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Anaphylaxis Flashcards

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USMLE® Step 1 flashcards
1
Q

Half of fatalities occur with in

A

First hour

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2
Q

Anaphylaxis caused by

A

Activation of mast cells + basophils through a mechanism crosslinking IgE and aggregation of high affinity receptors for IgE

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3
Q

Upon activation of mast cells and basophils

A

Several chemical mediations released, including histamine

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4
Q

Common systems involved in anaphylactic reaction

A

Heart lungs GI skin

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5
Q

4 routes of entry

A

Injection Ingestion Absorption Inhalation

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6
Q

3 ways to develop tolerance

A

Natural
Acquired
Artificially introduced

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7
Q

4 classes of immunogoblins (AKA antibodies)

A

Type 1 - IgE mediated
Type 2 - Tissue specific reactions
Type 3 - Immune-complexed mediated reactions
Type 4 - Cell mediated reactions

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8
Q

Antigens

A

Each have one antibody which will disable it, they were developed in a protective response by the body

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9
Q

IgE dependent

A

Normal ones

Nuts, seafood, milk, stings, MSG, penicillin, pets, NSAIDS

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10
Q

IgE INdependent reactions

A

Radio contract materials

Blood products

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11
Q

Non-immunologic

A

Opioids
Dextrans
Vancomycin

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12
Q

Primary response

A

Large amounts of IgE are produced, which bind to cell membranes of basophils and mast cells

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13
Q

IgE mediated hypersensitivity Type I

A

Ag induces crosslinking -

IgE binds to mast cells and basophils which release vasoactive mediators

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14
Q

IgG mediated cytotoxic Type II

A

Ab directed against cell surface antigens mediates cell destruction via complement activation
From blood transfusions, erthroblastosis fetalis, autoimmune hemolytic anemia

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15
Q

Type III Immune complex-mediated

A

Ag-Ab complexes deposited in various tissue induce complement activation and ensuing inflammatory response mediated by massive infiltration of neutrophils
Arthus reaction, serum sickness, necrotizing vasculitis, glomerulenephritis, RA and lupus

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16
Q

Ag =

A

Antigen generator

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17
Q

Ab =

A

Antibody

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18
Q

Arthus reaction

A

Localized vasculitis from type III reactions

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19
Q

Type IV Cell-mediated

A

Sensitized Th1 cells release cytokines that activate macrophages or Tc cells which mediate direct cellular damage
Contact dermitits, tubercular lesions, graft rejection

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20
Q

Histamines

A

Causes bronchoconstriction, increases intestinal motility, vasodilation, increased vascular permeability
Main culprit on anaphylaxis
Two classes H1 bronchoconstriction, contraction of intestines
H2 peripheral vasodilation and secretion of gastric acids

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21
Q

Leukotrienes

A

SRS-A (slow reacting substances of anaphylaxis)

Smooth muscle contraction and increased vasc perm, but takes longer than histamine to act

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22
Q

CNS effects

A 
Anxiety/agitated
Tremor
Sensation of cold
Dizziness
Weakness
Obtunded
Unconscious
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23
Q

Airway effects

A 
Stridor 
Hoarseness
Larygneal/epiglottic edema
Rhinorrhea
Bronchospasm 
Increased mucus production
Accessory muscle use
Wheezing
Decreased or absent air entry
24
Q

CVS effects

A

Tachy, hypotension, arrhythmias, shock, bradycardia, cvs collapse, cardiac arrest

25
Q

GI GU

A

N/V cramps diarrhea

26
Q

Integumentary

A

Angioedema, uticaria, pruritus (itchy), erythema

27
Q

Differential for anaphylaxis

A

Angioedema, PE/edema, asthma, epilgottitis, foregin body airway, poisoning, non-organic disease

28
Q

Tx keys

A

Early recognition, rapid evaluation, prompt intervention

29
Q

How does epi work

A

Reverses symptoms and inhibits release of mast cells/ basophils

30
Q

Epinephrine

A

1:1000 0.3mg IM q 5 max 0.9

31
Q

Benadryl

A

H1 antihistamine

25-50mg IM/IV/IO q 4-6 prn

32
Q

H2 blockers

A

Ranitidine or cimetidine after a severe reaction, or during episode if circulatory collapse

