ASTHMA

A. Definition of Asthma
Asthma is a chronic lung condition that affects the airways. Asthma makes
breathing difficult because the airways become swollen, produce too much mucus and the
muscles around the airways tighten. Asthma can range from mild to severe and can be life
threatening. Currently there is no cure for asthma, but it can be controlled by routine
medical care, which should include a management plan developed by a health care
provider, medication(s), avoidance of triggers, and good health habits.
Healthy People 2010, a national health promotion and disease prevention
initiative, reports that nationwide, asthma is responsible for 5,000 deaths and 134 million
days of restricted activity a year.
A person normally breathes in (inspiration) and out (expiration) without even
thinking about how the respiratory system works. The process of air moving in and out of
the lungs is called ventilation.
Air enters the respiratory system through the nose and mouth. The air is
humidified (moistened), filtered and temperature controlled in the nasal cavity and
pharynx (passageway from nasal cavity to larynx). The air travels through the larynx
(voice box), the trachea (windpipe) and the airways (bronchial tubes or bronchi).
Think for a minute about the structure of a tree. In a tree, nutrients are distributed
from the base of the tree, up the trunk, through the limbs, and out to the smaller branches,
twigs and leaves. The lower airways resemble an upside down or inverted tree. Oxygen
travels down the trachea where it can enter either the right or left lung through the
mainstem bronchi.The trachea and bronchi have linings that filter, trap and help remove
particles from the air. In each lung, the bronchi continue to divide and get progressively
smaller. The small bronchi are called bronchioles. In total, each mainstem bronchus
divides into more than 25 successively smaller branches and ends in balloon-like air sacs
called alveoli. From the alveoli, oxygen enters the blood and carbon dioxide is removed
from the blood and then exhaled. The primary muscle used in breathing is the diaphragm,
the large muscle that separates the abdominal cavity from the thoracic (chest)
cavity.When breathing becomes more difficult due to added work because of exercise or
lung disease, the body uses accessory muscles in the neck, chest and abdomen to assist in
breathing.

B. Etiology of and risk factors for asthma
Asthma comprises a range of heterogeneous phenotypes that differ in
presentation, etiology and pathophysiology. The risk factors for each recognized
phenotype of asthma include genetic, environmental and host factors. Although a family
history of asthma is common, it is neither sufficient nor necessary for the development of
asthma.
The substantial increases in the incidence of asthma over the past few decades
and the geographic variation in both base prevalence rates and the magnitude of the
increases support the thesis that environmental changes play a large role in the current
asthma epidemic. Furthermore, environmental triggers may affect asthma differently at
different times of a persons life, and the relevant risk factors may change over time.
Short-term studies of risk factors may suggest a lower likelihood of asthma,
whereas the same factors may be associated with greater risk if follow-up is more
prolonged. This pattern may relate to overlap between different wheezing phenotypes in
early childhood, only some of which persist as asthma in later childhood and adulthood.
Because of this phenomenon, we examine here the risk factors for persistent asthma at
different ages, specifically the prenatal period, infancy, childhood and, briefly, adulthood.

1. Genetics
Family and twin studies have indicated that genetics plays an
important role in the development of asthma and allergy, 15 likely through
several genes of moderate effect (i.e., genes associated with relative risks in
the range of 1.22).
Genome-wide linkage studies and casecontrol studies have
identified 18 genomic regions and more than 100 genes associated with
allergy and asthma in 11 different populations. In particular, there are
consistently replicated regions on the long arms of chromosomes 2, 5, 6, 12
and 13. Association studies of unrelated individuals have also identified more
than 100 genes associated with allergy and asthma, 79 of which have been
replicated in at least one further study. A recent genome-wide association
study identified a new gene, ORMDL3, that exhibited a highly significantly
association with asthma (p < 1012) (for single nucleotide polymorphism
rs8067378, odds ratio 1.84, 95% confidence interval 1.432.42) a finding that
has now been replicated in several populations.
Extensive heterogeneity in the genetic basis of asthma, and in gene-
by-environment interactions, is likely. Failure to identify and precisely
quantify environmental exposures and their timing may account for some of
the difficulty that researchers have had in replicating genetic associations.
2. Prenatal risk factors
Risk factors in the prenatal period are multifactorial. Assessment is
complicated by the variety of wheezing conditions that may occur in infancy
and childhood, only some of which evolve to classical asthma.
