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35 Cards in this Set
- Front
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AP II EXAM 2 ANAPHYLACTIC REACTIONS
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AP II EXAM 2 ANAPHYLACTIC REACTIONS
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4 hypersensitivity reactions
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Types 1-4
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Type I
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Immediate hypersensitivity
1. atopy 2. urticaria 3. angioedema 4. anaphylaxis |
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What are the immune reactants of Type I?
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IgE antibody
Th2 cells |
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Type IV
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Delayed hypersensitivity
1. pruritis 2. red weepy skin |
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Char of irritant contact dermatitis
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1. erythema, cracks and fissures
2. pruritis or pain |
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Anaphylaxis
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1. SEVERE allergic rxn (Type I).
2. rapid onset 3. mediated by antigen-antibody rxn. 4. requires prior exposure to antigen 5. circulatory collapse |
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Mechanism of anaphylaxis
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1. exposure to antigen
2. production of antigen IgE antibody. 3. antibodies fix to mast cells/basophils 4. re-exposure of antigen results in binding to antibodies and crosslinking. 5. chemical mediators released |
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What are the products of mast cells?
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1. granule proteins
2. cytokines 3. chemokines 4. LTC, PAF |
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Granule protein effects
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Damages epithelial
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Effects of cytokines
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1. attract eosinophils
2. airway remodelling, IgE 3. Th2 polarisation |
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Effects of chemokines
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Attract/activate eosinophils
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LTC4 and PAF effects
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1. mucus hypersecretion
2. airway narrowing 3. attract pro-inflammatory cells |
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Important mediators of anaphylaxis
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1. histamine
2. leukotrienes 3. prostaglandins |
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Histamine
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1. increased cap. perm.
2. peripheral vasodilation 3. bronchoconstriction |
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Leukotriene effects
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1. BRONCHOCONSTRICTION
2. inc. cap perm. 3. neg. iontropy |
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Prostaglandins
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1. bronchoconstriction
2. vasodilation |
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Anaphylactoid rxn
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1. NOT dependent on IgE antibodies
2. direct action on mast cells 3. MASSIVE release of histamine 4. may occur on first exposure 5. clinically INDISTINGUISABLE |
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Dispositions to anaphylactoid rxn?
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1. atopy (predisposed to having allergic rxn)
2. pregnancy 3. youth |
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Circulatory collapse due to allergic rxn
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1. profound VASODILATION (dec. SVR)
2. HYPOTENSION 3. tachy 4. dysrhythmias 5. pulm vasoconstriction--> HTN 6. cardiac arrest |
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Pulmonary insults
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1. wheezing
2. bronchospasm 3. inc. PIP 4. stridor/ laryngeal edema 5. pulm. edema 6. ARF/hypoxia |
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Cutaneous signs
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1. urticaria (hives)
2. flushing 3. periorbital edema 4. perioral edema |
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Treatment for anaphylaxis?
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1. stop adm. of antigen
2. 100% O2 and PPV 3. discontinue anesthetic agents (volatile) 4. use colloid (intravascular vol. expansion) 5. Epi (1/10,000 0.1 cc/kg IV) 6. external cardiac massage |
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Role of Epi
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1. it increases in cAMP, stabilizing cell membranes
2. relaxes bronchial smooth muscle 3. alpha agonist effect vasoconstricts vessels |
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What are some common offenders for an allergic rxn?
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1. muscle relaxants (sux, atracurium)
2. barbituates 3. propofol 4. opioids (morphine, meperidine: histamine release and arterial and venodilatation) 5. PABA ester local anesthetics 6. antibiotics 7. latex |
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Local anesthetic role in allergic rxn
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Ester LA metabolized to PABA
a. IgE mediated rxns exist b. cross reactivity occurs Amide LA- preservatives antigenic True allergic rxn rare |
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Antibiotics
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Most are true anaphylaxis
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Which antibiotics are the biggest offenders in causing anaphylaxis?
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1. PCN (anaphylaxis--> 50%)
2. cephalosporins |
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PCN and Cephalosporin
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1. cross reactivity only 1-7%
2. anaphylaxis to PCN- 50% |
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Vancomycin
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Produces both rxns
1. anaphylactoid rnx more common. 2. Redman's syndrome- histamine release |
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Latex
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Contact dermititis
True anaphylactic rxn Delayed onset |
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Which conditions lead to the highest risk with Latex?
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1. spina bifida
2. spinal cord injury 3. healthcare workers |
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Allergic to anesthetic agents
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True anaphylaxis is rare (IgE mediated)
Anaphylactoid rnxs more common, i.e. Red man's sydrome. |
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Which drugs can cause nonimmunologic histamine release?
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1. antibiotics
2. opioids 3. muscle relaxants |
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Preventing death in the OR
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1. suspicion
2. recognition 3. treatment 4. aggressive treatment |