Diseases of the Cornea — MCQs

Diseases of the Cornea Indian Medical PG Practice Questions and MCQs

Question 271: Herpes virus causes which type of corneal ulcer?

A. Dendritic ulcer (Correct Answer)
B. Serpiginous ulcer
C. Hypopyon corneal ulcer
D. Corneal erosion

Explanation: **Explanation:** **Herpes Simplex Keratitis (HSK)** is a leading cause of corneal blindness. The hallmark of epithelial HSK is the **Dendritic Ulcer**. This occurs due to active viral replication in the corneal epithelium, leading to cell lysis. The ulcer is characterized by a linear, branching (arborescent) pattern with terminal bulbs (knobs) that contain live virus. These ulcers stain brilliantly with **Fluorescein** (the floor) and **Rose Bengal** (the devitalized margins). **Analysis of Incorrect Options:** * **Serpiginous Ulcer:** This is a characteristic feature of bacterial keratitis, most commonly caused by *Streptococcus pneumoniae*. It is a creeping ulcer that spreads centrally while healing peripherally. * **Hypopyon Corneal Ulcer:** While many organisms can cause a hypopyon (pus in the anterior chamber), it is most classically associated with fungal keratitis (filamentous fungi) or virulent bacteria like *Pseudomonas* and *Pneumococcus*. Viral ulcers are typically "dry" and rarely present with a sterile hypopyon unless there is secondary bacterial infection or severe disciform keratitis. * **Corneal Erosion:** This refers to the sloughing off of the epithelium, often due to trauma or basement membrane dystrophies, rather than a primary viral infection. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Sign:** Terminal bulbs are present in Dendritic ulcers (HSV) but **absent** in Pseudodendrites (seen in Acanthamoeba or Herpes Zoster). * **Sensation:** Corneal sensations are characteristically **diminished or absent** in HSV keratitis. * **Treatment:** Topical **Acyclovir (3%)** or Ganciclovir gel. **Steroids are strictly contraindicated** in epithelial (dendritic) ulcers as they can lead to a "Geographic ulcer." * **Recurrence:** HSV remains latent in the **Trigeminal Ganglion**.

Question 272: Megalocornea is not seen in which of the following conditions?

A. Marfan Syndrome
B. Congenital Rubella (Correct Answer)
C. Alport syndrome
D. Down's syndrome

Explanation: **Explanation:** **Megalocornea** is a non-progressive, bilateral condition characterized by an increased corneal diameter (typically >13 mm) at birth, in the absence of elevated intraocular pressure. **Why Congenital Rubella is the correct answer:** Congenital Rubella Syndrome (CRS) is classically associated with **Microcornea** (corneal diameter <10 mm) and **Microphthalmos**, rather than Megalocornea. While CRS can cause "Infantile Glaucoma" (which might lead to secondary corneal enlargement or *Buphthalmos*), the primary developmental anomaly associated with Rubella is a small cornea. **Analysis of Incorrect Options:** * **Marfan Syndrome:** This is a well-known systemic association of Megalocornea. Patients often present with large corneas, flat curvatures (*Cornea Plana*), and ectopia lentis. * **Alport Syndrome:** This hereditary nephritis is associated with several ocular features, including anterior lenticonus and Megalocornea. * **Down’s Syndrome (Trisomy 21):** While Keratoconus is the most common corneal association in Down’s syndrome, Megalocornea is also a documented clinical finding in these patients. **High-Yield Clinical Pearls for NEET-PG:** 1. **Megalocornea vs. Buphthalmos:** In Megalocornea, the intraocular pressure (IOP) is normal, the optic disc is healthy, and the cornea is clear. In Buphthalmos (Congenital Glaucoma), the cornea is large but associated with high IOP, Haab’s striae, and optic disc cupping. 2. **Inheritance:** Simple Megalocornea is most commonly **X-linked recessive** (90% of cases occur in males). 3. **Other Associations:** Megalocornea is also seen in **Osteogenesis Imperfecta**, **Ehlers-Danlos Syndrome**, and **Mucopolysaccharidosis**. 4. **Surgical Risk:** Patients with Megalocornea have a very deep anterior chamber, making them prone to lens subluxation and vitreous loss during cataract surgery.

