Diseases of the Cornea Practice Questions

Q: Where are stem cells located in the cornea?

Limbus. **Explanation:** The correct answer is **Limbus**. **1. Why Limbus is Correct:** The corneal epithelium is a self-renewing layer that undergoes constant turnover. The source of these new cells is a population of **Limbal Epithelial Stem Cells (LESCs)** located in the **Palisades of Vogt** within the limbus (the junction between the clear cornea and the opaque sclera). These stem cells divide to produce transient amplifying cells, which migrate centripetally toward the center of the cornea and superficially to replace shed epithelial cells. This "Limbal Barrier" also prevents the conjunctival epithelium from growing onto the transparent cornea. **2. Why Other Options are Incorrect:** * **Stroma:** This is the thickest layer of the cornea, composed primarily of organized collagen fibers and keratocytes. It does not harbor epithelial stem cells. * **Epithelium:** While the epithelium contains the progeny of stem cells, the actual "mother" stem cells reside at the periphery (limbus) to remain protected in a vascularized niche. * **Descemet's Membrane:** This is the basement membrane of the endothelium. It is an acellular layer and does not possess regenerative stem cell properties. **3. Clinical Pearls for NEET-PG:** * **Limbal Stem Cell Deficiency (LSCD):** Caused by chemical burns (alkali), Stevens-Johnson Syndrome, or ocular cicatricial pemphigoid. It leads to "conjunctivalization" of the cornea, resulting in vascularization and loss of transparency. * **XYZ Hypothesis:** Describes corneal epithelial dynamics: **X** (proliferation of basal cells), **Y** (centripetal migration of limbal cells), and **Z** (desquamation of surface cells). * **High-Yield Fact:** The corneal **endothelium** does not regenerate; it heals by the enlargement and migration of existing cells (pleomorphism and polymegethism).

Q: What is the definition of Keratoconus?

Cornea thins near the center and bulges forwards. **Explanation:** **Keratoconus** is a non-inflammatory, progressive ectatic dystrophy of the cornea. The correct answer is **C** because the hallmark of the disease is the progressive **thinning and weakening of the corneal stroma**, which causes the cornea to lose its spherical shape and bulge forward into a **cone-like configuration**. This typically occurs paracentrally (usually inferonasally), leading to high irregular myopic astigmatism. **Analysis of Incorrect Options:** * **Option A:** Degeneration of the conjunctiva refers to conditions like **Pinguecula** or **Pterygium**, which do not involve the corneal curvature or thickness. * **Option B:** Cornea undergoing necrosis due to Vitamin A deficiency is the definition of **Keratomalacia**, a severe stage of Xerophthalmia. * **Option C:** Recurrent corneal ulcerations are characteristic of conditions like **Herpes Simplex Keratitis** or recurrent corneal erosion syndrome, not structural ectasia. **High-Yield Clinical Pearls for NEET-PG:** * **Early Signs:** Fleischer’s ring (iron deposition at the base of the cone) and Vogt’s striae (vertical stress lines in the stroma). * **Late Signs:** Munson’s sign (indentation of the lower lid on down-gaze) and Rizutti’s sign (conical reflection on the nasal iris). * **Acute Hydrops:** Caused by a rupture in **Descemet’s membrane**, leading to sudden corneal edema. * **Management:** Rigid Gas Permeable (RGP) lenses for vision; **Collagen Cross-linking (CXL/C3R)** to stop progression; Keratoplasty for advanced cases. * **Association:** Often associated with Down syndrome, Atopy (eye rubbing), and Marfan syndrome.

Q: All of the following are true about blood staining of the cornea except?

