Diseases of the Cornea Practice Questions

Q: Which of the following is not an indication for keratoplasty?

None of the above. **Explanation:** The correct answer is **None of the above** because all three conditions listed (A, B, and C) are standard, well-established indications for **Keratoplasty** (Corneal Transplantation). Keratoplasty is indicated when the cornea loses its transparency or structural integrity, leading to significant visual impairment or pain. * **Pseudophakic Bullous Keratopathy (PBK):** This is a common complication after cataract surgery where the corneal endothelium is damaged, leading to chronic edema and "bullae" (blisters). It is a leading **optical indication** for endothelial keratoplasty (like DSAEK or DMEK). * **Keratoconus:** This is a progressive non-inflammatory thinning of the cornea resulting in a cone-like bulge. When contact lenses or collagen cross-linking (CXL) can no longer provide functional vision, keratoplasty (usually DALK or PKP) is the definitive treatment. * **Corneal Dystrophies:** These are hereditary, bilateral, non-inflammatory opacities (e.g., Fuchs' endothelial dystrophy, Lattice, or Macular dystrophy). They require keratoplasty when the central visual axis is significantly obscured. **High-Yield Clinical Pearls for NEET-PG:** * **Indications Classification:** 1. **Optical:** To improve vision (e.g., PBK, Keratoconus, Dystrophies, Scars). 2. **Tectonic:** To restore structural integrity (e.g., Corneal perforation, Descemetocele). 3. **Therapeutic:** To eliminate active disease (e.g., Non-healing fungal keratitis). 4. **Cosmetic:** To improve the appearance of a disfigured eye (e.g., Leucomatous opacity in a blind eye). * **Success Rate:** Keratoconus has the highest success rate for graft survival. * **Gold Standard:** Penetrating Keratoplasty (PKP) involves full-thickness replacement, while Lamellar Keratoplasty (DALK/DMEK) replaces only specific diseased layers, reducing rejection risk.

Q: Not true regarding herpes keratitis?

Satellite lesions are seen. **Explanation:** **Satellite lesions** are the hallmark clinical feature of **Fungal Keratitis** (typically caused by *Aspergillus* or *Fusarium*), not Herpes Simplex Keratitis (HSK). These are small, isolated infiltrates surrounding the main ulcer, separated by a zone of clear cornea. **Analysis of Options:** * **A. Diminished corneal sensation:** This is a classic feature of HSK. The virus resides in the trigeminal ganglion; its reactivation and replication lead to neurotrophic changes and significant loss of corneal sensitivity. * **B. Can be recurrent:** HSK is characterized by its ability to remain latent in the sensory ganglia. Stress, fever, or UV exposure can trigger reactivation, leading to recurrent episodes. * **C. Satellite lesions (Correct Answer):** As mentioned, these are characteristic of fungal infections. HSK typically presents with dendritic or geographic ulcers. * **D. Punctate keratitis is seen:** The earliest stage of epithelial HSK often manifests as **SFCK (Small Fine Corneal Keratitis)** or coarse punctate epithelial keratitis before coalescing into a dendritic ulcer. **Clinical Pearls for NEET-PG:** * **Dendritic Ulcer:** The most characteristic lesion of HSK; it has **terminal bulbs** (which stain with Rose Bengal) and a floor that stains with Fluorescein. * **Treatment:** Topical **Acyclovir (3%)** or Ganciclovir. **Steroids are strictly contraindicated** in epithelial (dendritic) keratitis as they can lead to a "geographic ulcer." * **Disciform Keratitis:** An immune-mediated (Type IV hypersensitivity) endotheliitis seen in HSK, presenting with a central zone of stromal edema and Wessely ring.

Q: Cloudy cornea is seen in which of the following conditions?

