Dry eye disease Flashcards
what is dry eye disease
dry eye is a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film , and accompanied by ocular symptoms in which tear film instability , hyperosmatlorty, ocular surface inflammation and damage and neurosensory abnormalities play etiological roles
what are the two types of dry eye disease
evaporative dry eye (dysfunction of lipid layer)
aqueous deficient dry eye - aqueous dysfunction
how does covid 19 affect dry eye
covid 19 and therefore increased green time and online learning were associated with worsening pre-existing ocular surface diseases
what is evaporative dry eye due to
typically due to some type of meibomian gland dysfunction
what are causes of evaporative dry eye
anterior blepharitis
contact lens wear
seborrheic dermatitis
allergic eye disease
psoriasis
what are causes of aqueous deficiency dry eye
typically due to reduced lacrimal secretion
causes include
Sjogren syndrome dry eye systemic - autoimmune disease
rheumatoid arthiritis
systemic lupus erythematosus
stevens johnson syndrome /TEN
trigeminal nerve in jury
refractive surgery
how is tear hyperosmolarity related to dry eye disease
tear hyperosmalirty and tear film instability are the core drivers of dry eye disease
regardless of how its initiated patients end up in a vicious cycle where tear hyperosmolarity occurs which causes inflammatory proteins to activate and recruit other inflammatory mediators to affect the Hglycocalayx and cause epithelial cell apoptosis and goblet cells
the loss of glycolaxyl musician (exists between mucin and corneal layer) joins tear film and cornea probably ACCOUNTS FOR SOME OF THE CORNEAL STAINING WE SEE AND LEADS TO REDUCE CORENAL WETTING WHICH contributes to reduced tear break up time (uchino 2018)
how does tear film become damaged
a normal tear film consists of a lipid layer and aqueous layer in this order from the ocular surface
in dry eye the tear film is collapsed sometimes with decreased expression of membrane muffins in epithelial cells and disordered or lost epithelial cells
how to differentiate between evaporation dry eye and aqueous dry eye disease
to differentiate between the two causes history will need to be taken and a careful examination of the lids on slit lamp
aqueous dry eye disease tends to be worse during the day whereas evaporation dry eye is worse on waking
however there is often little correlation. between signs and symptoms
the usual symptoms of dry eye disease include ocular discomfort (gritty eyes) light sensitivity and epiphora
what is the first line of treatment for dry eye disease
first line of treatment is non pharmacological and is aimed at identifying any modifiable lifestyle factors
the aim of treatment should be to re - establish and maintain the ocular surface homeostasis that has been damaged by the vicious circle outline previously
what are signs of dry eye disease
reduced tear film break up time (without fluroscein is preferred)
schemers test (a test of the production od tears)
tear osmolarity not usually done in the nos clinic but is the most reliable indicator of dry eye disease
values greater than 308mOsm/litre (milie - osmole - is a measure of saltiness per litre are Indicative of dry eye disease as are asymmetries between the values od the two eyes
examination of the corneal epithelium using stains/dyes e.g. flurocein and lissamine green (staining goblet cells in the conjuctiva)
how are artificial tear preparations used
they are available but there is a wide variation of options and not all options are available at all local formularies
reviews have found that no single preparation is more effective than others
hyaluronic acid has been shown to be effective in a range of patients and across a range of severities. Optimal drop concentration = between 0.1 and 0.4% and optimal drop frequency is still lacking evidence
what are the types of artificial tears
hypromellose
carbomers
hydroxythycellulose
polyvinyl alchol
sodium hyaluronate (hylaruynoic acid)
carmellose
trehalose
what is the next line of treatment if artificial tears are not responsive
if disease severity is unresponsive got artificial tear supplements than further treatment options include a course of steroids to reduce the corneal inflammation and try and stop the vicious circle
further options include the use of cicilosporin eye drops or analogous serum eye drops but these need referral to the doctors
in cases of ADDE punctual plugs can be used to try and increase the tear reservoir
what structures are involved in the production of normal tear film
lacrimal gland is located underneath the eyebrow (innervated by the facial nerve which is the seventh nerve , tears are also produced by the meibomian gland
is the lacrimal gland under parasympathetic or sympathetic innervation
parasympathetic ally innervated
lacrimal gland involved primarily in the production of reflex tears
where is the meibomian gland located
located in the upper and lower lids
what do meibomian glands produce
they produce meiobom
prevents tear evaporation tear evaporation can cause dry spots on the cornea
in what other glands are the lipid layer produced in
- the glands of ziess and moll
where is the aqueous layer of tear film produced
the glands of Krauser and wolfring and are located in the tarsal plate
these are acessory glands and they are producing normal levels of aqueous
where is the mucin layer produced
goblet cells of the conjuctiva
mucin is composed of heavy weight molecules called glycoproteins
what is the role of mucin layer
increases wet ability of the tear film
if there was no mucin there would just be aqueous next to the cornea and it would not be dispersed out across the corneal surface - so the mucin layer is essential for a normal tear film
how are the structures that are responsible for the different tear film components neurally regulated
neural regulation is ongoing
there are neurosensory mechanisms that are undergoing constantly from the cornea and conjuctiva that influence the production of mucin , lipid and aqueous , constantly regulated and controlled , when the regulation and feedback breaks down and the glands become diseased/dirsupted gives rise to dry eye disease