It clears from the centre towards the periphery. **Explanation:** Corneal blood staining is a serious complication typically occurring after a traumatic **hyphema** (blood in the anterior chamber). It results from the breakdown of hemoglobin into **hemosiderin**, which penetrates the corneal stroma through a damaged endothelium. **1. Why Option B is the Correct Answer (The Exception):** Corneal blood staining clears **from the periphery towards the center**. The peripheral cornea clears first because of its proximity to the limbal blood vessels, which facilitate the removal of pigment. The central cornea is the last to clear. Therefore, the statement that it clears from the center to the periphery is incorrect. **2. Analysis of Other Options:** * **Option A:** Raised intraocular pressure (IOP) is the primary risk factor. High pressure forces red blood cell breakdown products through the endothelium into the stroma. * **Option C:** The clearing process is extremely slow. Depending on the density of the staining, it can take anywhere from **several months to 2 years or more** to resolve completely. * **Option D:** The visual prognosis is often poor because the staining can lead to **amblyopia** (especially in children) and is usually associated with severe ocular trauma and secondary glaucoma. **Clinical Pearls for NEET-PG:** * **Appearance:** Initially, the cornea looks rusty or greenish-brown; in late stages, it may resemble a "dislocated lens" in the anterior chamber. * **Management:** To prevent staining, a surgical wash-out of the hyphema is indicated if IOP remains >35 mmHg for 7 days or >25 mmHg for 1 day in patients with Sickle Cell Trait. * **Histology:** Staining is primarily due to **hemosiderin** granules in the stroma.

Q: A patient using contact lenses develops corneal infection. Laboratory diagnosis of Acanthamoeba keratitis was established. What is the best drug for its treatment?

Polyhexamethylene biguanide. **Explanation:** **Acanthamoeba keratitis** is a sight-threatening infection typically associated with contact lens wearers (due to poor hygiene or use of tap water). The organism exists in two forms: the active **trophozoite** and the highly resistant **double-walled cyst**. **Why Polyhexamethylene biguanide (PHMB) is the correct answer:** PHMB (0.02%) is a biguanide disinfectant that acts as a potent **cysticidal** agent. It disrupts the cytoplasmic membrane of the amoeba, leading to cell death. Because the cysts are notoriously resistant to most antibiotics and antifungals, biguanides (PHMB or Chlorhexidine) are considered the **first-line treatment** and the "gold standard" for medical management. **Analysis of Incorrect Options:** * **Propamidine (Brolene):** While used in the past (often in combination with biguanides), it is a diamidine. It is primarily effective against trophozoites but has poor cysticidal activity when used alone, leading to high recurrence rates. * **Neosporin:** This is a combination of Neomycin, Polymyxin B, and Bacitracin. While Neomycin has some anti-acanthamoebic activity, it is insufficient as monotherapy and is generally used as an adjunct to prevent secondary bacterial infection. * **Ketoconazole:** This is an antifungal agent. While some systemic antifungals (like Voriconazole) are used in refractory cases, Ketoconazole is not the primary treatment for Acanthamoeba. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Sign:** **Ring-shaped stromal infiltrate** (late stage) and **Radial Keratoneuritis** (early stage, pathognomonic). * **Pain-Feature Mismatch:** The patient often experiences severe pain that is out of proportion to the clinical signs. * **Culture Media:** Non-nutrient agar (NNA) enriched with *E. coli*. * **Stains:** Calcofluor white (fluorescent) or Periodic acid-Schiff (PAS).

Q: Which form of calcium is deposited in band-shaped keratopathy?

