CM- Food Allergy Flashcards

1
Q

What are the 8 common foods that cause allergic reactions?
[objective 1]

What 4 are more common in adults because they are least likely to be outgrown? [marked with *]

A
  1. milk
  2. egg
  3. peanut*
  4. tree nuts*
  5. fish*
  6. shellfish*
  7. wheat
  8. soy
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2
Q

What is the difference between a food intolerance and a food allergy?

A

Allergy = immune-mediated mechanism of eliciting an adverse health effect

Intolerance = non-immunologic mechanism leading to a reaction following food ingestion

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3
Q

What are the 4 types of food intolerances [non-immune mediated reactions to food]?

A
  1. metabolic
    - lactose intolerance
    - galactosemia
    - pancreatic insufficiency
    - gallbladder or liver disease
  2. pharmacologic
    - caffeine
    - alcohol
    - histamine, tyramine
    - capsaicin
  3. Toxic
    - scrombroid fish
    - bacterial food poisoning
    - heavy metal poisoning [mercury in tuna]
  4. Idiopathic/undefined
    - sulfite sensitivity
    - anorexia nervosa
    - auriculotemporal syndrome
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4
Q

What are 5 examples of metabolic food intolerance?

A
  1. lactose intolerance
  2. galactosemia
  3. pancreatic insufficiency
  4. liver disease
  5. gall bladder disease
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5
Q

What are 5 examples of pharmacologic food intolerance?

A
  1. caffeine
  2. histamine
  3. tyramine [wine/cheese]
  4. capsaicin
  5. alcohol
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6
Q

What are 3 examples of toxic food intolerance?

A
  1. scombroid fish
  2. heavy metal poisoning
  3. bacterial food poisoning
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7
Q

Food allergy is the result of immune-mediated response occurring AFTER FOOD EXPOSURE [must be sensitized] that can be classified in what 3 ways?

A
  1. IgE mediated
  2. Non-IgE mediated
  3. Mixed IgE and non-IgE mediated
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8
Q

What are the 5 signs of IgE-mediated food allergies?

A
  1. acute urticaria
  2. acute angioedema
  3. oral allergy syndrome
  4. GI anaphylaxis -rapid onset nausea/vomiting etc
  5. generalized anaphylaxis
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9
Q

What are the 3 non-IgE mediated food allergies?

A
  1. Celiac disease
  2. Dermatitis herpetiformis
  3. food-induced pulmonary hemosiderosis [Heiner’s syndrome]
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10
Q

What are the 3 mixed IgE/non-IgE food allergies?

A
  1. eosinophilic esophagitis
  2. eosinophilic gastroenteritis
  3. atopic dermatitis
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11
Q

What is the pathophysiology for IgE-mediated reaction to food?

A

prior exposure/sensitization must occur!

  1. ingestion of food
  2. Proteins taken up by M cells [epithelial cells] in gut
  3. APCs like dendritic cells acquire the protein and process it into fragments
  4. Peptide frags are presented on the cell surface by MHC class II molecules
  5. Antigen receptor on naive T-cell recognizes the peptide

NON-allergic –> Th1 response with cytokines IFNg
ALLERGIC–>Th2 with IL4, IL5, IL13

  1. allergic individuals have B-cells make IgE specific for the particular food
  2. IgE binds to the surface receptor on mast cells and basophils [FceRI]
    8 re-exposure to food causes IgE to cross-link the allergen and cause mast and basophils to release histamines, cytokines, leukotrienes
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12
Q

In the initial encounter with food, how do not allergic and allergic immune systems respond differently?

A

When the T-cell is introduces to MHCII on APC presenting the food,

  1. allergic people have Th2 rxn releasing IL4,5,13 which activates b-cells to make IgE
  2. non-allergic people have Th1 rxn releasing IFNg
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13
Q

Symptoms of an IgE mediated food allergy can present in any organ system , but are characteristically seen where?

A

Sites where mast cells are found

  1. respiratory tract
    - UPPER: sneezing, rhinorrhea, nasal congestion
    - LOWER: dyspnea, cough, wheeze
  2. GI tract
    - nausea, vomit, diarrhea, cramping
  3. cardiovascular system
    - hypertension
  4. skin
    - urticaria [hives]
    - flushing
    - angioedema
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14
Q

What 4 food allergies do children tend to develop a natural tolerance over time?
When does tolerance typically develop?

A

Milk, eggs, soy and wheat.

Tolerance is achieved by school-age

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15
Q

Which food allergy may not have developed until adulthood in 60% of allergic individuals?

A

shellfish

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16
Q

What is the gold standard for diagnosing a food allergy?

What is done more commonly by physicians?

A

Gold standard =Double-blind, placebo-controlled food challenge

Typical diagnostic strategies:

  1. specific IgE tests
    - in vitro quantification of IgE in response to food
  2. skin prick tests
    - puncture epidermis through an extract of food
  3. observed open oral food challenges
17
Q

Describe the procedure of the Skin Prick Test.
What must the results be interpreted in the light of?
What determines a positive skin test?
What is the NPV and PPV?

