Who is the ALLERGIC PATIENT?

- The allergic patient have an altered state of reactivity to common environmental

antigens
- They produce IgE antibodies to the antigens that trigger their illness
- Such individuals have a familial predisposition to allergic diseases that manifest as
hyperresponsiveness in their target organs such as the lung, skin, or nose
*Immunology:
2 types of immunity
1. Innate immunity:
- made up of epithelial barrier, cytokines, degrading cells, complement system and NK
cells
-the first line of defense of the body against infection/microbe or antigen
2. Adaptive immunity
-if the microbes penetrate the first line of defense, the adaptive immunity comes into play
-made up mostly of lymphocytes: B lymphocytes and T lymphocytes
-B cells/B lymphocytes: develop into plasma cells, which will produce antibodies
-T cells/T lymphocytes: develop into effector T cells
*How the adaptive immune system respond?
If you have an antigen X/microbe X, first your nave B cells will bind to this antigen X and
they are stimulated to develop into plasma cells, and plasma cells will produce antibodies
specific for this antigen X. Aside from developing into plasma cells they also form into memory T
cells, so that the next time that the body encounters the same antigen they will easily produce
reaction faster and softer than the first one.
Picture: If antigen X is introduced to the body together with another new antigen Y, you see the
primary response is small because thats the first time that the body encounters the antigen
while the secondary response to antigen is bigger and faster because of the presence of
memory T cells.
Allergic reaction:
For example, the initial contact with the egg protein/ egg allergen, B cells will bind into this
allergen and will be stimulated to develop into plasma cell which will produce antibodies specific
for the egg allergen. Now once the IgE antibodies are produced, they bind to their receptors on
the surfaces of the mast cells or basophils. So this process where IgE antibodies are produced
and binding with surfaces of mast cells are what we call sensitization. So the patient is now
sensitized with this allergen. For the first contact usually the patient will not have any physical
manifestation because the body is still preparing for the next allergen exposure. So when the
patient ingest egg again? In the subsequent contact with the allergen the IgE antibodies readily
react with the allergen and the allergen binds into at least 2 IgE antibodies, cross-linking
them. This cross linking of allergen triggers the degranulation of mast cells. Mast cells
degranulate, releasing histamine, and other chemicals, mediators and other inflammatory cells
which are responsible for the allergic reaction.
Phases of allergic reaction:
1. The immediate/early phase
- occurs within minutes of allergen exposure;
- during the binding of allergen to antibodies and degranulation of mast cells
-these are your histamine, leukotriene, _____ cell and they are responsible for immediate
reactions like evening
ithchyness, swelling, coughing
-antihistamine, antileukotriene for these reactions
2. The delayed phase
-occurs hours after the initial binding of antigen to the IgE antibodies
*So whenever you have an allergic patient, it is better to give antihistamines in 5-7 days than in
a daily basis so that it will prevent the delayed-phase reaction.

How to diagnose allergic patient?

Good history is important
- Ask about symptoms, its time and duration.
- When did the reaction start?
- Was it associated with ingestion of food? If yes, how many minutes after the patient eat
the food before the rashes appeared?
- For how long? If more than 24 hours, think of other diagnosis.
Ask exposure to common allergen:
- Insects (hymenoptera family)
- Pollen
- Food
- Medicine
- Furry animals
- Dust mites
Ask responses to previous therapy. How did he respond to nebulization?
Ask presence of other allergies. Usually multiple allergy occurs.
Ask history of family allergies (Familial/inherited)
Environmental survey
Physical examinations
Diagnostic tests:
a) CBC: + Eosinophils in blood (eosinophilia is the MC abnormality in the allergic
patient)
b) Serum IgE (IgE- the primary antibody associated with allergies)
c) In vivo test: ALLERGIC SKIN TEST- the primary procedure. Inject an allergen
extract in the superficial skin, after 20 min, if there is itchiness or erythema, a lump
appears, then the patient is allergic.
Other tests:
_________________
Metacholin challenge test asthma
____ challenge- For food allergy
ALLERGIC RHINITIS (AR)
an inflammatory disorder of the nasal mucosa characterized by nasal congestion,
rhinorrhea, and itching and often accompanied by sneezing and conjunctival irritation.
this may be classified as either seasonal or perennial (US)
Intermittent or persistent (Phil)
ARIA guidelines of classification:
Mild intermittent: normal activity, no sleep disturbance, no troublesome symptoms and
the symptoms occurs <4 days a week or less than 4 weeks
Mild persistent: >4 days a week of symptoms and more than 4 weeks (almost every
day in a month)
Moderate severe intermittent: abnormal skin, interrupment of daily activities,
abnormal work or school, troublesome symptoms in <4 days a week or less than 4 weeks
Moderate severe persistent: abnormal skin, interrupment of daily activities, abnormal
work or school, troublesome symptoms in >4 days a week or greater than 4 weeks
*Symptoms are mistakenly attributed to respiratory infection.
*The diagnosis of Allergic rhinitis is based on symptoms in the absence of URTI and
structural abnormalities.
Ex. Persistent cold without signs infection or fever