3. Prenatal tobacco smoke
Prenatal maternal smoking has been consistently associated with
early childhood wheezing, and there is a doseresponse relation between
exposure and decreased airway calibre in early life. Prenatal maternal
smoking is also associated with increased risks of food allergy, cytokine
responses in the cord blood and concentrations of nitric oxide in exhaled air
in newborns. Studies have shown a clear prenatal effect of smoking; this
effect is increased when combined with postnatal smoke exposure.
4. Diet and nutrition
Observational studies examining prenatal nutrient levels or dietary
interventions and the subsequent development of atopic disease have focused
on foods with anti-inflammatory properties (e.g., omega-3 fatty acids) and
antioxidants such as vitamin E and zinc. Several studies have demonstrated
that higher intake of fish or fish oil during pregnancy is associated with lower
risk of atopic disease (specifically eczema and atopic wheeze) up to age 6
years. Similarly, higher prenatal vitamin E and zinc levels have been
associated with lower risk of development of wheeze up to age 5 years.
However, no protective effect against the development of atopic disease in
infants has been shown for maternal diets that excluded certain foods (e.g.,
cows milk, eggs) during pregnancy. The authors of 2 recent studies reported
an inverse relation of maternal vitamin D levels with wheeze in early life, but
no relation with atopy or symptoms in later life.
5. Stress
A number of animal models have suggested that prenatal maternal
stress acts through regulation of the offsprings hypothalamicpituitary
adrenal axis to decrease cortisol levels, which may affect the development of
an allergic phenotype. Although there is a correlation between caregiver
stress early in the infants life and higher levels of immunoglobulin E in the
infant and early wheezing, no studies to date have shown an association with
asthma. Antibiotic use
The association between prenatal antibiotic treatment and subsequent
development of atopic disease has been examined in 2 ways: with treatment
as a dichotomous predictor (i.e., any antibiotic use) and by number of courses
of antibiotics during pregnancy. Longitudinal cohort studies examining any
antibiotic use showed a greater risk of persistent wheeze and asthma in early
childhood and a doseresponse relation between number of antibiotic courses
and risk of wheeze or asthma.
6. Mode of delivery
Development of atopy was 2 to 3 times more likely among infants
delivered by emergency cesarean section, although no such association
occurred with elective cesarean section. Potential reasons for these findings
include maternal stress and differences in the infants gut microflora
associated with different modes of delivery.

C. Pathophysiology of asthma
Asthma is a complex disease characterized by airway inflammation, airway
smooth muscle hyperresponsiveness, and symptomatic bronchoconstriction. Because the
most prominent clinical feature of asthma is bronchoconstriction, a simplistic approach to
understanding the disease focuses on airway smooth muscle contraction. At its most
fundamental level, however, asthma is an inflammatory disease of the airways, and
treatment of the underlying inflammation is crucial to maintain normal airway function.
Therefore, as detailed below, the treatment of asthma employs both bronchodilators and
anti-inflammatory agents.

1. Asthma as a Bronchoconstrictive Disease
The propensity of asthmatic airways to constrict in response to a wide
variety of stimuli, including allergens, environmental irritants, exercise, cold
air, and infections, is termed hyperresponsiveness. Two features of airway
hyperresponsiveness separate the asthmatic response to stimuli from the non-
asthmatic response:hypersensitivity and hyperreactivity. Hypersensitivity
describes a normal response at abnormally low levels of stimuli; i.e., the
airways of asthmatics constrict to stimuli that do not elicit a response in
normal individuals. Hyperreactivity describes an exaggerated response at
normal levels of stimuli; i.e., the airways of asthmatics respond too
vigorously. Hypersensitivity describes a shift of the stimulusresponse curve
to the left, while hyperreactivity describes an upward shift. The overall
asthmatic response represents the combination of hypersensitivity and
hyperreactivity.
The causes of airway hyperresponsiveness in asthma have not been
completely elucidated. The hyperreactive response may be explained by
alterations in airway smooth muscle mass due to the increase in size
(hypertrophy) and number (hyperplasia) of myocytes that occurs in response
to inflammation. The hypersensitivity response is due to alterations in smooth
muscle excitationcontraction coupling. Possible mechanisms of altered
coupling in asthma include greater responsiveness of intracellular calcium
release channels, increased calcium sensitization, and changes in the
expression of ion channels, receptors, and second messengers.
