SPUP AUXILIUM 2023 ALLERGY

PEDiATRiCS 1 DR. FRANCES ROSE R. PALABRiCA

AY 2020 – 2021 : 1ST SEMESTER FEBRUARY 24, 2021

TOPiC OUTLINE - 66% - both parents are allergic.

I. Diagnosis of allergic disease X. Adverse drug reaction • Thorough environmental survey should be
A. History A. Gell and coombs
B. Physical exam classification
performed.
C. Diagnostic testing B. Blistering § Age and type of the dwelling (how it is
II. Allergic rhinitis mucocutaneous heated or cooled)
A. Clinical manifestation disorders induced by § Use of humidifiers or air filtration units.
B. Differentials drugs
C. Occupational risk C. Improved outcomes of § Forced air heating may stir up dust mite,
D. Complications mucocutaneous fungi, and animal allergens.
E. Treatment syndromes § Irritant effects of wood-burning stoves,
III. Ocular allergies D. Treatment
A. Clinical manifestations XI. How will you manage allergic
fireplaces, and kerosene heaters –
B. Treatment reactions? provoke respiratory symptoms.
IV. Asthma XII. Environmental control § Increase humidity or water damage -
A. Clinical manifestation A. Environmental control of associated with greater exposure to dust
B. Differentials allergen exposure
C. Management XIII. Pharmacologic therapy mites and fungi.
V. Atopic dermatitis A. Adrenergic agents § Carpeting – serves as reservoir for dust
A. Clinical manifestation B. Anticholinergic agents mites, fungi, and animal dander.
B. Differentials C. Antihistamines
C. Treatment D. Chromones
VI. Insect allergy E. Glucocorticoids B. PHYSICAL EXAM
A. Clinical manifestation F. Leukotriene modifying • Look for evidence of atopic disease.
B. Clinical reaction agents
C. Treatment G. Theophylline
• Head to toe
VII. Urticaria H. Olopatadine HCL
A. Acute urticaria XIV. Allergen C. DIAGNOSTIC TESTING
B. Chronic urticaria immunotherapy
1. IN VITRO TESTS
C. Physical urticaria
D. Treatment • CBC – most common test performed.
VIII. Anaphylaxis • Eosinophilia
A. Differentials o > 500 eosinophils/ul
B. Treatment
IX. Food allergy
o Most common hematologic
A. Clinical manifestation abnormality of allergic patients
B. Treatment • IgE
o Primary antibody associated with
I. DIAGNOSIS OF ALLERGIC DISEASE immediate hypersensitivity reactions.
2. IN VIVO
A. HISTORY
• Allergen skin testing
• Obtaining a complete history from the allergic
o Primary in vivo procedure for the
patient involves eliciting a description of all:
diagnosis of allergic disease
o Symptoms and their timing and duration
o Histamine is the mediator most
o Exposure to common allergens
responsible for the immediate wheal
§ Insect sting
and flare reactions.
§ Pollens o Performed using prick/puncture
§ Medications example penicillin technique.
§ Dust mites o small drop of allergen is applied to the
§ Cats and other furry or hairy animals such skin surface, and a tiny amount is
as pig, dogs, horse, cat
introduced into the epidermis by lightly
§ Food such as peanuts, dairy products,
pricking the outer layer of the skin
seafoods and eggs
through the drop of extract with a
o Response to previous therapies small needle.
o Presence or absence of other allergic disease o Positive skin test result reveals a pruritic
§ Allergic rhino conjunctivitis wheal surrounded by erythema.
§ Asthma
§ Time course of reaction is
§ Food allergy
rapid in onset, reaching a
§ Eosinophilic esophagitis
peak within 10-20 mins and
§ Atopic dermatitis and urticaria usually resolving over the next
§ Drug allergy 30 min.
• Family history of allergic disease is common and 3. Provocation testing
one of the most important factors predisposing a
• performed to examine the association
child to the development of allergies.
between allergen exposure and the
§ Risk of allergic disease
development of symptoms.
- 50% - one parent is allergic.
• Methacholine challenge

