CARE OF CLIENTS WITH ALLERGIC DISORDERS
antigens, remove cells and other debris
Allergic Reaction
• manifestation of tissue injury resulting from
interaction between an antigen and antibody
• there are chemical mediators released during
allergic reactions that would produce symptoms
that would range from lid to life-threatening
Allergy
• is an inappropriate and often harmful response
of the immune system to normally harmless
substances (allergens – dust, pollen)
• in allergic reactions, the body encounters
allergens → proteins that body’s defenses
recognize as foreign → destroy them, and
remove them from the body
FUNCTIONS OF IMMUNOGLOBULINS
-antibodies formed by lymphocytes and plasma cells in
response to an immunogenic stimulus that constitute a
group of serum protein
• immunoglobulins of IgE
o Involved in allergic disorders and some
parasitic infections
o IgE – producing cells are located in the
respiratory and intestinal mucosa
• Two or more IgE molecules bind together to an
allergen and trigger the mast cells or basophils to
release chemical mediators – histamine,
serotonin, slow reacting substances of
anaphylaxis and neutrophil factor which
produces allergic reaction such as your asthma
and hay fever
• ATOPY – refers to IgE-mediated diseases, such as
allergic rhinitis
ROLE OF B CELLS
• Are programmed to produce one specific
antibody.
• On encountering a specific antigen → B cells
stimulate production of plasma cells (the site of
antibody production) → outpouring of
antibodies for the purpose of destroying and
removing the antigen
ROLE OF T CELLS
• Assist B cells in producing antibodies
• Secrete substances known as lymphokines that
encourage cell growth, promote cell activation
• Direct the flow of cell activity, destroy and digest
• Does not bind free antigens
• Stimulates the macrophages -macrophages
present the antigen to the T cells and initiate
immune response.
FUNCTION OF ANTIGENS
1. Complete protein antigens
• animal dander, pollen, and horse serum,
stimulate a complete humoral response
2. Low molecular weight substances
• medications, function as haptens
(incomplete antigens), binding to tissue
or serum proteins to produce a carrier
complex that initiates an antibody
response
➢ In an allergic reaction, the production of
antibodies requires active communication
between cells.
➢ When the allergen is absorbed through the
respiratory tract, gastrointestinal tract, or skin,
allergen sensitization occurs.
➢ Macrophages process the antigen and present it
to the appropriate cells.
➢ These cells mature into allergen-specific
secreting plasma cells that synthesize and
secrete antigen-specific antibodies.
FUNCTION OF CHEMICAL MEDIATORS
Mast cells: located in the skin and mucous membranes,
• play a major role in IgE-mediated immediate
hypersensitivity
• When mast cells are stimulated by antigens,
powerful chemical mediators are released,
causing a sequence of physiologic events that
results in symptoms of immediate
hypersensitivity
1. Primary mediators
▪ are preformed and are found in
mast cells or basophils
2. Secondary mediators
▪ inactive precursors that are
formed or released in response
to primary mediators
PRIMARY CHEMICAL MEDIATORS
1. HISTAMINE
• 1st chemical mediator in immune and
inflammatory responses
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 • Effects peak 5 to 10 mins after antigen
contact
• Erythema, localized edema in the form
of wheals: contraction of bronchial
smooth muscles → wheezing and
bronchospasm; dilation of small venules
and constriction of large vessels;
increased secretion of gastric and
mucosal cells → diarrhea
• Stimulates H1 (bronchiolar and vascular
smooth muscle cells) H2receptors
(gastric parietal cells)
• Diphenhydramine (Benadryl) - a
medication that displays an affinity for
H1 receptors.
• Cimetidine (Tagamet) and ranitidine
(Zantac) target H2 receptors - inhibit
gastric secretions in peptic ulcer disease.
2. EOSINOPHIL CHEMOTATCTIC FACTOR OF
ANAPHYLAXIS
• Eosinophil chemotactic factor of anaphylaxis
affects movement of eosinophils (granular
leukocytes) to the site of allergens. It is
preformed in the mast cells and is released
from disrupted mast cells.
3. PLATELET-ACTIVATING FACTOR
• responsible for initiating platelet
aggregation and leukocyte infiltration at
sites of immediate hypersensitivity
reactions.
• It also causes bronchoconstriction and
increased vascular permeability
4. PROSTAGLANDINS
• produce smooth muscle contraction as
well as vasodilation and increased
capillary permeability
• causes fever and pain that occur with
inflammation in allergic responses
SECONDARY CHEMICAL MEDIATORS
1. LEUKOTRIENES
• initiate the inflammatory response
• cause smooth muscle contraction,
bronchial constriction, mucus secretion
in the airways, and the typical wheal-
and-flare reactions of the skin.
• 100 to 1000 times more potent in
causing bronchospasm.
2. BRADYKININ
• has the ability to cause increased
vascular permeability, vasodilation,
hypotension, and contraction of many
types of smooth muscle, such as the
bronchi.
• Increased permeability of the capillaries
