Understanding Asthma: Etiology, Diagnosis, Pathogenesis, Treatment and Prevention

This article provides an in-depth understanding of asthma, including its etiology, diagnosis, pathogenesis, treatment, and prevention. It also includes a concept map for asthma.

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Name of the Student
Name of the University
Author Note

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Question 1
Jackson smith is an 18 years old male, having a history of asthma and who had been
admitted in to the ED with severe breathlessness. The signs and the symptoms of asthma
involves productive cough, chest tightness,, acute airway obstruction due to the narrowing of
the airway and the formation of the mucus plugs and wheezing due to the narrowing of the
airways.
The underlying pathophysiology behind the bronchoconstriction, airway hyper-
responsiveness and airway obstruction is the inflammation in the airways causing several
anatomical modifications in the airways (Brannan & Lougheed, 2012). The constriction is
mainly due to the contraction of the bronchial smooth muscle in response to a variety of
allergens.
Allergen induced bronchoconstriction is brought by the release of the IgE dependant
mediators from the mast cells which includes prostaglandins, leukotriene, histamines and
tryptase that contracts the muscles of the airways (Bonini & Usmani, 2015). Obstruction of
the airways gives rise to sounds of wheezing limiting the flow of air through the airways.
This is the main cause of the symptom of chest tightness in Mr. Smith. Wheezing is a kind of
musical sound that that is produced due to the limited airflow through the airways (Melen &
Pershagen, 2012).
Airway remodelling is the permanent changes that might occur due to inflammation.
Hypertrophy and hyperplasia of the airway smooth muscles can cause this change in the
airways and can be related to the progressive loss of the lung function that cannot be
reversible by the current therapy (Brannan & Lougheed, 2012). Furthermore the regulation,
repair and the remodelling process is still not well established. Airway hyper-responsiveness

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is also caused due to inflammation, dysfunctional neuro-regulation and the structural
changes.
The vital signs of Jackson Smith displays that he had a low oxygen saturation level,
which is a common symptom during an asthmatic attack. Low oxygen saturation can be
related to fact that less amount of oxygen reaches the blood for being carried to the cells.
Acute dyspnoea is also a common manifestation during the asthma exacerbations.
Jackson Smith was also found to be suffering from acute dyspnoea that is chest
tightness that was preventing him to talk. The intensity of the dyspnoea depends upon the
severity of the asthma, bronchoconstriction, dynamic hyperinflation, respiratory drive and
other physiological factors (Antoniu, 2010). According to a study Antoniu, (2010) chest
tightness was found to be associated with the mild bronchoconstriction and is attributed to the
vagal stimulation due to the increased resistance of the airways but not to the hyperinflation.
The respiratory rate of Mr. Smith was also found to be higher than the normal range, which
implies that the person has to take more breaths to meet the oxygen demand.
A diminished breath sound in asthma manifests the fluid or air accumulation round
the lungs or the thickening of chest walls, over inflation of the parts of the lungs or lessened
flow of the air flow in to the lungs (Melen & Pershagen, 2012). The chest x-ray displayed a
hyper-inflated lungs in asthmatic patients. Lung hyperinflation can be caused by the blockage
of the airway that resists the expulsion air from the lungs. However lung hyperinflation is
more common for the COPD patients and mild or moderate hyperinflation in the asthmatic
patients. A rise in the serum lactate levels can be found in the asthma patients (Melen &
Pershagen, 2012). This is due to the fact that when the oxygen level is low in the blood, the
carbohydrate breaks down for producing energy with a subsequent production of lactic acid.
As a result the lactate levels in the blood gets higher. Again it has been noticed that the

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administration of the Beta – agonist during the asthma treatment can also cause an abrupt
increase the concentration of the lactate in the blood (Rodrigo, 2014). Finally, the rapid pulse
rate of Jackson Smith is mainly due to the fact that the heart has to pump more quickly for
sending blood to different parts of the body due to the less oxygen concentration. Some
psychological factors comes in to play during asthmatic attacks that can be responsible for the
elevated pulse rate.
Question 2
Two high priority nursing interventions for managing the asthma attack in Jackson
Smith
 One of priority intervention is to increase the oxygen saturation level of Jackson Smith.
Since the oxygen saturation level of Jackson is not below 90 %, hence application of
oxygen therapy might not be helpful. It is necessary to assess the exacerbation by
monitoring the peak expiratory flow rates and forced expiratory volume as taken by the
respiratory therapist. Helping Jackson Smith to do a pursed lip breathing might increase
the oxygen saturation level.
 Rationale: Oxygen saturation refers to the fraction of the oxygen saturated haemoglobin
relative to the total haemoglobin present in the blood. The peak flow measure enables a
nurse to measure the airway obstruction and the severity of the exacerbations (Sue Jordan,
2011). Pursed lip breathing helps in increasing the oxygen saturation level by increasing
the probability of the entry of oxygen in the lungs.
 Another priority nursing strategy is the effective clearance of the airways. In Jackson
Smith it is necessary to clear the hyper-secreted mucus to get a clear airways. The
interventions include assessment of the respiratory rhythm, depth and rate, assessing for

