Diseases of the Cornea Practice Questions

Q: The thickness of the cornea is measured by using which instrument?

Pachymeter. **Explanation:** The measurement of corneal thickness is known as **Pachymetry**, and the instrument used is a **Pachymeter**. This is a critical clinical measurement because corneal thickness influences the accuracy of Intraocular Pressure (IOP) readings and determines candidacy for refractive surgeries like LASIK. **Why the correct answer is right:** * **Pachymeter:** It measures the distance between the corneal epithelium and endothelium. There are two main types: **Optical pachymeters** (using a slit lamp) and **Ultrasound pachymeters** (more common, using high-frequency sound waves). The average central corneal thickness (CCT) is approximately **540–560 μm**. **Analysis of incorrect options:** * **Schiotz tonometer:** Used to measure **Intraocular Pressure (IOP)** based on the principle of indentation. It is no longer the gold standard (which is Goldmann Applanation Tonometry). * **Keratometer:** Used to measure the **curvature** of the anterior corneal surface. It is essential for calculating IOL power and fitting contact lenses. * **Aesthesiometer:** Used to measure **corneal sensitivity** (e.g., Cochet-Bonnet aesthesiometer). Reduced sensitivity is seen in conditions like Herpes Simplex Keratitis or Diabetes. **High-Yield Clinical Pearls for NEET-PG:** 1. **IOP Correction:** If the cornea is thinner than average, the measured IOP is falsely low; if thicker, the IOP is falsely high. 2. **Keratoconus:** A thin cornea (usually <450–500 μm) with apical scarring is a hallmark of progressive keratoconus. 3. **Specular Microscopy:** While primarily used to count endothelial cells, it can also provide a measurement of corneal thickness.

Q: Kayser-Fleischer rings in Wilson's disease are seen at the level of which corneal layer?

Descemet's membrane. ### Explanation **1. Why Descemet’s Membrane is Correct:** Kayser-Fleischer (KF) rings are the hallmark ocular manifestation of **Wilson’s Disease** (hepatolenticular degeneration). The underlying pathophysiology involves a deficiency in ceruloplasmin, leading to excessive free copper deposition in various tissues. In the eye, copper ions are deposited specifically in the **periphery of Descemet’s membrane**. This occurs because copper ions from the aqueous humor diffuse into the posterior layers of the cornea. **2. Why Other Options are Incorrect:** * **Epithelium:** This layer is involved in conditions like *Hudson-Stahli lines* (iron deposition) or *Vortex keratopathy* (Amiodarone/Fabry’s disease), but not copper deposition in Wilson's. * **Endothelium:** While copper passes through the endothelium to reach Descemet’s membrane, it does not accumulate here. * **Stroma:** Copper deposition in the stroma is seen in *Chalcosis* (intraocular copper foreign body), resulting in a "sunflower cataract," but the KF ring specifically targets the basement membrane (Descemet’s). **3. High-Yield Clinical Pearls for NEET-PG:** * **Appearance:** KF rings appear as golden-brown, ruby-red, or green bilateral rings at the limbus. * **Examination:** They are best visualized using a **Slit-lamp examination** (Gonioscopy can help see the peripheral extent). * **Clinical Significance:** They are present in 95% of patients with neurological Wilson’s and 50-60% of those with hepatic presentation. * **Reversibility:** The KF ring is one of the few corneal deposits that **disappears** with systemic chelation therapy (e.g., D-Penicillamine). * **Differential Diagnosis:** Similar rings can rarely be seen in primary biliary cholangitis or chronic cholestasis due to systemic copper overload.

