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NCM 64 Care of Client’s with Problems in Inflammation, Immunologic Response,

Perception and Coordination

Mary Gold D. Jayme
Central Mindanao University
College of Nursing
Dr. Ellen Gay S. Intong, RN
February 14, 2018

Asthma is a Greek word which means ‘breathless’ or ‘to breathe with open mouth’.
The Global Strategy for Asthma Management and Prevention Guidelines define asthma
as ‘a chronic inflammatory disorder of the airways associated with increased airway
hyper-responsiveness, recurrent episodes of wheezing, breathlessness, chest tightness,
and coughing, particularly at night/early morning’. Asthma is often called Reactive Airway
disease (Morris, 2017).

One of the health problems that most Filipinos suffered from is asthma. The most
common chronic respiratory disease among children, it has no known cure but it can be
controlled and effectively treated. The “Asthma Awareness, Education and Treatment Act
of 2005” shares this information: “According to the United Nations Daily Highlights,
asthma kills over 180,000 people globally ever year. In the Philippines asthma affects
over 6 million children. The Philippines is ranked 32nd in ‘self-reported asthma.’ The
country has a prevalence rate of about 12 percent. A nationwide study conducted by the
University of Santo Tomas showed that about 12.4 percent of children aged 14 to 15
years old are afflicted with asthma. Most of these children come from low-income families
or communities.” The 2014 Global Asthma Report said about 300 million people around
the world are affected by asthma. In the Philippines one out 10 people is suffering from
this debilitating disease (Tacio, 2016).

The Merck Manual of Medical Information explains. “Cells lining the bronchi have
microscopic structures, called receptors. These receptors sense the presence of specific
substances and stimulate the underlying muscles to contract and relax, thus, altering the
flow of air.” Medical authorities say asthma is due to the inflammation of the air passages
in the lungs and affects the sensitivity of the nerve endings in the airways so they become
easily irritated. In an attack, the lining of the passages swell, causing the airways to
narrow and reducing the flow of air in and out of the lungs (Tacio, 2016).

 Anatomy

The airways of the lungs consist of the cartilaginous bronchi, membranous bronchi,
and gas-exchanging bronchi termed the respiratory bronchioles and alveolar ducts. While
the first 2 types function mostly as anatomic dead space, they also contribute to airway
resistance. The smallest non-gas-exchanging airways, the terminal bronchioles, are
approximately 0.5 mm in diameter; airways are considered small if they are less than 2
mm in diameter.

Airway structure consists of the following:

 Mucosa, which is composed of epithelial cells that are capable of specialized

mucous production and a transport apparatus
 Basement membrane
 A smooth-muscle matrix extending to the alveolar entrances
 Predominantly fibrocartilaginous or fibroelastic-supporting connective tissue.

Cellular elements include mast cells, which are involved in the complex control of
releasing histamine and other mediators. Basophils, eosinophils, neutrophils, and
macrophages also are responsible for extensive mediator release in the early and late
stages of bronchial asthma. Stretch and irritant receptors reside in the airways, as do
cholinergic motor nerves, which innervate the smooth muscle and glandular units. In
bronchial asthma, smooth muscle contraction in an airway is greater than that expected
for its size if it were functioning normally, and this contraction varies in its distribution.

 Pathophysiology

The underlying pathology in asthma is reversible and diffuse airway inflammation. The
inflammation leads to obstruction due to following factors:
 Swelling of the membranes that line the airways (mucosal edema), which
reduces the airway diameter.
 Contraction of the bronchial smooth muscle that encircles the airways (
bronchospasm), which causes further narrowing
 Increase mucus production, which diminishes airway size and may entirely plug
the bronchi.
The bronchial muscles and mucous glands enlarge; thick, tenacious sputum is
produced and the alveolar hyperinflate. Some patients have airway subbasement
membrane fibrosis. This is called airway “remodelling” and occurs in response to chronic
inflammation. The fibrotic changes in the airway lead to airway lead to airway narrowing
and potentially irreversible airflow limitation. (Expert Panel Report, 2003)
Cells that play a key role in the inflammation of asthma are mast cells, neutrophils,
eosinophils, and lymphocytes. Mast cells, when activated, release several chemicals
called mediators. These chemicals, which include histamine, bradykinin, prostaglandins,
and leukotrienes, perpetuate the inflammatory response, causing increased blood flow,
vasoconstriction, fluid leak from the vasculature, attraction of white blood cells to the area
and bronchoconstriction ( Expert Panel Report, 2003). Regulation of these chemicals is
the aim of much of the current research regarding pharmacologic therapy for asthma.
In addition, alpha and beta2 adrenergic receptors of the sympathetic nervous system
located in the bronchi play a role. When the alpha-adrenergic receptors are stimulated,
bronchoconstriction occurs. When the beta2-adrenergic receptors are stimulated,
bronchodilation occurs. The balance between alpha and beta2-adrenergic receptors is
controlled primarily by cyclic adenosine monophosphate (Camp). Alpha-adrenergic
receptor stimulation results in a decrease in cAMP, which leads to an increase of chemical
mediators released by the mast cells and bronchoconstriction. Beta-adrenergic
stimulation results in increased levels of cAMP, which inhibits the release of chemical
mediators and causes bronchodilation (Smeltzer et al., 2007).

