Transcript Allergic Diseases - Lock Haven University of Pennsylvania

Allergies and Children
Richard E. Freeman MD MPH
Korin Trumpie, PA-C
Lock Haven University
2013

Includes
◦Asthma
◦Food allergies
◦Atopic dermatitis (eczema)
◦Allergic rhinitis
◦Urticaria
Allergic Diseases
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Allergies:
(allos=other & ergon=reaction)
◦ Used the term when referring to his patients who
expressed an “altered state of reactivity” to
common environmental antigens
 Clements von Pirquet- Austrian Pediatrician 1906

1960’s discovered that most patients with
allergy problems produced IgE in response to
antigens
Allergy
ALLERGEN:
 a type of antigen that produces an
abnormally vigorous immune response in
which the immune system fights off a
perceived threat that would otherwise be
harmless to most persons
 by stimulating a type-I hypersensitivity
reaction in atopic individuals through
Immunoglobulin E (IgE) responses

ATOPY:
 /ˈætəpi/; Greek ἀτοπία - placelessness,
out of place, special, unusual,
extraordinary)
 Hereditary (familial) predisposition in
which a individual responds to several or
many common environmental allergens
but only after sensitization.
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BUT NOT ALL Allergic REACTIONS ARE
ATOPIC
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Not all allergic reactions are IgE mediated
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Non IgE mediated
◦ More poorly understood
◦ T-cell mediated (Th1)
◦ Usually delayed in onset 4-28 hours after
exposure
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Non-allergic rhinitis
THE ALLERGIC PATHWAY

Antigen-presenting cells
◦ Dendritic cell, Landerhan cells, macrophages
◦ Induce allergic inflammation by “presenting”
allergens to T- cells
 Dendritic and Langerhan cells can “prime” naïve
T-cells
◦ Dendritic cells in skin, intestine and lung are
immature
 Actively phagocytize antigens
 Cells migrate to area lymph nodes
 Antigens are fully processed & converted
◦ Causing T-cells to proliferate and differentiate
Antigen Presenting Cells-Step1
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T helper cells Type 2 (TH2)
◦ Atopic persons respond by activation of TH2
helper cells
◦ Secrete cytokines that favor IgE mediated
responses
◦ Also secrete interleukins which
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T
Switch immunoglobulin isotypes to IgE
Enhance IgE synthesis
Differentiate and develop eosinophils (from stem cells)
Contribute to mast cell development
◦ Th2 thought to play big role in development of
asthma and
allergies
helper
Cell
Type 2 (TH2)
Step 2
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T helper cells Type 1 (TH1)
 Non-atopic person:
 responds to exposure to potential allergens by making
TH1 cells
 Secrete cytokines that stimulate IgG responses
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IgE
◦ Derived from Plasma cells (activated
Lymphocytes)
◦ memory
◦ Acute allergic response is dependent on IgE
and its ability to bind to allergen
◦ Binding initiates intracellular cascade
IgE – it’s role: STEP 3
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Eosinophils
◦ Help defend against parasites
◦ Found in peripheral blood and tissue
◦ Accumulate where allergic rxns take place
◦ Contain intracellular granules that are
sources of inflammatory proteins
 These proteins
◦ Damage epithelial cells
◦ Induce airway hyper-responsiveness
◦ Degranulate basophils and mast cells
EOSINOPHILS-
Step 4
Eosinophils
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Mast cells
◦ Derived from cells in bone marrow
◦ Enter circulation and travel to peripheral tissues where
they undergo tissue specific maturation
◦ Mature mast cells do not circulate
◦ Located throughout connective tissue and lie next to
vessels
◦ Mast cell and basophil degranulate
◦ Releasing mediators of allergenic inflammation:
histamine,serine proteases and proteolytics,
lipids, cytokines, and chemokines
=
Allergic Response
MAST CELLS-
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Three patterns of inflammatory reactions
◦ EARLY PHASE RESPONSE
◦ LATE PHASE RESPONSE
◦ CHRONIC RESPONSE
Mechanisms of Allergic Inflammation
◦ IMMEDIATE (from mast cell
degranulation)
◦ Occurs within minutes of allergen
exposure
◦ Resolves within 1 to 3 hours
◦ Associated with increased local vascular
permeability
 Tissue swelling
 Increased blood flow
 Itching
Sneezing
Wheezing
Abdominal cramps
Early Phase Response
◦ Occur within hours of exposure
◦ Reach peak at 6 to 12 hours
◦ Resolve by 24 hours
◦ Associated with infiltration of neutrophils
and eosinophils, then basophils,
monocytes,macrophages and TH2 cells
 Skin – redness, edema, induration
 Nose - sustained nasal blockage
 Lungs - wheezing
Late Phase Response
◦ Persist for days to years
◦ Seen in patients with chronic allergic
diseases
◦ Contributing factors
 Recurrent exposure to allergens and
microbial agents
 Tissue remodeling leading to
irreversible changes in target organs
 TH2 cytokines can maintain active
inflammation
Chronic Response
Familial pre-disposition seen
 Environment plays a big role