*Typical Complaints:
1. Patient may have intermittent nasal congestion, leading to mouth breathing and later
on snoring.
2. Itching of the nose and even eyes. Manipulation of the nose can lead to epistaxis or
nosebleeds.
*Symptoms:
Sneezing
Clear rhinorrhea
Conjunctival irritation
Allergic salute: Upward rubbing of the nose, can lead to transverse nasal crease
Transverse nasal crease- horizontal skinfold over the nasal bridge of the nose
Allergic shiners- blue-gray to purple discoloration beneath the lowers eyelids attributed
to venous stasis
Denie lines/Denie morgan folds-prominent symmetric skin folds that extend in an arc
from the inner canthus beneath and parallel to the lower lid margin
*Other manifestations:
Abnormality of facial development
Dental malformations
Allergic gape
Continuous open mouth breathing
Chapped lips
Conjunctival edema, Itching, tearing and hyperemia
Swollen turbinate
*Nasal exam: boggy, edematous and bluish mucus membrane
Swollen turbinate
*Differential Diagnosis:
Nonallergic inflammatory rhinitis with eosinophils (NARES): imitates AR in presentation
and response to treatment, but the patients do not have elevated IgE antibodies.
Vasomotor rhinitis: characterized by excessive responsiveness of the nasal mucosa to
physical stimuli.
Infectious rhinitis
Comon colds
Structural abnormalities/anatomic abnormalities including nasal polyps and septal
deviation, rhinitis medicamentosa (which is caused by overuse of topical
vasoconstrictors), hormonal rhinitis associated with pregnancy or hypothyroidism,
neoplasms, vasculitides, and granulomatous disorders.
*Complications:
- chronic sinusitis-common complication of AR
- asthma
- persistent/recurrent cough/cold
- Obstruction of the eustachian tube and middle-ear effusion are frequent complications.
- Chronic allergic inflammation causes hypertrophy of adenoids and tonsils that may be
associated with eustachian tube obstruction, serous effusion, otitis media, and
obstructive sleep apnea.
- AR in children is strongly associated with snoring, sleep abnormalities, and daytime
fatigue.
ALLERGIC CONJUNCTIVITIS

closely associated to allergic rhinitis

most common hypersensitivity response of the eye,
caused by direct exposure of the mucosal surface of the eye to the allergen
Common symptoms: Itchiness with increased tearing
Clinical signs: bilateral infected conjunctivae with vascular congestion that may progress
to chemosis or conjunctival swelling and watery discharge