2M.4.PED1 CABULAY, ELEPANIO, FLORES, MAMAUAG, PUNO PAGE 1 OF 11

 o Bronchial provocation test most
frequently performed.
o Caused potent bronchoconstriction of
asthmatic but not of normal airways.
4. Oral food challenges
• Performed to determine whether a
specific food causes symptom or whether
a suspected food can be added to the
diet.
• Performed when the history and results of
skin test and immunoassay for sIgE fail to
clarify the diagnosis of allergy.
II. ALLERGIC RHINITIS
• Common chronic disease affecting 20-30% of
children.
• Inflammatory disorder of the nasal mucosa marked
by nasal congestion, rhinorrhea, and itching, often
accompanied by sneezing and conjunctival
inflammation.
• May be seasonal or perennial.
• Can be categorized as
o Mild-intermittent
o Moderate-severe intermittent
o Mild persistent
o Moderate severe persistent
Moderate to severe persistent allergic rhinitis
• child patient with more than 2 months symptoms
and has abnormal sleep, and impairment of
daily activities.
Mild intermittent
• occasional runny nose for 3 days, normal sleep
and daily activities
A. CLINICAL MANIFESTATION
• mistakenly attributed to a respiratory infection
• diagnosis is based on symptoms in the absence of
an upper respiratory tract infection and structural
abnormalities.
• typical complaints:
o intermittent nasal congestion
o itching that may lead to epistaxis because
of continuous rubbing of the nose.
o Sneezing
o Rhinorrhea
o Conjunctival irritation
2.M.4.PED1 ALLERGY
• Patient may lose their sense of smell and taste
because symptoms increase with greater exposure
to responsible allergen.
• Nasal congestion is more severe at night, inducing
mouth breathing and snoring , interfering with
sleep, and rousing irritability
• Allergic salute
o Upward rubbing of the nose with an open
palm or extended index finger
o This maneuver relieves itching and briefly
unblocks the nasal airway.
• Nasal crease
o Horizontal skin fold over the bridge of the
nose
• Allergic shiners
o Blue gray to purple discolorations beneath
the lower eyelid’s, attributed to venous
statis.
• Dennie-Morgan folds (Dennie lines)
o Prominent symmetric skin folds that extend
in an arc from the inner canthus beneath
and parallel to the lower lid margin
• Signs on physical examinations
o Abnormalities of facial development
o Dental malocclusion
o Allergic gape (continuous open mouth
breathing)
o Chapped lips
o Conjunctival edema
o Itching
o Tearing
o Hyperemia
o Clear nasal secretion
o Edematous, boggy, and bluish mucus
membranes with little or no erythema
o Swollen turbinates that may block the
nasal airway
B. DIFFERENTIAL DIAGNOSIS
• Nonallergic inflammatory rhinitis with eosinophils
(NARES)
o imitates AR in presentation and response
to treatment but without elevated IgE
antibodies.
• Vasomotor rhinitis
o excessive responsiveness of the nasal
mucosa to physical stimuli.
• Other non-allergic conditions
o Infectious rhinitis
o Structural problems (nasal polyps, septal
deviation)
o Rhinitis medicamentosa (due to overuse of
topical vasoconstrictors)
o Hormonal rhinitis associated with
pregnancy of hypothyroidism.
o Neoplasms
o Vasculitis
o Granulomatous disorders
PAGE 2 OF 11
 C. OCCUPATIONAL RISK • Clinical sign: bilateral injected conjunctivae with
• Exposure to allergens (grain dust, insects, latex, vascular congestion that may progress to
enzymes) chemosis– conjunctival swelling, watery discharge
• Exposure to irritants (wood dust, paint, smoke, • When associated with allergic rhinitis: Allergic
solvents, cold air) rhinoconjunctivitis

