Diseases of the Cornea — MCQs

Diseases of the Cornea Indian Medical PG Practice Questions and MCQs

Question 171: Which of the following is not an indication for keratoplasty?

A. Pseudophakic bullous keratopathy
B. Keratoconus
C. Corneal dystrophies
D. None of the above (Correct Answer)

Explanation: **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.

Question 172: Not true regarding herpes keratitis?

A. Diminished corneal sensation
B. Can be recurrent
C. Satellite lesions are seen (Correct Answer)
D. Punctate keratitis is seen

Explanation: **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.

Question 173: A 48-year-old diabetic with orbital cellulitis presented with a corneal ulcer. An aqueous tap showed branched hyphae. What is the diagnosis?

A. Herpetic ulcer
B. Mycotic Ulcer (Correct Answer)
C. Bacterial Ulcer
D. Anterior staphyloma

Explanation: ### Explanation **Correct Answer: B. Mycotic Ulcer** The diagnosis is established by the direct visualization of **branched hyphae** in the aqueous tap/corneal scraping. Fungi are broadly classified into yeasts (e.g., *Candida*) and filamentous fungi (e.g., *Aspergillus*, *Fusarium*). The presence of hyphae is a pathognomonic microscopic finding for **filamentous fungal keratitis**. Furthermore, the patient’s **diabetic status** represents a significant immunocompromised state, which is a major predisposing factor for opportunistic fungal infections. In cases of orbital cellulitis or deep keratitis, fungi can penetrate Descemet’s membrane, necessitating an aqueous tap for diagnosis. **Why other options are incorrect:** * **A. Herpetic Ulcer:** Typically presents with a characteristic "dendritic" (branching) pattern on the epithelium, but this refers to the macroscopic lesion shape, not microscopic hyphae. It is caused by the Herpes Simplex Virus (HSV). * **C. Bacterial Ulcer:** Microscopic examination would reveal cocci or bacilli (rods) and a dense polymorphonuclear leucocyte response, rather than hyphae. Bacterial ulcers usually have a more acute, suppurative presentation. * **D. Anterior Staphyloma:** This is a late complication of a perforated corneal ulcer where the iris tissue prolapses and becomes incorporated into a scarred, ectatic cornea. It is a structural end-stage finding, not an active infective process identified by hyphae. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Potassium Hydroxide (KOH) wet mount is the fastest way to identify hyphae. * **Culture Media:** Sabouraud’s Dextrose Agar (SDA) is the specific medium for fungi. * **Clinical Signs:** Look for "feathery margins," "satellite lesions," and a "dry, leathery" appearance. Fungal ulcers often have a slow onset but are notoriously difficult to treat. * **Drug of Choice:** Natamycin (5%) is the first-line topical treatment for filamentous fungi.

Question 174: Cloudy cornea is seen in which of the following conditions?

A. Klinefelter syndrome
B. Turner syndrome
C. Megalocornea
D. Mucopolysaccharidosis (Correct Answer)

Explanation: **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.

Question 175: Deposition of which of the following is seen in the Descemet's membrane in Kayser-Fleischer rings?

A. Copper (Correct Answer)
B. Arsenic
C. Iron
D. Mercury

Explanation: **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.

Question 176: All of the following are true regarding keratoconus except?

A. Munson sign is present
B. Hypermetropia is seen (Correct Answer)
C. Thinning of central cornea
D. Contact lens is used as treatment

Explanation: **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.

Question 177: Cogan Syndrome is associated with all of the following EXCEPT:

A. Splenomegaly (Correct Answer)
B. Interstitial keratitis
C. Vestibuloauditory symptoms
D. Aortic valvular insufficiency

