Clinical Pearls for NEET-PG:** * **The Triad:** Interstitial Keratitis + Vertigo/Tinnitus/Hearing loss + Systemic Vasculitis. * **Systemic Association:** Up to 10% of patients develop **Aortitis**, which can lead to life-threatening aortic insufficiency or aneurysms. * **Differential Diagnosis:** Always rule out **Syphilis** (the most common cause of IK) using FTA-ABS or VDRL tests. * **Treatment:** Topical steroids for ocular symptoms; systemic steroids or immunosuppressants (e.g., Cyclophosphamide) for auditory and systemic involvement. Early treatment is critical to prevent permanent deafness.
Question 147: Schwalbe's line represents:
- A. The junction of the choroid and retina
- B. The termination of Descemet's membrane (Correct Answer)
- C. The division between bulbar and palpebral conjunctiva
- D. The upper limit of the macula
Explanation: **Explanation:** **Schwalbe’s line** is a critical anatomical landmark in the anterior chamber angle. It represents the **peripheral termination of Descemet’s membrane** (the basement membrane of the corneal endothelium). Structurally, it marks the transition point where the corneal endothelium ends and the trabecular meshwork begins. **Analysis of Options:** * **Option B (Correct):** As the Descemet’s membrane reaches the limbus, it thickens and ends abruptly, forming a faint white ridge known as Schwalbe’s line. * **Option A:** The junction of the choroid and retina is the **Ora Serrata**, which marks the transition from the non-photosensitive ciliary epithelium to the photosensitive retina. * **Option C:** The division between the bulbar and palpebral conjunctiva is the **Conjunctival Fornix**. * **Option D:** There is no specific anatomical line named "Schwalbe's" for the macula; the macula is defined by its high density of xanthophyll pigment and cones. **Clinical Pearls for NEET-PG:** 1. **Gonioscopy:** Schwalbe’s line is the **most anterior (uppermost) structure** visible during gonioscopy. Identifying it is the first step in grading the angle. 2. **Sampaolesi Line:** In Pigmentary Glaucoma or Pseudoexfoliation Syndrome, pigment may deposit on or anterior to Schwalbe’s line, forming a "Sampaolesi line." 3. **Posterior Embryotoxon:** If Schwalbe’s line is thickened and anteriorly displaced (visible on slit-lamp exam without a goniolens), it is called Posterior Embryotoxon, often associated with **Alagille syndrome** or **Axenfeld-Rieger syndrome**.
Question 148: Bowman's membrane is seen in which structure?
- A. Conjunctiva
- B. Cornea (Correct Answer)
- C. Lens
- D. Iris
Explanation: **Explanation:** The **Cornea** is the correct answer because Bowman’s membrane is one of its five primary histological layers. To remember the layers of the cornea from anterior to posterior, use the mnemonic **"ABCDE"**: 1. **A**nterior Epithelium 2. **B**owman’s Membrane (Anterior limiting membrane) 3. **C**orneal Stroma (Substantia propria) 4. **D**escemet’s Membrane (Posterior limiting membrane) 5. **E**ndothelium **Bowman’s membrane** is an acellular, condensed layer of collagen fibers. Its most significant clinical characteristic is that **it does not regenerate**; if damaged by trauma or ulceration, it heals by permanent scarring (opacification), which can lead to visual impairment. **Why other options are incorrect:** * **Conjunctiva:** This is a mucous membrane consisting of non-keratinized stratified columnar epithelium and a lamina propria (adenoid and fibrous layers), but it lacks a Bowman’s layer. * **Lens:** The lens consists of a capsule, anterior epithelium, and lens fibers. It is an avascular, transparent structure but does not contain Bowman’s membrane. * **Iris:** Part of the uveal tract, the iris consists of the anterior limiting layer, stroma, and posterior pigmented epithelium. **High-Yield Clinical Pearls for NEET-PG:** * **Regeneration:** Descemet’s membrane *can* regenerate (secreted by the endothelium), whereas Bowman’s membrane *cannot*. * **Keratoconus:** Characterized by early breaks in Bowman’s membrane. * **Reis-Bücklers Dystrophy:** A superficial corneal dystrophy specifically affecting Bowman’s layer. * **Thickness:** Bowman's membrane is approximately 8–14 microns thick.