Question 273: Munson's sign is seen in which of the following conditions?

A. Keratoconus (Correct Answer)
B. Keratoglobus
C. Microcornea
D. All of the above

Explanation: **Explanation:** **Munson’s sign** is a classic clinical feature of **Keratoconus**, a non-inflammatory, progressive thinning and cone-like protrusion of the cornea. It refers to the V-shaped indentation of the lower eyelid when the patient looks downward, caused by the protrusion of the conical cornea. **Why the correct answer is right:** In Keratoconus, the cornea undergoes paracentral thinning and ectasia. As the disease advances, the corneal apex becomes significantly pointed. When the patient attempts to look down, this "cone" pushes against the lower eyelid margin, creating the characteristic V-shaped notch known as Munson’s sign. This is typically a late-stage clinical finding. **Why the incorrect options are wrong:** * **Keratoglobus:** While this is also an ectatic dystrophy, the thinning is global and hemispherical rather than focal and conical. The cornea is globular, not pointed, so it does not typically produce the V-shaped indentation seen in Munson’s sign. * **Microcornea:** This refers to a cornea with a diameter of less than 10 mm. It is a structural size abnormality without ectasia or protrusion, thus Munson's sign is absent. **High-Yield Clinical Pearls for NEET-PG:** * **Other Signs of Keratoconus:** * **Fleischer’s Ring:** Iron deposition at the base of the cone (best seen with Cobalt blue filter). * **Vogt’s Striae:** Vertical stress lines in the deep stroma/Descemet’s membrane. * **Rizutti’s Sign:** Conical reflection on the nasal cornea when light is shone from the temporal side. * **Oil Droplet Sign:** Seen on distant direct ophthalmoscopy. * **Acute Hydrops:** Caused by a rupture in Descemet’s membrane, leading to sudden corneal edema. * **Management:** Early stages use spectacles/RGP lenses; **CXL (Corneal Collagen Cross-linking)** stops progression; advanced cases require Penetrating Keratoplasty (PK).

Question 274: Brown discoloration of the cornea is seen in which of the following conditions?

A. Siderosis
B. Mustard gas exposure
C. Chalcosis
D. All of the above (Correct Answer)

Explanation: **Explanation:** Brown discoloration of the cornea (keratopathy) occurs due to the deposition of metallic particles or chemical pigments within the corneal layers. 1. **Siderosis (Iron deposition):** When an intraocular iron-containing foreign body is retained, it undergoes oxidation. The resulting iron salts deposit in the corneal stroma and epithelial cells, leading to a characteristic **rusty-brown** discoloration. 2. **Mustard Gas Exposure:** Delayed keratitis is a known complication of mustard gas (sulfur mustard) exposure. It leads to a "marbled" appearance of the cornea with **brownish pigmentation**, often associated with vascularization and fatty degeneration. 3. **Chalcosis (Copper deposition):** While copper is classically associated with the "Sunflower cataract" and the "Kayser-Fleischer (KF) ring" (a golden-brown ring in Descemet’s membrane), heavy copper deposition can result in a generalized **greenish-brown** hue to the cornea. **Clinical Pearls for NEET-PG:** * **Kayser-Fleischer (KF) Ring:** A pathognomonic sign of **Wilson’s Disease** (Hepatolenticular degeneration). It is a golden-brown/greenish deposit of copper in the **Descemet’s membrane**, starting at the 12 and 6 o'clock positions. * **Hudson-Stahli Line:** A horizontal brown line of **iron deposition** seen at the junction of the upper 2/3 and lower 1/3 of the cornea (physiologic aging). * **Flecked/Vortex Keratopathy (Cornea Verticillata):** Golden-brown whorl-like deposits in the basal epithelium, seen in **Fabry’s disease** or chronic **Amiodarone/Chloroquine** use. * **Stocker’s Line:** Iron line seen at the head of a **Pterygium**. * **Ferry’s Line:** Iron line seen at the edge of a **Filtering Bleb**.

Question 275: Ionic exchange in the corneal endothelium depends upon the metabolic rate. Which of the following can block ionic exchange in corneal endothelium?