results in edema.
• stimulates nerve cell fibers and produces
pain.
3. SEROTONIN
• acts as a potent vasoconstrictor and
causes contraction of bronchial smooth
muscle.
HYPERSENSITIVITY
-Although the immune system defends the host against
infections and foreign antigens, immune responses can
themselves cause tissue injury and disease.
• is a reflection of excessive or aberrant immune
response to any type of stimulus
• usually does not occur with the first exposure to
an allergen.
• reaction follows a re-exposure after
sensitization, or buildup of antibodies, in a
predisposed person.
SPECIFIC TYPES OF REACTIONS
1. Anaphylactic (Type I) Hypersensitivity
• most severe hypersensitivity reaction
• unanticipated severe allergic reaction
• characterized by edema in many tissues,
including the larynx
• often accompanied by hypotension,
bronchospasm, and cardiovascular
collapse in severe cases.
• is an immediate reaction beginning
within minutes of exposure to an
antigen
• Primary chemical mediators are
responsible for the symptoms of type I
hypersensitivity because of their effects
on the skin, lungs, and gastrointestinal
tract. If chemical mediators continue to
be released, a delayed reaction may
occur and may last for up to 24 hours.
• Clinical symptoms:
▪ the amount of the allergen
▪ the amount of mediator
released
▪ the sensitivity of the target
organ
▪ the route of allergen entry.
• Type I hypersensitivity reactions may
include both local and systemic
anaphylaxis. Examples include allergic
rhinitis, asthma, and severe allergic
response in people sensitized to
penicillin or latex.
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2. Cytotoxic (Type II) Hypersensitivity
• occurs when the system mistakenly
identifies a normal constituent of the
body as foreign.
• may be the result of a cross-reacting
antibody, possibly leading to cell and
tissue damage.
• MYASTHENIA GRAVIS
▪ the body mistakenly generates
antibodies against normal nerve
ending receptors.
• GOODPASTURE SYNDROME
▪ it generates antibodies against
lung and renal tissue, producing
lung damage and renal failure.
3. Immune Complex (Type III) Hypersensitivity
• involves immune complexes that are
formed when antigens bind to
antibodies.
• These complexes are cleared from the
circulation by phagocytic action.
• Immune complexes are deposited in
tissues or vascular endothelium
• two factors contribute to injury:
▪ the increased amount of
circulating complexes
▪ the presence of vasoactive
amines.
• Result:
▪ there is an increase in vascular
permeability and tissue injury
▪ associated with systemic lupus erythematosus,
rheumatoid arthritis, certain types of nephritis, and
some types of bacterial endocarditis.
4. Delayed-Type (Type IV) Hypersensitivity
• also known as cellular hypersensitivity
• occurs 24 to 72 hours after exposure to
an allergen.
• It is mediated by sensitized T cells and
macrophages rather than antibodies.
• s/s: itching, erythema, and raised lesions
• subcutaneous injection of antigen
• often used as and assay for cell-
mediated immunity
• assay for cell mediated immunity:
purified protein derivative skin test for
immunity to M. tuberculosis
• CONTACT DERMATITIS
▪ resulting from exposure to
allergens such as cosmetics,
adhesive tape, topical agents
(eg, povidone-iodine),
medication additives, and plant
toxins. Symptoms include
itching, erythema, and raised
lesions.
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HEALTH ASSESSMENT
• A comprehensive allergy history
• Thorough physical examination
o provide useful data for the diagnosis and
management of allergic disorders.
• Allergy assessment form
o useful for obtaining and organizing this
information
• TAKE NOTE:
o degree of difficulty and discomfort
experienced by the patient because of
allergic symptoms
o degree of improvement in those
symptoms with and without treatment
are assessed and documented
o relationship of symptoms to exposure
to possible allergens is noted.
• Allergy
o Type of allergens
o Symptoms experiences
o Seasonal variations in occurrence of
severity in the symptoms
• History of testing and treatments
• Prescribed OTC meds
o Previously taken
o Currently taking for those allergies
o Effectiveness of the treatment
• Continued assessment for potential allergic
Precautionary steps
reactions in the patient is vital
All medication and food allergies are listed on an allergy
alert sticker and placed on the front of the patient’s
health record or chart to alert others
DIAGNOSTIC EVALUATIONS
1. Blood tests
2. Smears of body secretions
3. Skin tests
4. Serum specific IgE test (RAST)
Types of Skin tests
➢ Results of laboratory blood studies provide
supportive data for various diagnostic
possibilities; however, they are not the major
criteria for the diagnosis of allergic disease.
1. COMPLETE BLOOD COUNT WITH DIFFERENTIAL
• white blood cell (WBC) count is usually
normal except with infection
• eosinophils (n=2% - 5%)
▪ 5% to 10% for patients with
allergic disorders
2. EOSINOPHIL COUNT
• obtained from blood samples or smears
of secretions