2. Asthma as an Inflammatory Disease
Although the primary symptoms (wheezing and shortness of breath)
of most asthmatic patients are due to bronchoconstriction, the underlying
cause of asthma is an allergic inflammation of the airways. The inflammatory
process is visible histologically as airway edema, goblet cell hyperplasia,
subepithelial fibrosis, mucus hypersecretion, and infiltration by a variety of
inflammatory cells, including TH2 lymphocytes, antigen-presenting cells,
plasma cells, mast cells, neutrophils, and eosinophils . Airway inflammation
can lead to a chronic cough in asthmatic individuals, even in those who do not
develop symptomatic bronchoconstriction (this diagnosis is known as cough
variant asthma). Many inflammatory mediators and cytokines govern the
interplay among the various immune cells. Anti-inflammatory medications,
particularly corticosteroids, are mainstays in the pharmacologic treatment of
asthma. As the complex pathophysiology of asthma is further elucidated, more
targeted therapies will be developed.
a. TH2 Cells and the Origin of Asthma
Although the exact causes of asthma are not fully understood, one theory
suggests that asthma (and other allergic diseases) is the result of an
immune imbalance favoring TH2 lymphocytes over TH1 lymphocytes.
TH2 lymphocytes contribute to asthma through three mechanisms. First,
in patients with a hereditary predisposition to atopy (from the Greek,
meaning out of place), an allergen can trigger a type I hypersensitivity
response. In normal (nonatopic) individuals, an allergen is phagocytosed
by antigen-presenting cells, stimulating a low-level TH1 response and the
production of appropriate amounts of IgG antibodies directed against the
allergen. In atopic individuals, however, the same allergen induces a
strong TH2 response mediated through the release of IL-4, which induces
B cells to produce exaggerated amounts of IgE antibodies directed
against the allergen. The IgE antibodies bind to high-affinity IgE
receptors on mast cells, and subsequent cross-linking of the IgE receptors
upon re-exposure to the allergen causes mast-cell degranulation and
triggers an allergic reaction. Second, TH2 cells can directly induce a type
IV hypersensitivity reaction through the production of IL-13 (and, to a
lesser degree, IL-4). In the airway, IL-13 causes goblet cell hyperplasia,
increased mucus production, and smooth muscle hyperplasia and/or
hypertrophy. Third, TH2 lymphocytes recruit eosinophils by producing
IL-5 as well as GM-CSF and IL-4. These cytokines (especially IL-5)
induce eosinophil proliferation and release from the bone marrow and
promote eosinophil survival in the circulation and tissues. As in many
patients with asthma, Mr. Y had a high level of circulating eosinophils
and elevated levels of serum IgE.
What causes the imbalance between TH1 and TH2 lymphocytes in
patients with asthma? Although the exact reasons remain to be fully
elucidated, they likely involve environmental effects on genetically
susceptible individuals. Epidemiologic studies have found that exposures
to tuberculosis and viruses such as measles and hepatitis A are protective
against the development of asthma. Having older siblings and/or
encountering other children through attendance at a day-care facility
(both of which are associated with increased exposure to infectious
agents) are also associated with a decreased incidence of asthma. Living
in a rural environment (where there is substantial contact with bacterial
endotoxins) is also protective. One leading theory suggests that a
Western lifestyle, including decreased exposure early in life to
microbes that engender TH1-lymphocyte responses, contributes to the
development of asthma and other allergic diseases in susceptible
individuals. Although this hygiene hypothesis is probably too
simplistic to explain the origins of a complex disease such as asthma, it
forms a useful model for thinking about the disease and is a possible
explanation for the dramatic rise in the incidence of asthma in the
Western hemisphere. It is impossible to know exactly what caused Mr.
Ys asthma; however, the fact that he had allergic rhinitis and elevated
levels of IgE suggests that he had an atopic predisposition triggered by
environmental allergens.
b. Plasma Cells, IgE, Mast Cells, and Leukotrienes
As noted above, an IgE-mediated type I hypersensitivity response is one
mechanism by which allergens cause the pathologic and clinical
manifestations of asthma 3. The allergic response is initiated when a
dendritic cell phagocytoses an inhaled allergen. The dendritic cell
presents the processed allergen to TH2 cells and activates them. The
activated TH2 cells bind to and activate B lymphocytes via CD40 on the
B-cell surface. Activated TH2 cells also generate IL-4 and IL-13, which
induce B-cell transformation into IgE-producing plasma cells.
IgE circulates briefly in the bloodstream before binding to high-affinity
IgE receptors (FcRI) on mast cells. Upon re-exposure, the allergen binds
to mast cell-bound IgE and cross-links the FcRI receptors, thereby
activating the mast cell. The activated mast cell degranulates, releasing its
preformed inflammatory mediators. These molecules include histamine,
proteolytic enzymes, and certain cytokines (such as platelet-activating
factor). The activated mast cell also releases arachidonic acid from its
plasma membrane and produces leukotrienes and prostaglandin D2 .
