W3 DED Flashcards by Dyllan Nye

Layers of tear film:

Lipid
Aqueous
Mucous
Glycolax
Ocular surface

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Lipid layer:

Thin outer meibum layer from sebaceous glands in tarsal plate (Meibomian glands) secreted during blink
Prevent evapouration, acts as surfactant (spreads film)
Non-polar cholesterol, esters, phospholipids, alcohols

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Aqueous layer Components:

Water, electrolytes, proteins, growth factors, pro-inflammatory interleukin cytokines (accumulate during sleep), Lysozyme, lactoferrin, urea, glucose, ions (Ca/Mg/Na/K), IgA

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Aqueous layer formation:

97% of film from lacrimal gland (95%) / Krause & Wolfring
From inner/upper lid

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Aqueous layer function:

O2 > Cornea
IgA / Lactoferrin / Lysozyme > Antimicrobial activity
Maintain moisture of non-keratinized corneal epith.
Leukocyte transport after injury
Smoothens optical surface
Flushes debris

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Mucin layer composition

Thinnest layer of mucus from goblet cells in conj. / plica semilunaris / glands of henle & Manz
Hydrophilic High mol. Wgt. Mucin glycoproteins (transmembrane or secretory)
Transmembrane mucins bind glycolax from corneal epith.
Secretory are soluble in aqueous forming gel

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Types of mucins:

MUC1/4/16: membrane bound, with galectin glue to glycolax
MUC7 / MUC5AC: secretory to prevent strands of mucous (light scatter)

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Mucin layer function

Turns hydrophobic corneal epith. Hydrophilic > corneal wetting
Attaches film to cornea, allows lubrication

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Lacrimation reflex:

Stimulation > CN5 sensation > brainstem > parasympathetic nucleus of CN7 / sympathetic of medulla > lacrimal gland / spinal cord > lacrimal gland

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Definition of dry eye disease (DEWS 2):

Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles

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Causes of ADDE:

Sjrogren’s syndrome (autoimmune against exocrine glands)
Lacrimal gland dysfunction: Primary (age/genetics) or secondary (AIDS/Lymphoma)
Lacrimal gland duct obstruction
Alteration in stimulation (reflex block)

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ADDE from secretion stimulation alteration:

Reflex hyposecretion from reflex sensory block (CLs/LASIK/herpes/diabetes) or reflex motor block (CN 7 lesion)
Blockage of para/sympathetic nerves to lacrimal gland
Decreased androgen from hormone loss (age)
Exposure to anti depressants/histamines

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Causes of EDE:

MGD
Infrequent blink
Environment
Ectropion / lagopthalmos
CLs via lipid layer loss
Mass lesions
Vit A def.
Defective mucins (infection)

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Meibomian gland dysfunction causes:

Drop out (age>50)
Gland replacement (Distichiasis)
Hypersecretory glands (Seborrhea / retinoid therapy)
Gland obstruction
Glaucoma medication (pilocarpine)

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Types of MGD:

Primary (age/acne): increased bacterial lipases > meibum cleavage > fatty acid formation > increased melting point > hardening
Secondary: diseases
Cicatrical: hyposecretion from damage / steven-johnson syndrome / allergies

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hyperosmolarity

Loss of aqueous or evaporation > hyperosmolarity > epithelial irritation > Mitogen-activated protein kinase (MAPK) & NFkB activation > inflammatory mediator release (IL-1 & TNF-1/MMPs) > Matrix metalloproteinases damage epithelium / goblet cells > epitheliopathy (corneal epithelium loss) > pain > reflex stimulation
ADDE > lack of watering > further hyperosmolarity
EDE > poor lipid layer > watering

Tear film instability:

Damage to goblet cells > glycolax/mucin dysfunction > friction on bling > discomfort/inflammation > hyperosmolarity

DED symptoms:

Pain/burn/grit/FBF
Watering (CN6 activation)
Hyperemia
Lid fatigue
Intermittent blur (better on blink)
Struggle on screen use (blink rate 11/m > 4/m)

Slit lamp examination of DED:

Lid hyperemia
Tear film debris
Conj. Hyperemia
SPEE (superficial punctate epithelial erosions)
Meibomian capping (MGD/bleph.)
Tear meniscus (reduced in ADDE)

Sodium Fluroescein function:

NaFl peak absorption at 493nm (blue), emits 520(green), instilled via strip (1% drop), viewed via wratten #12 (yellow-green) filter
Hydrophilic (doesn’t pass lipid bilayer epithelium or tight junctions), pools in corneal/conj. Areas of cell loss

Analysis via NaFl:

TBUT
Epithelial damage
Papillae/follicle assessment

Rose bengal and lissamine green:

Binds to damages cells which no longer secrete protective mucins.
Bengal is toxic, lissamine is not painful.