• During symptomatic episodes, smears
obtained from nasal secretions,
conjunctival secretions, and sputum of
allergic patients usually reveal
eosinophils, indicating an active allergic
response.
3. TOTAL SERUM IgE LEVELS
• High total serum IgE levels support the
diagnosis of allergic disease
4. SKIN TESTS – most accurate
• High total serum IgE levels support the
diagnosis of allergic disease
• several different solutions may be
applied at separate sites
• Positive (wheal-andflare) reactions are
clinically significant when correlated
with the history, physical findings, and
results of other laboratory tests.
• results of skin tests complement the
data obtained from the history
• indicate which of several antigens are
most likely to provoke symptoms and
provide some clue to the intensity of the
patient’s sensitization.
• dosage of the antigen (allergen) injected
is also important
• Most patients are hypersensitive to
more than one allergen. Under testing
conditions, they may not react (although
they usually do) to the specific allergens
that induce their attacks
• In cases of doubt about the validity of
the skin tests, a RAST or a provocative
challenge test may be performed
1. Testing is not performed during periods of
bronchospasm.
2. Epicutaneous tests (scratch or prick tests) are
performed before other testing methods, in an
effort to minimize the risk of systemic reaction
3. Emergency equipment must be readily available
to treat anaphylaxis.
4. Corticosteroids and antihistamines should be
stopped 48-96 hours before testing
1. prick skin tests
2. scratch tests
3. intradermal skin testing
▪ positive reaction (urticarial wheal,
localized erythema, pseudopodia –
irregular projection at the end of the
wheal)
▪ After negative prick or scratch tests, intradermal
skin testing is performed with allergens that are
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 suggested by the patient’s history to be
problematic.
▪ The back is the most suitable area of the body
5. PROVOCATIVE TESTING
6. SERUM SPECIFIC IgE TEST
Interpretation of reactions:
▪ Negative wheal soft with minimal erythema.
▪ 1 wheal present (5 to 8 mm) with associated
erythema.
▪ 2 wheal (7 to 10 mm) with associated erythema.
▪ 3 wheal (9 to 15 mm), slight pseudopodia
possible with associated erythema.
▪ 4 wheal (12 mm) with pseudopodia and diffuse
erythema.
The following guidelines are used for the interpretation
of skin test results:
▪ Skin tests are more reliable for diagnosing atopic
sensitivity in patients with allergic rhinitis
▪ Positive skin tests correlate highly with food
allergy.
▪ Negative results are helpful in ruling out food
allergy
▪ The use of skin tests to diagnose immediate
hypersensitivity to medications is limited,
because metabolites of medications, not the
medications themselves, are usually responsible
for causing hypersensitivity
• direct administration of the suspected allergen
to the sensitive tissue, such as the conjunctiva,
nasal or bronchial mucosa, or gastrointestinal
tract (by ingestion of the allergen), with
observation of target organ response.
• helpful in identifying clinically significant
allergens in patients who have a large number of
positive tests.
• Major disadvantages:
o limitation of one antigen per session
o risk of producing severe symptoms,
particularly bronchospasm, in patients
with asthma.
• formerly known as Radioallergosorbent Test
(RAST)
• radioimmunoassay that measures
allergenspecific IgE
• patient’s serum is exposed to a variety of
suspected allergen particle complexes.
• If antibodies are present, they will combine with
radiolabeled allergens.
• Test results are then compared with control
values, reported on a scale from 0 to 5 (>2 is
significant)
• advantages of RAST
o decreased risk of systemic reaction,
o stability of antigens
o lack of dependence on skin reactivity
modified by medications
• disadvantages
o limited allergen selection
o reduced sensitivity compared with
intradermal skin tests
o lack of immediate results
o higher cost
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MEDICAL MANAGEMENT
Goal: provide relief from symptoms
AVOIDANCE THERAPY
• every attempt is made to remove
allergens that act as precipitating factors
• examples:
▪ use of air conditioners and air
cleaners
▪ removal of dust-catching
furnishings
▪ removal of pets from home
▪ use of high-efficiency
particulate air (HEPA) purifiers
▪ changing clothing when coming
in from outside
▪ showering to wash allergens
from hair and skin
▪ using an OTC nasal irrigation
device or saline nasal spray to
reduce allergens in the nasal
passages
PHARMACOLOGIC AGENTS
a. Antihistamines (H1 receptor
antagonist/H1 blockers)
b. Adrenergic agents
• Vasoconstrictor of the mucosal
muscles
• Reduces local blood flow, fluid
exudation, mucosal edema
c. Mast cell stabilizers
• Stabilizes the mast cell
membrane thus reducing the
release of histamine and other
mediators
d. Corticosteroids
• Anti-inflammatory action
e. Leukotriene modifiers
• Block the action of leukotriene,
prevent the s/s of asthma
Antihistamines
