Diseases of the Cornea Practice Questions

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: Nummular keratitis is a feature of:

Herpes zoster keratitis. **Explanation:** **Nummular keratitis** is characterized by the presence of multiple, small, disc-shaped (coin-like) subepithelial opacities. 1. **Why Herpes Zoster is Correct:** In **Herpes Zoster Ophthalmicus (HZO)**, nummular keratitis typically appears about 10 days after the onset of the skin rash. These lesions represent a delayed hypersensitivity reaction to the viral antigen. They consist of granular deposits beneath the Bowman’s layer, often surrounded by a halo of stromal haze. While most commonly associated with HZO, it is also a classic late feature of **Adenoviral Keratoconjunctivitis** (Epidemic Keratoconjunctivitis). 2. **Why Other Options are Incorrect:** * **Fungal Keratitis:** Typically presents with a dry, gray-white infiltrate, **feathery margins**, and **satellite lesions**. * **Bacterial Keratitis:** Characterized by acute suppuration, dense stromal infiltrates, and often a hypopyon. * **Acanthamoeba Keratitis:** Classically associated with a **ring-shaped infiltrate** and disproportionately severe pain due to perineural infiltration (radial keratoneuritis). **High-Yield Clinical Pearls for NEET-PG:** * **Hutchinson’s Sign:** Vesicles on the tip or side of the nose (involving the external nasal nerve) indicate a high risk of ocular involvement in Herpes Zoster. * **Dendritic Ulcer:** While HZO causes "pseudodendrites" (tapered ends, no terminal bulbs), **Herpes Simplex Keratitis (HSV)** causes true dendritic ulcers (terminal bulbs, stains well with fluorescein). * **Treatment:** Nummular keratitis in HZO usually responds well to topical steroids, though systemic antivirals (Acyclovir) are required for the acute phase.

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: Corneal dystrophies are?

Primary and bilateral. **Explanation:** Corneal dystrophies are a group of genetically determined, progressive, and non-inflammatory disorders that affect specific layers of the cornea. **1. Why Option B is Correct:** * **Primary:** They are "primary" because they occur without any prior ocular inflammation, infection, or systemic disease. They are caused by genetic mutations (most commonly autosomal dominant). * **Bilateral:** Because they are genetic, they characteristically affect **both eyes** (bilateral) and are typically **symmetrical** in appearance. **2. Why Other Options are Incorrect:** * **Options A & D (Unilateral):** Corneal dystrophies are almost never unilateral. If a corneal opacity is unilateral, it is more likely a **corneal degeneration** (secondary to age or inflammation) or a result of trauma/infection. * **Option C (Systemic Disease):** By definition, dystrophies are limited to the cornea. If corneal deposits are associated with systemic conditions (e.g., Wilson’s disease or Mucopolysaccharidosis), they are classified as **corneal manifestations of systemic disease**, not primary dystrophies. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most are Autosomal Dominant (AD). **Exception:** Macular dystrophy is **Autosomal Recessive (AR)**—remember: *"Macular is Miserable"* (it is the most severe and the only AR one). * **Layer-wise Classification:** * **Epithelial:** Meesmann dystrophy. * **Stromal:** Granular (Hyaline), Lattice (Amyloid), Macular (Acid Mucopolysaccharide). *Mnemonic: **G**et **L**unch **M**onday / **H**is **A**nt **M**ary.* * **Endothelial:** Fuchs’ Endothelial Dystrophy (presents with *beaten metal* appearance/corneal guttata). * **Symptom:** Unlike degenerations, dystrophies usually manifest in the first or second decade of life.

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).

Q: Which of the following is NOT a layer of the cornea?

Keratinized squamous epithelium. The cornea is the transparent, avascular front part of the eye. To maintain its transparency, the corneal epithelium must remain **non-keratinized**. ### Why "Keratinized squamous epithelium" is the correct answer: The corneal epithelium is specifically **stratified non-keratinized squamous epithelium**. If the cornea becomes keratinized (a process called xerosis), it loses its transparency, leading to severe visual impairment. This is commonly seen in pathological states like Vitamin A deficiency (Bitot’s spots/Keratomalacia) or Stevens-Johnson Syndrome. ### Explanation of other layers (Incorrect Options): The cornea traditionally consists of five layers (recently updated to six with the discovery of Dua’s layer): 1. **Epithelium:** Non-keratinized stratified squamous type. 2. **Bowman’s Membrane (Option A):** An acellular, condensed superficial layer of the stroma. **Crucial Fact:** It does not regenerate; if damaged, it leaves a permanent scar. 3. **Stroma (Substantia Propria):** Makes up 90% of corneal thickness. 4. **Descemet’s Membrane (Option B):** The basement membrane of the endothelium. Unlike Bowman’s, it **can regenerate**. 5. **Endothelium (Option C):** A single layer of hexagonal cells that maintains corneal dehydration (deturgescence) via active Na+/K+ ATPase pumps. These cells **do not regenerate** in humans; they simply enlarge to fill gaps. ### High-Yield NEET-PG Pearls: * **Dua’s Layer:** The "6th layer" discovered in 2013, located between the stroma and Descemet’s membrane. * **Nerve Supply:** Long ciliary nerves (Trigeminal - V1). The cornea is the most sensitive tissue in the body. * **Transparency:** Maintained by the **lattice arrangement** of collagen fibrils (Maurice’s Theory) and the state of relative dehydration.

Q: What is the early ocular sign of herpes zoster?

