The Opaque Eye 1 Flashcards
Layers of the corneal epithelium
- Basal Cells
- Stems cells at the limbus (should persist forever) -> TransientAmplifyingCells capable of mitosis -> Basal cells -> differentiate to other layers - Wing cells
- no longer mitotic
- 2-4 layers - Squamous, non-keratinised epithelium
- slough off with blinking (weekly)
- replenished from below
What is necessary for permenant adhesions and healing to form?
- Basal lamina
What 2 ways does epithelium heal? How does new epithelium move? What effects may this have?
> sliding
- with abrasion of superficial epithelial lesion that does not reach basal lamina
- ~ 1mm/day
- dependant on corneal health (eg. KCS) limbal basal stem cell population, basal lamina, species and age.
- limbal stem cells act as barrier to conjunctival overgrowth and conjunctivalization
vertical movement
- first epithelial sliding then basal cell mitosis
- takes 1 week/cycle
- regains thickness
centripetal movement from limbus -> center, every layer moves like this
- happens more quickly if basal lamina present
- chronic corneal disease or irritation may drag pigment in from limbus -> blindness
- esp pugs and GSDs (pigmented limbus)
When may superficial pigment deposition occour?
- theory: irritants activate melanin production
- at limbus and paralimbal conjunctiva
- pigment deposited in new migrating epithelial cells -> central migration and in superficial stroma
- can be severe esp in pugs
Is the cornea vascular?
NO not if healthy (exception: manitees, rocky mountain goat)
- with epithelial wound healing neovascularisation can occour
- inflammation stimulus
- vessels can coalesce -> granulation tissue
- atrophy over time once stimuls removed
> VASCULARISATION IS A MARKER OF CHRONICITY
- Budding takes 2-4d
+ 1mm/2days
How may vascularisation of the cornea assist healing and your dx?
- superficial or deep (stromal)
- highlights area of damage
- stabilizing serum (ANTI - MMP and serum proteases, which unopposed can -> corneal melting [produced by bacteria, neutrophils and other cells])
- neutrients, growth factors, inflame cells
- structural support
What is the stroma made up of?
> collagen lamellae
- type 1 collagen fibrils (+ others)
- fibrils travel limbus to limbus
- united and ordered by GAGs (chondriotan, dermatan sulphate)
- dehydration/deturgenscence
- transparency
keratocytes
- relatively inactive fibrocytes
- low numbers for transparency
- contribute to lamellar creation and maintainance
- differentiate into fibroblasts and myofibroblasts (myofibrocytes with pseudopodia and a-sm-actin for cell movement)
chemical factors
- IL-1, EDGF, EGF, TNFa, TGFb, collagenases, metaloproteases etc.
- produced by corneal nn. and other cells (lacrimal glands, epithelium, keratocytes, leucocytes, BACTERA)
Which cells are involved in stromal healing? What is required for proper healing?
> cellular attraction - destruction and clean up
- monocytes and macrophages, neutrophils and leucocytes
keratocyte-mediated build up
- collagen fibrils
- ECM GAGs
- initially GAGs incorrect type and haphazardly laid down -> scar
BALANCE between these required for controlled healing
How quickly does stromal regeneration occour cf. epithelial? What stage follows reconstruction?
Slower
- remodelling follows reconstruction
- all transparency will eventually be regained (mostly)
- cats better at remodelling than dogs.
What is the first GAG to form?
Hyaluronic acid
- then others increase [] with time
What may occour during stromal regeneration?
Epithelium tries to ‘help’
- epithelial hyperplasia -> facet formation (flat edges to cornea)
- may remain for life
How is the endothelium layer arranged? Properties?
- one cell thick
- honeycomb appearance hexagonal cells
- v. sensitive (lens luxation touching endothelium -> destruction)
- NON REGENERATIVE
- actively pumps water out of cornea
- preserves fibre alignment and helps transparency
- strong intercellular junctions (as in epithelium) = natural barrier between cells
How can the endothelium repair? What can occour is this capacity is surpassed?
