Diseases of the Cornea Practice Questions

Q: All of the following clinical signs are seen in Keratoconus except?

Haab's striae. **Explanation:** The correct answer is **C. Haab's striae**. **Why Haab's striae is the correct answer:** Haab's striae are horizontal or curvilinear breaks in the **Descemet’s membrane** caused by increased intraocular pressure and globe enlargement. They are a hallmark clinical sign of **Primary Congenital Glaucoma**, not Keratoconus. In contrast, Keratoconus involves vertical stress lines in the deep stroma and Descemet’s membrane known as **Vogt’s striae**. **Analysis of incorrect options (Signs of Keratoconus):** * **Fleischer ring:** A partial or complete ring of **iron deposition** (hemosiderin) in the basal epithelium at the base of the cone. It is best visualized using a cobalt blue filter. * **Rizzuti sign:** A sharply focused triangle of light on the nasal iris when a penlight is shone from the temporal side. This occurs due to the conical shape of the cornea acting as a lens. * **Oil droplet reflex:** Seen during distant direct ophthalmoscopy; the protrusion of the cornea creates a dark shadow resembling a drop of oil against the red reflex. **High-Yield Clinical Pearls for NEET-PG:** * **Munson’s Sign:** V-shaped indentation of the lower eyelid on down-gaze. * **Vogt’s Striae:** Vertical stress lines that disappear upon applying digital pressure over the globe. * **Hydrops:** Acute corneal edema caused by a rupture in the Descemet’s membrane (managed conservatively, not with surgery initially). * **Treatment of Choice:** Collagen Cross-Linking (CXL/C3R) to arrest progression; Penetrating or Deep Anterior Lamellar Keratoplasty (DALK) for advanced cases.

Q: Which of the following is associated with Acanthamoeba keratitis?

Wearing of soft contact lenses. **Acanthamoeba keratitis** is a rare but vision-threatening parasitic infection of the cornea caused by a free-living amoeba. It is most commonly associated with **contact lens wearers** (accounting for approximately 85% of cases). ### **Explanation of Options** * **Option B (Correct):** The use of soft contact lenses, especially when combined with poor hygiene practices—such as using tap water for cleaning, swimming while wearing lenses, or using contaminated solutions—is the primary risk factor. The amoeba adheres to the lens surface and subsequently invades the corneal epithelium. * **Option A:** Trauma with vegetable matter is the classic risk factor for **Fungal Keratitis** (e.g., *Aspergillus* or *Fusarium*), not Acanthamoeba. * **Option C & D:** Dry eyes and Entropion (inward turning of the eyelid) can lead to corneal erosions and secondary bacterial infections, but they are not specific predisposing factors for Acanthamoeba. ### **High-Yield Clinical Pearls for NEET-PG** * **Classic Presentation:** The hallmark is **"Pain out of proportion to clinical findings"** (due to radial keratoneuritis). * **Early Sign:** **Radial Keratoneuritis** (infiltrates along the corneal nerves). * **Late Sign:** **Ring-shaped stromal infiltrate** (pathognomonic). * **Diagnosis:** * Gold standard culture: **Non-nutrient agar with E. coli overlay**. * Stain: **Calcofluor white** (shows double-walled cysts under fluorescence). * **Treatment:** Topical biguanides like **PHMB (Polyhexamethylene biguanide)** or **Chlorhexidine**. Propamidine isethionate (Brolene) is also used.

Q: What is true about fungal corneal ulcer?

Satellite lesion. **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.

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

Dendritic ulcers are a characteristic finding.. **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.

Q: All are true about Mooren's ulcer except?

It is caused by infection.. **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.

Q: What is the primary pathology observed in keratomalacia?

Breakdown of collagen fibers in the corneal stroma. **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). * **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.

Q: Keratic precipitates are found on which layer of the cornea?

