Food Allergy Flashcards

1
Q

A 10-year-old boy presents to the clinic complaining of tongue and mouth itching within a few minutes after eating apples. His mother states that he has not experienced these symptoms with other foods, but they occur every time he eats a fresh apple. He denies systemic symptoms, and the oral symptoms resolve within a few minutes. Other than allergic rhinitis (nasal inflammation) in the spring months, he is healthy. Of the following, you are MOST likely to advise his mother that:

A) allergy skin testing to fresh apples probably will have negative results.

B) cooking the apple will not alter its allergenicity.

C) her son should avoid eating all fruits.

D) her son should avoid milk products.

E) her son’s symptoms are related to his allergic rhinitis.

A

E) her son’s symptoms are related to his allergic rhinitis

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2
Q

You are the ER physician and you give the child epinephrine injectable, followed by the antihistamine diphenhydramine (Benadryl), and some intravenous fluids. The mother asks you how she is supposed to know if the peanut caused the reaction or if it was something else and you tell her:

A. peanuts don’t cause allergic reactions if they are baked in a cookie.

B. who knows, she should have just given him diphenhydramine (Benadryl) and see if he okay.

C. this was a minor allergic reaction and she should just avoid peanuts in the future.

D. this was anaphylaxis, possibly to peanut, the epinephrine injection likely saved his life, but he needs further testing to find out for sure if it was peanut or another ingredient in the cookie.

A

D. this was anaphylaxis, possibly to peanut, the epinephrine injection likely saved his life, but he needs further testing to find out for sure if it was peanut or another ingredient in the cookie

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3
Q

What is sensitization?

A

May not go on to proceed to a clinical disease.

proven by IgE immunocap testing, skin testing, or oral challenge

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4
Q

Define a clinical food allergy. What differentiates it from sensization?

A

Sensitized

-Exposure causes reproducible characteristic IgE-mediated symptoms

(swelling, angioedema, hives, wheezing, histamine driven)

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5
Q

Compare intolerance to Allergy

A

Intolerance: your body cannot break down the food, if you eat small amounts you are okay, like with lactose causing pain, bloating, diarrhea with milk

Allergy: Your body mistakes that foord for something harmful leading to IgE-mediated reaction, there is an immmune reponse, and can be triggered by a microscoptic amount even by touch or inhalation or particles.

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6
Q

Is the presence of an atopic dz, like latex allergy, associated w/ a higher or lower prevalence of food allergy?

A

Higher

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7
Q

What are some of the most prevalent food allergies in children?

A

Cow’s milk, Egg, Peanut

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8
Q

What is the most prevalent food allergies in adults?

A

Crustaceans (Shellfish)

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9
Q

Differentiate the symptoms/complications of IgE medaited reaction vs. Non-IgE/Cemm mediated

A

In contrast to food intolerance, food allergy defines adverse reactions to food protein mediated by the immune system. Food allergy can be further divided into those allergies that are mediated by IgE antibody and those which are not IgE mediated. The IgE mediated food allergies are typically acute in onset and examples include anaphylaxis or urticaria. The non-IgE mediated food allergies are generally slower in onset and primarily are gastrointestinal reactions.

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10
Q

What some complications associated with IgE-mediated food allergies?

A

anaphylaxis, urticaria, angioedema, oral allergy syndrome, acute rhinitis, acute asthma

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11
Q

What is the typical chemical moiety of allergens? What are rarely allergens?

A

Proteins or glycoproteins (generally heat resistant and acid stable)

Rarely: carbohydrates

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12
Q

Describe the sensitization process on a molecular level (start with allergen and end with mast cell).

A

allergen -> allergen phagocytosed by DC -> allergen presented to allergen specific T cell -> Th2 -> Release IL-4, IL-5, IL-13 -> B cell stimulation -> Allergen specific IgE production -> IgE binds mast cell via Fc(epsilon)RI

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13
Q

What is released from mast cells during degranulation that causes the symptoms that present in IgE-mediated responses?

A

Histamines

Leukotrienes

Cytokines

Prostaglandins

PAF

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14
Q

What are some symptoms that people wrongly attribute to IgE-mediated food allergys?