33
Q

Steroids - 3rd line

A

Clinical effect delayed 4-6 hours
Do reverse bronchospasm and skin effects
Don’t reverse cardiovascular effects
Can prevent biphasic

34
Q

Solumderol/Methylprenisolone

A

125mg IV/IO once

35
Q

Dexamethasone

A

8MG IM/IV/IO once

36
Q

Prenisone

A

50mg PO

37
Q

Epi 1:10 000

A

Refractory to 1st/2nd line therapies

0.1mg of 1:10000 SIVP/IO given q 2 prn max 1mg

38
Q

Epi infusion

A

Persistent symptoms greater than 30 min transport

1mcg/min titrate to BP 90 max dose 8mcg/min

39
Q

Glucagon

A

Hypotensive and on BB 1mg SIVP/IO q5 max 5mg

40
Q

Ventolin

A

2.5-5mg q 4-6 hours (thats silly)

41
Q

Nebbed epi

A

May help reduce laryngeal swelling, does not replace IM/IV

42
Q

BP

A

Lots of epi, lots of crystalloids consider pressors with alpha activity (levophed, epi, dope)
Consider glucagon if on BB

43
Q

Biphasic response

A

1-8 hours despite being asymptomatic, up to 36 hours

44
Q

Anaphylaxis tins pathology

A

IgE activates preformed mediators from secretory granules (histamine, tryptase, carboxypeptidase A, proteoglycans.
Downstream activation of phospholipase A2, followed by cyclooxygenases and lipoxygenases, produce AA metabolites including prostaglandins, leukotrienes, PAF.

45
Q

Histamine

A

Vasodilation, increased cap perm, increased heart rate and contraction, increased glandular secretion

46
Q

Prostaglandin

A

Bronchocontrictor
Pulm and coronary vasoconstrictor
Peripheral vasodilator

47
Q

AHS anaphylaxis criteria

A 
Exposure plus 1 of:
Sudden resp syndromes
Sudden hypotension or signs of end organ perfusion
OR BOTH:
Sudden skin & GI
48
Q

Timing of anaphylaxis

A

Quicker onset = more serious
1/2 of fatalities in first hour
Small risk for secondary reaction 8-11 hours later from cysteinyl leukotrienes 4-5% experience this (some studies say 20%)

49
Q

Differential for anaphylaxis

A 
Vasovagal
Myocardial ischemia, arrhythmias
Sever acute asthma, epiglottitis
Seizure
HAE
FBAO
non-IgE- mediated reactions
50
Q

Approach to anaphylaxis

A

Examine mouth, pharynx and neck for S&S of angioedema.
Assess for stridor, resp distress, hypoxia
If angioedema present consider tubing
Remove decontamination
EPI, benadryl, Neb, steroid,
2L fluid
1mg glucagon if on BB

51
Q

IV EPI

A

after 500mL 1mcg/min to 8mcg/min greater than 30 minute transport time

52
Q

IV EPI setup

A

1.5mg to 250mL D5W, concentration is 6mcg/mL

60 drop set, 1mcg/min = 10 drops per minute (Start at 10/min go to 80/min

53
Q

B blockers, CCB maybe

A

Severe hypotension due to unopposed alpha agonism so only B blockers need it

54
Q

Strongest to weakest steroid effects of mineralcorticoid

A

Hydrocortisone and cortisone are strongest, then pred followed by methylprednisolone and dex

55
Q

ACE inhibitor induced angioedema managament

A

Not IgE so standard meds don’t work
Tins says steroids won’t work either for this reason
Icartibant (bradykinin-2 antagonist) is tx
1000 IU of C1 esterase inhibitor may help as well

56
Q

Hereditary angioedema

A 
C1 esterase inhibitor deficiency 
Last from few hours to 1-2 days
Minor trauma often precedes attack
Stanozolol 2mg/d
C1 esterase inhibitor
FFP if no C1 available

Advanced medical (24 decks)

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