A. Inhibition of anaerobic glycolysis
B. Activation of anaerobic glycolysis (Correct Answer)
C. Activation of cAMP phosphodiesterase inhibitors
D. Interference with electron chain transport

Explanation: **Explanation:** The corneal endothelium is responsible for maintaining **corneal deturgescence** (state of relative dehydration) through an active metabolic pump mechanism. This pump primarily relies on **Na+/K+ ATPase**, which is an energy-dependent process. **Why Option B is Correct:** The corneal endothelium derives its energy (ATP) almost exclusively from **aerobic metabolism** (the Krebs cycle and Electron Transport Chain). While the corneal epithelium can tolerate anaerobic conditions, the endothelium is highly sensitive to oxygen deprivation. **Activation of anaerobic glycolysis** signifies a shift away from efficient aerobic respiration. This leads to a significant drop in ATP production and an accumulation of lactic acid. Insufficient ATP causes the failure of the Na+/K+ ATPase pump, leading to an influx of water into the corneal stroma (corneal edema) and a breakdown of ionic exchange. **Analysis of Incorrect Options:** * **A & D:** Inhibition of anaerobic glycolysis (A) or interference with the electron transport chain (D) would technically decrease energy, but the question specifically targets the metabolic shift. In clinical scenarios (like contact lens overwear), it is the *shift* to anaerobic pathways and subsequent lactic acidosis that disrupts the endothelial pump. * **C:** cAMP phosphodiesterase inhibitors (like caffeine or theophylline) actually *increase* intracellular cAMP levels. In the corneal endothelium, increased cAMP is known to **stimulate** the pump function and improve the barrier effect, rather than blocking it. **High-Yield Pearls for NEET-PG:** * **Endothelial Cell Count:** Normal is 2500–3000 cells/mm². Functional failure occurs when the count falls below **500 cells/mm²**. * **Pump-Leak Hypothesis:** Corneal hydration is a balance between the "leak" (passive entry of water from the aqueous) and the "pump" (active transport out by the endothelium). * **Pachymetry:** The gold standard for measuring corneal thickness; a thickening cornea is the first clinical sign of endothelial pump failure.

Question 276: Kayser-Fleischer ring is pathognomonic of:

A. Keratoconus
B. Wilson's disease (Correct Answer)
C. Lowe's syndrome
D. All of the above

Explanation: **Explanation:** The **Kayser-Fleischer (KF) ring** is a hallmark clinical sign of **Wilson’s disease** (Hepatolenticular degeneration). It is caused by the deposition of **copper** in the **Descemet’s membrane** of the cornea. **1. Why Wilson’s Disease is Correct:** Wilson’s disease is an autosomal recessive disorder involving a mutation in the *ATP7B* gene, leading to impaired biliary copper excretion. Excess copper accumulates in the liver, brain, and eyes. In the eye, copper ions deposit in the periphery of the Descemet’s membrane, appearing as a golden-brown, ruby-red, or greenish ring. It typically starts superiorly, then inferiorly, and eventually becomes circumferential. It is present in nearly 95% of patients with neurological involvement. **2. Why Other Options are Incorrect:** * **Keratoconus:** This condition is characterized by progressive thinning and cone-like protrusion of the cornea. The characteristic pigment sign here is the **Fleischer ring** (iron deposition at the base of the cone), which is often confused with the KF ring. * **Lowe’s Syndrome (Oculocerebrorenal syndrome):** This is an X-linked disorder characterized by congenital cataracts, glaucoma, and renal tubular dysfunction. It does not feature copper deposition or KF rings. **Clinical Pearls for NEET-PG:** * **Examination:** Best visualized using a **Slit-lamp examination**; it may be invisible to the naked eye in early stages. * **Reversibility:** The KF ring disappears with successful chelation therapy (e.g., D-Penicillamine). * **Sunflower Cataract:** Another ocular feature of Wilson’s disease involving copper deposition in the anterior lens capsule. * **Differential Diagnosis:** Similar rings can rarely be seen in primary biliary cholangitis or chronic cholestasis, but the term "pathognomonic" in exams traditionally links it to Wilson’s.