Acutely, mast-cell degranulation produces bronchoconstriction and
airway inflammation. Histamine released by the mast cells promotes
capillary leakage, leading to airway edema. Mast cells also release
leukotriene C4 (LTC4), which is subsequently converted into LTD4 and
LTE4 . These three leukotrienes, called cysteinyl leukotrienes, are central
to the pathophysiology of asthma because they induce marked
bronchoconstriction. Leukotriene D4 is 1,000 times more potent than
histamine in producing bronchoconstriction. Leukotrienes also cause
mucus hypersecretion, capillary leakage, and vasogenic edema, and
recruit additional inflammatory cells. The effect of the leukotrienes,
though slower in onset, is more powerful and sustained than that of the
preformed mediators. Because of their delayed yet potent inflammatory
effect, leukotrienes were once called slow-reacting substance of
anaphylaxis (SRS-A) before their actual structures were identified.
Mast cells recruit other inflammatory cells via the release of cytokines.
This produces a delayed reaction that develops 4 to 6 hours after
exposure to allergen . Mast cells also release tryptase, a protease that
activates receptors on epithelial and endothelial cells, inducing the
expression of adhesion molecules that attract eosinophils and basophils.
Tryptase is also a smooth muscle mitogen, causing hyperplasia of airway
smooth muscle cells and contributing to airway hyperresponsiveness. The
production of IL-1, IL-2, IL-3, IL-4, IL-5, GM-CSF, interferon-, and
TNF- by mast cells contributes to chronic inflammation and the chronic
asthmatic reaction. Finally, mast cells release proteases and
proteoglycans that act on supporting airway structures to produce chronic
changes in the airway (also called airway remodeling). Unlike the
reversible component of bronchoconstriction that characterizes the acute
asthmatic reaction, airway remodeling induced by chronic inflammation
may cause irreversible impairment in pulmonary function.
c. Eosinophils
The major physiologic role of eosinophils is to defend against parasitic
infections. Eosinophils originate in the bone marrow and are stimulated
by IL-4, IL-5, and GM-CSF produced by TH2 lymphocytes and mast
cells. Eosinophils migrate from the bloodstream to the airway by binding
to specific adhesion molecules, particularly VCAM-1, and by traveling
along chemokine gradients to sites of inflammation. Once recruited to the
airway, eosinophils have a complex, multifunctional role in asthma.
Activated eosinophils secrete cytotoxic granules that cause local tissue
damage and induce airway remodeling, lipid mediators and
neuromodulators that affect airway tone, and cytokines and chemokines
that recruit other inflammatory cells.
The toxic granules of eosinophils contain a number of cationic proteins
including major basic protein (MBP), eosinophilic cationic protein(ECP),
eosinophil peroxidase, and eosinophil-derived neurotoxinthat are
directly damaging to the bronchial epithelium. For example, ECP can
breach the integrity of target cell membranes by forming ion-selective,
voltage-insensitive pores, and eosinophil peroxidase catalyzes the
production of highly reactive oxygen species that oxidize target cell
proteins and induce apoptosis. Eosinophils also produce matrix
metalloproteinases that contribute to airway remodeling.
Eosinophils contribute both directly and indirectly to airway
hyperresponsiveness. MBP and ECP affect smooth muscle tone and
induce hyperresponsiveness by increasing intracellular calcium
concentrations and damaging inhibitory M2 muscarinic receptors, thereby
increasing vagal tone. Eosinophil-derived cysteinyl leukotrienes and
neuropeptides (such as substance P) increase vasodilation, vascular
permeability, mucus hypersecretion, and airway smooth muscle
contraction.
Finally, eosinophils are immunomodulatory cells that can amplify the
immune response in asthma. Eosinophils up-regulate endothelial
adhesion molecules and thereby recruit other inflammatory cells.
Eosinophils are also antigen-presenting cells capable of activating T
lymphocytes.
D. Outlook (Prognosis) of asthma
There is no cure for asthma, although symptoms sometimes improve over time.
With proper self-management and medical treatment, most people with asthma can lead
normal lives.