- Not regenerative
- 50% cells lost in adulthood
- cells grow when neighbouring cells die (polimegathism)
- lose hexagonal shape (pleo/policorphism)
- ^ no NaK pumps
- POINT OF DECOMPENSATION*
- > corneal oedema will occour after this point
- point of decomp varies 800-500c/mm2 in dogs
Causes of endothelial damage
- glaucoma, uveitis
- anterior lens luxation (contact w/ anterior lens belly)
- firect damage intraoperatively (instruments)
- chemical damge (injected into eye)
> PRIMARY endothelial degeneration (blisters of fluid in cornea, ulceration, common in ‘hunting breeds’ but not v common overall)
What 2 factors influence self repair?
- superficial v deep
- does the tissue know its ulceratied?
- cell cell communication
- corneal sensation (desensitisation, brachycephalic factor)
> affects keratocyte activation and production of tissue factors
How quickly does re-epithelialisation and stromal reconstruction occour?
> re-epithelialisation fast providing stroma is healthy
- re-anchoring to secrure the epithelium takes MONTHS
stromal regeneration starts immediately but takes longer to complete
- if unstable can -> melting (collagenolysis) d/t chronic inflame/irritation or 2* infection
- once melting starts, v hard to control
How soon after being presented with a superficial ulcer should you re-see an animal?
~3d - expect 3mm decrease in size
- if no improvement or worse, what is causing the imblanace?
What are the most common causes of non-healing ulcers?
2* > tear film problem (quantitative or qualitative) > eyelids, TE > repair process (brachycephalic factor, 2* infection, melting) 1* [VERY RARE] > SCCEDs > calcium deposits > FHV-1: 1* infection -> ulcerative dz
What 2 main thoughts should cross your mind if ulcer is taking too long to heal?
- what caused the ulcer in the 1st place - what am I missing?
- changing topical antibiotics is not the answer!!
oUTLINE DIAGNOSTIC TESTS USEFUL FOR CORNEAL ULCERATIVE DISEASE
- STT1
- eyelid exam
- eyelid function/structure
- cytology? (often not helpful, but can distinguish rods v cones)
- additional factors ( brachycephalic etc.)
What medical tx options are available?
- protect from self trauma (collar, tarsorrhaphy horizontal mattress suture with stents, TE flap [but not that great - no benefit over bandage lens and tarsorrhaphy, damages conjunctiva, prevents exit of debris and evaluatin of eye])
- Abx for PREVENTION
- atropine for comfort (mydirasis, relaxation of CB [cicloplegia] NB. will dry eye)
- ciclosporin (does not interfere with stromal/epithelial healing like steroids)
X Steroids X NOOOOO!!! also most NSAIDs no. - enhance collagenolsis, slow healing
Which abx are used in the eye?
> Fusidic acid gel for G+s BID
chloramphenicol eyedrops for G+, good penetration, TID
aminoglycosides (gentamycin and tobramycin TID) pseudomonas may be resistant and delay epithelial healing
Fluoroquinolones (exocin and ciloxin) good penetration for G+s
- big guns?? think resistance - really necessary?
- may interfere with healing
How may melting be prevented (or decreased slightly, but rarely ‘treated’)?
- serum eyedrops (antiproteases for serin proteases and MMP)
- frequent application TID/QID
- supports epithelial healing
What medical treatment can provide comfort in ulcerated eyes?
> mydriatic-clycloplegic, long acting: atropine
- BID for ~2d smallies, longer horses
- temporary dryness and gut stasis in horses
mydriatic but POOR cycloplegic, short acting: Tropicamide (midriacyl)
long term preservative free viscous tears
How quickly can a melting ulcer destroy the cornea? Exceptions?
A week - do not wait longer than 3-5d to see
- rare excpetion = SCCEDs.
What type of ulcer must be referred and assessed for surgery?
- > 50% depth ‘pot-hole’ look
general tx rules - what is healing aided by?
- stabilisaing serum
- granulation tissue bed
- but healing does not depend on it - ULCER DEEPENING IS FASTER
