Diseases of the Cornea — MCQs

Diseases of the Cornea Indian Medical PG Practice Questions and MCQs

Question 81: KF ring is seen in which of the following conditions?

A. Chalcosis (Correct Answer)
B. Diabetes mellitus
C. Keratoconus
D. Anterior Uveitis

Explanation: **Explanation:** The **Kayser-Fleischer (KF) ring** is a characteristic clinical sign caused by the deposition of **copper** in the **Descemet’s membrane** of the peripheral cornea. It typically appears as a golden-brown or greenish-yellow ring. 1. **Why Chalcosis is correct:** Chalcosis refers to the presence of intraocular copper (usually from a retained copper-containing foreign body). Since the KF ring is a manifestation of copper deposition, it is classically seen in Chalcosis. However, it is most famously associated with **Wilson’s Disease** (hepatolenticular degeneration), where a deficiency in ceruloplasmin leads to systemic copper overload. 2. **Why other options are incorrect:** * **Diabetes mellitus:** Associated with corneal changes like decreased sensitivity and delayed wound healing (diabetic keratopathy), but not copper rings. * **Keratoconus:** Characterized by **Fleischer’s ring**, which is an iron deposition (hemosiderin) at the base of the cone. Do not confuse *Fleischer* (Iron/Keratoconus) with *Kayser-Fleischer* (Copper/Wilson's). * **Anterior Uveitis:** Associated with Keratic Precipitates (KPs) on the endothelium, but not pigmentary rings in the Descemet’s membrane. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** KF rings start at the **12 o'clock** position, then 6 o'clock, and eventually become circumferential. * **Examination:** They are best visualized using a **Slit-lamp examination**; early rings may only be visible via **Gonioscopy**. * **Reversibility:** The ring disappears once the systemic copper levels are managed (e.g., with Penicillamine). * **Sunflower Cataract:** Another ocular feature of copper deposition (Chalcosis/Wilson's) involving the anterior capsule of the lens.

Question 82: Corneal deposits are seen in all of these conditions except?

A. Hurler's syndrome
B. Morquio's syndrome
C. Myeloma
D. Sanfilippo's syndrome (Correct Answer)

Explanation: **Explanation:** The question tests your knowledge of **Mucopolysaccharidoses (MPS)** and their ocular manifestations. MPS are lysosomal storage disorders caused by the deficiency of enzymes required to break down Glycosaminoglycans (GAGs). **Why Sanfilippo’s Syndrome is the correct answer:** Sanfilippo’s syndrome (**MPS III**) is unique among the mucopolysaccharidoses because it primarily presents with severe progressive intellectual disability and neurological degeneration, but **lacks corneal clouding**. In this condition, the accumulated GAG (Heparan sulfate) does not typically deposit in the corneal stroma. **Analysis of Incorrect Options:** * **Hurler’s Syndrome (MPS IH):** This is the prototype for corneal clouding. Severe ground-glass opacification of the cornea occurs early in life due to the accumulation of Dermatan and Heparan sulfate. * **Morquio’s Syndrome (MPS IV):** Characterized by severe skeletal dysplasia and **fine, diffuse corneal clouding** that usually appears after age 10. * **Myeloma:** In Multiple Myeloma, immunoglobulin light chains can deposit in the cornea, a condition known as **crystalline keratopathy**. **NEET-PG High-Yield Pearls:** 1. **MPS with Corneal Clouding:** Hurler (MPS I), Scheie (MPS IS), Morquio (MPS IV), and Maroteaux-Lamy (MPS VI). 2. **MPS WITHOUT Corneal Clouding:** Hunter’s (MPS II) and Sanfilippo (MPS III). *Mnemonic: The "Hunter" needs clear vision to "San-fill" (aim) his target.* 3. **Hunter’s Syndrome** is the only MPS that is **X-linked Recessive**; all others are Autosomal Recessive. 4. **Cherry Red Spot** is NOT seen in MPS; it is a feature of Sphingolipidoses (like Tay-Sachs or Niemann-Pick).

Question 83: Which of the following is NOT true regarding the treatment of bacterial corneal ulcer?