Calcium hydroxyapatite. **Explanation:** **Band-shaped Keratopathy (BSK)** is a degenerative condition characterized by the deposition of calcium salts in the sub-epithelial layers of the cornea, specifically within the **Bowman’s membrane**, the anterior stroma, and the epithelial basement membrane. 1. **Why Calcium Hydroxyapatite is Correct:** The specific chemical form of these deposits is **Calcium Hydroxyapatite** $[Ca_{10}(PO_4)_6(OH)_2]$. This occurs due to the precipitation of calcium salts in the interpalpebral fissure. The process is driven by the evaporation of tears, which increases the local concentration of salts, and the relative alkalinity of the exposed ocular surface (due to the loss of $CO_2$), which decreases the solubility of calcium phosphate. 2. **Why Incorrect Options are Wrong:** * **Calcium chloride:** This is a highly soluble salt and does not precipitate in ocular tissues under physiological conditions. * **Calcium cyanide:** This is a potent systemic toxin and is not a biological mineral found in human tissue. * **Sodium hydroxyapatite:** This is a chemically incorrect term; hydroxyapatite is inherently a calcium-phosphate mineral. **High-Yield Clinical Pearls for NEET-PG:** * **Appearance:** Characterized by a "Swiss-cheese" appearance (holes represent areas where corneal nerves pierce the Bowman’s membrane). * **Location:** Deposits begin at the limbus (3 and 9 o'clock positions) but are separated from the limbus by a **clear zone**. * **Etiology:** * *Chronic Uveitis* (most common cause in children, often associated with Juvenile Idiopathic Arthritis). * *Metabolic:* Hypercalcemia, Hyperphosphatemia, Chronic Renal Failure. * *Ocular:* Silicone oil in the vitreous cavity, Phthisis bulbi. * **Treatment:** The treatment of choice is **Chelation** using **EDTA** (Ethylenediamine tetra-acetic acid) after removing the corneal epithelium.

Q: Dendritic ulcer is seen in:

Herpes simplex keratitis. **Explanation:** **Herpes Simplex Keratitis (HSK)** is the most common cause of corneal blindness in developed nations. The hallmark of primary or recurrent epithelial HSK is the **Dendritic Ulcer**. This occurs due to active viral replication in the corneal epithelium, leading to cell lysis in a linear, branching pattern. **Key Features of the Dendritic Ulcer in HSK:** * **Morphology:** True branches with characteristic **terminal bulbs** (knobs) containing live virus. * **Staining:** The floor of the ulcer stains with **Fluorescein** (denuded epithelium), while the margins stain with **Rose Bengal** or Lissamine Green (devitalized cells). * **Sensation:** Significantly **reduced corneal sensations** (hypesthesia) due to trigeminal nerve involvement. **Why other options are incorrect:** * **Fungal Keratitis:** Typically presents with a "dry" looking ulcer, **feathery margins**, satellite lesions, and often a fixed hypopyon. * **Chlamydial Keratitis:** Usually presents as follicular conjunctivitis with superior epithelial keratitis or pannus, but not dendritic ulceration. * **Herpes Zoster Keratitis:** Characterized by **Pseudodendrites**. Unlike HSK, these are elevated (plaque-like), lack terminal bulbs, and do not stain deeply with fluorescein. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment:** Topical **Acyclovir (3%)** or Ganciclovir. **Steroids are strictly contraindicated** in epithelial (dendritic) keratitis as they can lead to a "Geographic Ulcer." * **Recurrence:** Triggered by stress, fever, or UV exposure. * **Disciform Keratitis:** An endotheliitis (Type IV hypersensitivity) causing central stromal edema without an active epithelial ulcer.

Q: Pathologically, what deposits are associated with lattice corneal dystrophy?

Amyloid. **Explanation:** Corneal dystrophies are a group of genetic, non-inflammatory, bilateral opacifications. The correct answer is **Amyloid** because Lattice Corneal Dystrophy (Type 1) is characterized by the deposition of amyloid fibrils within the corneal stroma. These deposits create the characteristic "lattice" pattern of branching, refractile lines. **Analysis of Options:** * **Amyloid (Correct):** Associated with **Lattice Dystrophy**. These deposits stain with **Congo Red** and exhibit **apple-green birefringence** under polarized light. * **Glycosaminoglycans (Incorrect):** These are associated with **Macular Corneal Dystrophy**. They stain with **Alcian Blue** or Colloidal Iron. * **Hyaline (Incorrect):** Hyaline material (granular protein) is associated with **Granular Corneal Dystrophy**. It stains bright red with **Masson Trichrome**. * **Cholesterol crystals (Incorrect):** These are seen in **Schnyder Corneal Dystrophy**, often associated with systemic hyperlipidemia. **High-Yield Clinical Pearls for NEET-PG:** To remember the common stromal dystrophies and their stains, use the mnemonic **"Marilyn Monroe Got Hers in Los Angeles"**: 1. **M**acular – **M**any (**G**lycosaminoglycans) – **A**lcian Blue 2. **G**ranular – **H**yaline – **M**asson Trichrome 3. **L**attice – **A**myloid – **C**ongo Red * **Inheritance:** Most stromal dystrophies (Granular, Lattice) are **Autosomal Dominant**, except Macular, which is **Autosomal Recessive** (the most severe type). * **Gene:** Lattice Dystrophy is linked to the **TGFBI** gene (Transforming Growth Factor Beta Induced) on chromosome 5q31.