what muscles control blinking
obicularis oculi
controlled by cranial nerve e7 (facial nerve)
what opens the lid ( parasympathetic)
levator muscle and is innervated by the third
what opens the lid (sympathetic control)
mullers muscle e.g. if someone is given too much phenelephrin
what is a characteristic symptom of dry eye disease
gritty eyes (suggestive of something affecting the tear film) and in the absence of infection it will be dry eye disease
what is hyperosmolarity
osmolarity= a measure of the salt concentration
hyperosmolarity refers to an increase in the salt concentration
there are machihienes that get measure the osmolarity of the tear film as a result of hyperosmolarity e.g. high conc of salt in the tear film it draws water from the corneal epithelium resulting in epithelial apopotisis
what happens if epithelial apoptosis occurs due to hyperosmolarity
these epithelial cells are responsible for the normal regulation of tear film , if we are killing these neurosensory cells then it will feedback into the system and correct tears will not be produced
chain of events - hyperosmolarity - neurosensory abnormalitties- tear film instability - crappy tears
what part of the tear film is affected with aqueous deficient dry eye
something is wrong with the aqueous layer - not producing the correct amount of aqueous
what part of the tear film layer is affected with evaporative dry eye
something is wrong with the tear film layer and therefore tears are evaporating
what happens to blink rate as you look close up
you blink less
what is anterior blepharitis
inflammation of the lids and crusting
how is sjogrens syndrome related to dry eye
shortens syndrome is a systemic disease which is a autoimmune condition that inside of lacrimal glands
why is refractive surgery associated Wirth aqueous deficiency dry eye
in order to get to the cornea you have take off the epithelium - have to cut itnto neurosensory fibres which regulate tear production
what is a glycocalyx
the glycocalyx is a intermediate layer between the mucin layer and the corneal epithelium related to the corneal epithelium micropilthey
acts as join between the tear film and the mucin layer itself , evolved in the wetting and transmission of some of the nutrients , when we see it dissapera then we see formation of dry areas on the cornea and reduced tear break up time
what happens if you lose glycolayx
you get cell death , dry spot formation and problems with the glycolayx and mucin layer
where does the grittiness in dry eye disease come from
what happens when our patient blinks?
- instead of having lubrication of the lid over the tear film there will be contact between the lid and the epithelium so you feel the lid action of the cornea
what are factors for evaporative dry eye disease
MGD- mebiomian gland dysfunction
anterior belpharitis
deficient or unstable tear film lipid layer
vitamin a deficiency
allergies
contact lense wearer
these are all disrupters to tear film stability
if you have evaporative dry eye disease what happens
if you have evaporative then you have high evaporation of the tears (of the aqueous component of the tears) this leads to the tear hyperosmolarity - leads to high evaporttion which leads to tear hyperosmolarity
what are factors for aqueous deficiency dry eye disease
non sorjens dry eye disease
KCS- keratoconjuctivits sica
(dry eye disease)
SSDEautominune (sorjens syndrome dry eye disease)
systemic drugs
these all affect aqueous input meaning low flow in i.e. not much of the aqueous is going in - compared with losing aqueous in evaporative dry eye disease
what is the main driver of dry eye disease
tear hyperosmolarity is the main driver
what its acute epitheliel
MAPK
these are intermediate signalling molecules - it leads to goblet cell and glycol calyx mucin loss - epithelieel and cell apoptosis this leads to tear film instability because you ar losing the neurosensory control - this leads to tear hyperomsolarity
how does DED cause epiphora
reflex tears to the itchiness and grittiness
if symptoms are worse in the morning what type of dry eye disease is that
evaporative dry eye disease if worse during evening or morning = aqueous
why do you measure tear film break up time without fluroscein if possible first
disrupts tear film
what is schimers test for
measuring aqueous production
it is a little strip of paper that you hook into the lower fornix and you measure how far along the schirmer strip the tears have progressed
what are the aims of dry eye disease treatment
aims are to reduce tear hyperosmolarity using aqueous supplements , to increase tear film stability and to let the cornea recover to redevelop normal neurosensory control
what should be considered about artificial free preperations
things that contain preservatives are harmful to the front of the eye in particular benzayl conium chloride so if you have someone with an anterior surface pathology you shouldn’t but that
preservative free tends to be More expensive
what things need to be balanced when considering type of artificial tear preparations
the viscosity and effect on vision vs the treatment efficiency -
risk factors of dry eye disease include
age , hormonal disorders. lifestyle, allergies, glaucoma , belpharitis , contact lense wear
symptoms of dry eye disease include
dryness, blurry vision, foreign body sensation , photophobia, achiness , pain
what inevstigatice techniques can be used to investigate dry eye disease
tear stability, tear volume , ocular surface damage , dermodex
what is glycolayx and why is it important
The keratoconjunctival epithelium surface has protruding structures known as microplicae, whose tips include highly expressed membrane mucins that take the form of lawn patterns
In patients with dry eye, the MUC16 protein expression decreased, the barrier was broken, and galectin 3, which should otherwise form the glycocalyx, was released into the tear fluid at increased levels. In addition, in cases of severe dry eye with intense barrier collapse,