• Bind selectively to H1 receptors, preventing the
action of histamine at these sites
• FOR MILD ALLERGIC DISORDERS
o They do not prevent the release of
histamine from mast cells or basophils
• Oral antihistamines are most effective when
given at the first occurrence of symptoms
o Effectiveness is limited to certain
patients with hay fever, vasomotor
rhinitis, urticarial and mild asthma
• Major class of meds prescribed for the
symptomatic relief of allergic rhinitis
• Major side effect: DROWSINESS AND DRY
MOUTH
• Other side effects
o Anxiety
o Agitation
o Urinary retention
o Blurred vision
o Anorexia
o Nausea and vomiting
• Contraindications:
o Intake during the third trimester
o In nursing mothers
o Newborns and children
o Older patients
o Patient with asthma, urinary retention,
open-angle glaucoma, HPN and prostatic
hyperplasia
• Second-generation H1-receptor antagonists
o Nonsedating (does not cross the blood-
brain barrier)
o Examples: Loratadine, Cetirizine,
Fexofenadine
• May be combined with decongestants to reduce
nasal congestions
o Examples:
▪ Loratadine/Pseudoephedrine
(Claritin D)
▪ Cetirizine/Pseudoephedrine
(Zyrtec-D)
• Decongestants can cause increase in blood
pressure
Adrenergic agents
• Vasoconstrictors of the mucosal vessels
• Used for relief of nasal congestion
• Activate the alpha-adrenergic receptor sites of
the smooth muscle of the nasal mucosal blood
vessels causing reduction of
o Local blood flow
o Fluid exudation
o Mucosal edema
• Used topically in nasal (Afrin) and ophthalmic
(Alphagan P) formulations in addition to oral
route (Pseudoephedrine (Sudafed))
• Topical preparations have less side effects
• However, should be limited to a few days to
avoid rebound congestion
• potential side effects:
o Hypertension
o Dysrhythmias
o Palpitations
o CNS stimulation
o Irritability
o Tremor
o Tachyphylaxis (acceleration of
hemodynamic status)
Mast cell stabilizers
• Stabilizes the mast cell membrane, thus reducing
the release of histamine and other mediators
• Inhibits macrophages, eosinophils, monocytes,
and platelets involved in immune response
• Used prophylactically to prevent the onset of
symptoms and to treat the symptoms once they
appear
• Used therapeutically for chronic allergic rhinitis
• Intranasal Cromolyn Sodium
o Effective as antihistamines but less
effective than nasal corticosteroids in
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 the treatment of seasonal allergic
rhinitis
• Adverse effects are usually mild:
o Sneezing
o Local stinging
o Burning sensations
Corticosteroids
• Indicated for more severe cases of allergic and
perennial rhinitis
• Example:
o Beclomethasone (Beconase, Qnasl)
o Budosenide (Rhinocort)
o Flunisolide (AeroSpan)
o Triamcinolone (Nasocort)
• Full benefit may not be achieved for several days
to 2 weeks
• Adverse effects
o Drying of the nasal mucosa
o Burning and itching sensations
• Systemic effects are more likely with
Dexomethasone
• Use of this medication should be limited only up
to 30 days
• Suppresses the host defenses, must be used with
caution in patients with tuberculosis or
untreated bacterial infections
• Inhaled corticosteroids DO NOT affect the
immune system to the same degree as systemic
corticosteroids
• Because the response to corticosteroids is
delayed, they have little or o value in acute
therapy for severe reactions such as anaphylaxis
• Patients who receive high-dose or long-term
corticosteroid therapy must be cautioned not to
stop taking the medication suddenly. Doses are
tapered when discontinuing this medication to
avoid adrenal insufficiency
• Side effects
o Fluid retention
o Weight gain
o Hypertension
o Gastric irritation
o Glucose intolerance
o Adrenal suppression
reached that is effective in reducing disease
severity from natural exposure
• Used when avoidance of allergen is impossible
• Most common method: serial injection of one or
more antigen
• Goals:
o Reduce level of circulating IgE
o Increase level of blocking IgG
o Reduce mediator cell sensitivity
• Effective for ragweed pollen, grass, tree pollen,
cat dander and house dust mites
• Evidence of failure:
o No decrease in symptoms within 12-24
months
o Failure to develop increased tolerance
to known allergens
o Failure to decrease the use of meds to
reduce symptoms
• Begin with very small amount
• Gradually increased, usually on a weekly
interval, until a maximum tolerated dose is
achieved
• Maintenance booster injections are
administered at 2-4-week interval
• Contraindications:
o Patients using beta-blocker or ACE
inhibitors
o With significant pulmonary or cardiac
disease or organ failure
o Inability of the patient to recognize/
report signs of systemic reaction
o Nonadherence of the patient
o Absence of any equipment or adequate
personnel to respond to allergic reaction
o Should be initiated during pregnancy
• Nursing responsibilities:
o Monitor px after administration of
immunotherapy
o Should not be administered by a lay
person/patient
o Px must remain in the office or clinic for
30 minutes
o If px develops local swelling, the next
dose should not be increased