A. Fortified antibiotic eye drops
B. Cycloplegic and mydriatic agents to relieve pain
C. Cyanoacrylate glue is indicated in the treatment of small perforations
D. Steroids are usually given in persistent epithelial defects (Correct Answer)

Explanation: **Explanation:** In the management of bacterial corneal ulcers, the primary goal is to eliminate the pathogen and promote healing. **Option D is the correct answer (the false statement)** because steroids are generally **contraindicated** in the presence of an active infection or a persistent epithelial defect. Steroids inhibit collagen synthesis and fibroblast activity, which delays epithelialization and increases the risk of corneal melting and perforation. They should only be considered under strict supervision once the infection is controlled and the epithelium is intact. **Analysis of other options:** * **Option A:** Fortified antibiotics (e.g., Tobramycin 1.4% or Cefazolin 5%) are the **gold standard** for treating severe bacterial ulcers, providing higher drug concentrations than commercially available drops. * **Option B:** Cycloplegics (like Atropine or Homatropine) are essential to relieve ciliary spasms (reducing pain) and to prevent the formation of posterior synechiae by keeping the pupil mobile. * **Option C:** For small corneal perforations (<2mm) or impending perforations, **Cyanoacrylate glue** (tissue adhesive) with a bandage contact lens is a standard intervention to maintain anterior chamber integrity. **NEET-PG High-Yield Pearls:** * **Most common causative organism:** *Staphylococcus aureus* (overall); *Pseudomonas* (contact lens users). * **Hypopyon** in bacterial ulcers is typically **sterile** (due to toxins, not direct bacterial invasion). * **Steroid use rule:** Never use steroids if the ulcer is fungal or if a dendritic (Herpetic) lesion is present. * **Vitamin C** supplementation is often given to promote collagen synthesis and healing.

Question 84: Keratomalacia includes the following except?

A. Night blindness
B. Severe pain in the eye (Correct Answer)
C. Xerosis of the cornea
D. Perforation of cornea

Explanation: **Explanation:** **Keratomalacia** is the most severe stage of Vitamin A deficiency (Xerophthalmia), characterized by the liquefactive necrosis of the cornea. **Why "Severe pain in the eye" is the correct answer:** The hallmark of Keratomalacia is that it is a **painless** condition. This occurs because Vitamin A deficiency leads to **corneal xerosis (dryness)** and a loss of corneal sensation (anesthesia). Because the cornea becomes insensitive, even extensive melting and perforation occur without the typical inflammatory pain associated with other types of keratitis. **Analysis of Incorrect Options:** * **Night Blindness (Nyctalopia):** This is the earliest clinical symptom of Vitamin A deficiency (WHO Grade XN). It occurs due to the failure of rhodopsin regeneration in the rod cells. * **Xerosis of the Cornea:** This is a precursor to Keratomalacia. The cornea appears dull, lusterless, and "dry-leather" like due to the loss of goblet cells and keratinization of the epithelium. * **Perforation of Cornea:** Keratomalacia involves rapid "melting" of the corneal stroma. If untreated, this leads to descemetocele formation and eventual perforation, often resulting in endophthalmitis or phthisis bulbi. **Clinical Pearls for NEET-PG:** * **WHO Classification of Xerophthalmia:** * X1A: Conjunctival xerosis * X1B: **Bitot’s spots** (foamy deposits on bulbar conjunctiva) * X2: Corneal xerosis * X3A: Keratomalacia (<1/3rd corneal surface) * X3B: Keratomalacia (>1/3rd corneal surface) * **Treatment:** Immediate administration of Vitamin A (200,000 IU orally on days 0, 1, and 14). * **Key Differentiator:** Unlike bacterial ulcers, Keratomalacia presents with a **quiet eye** (no redness or ciliary congestion) despite the severity of the melting.

Question 85: Keratomalacia is a clinical manifestation associated with which of the following conditions?

A. Varicella infection
B. Mumps
C. Diarrheal diseases (Correct Answer)
D. All of the above

Explanation: **Explanation:** **Keratomalacia** is the most severe ocular manifestation of **Vitamin A deficiency (Xerophthalmia)**, characterized by rapid, liquefactive necrosis of the corneal stroma. **Why Diarrheal Diseases are correct:** Vitamin A is a fat-soluble vitamin that requires adequate intestinal absorption and a healthy liver for storage (as retinol palmitate). **Diarrheal diseases**, particularly chronic diarrhea or malabsorption syndromes (like Celiac disease or cystic fibrosis), lead to a significant loss of nutrients and impaired absorption. In children, acute gastroenteritis often acts as a "precipitating factor" that depletes already low Vitamin A stores, leading to the rapid onset of keratomalacia. **Why other options are incorrect:** * **Varicella (Chickenpox):** While it can cause viral keratitis or uveitis, it is not a primary cause of the systemic nutritional deficiency required to produce keratomalacia. * **Mumps:** This typically presents with dacryoadenitis (inflammation of the lacrimal gland) or optic neuritis, but does not cause corneal liquefaction. **Clinical Pearls for NEET-PG:** * **WHO Classification of Xerophthalmia:** Keratomalacia is classified as **X3A** (involving <1/3 of the cornea) and **X3B** (involving >1/3 of the cornea). * **Bitot’s Spots (X1B):** These are triangular, foamy, silvery-white patches on the bulbar conjunctiva (usually temporal) caused by *Corynebacterium xerosis*. * **The "Silent" Ulcer:** Keratomalacia is often painless and lacks significant inflammation (ciliary congestion) because the cornea is necrotic and the eye is "quiet." * **Treatment:** Immediate administration of Vitamin A (200,000 IU orally on days 0, 1, and 14) is critical to save the fellow eye and the child's life, as keratomalacia is a marker of high systemic mortality.