Mucopolysaccharidosis. **Explanation:** **Mucopolysaccharidoses (MPS)** are a group of lysosomal storage disorders characterized by the deficiency of enzymes required to break down glycosaminoglycans (GAGs). The accumulation of these GAGs (such as dermatan sulfate and keratan sulfate) within the corneal stroma disrupts the regular arrangement of collagen fibrils, leading to **corneal clouding**. * **High-Yield Note:** MPS Type I (Hurler), Type VI (Maroteaux-Lamy), and Type VII (Sly) typically present with significant corneal clouding. **MPS Type II (Hunter syndrome)** is the classic exception where the cornea remains clear. **Analysis of Incorrect Options:** * **Klinefelter (47, XXY) and Turner (45, XO) Syndromes:** These are chromosomal anomalies. While they may have associated ocular features (e.g., strabismus or ptosis in Turner), they are not typically associated with corneal opacification or storage-related clouding. * **Megalocornea:** This is a non-progressive condition defined by a corneal diameter of ≥13 mm at birth or in an adult. Crucially, the cornea in simple megalocornea remains **clear** and has normal thickness, which helps differentiate it from infantile glaucoma (where the cornea is enlarged but cloudy due to edema). **Clinical Pearls for NEET-PG:** 1. **Clear Cornea in Hunter:** Remember "The Hunter needs clear vision to hit the target" (Hunter syndrome = Clear cornea). 2. **Differential Diagnosis of Cloudy Cornea at Birth (STUMPED):** **S**clerocornea, **T**rauma, **U**lcer, **M**etabolic (MPS), **P**eters anomaly, **E**ndothelial dystrophy (CHED), and **D**ermoid. 3. **Wilson’s Disease:** Causes a KF ring (peripheral), not generalized clouding.

Q: Deposition of which of the following is seen in the Descemet's membrane in Kayser-Fleischer rings?

Copper. **Explanation:** The **Kayser-Fleischer (KF) ring** is a hallmark clinical sign of **Wilson’s Disease** (Hepatolenticular degeneration). In this condition, a deficiency of the enzyme *ceruloplasmin* leads to impaired biliary excretion of copper, resulting in systemic accumulation. In the eye, **Copper** is deposited specifically in the **peripheral Descemet’s membrane** of the cornea. It typically appears as a golden-brown or greenish-brown ring, starting superiorly, then inferiorly, and eventually becoming circumferential. It is best visualized using a **slit-lamp biomicroscope**, though it may be visible to the naked eye in advanced cases. **Analysis of Incorrect Options:** * **B. Arsenic:** Arsenic poisoning does not manifest with corneal rings; it is more commonly associated with dermatological changes (Mees' lines, hyperkeratosis) and systemic toxicity. * **C. Iron:** Iron deposition in the cornea is seen in **Flecked/Pigmented lines** such as **Hudson-Stahli lines** (age-related), **Fleischer rings** (at the base of the cone in Keratoconus), or **Stockers lines** (at the head of a Pterygium). Note: Do not confuse *Fleischer* (Iron) with *Kayser-Fleischer* (Copper). * **D. Mercury:** Chronic exposure to mercury vapor can lead to **Mercurialentis**, which is a dull ash-grey or rose-brown discoloration of the anterior lens capsule, not the cornea. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** KF rings are always in the **Descemet’s membrane**. * **Reversibility:** The ring may disappear with successful chelation therapy (e.g., D-Penicillamine). * **Sunflower Cataract:** Another ocular manifestation of Wilson's disease involving copper deposition in the anterior lens capsule. * **Diagnostic Triad:** Liver disease, Basal ganglia symptoms (Parkinsonian features), and KF rings.

Q: All of the following are true regarding keratoconus except?

Hypermetropia is seen. **Explanation:** Keratoconus is a non-inflammatory, progressive ectatic dystrophy characterized by localized thinning and protrusion of the cornea, typically starting at or near the center. **Why Option B is the Correct Answer (The False Statement):** In keratoconus, the cornea assumes a conical shape, which significantly **increases the refractive power** of the eye. This leads to **progressive high irregular myopia** and irregular astigmatism, not hypermetropia. Hypermetropia (farsightedness) occurs when the refractive power is too low or the axial length is too short, which is the opposite of what occurs in keratoconus. **Analysis of Other Options:** * **A. Munson sign:** This is a classic clinical sign where the lower eyelid bulges in a V-shape when the patient looks downward, caused by the cone-shaped cornea. * **C. Thinning of central cornea:** The hallmark pathophysiology of keratoconus is the progressive thinning of the corneal stroma (usually inferior-paracentral), leading to secondary protrusion (ectasia). * **D. Contact lens:** Rigid Gas Permeable (RGP) or Scleral contact lenses are the mainstay of optical treatment. They provide a regular refracting surface by neutralizing the irregular corneal astigmatism. **High-Yield Clinical Pearls for NEET-PG:** * **Early Sign:** "Scissoring reflex" on retinoscopy and "Oil droplet sign" (Charleux sign) on distant direct ophthalmoscopy. * **Slit Lamp Signs:** **Vogt’s striae** (vertical stress lines), **Fleischer’s ring** (iron deposition at the base of the cone), 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. * **Gold Standard Diagnosis:** Corneal Topography (Pentacam). * **Treatment to stop progression:** Corneal Collagen Cross-linking (CXL/C3R) using Riboflavin and UVA light.