Leukotriene modifiers
• Block the synthesis or action of leukotriene
• For long term use
• Should be taken daily
• Examples:
o Zileuton
o Zafirlukast (Accolate)
o Montelukast (Singulair)

IMMUNOTHERAPY
• “allergen desensitization” / “allergen
immunotherapy” / “hyposensitization” /
“allergen vaccine therapy”
• Administration of gradually increasing quantities
of specific allergens to the patient until a dose is

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Types of Allergies
An allergy occurs when your body’s immune system sees a certain substance as harmful. It reacts by causing an
allergic reaction. Substances that cause allergic reactions are allergens.

There are many types of allergies. Some allergies are seasonal and others are year-round. Some allergies may be
life-long.

It is important to work with your health care provider to create a plan to manage your allergy. Avoiding your
allergens is the best way to prevent an allergic reaction.

t is important to work with your health care provider to create a plan to manage your allergy. Avoiding your allergens
is the best way to prevent an allergic reaction.

Drug Allergy True allergies to drugs (medicines) occur in only a small number of people. Most drug reactions are
not allergic, but are side effects of the properties of the medicine. A diagnosis of the cause of the drug reaction is
usually based only upon the patient’s history and symptoms. Sometimes skin testing for drug allergy is also done.
Food Allergy
There are different types of allergic reactions to foods. There are differences between IgE-mediated allergies, non-IgE
mediated allergies and food intolerances.

