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What is a type I reaction?

occur promptly after sensitized individual is exposed to an antigen, mediated by specific IgE antibody. cross-plinking of IgE on the surface of mast cells an basophils lead to histamine release/other inflammatory mediators release
examples: immediate hypersensitivity - allergic rhinitis and urticaria
anaphylactoid reactions - similar, but caused by degranulation of mast cells ann basophils WITHOUT specific IgE


What is Type II reactions?

Antibody against antigen components of blood or tissue cells or foreign antigens, results in cell destruction.
can be IgM, IgG or IgA antibodies, they bind to the cell surface and activate the entire complement pathway , triggers mast cell degranulation, leads to inflammatory mediator release
examples: autoimmune hemolytic anemia and Rh/ABO hemolytic disease of the newborn; other examples (from baby Nelson): thrombocytopenia, basement membrane molecules in the kidney (GOodpasture), myasthenia gravis, Graves disease
IgG or IgM involved, complement is the mediator


What are type III reactions?

antigen-Ab complexes form, deposited in the lining of blood vessels, and filtering organs (i.e. liver, spleen, kidney)
activate the complement cascade, recruit neutrophils, leads to inflammation
ie: serum sickness and immune complex-mediated renal diseases (i.e. PSGN), also hypersensitivity pneumonitis
complement and anaphylatoxin are mediators
Timing (baby nelson ) 1-3 hours after drug exposure (i.e. for serum sickness), arthrus reaction can happen earlier after


Type IV reactions?

involve T cell-mediated tissue inflammation and typically occur 24-48 hours after exposure (baby Nelson says 2-7 days after drug exposure)
ie: tuberculin reactions, contact dermatitis , graft vs host disease
lymphocytes involved, cytoins are mediators (include IFN alpha, TNF, alpha, GMCSF)


What is the best biological marker for anaphylaxis?

tryptase, although it is still rather insensitive
early mediators of anaphylaxis: histamine, tryptase, chymas, heparin, proteases
late mediates: prostaglandings, leukotriene and cytokines

steps of type I hypersensitivity:
develop depends on :
hereditary predisposition, sensitization by exposure, subsequent reexposure to the antigen
IgE towards specific allergens bound o receptors on mast cells an dbasophils, cell gets activated by cross linking IgE antibodies and leads to the release of mediators


Examples of type I hypersensitivity

alergic rhinitis (most common)
anaphylaxis (most severe)


How is type I hypersensitivity diagnosed?

skin testing
percutaneous skin test - in vivo method to detect IgE antibody to specific allergens ; how it works, the IgE cross links and causes mast cell degranulation leads to histamine release
skin prick test - safest and most specific test: correlates best with symptoms
- interpret by measuring maximal diameter of wheal and flare 15-20 minutes after infecting with the allergen (via prick/puncture or intradermal infection)
- intradermal thought to be more sensitive than prick tests, but specificity is poor , should only use when ruling out allergic disease is essential (i.e. skin prick test is better)
- compare with negative control (saline) and positive control (histamine)


What are 4 contraindications to allergic skin testing:

1) recent use of anti-histamines (histamine control will be negative)
2) skin disease limits the area available for testing (i.e. dermatographism or extensive dermatitis)
3) during an asthma exacerbation or episode of anaphylaxis
4) when a patient is taking a beta blocker, because this could interfere with epi to treat test-induced anaphylaxis

in these cases, in vitro testing is a good alternate
can do with a few millilitres of blood


Which are more sensitivite, in vitro tests or skin prick tests for allergy?

in vitro tests are
1) less sensitive than allergy prick tests (especially less sensitive for aeroallergens, drugs and hymenoptera)
2) more expensive than allergy prick tests
see table on pg 113 for comparisons
also, in vitro not affected by any drugs, including steroids, vs skin test will be affected by antihistamines and not usually affected by corticosteroids**
(also baby nelson pg 273 comparison)


What organ is most commonly involved in anaphylaxis?

the skin


True or false - skin testing is commonly affected by steroids

false - not commonly affected by steroids


True or false - life-threatening reaction to hymenoptera is common in childhood

false - not common in childhood, compared to common opinion.
most common are large local reactions or generalized urticaria


A child presents with a large local reaction after a bee sting. The parents want to know how long it will last. What do you tell them?