Q: What is the toughest layer of the cornea?

Pre-Descemet's membrane. **Explanation:** The correct answer is **Pre-Descemet’s membrane (Dua’s Layer)**. **Why it is correct:** Discovered by Harminder Dua in 2013, the Pre-Descemet’s membrane is a distinct, acellular, and extremely tough layer located between the corneal stroma and Descemet’s membrane. It is approximately **10–15 microns** thick but remarkably strong, capable of withstanding pressures up to **1.5 to 2 bars**. Its toughness is attributed to the dense, transverse arrangement of collagen fibers. In clinical procedures like Deep Anterior Lamellar Keratoplasty (DALK), this layer is crucial for the "Big Bubble" technique. **Why other options are incorrect:** * **Descemet’s membrane:** While it is highly resistant to chemical agents and proteolysis (and remains intact in a *Descemetocele*), it is elastic and thin, not the mechanically toughest layer. * **Endothelium:** This is a single layer of metabolic pump cells. It is fragile and does not provide structural strength. * **Connective tissue stroma:** This makes up 90% of the corneal thickness. While it provides the bulk of structural integrity, it is not as pressure-resistant or "tough" per unit of thickness as Dua’s layer. **High-Yield Clinical Pearls for NEET-PG:** * **Layers of Cornea (New Order):** Epithelium $\rightarrow$ Bowman’s $\rightarrow$ Stroma $\rightarrow$ **Dua’s Layer** $\rightarrow$ Descemet’s $\rightarrow$ Endothelium. * **Type 1 Bubble:** Occurs when air is injected between the stroma and Dua’s layer (stronger, well-defined). * **Type 2 Bubble:** Occurs between Dua’s layer and Descemet’s membrane (thinner, more prone to rupture). * **Regenerative Capacity:** Bowman’s layer and Descemet’s membrane do **not** regenerate (though Descemet's is secreted by the endothelium); the Epithelium regenerates rapidly.

Q: In the given condition, what is the cause of defective vision?

Visual axis is obscured. ***Visual axis is obscured*** - In conditions like **central corneal opacity** (leucoma) or **dense cataract**, the **visual axis** is physically blocked, preventing light from reaching the retina properly. - This mechanical obstruction causes **defective vision** by blocking the path of light rays, not by altering their focus or creating refractive errors. *Astigmatism* - This is a **refractive error** caused by irregular curvature of the cornea or lens, leading to blurred vision at all distances. - The **visual axis remains clear** in astigmatism; the problem is with **uneven light focusing** rather than physical obstruction. *Hypermetropia* - This is a **refractive error** where distant objects are seen clearly but near objects appear blurred due to **short axial length** or **weak refractive power**. - The **visual axis is not obstructed**; light reaches the retina but focuses **behind it** rather than on it. *Diplopia* - This refers to **double vision** caused by misalignment of the eyes due to **extraocular muscle weakness** or neurological issues. - The **visual axis remains clear** in both eyes; the problem is with **binocular coordination** rather than obstruction of light transmission.

Q: Neuroparalytic keratitis is most commonly associated with damage to which cranial nerve?

Trigeminal nerve (CN V). **Explanation:** **Neuroparalytic keratitis** (also known as neurotrophic keratopathy) occurs due to the loss of sensory innervation to the cornea. The **Trigeminal nerve (CN V)**, specifically its ophthalmic division (V1) via the long ciliary nerves, provides this sensory supply. When CN V is damaged, the cornea loses its protective sensations and trophic factors. This leads to a decrease in the blink reflex, reduced tear film stability, and impaired epithelial healing, ultimately resulting in persistent epithelial defects and corneal ulceration. **Analysis of Incorrect Options:** * **Oculomotor nerve (CN III):** Damage leads to ptosis and extraocular muscle palsy. While a drooping eyelid might actually protect the cornea (pseudoptosis), it does not cause neuroparalytic keratitis. * **Abducens nerve (CN VI):** This nerve supplies the lateral rectus muscle. Damage causes esotropia (inward deviation) and diplopia, but has no effect on corneal sensation or integrity. * **Facial nerve (CN VII):** Damage to CN VII leads to **Exposure Keratitis**. This is due to the paralysis of the orbicularis oculi muscle, resulting in lagophthalmos (inability to close the eye), which causes the cornea to dry out. It is a motor deficit, whereas neuroparalytic keratitis is a sensory deficit. **High-Yield Clinical Pearls for NEET-PG:** * **Key Distinction:** Remember **"S"** for **S**ensory/Trigeminal = Neuro**p**aralytic; **"M"** for **M**otor/Facial = **E**xposure Keratitis. * **Common Causes:** CN V damage can occur due to Herpes Zoster Ophthalmicus, acoustic neuroma (at the cerebellopontine angle), or surgical trauma during trigeminal neuralgia procedures. * **Clinical Feature:** A hallmark of neuroparalytic keratitis is a **painless** corneal ulcer with characteristic rolled-up epithelial edges.