D. COMPLICATIONS OTHER OCULAR ALLERGIES:

• Chronic sinusitis VERNAL KERATOCONJUNCTIVITIS
• Coexistence of asthma • severe bilateral chronic inflammatory process of
• Persistent or recurrent cough due to postnasal drip the upper tarsal conjunctival surface that occurs in
• Eustachian tube obstruction and middle ear a limbal or palpebral form
effusion • may threaten eyesight if there is corneal
• Hypertrophy of tonsils and adenoids; snoring involvement
• Impairment of quality of life • not IgE mediated, but occurs frequently in children
with seasonal allergies, asthma or atopic dermatitis
E. TREATMENT • Symptoms:
• Environmental allergen control o Sever ocular itching exacerbated by
• Oral antihistamines exposure to irritants, light or perspiration
o help reduce sneezing, rhinorrhea, and o Severe photophobia
ocular symptoms. o Foreign body sensation
o Administered as needed, o Lacrimation
o for mild-intermittent disease • Signs
o Second generation are preferred because o Giant papillae on the upper tarsal plate
they cause less sedation. “clobberstoning”
o Stringy, thick or ropey discharge
1st gen 2nd gen o Cobblestone papillae
Chlorpheniramine Desloratadine o Transient yellow-white points in the limbus
maleate Levocetirizine (trantas dots) and conjuctive (Horner
Hydroxyzine Cetirizine points)
Promethazine Loratadine o Corneal “shield ulcers
Fexofenadine o Dennie Lines

• Anticholinergic nasal spray ATOPIC KERATOCONJUNCTIVITIS

o Ipratropium bromide -effective for serous
rhinorrhea
• Intranasal decongestants
o Oxymetazoline and phenylephrine
o Used for <5 days.
o Should NOT be repeated more than once
a month to avoid rebound nasal
congestion.
• Intranasal corticosteroid
o For persistent severe symptoms
o Most effective therapy for AR
III. OCULAR ALLERGIES
Eye: a common target because of its marked
vascularity and direct contact with allergens
Conjunctiva: the most immunologically active
tissue of the external eye
Allergies can occur as an isolated target organ
disease or more commonly in conjunction with
nasal allergies
• Chronic inflammatory ocular disorder most
commonly involving the lower tarsal conjunctiva
• May threaten eyesight if there is corneal
involvement
• Almost all patients have atopic dermatitis; a
significant number have asthma
Symptoms
• Severe bilateral ocular itching
• Burning sensation
• Photophobia
• Tearing with mucoid discharge more severe than
allergic conjunctivitis and persist throughout the
year
Signs
• Bulbar conjunctivitis is injected and chemotic
• Cataracts may occur
• Trantas dots or giant papillae may be present
• Eyelid eczema – may extend to periorbital skin and
cheeks
• Secondary staphylococcal blepharitis is common
because of eyelid induration and maceration

A. CLINICAL MANIFESTATION GIANT PAPILLARY CONJUNCTIVITIS

ALLERGIC CONJUNCTIVITIS
• Most common hypersensitivity response of the eye
• Caused by direct exposure of the mucosal surfaces
of the eye to environmental allergens
• Usually associated with allergic rhinitis
• Common symptoms: itchiness with increased
tearing
• linked to chronic exposure to foreign bodies
(contact lenses, ocular prostheses, sutures)
Signs and Symptoms:
• Mild bilateral ocular itching
• Tearing
• Foreign body sensation
• Excessive ocular discomfort

2.M.4.PED1 ALLERGY PAGE 3 OF 11

 • Trantas dots, limbal infiltration, bulbar conjunctival • Refractory asthma
hyperemia and edema
A. CLINICAL MANIFESTATION
CONTACT ALLERGY • Intermittent dry coughing and expiratory wheezing
• involves the eyelids but can also involve the are the most
conjunctivae • common chronic symptoms of asthma
• associated with increased exposure to topical Older children and adults report associated
medications, contact lens solutions and shortness of breath and chest tightness;
preservatives • Younger children are more likely to report
intermittent, non-focal chest pain.
B. TREATMENT • Respiratory symptoms can be worse at night
• Primary: avoidance of allergens, cold compress • Daytime symptoms, often linked with physical
and lubrication activities or play
• Secondary: use of the following: • Self-imposed limitation of physical activities,
o Oral or topical antihistamines • General Fatigue (possibly due to sleep
o If necessary – topical decongestants, mast disturbance)
cell stabilizers and anti-inflammatory • Difficulty keeping up with peers in physical
agents activities.
• Tertiary: topical/oral corticosteroids (see an • Routine clinic visits: may have normal auscultatory
ophthalmologist) findings
• During asthma exacerbations, expiratory wheezing
IV. ASTHMA and a prolonged expiratory phase
chronic inflammatory condition of the lung airways resulting • Decreased breath sounds in right lower posterior
in episodic airflow obstruction lobe consistent with regional hypoventilation owing
– airways hyper responsiveness (AHR) to airways obstruction.
• May also hear crackles