Insect Allergy
Bees, wasps, hornets, yellow jackets and fire ants are the most common stinging insects that cause an allergic
reaction.

Non-stinging insects can also cause allergic reactions. The most common are cockroaches and the insect-like dust
mite. Allergies to these two insects may be the most common cause of year-round allergy and asthma.

Latex Allergy
A latex allergy is an allergic reaction to natural rubber latex. Natural rubber latex gloves, balloons, condoms and other
natural rubber products contain latex. An allergy to latex can be a serious health risk.

Mold Allergy
Mold and mildew are fungi. Since fungi grow in so many places, both indoors and outdoors, allergic reactions can
occur year round.

Pet Allergy
Allergies to pets with fur are common. It is important to know that an allergy-free (hypoallergenic) breed of dog or cat
does not exist.

Pollen Allergy
Pollen is one of the most common triggers of seasonal allergies. Many people know pollen allergy as “hay fever,” but
experts usually refer to it as “seasonal allergic rhinitis.”

Source:

AAFA. (n.d.). Retrieved October 05, 2020, from https://www.aafa.org/types-of-allergies/

 ALLERGIC DISORDERS 1. Local Reaction
 At the site of antigen exposure, rarely
two types of IgE-mediated allergic reactions: fatal
 Atopic 2. Systemic Reaction
o Intrinsic  Involve cardiovascular, respiratory, GI,
o characterized by a hereditary predisposition and integumentary organ systems
and production of a local reaction to IgE
antibodies, which manifests in one or more Common Causes
of the following three atopic disorders: 1. Foods
allergic rhinitis, asthma, and atopic  Peanuts, tree nuts (eg. Walnuts, pecans,
dermatitis/eczema cashews, almonds), shellfish (shrimp,
 Nonatopic disorders lobster, crab), fish, milk, egg, soy
o extrinsic 2. Medications
o lack the genetic component and organ  Antibiotics- penicillin and sulfa
specificity of the atopic disorders antibiotics, allopurinol
o nonatopic asthma  Radiocontrast agents, anesthetic agents
o nonatopic dermatitis (lidocaine, procaine), vaccines,
hormones (insulin vasopressin,
Although the underlying immunologic reactions of the adrenocorticotropic hormone), aspirin,
two types of disorders are the same, the predisposing nonsteroidal anti-inflammatory drugs)
factors and manifestations are different. 3. Other pharmaceutical/ biologic agents
 Animal serums (tetanus antitoxin, snake
ANAPHYLAXIS venom antitoxin, rabies antitoxin),
 a clinical response to an immediate (type I antigens used in skin testing
hypersensitivity) immunologic reaction between  Insect stings
a specific antigen and an antibody.  Bees, wasps, hornets, yellow jackets,
 The reaction results from a rapid release of IgE- ants (including fire ants)
mediated chemicals, which can induce a severe,  Latex
life-threatening allergic reaction.  Medical and nonmedical products
containing latex
Pathophysiology
 caused by the interaction of a foreign antigen
with specific IgE antibodies found on the surface
membrane of mast cells and peripheral blood
basophils.
 The subsequent release of histamine and other
bioactive mediators causes activation of
platelets, eosinophils, and neutrophils.
 Histamine, prostaglandins, and inflammatory
leukotrienes are potent vasoactive mediators
that are implicated in the vascular permeability
changes, flushing, urticaria, angioedema,
hypotension, and bronchoconstriction that
characterize anaphylaxis.
 Smooth muscle spasm, bronchospasm, mucosal Clinical Manifestations
edema and inflammation, and increased “the faster the onset, the more severe the reaction”
capillary permeability result.
 Substances that most commonly cause Categories:
anaphylaxis include: foods, medications, insect 1. Mild
stings, and latex  peripheral tingling
 Foods that are common causes of anaphylaxis  sensation of warmth
include peanuts, tree nuts, shellfish, fish, milk,
 sensation of fullness in the mouth and
eggs, soy, and wheat.
throat
 antibiotics (eg, penicillin), radiocontrast agents,
 Nasal congestion
intravenous (IV) anesthetic agents, aspirin and
 periorbital swelling
other nonsteroidal antiinflammatory drugs
 pruritus
(NSAIDs), and opioids.
 sneezing
 tearing of the eyes
 Onset of symptoms begins within the
first 2 hours after exposure

