Term
Describe gender and age effects on the incidence of anaphylaxis
Know the geographic risk factors and possible hypothesis |
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Definition
MAles > Females under age 15
Females > Males after age 15
Females > Males for latex, muscle relaxants, asa, idiopathic and overall rates of anaphylaxis
More Epi Rx's are written in the North than the South in N America. Hypothesis is that there is an inverse relationship with sunlight, therefore, Vitamin D levels |
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Term
| For which triggers is atopy a risk factor for anaphylaxis? |
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Definition
Triggers for which atopy is a risk factor: oral agents, idiopathic, exercise, latex, RCM
Triggers for which atopy is not a risk factor: most parentally administered agents, penicillin, insulin, hymenoptera |
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Term
| Know the physiologic effects of the 3 Histamine Receptors |
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Definition
H1: coronary artery vasoconstriction, bronchial constriction
H2: Coronary vasodilation, ventricular ionotropy, atrial and ventricular chronotropy
Together, H1 and H2 affect pulse, pulse pressure (increase), diastolic BP (decrease), headache, flushing. This is why you should use both H1 and H2 blockers to tx hypotension in anaphylaxis.
H3: autonomic receptor downregulator (turns off norepinephrine, which is a compensatory response to hypotension) |
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Term
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Definition
PAF is increased
PAF levels positively correlate with severity of anaphylaxis
If PAF acetylhydrolase is inhibited, PAF metabolism decreases and anaphylaxis will be more severe. |
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Term
Which cytokines/mediators correlate with hypotension?
Which peaks first? |
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Definition
IL-6, TNF receptor I, mast cell tryptase and histamine.
HIstamine peaks first. |
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Term
| Know how mast cell triggers the contact, coagulation and complement systems during anaphylaxis |
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Definition
Release of trypsin activates complement
Release of kallikrein activates contact system, which in turn, leads to activation of coagulation pathway. |
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Term
| Which drugs predispose to anaphylaxis? |
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Definition
Beta blockers
ACE inhibitors
ACE receptor blockers
Tricyclics (block re-uptake of epi)
MAO inhibitors (block re-uptake of epi)
Thus, these are relatively contraindicated in patients at risk for anaphylaxis. |
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Term
| Pretreatment is effective for which triggers of anaphylaxis? |
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Definition
RCM
Cold (used in bypass surgery)
Fluorescein
NOT Latex! |
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Term
| Bradycardia in anaphylaxis: does it occur? |
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Definition
| In the setting of a sting challenge, all subjects who became hypotensive had initial tachycardia f/b bradycardia. Therefore, do not use bradycardia as a way to distinguish vasovagal responses from anaphylaxis. |
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Term
Lab tests in the diagnosis of anaphylaxis
Know the time course of histamine, tryptase and urinary histamine metabolites
Do histamine and tryptase always correlate in anaphylaxis? |
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Definition
Histamine: peaks within minutes; gone within an hour. Don't order this test!
Serum tryptase: peaks at 60 minutes, remains elevated for several hours
Urinary histamine metabolites: last to peak (around 3 hours) but remain elevated the longest.
No. There are settings in which histamine is elevated while tryptase is not (food induced anaphylaxis) |
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Term
Pro- Beta Tryptase vs Mature Beta-Tryptase
1. Which is secreted constitutively?
2. Which is secreted during degranulation?
3. What the ratio of total tryptase (pro plus mature) in mastocytosis? In other causes of anaphylaxis? |
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Definition
1. Pro-beta
2. Mature-beta
3. Mastocytosis > 20. Other causes < 10. |
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Term
| WHich correlates better with symptoms and signs of anaphylaxis: histamine or tryptase? |
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Definition
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Term
| HOw can you differentiate exercise-induced anaphylaxis from cholinergic urticaria? |
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Definition
Giant hives (exercise) vs pinpoint (cholinergic)
Any stimuli causing sweating vs exercise
Cholinergic hives are caused by anything that triggers sweating, including emotional upset! |
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Term
| If systemic vascular resistance is increased in the face of hypotension, what treatment should be given? |
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Definition
| Volume expanders (epi doesn't work well in this setting) |
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Term
| Name the 4 endogenous compensatory mechanisms in anaphylaxis |
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Definition
epinephrine
Angiotensin 1 and 2
Norepinephrine
Endothelin |
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Term
| What do oversulfated heparin (a contaminated drug) and chondroitin sulfate do to kallikrein activity? |
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Definition
| They increase kallikrein, which leads to anaphylaxis, mostly manifest as angioedema |
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Term
| Idiopathic Anaphylaxis: Be familiar with immunologic discoveries |
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Definition
1. Autoantibody, response to anti-leukotriene
2. Increased skin response to codeine
3. Increased activated T cells
4. Increased production of IL4, IL5, IL13 by PBMC.
5. c-kit mutation (D816>V)...undiagnosed mastocytosis |
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Term
Galactose-alpha-1,3-Galactose (aka alpha-gal)
1. What drug is it present in?
2. What is the normal human response to it? (Clue: alpha-gal is found in non-primate mammals)
3. What is its relevance in transplants?
4. What allergic condition does it cause? |
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Definition
1. Cetuximab
2. Humans have natural IgG to it
3. It is the major antigen preventing transplants.
4. Delayed anaphylaxis to meat (beef, pork). Need to skin test with fresh meat, not extract. |
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Term
| How do you treat anaphylaxis in a beta blocked patient? |
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Definition
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Term
| What is the mean time to peak concentration for IM epi vs sq epi? |
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Definition
IM: 8 minutes
SQ: 34 minutes |
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Term
Death in Anaphylaxis
1. Know the importance of lying down
2. Know the major causes (organ systems) of death |
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Definition
1. In Pumphrey's paper, 4 of 10 fatalities were assoc with upright position, which indicated "empty heart" with pulseless electrical activity
2. Shock, asphyxia, DIC. Minority due to epi overdose.
NOTE: severity of prior reaction was not predictive. |
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Term
| Which tends to be more severe: anaphylaxis or anaphylactoid reactions? |
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Definition
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