B. DIFFERENTIAL DIAGNOSIS
Gastroesophageal reflux (GER)
Rhinosinusitis.

YOUNGER CHILDREN:
• Recurrent aspiration
• tracheobronchomalacia
• congenital anatomic abnormality of the airways
• foreign body aspiration
• cystic fibrosis
• bronchopulmonary dysplasia

MAIN TYPES OF CHILDHOOD ASTHMA: OLDER CHILDREN

§ RECURRENT WHEEZING in early childhood, primarily
triggered
• by common viral infections of the respiratory tract.
• Usually resolved during pre-school/lower school
age years
§ CHRONIC ASTHMA associated with allergy that
persists into later childhood and often adulthood.
TYPE OF ASTHMA ACCORDING TO DISEASE SEVERITY
• Intermittent
• Persistent (mild, moderate severe)
TYPES OF ASTHMA ACCORDING BY CONTROL (USED WHEN
TREATING THE PATIENT)
• Well controlled
• Not well controlled
• Very poorly controlled
• vocal cord dysfunction: may manifest as
intermittent daytime wheezing
C. ASTHMA MANAGEMENT
COMPONENTS:
• Assessment and monitoring of disease activity
• Education to enhance patient and family
knowledge and skills for self-management
• Identification and management of precipitating
factors and comorbid conditions
• Appropriate selection of medications
• Long term goal: optimal asthma control
• Preferred treatment for patients with persistent
asthma: inhaled corticosteroids (monotherapy or in
combination with adjunctive therapy)

TYPES OF ASTHMA ACCORDING TO TREATMENT RESPONSE

• Easy to treat
• Difficult to treat
• Exacerbators

2.M.4.PED1 ALLERGY PAGE 4 OF 11

 o Excessive sweating
o Irritants

INFANCY
• Face, scalp and extensor surfaces of the
extremities
• Diaper area is usually spared
CHILDREN
• Infragluteal involvement is common

V. ATOPIC DERMATITIS
• ECZEMA
• most common chronic relapsing skin disease seen
in infancy and childhood
• Infants with AD are predisposed to development of
allergic rhinitis and/or asthma later in childhood, a B. DIFFERENTIAL DIAGNOSIS
process called “the atopic march.” Differential diagnosis of atopic dermatitis
Congenital disorders
ETIOLOGY • Netherhorn syndrome
• defective skin barrier • Familial keratosis pilaris
• reduced skin innate immune responses Chronic dermatoses
• exaggerated T-cell responses to environmental • Seborrheic dermatitis
allergens and microbes • Contact dermatitis (allergic or irritant)
• polarized adaptive immune responses to • Nummular eczema
environmental allergens and microbes • Psoriasis
• ichthyoses
A. CLINICAL MANIFESTATION Infections and infestations
• typically begins in infancy • scabies
• Cardinal features: • HIV associated dermatitis
o Intense pruritus (especially at night) • Dermatophytosis
o Cutaneous reactivity • Onsect bites
• Triggers of pruritis and scratching: • onchocerciasis
o Food Malignancies
o aeroallergens • cutaneous T-cell lymphoma (mycosis
o Bacterial infection fungoides/Sezary syndrome
o Reduced humidity • letterer – sive disease