Q: Which type of refractive error is seen in keratoconus?

Irregular astigmatism. **Explanation:** **Keratoconus** is a progressive, non-inflammatory thinning and protrusion of the central or paracentral cornea, resulting in a cone-like shape. 1. **Why Irregular Astigmatism is correct:** In keratoconus, the cornea thins and bulges unevenly. This creates an asymmetrical, non-spherical surface where the curvature varies significantly across different points of the same meridian. Unlike regular astigmatism, these principal meridians are not 90 degrees apart, leading to **irregular astigmatism**. This results in distorted images that cannot be fully corrected with standard spectacles. 2. **Why other options are incorrect:** * **Regular Astigmatism:** Here, the two principal meridians are at right angles. While early keratoconus may mimic regular astigmatism, the hallmark of progressive disease is its irregularity. * **Myopia:** While patients often develop **progressive high myopia** due to the increased curvature (steepening) of the cornea, the most *characteristic* and diagnostic refractive error defining the pathology is the irregular astigmatism. * **Hypermetropia:** This is incorrect as the steepening of the cornea increases the refractive power, shifting the focus in front of the retina (myopic shift), not behind it. **High-Yield Clinical Pearls for NEET-PG:** * **Early Sign:** Retinoscopy shows an **"Oil droplet sign"** or **"Scissor reflex."** * **Slit Lamp Signs:** **Fleischer’s ring** (iron deposition at the base), **Vogt’s striae** (vertical stress lines), and **Munson’s sign** (indentation of the lower lid on downgaze). * **Diagnosis:** **Corneal Topography** (Videokeratography) is the gold standard for early detection. * **Treatment:** **RGP (Rigid Gas Permeable) lenses** are the mainstay for irregular astigmatism. **CXL (Corneal Collagen Cross-linking)** is used to arrest progression.

Q: Which ocular symptom is NOT seen in Herpes zoster?

Satellite lesions. **Explanation:** The correct answer is **D. Satellite lesions**. **1. Why Satellite Lesions are the correct answer:** Satellite lesions (small infiltrates surrounding a primary lesion) are a hallmark clinical feature of **Fungal Keratitis**, not Herpes Zoster. In fungal infections, these represent the spread of fungal hyphae into the corneal stroma. Herpes Zoster Ophthalmicus (HZO) is caused by the reactivation of the Varicella-Zoster Virus (VZV) and presents with distinct viral patterns rather than satellite infiltrates. **2. Why the other options are seen in Herpes Zoster:** * **Nummular Keratitis (A):** This is a classic manifestation of HZO. It presents as multiple, granular, coin-shaped subepithelial opacities. * **Glaucoma (B):** Secondary glaucoma is common in HZO, usually occurring due to trabeculitis (inflammation of the drainage angle) or as a complication of chronic uveitis. * **Uveitis (C):** HZO frequently causes a hypertensive anterior uveitis characterized by patchy iris atrophy and keratic precipitates. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hutchinson’s Sign:** Vesicles on the tip, side, or root of the nose (involving the external nasal nerve) indicate a high risk of ocular involvement in HZO. * **Pseudodendrites:** Unlike the true dendrites of Herpes Simplex (which have terminal bulbs and central ulceration), HZO produces "pseudodendrites" which are elevated, lack terminal bulbs, and stain poorly with fluorescein. * **Neurotrophic Keratopathy:** A serious late complication of HZO due to loss of corneal sensations (Trigeminal nerve damage). * **Treatment:** Oral Acyclovir (800 mg 5 times daily for 7–10 days) is the standard systemic therapy.