Vesicles on eyelids. **Explanation:** Herpes Zoster Ophthalmicus (HZO) is caused by the reactivation of the Varicella-Zoster virus (VZV) in the trigeminal ganglion, specifically involving the ophthalmic division ($V_1$). **Why "Vesicles on eyelids" is correct:** The earliest clinical manifestation of HZO is a prodromal phase of fever and malaise, followed rapidly by a **painful vesicular skin rash**. These vesicles appear on the eyelids and forehead, strictly following the dermatomal distribution of the $V_1$ nerve (respecting the midline). Ocular involvement (keratitis or uveitis) typically occurs *after* or concurrent with the skin eruption, making the eyelid vesicles the earliest visible ocular-related sign. **Analysis of Incorrect Options:** * **Punctate keratitis:** While this is the earliest *corneal* sign (appearing within 2 days of the rash), it occurs after the initial skin vesicles have already formed. * **Follicular keratitis:** This is not a characteristic feature of Herpes Zoster. Follicles are more commonly associated with viral conjunctivitis (e.g., Adenovirus) or Chlamydial infections. * **Dendritic ulcer:** This is the classic sign of **Herpes Simplex Keratitis (HSV)**. In HZO, the lesions are "pseudodendrites," which are smaller, more elevated, and lack the terminal bulbs seen in HSV. **High-Yield Clinical Pearls for NEET-PG:** * **Hutchinson’s Sign:** Vesicles on the tip or side of the nose indicate involvement of the nasociliary nerve, which strongly predicts a higher risk of intraocular complications. * **Pseudodendrites:** Unlike HSV dendrites, HZO pseudodendrites are peripheral, lack central ulceration (they are plaques), and do not stain well with fluorescein. * **Treatment:** Oral Acyclovir (800 mg 5 times daily for 7–10 days) is the mainstay, ideally started within 72 hours of the rash.

Q: Ulcus serpens is caused by?

Pneumococcus. **Ulcus Serpens** (also known as Hypopyon Corneal Ulcer) is a clinical entity characterized by a rapidly spreading, grayish-white or yellowish disc-shaped ulcer. **1. Why Pneumococcus is the correct answer:** The term "Ulcus Serpens" specifically refers to the **creeping nature** of the ulcer. It is classically caused by **Streptococcus pneumoniae (Pneumococcus)**. The bacteria produce toxins that cause the ulcer to spread superficially in one direction while healing in the other, giving it a "serpentine" or "creeping" appearance. It is frequently associated with chronic dacryocystitis, which acts as a reservoir for the infection. **2. Why other options are incorrect:** * **Pseudomonas pyocyaneus:** While it causes the most fulminant and destructive corneal ulcers (often associated with contact lens wear), it is characterized by a greenish-blue discharge and rapid liquefactive necrosis, not the specific "creeping" morphology of Ulcus Serpens. * **Corynebacterium diphtheriae & Neisseria gonorrhoeae:** These are unique because they can penetrate a **healthy, intact corneal epithelium**. However, they do not typically present as Ulcus Serpens. **3. Clinical Pearls for NEET-PG:** * **The "Creeping" Edge:** The advancing edge of Ulcus Serpens is packed with active bacteria and shows more infiltration, while the trailing edge shows signs of cicatrization (healing). * **Hypopyon:** It is usually associated with a sterile hypopyon due to the release of bacterial toxins into the anterior chamber. * **Predisposing Factor:** Always check the lacrimal sac; **Chronic Dacryocystitis** is the most common predisposing factor for Pneumococcal corneal ulcers. * **Treatment:** Intensive topical antibiotics (e.g., fortified cephalosporins or fluoroquinolones) and treatment of the underlying dacryocystitis.

Question 1

Pathologically, what deposits are associated with lattice corneal dystrophy?

Accepted Answer

Amyloid

Answer

Glycosaminoglycan

Answer

Cholesterol crystals

Answer

Hyaline

Question 2

Which type of refractive error is seen in keratoconus?

Accepted Answer

Irregular astigmatism

Answer

Regular astigmatism

Answer

Myopia

Answer

Hypermetropia

Question 3

Nummular keratitis is a feature of:

Accepted Answer

Herpes zoster keratitis

Answer

Fungal keratitis

Answer

Bacterial keratitis

Answer

Acanthamoeba keratitis

Question 4

Which ocular symptom is NOT seen in Herpes zoster?

Accepted Answer

Satellite lesions

Answer

Nummular keratitis

Answer

Glaucoma

Answer

Uveitis

Question 5

Corneal dystrophies are?

Accepted Answer

Primary and bilateral

Answer

Primary and unilateral

Answer

Primary, bilateral with systemic disease

Answer

Primary, unilateral without systemic disease

Question 6

Which of the following are types of corneal dystrophies?

Accepted Answer

All of the above

Answer

Macular

Answer

Granular

Answer

Lattice

Question 7

Keratomalacia is associated with which of the following conditions?

Accepted Answer

Measles

Answer

Mumps

Answer

Rubella

Answer

Chickenpox

Question 8

Which of the following is NOT a layer of the cornea?

Accepted Answer

Keratinized squamous epithelium

Answer

Bowman's membrane

Answer

Descemet's membrane

Answer

Endothelium

Question 9

What is the early ocular sign of herpes zoster?

Accepted Answer

Vesicles on eyelids

Answer

Punctate keratitis

Answer

Follicular keratitis

Answer

Dendritic ulcer

Question 10

Ulcus serpens is caused by?

Accepted Answer

Pneumococcus

Answer

Pseudomonas pyocyaneus

Answer

Corynebacteria

Answer

Neisseria gonorrhoeae

Diseases of the Cornea — MCQs

Diseases of the Cornea — MCQs

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