Question 86: In Keratoconus, all are seen except?

A. Munson's sign
B. Thinning of cornea in the center
C. Distortion of corneal reflex at the center
D. Hypermetropic refractive error (Correct Answer)

Explanation: **Explanation:** **Keratoconus** is a non-inflammatory, progressive ectatic dystrophy characterized by localized thinning and protrusion of the cornea, typically assuming a conical shape. **Why Option D is the correct answer:** In Keratoconus, the cornea becomes increasingly **steep** and conical. According to optical principles, a steeper corneal curvature increases the refractive power of the eye, leading to **Progressive Myopia** and **Irregular Astigmatism**. Hypermetropia (farsightedness) is not a feature of keratoconus; rather, it is the opposite of the refractive change observed. **Analysis of incorrect options:** * **Munson’s Sign (Option A):** This is a classic late-stage clinical sign where the lower eyelid bulges in a V-shape when the patient looks downward, caused by the cone-shaped cornea. * **Thinning of the cornea (Option B):** The hallmark of the disease is progressive **stromal thinning**, most commonly involving the paracentral or central area, leading to corneal protrusion. * **Distortion of corneal reflex (Option C):** Due to the irregular curvature (ectasia), the normal circular corneal light reflex becomes distorted. This is easily visualized using a Placido disc or Keratoscopy (showing irregular, crowded mires). **High-Yield Clinical Pearls for NEET-PG:** 1. **Early Sign:** "Scissoring reflex" on retinoscopy and "Oil droplet sign" (Charleux sign) on distant direct ophthalmoscopy. 2. **Vogt’s Striae:** Vertical stress lines in the deep stroma/Descemet’s membrane that disappear with digital pressure. 3. **Fleischer’s Ring:** Iron deposition in the basal epithelium at the base of the cone (best seen with a cobalt blue filter). 4. **Hydrops:** Sudden profound vision loss due to a rupture in Descemet’s membrane, leading to acute corneal edema. 5. **Associations:** Down syndrome, Atopy (eye rubbing), Marfan syndrome, and Ehlers-Danlos syndrome.

Question 87: What is the diagnostic test for a corneal ulcer?

A. Methylene blue
B. Sodium fluorescein dye (Correct Answer)
C. Alcian blue
D. Rose Bengal

Explanation: **Explanation:** The diagnosis of a corneal ulcer (epithelial defect) is clinically confirmed using **Sodium Fluorescein dye (2%)**. **1. Why Sodium Fluorescein is the Correct Answer:** The corneal epithelium is lipophilic and normally acts as a barrier to water-soluble dyes. When there is a breach in the epithelium (as seen in a corneal ulcer), the underlying **hydrophilic stroma** is exposed. Fluorescein dye, being water-soluble, is absorbed by the stroma and glows a **brilliant green** under cobalt blue light. This clearly demarcates the area of the ulcer. **2. Analysis of Incorrect Options:** * **Methylene Blue:** This is primarily used to stain the lacrimal sac during Dacryocystorhinostomy (DCR) or to mark the skin before surgery. It is not used for routine corneal staining. * **Alcian Blue:** This dye has an affinity for mucin. It is used to stain excess mucus in the tear film, often seen in cases of Keratoconjunctivitis Sicca (Dry Eye). * **Rose Bengal:** This dye stains **devitalized (dead/dying) cells** and mucus. While it can stain the edges of a dendritic ulcer (Herpes Simplex Keratitis), it is highly irritating to the eye and has largely been replaced by Lissamine Green. **3. High-Yield Clinical Pearls for NEET-PG:** * **Dendritic Ulcer:** Stains with Fluorescein (the floor/bed of the ulcer) and Rose Bengal (the swollen epithelial cells at the margins). * **Seidel’s Test:** Uses Fluorescein to detect aqueous leakage from a penetrating ocular injury (positive if the dye is diluted/washed away by clear fluid). * **Lissamine Green:** Similar to Rose Bengal (stains dead cells) but is much better tolerated and preferred for diagnosing Dry Eye Syndrome.

Question 88: Marginal catarrhal corneal ulcer is caused by which of the following?

