11/3- Pediatric Allergic Disease Flashcards

1
Q

What is another name for atopic dermatitis?

A

Eczema

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2
Q

What is the “Atopic (Allergic) March”?

A

The typical progression of allergic diseases that begin early in childhood

  • Atopic dermatitis (eczema) (birth+)
  • Food allergy
  • Allergic rhinitis (3-5 yo)
  • Asthma
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3
Q

What is atopic dermatitis?

  • Genetic component
  • Prevalence
A

Chronic, inflammatory skin disease

  • Involves a genetic defect in the proteins supporting the epidermal barrier
  • Relapsing, itchy skin condition
  • Affects 15-20% of children
  • Also known as “eczema” or “atopic eczema”
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4
Q

Describe the natural history of atopic dermatitis?

  • Onset
  • Progression
A

Onset

  • 60% in 1st yr
  • 85% before 5 yo

Remission

  • 70% before adolescence

IgE sensitization

  • Only 50% of children < 2 yo
  • 80% of older children and adults
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5
Q

T/F: there is a genetic predisposition to atopic dermatitis?

A

True

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6
Q

What are major genetic components/mutations contributing to atopic dermatitis?

A

Filaggrin mutations

  • Atopic dermatitis
  • Allergic asthma
  • Peanut allergy
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7
Q

What are causes of the following clinical features?

A
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8
Q

What are consequences of these causes?

A
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9
Q

What is seen here?

A

Ichthyosis

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10
Q

What is seen here?

A

Excoriation/lichenification

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11
Q

Secondary infection may also occur with atopic dermatitis/eczema. List some of these:

  • Bacterial
  • Viral
  • Mycotic
A

Bacterial

  • Impetiginization
  • Polyclonal activation of T-lymphocytes by bacterial exotoxins

Viral

  • Localize: human papilloma, molluscum, herpes
  • Systemic: eczema herpeticum

Mycotic

  • Malassezia
  • Dermatophytes, candida
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12
Q

What are some trigger factors of atopic dermatitis?

A
  • Irritants (wool, detergents, disinfectants, cosmetics)
  • Microbial agents (Staph aureus, other bacteria, Malassezia furfur, viral infxns)
  • Emotional (stress)
  • Food allergens (cow’s milk, wheat, egg, soy)
  • Aeroallergens (house dust mite, animal dander, tree and grass pollen, mold/fungal allergies)
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13
Q

What are the basic principles of therapy with atopic dermatitis?

A

Recall AD is associated with:

  • Epidermal barrier dysfunction
  • Immunological dysregulation

Long-term management involves

  • Moistures for skin hydration
  • Anti-inflammatory medication
  • Flare prevention by avoidance of proven allergens

For the most severe cases, may use cyclosporin or UV therapy, but the mainstay of treatment are anti-inflammatories and moisturizers

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14
Q

What is the definition of a food allergy?

A

FA is an adverse health effect arising from a specific immune response that occurs reproducibly upon exposure to a given food

Two important points:

  • FA is defined as an adverse health effect, not simply having a positive skin prick test or elevated IgE (need hives, vomiting, diarrhea…)
  • FA arises from a specific immune response, thus distinguishing it from food intolerance
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15
Q

What are common food allergens?

A

Proteins or glycoproteins (not fat or carbs)

  • Generally heat resistant, acid stable

Major allergenic foods (>85% of food allergies):

  • Children: mlik, egg, soy, wheat, peanut, tree nuts
  • Adults: peanut, tree nuts, shellfish, fish, fruits, and vegetables
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16
Q

What is the prevalence of food allergies?

  • Adults vs. kids
  • Prevalence higher in what populations
  • Prevalence increasing or decreasing
A
  • Public perception: 20-25%
  • Confirmed allergy (oral challenge)
  • Adults: 2-3.5%
  • Infants/children: 6-8%
  • Specific allergens depend upon societal eating and cooking patterns
  • Prevalence is higher in those with:
  • Atopic dermatitis
  • Certain pollen allergies
  • Latex allergies
  • Prevalence seems to be increasing
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17
Q

What are the immune mechanisms behind food allergies?

A
  • Protein digestion, antigen processing, and some Ag enters blood
  • APC is responsible for non-IgE mediated reactions (delayed)
  • TNF-a and IL-5
  • Activates T cell and B cell to produce IgE
  • IgE binds mast cell and causes release of histamine
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18
Q

What are signs/symptoms of IgE and non-IgE allergic reactions?

A

IgE (acute):

  • Skin: urticaria, angioedema, atopic dermatitis
  • Respiratory: throat tightness, asthma
  • Gut: vomit, diarrhea, pain
  • Anaphylaxis

Non-IgE (chronic):

  • Atopic dermatitis
  • Gut: vomit, diarrhea, pain
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19
Q

What is the #1 cause of anaphylaxis in the ED?

A

Food allergies

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20
Q

What is food-induced anaphylaxis?