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 2. Moderate
 Flushing
 Warmth
 Anxiety
 itching
 in addition to any of the milder
symptoms
 bronchospasm
 edema of the airways or larynx with
dyspnea, cough, and wheezing
 the onset of symptoms is the same as for
a mild reaction
3. Severe
symptoms progress rapidly to:
 Bronchospasm
 laryngeal edema  Screening for allergies before a medication is
 severe dyspnea prescribed or first administered
 cyanosis o careful history of any sensitivity to
 hypotension suspected antigens must be obtained
 Dysphagia (difficulty swallowing) o ask about previous exposure to contrast
 abdominal cramping agents used for diagnostic tests and any
 vomiting allergic reactions, as well as reactions to
 diarrhea any medications, foods, insect stings,
and latex.
 seizures can also occur
o If predisposed to anaphylaxis, wear
 Cardiac arrest and coma may follow.
some form of identification, such as a
MedicAlert bracelet, which names
Prevention
allergies to medications, food, and other
 Strict avoidance of potential allergens
substances.
o Insect stings
 Should avoid areas populated by
Immunotherapy/Desensitization
insects
 Those who are allergic to insect venom
 Use appropriate clothing
o Very effective in the reduction of risk of
 use of insect repellant
anaphylaxis in future stings
 caution to avoid further stings
 Effective also for insulin-allergic patients with
 If avoidance of exposure to allergens is
diabetes and those who are allergic to penicillin
impossible, the patient should be instructed to
 USED AS A CONTROL MEASURE, NOT CURE
carry and administer epinephrine to prevent an
anaphylactic reaction in the event of exposure to
Medical Management
the allergen.
 CPR if cardiac arrest is noted
EpiPen Auto-Injector  Supplemental oxygen
 a commercially available first-aid device that o Provided during CPR or if the patient is
delivers premeasured doses of 0.3 mg (EpiPen) cyanotic, dyspneic, or wheezing
or 0.15 mg (EpiPen Jr.) of epinephrine  Administer epinephrine
 requires no preparation o 1:1000 dilution; administered SC in the
upper extremity or in the thigh
 self-administration technique is not
o May also be followed through
complicated.
continuous IV infusion
Who should bring?  Antihistamine and corticosteroids
o To prevent recurrence of the reaction
 Those who are
o Treat urticarial and angioedema
sensitive to insect
bites and stings  IV fluids, volume expanders and vasopressor
agents
 Those who have
o To maintain BP and normal
experienced food or
hemodynamic status
medication reactions
 Aminophylline
 Those who have
o To improve airway patency, esp. those
experienced
with bronchospasm and history of
idiopathic pr exercise-
asthma and COPD
induced anaphylactic
reactions  Patients should also be transported immediately
to the local emergency dept for observation and
monitoring because of the risk of “rebound” or
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 delayed reaction 4 to 8 hours after the initial
reaction
 Monitoring should be done for the next 12 to 14
hours
Nursing Management
 Assess for s/s of anaphylaxis
o Airway, breathing patterns and vital
signs
o Increasing edema
o Respiratory distress
 Prompt notification of the rapid response team
and/or provider
 Rapid initiation of emergency measures
o Intubation
o Administration of emergency
medications
o Insertion of IV lines
o Fluid administration
 Documentation of interventions done patient’s
vital signs and response to the treatment
o Explanation to the patient of what has
occurred
o Give instructions about avoiding future
reactions and about how to administer
emergency medications
o Make sure the patient has received a
prescription of preloaded syringes of
epinephrine
ALLERGIC RHINITIS
 most common form of respiratory allergy
 presumed to be mediated by an immediate (type
I hypersensitivity) immunologic reaction
 Occurrence increases as one ages
 Occurs with other conditions
o Allergic conjunctivitis
o Sinusitis
o Asthma
 Induced by airborne pollens or molds
 in temperature areas that does not experience
freezing temps., molds can persist through the
year
o Early spring—tree pollen (oak, elm,
poplar)
o Early summer—rose pollen (rose fever),
grass pollen (Timothy, red-top)
o Early fall—weed pollen (ragweed)
Pathophysiology
 by ingestion or inhalation of an antigen.
 On re-exposure, the nasal mucosa reacts by
o the slowing of ciliary action
o edema formation
o leukocyte (primarily eosinophil)
infiltration
Histamine is the major mediator of allergic reactions in
the nasal mucosa. Tissue edema results from
vasodilation and increased capillary permeability
Clinical Manifestations
 sneezing and nasal congestion
 clear, watery nasal discharge
 nasal itching
 Drainage of nasal mucus into the pharynx results
in multiple attempts to clear the throat and
results in a dry cough or hoarseness
 Headache
 pain over the paranasal sinuses
 epistaxis
Assessment and Diagnostic Findings
 history and PE
 nasal smears
 peripheral blood smears
 total serum IgE – increased
 epicutaneous (on the skin) and intradermal
testing
 RAST – presence of IgE
 Food elimination and challenge
 Nasal provocation test
Medical Management
 Avoidance Therapy
 Pharmacologic Therapy
o Antihistamines
o Adrenergic agents
o Mast cell stabilizers
o Corticosteroids
o Leukotriene modifiers
 Immunotherapy
Nursing Diagnoses
 Ineffective breathing pattern related to allergic
reaction
 Deficient knowledge about allergy and the
recommended modifications in lifestyle and self-
care practices
 Ineffective individual coping with chronicity of
condition and need for environmental
modifications
Nursing Interventions
 Assist in modifying environment
 Reduce exposure to people with respiratory
infections
 If with upper respiratory infection, instruct deep
breaths and to cough frequently
 Reinforce adherence to medication schedules
and other treatment regimen
 Instruct to seek medical attention if both upper
respiratory infection and allergic rhinitis are
present
 Remind about the desensitization schedules
 Explain the difference of each medication
 Encourage client to verbalize feelings and
concerns
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CONTACT DERMATITIS
 a type IV delayed hypersensitivity reaction, is an
acute or chronic skin inflammation that results
from direct skin contact with chemicals or
allergen
 has a sensitization period of 10-14 days
 4 basic types
o Allergic
o Irritant
o Phototoxic
o Photoallergic