◦ ie. Hygiene hypothesis
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Genetic basis
◦ Controversial
◦ Genetic coding controls
 systemic expressions of atopy,
 increased IgE synthesis and
 eosinophilia
◦ Control local inflammatory response, asthma
and atopic dermatitis
Genetic Basis for Atopy
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THE CLEANER OR MORE STERILE THE
ENVIRONMENT THE HIGHER THE RISK OF
ALLERGIC DISORDERS.
MORE CHILDREN in house – LESS
ALLERGIES
 PLAYING IN DIRT/OUTSIDE EARLIERLESS ALLERGIES
 FREQUENT BATHING/ANTIBACTERIAL
SOAPS
◦
MORE ALLERGIES
HYGIENE HYPOTHESIS
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HISTORY
◦ A careful History and P/E remain the most
effective diagnostic means of diagnosis.
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Description of symptoms- severity
Triggers- inhaled, food, pets,
Place-home, school, outside, bedroom,daycare
Age at presentation
 Infants and young children-- food, environment
 Older children-- seasonal
◦ Timing-Seasonal vs Perennial, night-time,
morning, activity
◦ - How long do the symptoms last?
Diagnosis of Allergic Disease
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DESCRIPTION OF SYMPTOMS
◦ HEENT:
 Congestion, rhinorrhea, type of nasal
discharge,, sneezing or pruritus of nose or
eyes
◦ Lungs:
 Wheezing, Cough, Shortness of Breath
◦ Skin:
 Rash, (eczema, contact dermatitis,
uricaria)
◦ GI tract:
 nausea, diarrhea, abdominal pain
◦ Other complaints:
 headache, fatigue, lethargy, impaired
concentration, and difficulty in learning.
◦?
◦ MEDICATIONS:
 Meds used and how he/she responds to them
◦ PAST MEDICAL HISTORY
 atopic conditions,( i.e. eczema), drug allergy, food allergy,
recurrent infections such as sinusitis and otitis media
◦ FAMILY HISTORY
 50% risk with one positive parent
 66% risk if both parents have positive history
ALLERGY HISTORY -cont
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Behaviors
◦ Allergic salute – rubs nose upward with palm of
hand
◦ Allergic click – tongue against roof of mouth to
scratch soft palate
◦ Rubbing of eyes
History
◦ PE: TOROUGH
◦ ALLERGIC FACIES
◦ Allergic shiner – gray purple color to lower
lids
 Found in 60% allergic patients
 Found in 40% of non-allergic patients
 Dennie-Morgan lines- creases from inner
canthus parallel and underneath rim of lower
lid
◦ Allergic transverse nasal crease
◦ Elongated facial structures mouth breathing
PE
Denne-Morgan lines
Allergic shiners &
Dennie-Morgan lines
Nasal crease
Transverse Nasal creaseProlonged nasal salute
Allergic Facies
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Physical Exam
◦ Allergic facies
◦ Skin – dry, urticaria, eczema
◦ Eyes - ropy discharge, cobblestoning of
conjunctivae
◦ Ears - check for serous fluid
◦ Nose – Turbinates- boggy, pale to purple
rather than beefy red
◦ Mouth-High arched palate from chronic
mouth breathing, and tongue thrusting
 Dental malocclusion
◦ Lungs – wheezing
PE
The Snotty Nose
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Eosinophilia;
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Total serum IgE:
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RAST – Radioallergosorbent test,
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ELISA
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Skin Allergy Testing –
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Methacholine Challenge Testbronchial provocation. Non-asthmatics do not
constrict. Requires 20% decrease in FEV-1
◦ peripheral smear and mucous of nose (Hensel Stain)
◦ Parasites/allergies
◦ Sometimes elevated (neither sensitive or specific)
◦ documents allergen specific IgE (less sensitive than skin
tests)
◦ inject allergen subq. Some patients have late phase
response
Diagnostic Testing
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Environmental Control
◦ Majority of our time spent indoors
◦ Improved building causes
 increase humidity and
 concentration of indoor allergens
◦ Dust mite
 In bedding, carpet, upholstered furniture
 Fecal pellets are source of allergen
 Do not survive in humidity <50%
 Emphasize control in bedroom
Treatment
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Environment
◦ PETS
 Cats more sensitizing than dogs
 Hair, dander, saliva main sources of allergens
 Remove pet – still takes 6 months to clear
allergens
 Keep one room pet free
◦ Insects and pests
 Mice, cockroaches
 Limit access to home and food
Treatment
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Environment
◦ Irritants
 Tobacco smoke
 Wood burning stove
 Kerosene heaters
◦ Fungi
 Aspergillis and Penicillium
 Keep humidity < 50%
 Wipe down walls and floors
Treatment
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PHARMACOLOGIC
◦ Adrenergic agents◦ 2 adrenergic receptor sites
 Alpha-adrenergics
◦ Constriction of small blood vessels in the bronchial mucosa
◦ Used for nasal congestion: pseudoephedrine (CAUTION)
 Beta-adrenergics- short and long action
◦ Used in treatment of asthma
◦ B-2 produces bronchodilation
 Epinephrine has alpha and beta effects
 DRUG OF CHOICE FOR ANAPHYLAXIS
Treatment
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Pharmacologic
◦ Anticholinergic agents
 Diphenhydramine (Benadryl)
◦ Use: Skin manifestations- urticaria, itching
◦ Sedating,
◦ Avoid in asthma
 Ipratroprium bromide (atrovent) – atropine-like
◦ Inhibits vagally mediated responses
◦ MDI or nebulized for asthma
◦ Nasal spray,
◦
limited to severe cases,
 does not alleviate sneezing, congestion or pruritis
Treatment
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Pharmacologic
◦ Antihistamines
 Most frequently used
 H-1 receptor causes allergic inflammation, pain,
pruritis, vasodilation, increased mucous
production
 1st generation H-1 antihistamines cause
somnolence and impaired cognition – benadryl,
phenergan
 2nd generation negligible side effects and once a
day dosing- loratadine
Treatment
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Pharmacologic
◦ Chromones (chromoglycates)
 Inhibit mast cell degranulation/ mediator release
 Safe
 Usually require multiple dosing (short half life)
 Better for prophylaxis
 Cromolyn sodium
 Nedocromil sodium
Treatment
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Pharmacologic
◦ Glucocorticoids Widely used
 Block more mediators
 Topical
◦ Ophthalmic drops
◦ Nasal sprays
◦ Inhaled
 Oral or IV
Treatment