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any sort of colour change in nail beds, buccal mucosa and lips (Melen & Pershagen,
2012). A nurse should assess the effectiveness of cough as coughing is the natural way of
clearing secretion from the throat.
 Rationale: Assessment of the respiratory rate is necessary as it helps to determine any
signs of impending respiratory distress. Assessing the nail and the lip colour might help to
assess the presence of cyanosis that might indicate low oxygenation in the blood (Melen
& Pershagen, 2012). Effective coughing is important as mucus plugs, thick secretions and
respiratory muscle fatigue are due to ineffective cough.
Question 3
Nebulised Salbutamol- It works on the β2-adrenoreceptors situated on the smooth muscles of
the bronchi and stabilizes the receptor to its active state. More cAMP is generated as the
receptors remains in the active state. This generation of the cAMP activates the intercellular
cascade reducing the intracellular Ca2+, thus preventing the contraction of the smooth
muscles of the airways.
Nebulised Ipratropium- Ipratropium acts as an anticholinergic agent blocking the muscarinic
receptors of the acetyl choline and also helps to restrict the vagally mediated reflexes caused
by the antagonisation of the acetyl choline receptors released by the vagus nerves. The
anticholinergic action of the Ipratropium inhibits the effect of the cholinergic nerves
inhibiting smooth muscle contraction (Morales et al., 2012).
Hydrocortisone-It inhibits the release of the secreatagogue by the macrophages, thus
reducing the excessive secretion of the mucus in to the airways. It stops the late phase
reaction by inhibiting the chemotaxis and inflammatory response (Alangari, 2014).

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b) Careful surveillance of the arterial blood gases and the vital signs are necessary after
providing salbutamol to the patients. Dosage for the Salbutamol should be restricted to 5mg.
It is necessary to consider if the patient has history of hypersensitivity. Cardiac dysrhythmias
and tachycardia should be monitored. The patient should be assessed for mild tachycardia,
hypokalemia and nervousness. Before the application of the ipratropium, it is necessary to
adjust the dosage as per the body weight of the patient (Melani et al., 2012). A mouthpiece
can be used for the administration of the inhalers (Cates, Welsh & Rowe, 2013). Nurses
should be able to assess any signs of dizziness, tremors or shaking after the application of the
medicine.
Before administering hydrocortisone, the nurses should check on the vital signs and
should be mindful about how long the medicines will be continued as hydrocortisone can
cause long-term effects such as hypertension and peptic ulcer diseases (Alangari, 2014).

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References
Alangari, A. A. (2014). Corticosteroids in the treatment of acute asthma. Annals of Thoracic
Medicine, 9(4), 187–192. http://doi.org/10.4103/1817-1737.140120
Antoniu, S. A. (2010). Descriptors of dyspnea in obstructive lung diseases. Multidisciplinary
respiratory medicine, 5(3), 216.
Bonini, M., & Usmani, O. S. (2015). The role of the small airways in the pathophysiology of
asthma and chronic obstructive pulmonary disease. Therapeutic advances in
respiratory disease, 9(6), 281-293. https://doi.org/10.1177/1753465815588064
Brannan, J. D., & Lougheed, M. D. (2012). Airway Hyperresponsiveness in Asthma:
Mechanisms, Clinical Significance, and Treatment. Frontiers in Physiology, 3, 460.
http://doi.org/10.3389/fphys.2012.00460
Cates, C. J., Welsh, E. J., & Rowe, B. H. (2013). Holding chambers (spacers) versus
nebulisers for beta‐agonist treatment of acute asthma. The Cochrane Library.
http://dx.doi.org/10.1136/thoraxjnl-2012-202071
Melani, A. S., Canessa, P., Coloretti, I., DeAngelis, G., DeTullio, R., Del Donno, M., ... &
Vaghi, A. (2012). Inhaler mishandling is very common in patients with chronic
airflow obstruction and long-term home nebuliser use. Respiratory medicine, 106(5),
668-676. https://doi.org/10.1016/j.rmed.2011.11.016

