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Disease > Ocular Allergy (Cale) > Flashcards

Ocular Allergy (Cale) Flashcards

1
Q

Atopy

A

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

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2
Q

ocular allergic conditons

A

seasonal allergic conjunctivitis, perennial allergic conjunctivitis, atopic keratoconjunctivitis, vernal keratoconjunctivitis, Giant papillary conjunctivitis, contact dermatitis

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3
Q

Hypersensitivity

A

excessive immune response to antigen often causing tissue damage. mediated by adaptive immune system in all cases. immune memory establishes long term sensitivity

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4
Q

hypersensitivity reactions

A

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)

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5
Q

Mast Cell

A

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*

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6
Q

Mast cell degranulation: early inflammatory response

A

Early phase: immediate release of preformed mediators (histamine) from mast cell lasts 20-30min
intervension: and (antihistamine)

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7
Q

histamines

A

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)

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8
Q

Mast cell degranulation: late inflammatory cascade

A

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
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9
Q

inflammatory mediators

A

include cytokines and chemotactic factors which attract other inflammatory cells such as eosinophils, neutrophils, macrophages, monocytes- diapedesis prolonged inflammation, tissue damage

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10
Q

eosinophils

A

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

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11
Q

differential diagnosis

A

allergic conditon
dry eye
infectious (microbial, viral, chlamydial)
episcleritis or scleritis
other non-infectious inflammatory conditions

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12
Q

one atopic parent vs two atopic parents

A

one= 4x risk of developing allergy

two=10x risk of developing allergy

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13
Q

seasonal allergic cong

A

itching, conjunctival papillae, hyperemia, burning, conjunctival chemosis, clear watery (serous) discharge, lid edema, allergic “shiners” (hyperpigmented periorbital), exacerbated in dry, hot climates

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14
Q

papillae

A

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)

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15
Q

follicles

A

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

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16
Q

treatment seasonal and perennial allergic

A

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

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17
Q

mast cell stabilizer

A

pemirolast (alamast), nedocromil (alocril), lodoxamide (alomide), cromolyn sodium (crolom)

18
Q

antihistamine

A

emedastine (emadine) and levocabastine (livostin), combo with decongenstant: pheneramine maleate (NaphconA), OpcomA

19
Q

combined mast cell stabilizer+antihistamine

A

ketotifen (Alaway, Zaditor), azelastine (Optivar), olopatadine (Patanol, Pataday), bepotastine (Bepreve), epinastine (Elestat), alcaftadine (Lastacaft)

20
Q

NSAID

A

Keratolac (Acular)

21
Q

Steroid

A

lotoprednol (Lotemax, Alrex), prednisone

22
Q

Atopic disease and Atopic keratoconjunctivitis

A
  • 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
23
Q

AKC signs

A

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)

24
Q

Dennie-Morgan Lines

A

extra creases in eyelid

25
Q

Canthal fissuring

A

ulceration due to chronic tearing

26
Q

chronick AKC inflammation

A

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

27
Q

symblepharon

A

adhesion of palpebral and bulbar conj

28
Q

AKC treatment

A
  • Ocular
  • multidisciplinary approach for improved control
  • systemic immunosuppression
29
Q

AKC ocular treatment

A

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)

30
Q

multidisciplinary approach for improved control

A

internist, allegist, dermatologist

31
Q

systemic immunosuppresion

A

cyclosporine- suppress T lympocytes

balance with additional risk of infection

32
Q

Vernal Keratoconjunctivitis

A

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

33
Q

Giant papillary conj hallmarks

A

iching, redness, burning, mucous

34
Q

GPC in CL wear

A

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

35
Q

GPC treatment

A

remove offending agent or reduce contact time. change CL material, replacement regimen. Use steroids, mast cell stabilizers, NSAID

36
Q

GPC pathophysiology in CL wear

A

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

37
Q

allergic eyelid disorders

A

contact dermatitis
acute allergy with eyelid edema
atopic dermatitis (eczema)

38
Q

contact dermatitis

A

exposure to meds, cosmetics, chemicals, type IV, erythema, scaling, edema, itching, papillary conj
tx: avoidance, cold compresses, topical steroid

39
Q

acute allergy with eyelid edema

A

pollen or insect bites

tx: antihistamine

40
Q

atopic dermatitis

A

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

Disease (11 decks)

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