Staining patterns in DED:

Interpalpebral staining of ocular surface > DED
Sup. Conj. Stain > sup. Limbic keratoconjunctivitis
Inf. Corneal / conj. > poor blink exposure / blepharitis

Grading conj./corneal stains:

CCLRU grading:
Type/area (2>1>3^4≥5)
Depth
Extent
Conj. Staining

Schirmer test:

5mm fold in Whatman filter inserted under lower lid (temporal side), don’t touch cornea/lash Px closes eyes over filter Remove paper after 5min <10mm without anesthesia / <6 with ana. Indicates abnormal

TFBUT:

NaFl instilled with Wratten #12 cobalt filter lens Px blinks before holding eyes open Timed appearance of black spots <10s abnormal, repeated breakup in given area indicates localized surface abnormality

Ocular protective index:

TBUT/time between blinks: <1 indicates oculur surface exposure

Other diagnostic tests for DED:

Osmolarity (>317mOsm/L) Phenol red (pH dye on string like schirmers) Lactoferrin test (lacrimal Gland production) Meibometry Impression cytology (goblet population)

DED severity classification:

Incresing degrees of symptoms from level 1-4: Discomfort, visual symptoms, Conj. Injection, conj. Staining, corneal staining, corneal damage, tear film stability (debris/meniscus/mucus clumps), lid/meibomian health, TFBUT (>10, <10, <5, <2), schirmers (>10, <10, <5, <2)

Goals of DED management:

Eliminate exacerbating factors Lubricate ocular surface Minimize exposure Restore normal osmolarity Prevent inflammatory mediator/enzyme production Improve film stability

Eye drop preservatives:

BAK: toxic to cell junctions / microvilli > necrosis of outer epith. Disodium (EDTA): stronger (less needed) Polyquad: less toxic Sodium chlorite: degrades to Cl- / water via UV Sodium perobate: converts to water / O2 on contact with tear film

Electrolyte function in lubricating drops:

K+: maintains corneal thickness Bicarbonate: maintains epith. Ultrastructures (mucin layer) / ^recovery of epithelial defence Hypotonic: decrease osmolarity (TheraTears)

Compatible solutes in lubricating drops:

Glycerin, erythritol, levocarnitine: distribue between intracellular fluid to protect epith.

Viscosity agents in lubricating drops:

Increase tear residency and protects damaged epith. Hydroxypropyl(HP)-guar: gel with glycol 400 / propylene glycol Hyaluronic acid Polyvinyl alcohol Carmellose (CMC) Hydroxymethylcellulose (HPMC)

Blepharitis:

Lid inflammation from Staphyloccal or dermatitis Ant. Affects zeis glands/lash follicles (crusty scales) > bleph debris decreases tear quality Pos. affects meibomian glands (meibum capping) > EDE + inflammatory mediator passage from lid

Blepharitis management:

Ant. > lid scrubs decrease bac. Load or 1/3 shampoo Pos. > warm compress + massage > melts meibum caps and expresses

Punctal occlusion:

Temporary plugs: dissolve in 2w Prolonged: removed in 6m (risks granuloma) Permenant occlusion: opthal for cautery

Anti-inflammatory treatment of DED:

Fluromethalone alcohol/acetate (FML/Flarex): 0.1% qid > 1week with lubricants Topical ciclosporin (cequa/ikervis): 0.05% bid for ADDE, reduces T-cell inflammation (requires oxford grading scale = 4) Topical lifitegrast (Xiidra 5%): lymphocyte function-associated antigen (LFA-1) antagonist, blocks LFA-1 on lymphocytes from intercellular adhesion molecule-1 (ICAM-1) on epith.

Uncommon DED treatments:

Manuka honey Systemic tetracyclines: alters meibum for rosacea/bleph. Omega 3 fatty acid supp.: decreases inflammation systematically CLs: occlusive GP scleral CLs provide saline reservoir Lacrisert: plastic insert placed in lower lid to hold artificial tears Palpebral tarsorrhaphy: stich lids closer together