ASTHMA
- Chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction
- Airway responsiveness (AHR)
*Normal bronchus: cartilage, mucous gland and muscle layer.
*If the patient is exposed to the asthma triggers, the bronchus become inflamed, the smooth
muscle layer constrict/ contract reducing the airways. At the same time, the mucous glands
are activated so they produce more mucous and further reducing the airway of the lungs. This
will cause dyspnea or difficulty of breathing or always coughing
*2 types of childhood asthma:
1. Recurrent wheezing
- in early childhood,
- primarily triggered by common viral infections of the respiratory tract.
- Common in early preschoolers and tend to resolve during preschool years without
risk for asthma in later life
2. Chronic asthma
- assoc with allergy that persists into later childhood and often adulthood
- assoc with atopy, so the patient have clinical typical manifestation of atopic
dermatitis, allergic rhinitis or burning sensitization of allergens.
- The serum Ig is high, so this patients have the highest risk for persistence in
childhood and adulthood asthma
*Clinical Manifestation of asthma
Intermittent dry coughing and or expiratory wheezing- the most common chronic
symptom of asthma
- In pediatric patient, usually cough and you dont always see DOB, because this is more
seen in adulthood
- In older children they may complain of shortness of breath and chest tightness
- In younger children, intermittent nonfocal chest pain
- Respiratory symptoms are recognized so we always have to ask about the occurrence of
the cough.
Does it always occur at night? If present at night, does patient wake up at night due to
coughing? If yes, then probably, the patient has asthma.
- Daytime symptoms are also frequent in children and assoc with typical activity or play
- Patient may also have self imposed limitation of physical activities, general fatigue due to
sleep disturbance and difficulty of keeping up with peers in physical activity
- Seen during asthma exacerbation: Expiratory wheezing and prolonged expiratory wheeze,
dec breath sounds Right lower posterior lobe are consistent with regional hypoventilation
owing to airway obstruction; and may also hear crackles.
-

*Diff diagnosis:
- GERD-infant
- Rhinosinusitis-younger children
- Vocal cord dysfunction in older children and adolescent
ATOPIC DERMATITIS (ECZEMA)

this is the most common chronic anaphylactic skin disease seen in infancy and
childhood,so pabalik balik on off on off
response are predisposed to the development of allergic rhinitis or asthma childhood
disease also known as ATOPIC MARCH
*ETIOLOGY
1. defective skin barrier
2. reduced skin innate immune response
3. exaggerated T cell response to the environmental allergen and microbes
CARDINAL/MAJOR FEATURES:
1. INTENSE PRUTITUS
o especially at night and cutaneous reactivity
o ITCH-SCRATCH -usually itchiness first then patient scratches. If the patient
scratches the itchiness spread, so the cycle goes on.
*TRIGGERING FACTORS:
food
allergen
infection
reduced immunity
excessive sweating
irritants
2. DISTRIBUTION OF ERYTHEMATOUS LESION
INFANTS:
Face
Mouth
Extensor surfaces
**DIAPER AREA(spared!) if rash is present think of other diagnosis
OLDER CHILDREN/ADOLESCENT
Flexor surfaces
Elbow
neck
Inguinal area
3. CHRONIC/RELAPSING dapat pabalik balik
4. Personal and family history of atopic dermatitis (OPTIONAL!)
CLASSIFICATIONS OF ATOPIC DERMATITIS:
A. ACUTE AD
- Intense deep pruritic with erythematous papules (crust) in the skin.
- If not treated properly it will become sub acute AD.
B. SUBACUTE AD
- patient has erythematous excoriated bleeding papules -pumapangit na lalo ang skin
C. CHRONIC AD
- you now have presence lichenification (thickening of the skin with accentuated markings
and fibrotic marking
- chronic AD, acute AD and subacute AD may also coexist
*Differential diagnosis
1. Immunodeficiencies - because some immunodeficiencies can present the same
manifestation
- Ex: wisKotts aldrich syndome , SCIDS, Hyper Ig
2. Chronic dermatosis such as seborrheic dermatitis
3. Infections particularly in scabies

*If patient has been treated by several cream, lotion, antihistamine and the rashes wont go
away ask if there is a member of the family who has itchiness/pruritus, most probably its
SCABIES.
INSECT ALLERGY
- Varies from localized cutaneous reaction to systemic anaphylaxis
- May manifest also with acute and chronic respiratory symptoms, rhinitis, conjunctivitis and
asthma when there is inhalation of airborne particles of insect origin
- Localized skin responses are caused by vasoactive or irritant materials derived from insect
saliva. (No IgE)
*Most common allergen
- Hymenoptera family
*Hymenoptera venom contains vasoactive substances such as histamine, acetylcholine,
and kinins; enzymes such as phospholipase and hyaluronidase; apamin; melittin; and
formic acid; Majority of patient who had systemic reaction has IgE-mediated sensitivity to
the antigenic substances in the venom.