Q: Corneal lesion seen in Hutchinson triad associated with congenital syphilis is:

Interstitial keratitis. **Explanation:** **Interstitial Keratitis (IK)** is the correct answer because it is a hallmark ocular manifestation of **late congenital syphilis**. It is an immune-mediated inflammation of the corneal stroma without involvement of the epithelium or endothelium. In syphilis, it typically presents bilaterally and is a key component of **Hutchinson’s Triad**, which consists of: 1. **Interstitial Keratitis** 2. **Hutchinson’s Teeth** (notched incisors) 3. **Sensorineural Deafness** (8th cranial nerve palsy) **Analysis of Incorrect Options:** * **Disciform Keratitis:** This is a deep, circular corneal edema typically caused by a delayed hypersensitivity reaction to the **Herpes Simplex Virus (HSV)**. It is not associated with the Hutchinson triad. * **Phlyctenular Keratitis:** This is a nodular inflammation (allergic response) of the cornea/conjunctiva, most commonly triggered by **Tuberculosis** (endogenous staphylococcal proteins). * **Mooren Ulcer:** This is an idiopathic, peripheral ulcerative keratitis that is painful and progressive, often associated with autoimmune triggers, but unrelated to congenital syphilis. **High-Yield Clinical Pearls for NEET-PG:** * **Salmon Patch:** During the active phase of syphilitic IK, deep vascularization gives the cornea a characteristic pinkish-orange appearance. * **Ghost Vessels:** After the inflammation subsides, the empty, non-perfused vessels remain in the stroma, visible on slit-lamp examination. * **Wessely Ring:** An immune ring seen in the cornea, often associated with disciform keratitis or fungal infections, but distinct from the diffuse stromal involvement of IK.

Q: What happens to the corneal endothelium after injury?

Never regenerates. **Explanation:** The corneal endothelium is a single layer of hexagonal cells that plays a critical role in maintaining corneal transparency by regulating stromal hydration through an active "pump-leak" mechanism. **1. Why "Never regenerates" is correct:** In humans, corneal endothelial cells are considered **post-mitotic**. They are arrested in the G1 phase of the cell cycle and do not undergo mitosis to replace lost cells. When the endothelium is injured (due to trauma, surgery, or disease), the defect is healed not by cell division, but by the **enlargement (pleomorphism)** and **migration** of existing neighboring cells to cover the bare area. This leads to a progressive decrease in endothelial cell density over time. **2. Why other options are incorrect:** * **A & B (Regeneration):** Unlike the corneal epithelium, which possesses limbal stem cells and regenerates rapidly, the endothelium lacks this regenerative capacity. * **D (Forms a scar):** Scarring (fibrosis) is a feature of the corneal stroma. When the endothelium fails, it leads to **corneal edema** and bullous keratopathy rather than traditional scar tissue formation. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Cell Count:** Approximately 3,000 cells/mm² in young adults. * **Critical Threshold:** If the count falls below **500–700 cells/mm²**, the pump mechanism fails, leading to irreversible corneal edema (Pseudophakic Bullous Keratopathy). * **Specular Microscopy:** The gold standard investigation to assess endothelial cell count and morphology (Polymegathism and Pleomorphism). * **Hassall-Henle bodies:** Physiological hyaline outgrowths of Descemet’s membrane seen in the periphery; when seen centrally, they are called **Guttae** (characteristic of Fuchs’ Endothelial Dystrophy).

Q: Vogt's striae are seen in which of the following conditions?

Keratoconus. **Explanation:** **Vogt’s striae** are a classic clinical sign of **Keratoconus**, a non-inflammatory, progressive thinning and cone-like protrusion of the cornea. These are fine, vertical (stress) lines located in the deep posterior stroma and Descemet’s membrane. They are caused by the mechanical stretching of the corneal lamellae due to the ectasia. A key diagnostic feature is that these striae **disappear** temporarily when external pressure is applied to the globe. **Analysis of Options:** * **Keratoconus (Correct):** In addition to Vogt’s striae, other hallmark signs include **Fleischer’s ring** (iron deposition at the base of the cone), **Munson’s sign** (indentation of the lower lid on downgaze), and **Rizutti’s sign**. * **Congenital Glaucoma (Incorrect):** This condition is associated with **Haab’s striae**, which are horizontal or curvilinear breaks in Descemet’s membrane caused by increased intraocular pressure and globe enlargement (buphthalmos). * **Aphakia (Incorrect):** This refers to the absence of the crystalline lens. While it may lead to corneal edema or bullous keratopathy post-surgery, it does not feature Vogt’s striae. * **Subluxated Lens (Incorrect):** This is the partial displacement of the lens (e.g., in Marfan syndrome). It affects refraction and accommodation but does not typically involve structural corneal striae. **High-Yield Clinical Pearls for NEET-PG:** * **Vogt’s Striae:** Vertical lines in Keratoconus (disappear with pressure). * **Haab’s Striae:** Horizontal/Curvilinear lines in Congenital Glaucoma (permanent). * **Hydrops:** An acute complication of Keratoconus caused by a rupture in Descemet’s membrane, leading to sudden corneal edema. * **Treatment Gold Standard:** Rigid Gas Permeable (RGP) contact lenses for vision; Collagen Cross-linking (CXL/C3R) to halt progression.

