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18 Cards in this Set

  • Front
  • Back
Type 1 Hypersensitivity
IgE mediated response to foreign proteins

requires prior exposure

rapid onset

20% of population affected
Pathophysiology of Type 1 hypersensitivity
sensitization phase - exposer/processing/IgE production

IgE bing mast cells and basophils

Clinical phase - rexposure - binds IgE - degranulation - chemotactic factors - cellular inflammatory respose
Hygiene Hypothesis
lack of childhoods exposure to infectious agents increase susceptibility to allergic diseases by modulating immune system development

allergic diseases are driven by inappropriate TH2 mediated immune response

bacteria and viruses elicit a TH1 response which down regulate TH2 responses
Case 1 - Primarily RT pollens and molds

Findings - EYES - allergic shiners, dennie lines, conjuctivitis, cobblestoning, clear/stringy discharge
NOSE - pale mucosa, edamatous mucosa, THROAT - cobblestoning

Symptoms - itchy eyes, redness, drainage, sneezing, post nasal drip (early)
- congestion (late)

DDx?
Recurrent URI, Rhinitis, sinusitis, deviated septum, cystic fibrosis, immotile cilia, foreign body

Diagnosis - use HandP
allergy skin tests, RAST tests
also can measure IgE

Management - avoidance of allergens, antihistamines, steroids, immunotherapy
Corticosteroids
most are inhaled,

except prednisone and prednisolone
antihistamines
oral
1rst gen - ends in amine or stine
2nd gen - ends in adine or zine

Nasal - Azelastine
Other Anti Allergy Meds
inhaled mast cell stabilizers - Cromolyn sodium

leukotriene receptor antagonists - monolukast

oral decongestants - pseudophedrine, phenylephrine

inhaled anticholinergic - ipratropium bromide
immunotherapy
increasing amounts of allergen extract

usually effective in most people
induces shift from TH2 to TH1 cytokine production
Case 2
Perennial AR - Indoor allergens, rarely foods
diagnosis same for seasonal allergic rhinitis

avoid dust mites
remove animal dander
Caae 3
Food Allergy
Symptoms - Gi problems, Urticaria, angioedema, respiratory probs

runny nose alone does not occur in food allergy

there is a connection between food allergy and dermatitis

prognosis - infants usually outgrow allergies. exception: peanut allergy is life long

Dx:skin testing or immunoCAP
-watch out for false positives

intradermal testing is CONTRAINDICATED

Negative tests can be relied on

Vaccines and egg allergy - MMR is not contraindicated
Flu and Yellow Fever IS contraindicated

Tx: strict avoidance
Dx for Asthma
H and P
CXR
Spirometry (w/ and w/o)
Methacholine challange
exercise challange
CXR in Asthma
hyperinflation
widening of rib spaces
flattening of diaphragm
stelectasis
pneumothorax
Asthma Classification
mild intermittent: around 2 times a week
nocturnal symptoms
no daily medication
beta 2 agonist for emergencies

mild persistent: 3-6 times a week
nocturnal symptoms 4 times a month

Low dose corticosteroids
or mast stabilizers
or theophyline
or leukotriene inhibitors

moderate persistent:5 times a month but with more severe loss in function

medium dose ICS or combo with beta 2 agonist
also use typical alternatives

severe persistent: continual, every night symptoms, large loss in function

high dose ICS or long acting beta 2 agonists, theophyline, LI
Case 6
Allergic Asthma
seasonal or perennial allergies

USE immunotherapy
also use anti-IgE
Case 7
Anaphylaxis
multisystem mast cell mediator release
acute onset
can be fatal

caused by: food allergy, insect sting, medications, radio contrast, latex, immunotherapy, idiiopathic
Symptoms of Anaphylaxis
tachycardia, hypotension, volume loss, MI

bronchoconstriction,
rhinitis, throat edema

cutaneous, GI, occular and GU symptoms
Mechanism of Anaphylaxis
IgE mediated (food, medicine, insects, latex)
complement mediated (radiocontrast)
direct mast cell activations (Vanc, opiates, exercise)
Diagnosis and treatment of Anaphylaxis
elevated tryptase
H and P

give O2, epi, IV fluids, H1 and H2 antihistamines, vasopressors

corticosteroids