Q: Corneal ulcer can lead to which of the following complications?

Anterior staphyloma. **Explanation:** A corneal ulcer, particularly if it progresses to perforation, can lead to the formation of an **Anterior Staphyloma**. When a corneal ulcer causes a large perforation, the iris prolapses through the defect. Over time, this prolapsed iris becomes covered by a thin layer of fibro-cicatricial tissue (pseudocornea). Due to the weakness of this new tissue and the associated rise in intraocular pressure (secondary glaucoma), the area bulges forward, resulting in a slate-colored protrusion known as an anterior staphyloma. **Analysis of Incorrect Options:** * **Posterior Staphyloma:** This is a protrusion of the weakened sclera lined by uveal tissue at the posterior pole of the eye. It is a hallmark of **Pathological Myopia**, not corneal ulceration. * **Lenticonus:** This is a congenital localized cone-shaped protrusion of the anterior or posterior lens surface. Anterior lenticonus is classically associated with **Alport Syndrome**. * **Keratoconus:** This is a non-inflammatory, progressive thinning and ectasia of the central or paracentral cornea. While it involves corneal bulging, it is a degenerative condition and not a direct complication of an acute infectious corneal ulcer. **High-Yield Clinical Pearls for NEET-PG:** * **Descemetocele:** This occurs when a corneal ulcer erodes everything except Descemet’s membrane; it appears as a transparent, bulging vesicle and is a precursor to perforation. * **Secondary Glaucoma:** This is the most common cause of the "bulge" in an anterior staphyloma. * **Management:** A small perforation is managed with Cyanoacrylate glue, while a large perforation requires a tectonic keratoplasty.

Question 1

Which of the following is not an indication for keratoplasty?

Accepted Answer

None of the above

Answer

Pseudophakic bullous keratopathy

Answer

Keratoconus

Answer

Corneal dystrophies

Question 2

Not true regarding herpes keratitis?

Accepted Answer

Satellite lesions are seen

Answer

Diminished corneal sensation

Answer

Can be recurrent

Answer

Punctate keratitis is seen

Question 3

A 48-year-old diabetic with orbital cellulitis presented with a corneal ulcer. An aqueous tap showed branched hyphae. What is the diagnosis?

Accepted Answer

Mycotic Ulcer

Answer

Herpetic ulcer

Answer

Bacterial Ulcer

Answer

Anterior staphyloma

Question 4

Cloudy cornea is seen in which of the following conditions?

Accepted Answer

Mucopolysaccharidosis

Answer

Klinefelter syndrome

Answer

Turner syndrome

Answer

Megalocornea

Question 5

Deposition of which of the following is seen in the Descemet's membrane in Kayser-Fleischer rings?

Accepted Answer

Copper

Answer

Arsenic

Answer

Iron

Answer

Mercury

Question 6

All of the following are true regarding keratoconus except?

Accepted Answer

Hypermetropia is seen

Answer

Munson sign is present

Answer

Thinning of central cornea

Answer

Contact lens is used as treatment

Question 7

What is the toughest layer of the cornea?

Accepted Answer

Pre-Descemet's membrane

Answer

Descemet's membrane

Answer

Endothelium

Answer

Connective tissue stroma

Question 8

In the given condition, what is the cause of defective vision?

Accepted Answer

Visual axis is obscured

Answer

Astigmatism

Answer

Hypermetropia

Answer

Diplopia

Question 9

Neuroparalytic keratitis is most commonly associated with damage to which cranial nerve?

Accepted Answer

Trigeminal nerve (CN V)

Answer

Oculomotor nerve (CN III)

Answer

Abducens nerve (CN VI)

Answer

Facial nerve (CN VII)

Question 10

Corneal ulcer can lead to which of the following complications?

Accepted Answer

Anterior staphyloma

Answer

Posterior staphyloma

Answer

Lenticonus

Answer

Keratoconus

Diseases of the Cornea — MCQs

Diseases of the Cornea — MCQs

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