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Respiratory Block > Allergies > Flashcards

Flashcards in Allergies Deck (26):

1. Describe the components of immediate hypersensitivity reactions.

antigen from the environment is processed by an antigen presenting cell APC, a TH2 response dominates which drives IgE , IgE binds to receptors on mast cells and basophils

IgE on mast cells results in release of mediators the produce end organ response


2. Identify the major difference between mast cells and basophils (location, histamine content, steroid effects, cyclooxygenase inhibition)

Mast: located in tissues and contain much more histamine, minimal steroid effects, no effect from cylcooxygenase pathway inhibition (immediate-predominate rxn.)

basophils: in the peripheral blood, steroids inhibit mediator release, and COO pathway inhibition augments mediator release, lesser histamine content (late-predominant reaction


3. Describe the mechanisms and agents responsible for mast cell activation/secretion.

cross linking of IgE receptors is essential for mast cell/basophil activation (allergen binds at least two IgE molecules)

secretion can be triggered by IgE, endogenous stimulus (complement, neuropeptides, ATP, adenosine, cytokines etc.) and exogenous factors (anesthetic agents, antibiotics, narcotics and iodinated contrast material)


4. List the principal preformed and generated mast cell mediators.

preformed: vasoactive amines (histamine, serotonin), proteoglycans (heparin), neutral proteases (tryptase, chymotrypitc proteases), acid hydrolyses (B hyxosaminidase and B glucoronidase, chemotactic factors for eos and polys and peroxdase/superoxide


5. Describe late-phase reactions.

over hours cytokines are produced and released, speficially IL-4, IL-13


6. Compare the skin test and serum IgE procedures for sensitivity testing.

allergen hypersensitivity on skin- detects IgE on skin mast cells (most common and most sensitive test used clinically)

immunoassays for specific Ig (ie. RAST or ELISA)
Provocation studies "challenge"- tests tolerance
basophil/mast cell histamine release- tests activation


7. Describe the signs and symptoms of allergic rhinitis.

congestion, post nasal drip and rhinorrhea, pruritus, sneezing, ocular congestion, redness, itching

complications: sinusitis, nasal polyposis, otitis media and allergic conjunctivitis


8. Describe the pathogenesis of allergic rhinitis. (immediate and late phase)

binding of allergen to allergen specific IgE on mast cells causes mediator release (preformed: histamine and proteases; De novo: arachidonic acid metabolites and cytokines)

late phase inflammation involves increased expression of cell adhesion molecules by endothelium, local release of cytokines and chemotactic factors and eosinophils, basophils and activated lymphocytes


9. Discuss the methods to diagnose allergic rhinitis.

hx: seasonal or perennial pattern of allergen
PE: swelling of nasal mucosa, conjunctival inflammation, allergic shiners, Dennies lines, nasal crease, mouth breathing

dx. tests (when needed): Serum IgE, skin tests,


10. Discuss the different modes of therapy for allergic rhinitis.

environmental control measures

mediator antagonists (antihistamines, topical anticholinergics, leukotriene inhibitors and antagonists, decongestants)
anti-inflammatory agents
mast stabilizers


11. Describe the pathogenesis of allergic asthma.

TH2 shift magnifies sensitization and allergic response leading to airway inflammation and eventually airway remodeling


12. Define the following terms: atopy and allergen.

allergen is an antigen capable of eliciting an IgE antibody response
Atopy- a genetic predisposition to the formation of increased levels of IgE antibody (factors that play a role: changes in allergen levels, increased environmental pollution, dietary changes, alterations in exposure to microbial pathogens)

IL-4, IL-13 will increase IgE production while INF gama will decrease IgE


13. Differentiate food allergy and food intolerance.

allergies have immunological mechanism
food intolerance is due to non-immunologic cause (ie. metabolic, food poisoning, pharmacologic etc. )


14. Discuss the clinical manifestations of food allergy.

cutaneous manifestations (hives, pruritus, eczema)
GI (itching, nausea, vomiting diarrhea, abdominal pain)
respiratory (rhinoconjuctivitis, wheezing, hoarseness)
neurologic manifestation (feeling of dread)


15. Differentiate drug allergy from other adverse reactions to drugs.

food allergies are reproducible, and are eliminated if food is eliminated

drug reactions can be predictable (occur in most normal individuals) or unpredictable (occurring in a small subset of the population- idiosyncratic or immunologic)


16. Describe the various mechanisms (Type I-IV) that produce drug hypersensitivities.

I) immediate hypersensitivity: penicillin, radioconrast
II) cytotoxic: penicillin-induced hemolytic anemia
III) immune complex: cephlosporin
IV) delayed type hypersensitivity: neomycin-induced contact dermatitis


17. Describe the clinical manifestations of anaphylaxis.

can be incited by: food, medications, physical, autoimmune, idiopathic resulting in a systemic allergic reaction with urticaria, angioedema, nausea, vomiting, diarrhea, wheezing, shortness of breath, arrhythmias, hypotensionand death


18. Describe the treatment of anaphylaxis. (drug/dose/route)



Name features of inhaled allergens that may promote the priming of TH2 cells that drive IgE responses.

enzymatically active
low dose
low molecular weight
high solubility
contains peptides that bind host MHC class II


When do antigen specific IgE antibody formation begin?

18mo- 2 years aeroallergens


IgE production requires cytokines that are released by TH_ cells in particular IL-_.

TH2, IL-4


Name the principal receptor that binds IgE on mast cells and basophils.

Fc epsilon RI, present on mast and basophils including a alpha, beta and gamma


The describe how the pulmonary dual response to allergen exposure is a potential mechanism for the development of chronic asthma.

the late response to allergens is a due to tissue inflammation that was initiated or exacerbated by mast cell activation, it is recognized now as an important feature in many allergic diseases: asthma, allergic rhinitis, and atopic dermatitis and urticaria


Contrast seasonal and perennial allergens.

seasonal allergens: spring-trees, mid-summer-grassses and fall-weeds and molds


What is oral allergy syndrome?

fresh fruits and vegetables cross react with pollen allergens (ie. birch/apple; ragweed/melon)


What options of treatment exist to address medication allergy?

stop the drug, pick an alternative
treat symptoms with antihistamine
desensitization (best for IgE mediated reactions
treat through

make sure patient does not get drug in future