Pharmacologic
◦ Leukotriene inhibitors
 Inhibit either production or receptor binding of
leukotrienes
 Mild anti-inflammatory and bronchodilator effect
 Mainly used in asthma
 Singulair
◦ Asthma
◦ Allergic rhinitis
◦ Exercise induced asthma
Treatment
◦IMMUNOTHERAPY
◦ (ALLERGY SHOTS)
◦ Reserved for diseases that responds to
this form of treatment
◦.
◦ Insect anaphylaxis-highly recommend
◦ DRAW BACKS:
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◦
 Expensive-usually under Allergist
supervision (initiation phase)
painful,
long-term treatment
 Not for food or latex allergies
◦ Anaphylaxis risk
◦ ALWAYS-
ALLERGY SHOTS
 ANAPHYLAXIS RISK
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Initiation of new regimen
Dosage/allergen change
Local reaction at the last injection site (worse)
Hx of anaphylaxis to allergen in shot
ALWAYS ALWAYS ALWAYS
 Check patients name, dose, last reaction in chart. Name
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on bottle matches patient
Have a second person check dosage
Keep patient for designated time post-shot
Have Anaphylaxis meds readily available
Educate staff in all aspects
ANY questions call Allergist
ALLERGIC RHINITIS
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Two factors needed for diagnosis
◦ Sensitivity to allergen
◦ Presence of allergen in environment
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Itchy nose, mouth, eyes, throat, skin, or
any area
Problems with smell
Runny nose
Sneezing
Tearing eyes
ALLERGIC RHINITIS
◦ SEASONAL ALLERGIC RHINITIS
(SAR)
◦ 20%
 Itching of ears, nose, palate or throat
is the prominent feature
 Sneezing with tearing of eyes is
common
 Runny and/or stuffy nose with a nonproductive cough 2o to post-nasal
drainage
 Sinus headache or earache with altered
smell and taste
◦ PERENNIAL ALLERGIC RHINITIS
(PAR)
◦ 40%
 Persistent, chronic and generally less
severe than SAR
 Nasal congestion is the most common
symptom
 Patient complains of a “persistent cold”
or “chronic sinusitis”
ATOPIC DERMATITIS (ECZEMA)
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Pruritic skin disease
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Occurs in 10% of population
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80% with AD develop allergic rhinitis and/or
asthma
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Pathology
◦ “itch that rashes”
◦ T-cells in skin produce decrease in interferon
◦ Develops intercellular edema in acute lesions
◦ Chronic lesions have hyperplastic epidermis,
◦ hyperkeratosis and decreased intercellular edema
Genetics suggest strong maternal influence
Atopic Dermatitis
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Atopic Dermatitis
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Usually begins in infancy
◦ 50% by 1 year
◦ Additional 30% between 1 and 5 years
Pruritis is worse at night
 Scratching leads to eczematous lesions
and secondary infections
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Diagnosis
◦ Main features
 Pruritis
 Facial or extensor eczema in infants
and children
 Flexural eczema in adolescents
(elbows, knees, wrists)
 Chronic or relapsing dermatitis
 Personal or family history of atopic
disease
Atopic Dermatitis
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Treatment
◦ Identify and eliminate triggers
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Irritants – soaps, chemical, smoke, abrasive clothing
Foods – must take careful history, milk protein
Aero-allergens – fungi, dander, grass, ragweed
Infection – viral, bacterial or fungal
◦ Systemic
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Antihistamines
Glucocorticoids
Cyclosporine (psoriasis)
Interferon
Atopic Dermatitis
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Treatment
◦ Topical
 Hydration of skin
 Glucocorticoids
 Immunomodulators – Elidel (primecrolimus)
 Tar preparations
 Phototherapy
Atopic dermatitis
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Complications
◦ Repeated infections
◦ Chickenpox, herpes can spread over body
◦ Smallpox vaccination can be fatal
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Prognosis
◦ Spontaneous remission after age 5 yrs in some
◦ Poor prognosis
 Widespread AD in childhood Early onset of AD
 Allergic rhinitis or asthma
Only child
 Family history
Very high IgE
Atopic Dermatitis
Other Allergic Disorders
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ANAPHYLAXIS
◦ Outside hospital
 usually due to food peanuts, seafood,
 insect stings
 Peanut Butter and schools
◦ Inside hospital
 due to meds or latex
◦ Clinical manifestations
 Usually very apparent
 Diffuse Edema – facial, oral, laryngeal
 Hypotension & Tachycardia SHOCK like state
 Sometimes nausea and abdominal cramps are
presenting symptoms
Other Allergic Disease
ANAPHYLAXIS:
 TREATMENT:
 Oxygen, Fluids, monitor

