CL Sequencing Physiology Flashcards
Why are central K readings misleading indicators of overall corneal topography?
Because cornea should be spherical which is not the case.
It tells you central is 4mm only, nothing about spherical
- Is the cornea symmetrical?
2. The curvature flattens towards which part of the cornea?
- Not symmetrical
2. Periphery
What is the normal HVID?
~12mm
What are the 4 topographic zones?
- Central (4mm spherical)
- Paracentral (~ diameter of scotopic pupil)
- Peripheral (flattest and aspheric)
- Limbal
Cornea provides how much refractive power of the eye?
2/3
Why is cornea curved, transparent with clear optics?
It all thanks to cellular organisation and the air TF interface
Slight irregularities can be compensated by?
Overlying TF
What allows cornea to withstand shear forces of blinking, EM, microbial infection and FB?
- cell specialisation
- cell turnover
- tight junctions
- surface glycocalyx
- TF
How many layers does cornea have? What are they?
5 layers!
- Epithelium
- BOwman’s layer
- Stroma
- Descemet’s membrane
- Endothelium
How many cells does epithelium have? What are they?
3 cell types!
- Basal cells
- Wing cells
- Squamous cells
Microplicae and microvilli on the epithelium surface play a role in TF by doing what?
Anchoring the mucus layer (glycocalyx)
How long is cell shedding and turnover (basal to the surface) without CL wear?
~7 days
Does epithelium negatively or positively impacted by CL wear?
NEGATIVE!
Epithelium is a permeability barrier to what?
Adjacent cells are connected by what?
- water
- ions
- most hydrophilic molecules (eg. fluorescein)
- infective pathogens through tight junctions (desmosomes)
- Aquaporins (water channels)
- Gap junctions (ion transport)
In the stroma, how do intermediate filaments in the cytoskeleton are linked through?
Linked through the hemidesmosomes via anchoring fibrils to anchoring plaques
CL wear can reduce the epithelial barrier function related to what?
- Hypoxia dose
2. Overnight wear
How thick is the stroma and it is how many % of the cornea?
Thickness: 0.50mm thick/ 500 microns
It is 90% of the cornea
What does stroma contain?
2-3% keratocytes (fibroblasts) and 1% ground substance (GAGs) interspersed between lamellae
What are keratocytes in the stoma?
They are:
- thin
- flat cells
- tight junctions
- 10 microns in diameter with long processes
What are GAGs in the stroma?
They are:
- proteoglycans
- poly-ionic
- induce water retention
- influence fibril arrangement
What are stromal Lamellae?
A regular arrangement of collagen fibrils within each lamellae provides optical clarity
What happens when there’s infection and/or irritation in stromal lamellae?
Leads to epithelial cells will release cytokines and chemokines to begin immune defence
What kinds of WBC will go to the infected site in stromal lamellae?
- Limbal vasodilation
- Keratocyte migrate
- Interferon
- Neutrophils
- Natural Killer cells
- Macrophages
What happens when there’s corneal insult in stromal lamellae?
Leads to:
- Disorganised spacing
- Oedema (Striae)
- Tissue loss (ulcer)
- Clarity loss (infiltrate + scarring)
What is the corneal endothelium?
Do endothelial cells lost with age?
A mono-layer of squamous cells 500,000 cells at birth (4,500 cells/mm2)
Yes, it loses with age
What does corneal endothelium have/do?
- Inter-locking irregular edges, tight junctions, lots of organelles, metabolic activity
- allows passage of ions and small molecules
- Maintains osmotic gradient by metabolically driven pumping ions out of the stroma into the aqueous
Endothelium function
- Pumping function: maintains 78% corneal hydration for optimal transparency & normal thickness
- Minimal endo cell count: 1000 cells/mm2 - needed to maintain this state
In endothelium:
Age, pathology, trauma, oxygen deficiency (hypoxia) can lead to?
- loss of pumping ability
- corneal oedema
- corneal striae
- polymegethism (size)
- polymorphism (shape)
of the cells
What does innervation do?
- There’s 50-80 myelinated and unmyelinated precorneal nerve trunks -> enters mid stroma -> lose myelin at the cornea and branch anterior centrally
- Dense subepithelial plexus, unsheathed nerve endings enter the epithelium and branch out among basal cells
- Richly innervation, initiates blink reflex, wound healing (trophic role), and tear secretion
What is the transition zone between cornea and conjunctiva/sclera?
1.5mm Horizontal
2mm Vertical
- Surgical reference point and significant change between steeper corneal curvature and flatter sclera
Why do you need to respect the limbus?
Because it has a:
- minor role in corneal nutrition
- Important role for defence
- location of limbal stem cells
So… need to avoid CL touch, interaction or pressure on this area
Terminal arteries of limbus have distinctive looping, so what do you have to look out for?
- Engorgement
- NVZ
with CL wear
What does the cornea need to maintain tissue health and control hydration?
These nutrients are supplied by what?