Q: Which of the following are types of corneal dystrophies?

All of the above. Corneal dystrophies are a group of genetic, bilateral, symmetric, and slowly progressive disorders that are not associated with inflammation or systemic disease. They are classified based on the specific layer of the cornea they affect. **Explanation of Options:** The options provided represent the three classic **Stromal Corneal Dystrophies**, which are high-yield for NEET-PG: * **Granular Dystrophy (Type 1):** Characterized by "crumb-like" opacities in the stroma. It is Autosomal Dominant (AD) and associated with **Hyaline** deposits (stains with Masson Trichrome). * **Lattice Dystrophy (Type 1):** Characterized by branching, spider-like filaments. It is Autosomal Dominant and associated with **Amyloid** deposits (stains with Congo Red; shows apple-green birefringence). * **Macular Dystrophy:** Characterized by ill-defined opacities that extend to the periphery. Unlike the others, it is **Autosomal Recessive (AR)** and associated with **Acid Mucopolysaccharide** deposits (stains with Alcian Blue). Since all three are established types of stromal corneal dystrophies, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Deposits:** **M**any **A**mes **L**ove **C**andy **G**et **H**it ( **M**acular-**A**lcian Blue; **L**attice-**C**ongo Red; **G**ranular-**H**yaline/Masson Trichrome). * **Inheritance:** Most dystrophies are Autosomal Dominant, **except Macular Dystrophy**, which is Autosomal Recessive and often the most severe. * **Layer Involvement:** * *Epithelial:* Meesmann’s. * *Bowman’s:* Reis-Bücklers. * *Endothelial:* Fuchs’ Endothelial Dystrophy (presents with "beaten metal" appearance/corneal guttata).

Question 1

Where are stem cells located in the cornea?

Accepted Answer

Limbus

Answer

Stroma

Answer

Epithelium

Answer

Descemet's membrane

Question 2

What is the definition of Keratoconus?

Accepted Answer

Cornea thins near the center and bulges forwards

Answer

Degeneration of conjunctiva

Answer

Cornea undergoes necrosis due to vitamin A deficiency

Answer

Recurrent corneal ulcerations of the cornea

Question 3

All of the following are true about blood staining of the cornea except?

Accepted Answer

It clears from the centre towards the periphery

Answer

Its occurrence is hastened by the raised intraocular pressure

Answer

Its clearance may take 2 years or more

Answer

Visual prognosis is usually poor in such cases

Question 4

A patient using contact lenses develops corneal infection. Laboratory diagnosis of Acanthamoeba keratitis was established. What is the best drug for its treatment?

Accepted Answer

Polyhexamethylene biguanide

Answer

Propamidine

Answer

Neosporin

Answer

Ketoconazole

Question 5

Which form of calcium is deposited in band-shaped keratopathy?

Accepted Answer

Calcium hydroxyapatite

Answer

Calcium chloride

Answer

Calcium cyanide

Answer

Sodium hydroxyapatite

Question 6

Dendritic ulcer is seen in:

Accepted Answer

Herpes simplex keratitis

Answer

Fungal keratitis

Answer

Chlamydial keratitis

Answer

Herpes zoster keratitis

Question 7

Pathologically, what deposits are associated with lattice corneal dystrophy?

Accepted Answer

Amyloid

Answer

Glycosaminoglycan

Answer

Cholesterol crystals

Answer

Hyaline

Question 8

Which type of refractive error is seen in keratoconus?

Accepted Answer

Irregular astigmatism

Answer

Regular astigmatism

Answer

Myopia

Answer

Hypermetropia

Question 9

Which ocular symptom is NOT seen in Herpes zoster?

Accepted Answer

Satellite lesions

Answer

Nummular keratitis

Answer

Glaucoma

Answer

Uveitis

Question 10

Which of the following are types of corneal dystrophies?

Accepted Answer

All of the above

Answer

Macular

Answer

Granular

Answer

Lattice

Diseases of the Cornea — MCQs

Diseases of the Cornea — MCQs

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