1. Allergic
 Results from contact of skin and
allergenic substances
 Clinical manifestations
o Vasodilation and perivascular
infiltrates on the dermis
o Intracellular edema
o Usually seen on the dorsal Treatment
aspects of hand 1. Allergic
2. Irritant  Avoidance of offending material
 Results from contact with a substance  Burow’s solution or cool water compress
that chemically or physically damages  Systemic corticosteroids (prednisone)
the skin on a nonimmunologic basis. for 7–10 days
 Occurs after first exposure to irritant or  Topical corticosteroids for mild cases
repeated exposures to milder irritants
 Oral antihistamines to relieve pruritus
over an extended time.
2. Irritant
 Clinical manifestations
 Identification and removal of source of
o Dryness lasting days to months
irritation
o Vesiculation, fissures, cracks
 Application of hydrophilic cream or
o most common areas: Hands
petrolatum to soothe and protect
and lower arms
 Topical corticosteroids and compresses
3. Phototoxic
for weeping lesions
 Resembles the irritant type but requires
 Antibiotics for infection and oral
sun and a chemical in combination to
antihistamines for pruritus
damage the epidermis.
3. Phototoxic and Photoallergic
4. Photoallergic
 Same as for allergic and irritant
 Resembles allergic dermatitis but
dermatitis
requires light exposure in addition to
allergen contact to produce
immunologic reactivity

Clinical Manifestations
 Itching
 Burning
 Erythema
 Skin lesions (vesicles)
 Edema
 Followed by:
o Weeping, crusting, and drying and
peeling of the skin
 Hemorrhagic bullae may develop
 Repeated reactions may be accompanied by
thickening of the skin
 Secondary infection may develop

Assessment and diagnostic findings

 History
 Patch test
o Thin-layer Rapid Use Epicutaneous Test
(T.R.U.E. Test)
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