honeybee,

yellow jacket,

yellow hornet,

white-faced hornet

wasp
*Clinical manifestation:

usually urticarial but may be papular or vesicular

IgE antibodyassociated immediate- and late-phase allergic responses

sometimes mimic cellulitis.
*Clinical reactions to stinging venomous insects are categorized as local, large local,
generalized cutaneous, systemic, toxic, and delayed/late.
*6 categories of insect bites:
1. Simple local reactions -involve limited swelling and pain, and generally last <24 hr.
2. Large local reactions -develop over hours and days, involve swelling of extensive areas
(>10 cm) that are contiguous with the sting site, and may last for days.
3. Generalized cutaneous reactions -typically progress within minutes and include
cutaneous symptoms of urticaria, angioedema, and pruritus beyond the site of the sting.
4. Systemic reactions- are identical to anaphylaxis from other triggers and may include
symptoms of generalized urticaria, laryngeal edema, bronchospasm, and hypotension.
5. Toxic reactions- develop from stings from a large number of insects at once may result in
of fever, malaise, emesis, and nausea due to the chemical properties of the venom in large
doses.
6. Delayed/late reactions- they may have serum sickness, nephrotic syndrome, vasculitis,
neuritis, or encephalopathy
URTICARIA (HIVES) AND ANGIOEDEMA
URTICARIA
- transient, pruritic, erythematous, raised wheals, with flat tops and edema that may
become tense and painful.
- The lesions may coalesce and form polycyclic, serpiginous, or annular lesions which only
last 20 min to 3 hr, and rarely more than 24 hr.

The lesions often disappear and only to reappear to the other side

ANGIOEDEMA
- involves the deeper subcutaneous tissues such as the eyelids, lips, tongue, genitals, and
dorsum of the hands or feet
* CLASSIFICATION OF URTICARIA
1. ACUTE URTICARIA episodes less than 6 weeks
Etiology:
o Foods
o Medications
o Insect stings
o Infections
o Contact allergy
o Transfusion reactions
- * Acute urticaria and angioedema are often caused by an allergic IgE-mediated
reaction. This is self-limited process that occurs when an allergen activates mast cells in
the skin.
- *Acute urticaria can also result from nonIgE-mediated stimulation of mast cells
caused by radiocontrast agents (CT scan, MRI), viral agents including hepatitis B and
Epstein-Barr virus, opiates, and nonsteroidal anti-inflammatory agents (NSAID).
-

So ask the patient what food they ate prior to appearance of urticaria, are they taking
maintenance medication, painkillers ,after 1 day of antibiotic then presented rash.
- Infection, contact, transmission can also cause acute urticaria
2. CHRONIC URTICARIA
episodes occur at least twice a week or more than 6 weeks,
A lot of patient have each problem of recurrent urticaria. Lullaby in tagalog
You always have to ask since when did the urticaria appear.
- Often accompanied by angioedema.
- Most cases are idiopathic (75-90%) (unknown cause), this is the most common diagnosis
but still we have to rule out the other causes.
Etiology:
A. PHYSICAL
1. Dermatographism (also called dermographism or urticaria factitia),
- The ability to write on skin
can occur as an isolated disorder or accompany chronic urticaria or other physical
urticaria such as cholinergic and cold urticaria.
- diagnosed by observing the skin after stroking it with a tongue depressor or
fingernail. In such patients, a linear response occurs secondary to reflex
vasoconstriction, followed by pruritus, erythema, and a linear wheal.
2. Cholinergic Urticaria- onset of small punctate wheals surrounded by a prominent erythematous flare
- associated with exercise, hot showers, and sweating.
- When the patient cools down, the rash usually subsides in 3060 min.
3. Cold
- rapid onset of localized pruritus, erythema, and urticaria/angioedema after exposure
to a cold stimulus
- ice cube placed on the patient's skin for 1015/30 min. Patients with cold urticaria
have a positive reaction on rewarming of the chilled skin. (+) formation of wheals
4. Pressure urticaria and angioedema
- Pressure-induced urticaria differs from most types of urticaria or angioedema in that
symptoms typically occur 46 hr after pressure has been applied.