Epinephrine-SQ
 Benadryl- IV IM
 Corticosteriods - IV
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URTICARIA AND ANGIOEDEMA
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IgE mediated reaction
Usually self-limited
Chronic if symptoms last > 6 weeks
Treatment: Usually requires systemic meds
Antihistamines
steroids
Other Allergic Disease
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DRUG REACTIONS
◦ True allergic response requires prior
sensitization
◦ Pseudo-allergic reactions – immune
mechanisms not involved
◦ Ampicillin/EB viral eruption- labeled as allergic
◦ Treatment:
◦ STOP offending MED
◦ Systemic meds
Other Allergic Diseases
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SERUM SICKNESS
◦ Immune complex mediated vasculitis
◦ Begins 7 to 21 days after injection of foreign
protein
◦ Original site may become red and swollen
◦ Sx – fever, malaise, rash, may have joint pain
◦ Rashes are morbilliform and urticarial
◦ Treat with antihistamines and glucocorticoids
Other Allergic Diseases
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Old way of thinking was that certain foods are
more likely to cause a rxn in infants and should be
avoided until after 12 months
◦ Eggs, nuts, seeds, legumes, wheat, corn, citrus fruits
and juices, seafood-shellfish
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However there is no evidence to support this
theory, and it is now thought that WAITING to
begin foods can INCREASE the likelihood of
developing food allergies
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Whole Cow’s milk can be started at 1 y/o
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No honey (carries the risk of botulism)
Foods that may cause a reaction
~
Questions?