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35 Cards in this Set

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AP II EXAM 2 ANAPHYLACTIC REACTIONS
AP II EXAM 2 ANAPHYLACTIC REACTIONS
4 hypersensitivity reactions
Types 1-4
Type I
Immediate hypersensitivity

1. atopy
2. urticaria
3. angioedema
4. anaphylaxis
What are the immune reactants of Type I?
IgE antibody

Th2 cells
Type IV
Delayed hypersensitivity

1. pruritis
2. red weepy skin
Char of irritant contact dermatitis
1. erythema, cracks and fissures
2. pruritis or pain
Anaphylaxis
1. SEVERE allergic rxn (Type I).
2. rapid onset
3. mediated by antigen-antibody rxn.
4. requires prior exposure to antigen
5. circulatory collapse
Mechanism of anaphylaxis
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
What are the products of mast cells?
1. granule proteins
2. cytokines
3. chemokines
4. LTC, PAF
Granule protein effects
Damages epithelial
Effects of cytokines
1. attract eosinophils
2. airway remodelling, IgE
3. Th2 polarisation
Effects of chemokines
Attract/activate eosinophils
LTC4 and PAF effects
1. mucus hypersecretion
2. airway narrowing
3. attract pro-inflammatory cells
Important mediators of anaphylaxis
1. histamine
2. leukotrienes
3. prostaglandins
Histamine
1. increased cap. perm.
2. peripheral vasodilation
3. bronchoconstriction
Leukotriene effects
1. BRONCHOCONSTRICTION
2. inc. cap perm.
3. neg. iontropy
Prostaglandins
1. bronchoconstriction
2. vasodilation
Anaphylactoid rxn
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
Dispositions to anaphylactoid rxn?
1. atopy (predisposed to having allergic rxn)
2. pregnancy
3. youth
Circulatory collapse due to allergic rxn
1. profound VASODILATION (dec. SVR)
2. HYPOTENSION
3. tachy
4. dysrhythmias
5. pulm vasoconstriction--> HTN
6. cardiac arrest
Pulmonary insults
1. wheezing
2. bronchospasm
3. inc. PIP
4. stridor/ laryngeal edema
5. pulm. edema
6. ARF/hypoxia
Cutaneous signs
1. urticaria (hives)
2. flushing
3. periorbital edema
4. perioral edema
Treatment for anaphylaxis?
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
Role of Epi
1. it increases in cAMP, stabilizing cell membranes
2. relaxes bronchial smooth muscle
3. alpha agonist effect vasoconstricts vessels
What are some common offenders for an allergic rxn?
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
Local anesthetic role in allergic rxn
Ester LA metabolized to PABA
a. IgE mediated rxns exist
b. cross reactivity occurs

Amide LA- preservatives antigenic

True allergic rxn rare
Antibiotics
Most are true anaphylaxis
Which antibiotics are the biggest offenders in causing anaphylaxis?
1. PCN (anaphylaxis--> 50%)
2. cephalosporins
PCN and Cephalosporin
1. cross reactivity only 1-7%
2. anaphylaxis to PCN- 50%
Vancomycin
Produces both rxns

1. anaphylactoid rnx more common.
2. Redman's syndrome- histamine release
Latex
Contact dermititis

True anaphylactic rxn

Delayed onset
Which conditions lead to the highest risk with Latex?
1. spina bifida
2. spinal cord injury
3. healthcare workers
Allergic to anesthetic agents
True anaphylaxis is rare (IgE mediated)

Anaphylactoid rnxs more common, i.e. Red man's sydrome.
Which drugs can cause nonimmunologic histamine release?
1. antibiotics
2. opioids
3. muscle relaxants
Preventing death in the OR
1. suspicion
2. recognition
3. treatment
4. aggressive treatment