Asthma Management

This document provides an overview of the pathophysiology of asthma, including inflammation of airways and the generation of airway hyper-responsiveness. It also discusses pharmacological interventions such as salbutamol, oral prednisolone, and ipratropium. The document concludes with management strategies for asthma.

Running head: ASTHMA MANAGEMENT
Asthma Management
Name of the Student
Name of the University
Author Note

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Pathophysiology of the disease
The main characteristics of asthma are inflammation of airways along with the
generation of airway hyper-responsiveness and hypersecretion in the mucus. This results in
the formation of obstructions and simultaneous development of dyspnoea, sensation of
tightness in chest, coughs and wheeze (Carpaij et al., 2019). This is the reason why the boy
Benji in the case study was showing audible wheeze at the time of admission in the hospital.
Asthma is associated with adverse immunological responses leading to predominance of
CD4+ T lymphocytes along with the secretion of type 2 T-helper cells (Th2) and other
inflammatory mediators like cytokines (IL-4. IL-5 and IL-13) (King et al., 2018). During
asthma, the pulmonary airways respond in an exaggerated way to irritants like physical
exercise. Exposure to physical exercise triggers type 1 hypersensitivity reaction like de-
granulation of mast cell followed by release of primary hypersensitivity mediators like
interleukins, prostaglandins histamine and nitric oxide. The primary inflammatory mediators
have vaso-dilution effects on the walls of the lungs followed by increased capillary
permeability. This cause in increase in the blood flow in the area and inflammatory cells
along with chemotactic factors move into the cells into the interstitial tissues of the lungs.
The movement of the chemotactic factors cause infiltration of the bronchial cells by the
eosinophills, neutrophills and lymphocytes. Eosinophills releases chemical causing
inflammation in the lung tissues. The inflammatory response generates muscle spasm in the
bronchial smooth muscle cells followed by vascular congestion and pulmonary oedema. This
ultimately thickens the bronchial line with mucus and impairs the muco-cilliary function and
hyper-responsiveness of the bronchial muscles. This change in the smooth muscles of
bronchioli hampers the normal functioning of the lungs along causing oxygen deprivation and
laboured breathing (Bonini & Usmani, 2015). This is the reason why Benji experiences

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difficulty while playing sports like soccer games and avoided running around with friends. In
asthma die to infiltration of the bronchial cells with inflammatory mediators, there occurs
constriction and obstruction in the airways leading to decrease in the flow of the air,
preliminary expiratory rates (King et al., 2018). For example, decrease in 10% of airway
calibre causes 2% increased resistance. The impaired exhalation leads trapping of air and
hyperinflation distal to the obstructions and thus causing laboured breathing. Intrapleural and
alveolar gas pressure increases casing reduced perfusion of the alveoli. These malfunctions
cause improper ventilation leading to hypoxaemia (reduction in the oxygen saturation in the
body). The receptors of the lungs trigger hyper-ventilation causing hyperinflation and
reduced the amount of dissolved carbon dioxide in the blood while increasing blood pH
(causing respiratory alkalosis). As the obstruction in the airways becomes severe, the
ventilation and perfusion of the total number of alveoli decreases. The trapping of air worsens
gradually and laboured breathing increases further followed by reduced tidal volume and
increased carbon dioxide retention (Gon & Hashimoto, 2018). Benji was diagnosed with
asthma at an age of 7. At present he is 11 years old. During this 4 years tenure, the prognosis
of the disease might have been negatively regulated worsening of the process of breathing.
This is the reason why he experiences laboured breathing during laugh and difficulty in
speaking in complete sentences.
Pharmacological interventions
Salbutamol 100 μg 12 puffs via a metered dose inhaler (MDI)
Salbutamol is a short-acting selective beta2-adrenergic receptor agonist. It is useful in
the treatment of asthma. Sulbutamol taken through MDI, gets absorbed through the nasal
airways and is released in the pulmonary cavities. It acts topically. vInside the pulmonary
cavities in the lungs, it acts as a bronchodilator. Inside the lungs, sulbutamol gets activated