Question 149: What is the initial treatment for a perforated corneal ulcer?
- A. Conjunctival flap grafting
- B. Tissue adhesive glue (Correct Answer)
- C. Contact lens
- D. Local anesthetic drops instillation
Explanation: **Explanation:** The management of a perforated corneal ulcer depends on the size of the perforation. For small perforations (typically <2 mm), the **initial and primary goal** is to restore the integrity of the anterior chamber and prevent further leakage of aqueous humor. **Why Tissue Adhesive Glue is Correct:** Cyanoacrylate tissue adhesive (glue) is the treatment of choice for small corneal perforations. It acts as a mechanical plug, allowing the underlying stroma to heal and preventing secondary infection. It is often applied in conjunction with a Bandage Contact Lens (BCL) to prevent the glue from irritating the eyelid. This procedure is minimally invasive and can be performed at the bedside or in a minor OT. **Analysis of Incorrect Options:** * **A. Conjunctival flap grafting:** This is a surgical procedure used for non-healing ulcers or larger defects. It is not the "initial" treatment for a simple perforation as it provides poor visual outcomes and makes subsequent monitoring of the ulcer difficult. * **C. Contact lens:** While a Bandage Contact Lens (BCL) is used *after* applying glue, a contact lens alone cannot seal a perforation; it is used for epithelial healing or small descemetoceles, not frank perforations. * **D. Local anesthetic drops:** These are strictly contraindicated for long-term use as they are epitheliotoxic and delay corneal wound healing. They are only used for brief diagnostic procedures. **NEET-PG High-Yield Pearls:** * **Size Matters:** If the perforation is **<2 mm**, use Tissue Adhesive Glue. If it is **>2 mm**, a **Penetrating Keratoplasty (PKP)** or "Patch Graft" is required. * **Seidel’s Test:** Used to diagnose corneal perforation. Fluorescein dye is applied; a positive test shows a "streaming" of clear aqueous through the orange-yellow dye under cobalt blue light. * **Emergency Management:** Until definitive repair, a pressure bandage or a shield should be applied to prevent further iris prolapse.
Question 150: Corneal dystrophy associated with acid mucopolysaccharidosis is:
- A. Lattice
- B. Granular
- C. Macular (Correct Answer)
- D. Peripheral
Explanation: **Explanation:** The correct answer is **Macular Corneal Dystrophy (MCD)**. **Why Macular Dystrophy is correct:** Macular corneal dystrophy is an autosomal recessive condition (unlike most other stromal dystrophies which are autosomal dominant). It is characterized by the systemic and localized accumulation of **Acid Mucopolysaccharides** (specifically Keratan Sulfate) within the corneal stroma, keratocytes, and endothelium. This occurs due to a defect in the carbohydrate sulfotransferase 6 (CHST6) gene, leading to the production of undersulfated keratan sulfate. **Analysis of Incorrect Options:** * **Lattice Dystrophy (Option A):** Associated with the deposition of **Amyloid** fibrils. It stains with Congo Red and shows apple-green birefringence under polarized light. * **Granular Dystrophy (Option B):** Associated with the deposition of **Hyaline** material. It stains bright red with Masson Trichrome. * **Peripheral Dystrophy (Option D):** This is not a standard classification for the primary stromal dystrophies mentioned above. **High-Yield Clinical Pearls for NEET-PG:** To remember the stains and deposits for stromal dystrophies, use the mnemonic **"Marilyn Monroe Always Gets Her Men in L.A."**: 1. **M**acular – **M**ucopolysaccharide – **A**lcian Blue/Colloidal Iron. 2. **G**ranular – **H**yaline – **M**asson Trichrome. 3. **L**attice – **A**myloid – **C**ongo Red. * **Inheritance Note:** Macular dystrophy is the **least common** but the **most severe** stromal dystrophy and is the only one that is **Autosomal Recessive**. * **Extent:** In Macular dystrophy, the opacities extend up to the **limbus**, whereas in Granular and Lattice, the peripheral cornea usually remains clear.
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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