A
  • # 1 cause of anaphylaxis in the ED
  • Rapid-onset, up to 30% biphasic
  • May be localized (single organ) or generalized
  • Potentially fatal
  • Any food, highest risk: peanut, tree nut, seafood (cow’s milk and egg in young children)
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21
Q

What is the natural history of food allergies?

A
  • Dependent on food and immunopathogenesis
  • ~ 85% of cases of cow milk, soy, egg and wheat allergy remit by age 3 yrs
  • Declining/low levels of specific-IgE predictive
  • IgE binding to conformational epitopes predictive
  • Non-IgE-mediated GI allergy
  • Infant forms resolve in 1-3 years
  • Toddler / adult forms more persistent
22
Q

What is the process for evaluating and diagnosing a food allergy?

A

History: most important

  • Sx, timing, reproducibility, treatment, and outcome
  • Concurrent exercise, NSAIDs, EtOH

Diet details/symptom diary

  • Subject to recall
  • “Hidden” ingredient(s) may be overlooked

Physical exam: assess for other allergic and alternative disorders

Identify general mechanism

  • Allergy vs. intolerance
  • IgE vs. non-IgE mediated

IF YOU SUSEPCT:

- IgE mediated:

  • Skin prick tests
  • In vitro tests for food-specific IgE

- non-IgE mediated:

  • Consider biopsy of gut, skin

- non-immune, (possibly just intolerance) consider:

  • Breath hydrogen
  • Sweat test
  • Endoscopy
23
Q

How do you manage a food allergy?

A
  • Complete avoidance of specific food trigger
  • Ensure nutritional needs are being met
  • Education
  • Anaphylaxis emergency action plan if applicable
  • Most accidental exposures occur away from home
24
Q

What is emergency treatment of anaphylaxis?

A

Epinephrine is the drug of choice

  • Self-administered Epi is readily available at all times
  • If administered, seek medical care IMMEDIATELY
  • Train patients, parents, contacts: indications/technique

Antihistamines are secondary therapy only

  • WILL NOT STOP anaphylaxis

Written Anaphylaxis Emergency Action Plan

  • Schools, spouses, caregivers mature sibs/friends
  • Emergency identification bracelet
25
Q

What is rhinitis?

A

Symptomatic disorder of the nose characterized by itching, nasal discharge, sneezing and nasal airway obstruction

26
Q

What is allergic rhinits?

A

Induction of rhinitis symptoms after allergen exposure by an IgE-mediated immune reaction; accompanied by inflammation of the nasal mucosa and nasal airway hyperreactivity

  • Recall, rhinits symptoms include: itching, nasal discharge, sneezing, and nasal airway obstruction
27
Q

What are clinical manifestations of allergic rhinitis?

A
  • Repetitive sneezing
  • Rhinorrhea
  • Nasal congestion/ obstruction
  • Nasal itching
  • Throat clearing
  • Postnasal drip, cough, irritability and fatigue
  • Symptoms of other co-morbidities
28
Q

What are co-morbidities of allergic rhinitis?

A
  • Conjunctivitis (itching, tearing, burning of eyes)
  • Sinusitis
  • Otitis Media
  • Cough
  • Asthma
29
Q

How can allergic rhinitis be classified?

A

Intermittent (seasonal):

  • Symptoms under 4 days/wk or
  • Symptoms under 4 wks

Persistent:

  • Symptoms >4 days/wk or
  • Symptoms > 4 wks

ALSO

Mild

  • Normal sleep
  • Normal daily activities (including sports)
  • Normal work-school activities
  • No severe Sx

Moderate-Severe

  • Disturbed sleep
  • Restricted daily activities
  • Disrupted work/school activities
  • Do have severe Sx
30
Q

What are globally important sources of allergens?

A
  • House dust mites
  • Pets
  • Cockroaches
  • Molds
  • Grass, tree, and weed pollen (seen a little later, ages 4-5 yo, because you need a couple exposures/seasons to develop; internal allergens seen earlier)
31
Q

How is allergic rhinitis diagnosed?

A
  • Detailed personal and family allergic history
  • Intranasal examination – anterior rhinoscopy
  • More pale, bluish, inflamed mucosa
  • Symptoms of other allergic diseases
  • Allergy skin prick tests and/or
  • In vitro specific IgE tests
32
Q

What is shown here?

A

Allergy skin prick testing

  • Right shows positive result
33
Q

How do in vitro IgE assays work?

A
  • Primary Ab measures specific IgE to different things
34
Q

How should allergic rhinitis be managed?

A

DEPENDS ON SEVERITY:

Mild intermittent:

  • Oral/local nonsedative antihistamines (H1 blocker)
  • Intranasal decongestant (under 10 days) or oral decongenstant
  • Leukotriene receptor antagonist
  • Avoidance of allergens, irritant, and pollutants

Moderate/severe intermittent:

  • All of the above
  • Add intranasal steroid
  • Possibly add immunotherapy (allergy shots)

Persistent (mild, moderate, severe)

  • All of the above
  • Immunotherapy (allergy shots)
35
Q

Describe allergen immunotherapy in children

A
  • Effective and well-tolerated in children
  • Prevents new onset of allergen sensitivities in monosensitized pts
  • Prevents progression from allergic rhinitis to asthma
  • Should be considered with pharmacotherapy and allergen avoidance in the mgmt of children with allergic rhinitis/conjunctivitis, allergic asthma and stinging insect hypersensitivity
36
Q

What is asthma?