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followed by the activation of beta-2-agrenergic receptors in the smooth muscles of the airway
causing the activation of adenyl cyclase. Increase in adenyl cyclase increases the
concentration of cyclic 3’,5’ adenosine monophosphate (cyclic AMP). c-AMP increases the
secretion of protein kinase A that prevents the down-stream phosphorylation of myosin and
decreases the intracellular concentration of calcium resulting in the relaxation of smooth
muscle cells of airways. Thus role of the Salbutamol is to function against broncho-
constrictor challenges (Bjermer, Abbott-Banner & Newman, 2019). The increased secretion
of c-AMP also inhibits the release of primary mediators and preventing degranulation of mast
cells. A measurable reduction in the airway resistance is observed within 5 to 15 minutes post
inhalation of salbutamol. Salbutamol is not metabolized in the lungs. It is transformed by the
hepatic cells into 4’-o-sulphate (salbutamol 4’-O-sulfate) ester, having minimal
pharmacologic activity. The salbutamol is released through urine within 24 hours post
administration. A small fraction is removed through faeces (Bjermer, Abbott-Banner &
Newman, 2019).
Oral Prednisolone 1mg
Prednisolone is gluco-cortocoid. It helps to control the severity of the type 1
hypersensitivity reaction by reducing the infiltration of the leukocyte at the site of
inflammation. The medicine interacts with mediators of inflammatory response and reduces
humoral immune responses. Prednisolone acts through phospholipase A2 inhibitory proteins
that controlss synthesis of prostaglandins and leukotrines. It also helps to prevent mast cell
degranulation and thus decrease the release of primary mediators and proinflammatory
cytokines. The oral medication of prednisolone is absorbed through gastrointestinal track and
its plasma concentration reach peak within 1 to 2 hours post administration. The medicine is
excreted through urine either in free form or as glucoconjugate (Sneeboer et al., 2016).

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Ipratropium 8 puffs
It is a quaternary ammonium compound and has anticholinergic effect. It is
administered through inhalation that helps in generating local effects without generating
significant systemic absorption. The medication helps in controlling the severe exacerbations
of asthma flares. The medication, though has short-acting effects reduces the parasympathetic
nervous system of the pulmonary airway. The overall medication effects last of 4 to 6 hours.
Ipratropium relaxes the smooth muscles of the bronchial airways that reverse the constriction
of airways and reducing the symptoms like wheezy breathing, tightness of chest and cough. It
mainly works through binding with acetylcholine receptors and inhibits the parasympathetic
nervous system (Nomura et al., 2017). Ipratropium is metabolised in the gastrointestinal tract
under the action of cytochrome P-450 isoenzyme. In case of oral administration at least 90%
of the dosage is excreted unchanged. The absorbed protein is metabolized partially through
ester hydrolysis to inactive metabolites, tropane and tropic acid. The medication is excreted
through urine (Nomura et al., 2017).

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References
Bjermer, L., Abbott-Banner, K., & Newman, K. (2019). Efficacy and safety of a first-in-class
inhaled PDE3/4 inhibitor (ensifentrine) vs salbutamol in asthma. Pulmonary
Pharmacology & Therapeutics, 101814.
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.
Carpaij, O. A., Burgess, J. K., Kerstjens, H. A., Nawijn, M. C., & van den Berge, M. (2019).
A review on the pathophysiology of asthma remission. Pharmacology & therapeutics.
Gon, Y., & Hashimoto, S. (2018). Role of airway epithelial barrier dysfunction in
pathogenesis of asthma. Allergology International, 67(1), 12-17.
King, G. G., James, A., Harkness, L., & Wark, P. A. (2018). Pathophysiology of severe
asthma: we’ve only just started. Respirology, 23(3), 262-271.
Nomura, O., Morikawa, Y., Hagiwara, Y., Ihara, T., Inoue, N., Sakakibara, H., & Akasawa,
A. (2017). Ipratropium bromide for acute asthma in children: A retrospective
trial. Arerugi=[Allergy], 66(7), 945-952.
Sneeboer, M. M., Majoor, C. J., de Kievit, A., Meijers, J. C., van der Poll, T., Kamphuisen, P.
W., & Bel, E. H. (2016). Prothrombotic state in patients with severe and
prednisolone-dependent asthma. Journal of Allergy and Clinical Immunology, 137(6),
1727-1732.