2.M.4.PED1 ALLERGY PAGE 5 OF 11

 Autoimmune disorders • 6 categories of clinical reactions: local, large local,
• dermatitis herperiformis generalized cutaneous, systemic, toxic and
• pemphigus foliasus delayed/late
• graft vs host disease
• dermatomyositis B. CLINICAL REACTIONS
Immunodeficiencies
• Wiskott-aldrich syndrome
• Severe combined immunodeficiency syndrome
• Hyper-immunoglobulin E syndrome
• Immunodysregulation polyendocrinopathy X-
linked (PEX) syndrome
Metabolic disorders
• Zinc deficiency
• Pyridoxine (vitamin B6) and niacin
• Multiple carboxylase deficiency
• Phenylketonuria

C. TREATMENT
ATOPIC DERMATITIS MANAGEMENT:
• Systemic multifaceted approach
• Skin moisturization
• Topical anti-inflammatory therapy
• Identification and elimination of flare factors
• If necessary, systemic therapy

VI. INSECT ALLERGY

• vary from localized cutaneous reactions to C. TREATMENT
systemic anaphylaxis. • Local cutaneous reactions
• May also manifest with acute and chronic o Cold compress
respiratory symptoms of rhinitis, conjunctivitis and o Topical meds to relieve itching
asthma when there’s inhalation of airborne o Systemic antihistamines and/or oral
particles of insect origin analgesics
• Localized skin responses to biting insects are • Systemic (anaphylaxis)
caused primarily by o Epinephrine is the DOC
• vasoactive or irritant materials derived from insect
saliva, and rarely occur from IgE-associated VII. URTICARIA (HIVES) AND ANGIOEDEMA
responses.
• Acute: episodes that last for <6wks
• Systemic responses: attributed to Ig-E mediated
• Chronic: episodes that occur on most days of the week
responses
for >6wks
o Yellow jacket
o Honeybee
o Paper wasp
o Hornet
o Fire ant
o
HYMENOPTERA VENOM
• Vasoactive substance (histamine, acetylcholine,
kinins)
• Enzymes (phospholipase and hyaluronidase)
• Apamin
• Melittin
• Formic acid
• Majority of patients who had systemic reactions
A. ACUTE URTICARIA AND ANGIOEDEMA
have IgE mediated
• often caused by an allergic immunoglobulin (Ig) E-
mediated reaction
A. CLINICAL MANIFESTATION
• self-limited process that occurs when an allergen
• Insect bites are usually urticarial but may be
activates mast cells in the skin
papular or vesicular.
• can also result from non-IgE-mediated stimulation of
• IgE-antibody associated immediate and late-
mast cells (radiocontrast agents, viral agents, opiates
phase allergic responses sometimes mimic cellulitis
and NSAIDs)

