Ocular Allergy (Cale) Flashcards
Atopy
Genetically determined predisposition to hypersensitivity reactions upon exposure to certain environmental antigens. Manifest in Various clinical presentations which almost universally include itching as a dominant component
ocular allergic conditons
seasonal allergic conjunctivitis, perennial allergic conjunctivitis, atopic keratoconjunctivitis, vernal keratoconjunctivitis, Giant papillary conjunctivitis, contact dermatitis
Hypersensitivity
excessive immune response to antigen often causing tissue damage. mediated by adaptive immune system in all cases. immune memory establishes long term sensitivity
hypersensitivity reactions
type I: immediate IgE
type II: cytotoxic IgG and IgM (myasthenia gravis, drug induced autoimmunity)
type III: Serum sickness IgG and IgM (Serum sickness)
type IV: delayed T-lymphocytes, chronic (contact derm, TB test, medication rash)
Mast Cell
Reside in superficial conj (substantia propria). each has high affinity receptors for IgE. Activation occurs when antigen binds to IgE mast cell complex, resulting in degranulation. Initiation of late-phase response gives a more prolonged response. Pretreating for anticipated allergy response is most effective*
Mast cell degranulation: early inflammatory response
Early phase: immediate release of preformed mediators (histamine) from mast cell lasts 20-30min
intervension: and (antihistamine)
histamines
bind to H1 and H2 receptors on target cell. H1 binds to nerve endings itching and burning. H2 binds to vessel walls vasodilation (hyperemia), increased vascular permeability, extravasation, edema (chemosis)
Mast cell degranulation: late inflammatory cascade
late phase starts 3-12 hours- mast cell synthesis of new mediators lasts 24 hours
- inflammatory mediators
- phospholipidase>arachidonic acid …. includes cyclooxygenase> prostaglandins and lipooxygenase>leukotrienes
inflammatory mediators
include cytokines and chemotactic factors which attract other inflammatory cells such as eosinophils, neutrophils, macrophages, monocytes- diapedesis prolonged inflammation, tissue damage
eosinophils
products are toxic to cells and may cause tissue damage, including corneal ulceration. abundance in conjunctival scraping is positive for allergic conjunctivitis since they are normally not present on the conj surface. absense of eosinophils does not rule out allergy
differential diagnosis
allergic conditon
dry eye
infectious (microbial, viral, chlamydial)
episcleritis or scleritis
other non-infectious inflammatory conditions
one atopic parent vs two atopic parents
one= 4x risk of developing allergy
two=10x risk of developing allergy
seasonal allergic cong
itching, conjunctival papillae, hyperemia, burning, conjunctival chemosis, clear watery (serous) discharge, lid edema, allergic “shiners” (hyperpigmented periorbital), exacerbated in dry, hot climates
papillae
present in allergic and bacterial or chlamydial conjunctivitis. raised tissue masses with central vessel tuft. focal infiltration of inflammatory cells upper and lower papebral conj (eosinophils greater in allergic, neutrophils greater in bacterial)
follicles
present in viral, chlamydial, toxic conj. blister-like with central avascular zone and normal conjunctival vasculature over the follicle. expansions of lymph system usually inferior palpebral conj. accompany preauricular adeopathy
treatment seasonal and perennial allergic
lubricants and cold compresses, vasoconstrictor, mast cell stabilizer which causes delayed symptomatic relief, antihistamine, combined mast cell stabilizer and antihistamine, NSAID, Steroid, Oral antihistamine with rhinitis or greater systemic involvement
mast cell stabilizer
pemirolast (alamast), nedocromil (alocril), lodoxamide (alomide), cromolyn sodium (crolom)
antihistamine
emedastine (emadine) and levocabastine (livostin), combo with decongenstant: pheneramine maleate (NaphconA), OpcomA
combined mast cell stabilizer+antihistamine
ketotifen (Alaway, Zaditor), azelastine (Optivar), olopatadine (Patanol, Pataday), bepotastine (Bepreve), epinastine (Elestat), alcaftadine (Lastacaft)
NSAID
Keratolac (Acular)
Steroid
lotoprednol (Lotemax, Alrex), prednisone
Atopic disease and Atopic keratoconjunctivitis
- Eczematous dermatitis- 5-20% of general population, greatest in peds
- ocular (AKC 25-40% of AD pt)- preceded by dermatitis, high incidence of asthma, rhinitis, occur most commonly age 20+, chronicity with visual complications greater in men
- genetic predispositon combined with antigen sensitization
- chronic throughout year with seasonal exacerbation
AKC signs
conjunctival edema, chemosis hyperemia, papillary hypertrophy, scarring, corneal epitheliopathy, haze, neovascularization, limbal infiltration, itching, tearing, irritation, stringy mucous discharge, lids sticking in AM, eyelids flaking, scaling, madarosis, periorbital hyerpigmentation, thickening margins (Dennie-Morgan lines and Canthal fissuring)
Dennie-Morgan Lines
extra creases in eyelid
Canthal fissuring
ulceration due to chronic tearing
chronick AKC inflammation
damaged and lost goblet cells (altered mucin production), tear film instability, epithelial disease, shield ulcer, reduced corneal sensitivity, structural lid changes from chronic bleph, edema, associated with keratoconus, subcapsular cataract
symblepharon
adhesion of palpebral and bulbar conj
AKC treatment
- Ocular
- multidisciplinary approach for improved control
- systemic immunosuppression
AKC ocular treatment
eliminate environmental antigens, treat bleph (scrubs, warm compresses) including antibiotic ung and alter with cool compresses, restasis, ocular lubricants, for lids use topical steroids, tacrolimus (immunosupressant)
multidisciplinary approach for improved control
internist, allegist, dermatologist
systemic immunosuppresion
cyclosporine- suppress T lympocytes
balance with additional risk of infection
Vernal Keratoconjunctivitis
younger age, burns out by late puberty, less sight threatening complications, spares skin, eyelid margins not involved, giant papillae, upper tarsus involved, cornea Horner- trantas dots at limbus
Giant papillary conj hallmarks
iching, redness, burning, mucous
GPC in CL wear
decreased CL tolerance, excess lens movement, FB sensation w/o CL, presence of giant papilla. soft CL start near upper tarsal plate and progress to all zones, RGP CL near lid margin
GPC treatment
remove offending agent or reduce contact time. change CL material, replacement regimen. Use steroids, mast cell stabilizers, NSAID
GPC pathophysiology in CL wear
antigen in coating of contact lens induce allergic reaction. supported by finding immunoglobulins in CL protein deposits and tear film, increase in number of normally present inflammatory cells
allergic eyelid disorders
contact dermatitis
acute allergy with eyelid edema
atopic dermatitis (eczema)
contact dermatitis
exposure to meds, cosmetics, chemicals, type IV, erythema, scaling, edema, itching, papillary conj
tx: avoidance, cold compresses, topical steroid
acute allergy with eyelid edema
pollen or insect bites
tx: antihistamine
atopic dermatitis
common idiopathic response in pt with asthma, hay fever. dermatitis, thickening, crusting, fissuring, associate with keratoconus, cataract, bleph
tx: emollient for hydration of skin, topical steroid