E. Complications
The complications of asthma can be severe, and may include:
1. Death
2. Decreased ability to exercise and take part in other activities
3. Lack of sleep due to nighttime symptoms
4. Permanent changes in the function of the lungs
5. Persistent cough
6. Trouble breathing that requires breathing assistance (ventilator).

F. Asthma Prevention
If you have asthma, you need to do what you can to reduce your exposure to
asthma triggers. Asthma triggers can aggravate your asthma symptoms -- coughing,
wheezing, and difficulty catching your breath. While theres no asthma cure, there are
steps you can take to keep your asthma in control and prevent an asthma attack
(worsening of asthma symptoms).
1. Identify Triggers for Asthma Prevention
Certain asthma triggers can set off the cascade of asthma symptoms. Some
asthma triggers may include:
a. Air pollution
b. Allergies
c. Cold air
d. A cold or flu virus
e. Sinusitis
f. Smoke
g. Fragrances
Its vital to learn to identify your asthma triggers and take steps to avoid
them. Keep track of your asthma symptoms in an asthma diary for several weeks,
detailing all the environmental and emotional factors that are associated with
your asthma. When you have an asthma attack, go back to your asthma diary to
see which factor, or combination of factors, might have contributed to it. Some
common asthma triggers are not always obvious, such as molds and cockroaches.
Ask your asthma specialist about allergy skin testing -- or RAST testing -- to
determine to which allergens you have become sensitized. You can then take
measures to minimize your exposure to those allergens.
If you have exercise-induced asthma or are planning vigorous exercise or
exercise in cold, humid, or dry environments, prevent exercise-induced asthma by
following your doctor's advice regarding asthma treatment (usually by using an
asthma inhaler containing the drug albuterol).
2. Allergies and Asthma Prevention
If you have allergies and asthma, its important to minimize your
exposure to allergens (substances to which you are allergic). Allergen exposure
can temporarily increase the inflammation of the airways in a person with asthma
making them more susceptible to an asthma attack. Avoiding or minimizing
contact with the substance you are allergic to can help prevent an asthma attack.
3. Avoid Smoke to Prevent Asthma
Smoke and asthma are a bad mix. Minimize exposure to all sources of
smoke, including tobacco, incense, candles, fires, and fireworks. Do not allow
smoking in your home or car, and avoid public places that permit smoking. If you
smoke cigarettes, get help to quit successfully. Smoking always makes asthma
worse.
4. Avoid Colds to Prevent Asthma
Do what you can to stay well. Avoid close contact with people who have
a cold or the flu since your asthma symptoms may worsen if you catch the
infection from them. Wash your hands thoroughly after touching items that may
have been handled by others with a respiratory infection.
5. Allergy-Proof Your Environment for Asthma Prevention
Whether youre at home, work, or traveling, there are specific measures
you can take to allergy-proof your environment and reduce the risk of having
asthma. For example, avoid eating in restaurants that are smoky or allow cigarette
smoking. Call ahead when traveling and ask for a smoke-free hotel room. And
bring your own bedding and pillows in case the hotel only supplies feather pillows
and down comforters, which may harbor dust mites and cause asthma symptoms.
6. Get a Flu Vaccine for Asthma Prevention
Get a flu shot every year to protect against the flu virus, which almost
always makes asthma much worse for days to weeks. People with asthma are more
likely to have complications from the flu, such as pneumonia, and are more likely
to be hospitalized because of the flu. Also get a pneumonia shot (called
Pneumovax) once every five to 10 years. People with asthma are about twice as
likely as others to get pneumococcal pneumonia, a common type of bacterial
pneumonia.
7. Consider Allergy Shots (Immunotherapy) for Asthma Prevention
If your doctor finds that you have allergies, allergy shots
(immunotherapy) may help prevent allergy symptoms and worsening of asthma.
With allergy shots, small doses of allergens are injected under your skin on a
regular schedule. Over a period of time, your body may become accustomed to the
allergen and less responsive to it upon exposure. This can help prevent a
worsening of asthma.
G. Tests and diagnosis
1. Physical exam
To rule out other possible conditions such as a respiratory
infection or chronic obstructive pulmonary disease (COPD) your doctor
will do a physical exam and ask you questions about your signs and
symptoms and about any other health problems.
2. Test to measure lung function
You may also be given lung (pulmonary) function tests to determine
how much air moves in and out as you breathe. These tests may include:
a. Spirometry.
This test estimates the narrowing of your bronchial tubes by
checking how much air you can exhale after a deep breath and how
fast you can breathe out.
b. Peak flow.
A peak flow meter is a simple device that measures how hard you
can breathe out. Lower than usual peak flow readings are a sign
your lungs may not be working as well and that your asthma may
be getting worse. Your doctor will give you instructions on how to
track and deal with low peak flow readings.
