Eye Pathology II - Cornea Flashcards
Normal cornea of eye
Cornea fundamental concepts (3)
- The cornea begins its life as skin + wants to return to being skin
- When subjected to injury, cornea has two responses:
- Acute + severe injury -> ulceration
- Mild + chronic injury -> cutaneous metaplasia - permits cornea to adapt + becomes histologically + functionally more skin-like = more resistant to injury
- There is no such thing as primary keratitis - due to cornea having no resident blood vessels/leucocytes - can’t undergo true inflammation
- Ulcerative keratitis truly means corneal ulceration -> infection taking advantage of loss of epithelial barrier across the eye
Corneal ulcer
Corneal oedema - segmented oedema due to endothelial degeneration, hazy blue-white material
What are the ways in which the corneal endothelium is damaged? (4)
What are the causes of corneal oedema? (4)
What are the different corneal opacities and how are they interpreted? (4)
Process of corneal ulceration - phases of epithelial injury (superficial epithelial wounds) (Slides 10-14) (4)
- Latent phase
- Apoptosis of cells damaged by wound stimulus
- Increased metabolic activity + cell structural changes
- Fibronectin polymerases onto wound bed - provisional anchoring of ECM
- Reduction in adhesion of basal cells to BM
- Migration phase
- Apoptosis of cells damaged by wound stimulus
- Migration of entire epithelial sheet over the wound bed
- Leading edge cells flatten out over wound area + develop filopodia (slender cytoplasmic projections that extend beyond the leading edge of lamellipodia in migrating cells) to move across
- No cell division at this stage
- Proliferation phase
- Cells at periphery of cornea undergo mitotic division while wound bed is migrated over
- Transformation of basal cells into the layers of stratified epithelium (normal corneal epithelium) and eventually squamous cells
- BM remodelling
- Attachement phase
- New hemidesmosome attachments formed - can take up to a year to form a complete new attachment
Process of corneal stomal wounding (deeper wounds) (6)
- Heals by fibrosis + granulation - transformation of keratocytes within stromal collagen -> fibroblasts, swelling of stroma + invasion of inflammatory cells recruited by conjunctiva vessels to site of injury
- Inflammatory cells = good, will protect against infection, bad = can contribute to tissue damage w/ types of cytokines produced
- Keratocytes (stromal cells) near wound apoptose
- Peripheral keratocytes differentiate into motile fibroblasts that repopulate the wounded area - migrate to wound
- Fibroblasts differentiate into myofibroblasts that close the wound
- Adherent myofibroblasts persist - no. keratocytes dec as wound heals, contracts + opacify -> corneal scar (takes weeks to years)
What is keratomalacia - how is it caused? (6)
- Bacterial or fungal infection (opportunistic) - pseudomonas strep, staph + fungi
- Inflammatory cells from tear film - cornea (sterile ulcers) - liquefy corneal stroma
- Proteinases and collagenases produced by bacteria and leucocytes by inflammatory cells
- Leads to keratomalacia ‘melting ulcer’ = deep ulceration + loss of stroma
- May be direct result of the severity of initial injury, more often result of neutrophil-mediated stromal lysis that was initially or later became septic
- Rapid time scale + can lead to globe rupture + require intevention
Melting ulcer
What are the clinical signs of corneal ulceration? (4)