Ch 119 Allergic Reactions

Front 1

Compare innate and adaptive responses to allergens

Back 1

Innate: recognize and clear standard antigens (mast cells, macrophages, dendritic cells, natural killer cells, compliment cytokines)

Adaptive: B and T cells mediated - has immune memory and amplifies cytokine response —> highly specific

T Cells mature in thymus —> CD4/8 helper cells

B Cells mature in lymphoid organs (BM, fetal liver)

Both have memory

Able to discern self from non-self

Front 2

Provide the clinical criteria for anaphylaxis

Back 2

1. antigen + hypotension

2. MM/Skin + one of: SOB, hypotension

3. 2 of: MM/Skin, Hypotension, SOB, N/V/D

Front 3

OLD

What are the 4 Coombs and Gel hypersensitivity reactions (give an example of each)

Back 3

1 : antigen recognised by IgE or IgG cells

2: cell bound antigen activates compliment system - Rh, graves, goodpastures, transfusion reaction (ABO),

3: immune complex floating around —> depositis in tissues i.e. GN, Serum Sickness, HSP,RA

4: Deayed rx - contact dermaitits, Td - PPD, EM, SJS, Tens, - antigen antibody

اللي تحت هو الصح

Front 4

Describe the anaphylactic process

Back 4

IgE is released by plasma cells and responds to novel antigen, causing sensitization. Re-exposure to the antigen leads to mast cell degranulation with up-regulated receptorMediators: histamine, tryptase, chymase, carboxypeptide A —> capillary permeability, vasodilation, smooth muscle contraction, myocardial depression

Front 5

Name 8 Sx of anaphylaxis?

5 ECG changes?

Back 5

ECG Changes:

1. ST,
   
2. PAC/PVC,
   
3. AF,
   
4. non-specific T wave changes,
   
5. RV strain
   

Front 6

Provide 10 DDx of anaphylaxis

Back 6

Front 7

What are the 3 indications for IV epinephrine in anaphylaxis?

Indication for glucagon?

Back 7

Glucagon if patient on BB (1mg bolus then 1-5mg/hr)

Front 8

Name 10 ways to reduce the mortality risk of anaphylaxis in patients in the ED

Back 8

Front 9

What is angioedema?

Tx?

Quincke's Disease?

Back 9

Edema of deeper dermal and subcutaneous tissues without pruritis

Quincke's = angioedema of the uvula

Tx: as per anaphylaxis

Front 10

OLD

Name 10 causes of serum sickness

Pathophysiology?

Back 10

Type III reaction, immune-complex deposition

4-10d after exposure: generalized lymphadeopathy with urticaria, joint pains, fever

Tx: stop agent, antihistamines, possible steroids

ABX: Amoxil, Septra

Anti-sz: Dilantin

Antivenoms

Hymenoptera

Transfusion

Front 11

How does radiocontrast dye cause a hypersensitivity reaction?

Risk Factors for contrast allergy?

Prevention?

Back 11

Direct mast-cell degranulation, not IgE mediated

RF:

Previous reaction

Atopy/asthma/allergic dz

Prevetion of Contrast Reaction (per UPTODATE)

NO TEST DOSING - this is not recomended

CHECK if different contrast material can be used

Accepted regimen if you have time:

1. Prednisone 50mg at 13, 7, 1 hr prior (or solumedrol)
   
2. Benadryl 1 hr prior
   
3. Ranitidine 3 hr prior
   
4. ephedrine prior —> weak evidence really not used anymore
   

In An Emergency:

1. Solumedrol 40mg IV
   
2. Benadryl 50mg IV one hour prior
   
3. epinephrine available in the event of a reaction
   

Front 12

Reasons to admit anaphylaxis?

Back 12

1. Hypotension in ED
   
2. Upper airway involvement
   
3. Prolonged bronchospasm
   
4. Beta-blockade
   

Front 13

OLD

What are possible causes of angioedema?

Treatment?

Mechanism of ACE-I angioedema?

Back 13

Causes:

ACEi

Anaphylaxis/anaphylactiod

Hereditary (C1 esterase inhibitor deficency)

Standard treatment: same tx as anaphylaxis (avoid this tx if hereditary)

If hereditary: Ruconest (recombinant C1-esterase inhibitor), FFP

ACEI angioedema in 0.1-0.2% 2° to inhibited metabolism of bradykinin and substance Pusually in the 1st month but can occur 10 years latertx supportive ? can try FFP

Front 14

Define Anaphylactoid Reaction

Back 14

Clinically similar to anaphylaxis but not IgE mediated mediated by direct mast cell and basophil degranulation

do not require prior sentisitazation so can occur at single exposure

Front 15

Anaphylaxis Risk Factors

Back 15

high SES

summer/early fall

female > 30

adults

IV/topical antigen > risk than oral

Atopy = increased risk for mucosal route of reactioncauses: Food, drug, insect stings, latex = majority of causes

Front 16

Treatmet of Anaphylaxis

Back 16

Remove stingers

benadryl 50 mg IV/PO

epinephrine sc 0.3-0.5 (kids 0.01mg/kg) IM or epi IV 1-10mcg/min IVP/minute (1ml of 1:10000 in 9cc NS or 0.1ml of 1:1000 in 9cc NS = 10 mcg/ml)dirty epi drip 1mg in 1000NS = 1mcg/ml (can pull push doses from the bag or run an infusion)

Ventolin/Atrovent for bronchospasm

Neb Epi 5ml of 1:1000 in NS (peds 0.5ml/kg max 5ml)

Steroids Methyl pred 125mg IV (Pred po)

Epi refractory —> norepi

Glucagon if poor response to epi or on beta blockade

Front 17

Biphasic Reactions = # patients?

Back 17

Can occur up to 3 days post rx

# clinically important biphasic reactions < 1%

Risk Factors

1. Severe initial sxs
   
2. Delayed tx with epi
   
3. Slow response to initial txingested antigens
   
4. B2 blockade
   
5. PMHx of same
   

UP TO DATE: no consensus on duration of observation (2016)those with the above risk factors should be observed for 12 hoursotherwise min. 2 hours some guidelines recomend 4-6 hours (world allergy organisation)

Front 18

What is Mastocytosis?

S/S?

Dx?

Tx?

Back 18

Disorders of too many mast cellscutaneous

sxs: urticaria pigmentosa

systemic: mast cell hyperplasia in BM, gut liver and spleen (pathologic #, AP, diarrhea, headache, flushing)

Dx

1. 24 hour urine histamine,
   
2. serum tryptase,
   
3. skin Bx
   

Tx:

1. Steroids,
   
2. H1/H2 blockers
   
3. Interferon
   

Front 19

OLD

Risk Factors for increased severity of anaphylaxis

6

Back 19

1. extremies of age
3. comorbid cardiac or lung disease
5. use of - B2Blockers,
7. ACE
9. ETOH
11. recent anaphylaxis

* List from UTD

Front 20

DDx for rash and joint pain

Back 20

1. discemminated gonococcal
   
2. serum sickness
   
3. Rheumatic Fever
   
4. HSP
   
5. Toxic Shock
   
6. Lyme (early disseminated)
   

Front 21

NSAID Anaphylaxis Mechanism

Back 21

Inhibition Cox - inhibits thromboxane production increased leukotriine production

Front 22

Epi MOA

Back 22