Q: Snow blindness is caused by which type of radiation?

Ultraviolet rays. **Explanation:** **Snow blindness**, clinically known as **Photokeratitis**, is an acute inflammatory condition of the cornea caused by exposure to high-intensity **Ultraviolet (UV) radiation**, specifically **UV-B rays** (wavelength 290–310 nm). Fresh snow reflects nearly 80% of UV radiation, significantly increasing the dose reaching the ocular surface. The corneal epithelium absorbs these rays, leading to protein denaturation and epithelial cell death (desquamation). This results in multiple punctate corneal erosions, causing severe pain, photophobia, and a foreign body sensation, typically occurring 6–12 hours after exposure. **Analysis of Options:** * **A. Ultraviolet rays (Correct):** As explained, UV-B is the primary causative agent for photokeratitis. This is also seen in "Welder’s Flash" (industrial arc welding). * **B. Infrared rays:** These are associated with **Glassblower’s cataract** (True exfoliation of the lens capsule) and thermal burns, but not snow blindness. * **C. Microwaves:** Prolonged exposure to microwaves is linked to **cataractogenesis** due to thermal effects on lens proteins, not acute corneal damage. * **D. Defect in mirror:** This is a distractor and has no clinical relevance to radiation-induced ocular injury. **High-Yield Clinical Pearls for NEET-PG:** * **Management:** Snow blindness is self-limiting. Treatment includes patching the eye, antibiotic ointment to prevent secondary infection, and systemic analgesics. **Topical anesthetics should be avoided** for long-term use as they inhibit epithelial healing. * **Eclipse Retinopathy:** Caused by **UV-A** and visible light (photochemical damage to the fovea). * **Wavelengths:** UV-C (<280 nm) is absorbed by the ozone layer; UV-B (280-315 nm) causes Keratitis; UV-A (315-400 nm) is linked to Cataracts and Macular Degeneration.

Q: Orange-skin cornea results due to:

Mustard gas. **Explanation:** **Mustard Gas (Correct Answer):** Mustard gas (sulfur mustard) is a potent alkylating agent used in chemical warfare. Ocular exposure leads to a delayed-onset keratitis that can manifest years after the initial insult. The characteristic **"Orange-skin cornea"** (also known as *peau d'orange* appearance) occurs due to chronic subepithelial changes, lipid deposition, and scarring that creates a granular, pitted, and orange-tinted texture on the corneal surface. This is often associated with "delayed mustard gas keratitis," characterized by vascularization and recurrent ulceration. **Incorrect Options:** * **A. Chalcosis:** This refers to the intraocular deposition of copper. In the cornea, it typically presents as a **Kayser-Fleischer (KF) ring** (golden-brown/greenish deposit in Descemet’s membrane) or a "sunflower cataract" in the lens. * **B. Siderosis:** This is caused by an iron-containing intraocular foreign body. It leads to rust-colored staining of the lens (anterior subcapsular) and iris, but not an orange-skin corneal texture. * **C. Ammonia burn:** This is a severe alkali burn. It causes rapid liquefactive necrosis, leading to corneal opacification ("ground glass" appearance), limbal ischemia, and potential perforation, rather than a chronic orange-skin texture. **Clinical Pearls for NEET-PG:** * **Mustard Gas:** Look for the triad of "delayed keratitis," "limbal ischemia," and "orange-skin cornea." * **Vossius Ring:** A circular ring of pigment on the anterior lens capsule following blunt trauma. * **Fleck Keratopathy:** Often confused with mustard gas changes but is a distinct congenital dystrophy. * **Hudson-Stahli line:** An iron deposit line seen at the junction of the upper 2/3 and lower 1/3 of the cornea in elderly patients (normal aging).