A. Staphylococcus
B. Moraxella
C. Haemophilus
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Marginal catarrhal corneal ulcer** (also known as a marginal keratitis) is not a direct infection of the cornea, but rather a **Type III hypersensitivity reaction** (antigen-antibody complex mediated) to bacterial exotoxins. **Why "All of the above" is correct:** The condition is most commonly associated with chronic blepharitis. The bacterial antigens from the lid margins trigger an immune response where complexes deposit in the peripheral cornea. While **Staphylococcus aureus** is the most frequent culprit, other organisms known to cause chronic blepharitis and subsequent marginal ulcers include **Moraxella lacunata** and **Haemophilus aegyptius**. Therefore, all three organisms listed are recognized etiological agents. **Clinical Mechanism:** The "lucid interval" (a clear space between the ulcer and the limbus) is a hallmark of this condition. This occurs because the high molecular weight antibodies (IgM) cannot easily diffuse to the extreme periphery, and the limbal blood vessels provide a constant supply of fresh complement and inflammatory cells that localize the reaction slightly away from the limbus. **High-Yield Clinical Pearls for NEET-PG:** * **Nature of Ulcer:** It is a sterile, "cold" ulcer (non-infectious). * **Key Feature:** Presence of a **clear zone (lucid interval)** between the limbus and the ulcer. * **Symptoms:** Mild irritation, photophobia, and lacrimation (less severe than bacterial keratitis). * **Treatment:** Unlike infectious ulcers, these respond rapidly to **topical steroids** combined with antibiotic coverage for the underlying blepharitis. * **Differential Diagnosis:** Must be distinguished from Mooren’s ulcer (which is idiopathic, painful, and lacks a lucid interval).

Question 89: The central nebular corneal opacity is best treated with which procedure?

A. Lamellar keratoplasty (Correct Answer)
B. Penetrating keratoplasty
C. Gas permeable contact lens
D. Soft contact lens

Explanation: ### Explanation **Correct Option: A. Lamellar Keratoplasty** The management of corneal opacities depends on the **depth** and **density** of the scar. A **nebular opacity** is a faint, superficial scar that involves only the epithelium and the superficial layers of the stroma. In **Lamellar Keratoplasty (LKP)**, only the diseased superficial layers of the cornea are removed and replaced with donor tissue, leaving the healthy host endothelium intact. Since a nebular opacity does not involve the deep stroma or endothelium, LKP is the treatment of choice as it carries a lower risk of graft rejection and shorter recovery time compared to full-thickness procedures. **Analysis of Incorrect Options:** * **B. Penetrating Keratoplasty (PKP):** This is a full-thickness transplant. While it would remove the opacity, it is unnecessarily invasive for a superficial scar. PKP is reserved for **macular or leucomatous opacities** that involve the full thickness of the stroma. * **C & D. Contact Lenses:** Nebular opacities cause significant visual impairment due to **irregular astigmatism** and light scattering (diffraction). While RGP lenses (Option C) can correct irregular astigmatism, they do not eliminate the light scattering caused by the opacity itself. Therefore, surgical removal is required for definitive treatment. **High-Yield Clinical Pearls for NEET-PG:** * **Grading of Opacities:** 1. **Nebula:** Faint, iris details clearly visible. 2. **Macula:** Translucent, iris details seen indistinctly. 3. **Leucoma:** Opaque/White, iris details not visible. * **PTK (Phototherapeutic Keratectomy):** If the nebular opacity is very superficial (Bowman’s layer/superficial stroma), Excimer laser PTK is an alternative modern treatment. * **Deep Anterior Lamellar Keratoplasty (DALK):** The preferred modern variant of LKP for opacities involving up to the pre-Descemet's layer.

Question 90: Diagnose the condition.

A. Keratoconus
B. Wilson's disease (Correct Answer)
C. Glaucoma
D. Williams syndrome

Explanation: ***Wilson's disease*** - The image shows **Kayser-Fleischer rings** - pathognomonic **golden-brown copper deposits** at the corneal periphery (Descemet's membrane). - These rings are virtually **diagnostic of Wilson's disease**, a copper metabolism disorder causing hepatic and neurological manifestations. *Keratoconus* - Presents with **cone-shaped corneal protrusion** and **Munson's sign** (lower eyelid bulging when looking down). - Does not cause **golden-brown rings** at the corneal periphery like shown in the image. *Glaucoma* - Characterized by **optic disc cupping** and **visual field defects**, not corneal ring findings. - May cause **corneal edema** in acute cases, but not the **golden-brown deposits** seen here. *Williams syndrome* - A **genetic disorder** causing distinctive facial features and **stellate iris pattern**. - Does not produce **Kayser-Fleischer rings** or corneal copper deposition.

Practice by Chapter

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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