The disorder is clinically heterogeneous in that some patients may complain of

swelling secondary to pressure with normal-appearing skin (no urticaria), so that the
term angioedema is more appropriate.
- Symptoms occur at sites of tight clothing; foot swelling is common after walking;
and buttock swelling may be prominent after sitting for a few hr.
5. Solar Urticaria
- Rare disorder in which urticaria develops within 13 min of sun exposure. (Vampires!)
- Typically, pruritus occurs 1st, in about 30 sec, followed by edema confined to the lightexposed area and surrounded by a prominent erythematous zone caused by an axon
reflex.
6. Aquagenic Urticaria
Patients with aquagenic urticaria develop small wheals after contact with
water, regardless of its temperature, and are therefore distinguishable from patients
with cold urticaria or cholinergic urticaria.
Direct application of a compress of water to the skin is used to test for its
presence.
B. RHEUMATOLOGIC SLE and juvenile rheumatoid arthritis
C. ENDOCRINE hyperthyroidism/ hypothyroidism
D. NEOPLASTIC lymphoma, mastocytosis, leukemia
E. ANGIOEDEMA hereditary angioedema (AD, def of Cl-esterase inhibitor
- acquired angioedema
- ACE inhibitors
ANAPHYLAXIS
- This is a serious allergic reaction that is rapid and onset and main cause of death.
- a sudden release of potent biologically active mediators from mast cells and basophils
leading to:
cutaneous (urticaria, angioedema, flushing),
respiratory (bronchospasm, laryngeal edema),
cardiovascular (hypotension, dysrhythmias, myocardial ischemia), and
gastrointestinal symptoms (nausea, colicky abdominal pain, vomiting,
diarrhea).
- so parang katulad ng mast cell degranulation ,pero bigger, madami, more mast cell,
more basophils, more mediatiors,
*Anaphylaxis is diagnosed if a patient fulfilled any of the 3 criteria:
1. There is an acute onset of illness which is for several hours, with involvement of the skin
and mucosal tissues, (so meaning the patient have generalized rash, pruritus or
flushing, hydrating of the lip, tounge and uvula)
And atleast one of the following: either patient have,
respiratory compromise
DOB
wheezing,
stridor,
reduced blood pressure or
associated symptoms of organ dysfunction (collapse, hypotonia, syncope,
incontinence)
- If the patient has this criteria you can read tb dx the px having anaphylaxis
2. Two or more of the following that occur rapidly after exposure to a likely allergen to that
patient.

There is involvement of the skin and mucosal tissue, respiratory compromise,

reduced blood pressure or persistent GI symptoms, such as abdmonial or
vomiting, so pwede ring magkaroon ng GI sa anaphylaxis