Endothelium. **Explanation:** **Keratic Precipitates (KPs)** are inflammatory cell deposits (leukocytes) that settle on the posterior surface of the cornea. These cells originate from the uveal tract (iris and ciliary body) and are shed into the aqueous humor during episodes of **anterior uveitis**. 1. **Why Endothelium is correct:** The corneal endothelium is the innermost layer of the cornea, directly in contact with the aqueous humor. Due to gravity and convection currents within the anterior chamber, inflammatory cells (lymphocytes, monocytes, or macrophages) adhere to the sticky, damaged endothelial cells. 2. **Why other options are incorrect:** * **Epithelium:** This is the outermost layer. Deposits here are usually foreign bodies or punctate erosions, not KPs. * **Stroma:** This is the thickest middle layer. While it can show edema or infiltration (keratitis), KPs are surface deposits, not parenchymal ones. * **Bowman’s Membrane:** This is a thin acellular layer between the epithelium and stroma; it does not come into contact with the aqueous humor. **Clinical Pearls for NEET-PG:** * **Arlt’s Triangle:** KPs typically settle in a triangular pattern on the inferior endothelium due to convection currents. * **Mutton-fat KPs:** Large, greasy-looking clusters of epithelioid cells and macrophages, pathognomonic for **Granulomatous Uveitis** (e.g., Sarcoidosis, TB). * **Small/Fine KPs:** Composed of neutrophils and lymphocytes, seen in **Non-granulomatous Uveitis**. * **Stellate KPs:** Star-shaped precipitates distributed over the entire endothelium, characteristic of **Fuchs’ Heterochromic Iridocyclitis** and Viral Uveitis.

Q: Which condition is always bilateral?

Megalocornea. ### Explanation **Correct Answer: B. Megalocornea** **1. Why Megalocornea is the correct answer:** Megalocornea is a non-progressive, non-glaucomatous condition characterized by an increased corneal diameter (typically >13 mm) at birth. It is almost **always bilateral and symmetrical**. It is most commonly inherited as an **X-linked recessive** trait (affecting males). Because it is a developmental anomaly of the anterior segment (specifically the ciliary ring), the enlargement is structural and inherent to both eyes from birth, without the involvement of elevated intraocular pressure (IOP). **2. Why the other options are incorrect:** * **A. Infantile Glaucoma:** While frequently bilateral (70-80% of cases), it can be **unilateral** in approximately 25-30% of patients. It is caused by developmental anomalies of the angle (trabeculodysgenesis) leading to high IOP and secondary corneal enlargement (buphthalmos). * **C. Acute Congestive Glaucoma:** This is a clinical manifestation of Primary Angle Closure Glaucoma. While the anatomical predisposition (shallow anterior chamber) is usually bilateral, the **acute attack** itself is almost always **unilateral** at the time of presentation. * **D. All of the above:** Incorrect because options A and C can present unilaterally. **3. NEET-PG High-Yield Pearls:** * **Megalocornea vs. Buphthalmos:** In Megalocornea, the IOP is normal, the optic disc is normal, and there are no Haab’s striae. In Buphthalmos (Infantile Glaucoma), IOP is high, the disc is cupped, and Haab’s striae are present. * **Associated Conditions:** Megalocornea is associated with lens subluxation (due to zonular stretching) and Marfan syndrome. * **Corneal Diameter:** Normal newborn diameter is ~10 mm; adult diameter is reached by age 2 (~11.7 mm). Megalocornea is diagnosed when the diameter exceeds 13 mm.

Q: Which of the following is true regarding corneal dystrophy?

Bilateral. ### Explanation Corneal dystrophies are a group of genetic, non-inflammatory disorders characterized by the accumulation of abnormal material within the corneal layers. **Why "Bilateral" is the Correct Answer:** Corneal dystrophies are **hereditary** (mostly autosomal dominant) conditions. Because they are rooted in a genetic mutation present in all cells of the corneal tissue, they characteristically manifest as **bilateral, symmetrical, and slowly progressive** opacities. They typically appear in the first or second decade of life and are not associated with systemic diseases. **Why Other Options are Incorrect:** * **A. Inflammatory:** By definition, dystrophies are **non-inflammatory**. If inflammation (redness, pain, or cellular infiltration) is present, the diagnosis is more likely a corneal *degeneration* or *keratitis*. * **B. Neovascularization:** Corneal dystrophies are **avascular**. The cornea remains clear of blood vessels unless a secondary complication (like a persistent epithelial erosions or infection) occurs. Neovascularization is a hallmark of degenerations or chronic inflammatory states, not primary dystrophies. **High-Yield Clinical Pearls for NEET-PG:** * **Dystrophy vs. Degeneration:** Dystrophies are bilateral, central, and hereditary; Degenerations are often unilateral, peripheral, and associated with aging or inflammation. * **Most Common Dystrophy:** Fuchs’ Endothelial Corneal Dystrophy (FECD). * **Staining Mnemonics (Very High Yield):** * **M**any **A**mericans **G**et **R**ocky **M**ountains: **M**acular = **A**lcian Blue; **G**ranular = **R**odent (Masson) Trichrome; **L**attice = **M**any (Congo) Red. * **Layer Involvement:** * *Epithelial:* Meesmann’s. * *Stromal:* Granular, Macular, Lattice (Lattice is the most common stromal dystrophy). * *Endothelial:* Fuchs’, CHED (Congenital Hereditary Endothelial Dystrophy).