Q: Keratic precipitates are most commonly seen in which condition?

Uveitis. **Explanation:** **Keratic Precipitates (KPs)** are inflammatory cell deposits on the **corneal endothelium**. They are a hallmark clinical sign of **anterior uveitis** (iridocyclitis). 1. **Why Uveitis is Correct:** In uveitis, the blood-aqueous barrier is breached, allowing inflammatory cells (leukocytes) and protein to enter the anterior chamber. These cells circulate via convection currents in the aqueous humor and eventually settle and adhere to the sticky, inflamed corneal endothelium, forming KPs. 2. **Why Other Options are Incorrect:** * **Corneal Ulcers:** These involve the corneal epithelium and stroma. While they may cause a secondary "sterile" aqueous flare, KPs are not their primary diagnostic feature. * **Nuclear Cataracts:** This is a degenerative/age-related change of the crystalline lens fibers and does not involve inflammatory deposits on the cornea. * **Keratoconus:** This is a non-inflammatory ectatic dystrophy characterized by corneal thinning and cone-shaped protrusion. Key signs include Munson’s sign, Fleischer’s ring, and Vogt’s striae, but not KPs. **High-Yield Clinical Pearls for NEET-PG:** * **Arlt’s Triangle:** KPs typically settle in a triangular distribution on the inferior part of the cornea due to gravity and convection currents. * **Mutton-fat KPs:** Large, greasy-looking precipitates (composed of macrophages) characteristic of **Granulomatous Uveitis** (e.g., Sarcoidosis, TB). * **Small/Fine KPs:** Composed of neutrophils and lymphocytes, seen in **Non-granulomatous Uveitis**. * **Stellate KPs:** Distributed over the entire endothelium; classic for **Fuchs’ Heterochromic Iridocyclitis** and Viral Uveitis.

Q: Treatment for dendritic ulcer includes all except:

Steroids. **Explanation:** Dendritic ulcers are the hallmark of **Herpes Simplex Keratitis (HSK)**, specifically the epithelial stage. The primary pathology is active viral replication within the corneal epithelial cells. **Why Steroids are Contraindicated (Correct Answer):** Topical steroids are strictly **contraindicated** in the presence of an active dendritic ulcer. Steroids suppress the local immune response and promote viral replication. This can lead to the expansion of the ulcer into a "geographic ulcer" and may facilitate stromal invasion or corneal perforation. **Analysis of Other Options:** * **Acyclovir (3% Ointment):** This is the standard antiviral treatment. It works by inhibiting viral DNA polymerase, thereby stopping replication. * **Debridement:** Mechanical debridement of the ulcer edges (which contain the highest load of live virus) helps reduce the viral load and allows for faster healing and better penetration of antiviral drugs. * **Penetrating Keratoplasty (PK):** While not the first-line treatment for an *active* ulcer, "therapeutic PK" may be indicated in cases of impending or actual corneal perforation resulting from complications of the ulcer. **NEET-PG High-Yield Pearls:** * **Morphology:** Dendritic ulcers have a linear, branching pattern with characteristic **terminal bulbs** (knobs) that stain with Fluorescein. The bed stains with Fluorescein, while the margins (containing virus) stain with **Rose Bengal**. * **Sensation:** Corneal sensations are typically **reduced or absent** (hypoesthesia) in HSK. * **Steroid Exception:** Steroids are only used in HSK for **Disciform Keratitis** (stromal involvement), which is an immune-mediated reaction, but *only* under the cover of topical antivirals.