A

Puncture the epidermis of the patient with a needle, probe or lancet that has food extract on it.

Interpret results in light of historical reactions.
Positive reactions are a wheal 3mm or larger than the negative control.

Negative results: greater than 95% NPV
PPV = 50% [although the larger the wheal, the greater the PPV]

18
Q

What is treatment for a food allergy?

A
  1. avoidance of the food allergen
  2. education about cross-contamination and cross-reacting foods
  3. education about nutritional supplementation
19
Q

It is recommended that 2 doses of auto-injectable epi be carried by all allergic individuals that meet what criteria?

A
  1. history of prior systemic allergic reaction
  2. food allergy and asthma
  3. allergy to peanuts, shellfish, tree nuts, fish
20
Q

What are the 7 major risk factors for a fatal or near fatal food-induced allergic reaction?

A
  1. concomitant asthma with adrenal suppression [from glucocorticoids]
  2. delayed epi administration
  3. denial of symptoms
  4. lack of skin symptoms
  5. concomitant alcohol [increased absorption of allergen]
  6. reliance on oral antihistamines alone
  7. peanuts, tree nuts, shellfish, fish
21
Q

What typically precedes the appearance of the eczematous lesion associated with atopic dermatitis?

A

chronic pruritis

AD is the “itch that rashes”

22
Q

What percent of cases of atopic dermatitis arise:

  1. within the first 6 months of life
  2. first year
  3. before the age of 5

What percent of atopic dermatitis cases go to remission before adolescence?

A
  1. 45%
  2. 60%
  3. 85%

70% will be in remission by adolescence

23
Q

What is the pathogenesis of atopic dermatitis?

[What factors are elevated and decreased?]

A

Acute atopic dermatitis:

  1. expansion of Th2 that release IL4, IL10, IL13 [pro-inflammatory]
  2. decrease in Th1 [decreased IFNg]
  3. elevated IgE [level does NOT correlate with disease activity]
  4. Eosinophils degranulate in the dermis releasing MBP which induces histamine from basophils and mast cells
24
Q

What is the role of eosinophils in atopic dermatitis?

A

They are NOT accumulated in tissue, however, degranulation occurs in the dermis releasing MBP which activates basophils and mast cells to release histamine leading to:

  1. itching
  2. irritation
  3. lichenification
25
Q

Typically there is not 1 factor that causes a child with atopic dermatitis to have a skin flare, but rather numerous contributing factors.
What 7 factors contribute to flares?

A
  1. temperature change, sweating
    - leaving hot shower to lower temp
  2. decreased humidity
    - colder temperatures
  3. contact with irritants
  4. aeroallergens
  5. microbic agents [s. aureus]
  6. food
  7. emotional stress
26
Q

What areas of the body are prone to itching of atopic dermatitis?

A

antecubital fossa

popliteal fossa

27
Q

What are common irritants that can contribute to AD flares?

A
  1. wool
  2. scented detergents, soaps, lotions
  3. cigarette smoke
  4. household chemicals
28
Q

What aeroallergens contribute to AD flares?

A
  1. dust mites [most common]
  2. pet dander
  3. mold
29
Q

50-80% of children with atopic dermatitis will ALSO have one of what 3 things?

What is the “Atopic Triad”?

A

They will have another atopic disease like:

  1. asthma
  2. allergic rhinitis
  3. food allergy

Triad = AD, asthma, allergic rhinitis

30
Q

S. aureus is common on skin, however people with atopic dermatitis tend to have increased colonization and their ability to fight infection is impaired. What are 3 reasons why?

A
  1. reduced antimicrobial peptide levels
  2. diminished recruitment of cells to skin
  3. Toll-Like receptor defects with epidermal barrier defects
31
Q

What is the food that most commonly provokes atopic dermatitis?

A

Eggs

32
Q

In atopic dermatitis, itching leads to acute inflammation. What is the progression of how symptoms present?

A
  1. erythematous papules [can be associated with excoriations, erosion, serous exudate]
  2. coalesce to form plaques [weeping, scaling, crusting]
  3. chronic dermatitis –> thickened skin, lichenifications, fibrotic papules
  4. dry, scaly, xerosis
33
Q

What is the distribution of atopic dermatitis in infants and toddlers?
[obj 4]

A

eczematous plaques on:

  1. forehead, cheeks
  2. scalp
  3. extensor surfaces
34
Q

What is the distribution of atopic dermatitis in older children and adolescents?
[obj 4]

A

lichenified, eczematous plaques on:

1. flexural areas [neck, elbows, wrist, ankles]

35
Q

What is the distribution of atopic dermatitis in adults?

[obj 4]

A

lichenification in flexural regions of:

hands, wrist, ankles feet face

36
Q

What is treatment for atopic dermatitis?

A
  1. intense moisturization
    - bathe no more than 1x daily, pat dry, use lotion within 3 minutes before water evaporates
  2. eliminate triggering factors
  3. topical steroids and NSAIDs [tacrolimus]