Q: Interstitial keratitis may be associated with which of the following conditions?

All of the above. **Explanation:** **Interstitial Keratitis (IK)** is a chronic non-ulcerative inflammation of the corneal stroma, characterized by cellular infiltration and vascularization without primary involvement of the epithelium or endothelium. It is typically an **immune-mediated response** to a systemic infection or inflammatory condition rather than a direct infection of the cornea. 1. **Congenital Syphilis (Option A):** This is the **most common cause** of IK (responsible for ~90% of cases historically). It typically presents bilaterally in late childhood or adolescence as part of the late manifestations of congenital syphilis. 2. **Malaria (Option B):** While rare, protozoal infections like Malaria and Leishmaniasis are documented systemic causes of IK. 3. **Sarcoidosis (Option C):** Non-infectious systemic granulomatous diseases, including Sarcoidosis and Cogan’s syndrome, are well-recognized etiologies of interstitial keratitis. Since all three conditions listed can trigger the immune-mediated stromal response characteristic of IK, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Hutchinson’s Triad:** A classic sign of late congenital syphilis consisting of Interstitial Keratitis, Hutchinson’s teeth (notched incisors), and Sensorineural deafness (8th nerve deafness). * **Salmon Patch Appearance:** In the active stage of IK, deep vascularization gives the cornea a pinkish-orange hue. * **Ghost Vessels:** After the inflammation subsides, the cleared vessels remain as empty channels in the stroma, visible on slit-lamp examination. * **Wessely Ring:** An immune ring of precipitate often seen in the stroma during the acute phase. * **Other Causes:** Tuberculosis, Leprosy, Herpes Simplex (most common viral cause), and Lyme disease.

Question 1

All of the following clinical signs are seen in Keratoconus except?

Accepted Answer

Haab's striae

Answer

Fleischer ring

Answer

Rizzuti sign

Answer

Oil droplet reflex

Question 2

Which of the following is associated with Acanthamoeba keratitis?

Accepted Answer

Wearing of soft contact lenses

Answer

Trauma with vegetable matter

Answer

Dry eyes

Answer

Entropion

Question 3

What is true about fungal corneal ulcer?

Accepted Answer

Satellite lesion

Answer

Symptoms are disproportionately severe compared to signs

Answer

Purulent ulcer

Answer

All of the above

Question 4

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

Accepted Answer

Dendritic ulcers are a characteristic finding.

Answer

Frontal nerve is the most commonly involved nerve.

Answer

Punctate epithelial keratitis may be present.

Answer

Other cranial nerves can be involved.

Question 5

All are true about Mooren's ulcer except?

Accepted Answer

It is caused by infection.

Answer

It is a superficial ulcer.

Answer

It spreads circumferentially.

Answer

Whitish overhanging margins are seen.

Question 6

What is the primary pathology observed in keratomalacia?

Accepted Answer

Breakdown of collagen fibers in the corneal stroma

Answer

Accumulation of desquamated debris

Answer

Absence of mucus

Answer

Infection with Corynebacterium xerosis

Question 7

Keratic precipitates are found on which layer of the cornea?

Accepted Answer

Endothelium

Answer

Epithelium

Answer

Stroma

Answer

Bowman's membrane

Question 8

Which condition is always bilateral?

Accepted Answer

Megalocornea

Answer

Infantile glaucoma

Answer

Acute congestive glaucoma

Answer

All of the above

Question 9

Which of the following is true regarding corneal dystrophy?

Accepted Answer

Bilateral

Answer

Inflammatory

Answer

Neovascularization

Answer

All of the above

Question 10

Interstitial keratitis may be associated with which of the following conditions?

Accepted Answer

All of the above

Answer

Congenital syphilis

Answer

Malaria

Answer

Sarcoidosis

Diseases of the Cornea — MCQs

Diseases of the Cornea — MCQs

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