 Etiology
Factors that can contribute to asthma or airway hyperreactivity may include any of the
 Environmental allergens ( house dust mites; animal allergens, especially cat and
dog; cockroach allergens; and fungi)
 Viral respiratory tract infections
 Exercise, hyperventilation
 Gastroesophageal reflux disease
 Chronic sinusitis or rhinitis
 Aspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity, sulfite
 Use of beta-adrenergic receptor blockers (including ophthalmic preparations)
 Obesity
 Environmental pollutants, tobacco smoke
 Occupational exposure
 Irritants ( household sprays, paint fumes)
 Various high- and low-molecular-weight compounds ( insects, plants, latex, gums,
diisocyanates, anhydrides, wood dust, and fluxes; associated with occupational
 Emotional factors or stress
 Perinatal factors (prematurity and increased maternal age; maternal smoking and
prenatal exposure to tobacco smoke; breastfeeding has not been definitely shown
to be protective)

 Clinical Manifestation
Three most common symptoms:
1. Cough with or without mucus production
2. Generalized chest tightness and dyspnea
3. Wheezing; first on expiration then possibly during inspiration as well.
 Often occurs at night or early in the morning, possibly because of circadian
variations that influence airway receptor threshold.
 Begin abruptly but most frequently is preceded by increasing symptoms over
the few days.
 Expiration requires effort and becomes prolonged
 As the exacerbation progresses, diaphoresis, tachycardia, and a widened
pulse pressure may occur along with hypoxemia and central cyanosis.

 Assessment and Diagnostic Findings

1. Complete family, environmental and occupational history

2. Health care providers must determine the periodic symptoms of airflow
 A positive family history and environmental factors, including seasonal changes,
high pollen counts, mold, pet dander, climate change, and air pollution are primary
associated with asthma.
3. Sputum and blood test for acute episodes may disclose eosinophilia
4. Arterial blood gas analysis and pulse oximetry reveals hypoxemia
 Prevention

 Should undergo test to identify the substances that precipitate the

 Patient are instructed to avoid causative factors
 Knowledge is the key to quality asthma care

 Complications

 Status asthmaticus
 Respiratory failure
 Pneumonia
 Atelectasis
 Airways obstruction results from hypoxemia, requiring the administration of oxygen
and monitoring pulse oximetry and arterial blood gases.
 Fluid administered, because people with asthma are frequently dehydrated from
diaphoresis and insensible fluid loss with hyperventilation.

 Medical management

 Pharmacological therapy

 Long-acting Control Medication- corticosteroids are the most potent and effective
anti-inflammatory medications currently available.
1. Cromolyn sodium ( Intal) and nedocromil ( Tilade) – mild to moderate anti-
inflammatory agents used more commonly in children.
2. Long-acting beta2-adrenergic agonist – used with anti-inflammatory
medication to control asthma symptoms, particularly those that occur during
3. Leukotrines- synthesized from membrane phospholipids through a cascade
of enzymes, are potent bronchoconstrictors that also dilate blood vessels
alter permeability.
 Quick relief medications for treatment of asthma symptoms and exacerbation
 Peak Flow Monitoring
 Measures the highest airflow during a forced expiration.
 Recommended for all patients with moderate or severe asthma, because it helps
measure asthma severity and when added to symptom monitoring, indicates the
current degree of asthma control.
 Patient is instructed in the proper technique, particularly about giving maximal
effort, and peak flows are monitored for 2 or 3 weeks after receipt of optimal
asthma therapy.

 Nursing Management
 Obtains a history of allergic reactions to medication before administering
 Identifies medications the patient is currently taking
 Administers medications as prescribed and monitors the patient’s response
to those medication. An antibiotic may be prescribed if the patient has an
underlying respiratory infection.
 Administers fluids if the patient is dehydrated.

Tacio, H. D. (2016). Asthma: Take your breath away. Retrieved from
Adams, R.J., Wilson, D.H., Taylor, A.W., et al. (2004). Psychological factors and
asthma quality of life: A population based study. Thorax, 59 (11), 930-935.
Centers for Disease Control and Prevention. (2004). Fast stats sheet: Asthma.
Atlanta: National Center for Health Statistics.
Sin, D. D., Man, J., Sharpe, H., et al. (2004). Pharmacological management to
reduce exacerbation in adults with asthma: A systematic review and meta-analysis.
Journal of the American Medical Association, 293 (2), 367-376.
Smeltzer, S. C., Bare, B.G., Hinkle, J.L., et al. (2007). Brunner and Suddarth’s
textbook of medical-surgical nursing (11th ed.) Lippincott Williams and Wilkins 610.73
(22), 709-716.
Pathophysiology of Asthma Attack