A

Chronic inflammatory lung disease characterized by:

  • Symptoms of cough, wheezing, dyspnea and chest tightness
  • Symptoms occur in paroxysms and are usually related to specific triggers
  • Airway narrowing is partially or completely reversible
  • Increased airways responsiveness to a variety of stimuli
37
Q

What are the 3 defining components of asthmatic airflow obstruction?

A
  • Airway inflammation
  • Reversible airflow obstruction
  • Airway hyperresponsiveness
38
Q

What are the major symptoms of asthma?

  • Describe the timing/aggravating factors of symptoms
A
  • Wheezing (during cold/other illness, when laughing/crying, in response to allergens/irritants)
  • Breathlessness
  • Chest tightness
  • Cough (frequent, especially at night; may be only sign in kids; when laughing/crying; in response to allergens/irritants)
  • Likely to occur at night and early in the morning
  • Likely to increase with activity and exercise (especially in cold weather)
39
Q

What are precipitating factors/triggers of asthma?

A
  • Allergens: pollens, animals, molds
  • Respiratory infections : viruses (mostly)
  • Irritants : cigarette smoke, odors, occupational exposures, chemicals, ozone, sulfites, sulfur dioxide
  • Exercise
  • Upper airway inflammation: sinusitis, rhinitis
  • Meteorologic factors: humidity, barometric pressure change, temperature, wind, cold air
  • Gastroesophageal reflux
40
Q

How is asthma diagnosed?

A
  • History of episodic or chronic symptoms of airflow obstruction
  • Spirometry or Pulmonary Function Testing (in children >5 years of age)
  • Other studies:
  • Bronchoprovocation testing (methacholine, exercise)
  • Chest X-ray
  • Sweat chloride
  • Allergy testing
41
Q

Describe spirometry and especially, it’s findings in an obstructive airway disease (like asthma)

  • What does spirometry measure
  • How is airflow obstruction defined in spirometry?
A
  • Spirometry helps assess severity of airflow obstruction and aids in the DDx of asthma
  • Obstructive vs. restrictive airway dz
  • Reversibility of airflow obstruction
  • Spirometry measurements include:
  • Forced vital capacity (FVC)
  • Forced expiratory volume in 1 s (FEV1)
  • Airflow obstruction is defined as:
  • FEV1 < 80% predicted and
  • FEV1/FVC < 85%
42
Q

T/F: It is essential to classify the severity of an asthmatic patient

A

True!

  • It determines their method of treatment
43
Q

How is asthma classified (children 5-11 yo)?

A

Intermittent

Persistent

  • Mild
  • Moderate
  • Severe
44
Q

Describe an intermittent asthmatic

A
  • Sx 2 or less days/wk
  • Nighttime awakenings < 2/mo
  • Short acting B2 agonist used < 2 days/wk
  • No interference with normal activity
  • Normal FEV1 between exacerbations and FEV1 > 80%; FEV1/FVC > 85%
45
Q

Describe a mild persistent asthmatic

A
  • Sx > 2 days/wk
  • Nighttime awakenings 3-4/mo
  • Short acting B2 agonist used > 2 days/wk
  • Minor limitation of normal activity
  • FEV1 < 80% but FEV1/FVC > 80%
46
Q

Describe a moderate persistent asthmatic

A
  • Sx daily
  • Nighttime awakenings >1/wk (but not nightly)
  • Short acting B2 agonist used daily
  • Some limitation of normal activity
  • FEV1 > 60% but < 80%; FEV1/FVC 75-80%
47
Q

Describe a severe persistent asthmatic

A
  • Sx throughout the day
  • Nighttime awakenings often; 7/wk
  • Short acting B2 agonist used several times/day
  • Extremely limited normal activity
  • FEV1 < 60%; FEV1/FVC < 75%
48
Q

In addition to the intermittent/persistent classifications, how else must a patient’s asthma be classified?

A
  • Well-controlled
  • Not well-controlled
  • Very poorly controlled
49
Q

What are the main components of asthma management?

A

Initial Assessment and Continuous Monitoring

  • Monitor symptoms, exacerbations, quality of life
  • Periodic pulmonary function tests

Control of Triggers

  • Cigarette smoke
  • Irritants (at work or at home)
  • Air Pollutants
  • Allergens
  • Rx of diseases exacerbating diseases: GERD, allergic rhinitis, sinusitis

Pharmacotherapy Asthma Education

50
Q

What are long-term control and quick relief pharmacotherapy agents?

A

Long-term control:

  • Inhaled Corticosteroids
  • Cromolyn/nedocromil
  • Leukotriene modifiers
  • Long-acting beta2-agonists
  • Methylxanthines

Quick relief:

  • Short-acting inhaled beta2-agonists
  • Anticholinergics
  • Systemic corticosteroids