3. Just reduced BP following exposure to a test known allergen .

Ex. The patient was allergy tested for food aller test for shrimp, the patient
accidentially eat that shrimp and he suddenly collapsed, so yun palang he already
satisfy the third criteria.
*Common anyphylactic allergen to children
1. food
2. drug
3. hymenoptera venom
4. related allergy
5. allergen immunotherapy
6. exercise
7. Vaccinations
8. Contrast media
*Differential Diagnosis:
The differential diagnosis includes:
other forms of shock (hemorrhagic, cardiogenic, septic),
vasopressor reactions including flush syndromes such as carcinoid syndrome, excess
histamine syndromes (systemic mastocytosis),
ingestion of monosodium glutamate (MSG),
scombroidosis (eg point fish),
Point fish- contains a lot of histamine, may present symptoms that may mimic
anaphylaxis, eto na yung bigla nalang may angioedema
heriditary angioedema
ADVERSE REACTION TO FOODS
- Adverse reactions to foods consist of any untoward reaction following the ingestion of a
food or food additive and are classically divided into:
o food intolerances, which are adverse physiologic responses, and
o food hypersensitivities, which include adverse immunologic responses and allergies
- Up to 6% of children experience food allergic reactions in the 1st 3 yr of life
CLASS 1: allergens penetrating the gastrointestinal barrier,
e.g egg, peanut, peas soy and bean cause 90% of food allergy during childhood
CLASS 2: by partially homologous allergens penetrating the respiratory tract,
e.g plant pollens
ADVERSE REACTION TO DRUG
- can be divided into predictable and unpredictable reactions.
- Predictable drug reactions, including drug toxicity, drug interactions, and adverse
effects, are dose dependent, can be related to known pharmacologic actions of the drug,
and occur in patients without any unique susceptibility.
- Unpredictable drug reactions are dose independent, often not related to the
pharmacologic actions of the drug, and occur in patients who are genetically predisposed.
These include idiosyncratic reactions, allergic (hypersensitivity) reactions, and
pseudoallergic reactions. Allergic reactions require prior sensitization, manifest with signs
or symptoms characteristic of an underlying allergic mechanism such as anaphylaxis or
urticaria, and occur in genetically susceptible individuals. They can occur at doses
significantly below the therapeutic range.

Pseudoallergic reactions resemble allergic reactions but are distinguished by the fact
that an immunologic mechanism is not involved.
Adverse Reactions can also be classified according to Gell and Coombs Classification:
i. Type I: immediate hypersensitivity reactions occur when a drug or drug
metabolite interacts with preformed drug-specific IgE antibodies that are bound to the
surfaces of tissue mast cells and/or circulating basophils; manifests as urticaria,
bronchospasm and anaphylaxis.
ii. Type II: cytotoxic antibody reactions involve the IgG or IgM antibodies that
recognize drug antigen on cell membrane. In the presence of serum complement, the
antibody coated cells is either cleared by the monocyte-macrophage system or is
destroyed. E.g., drug-induced hemolytic anemia and thrombocytopenia
iii. Type III: immune complex reactions caused by soluble complexes of drug or
metabolite in slight antigen excess with IgG or IgM antibodies. The immune complex is
deposited in blood vessel walls and causes injury by activating the complement cascade,
as seen in Serum Sickness fever, urticaria, rash, lymphadenopathy, and arthralgias.
Symptoms typically appear 1-3 weeks after last dose of offending drug and subside when
the drug and/or its metabolite is cleared from the body
iv. Type IV: delayed-type hypersensitivity reactions mediated by drug-specific T
lymphocytes. Sensitization usually occurs via the topical route neomycin and local
anesthetics resulting in allergic contact dermatitis; also PPD

1.
2.
3.
4.
5.

MANAGEMENT OF ALLERGIC REACTIONS

Avoid allergen exposure
Appropriate medication
Continuous allergy education
Environmental control
Pharmacologic Therapy:
a. Adrenergic Agents :
Alpha-Adrenergics (pseudoephedrine, phenylephrine) causes vasoconstriction and are
effective in the treatment of allergic nasal disease because of their decongestant effects.
Beta Adrenergics ( albuterol, salmetrol, formeterol) have been used in the treatment of
asthma because of their potent bronchodilator effects
b. Anticholinergic Agents (Ipratropium bromide) inhibit vagally mediated reflexes by
antagonizing the action of acetylcholine at muscarinic receptors. Lower onset
bronchodilator
c. Antihistamines treatment of allergic diseses. H1-Antihistaimes
d. Chromones ( Cromolyn sodium, neodocromil sodium) mast cell and mediator release
inhibitors
e. Glucoccorticoids anti-inflammatory actions
f. Leokotriene- Modifying Agents inhibit leukotriene production or block receptor
binding
g. Theophylline bronchodilating effects; IV route, toxic >20mg/mL
h. Olopatidine Hydrochloride in combination as nasal spray, both a mast cell
stabilizer and H1-receptor antagonist in relieving signs and symptoms of allergic
conjunctivitis after topical instillation.

i.

New therapies: Recombinant Soluble Receptors, Specific Cytokine Receptor Agonists,

and Humanized Monoclonal Anti-cytokine Antibodies