Explanation: **Cogan Syndrome** is a rare autoimmune vasculitis primarily affecting young adults. It is characterized by the clinical triad of non-syphilitic interstitial keratitis, vestibuloauditory dysfunction, and systemic vasculitis. ### **Explanation of Options:** * **A. Splenomegaly (Correct Answer):** Splenomegaly is **not** a recognized feature of Cogan Syndrome. While it is a systemic disease, the vasculitis typically involves the large vessels (like the aorta) rather than the reticuloendothelial system. * **B. Interstitial Keratitis:** This is a hallmark ocular finding. Patients present with sudden onset of corneal opacification (stromal inflammation), photophobia, and blurred vision. Unlike syphilitic keratitis, it is usually bilateral and associated with rapid progression. * **C. Vestibuloauditory symptoms:** These symptoms mimic Meniere’s disease and include sudden sensorineural hearing loss, tinnitus, and vertigo. If left untreated, it often leads to permanent deafness. * **D. Aortic valvular insufficiency:** Approximately 10% of patients develop systemic manifestations, most commonly **aortitis**. This can lead to life-threatening aortic aneurysm or aortic valvular insufficiency (regurgitation), requiring surgical intervention. ### **High-Yield Clinical Pearls for NEET-PG:** 1. **The Triad:** Interstitial Keratitis + Vertigo/Hearing Loss + Large vessel vasculitis. 2. **Differential Diagnosis:** Always rule out **Syphilis** (which also causes interstitial keratitis and deafness) using FTA-ABS or VDRL tests. 3. **Treatment:** High-dose systemic corticosteroids are the mainstay. Urgent treatment is required to prevent permanent hearing loss. 4. **Association:** It is often associated with other autoimmune conditions like Polyarteritis Nodosa (PAN) or Wegener’s Granulomatosis.

Question 178: What is the toughest layer of the cornea?

A. Descemet's membrane
B. Endothelium
C. Connective tissue stroma
D. Pre-Descemet's membrane (Correct Answer)

Explanation: **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.

Question 179: A 17-year-old girl presents with keratitis and severe eye pain, with suspected Acanthamoeba keratitis. Which of the following is NOT a risk factor for Acanthamoeba keratitis?

A. Extended wear contact lens
B. Exposure to contaminated water
C. Corneal trauma
D. Squamous blepharitis (Correct Answer)

Explanation: **Explanation:** *Acanthamoeba* keratitis is a rare but sight-threatening infection caused by a free-living ubiquitous amoeba. The pathogenesis typically involves a breach in the corneal epithelium followed by the introduction of the organism. **Why Squamous Blepharitis is the Correct Answer:** Squamous blepharitis is a chronic inflammatory condition of the eyelid margins, often associated with seborrheic dermatitis. While it can cause secondary ocular surface irritation or staphylococcal hypersensitivity (marginal keratitis), it is **not** a recognized risk factor for *Acanthamoeba* infection. Unlike the other options, it does not typically provide a direct mechanism for the introduction of *Acanthamoeba* cysts or trophozoites into the corneal stroma. **Analysis of Incorrect Options:** * **Extended wear contact lens (A):** This is the **most common risk factor** (approx. 90% of cases). Poor hygiene, such as using tap water for cleaning lenses or "topping off" solutions, facilitates amoebic colonization. * **Exposure to contaminated water (B):** *Acanthamoeba* is found in tap water, swimming pools, hot tubs, and soil. Direct exposure to these sources, especially while wearing lenses, is a major risk. * **Corneal trauma (C):** In non-contact lens wearers, minor trauma (often with organic matter or soil) provides the epithelial defect necessary for the organism to invade the cornea. **High-Yield Clinical Pearls for NEET-PG:** 1. **Classic Presentation:** Severe ocular pain that is **out of proportion** to the clinical signs. 2. **Pathognomonic Sign:** **Radial Keratoneuritis** (infiltrates along the corneal nerves). 3. **Late Sign:** Ring-shaped stromal infiltrate. 4. **Diagnosis:** Culture on **Non-nutrient agar with E. coli overlay**. 5. **Treatment:** Topical biguanides (PHMB 0.02%) or Diamidines (Propamidine/Brolene).

Question 180: Neuroparalytic keratitis is most commonly associated with damage to which cranial nerve?

A. Oculomotor nerve (CN III)
B. Trigeminal nerve (CN V) (Correct Answer)
C. Abducens nerve (CN VI)
D. Facial nerve (CN VII)

Explanation: **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.

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Corneal Anatomy and Physiology

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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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