- Oxygen
- Glucose
- Vitamins
- Amino acids
- Other metabolites
These nutrients are supplied by (oxygen supply):
- Peri-limbal vasculature - 55mmHg O2 tension
- TF - 155mmHg O2 tension
- Aqueous humour - 30-40mmHg O2 tension
- Palpebral vasculature - 55mmHg O2 tension
How much is corneal influx on average?
6microlitres/cm2/hr
If you wear CL, it reduces or increases oxygen availability to the cornea?
REDUCES
What permits corneal flux through the CL?
CL oxygen permeability (Dk)
What is Dk?
What is Dk/t?
Dk: measures oxygen permeability of CL
- means: how much oxygen is passing through the material under certain given conditions
Dk/t: measures oxygen transmissibility of CL
- Dk/t calculated using Dk of CL material and thickness. Usually refers to a CL with certain power
** Higher these values, better Dk/t of the material. Higher oxygen flow to the cornea and can improve comfort and longer-term tolerance
- Dk/t is dependent on CL thickness
- Local Dk/t is important. There’s a significant impact on central and peripheral CL thickness, especially for higher powers
What happens to the cornea when we sleep?
5% overnight oedema (increase in corneal thickness) in NORMAL eyes is observed WITHOUT CL wear
What happens when there’s a 5% increase in corneal hydration?
Leads to light scatter
- increase water uptake of GAGs between fibrils causes fibre aggregation
–> seen as striae after overnight eye closure even w/o CL wear
But return to normal/ baseline within 1 hour of waking
Think about the impact of CL EW, or even long-day wear of low Dk/t CL on the diffusion of CO2 and O2
We all know eye closure + CL wear will reduce oxygen tension.
So, low O2 tension leads to?
Build up of:
- Lactic Acidosis
- Increased osmotic load
- increase water intake into cornea
- –> OEDEMA!
** Long term –> tissue change
What are the signs you can see/ complications from CL?
What are they and what causes them?
- Corneal NVZ
What are they?
Causes:
- Epithelial Microcysts
What are they?
Causes:
- Corneal Striae What are they?
Causes:
- Endothelial polymegethism
What are they?
Causes:
- Endothelial Blebs
What are they?
Causes:
What has a significant impact on TF flow and CL fitting, movement, insertion, and removal?
- Lid action
- Aperture Size
- Gravity
What is a TF?
Tears:
- a complex, structured, surface film secreted by lacrimal and accessory glands
- which protects and nourishes the OS and provide goof optical front surface
What are the roles of the TF?
- Optical:
- TF maintains an optically uniform interface between the air and anterior surface of CL - Mechanical:
- TF acts as a vehicle for the continual blink-mediated removal of intrinsic and extrinsic debris and particulate matter from the front and underneath the CL - Lubricant:
- TF ensures a smooth movement of eyelids over the front surface of the CL, and CL over the globe, during blinking - Bactericidal:
- TF contains defence mechanisms in the form of proteins, antibodies, phagocytotic cells, and other immunodefence mechanisms that prevent CL-induced infections. - Nutritional:
- TF supplies epithelium with necessary supplies of oxygen, glucose, AA, and vitamins underneath CL via lid-lens tear pump - Waste Removal:
- TF acts as intermediate reservoir for removal of corneal metabolic byproducts (CO2, lactate) from underneath the CL via lid-lens tear pump.
TF vs CL thickness
And what are the things you should consider?
5 microns vs 100 microns
*CL are highly disruptive to the TF structure
Consider:
- Impact of lens edge design and movement
- Pre-lens TF - especially the lipid layer
- Post-lens TF - tear exchange, aqueous, and mucins
CL-associated keratitis can result from many mechanisms like what?
- Infection
- Toxic solutions
- Bacterial endotoxicity
- Immunological rxn
- Trauma
- Hypoxia
- Metabolic Disturbance
Other aetiological factors:
- Breakdown of trapped post-lens TF debris
- Lens deposits
- Poor px hygiene
What does the chemical messages in the immune cascade lead to?
- Redness
2, Recruit inflammatory cells (WBC)
into the cornea
Why do we avoid CL edge touch with the limbal area?
Don’t want lens edge to interact with area bcoz can induce NVZ
(The vessels can grow into the cornea and can leak to the stroma)
What are the 4 clinical signs associated with corneal hypoxia?
How is corneal thickness impacted by CL wear?
- Epithelial blebs
- Stroma oedema
- Polymegethism
- Corneal striae
- NVZ ingrowth BV in cornea
What are the key influences of the eyelid on CL fit?
Rotational force on CL
Push CL down and back
What impact does CL wear have on the corneal TF?
Highly disruptive TF, consider pre and post-lens TF, the impact of lens edge design and movement?
What are the functions and composition of the TF?
Lipid, aqueous and mucin
- Each of them can affect CL position, deposition differently
What is the immune response to corneal insult?
Breakdown of the post-lens TF debris, deposits in lens and poor px hygiene –> can cause redness, inflammatory cells into cornea