Q: A patient presents to the OPD with a recent onset of photophobia within 24 hours and a sloughing corneal ulcer. There is a greenish ulcer base. Which of the following can be the causative organism?

Pseudomonas. **Explanation:** The clinical presentation of a rapidly progressing, sloughing corneal ulcer with a characteristic **greenish-yellow discharge** or base is a classic hallmark of **Pseudomonas aeruginosa** keratitis. **1. Why Pseudomonas is correct:** Pseudomonas is a Gram-negative aerobe known for its high virulence. It produces enzymes like **proteases and elastases** that cause rapid liquefactive necrosis of the corneal stroma (sloughing). The distinctive greenish hue is due to the production of pigments, primarily **pyocyanin**. It is the most common cause of corneal ulcers in contact lens wearers and can lead to corneal perforation within 24–48 hours if not treated aggressively. **2. Why other options are incorrect:** * **Acanthamoeba:** Typically presents with a **ring-shaped infiltrate** and pain out of proportion to clinical findings. It has a much more chronic, indolent course compared to the rapid onset described here. * **Nocardia:** Usually presents with a "wreath-like" or **patchy infiltrate** and is often associated with trauma involving soil or post-LASIK infections. It does not produce a greenish slough. * **Herpes (HSV):** Characterized by **dendritic ulcers** (with terminal bulbs) and decreased corneal sensations. It does not cause a purulent, sloughing greenish ulcer. **Clinical Pearls for NEET-PG:** * **Pseudomonas:** Rapidly spreading, greenish discharge, common in contact lens users. * **Staphylococcus aureus:** Localized, round/oval ulcer with clear margins. * **Streptococcus pneumoniae:** Often associated with chronic dacryocystitis; causes a "hypopyon ulcer" (Ulcus Serpens). * **Fungal Keratitis:** Feathery margins, satellite lesions, and a dry, leathery appearance.

Question 1

The thickness of the cornea is measured by using which instrument?

Accepted Answer

Pachymeter

Answer

Schiotz tonometer

Answer

Keratometer

Answer

Aesthesiometer

Question 2

Kayser-Fleischer rings in Wilson's disease are seen at the level of which corneal layer?

Accepted Answer

Descemet's membrane

Answer

Epithelium

Answer

Endothelium

Answer

Stroma

Question 3

Corneal lesion seen in Hutchinson triad associated with congenital syphilis is:

Accepted Answer

Interstitial keratitis

Answer

Disciform keratitis

Answer

Phylectenular keratitis

Answer

Mooren ulcer

Question 4

What happens to the corneal endothelium after injury?

Accepted Answer

Never regenerates

Answer

Slowly regenerates

Answer

Regenerates rapidly

Answer

Forms a scar

Question 5

Vogt's striae are seen in which of the following conditions?

Accepted Answer

Keratoconus

Answer

Congenital glaucoma

Answer

Aphakia

Answer

Subluxated lens

Question 6

Snow blindness is caused by which type of radiation?

Accepted Answer

Ultraviolet rays

Answer

Infrared rays

Answer

Microwaves

Answer

Defect in mirror

Question 7

Orange-skin cornea results due to:

Accepted Answer

Mustard gas

Answer

Chalcosis

Answer

Siderosis

Answer

Ammonia burn

Question 8

Keratic precipitates are most commonly seen in which condition?

Accepted Answer

Uveitis

Answer

Corneal ulcers

Answer

Nuclear cataracts

Answer

Keratoconus

Question 9

Treatment for dendritic ulcer includes all except:

Accepted Answer

Steroids

Answer

Penetrating keratoplasty

Answer

Acyclovir

Answer

Debridement of the edges of the ulcer

Question 10

A patient presents to the OPD with a recent onset of photophobia within 24 hours and a sloughing corneal ulcer. There is a greenish ulcer base. Which of the following can be the causative organism?

Accepted Answer

Pseudomonas

Answer

Acanthamoeba

Answer

Nocardia

Answer

Herpes

Diseases of the Cornea — MCQs

Diseases of the Cornea — MCQs

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