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21 Cards in this Set
- Front
- Back
- 3rd side (hint)
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local and systemic diseases
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local: urticaria (hives), angioedema (lips, tongue, eyes), allergic rhinitis/conjunctivitis (hay fever), allergic gastroenteritis, asthma
systemic anaphylaxis |
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immediate and late response of type I
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immediate: vasodilation, vascular leakage, smooth muscle spasm
late: leukocyte infiltration, epithelial damage, bronchospasm |
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primary and secondary mediators produced by mast cells and basophils
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primary: biogenic amines (histamine), enzymes (proteinase and hydrolase), proteoglycans
secondary: lipid-derived mediators (from membrane phospholipids) - leukotrienes, prostaglandin, platelet activating factor cytokines |
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Biogenic amines (histamine)
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smooth muscle contraction
increased vascular permeability increased secretion by nasal, bronchial and gastric glands |
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enzymes (protease, hydrolase)
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tissue damage
generate kinins and activate complements |
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proteoglycans (heparin)
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serve to package and store other mediators
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leukotrienes
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increase vascular permeability and bronchial smooth muscle contraction
chemotactic for eosinophils |
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prostaglandin
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bronchspasm
increased mucus secretion |
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platelet activating factors (PAF)
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platelet aggregation
release of histamine chemotactic for eosinophils |
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cytokines
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participate in late phase response
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urticaria (hives, wheals)
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edema of superficial dermis
lesions appear rapidly and fade within hrs - episodes may last for days |
pruritic slightly elevated areas on the skin which are redder or paler than the surrounding skin
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angioedema
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deeper edema of both dermis and subcutaneous fat (lips, tongue and eyes)
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hereditary angioneurotic edema
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C1 inhibitor deficiency
not related to Type I hypersensitivity |
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allergic rhinitis/allergic conjunctivitis (hay fever)
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affects 20% of population
mucosal edema, redness and mucous secretion secretions and mucosa contain numerous eosinophils |
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bronchial asthma (extrinsic)
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most common type of asthma
hyperreactive airways leading to bronchoconstriction - dyspnea, couphing, wheezing triggered by bronchospasm overdistended lungs, occlusion of bronchioles with mucous plus edema, increased submucosal glands, hypertrophy of bronchial wall musle, esosinophils |
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neutral proteases
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activation of complement and kinins contributes to mast cell degranulation
causes tissue damage |
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systemic anaphylaxis
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widespread edema, respiratory distress, vascular shock
loss of consciousness hives swelling of tongues, inability to swallow rapid swelling of throat tissues (laryngeal edema) hypotension and dizziness |
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anaphylaxis treatment with ABC
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A - adrenalin (reverse histamine response)
B - Benadryl (anti histamine) C - corticosteroids |
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epinephrine and theophylline
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drug of choice for acute emergency Tc
vasoconstriction via alpha1 bronchodilation and blocks degranulation through beta 2 |
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corticosteroids is for
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for recurrent patients
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antihistamines given when?
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given after pt is stabilized
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