Lung function tests often are done before and after taking a
bronchodilator (brong-koh-DIE-lay-tur), such as albuterol, to open your
airways. If your lung function improves with use of a bronchodilator, it's
likely you have asthma.
3. Additional Test
Other tests to diagnose asthma include:
a. Methacholine challenge.
Methacholine is a known asthma trigger that, when inhaled, will
cause mild constriction of your airways. If you react to the
methacholine, you likely have asthma. This test may be used even if
your initial lung function test is normal.
b. Nitric oxide test.
This test, though not widely available, measures the amount of the
gas, nitric oxide, that you have in your breath. When your airways
are inflamed a sign of asthma you may have higher than
normal nitric oxide levels.
c. Imaging tests.
A chest X-ray and high-resolution computerized tomography (CT)
scan of your lungs and nose cavities (sinuses) can identify any
structural abnormalities or diseases (such as infection) that can cause
or aggravate breathing problems.
d. Allergy testing.
This can be performed by skin test or blood test. Allergy tests can
identify allergy to pets, dust, mold and pollen. If important allergy
triggers are identified, this can lead to a recommendation for allergen
immunotherapy.
e. Sputum eosinophils.
This test looks for certain white blood cells (eosinophils) in the
mixture of saliva and mucus (sputum) you discharge during
coughing. Eosinophils are present when symptoms develop and
become visible when stained with a rose-colored dye (eosin).
f. Provocative testing for exercise and cold-induced asthma.
In these tests, your doctor measures your airway obstruction before
and after you perform vigorous physical activity or take several
breaths of cold air.
H. Asthma Management
The focus of treatment is to return the respiratory status to normal, deliver
adequate oxygen, and limit the number of recurrences. Patient education should focus on
understanding the disease, its management, and when emergency care may be necessary.
1. Nursing Management
a. The nurse assesses the patients respiratory status by monitoring the
severity of symptoms, breath sounds, peak flow, pulse oximetry, and vital
signs.
b. The nurse obtains a history of allergic reactions to medications before
administering medications and identifies the patients current use of
medications.
c. The nurse administers medications as prescribed and monitors the
patients responses to those medications.
d. Fluids may be administered if the patient is dehydrated, and antibiotic
agents may be prescribed if the patient has an underlying respiratory
infection. Give patient 3 liters/day of fluid to help liquefy any secretions.
e. If the patient requires intubation because of acute respiratory failure, the
nurse assists with the intubation procedure, continues close monitoring of
the patient, and keeps the patient and family informed about procedures.
f. Administer supplemental oxygen to help meet bodys needs.
g. Identify and remove allergens and known triggers to avoid causing an
asthma attack.
2. Medical management (Pharmacologic therapy)
a. Administer short-acting beta 2 -adrenergic drugs to bronchodilate:
albuterol, pirbuterol, metaproterenol, terbutaline, levalbuterol
b. Administer long-acting beta 2 -adrenergic drugs to manage symptoms
day to day; keep airways open, not for acute symptoms: salmeterol,
formoterol
c. Administer leukotriene modulators to reduce local inflammatory response
in lung to reduce exacerbations; does not have immediate effect on
symptoms: zafirlukast, zileuton, montelukast
d. Administer anticholinergic drugs ipratropium inhaler, tiotropium
handihaler
e. Administer antacid, H2 blocker, or proton pump inhibitor to decrease the
amount of acid in the stomach, reducing the possibility of ulcers due to
stress of disease or medication effects.
1) Antacids: aluminum hydroxide/magnesium hydroxide, calcium
carbonate
2) H2 blockers: ranitidine, famotidine, nizatidine, cimetidine
3) Proton pump inhibitors: omeprazole, lansoprazole, esomeprazole,
rabeprazole, pantoprazole
f. Administer mast cell stabilizer to retain an early component of the initial
response to allergens, which will prevent further reactions from
occurring; this is not for acute symptoms. This is useful for pretreatment
for allergen exposure or chronic use to improve control of symptoms.
cromolyn, nedocromil
g. Administer steroids to decrease inflammation, which will help open
airways; these are not for acute symptoms : hydrocortisone,
methylprednisolone intravenously, beclomethasone, triamcinolone,
fluticasone, budesonide, flunisolide, mometasone inhalers, prednisolone,
prednisone orally
h. Administer methylxanthines to assist with bronchodilation, often used
when other medications not effective : aminophylline, theophylline.
















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