- continuous with sting, starts 12-24 hours after sting, peaks in 2-3 days, lasts 1 week and should be treated with antihistamines and NSAIDs


The same parents want to know if their kid needs an epi pen.

excellent long-term prognosis, do not need allergy testing, do not need to carry epi
**the risk for systemic anaphylaxis from stinging insets in children with symptoms confined only to the skin is equal to the risk in the general population


Two day's later, the child's sibling presents with generalized urticaria after a bee sting. They really need to get rid of the bees. Does this kid need epi?

Yes, at present, the consensus among allergists suggests that children with a history of generalized urticaria from stinging insects carry epi

these kids don't need skin testing or desensitization

**ps all from Zitelli


That night on call, the neighbour of the first two kids arrives with an anaphylactic reaction. After he is stabilized and being prepared for discharge, what do you tell the parents about follow up and treatment ?

anaphylaxis after sting: should get allergy testing and if positive, should get immunotherapy
testing should be done 4 or more weeks after reaction (if you do it too soon, risk of false negative)
immunotherapy protects from anaphylaxis in 95-100% of patients (for wasps, yellow jackets,hornet etc), less for honeybees (80%)

(unrelated immunotherapy also works for desensitization of pollens, dust mites, and cat and dog proteins)


What bug is the most common cause of hymenoptera anaphylaxis in US

yellow jackets


What are the two big categories of food allergy? (zitelli figure 4-9)

1) IgE mediated hypersensitivity (anaphylaxis, oral allergy)
2) non IgE mediated


What are some examples of non igE mediated food allergy?

- food protein enteropathy, milk protein enterocolitis, lactose intolerance

from either mechanism: eosinophilic gastroenteritis, atopic dermatitis


True or false - most kids will outgrow type I reactions to milk and egg

true - these reactions usually more mild (i.e. urticaria) and in first year of life, usually outgrow them


What percentage of kids will outgrow a type I hypersensitivity peanut allergy?



What is oral allergy syndrome?

aka pollen food syndrome
patients have underlying seasonal allergic rhinitis and develop pruritus and angioedema of the oropharynx when ingesting fresh fruits and veggies - cross reactivity between proteins in some fruits and veggies and outdoor seasonal pollens , can eliminate the reaction by heating the veggie/fruit


True or false - milk protein enterocolitis is IgE mediated

no, bloody diarrhea in few months, improves with removing milk proteins front eh diet.
non IgE mediated so neither allergy skin prick nor in vitro helps (i do think there is aIgE form too, will need to read more about this)


What is the time of onset of each of the hypersensitivity types?

type 1: <30 min (immediate) 2-12 hours (late phase
type II: minutes/hours
III: 4-8 hours
IV: delayed type 24-48 hours


what is the major determinant in penicillin?

once penicillin enters the body, it is converted to a reactive intermediate, binds to nearby proteins, forming penicilloyl amides
these are called the major antigenic determinant
small amount is in the body as a minor determinant
Skin testing with the major determinant, penicillin and minor determinant - negative predictive value of 100% , 10-20% of skin tests from minor determinant


How long after drug exposure does serum sickness start?

1-3 weeks after drug exposure, involves fever, malaise, arthralgia, arthritis, urticaria, lymphadenopathy
many patients have a characteristic serpiginous, erythematous or purpuric rash
decreased C3 and C4, immune complexes
triggers (baby Nelson): blood products, foreign proteins (i.e. antithymocyte globulin and antivenins)
medications: penicillin, sulfonamides, minocycline, cefaclor, hydantoins, thiazides
can happen more soon in a patients who was previously sensitized
rare complications: carditis, GN, Guillain Barre, encephalomyelitis, peripheral neuritis


What is the treatment for serum sickness

baby Nelson: self-limited should resolve in 1-2 weeks, treatment is symptomatic
antihistamines for pruritus, NSAIDS for fever and joint pain , if needed can give prednisone
allergy skin testing doesn't predict serum sickness

antihistamines steroids if doesn't work
should resolve within a few weeks


Common trigger for TEN

almost always drug induced


Comon trigger for SJS

drugs (1-3 weeks before)
infection: mycoplasma, HSV
no universal therapy: some say IVIG


Can we use steroids for SJS?

no, relatively contraindicated some studies have shown a deleterious effect