2.M.4.PED1 ALLERGY PAGE 6 OF 11


B. CHRONIC URTICARIA
• established when lesions occur on most days of the
week for >6wk and are not physical urticaria or
recurrent acute urticaria with repeated exposures to a
specific agent
• often accompanied by angioedema
C. PHYSICAL URTICARIA
• Cold Urticaria
o rapid onset of localized pruritis, erythema and
urticaria/angioedema after exposure to a cold
stimulus
• Cholinergic Urticaria
o onset of small punctate wheals surrounded by a
prominent erythematous flare associated with
exercise, hot showers and sweating
• Dermatographism (urticaria factitia)
o Ability to write on skin
o Isolated disorder or may accompany chronic
urticaria or other physical urticaria (cholinergic,
cold)
o Linear response occurs secondary to reflex
vasoconstriction, followed by pruritis, erythema
and a linear wheal
2.M.4.PED1 ALLERGY
• Pressure-Induced Urticaria and Angioedema
o Symptoms typically occur 4-6 hrs after pressure has
been applied.
o Some may only have swelling secondary to
pressure with normal-appearing skin (no urticaria),
others are predominantly urticarial with no
significant swelling
o Occurs at sites of tight clothing
• Solar Urticaria
o Rare; urticaria develops within 1-3 mins of sun
exposure
o Pruritus occurs first (30 secs) followed by edema
confined to the light-exposed area, and
surrounded by a prominent erythematous zone
caused by an axon reflex
• Aquagenic Urticaria
o Small wheals after contact with water, regardless
of its temperature
D. URTICARIA TREATMENT
• Acute Urticaria
o Antihistamines and avoidance of any identified
trigger
• Physical Urticaria
o Avoidance of the stimulus;
• Chronic Urticaria
o Dietary manipulation; antihistamines
VII. ANAPHYLAXIS
• Serious allergic reaction that is rapid in onset and may
cause death
• Sudden release of potent biologically active mediators
from mast cells and basophils → cutaneous, respiratory,
cardiovascular and gastrointestinal symptoms
PAGE 7 OF 11
 A. CLINICAL MANIFESTATION
Gastrointestinal manifestation
● Often the 1st form of allergy to affect infants and
young children
● Manifest as irritability, vomiting or “spitting up”,
diarrhea and poor weight gain
● Food protein-induced enterocolitis syndrome, food
protein-induced proctocolitis, food protein-
induced enteropathy, allergic eosinophilic
esophagitis, allergic eosinophilic gastroenteritis,
oral allergy syndrome and acute gastrointestinal
allergy
Skin manifestation
● Common in infants and young children
● Atopic dermatitis, acute urticaria and
angioedema
Respiratory manifestation
● Uncommon as isolated symptoms
A. DIFFERENTIAL DIAGNOSIS
● Food-induced rhinoconjunctivitis, food-associated
• Other forms of shock (hemorrhagic, cardiogenic,
exercise-induced anaphylaxis
septic)
● For example, a child eats peanuts, then after
• Vasopressor reactions including flush syndromes (e.g.
eating he plays basketball, then develops signs
carcinoid syndrome), excess histamine syndromes
and symptoms of anaphylaxis. But when the child
(systemic mastocytosis) and ingestion of MSG
eats peanuts and does not play basketball or any
• Scombroidosis
physical activity, the child will not manifest any
• Hereditary angioedema
signs of allergy at all.
B. TREATMENT
B. TREATMENT
• Anaphylaxis is a medical emergency requiring
● Appropriate identification and elimination of food
aggressive management with IM epinephrine
responsible for food hypersensitivity reactions are
(1:1000 amp, 0.01 mg/kg or 0.1-0.3 ml)
the only validated treatment for food allergies
• Adjunct treatments
● That’s why we do allergy skin testing and oral food
o Antihistamines
challenges, we can’t tell the mother to remove the
o Oxygen
food from the child's diet because it can result in
o IV fluids
malnutrition. If the child has an allergy, the child has
o Inhaled B2 agonists
to be seen by an allergist, to do some diagnostic
o Corticosteroids
test.
XI. FOOD ALLERGY
X. ADVERSE DRUG REACTION
CLASS 1 FOOD ALLERGENS:
Predictable (Type A)
● food allergens penetrating the GI barrier
● Dose-dependent
● egg, milk, peanuts, tree nuts, fish soy, wheat (90%
● Can be related to known pharmacologic actions
of food allergies during childhood)
of the drug
● Occur in patients without any unique susceptibility
CLASS 2 FOOD ALLERGEN:
● Drug toxicity, drug interactions, adverse effects
● Partially homologous allergens (e.g. Plant pollens)
Unpredictable (Type B)
penetrating respiratory tract
● Dose independent
● Plant or fruit proteins that are partially homologous
● Not related to the pharmacologic actions of the
with pollen proteins
drug
● Birch, grass, ragweed
● Occur in patients who are genetically predisposed
● For example, you have a child allergic to grass
● Idiosyncratic reactions, allergic reactions,
pollen, then a child eats apple, the apple has a
pseudoallergic reactions
structure similar to grass pollen, such that when the
Cutaneous reactions:
child eats the apple because she has allergy to
● Most common form of adverse drug reactions
grass pollen and that has similarity of protein
● Ampicillin, amoxicillin, penicillin and trimethoprim-
structure as the apple, the child will develop a
sulfamethoxazole
reaction to apple. Not because the child is allergic
to apple but because it has a similar structure to
the grass pollen where the child is allergic to. A. GELL AND COOMBS CLASSIFICATION
● Usually manifestation is swelling of the lips and ● Type I: immediate hypersensitivity reaction
itchiness of the lips. (oral allergy) ● Type II: cytotoxic antibody reactions
● Type III: immune complex reaction
● Type IV: delayed-type hypersensitivity reaction