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Melen, E., & Pershagen, G. (2012). Pathophysiology of asthma: lessons from genetic
research with particular focus on severe asthma. Journal of internal medicine, 272(2),
108-120. https://doi.org/10.1111/j.1365-2796.2012.02555.x
Morales, D. R., Jackson, C., Fielding, S., & Guthrie, B. (2013). Long-acting β-agonist
prescribing in people with asthma in primary care. Thorax, 68(2), 192-194.
Rodrigo, G. J. (2014). Serum lactate increase during acute asthma treatment: a new piece of
the puzzle. Chest, 145(1), 6-7. DOI: https://doi.org/10.1378/chest.13-2042
Sue Jordan, M. B. (2011). Bronchodilators: implications for nursing practice. DOI
10.7748/ns2011.03.15.27.45.c2999

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Concept map for Asthma
Common chronic disorder of the airways, which is complex and
characterized by airflow obstruction, bronchial hyper-responsiveness and
inflammation (1).
Etiology: The etiology and the risk factors of asthma are- Allergens like dust
mites, pet dander, family history, atopy, prenatal tobacco smoke, nutrition, stress,
smoking, antibiotic use, congestive heart failure, obesity and GERD (2).
Pathogenesis
 Bronchoconstriction- Contraction of the
bronchial smooth muscles due to the release of
the chemical mediators.
 Airway edema-Inflammation causes mucus
hyper-secretion and edema (5).
 Airway hyper-responsiveness
 Airway remodeling- Airway hyperplasia and
airway hypertrophy causes changes in the
airways
 Bronchospasm causing chest tightedness (1).
Asthma
Clinical manifestation- Bronchospasm,
wheezing, dyspnea, hyperinflation of the
lungs, mucus production, edema in the
bronchial mucosa (3).
Diagnosis- physical examination, Spirometry test,
peak flow, allergy testing, pulmonary function
testing, imaging testing, Methacholine changes (1).
Treatment- Inhaled
Corticosteroids, long acting
Beta-agonists, Ipratropium,
bronchodilators,
Anticholinergic, Air humidifiers
(6) Prevention- Avoiding the
asthma triggers such as food
allergens, maintaining the
optical humidity, being
vaccinated to prevent from flu
from triggering the asthma flare-
ups, decontamination inside the
household, use of inhalers (6).
Prognosis-
 Symptoms are resolved after the triggering
agent is removed (3).
 Permanent impairment of the lung function
can be caused
 Smokers are at the highest risk.
 Patients with previous hospital admissions to
intensive care units, patients with family
history are at the risk (4).
 Patients having brittle asthma are susceptible
to lung failure.
Progression of the disease
Without treatment-
 Airway function declination
 Bronchospasm, bronchoconstriction, airway hyper-responsiveness, airway remodeling, airway edema
 Thickened basement membrane, airway desquamatisation (4)

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References
1. Khan, D. A. (2014, September). Allergic rhinitis and asthma: epidemiology and common
pathophysiology. In Allergy & Asthma Proceedings (Vol. 35, No. 5).
https://web.a.ebscohost.com/abstract?
direct=true&profile=ehost&scope=site&authtype=crawler&jrnl=10885412&AN=978283
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%3d&crl=c&resultNs=AdminWebAuth&resultLocal=ErrCrlNotAuth&crlhashurl=login.a
spx%3fdirect%3dtrue%26profile%3dehost%26scope%3dsite%26authtype%3dcrawler
%26jrnl%3d10885412%26AN%3d97828349
2. Beasley, R., Semprini, A., & Mitchell, E. A. (2015). Risk factors for asthma: is
prevention possible?. The Lancet, 386(9998), 1075-1085. https://doi.org/10.1016/S0140-
6736(15)00156-7
3. Andersson, M., Hedman, L., Bjerg, A., Forsberg, B., Lundbäck, B., & Rönmark, E.
(2013). Remission and persistence of asthma followed from 7 to 19 years of age.
Pediatrics, peds-2013. DOI: 10.1542/peds.2013-0741
4. Carolan, B. J., & Sutherland, E. R. (2013). Clinical phenotypes of chronic obstructive
pulmonary disease and asthma: recent advances. Journal of Allergy and Clinical
Immunology, 131(3), 627-634. https://doi.org/10.1016/j.jaci.2013.01.010
5. Lambrecht, B. N., & Hammad, H. (2015). The immunology of asthma. Nature
immunology, 16(1), 45. https://www.nature.com/articles/ni.3049

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6. Gilliland, F. D. (2009). Outdoor air pollution, genetic susceptibility, and asthma
management: opportunities for intervention to reduce the burden of asthma. Pediatrics,
123(Supplement 3), S168-S173.
http://pediatrics.aappublications.org/content/123/Supplement_3/S168.full

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