Respiratory Disorders

Respiratory Disorders

Case Study

Asthma is a complicated complication that affects the respiratory system; it is characterized by hyperresponsiveness, bronchoconstriction, and chronic inflammation. The main signs and symptoms of the condition-coughing, wheezing, and dyspnea- are brought about by mucus, edema, and bronchoconstriction (Loerbroks et al., 2016). Among the affected individuals the severity of the disease varies along a range, the typical scenario is the interplay between inflammation of the airway and the clinical symptoms (Lockey & Ledford, 2014). This paper will describe the condition in details touching on the alternative drugs available for treatment, its pathophysiology and possible complications that arise from the situation. Click here to see a custom concept of brain disorders paper.

Homeostasis is simply the maintenance of a constant internal environment in the body, tissue or the cell. The consistent environment is the only one that can support physiological function. The body’s defensive mechanisms thus strive to maintain this environment without any alterations. The body’s immune reaction can tend to overdo things in its bid to keep the constant environment, case in point, asthma. Asthma is a case of the body immunity trying too much to retain the context of the respiratory system as it was. The hyperresponsiveness becomes harmful to the patient (Lockey & Ledford, 2014). Homeostasis is the entry of allergens into the airway when they do get in it initiates defense mechanisms that impede the free flow of air. Click here to see a custom concept of brain disorders paper.

Ciclesonide, fluticasone, beclomethasone and budesonide are some of the inhaled corticosteroids that are available in inhaled form. Among these, beclomethasone is the least potent while fluticasone is the more potent. All the drugs fall under the category of corticosteroid drugs; Corticosteroids are potent anti-inflammatory agents. Despite their potency in reducing the inflammatory process, they come with multiple serious systemic side effects that result from systemic administration of the drugs. The alternative is inhaling the agents into the bronchial pathway significantly diminishes the systemic side effects. Inhaled corticosteroids are very effective in reducing hyperresponsiveness and airway inflammations.

Mechanism of Action

Corticosteroids are anti-inflammatory agents. The corticosteroids inhibit the rupture of the mast cells and reduce the synthesis of the inflammatory mediators. In addition to that, the production of new antibodies is stopped, and there is suppression of the immune cell (especially macrophages and lymphocytes) activity (Hossny et al., 2016).  Inhibition of these actions subsequently leads to blockage of the pathophysiological symptoms such as the mucus production, edema, and the bronchoconstriction. These clinical effects do not happen immediately but take many hours after the administration of the drug through inhalation.  This class of medications is particularly useful in treating the late phase of an acute asthma attack in addition to the chronic inflammation that may develop (Pino-Yanes et al., 2015).

To be more specific, these categories of drugs are the best choice for any patient who has persistent asthma. Corticosteroids inhibit the production of arachidonic acid via phospholipase An inhibition. The result is a direct anti-inflammatory effect in the patient’s airways. The drugs do not achieve their effect by directly acting on the smooth muscles of the airway; they target the airway inflammation that is underlying (Hossny et al., 2016). They do this by decreasing the inflammatory cascade (T lymphocytes, eosinophils, macrophages) thereby decreasing the permeability of capillaries, reverse of mucosal edema, ad inhibiting the release of leukotrienes. After a long-term use of corticosteroids, the drugs reduce the hyperresponsiveness of the client’s airway to different bronchoconstriction stimulants such as cold air, dust, allergens and exercise.

The selective β2 agonists currently available include terbutaline, formoterol, indacaterol, and salbutamol.  The agents can be inhaled, taken orally, injected. Salbutamol and terbutaline are short-acting beta agonists (SABAs) while indacaterol and eformoterol are long-acting beta agonists (LABA).  The β2 agonists relax the smooth muscles of the airway directly. This effect will reduce the bronchoconstriction caused by the inflammation. The drug is used to bring about quick relief in patients who have asthma attacks (Zaslau, 2014). The SABA has a rapid onset of action ranging between five and thirty minutes.  Click here to see a custom paper on Learners with emotional and behavioral disorders. The β2 agonists have no anti-inflammatory effects rather they work by relaxing the smooth muscles in the bronchi thus relieving the bronchoconstriction which allows for easier passage of air into the lungs (Hossny et al., 2016).

Severe or persistent asthma is one that does not respond to the usual therapy. The asthma attacks could last as long as 24 hours or even more. Such long hours of the attack may lead to the patient becoming fatigued (Shah & Saltoun, 2012). During the attacks, the client experiences the usual symptoms of asthma and a decrease in the bronchial diameter are evident during an asthma attack. An abnormality in ventilation-perfusion develops leading to hypoxemia and respiratory alkalosis at the start and eventually developing to respiratory acidosis (Loerbroks et al., 2016).

Moreover, the patient, therefore, starts feeling tired because not enough oxygen can reach his tissues. Partial pressures of oxygen reduce during the respiratory alkalosis with low partial pressures of carbon (IV) oxide and a high pH value. As severe asthma exacerbates, the partial pressures of carbon (IV) oxide go up, and the pH value decreases leading to respiratory acidosis. Prolonged exhalation, labored breathing for long hours render the patient exhausted (Shah & Saltoun, 2012).

