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SS&OFMP > Dry eye disease > Flashcards

Dry eye disease Flashcards

1
Q

what is dry eye disease

A

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

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2
Q
A
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3
Q

what are the two types of dry eye disease

A

evaporative dry eye (dysfunction of lipid layer)

aqueous deficient dry eye - aqueous dysfunction

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4
Q

how does covid 19 affect dry eye

A

covid 19 and therefore increased green time and online learning were associated with worsening pre-existing ocular surface diseases

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5
Q

what is evaporative dry eye due to

A

typically due to some type of meibomian gland dysfunction

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6
Q

what are causes of evaporative dry eye

A

anterior blepharitis

contact lens wear

seborrheic dermatitis

allergic eye disease

psoriasis

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7
Q

what are causes of aqueous deficiency dry eye

A

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

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8
Q

how is tear hyperosmolarity related to dry eye disease

A

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)

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9
Q

how does tear film become damaged

A

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

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10
Q

how to differentiate between evaporation dry eye and aqueous dry eye disease

A

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

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11
Q

what is the first line of treatment for dry eye disease

A

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

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12
Q

what are signs of dry eye disease

A

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)

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13
Q

how are artificial tear preparations used

A

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

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14
Q

what are the types of artificial tears

A

hypromellose

carbomers

hydroxythycellulose

polyvinyl alchol

sodium hyaluronate (hylaruynoic acid)

carmellose

trehalose

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15
Q

what is the next line of treatment if artificial tears are not responsive

A

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

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16
Q

what structures are involved in the production of normal tear film

A

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

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17
Q

is the lacrimal gland under parasympathetic or sympathetic innervation

A

parasympathetic ally innervated

lacrimal gland involved primarily in the production of reflex tears

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18
Q

where is the meibomian gland located

A

located in the upper and lower lids

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19
Q

what do meibomian glands produce

A

they produce meiobom

prevents tear evaporation tear evaporation can cause dry spots on the cornea

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20
Q

in what other glands are the lipid layer produced in

A
  • the glands of ziess and moll
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21
Q

where is the aqueous layer of tear film produced

A

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

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22
Q

where is the mucin layer produced

A

goblet cells of the conjuctiva

mucin is composed of heavy weight molecules called glycoproteins

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23
Q

what is the role of mucin layer

A

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

24
Q

how are the structures that are responsible for the different tear film components neurally regulated

A

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

25
Q

what muscles control blinking

A

obicularis oculi

controlled by cranial nerve e7 (facial nerve)

26
Q

what opens the lid ( parasympathetic)

A

levator muscle and is innervated by the third

27
Q

what opens the lid (sympathetic control)

A

mullers muscle e.g. if someone is given too much phenelephrin

28
Q

what is a characteristic symptom of dry eye disease

A

gritty eyes (suggestive of something affecting the tear film) and in the absence of infection it will be dry eye disease

29
Q

what is hyperosmolarity

A

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

29
Q

what happens if epithelial apoptosis occurs due to hyperosmolarity

A

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

30
Q

what part of the tear film is affected with aqueous deficient dry eye

A

something is wrong with the aqueous layer - not producing the correct amount of aqueous

30
Q

what part of the tear film layer is affected with evaporative dry eye

A

something is wrong with the tear film layer and therefore tears are evaporating

31
Q

what happens to blink rate as you look close up

A

you blink less

32
Q

what is anterior blepharitis

A

inflammation of the lids and crusting

33
Q

how is sjogrens syndrome related to dry eye

A

shortens syndrome is a systemic disease which is a autoimmune condition that inside of lacrimal glands

34
Q

why is refractive surgery associated Wirth aqueous deficiency dry eye

A

in order to get to the cornea you have take off the epithelium - have to cut itnto neurosensory fibres which regulate tear production

35
Q

what is a glycocalyx

A

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

36
Q

what happens if you lose glycolayx

A

you get cell death , dry spot formation and problems with the glycolayx and mucin layer

37
Q

where does the grittiness in dry eye disease come from

A

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
38
Q

what are factors for evaporative dry eye disease

A

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

39
Q

if you have evaporative dry eye disease what happens

A

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

40
Q

what are factors for aqueous deficiency dry eye disease

A

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

41
Q

what is the main driver of dry eye disease

A

tear hyperosmolarity is the main driver

42
Q

what its acute epitheliel

MAPK

A

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

43
Q

how does DED cause epiphora

A

reflex tears to the itchiness and grittiness

43
Q

if symptoms are worse in the morning what type of dry eye disease is that

A

evaporative dry eye disease if worse during evening or morning = aqueous

44
Q

why do you measure tear film break up time without fluroscein if possible first

A

disrupts tear film

45
Q

what is schimers test for

A

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

46
Q

what are the aims of dry eye disease treatment

A

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

47
Q

what should be considered about artificial free preperations

A

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

48
Q

what things need to be balanced when considering type of artificial tear preparations

A

the viscosity and effect on vision vs the treatment efficiency -

49
Q

risk factors of dry eye disease include

A

age , hormonal disorders. lifestyle, allergies, glaucoma , belpharitis , contact lense wear

50
Q

symptoms of dry eye disease include

A

dryness, blurry vision, foreign body sensation , photophobia, achiness , pain

51
Q

what inevstigatice techniques can be used to investigate dry eye disease

A

tear stability, tear volume , ocular surface damage , dermodex

52
Q

what is glycolayx and why is it important

A

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,

SS&OFMP (11 decks)

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