Question 277: Neurotrophic keratopathy is caused by damage to which nerve?

A. Facial nerve (Cranial nerve VII)
B. Trigeminal nerve (Cranial nerve V) (Correct Answer)
C. Both trigeminal and facial nerves
D. Trochlear nerve (Cranial nerve IV)

Explanation: **Explanation:** **Neurotrophic Keratopathy (NK)** is a degenerative corneal disease caused by an impairment of corneal innervation. The correct answer is the **Trigeminal nerve (CN V)**, specifically its **Ophthalmic division (V1)** via the long ciliary nerves. The underlying medical concept is that sensory nerves do more than just transmit pain; they provide **trophic support** to the corneal epithelium. They release neuropeptides (like Substance P and Nerve Growth Factor) that are essential for epithelial cell turnover, wound healing, and maintaining the tear film reflex. When CN V is damaged, the cornea becomes anesthetic, leading to epithelial breakdown, poor healing, and eventually painless corneal ulcers. **Analysis of Incorrect Options:** * **Facial nerve (CN VII):** Damage to this nerve causes **Exposure Keratopathy** due to lagophthalmos (inability to close the eyelid). While it affects corneal health, it is a mechanical/exposure issue, not a neurotrophic one. * **Trochlear nerve (CN IV):** This is a motor nerve supplying the Superior Oblique muscle. Damage results in diplopia (double vision), not corneal pathology. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Cause:** Herpes Simplex (HSV) or Herpes Zoster Ophthalmicus (HZO) infections. Other causes include acoustic neuroma (damaging the CN V ganglion) and diabetes. * **Hallmark Sign:** A **painless** corneal ulcer with "rolled-up" epithelial edges. * **Staging:** Uses the **Mackie Classification** (Stage 1: Epithelial irregularity; Stage 2: Persistent epithelial defect; Stage 3: Corneal ulcer/perforation). * **Treatment Tip:** Avoid preservatives; use lubricants. Severe cases may require **Tarsorrhaphy** or the newer recombinant human nerve growth factor (**Cenegermin**).

Question 278: Which organism can penetrate a normal cornea?

A. Mycobacterium tuberculosis
B. Neisseria gonorrhoeae (Correct Answer)
C. Neisseria meningitidis
D. Mycobacterium leprae

Explanation: **Explanation:** The corneal epithelium acts as a formidable mechanical barrier against most pathogens. Most bacteria require a pre-existing epithelial defect (trauma or ulceration) to cause infection. However, a select group of organisms possesses specific virulence factors (proteolytic enzymes) that allow them to invade an **intact/normal corneal epithelium**. **Why Neisseria gonorrhoeae is correct:** *Neisseria gonorrhoeae* is the classic example of an organism that can penetrate a healthy cornea. It produces potent proteases that degrade the epithelial cell junctions. In neonates (Ophthalmia neonatorum) or sexually active adults, it can cause hyperacute purulent conjunctivitis which, if untreated, leads to rapid corneal perforation. **Analysis of Incorrect Options:** * **Neisseria meningitidis:** While it is also capable of penetrating an intact cornea (along with *Corynebacterium diphtheriae*, *Listeria*, and *Haemophilus aegyptius*), *N. gonorrhoeae* is the more frequently tested and clinically significant cause in this context. * **Mycobacterium tuberculosis & Mycobacterium leprae:** These are acid-fast bacilli that typically involve the cornea through secondary immune-mediated responses (interstitial keratitis) or chronic granulomatous spread, rather than direct acute penetration of a healthy epithelium. **High-Yield NEET-PG Pearls:** * **Mnemonic for organisms penetrating intact cornea:** "**CHNL**" (**C**orynebacterium diphtheriae, **H**aemophilus aegyptius, **N**eisseria gonorrhoeae/meningitidis, **L**isteria monocytogenes). Some also include *Shigella*. * **Clinical Presentation:** *N. gonorrhoeae* causes "Hyperacute Conjunctivitis" characterized by massive chemosis and profuse purulent discharge ("Pus-producing"). * **Management:** Systemic Ceftriaxone is mandatory because of the risk of rapid corneal melting and perforation.