2.M.4.PED1 ALLERGY PAGE 8 OF 11

Type I
● When a drug of drug metabolite interacts with
preformed drug-specific IgE Abs that are bound to
the surfaces of tissue mast cells or circulating
basophils
● Urticaria, bronchospasm, anaphylaxis
Type II
● IgG or IgM antibodies that recognize drug antigen
on cell membrane
● In the presence of serum complement, the Ab-
coated cell is either cleared by the monocyte-
macrophage system or is destroyed
● Drug-induced hemolytic anemia and
thrombocytopenia
Type III
● Caused by soluble complexes of drug or
metabolite in slight antigen excess with IgG or IgM
antibodies
● Immune complex is deposited in blood vessel walls
and causes injury by activating the complement
cascade (e.g. Serum sickness)
● Fever, urticaria, rash, lymphadenopathy,
arthralgias
● Symptoms appear 1-3 weeks after the last dose of
an offending drug and subside when the drug and
its metabolite is cleared from the body
Type IV
● Mediated by drug specific T Lymphocytes
● Sensitization usually occurs via the topical route of
administration
● Allergic contact dermatitis
● Neomycin and local anesthetics

B. Blistering mucocutaneous disorders induced by

drugs
● Stevens Johnson syndrome(SJS)
● Toxic Epidermal necrosis(TEN)
SJS
● Epidermal detachment less 10%
● Confluent purpuric macules on face and trunk
● Severe, explosive mucosal erosions, at more than 1
mucosal surface
● (+) fever and constitutional symptoms
● Ocular involvement
● Liver, kidney and lungs may be involved
TEN
● Epidermal detachment 30% or more
● Widespread areas of confluent erythema followed
by epidermal necrosis and detachment with
severe mucosal involvement
● SJS=less 10% involvement
● TEN= more than 30 % involvement
● Overlap of SJS-TEN=10 to 30 %
C. Improved outcomes of mucocutaneous syndromes
● Immediate withdrawal of the implicated drug
● Early transfer to an intensive care or burn unit
● Aggressive supportive care
D. Treatment
● Avoidance of the drug (identify the trigger and
avoid it)
● If there are no alternative drugs → specific
desensitization (this can only be done if it did not
have mucocutaneous syndrome like SJS and TEN, if
nagka-urticaria because of paracetamol)
○ Progressive administration of an allergen to
render effector cells less reactive
○ Only effective while the drug continues to
be administered; if discontinued or
interrupted, hypersensitivity can recur
○ Example, patients with TB, if they are taking
anti TB drugs (rifampicin, ethambutol,
isoniazid), if they are allergic to drugs like
rifampicin, ethambutol, they can undergo
desensitization, so the patient can tolerate
the drugs, but only effective of taken
continuously. If for pain relievers, like
paracetamol, it can’t be used for long
period, so better to look for alternative.