The patient has more work to do during breathing during an episode of severe asthma. The patient, therefore, requires more energy further increasing the oxygen demands leading to them feeling physically fatigued. Breathing through a normal airway would make the process less tiring (Shah & Saltoun, 2012). The bronchospasm, edema of the bronchial mucosa and the excessive production of mucus plug the usually clear airway. Consequently, the patient has a narrow airway that makes the process of expiration to become longer than normal (Lockey & Ledford, 2014). Also, the volume of air that could normally be exhaled by force in a second and the peak expiratory flow rate is reduced.

When the client has a severe asthma attack, inhaled air gets trapped behind the narrowed, occluded, and mucus plugged bronchial pathway thereby hyperinflating the lungs. Hyperinflation of the lungs implies an increment in the residual volume plus a decrease in the inspiratory reserve capacity and the forced vital capacity. This patient has no option but to breathe near their functional residual capacity. The physical fatigue will most likely set in since there is more work in breathing. Therefore, more energy expenditure is needed to overcome the tension that is in the lungs. More power is also necessary to overcome the tension in the accessory muscles so as to maintain ventilation and gaseous exchange (Shah & Saltoun, 2012).

Furthermore, Hypercapnia and hypoxemia in the body tissues contribute to fatigue as the condition goes on. The alveoli are no longer active in ventilation; the ventilation fails to match perfusion (Shah & Saltoun, 2012). Hypercapnia refers to elevated levels of carbon (IV) oxide in an individual’s bloodstream and hypoxemia which relates to reduced levels of oxygen in a person’s blood. Both are manifestations of persistent asthma that continue, and respiratory fatigue follows. Typically the human body would attempt to compensate for the excess C02 in the blood by increasing its elimination via the respiratory system. Click here to see a custom concept of brain disorders paper. This compensatory mechanism is however compromised by the fact that the patient has severe asthma. Worth noting is the fact that CO2 readily crosses the blood brain barriers; the central nervous complications that will likely follow are due to the entry of CO2 (Shah & Saltoun, 2012). Entry of CO2 into the blood brain barrier will cause complications that are linked to the fact that the pH of the brain fluids will be lowered.

An increase in CO2 concentration in the brain will lead to vasodilation of the blood vessels in the brain causing muscle twitching, blurring in vision, headache, and psychological disturbances. Also, through the normal physiologic compensatory mechanism, the body compensates for respiratory acidosis by reabsorbing more bicarbonate through the kidneys.  Elevated levels of C02 cause the cerebral blood vessels to dilate subsequently causing the client to experience a headache. In some cases, the cerebrospinal fluid pressure may go up, and a rare papilledema may occur (Shah & Saltoun, 2012). Also, hypercapnia is also affected the neurological function of the client. Hypercapnia brings about an almost sedative effect on the central nervous system of the body leading to disorientation, somnolence and in urgent cases, the patient may slip into a coma or even die.

In conclusion, asthma is a complex complication that affects the respiratory system; it is characterized by hyperresponsiveness, bronchoconstriction and chronic inflammation. The main signs and symptoms of the condition-coughing, wheezing, and dyspnea- are brought about by mucus, edema, and bronchoconstriction. Among the affected individuals the severity of the disease varies along a range, the typical scenario is the interplay between inflammation of the airway and the clinical symptoms. This paper has described the mechanism of action for two classes of drugs that are used in the treatment of asthma. Click here to see a custom concept of brain disorders paper.

The beta-agonists work by reversing the bronchoconstriction. The drugs possess no anti-inflammatory properties like the corticosteroids do. Examples of the beta agonists include salbutamol and terbutaline which are short acting beta agonists that could take between 5 to 30 minutes to act. The other types include indacaterol which is a long-term beta agonist that is used as a long term drug to sustain the treatment. Inhaled corticosteroids are the other option that, they function primarily as anti-inflammatory agents. They hinder the inflammatory process by impeding the functions of immune cells such as macrophages and leukotrienes. The paper has also discussed Hypercapnia which is the elevation in CO2 levels in the patient’s blood stream. It results from severe asthma which as discussed occurs when the asthma is unresponsive to conventional therapy.

The Hypercapnia can have far-reaching consequences, especially in the central nervous system. Persistence can cause a headache, disorientation, elevated CSF pressure and even the patient going into a coma and die. Fatigue also sets in for patients in severe asthma owing to the extended periods of labored breathing and reduced oxygen supply to the tissues. Asthma should be properly managed to avoid the serious complications arising.





Hossny, E., Rosario, N., Lee, B., Singh, M., El-Ghoneimy, D., SOH, J., & Le Souef, P. (2016). The use of inhaled corticosteroids in pediatric asthma: update. World Allergy Organization Journal9(1).

Lockey, R. & Ledford, D. (2014). Asthma (1st ed.).

Loerbroks, A., Sheikh, A., Leucht, V., Apfelbacher, C., Icks, A., & Angerer, P. (2016). Determinants of patients’ needs in asthma treatment: a cross-sectional study. Npj Primary Care Respiratory Medicine,26, 16044.

Pino-Yanes, M., Thakur, N., Gignoux, C., Galanter, J., Roth, L., & Eng, C. et al. (2015). Genetic ancestry influences asthma susceptibility and lung function among Latinos. Journal Of Allergy And Clinical Immunology135(1), 228-235.

Shah, R. & Saltoun, C. (2012). Chapter 14: Acute severe asthma (status asthmaticus). Allergy And Asthma Proceedings33(3), 47-50.

Zaslau, S. (2014). Lippincott’s illustrated Q & A review of pharmacology (1st ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.