A

Migraines, Behavioral / Developmental disorders, Arthritis, Seizures, Chronic fatigue, Inflammatory bowel disease

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15
Q

What do non-IgE medaited reactions primaryl manifest as?

A

Gastrointestinal symptoms like abdominal pain, vomiting, and diarrhea.

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16
Q

Describe these aspects of pollen-food syndrome aka oral allergy syndrome: Clinical features, Epidemiology, Key foods, and Allergens.

A

Clinical features: rapid onset oral pruritus, rarely progressive

Epidemiology: rhinitis due to prior sensitization to pollen

Key foods: raw fruits and vegetables

Allergens: Profilins (heat labile)

17
Q

What are some common fruits indicated in latex-food syndrome?

A

Banana, avocado, kiwi, chestnut but other fruits and nuts have been reported

18
Q

IgE enhances the expression of what receptor on mast cells and basophils?

A

FcεR1

19
Q

In a non-IgE-mediated anaphylaxis, what are some of the substances that could be activating the mast cells and basophils?

A

Complement anaphylatoxin activation (C3a/C5a), neuropeptide release (substance P), cytotoxic mechanisms, IgG and IgM, immune complexes, T cell activation

20
Q

What are some non-immunologic activators of mast cells and basophils?

A

venoms, contrast media, opiates, COX-1 inhibitors, vancomycin, NSAIDs, physical factors: cold or exercise

21
Q

What is mastocytosis? What mutation is associated with this condition?

A

Mastocytosis: Increased expression/production of mast cells, which leads to greater risk of IgE and non-IgE dependent anaphylaxis.

A GOF mutation is C-kit, which is transmembrane tyrosine kinase receptor for SCF that is responsible for promoting growth, differentiation, and survival of mast cells

22
Q

What are some of product classes produced by mast cells?

A

histamine, proteoglycans, proteases (tryptase), cytokines (IL-4, IL-8, IL-13), ang lipid mediators (leukotriene)

23
Q

What are the clinical criteria for anaphylaxis?

A

One out of three – highly likely

§Acute onset with skin, mucosal tissue or both involved AND at least 1 of the following:

§Respiratory compromise

§Hypotension or end organ dysfunction

§2+ of the following rapidly after exposure

§Involvement of the skin-mucosal tissue

§Respiratory compromise

§Hypotension

§Persistent symptoms

§Hypotension after exposure

§Low BP or greater than 30% decrease from baseline

24
Q

Why are histamine studies not very reliable if patient is currently under an attack? What are the two histamine studies?

A

Histamine has a very short half-life.

Histamine tests: Plasma histamine and 24 hour urine histamine

25
Q

Aside from histamine tests, what is another test to determine whether a patient underwent an anaphylactic episode?

A

Total serum or plasma tryptase (another product released by mast cells)

26
Q

How long must one wait before performing a sensitization test (skin prick test, inradermal)? Why?

A

3-4 wks. It allows the local mast cells to rebuild their granules

27
Q

What is considered negative in a immunocap test? postive?

A

Negative: class 0

Positive: class 2+

28
Q

What are some important aspects of managing a food allergy?

A

Ensure nutritional needs are being met

Education (all surrounding family/friends, etc)

Anaphylaxis Emergency Action Plan

Avoidance is the only effective therapy

29
Q

What are some factors to consider when deciding whether to to re-challenge an allergy?

A

§Type of food allergy (IgE vs non-IgE)

§Severity of previous symptoms

§Allergen/Prognosis (cow’s milk vs peanut)

§Age of the child

§Skin prick test/in vitro specific IgE should be negative prior to challenge

§Decline in concentration of food specific-IgE is suggestive of development of tolerance

30
Q

When should you administer epinephrine to a patient who is undergoing anaphylaxis?

A

If you think about it, administer it. (Basically, there is never a bad time to administer epinephrine to these patients. Also, the sooner the better b/c epinephrine can actually block mast cell degranulation)

31
Q

What are the 3 mechanisms of action of Epinephrine?

A

alpha 1 adrenegic vasoconstrictors - decreases mucosal edema, prevents hypotension, increased cardiac output

Beta 1 adrenergic- incresed force and rate of cardiac contractions

Beta 2 bronchodilation- decreases release of mediators form mst cells and basophils (fixes pulomarny problems and stops continuation of reaction)

32
Q
A