2.M.4.PED1 ALLERGY PAGE 9 OF 11

 XI. HOW WILL YOU MANAGE ALLERGIC REACTIONS?
• Avoid allergens.
• Medications
• Allergy shots (immunotherapy)
• Continue allergy education.
XII. ENVIRONMENTAL CONTROL
A. ENVIRONMENTAL CONTROL OF ALLERGEN EXPOSURE
ALLERGEN CONTROL MEASURES
Dust mites • Encase bedding in airtight, allergen
impermeable covers.
• Wash bedding weakly in water at
temp >130 F.
• Remove wall to wall carpeting.
• Replace curtains with blinds.
• Remove upholstered furniture.
• Reduce indoor humidity
Animal • Avoid furred pets.
dander • Keep animals out of patient’s
bedroom.
Cockroaches • Control available food and water
sources.
• Keep kitchen or bathroom surfaces
dry and free of standing water.
• Seal cracks in walls
• Use professionally extermination
services; safe pesticide should be
used in baits.
Mold • Repair moisture prone area.
• Avoid high humidity in patient’s
bedroom.
• Use High efficient particulate air
(HEPA) filters in living areas.
• Repair water leaks.
• Replace carpets with hardwood
floors.
• Regularly check basements, attics,
and crawl spaces for standing water
and mold.
Pollen • Keep automobile and house
windows closed.
• Control timing of outdoor exposure
• Restrict camping, hiking and leaf
raking.
• Drive in an air-conditioned
automobile.
• Air-conditioned the home.
• Install portable HEPA filters.
XIII. PHARMACOLOGIC THERAPY
A. ADRENERGIC AGENTS
Stimulates cell surface alpha- and beta-adrenergic
receptors in a variety of target tissues.
1. α-adrenergic agents
• effective in the treatment of allergic nasal
disease because of their decongestant effect
• vasoconstriction
• psuedoepinephrine and phenylephrine,
oxymetazoline
2. β-adrenergic agents
• Used in the treatment of asthma because of
their potent bronchodilator effects.
• short acting (eg. Salbutamol) and long acting
(eg.Salmeterol)
• improve mucociliary clearance, decrease
microvascular permeability, inhibit cholinergic
nerve transmission, and reduce mediator
release in mast cells, basophils, and
eosinophils.
B. ANTICHOLINERGIC AGENTS
• inhibit vagally mediated reflexes by antagonizing
the action of acetylcholine at muscarinic
receptors.
• ipratropium bromide is the most used.
• slower onset of action than short-acting inhaled
beta agonist
C. ANTIHISTAMINES
• Frequently used for treatment of allergic disease
• Histamine exerts its effects through binding with
one of its four receptors: H1.
• Prevent effects of H1 receptors activation through
reversible, competitive inhibition of histamine by
bind into the H1 receptor.
D. CHROMONES
• Cromolyn sodium and nedocromil sodium
• Should be applied topically to the mucosal
surface of the target organ to be effective.
• Inhibit mast cell degranulation and mediator
release.
E. GLUCOCORTICOIDS
• Anti-inflammatory actions are mediated via the
glucocorticoid receptor, which is present in all
inflammatory affector cells, as well as by direct
inhibition of cytokines and mediators.
F. LEUKOTRIENE MODIFYING AGENTS
• exert their clinical effects either by inhibiting
leukotriene production or by blocking receptor
binding site.
• mild anti-inflammatory properties exhibit
bronchodilator effects.
G. THEOPHYLLINE
• Broncho dilating effect.
• Nonspecific inhibition of phosphodiesterase
isozymes and antagonism of adenosine receptors.
• Often used intravenously when used for the
treatment of severe acute asthma.
• Has Toxic effects
H. OLOPATADINE HCL
• Both a mast cell stabilizer and an H1 receptor
antagonist.
• Relieving signs and symptoms of allergic
conjunctivitis.
• At least 3 y/o

2.M.4.PED1 ALLERGY PAGE 10 OF 11

 XIV. ALLERGY IMMUNOTHERAPY (AIT)
• Administering gradually increasing doses of
allergens to a person with allergic disease for the
purpose of reducing or eliminating the patient’s
adverse clinical response to subsequent natural
exposure to those allergens
• Indications
o Allergic rhino conjunctivitis
o Asthma
o Insect venom sensitivity

XV. SUBLINGAUL IMMUNOTHERAPY (SLIT)

• Alternative way to treat allergies without injections.
• Keep under tongue for 1 to 2 mins and then
swallow.
• Repeated between 3 days a week to as often as
daily, with recommendations the therapy is
continued for 3 to 5 years to develop a lasting
immunity.
• For grass and ragweed -take tablet before and
during the allergy season.
• For dust mite allergy – take tablet year round

REFERENCES
1. Palabrica, Frances Rose 2021. Allergy PowerPoint
(2021)
2. Nelsons textbook of Pediatrics, 21E (2020)
3. Sidenotes

2.M.4.PED1 ALLERGY PAGE 11 OF 11