Question 279: Giant dendritic ulceration on the cornea is typically seen in which of the following conditions?

A. Fungal infection
B. Chlamydial infection
C. Herpes Simplex Virus (HSV) infection (Correct Answer)
D. Pneumococcal infection

Explanation: **Explanation:** The correct answer is **Herpes Simplex Virus (HSV) infection**. **1. Why HSV is correct:** The hallmark of **Herpes Simplex Keratitis (HSK)** is the formation of a **dendritic ulcer**. This occurs due to the active replication of the virus in the corneal epithelium, leading to cell death in a linear, branching pattern. These ulcers have characteristic **terminal bulbs** (knob-like ends) and stain brilliantly with **Fluorescein** (the floor of the ulcer) and **Rose Bengal** (the devitalized margins). If left untreated or if topical steroids are inappropriately used, these dendrites can enlarge to form a **Geographic (Giant) ulcer**. **2. Why other options are incorrect:** * **Fungal infection:** Typically presents with a "dry" looking infiltrate, **feathery margins**, and **satellite lesions**. It does not form branching dendritic patterns. * **Chlamydial infection:** Usually presents as chronic follicular conjunctivitis or **Trachoma**, characterized by Arlt’s line, Herbert’s pits, and pannus, rather than epithelial ulceration. * **Pneumococcal infection:** *S. pneumoniae* is a common cause of **Hypopyon corneal ulcers** (Ulcus Serpens). It typically causes a deep, purulent, rapidly progressing oval ulcer with a shaggy base, not a dendritic pattern. **Clinical Pearls for NEET-PG:** * **Dendritic ulcer with terminal bulbs:** Pathognomonic for HSV. * **Pseudodendrite:** Seen in **Acanthamoeba keratitis** and **Herpes Zoster Ophthalmicus (HZO)**. Unlike HSV, these lack terminal bulbs and are slightly elevated. * **Corneal Sensations:** Characteristically **decreased or absent** in HSV keratitis (tested using a wisp of cotton). * **Treatment:** Topical **Acyclovir (3%)** or Ganciclovir gel. **Topical steroids are strictly contraindicated** in epithelial (dendritic) disease as they can trigger a geographic ulcer.

Question 280: Munson sign is seen in:

A. Corneal dystrophy
B. Perforated corneal ulcer
C. Keratoconus (Correct Answer)
D. Marfan syndrome

Explanation: **Explanation:** **Munson sign** is a classic clinical finding in advanced **Keratoconus**. It refers to the V-shaped bulging or indentation of the lower eyelid when the patient looks downward. This occurs because the progressive thinning and ectasia of the central cornea cause it to assume a conical shape; this cone physically displaces the lower lid margin during downgaze. **Analysis of Options:** * **A. Corneal dystrophy:** These are typically bilateral, genetic, non-inflammatory opacifications (e.g., Fuchs’ or Lattice dystrophy). While they affect corneal clarity, they do not cause the structural "coning" required to produce Munson sign. * **B. Perforated corneal ulcer:** This is an ocular emergency characterized by a full-thickness defect and often a flat anterior chamber. While the cornea is deformed, it is due to tissue loss and hypotony, not the progressive ectasia seen in Munson sign. * **C. Keratoconus (Correct):** The hallmark of this condition is progressive non-inflammatory thinning of the corneal stroma, leading to a cone-like protrusion and irregular astigmatism. * **D. Marfan syndrome:** While Marfan syndrome is associated with ocular issues like *Ectopia lentis* (superior-temporal subluxation) and flat corneas (*Cornea plana*), it is not a primary cause of Munson sign. **High-Yield Clinical Pearls for Keratoconus:** * **Fleischer’s ring:** Iron deposition at the base of the cone (best seen with cobalt blue filter). * **Vogt’s striae:** Vertical stress lines in the deep stroma/Descemet’s membrane. * **Rizutti’s sign:** A conical reflection on the nasal cornea when light is shone from the temporal side. * **Hydrops:** Acute corneal edema due to a rupture in Descemet’s membrane. * **Management:** Rigid Gas Permeable (RGP) lenses for vision; Collagen Cross-linking (CXL) to stop progression; Keratoplasty for advanced cases.

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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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