401210 Health Variations

1.Pathogenesis and clinical manifestations explained

Asthma is an airway disease, characterized by its chronicity. The hallmark of asthma is airway hypersensitivity to normal environmental allergens, reversible airflow and a variable course of airway obstruction (Maslan & Mims, 2014.) Asthma’s pathogenesis involves environmental and genetic factors. Environmental factors involve exposure to allergens like pollen, dust and perfumes. Other aspects are housing conditions like cooking using firewood, poor ventilation and presence of pets like cats in the house. Non-environmental factors not including genetics include diet and drugs. Drugs like aspirin and oral contraceptives have been shown to predispose one to asthma (Ojo et al., 2014). Diets low in anti-oxidants like Vitamin E and Vitamin C has also been associated with developing asthma. Genetic factors like atopy, gender and ethnicity have been implicated to enhance progression of asthma. Others include positive family history of asthma and polygenic intolerance.

In Jackson’s case, asthma attack can be traced back to positive family history and atopy. This may have been triggered by an allergen. It is therefore correct to say that both genetic and environmental factors may have played a role in Smith’s asthma attack. The two factors combined cause airway remodeling especially in repeated exposure to an allergen (Ojo et al., 2014).

The major etiological agent for asthma is attributed to genetic predisposition that induces a type 1 hypersensitive reaction. Numerous inflammatory cells and interleukins play a role in the cascade. Inflammatory cells involved are neutrophils and eosinophils. Atopic patient demonstrates a high level of T_H2 cells production. (Ojo et al., 2014).These cells stimulate production of interleukin 4 (IL-4) that promotes the release of IgE. B cells are also responsible for production of IgE. These B cells are usually activated by IL-13 which also oversees production of mucus in the bronchial smooth muscles as described by Chung, (2015).  Eosinophils are usually activated by IL-5. Upon exposure to an allergen, the IgE coats mast cells and cause degranulation to release histamine.

An early and late wave of reactions have been documented. The former is evident during the degranulation phase of mast cells. Early wave has bronchus constriction, marked mucus production and variable vasodilation (Lougaris et al., 2017). Epithelial vagal receptors mediate bronchoconstriction. T-cell, eosinophil and neutrophil activation caused by inflammation is characteristic of late phase. Airway remodeling occur when there is repeated exposure to allergen. This included bronchial smooth muscle hypertrophy, hypertrophy of mucus gland, vascularization and collagen deposition in sub epithelium (Craft et al, 2015).

One of the findings was that Smith had an increased blood pressure and heart rate. This was a physiological response to increase oxygen delivery to tissues at a time. Physical examination also revealed reduced breath sounds and wheeze. Wheeze was experienced due to narrowed bronchial lumen that caused turbulent flow of air as it rushed through a narrow space. Breath sounds were reduced on auscultation because air entry was limited as a result of narrowing of bronchial muscles (Kumar, Abbas & Aster, 2013).

Arterial blood gas showed compensated respiratory acidosis (renal compensation). This is shown by high partial pressures of carbon dioxide at 50 mmHg. This is suggestive of long respiratory distress as described by a book VENTILATOR, (2016). When carbon dioxide is in excess in blood, it dissolves to form weak carbonic acid that disintegrates to release hydrogen ions that lowers the blood pH. Short term solution for this is increased respiratory effort to wash out the excess carbon dioxide. This is why his respiratory rate was high (at 32 breaths per minute). Long term solution for respiratory acidosis is renal compensation. In this case, there is increased absorption of bicarbonate ions by the kidneys to act as a buffer (Johnson, 2017).

Smith’s also presents with severe dyspnea. This is because of acute excercubation of asthma (ASA). ASA does not respond to standard treatment with bronchodilators and corticosteroids. Dyspnea is due to airway obstruction that is overseen by increased mucus production as a result of hypertrophy of mucus glands. Airway narrowing is also contributed by bronchoconstriction secondary to inflammation and airway narrowing due to remodeling that results into hypertrophy of bronchial smooth muscles VENTILATOR, (2016). These three factors result into reduced air entry making the patient dyspneic. As a result, there is increased respiratory effort to try bring more air rich in oxygen and expel carbon dioxide accumulating in the blood. Poor oxygenation due to dyspnea is the reason why Smith was saturating at 90% at room air.

2.Priority nursing strategies

Initiation of a short acting bronchodilator and oxygen therapy are the two high priority interventions that should be undertaken by nurses to manage Smith’s ASA. Severity of the asthma attack should be assessed in order to determine the extent of initiating these procedures. This is described in the book National Asthma Council Australia, (2017).

Bronchodilation is best achieved by giving a short acting beta agonist like salbutamol. 12 puffs equivalent to 100 mcg per actuation using pressurized metered dose inhaler (pMDI) and a spacer is adequate (Carotenuto, Perfetti, Calcagno, & Meriggi, 2018). A nebulizer with 5mg of salbutamol is used in cases where the patient cannot breathe. Oxygen should also be given via a high pressure flow (venturi) system and target a saturation of above 94% in young patients like Smith (National Asthma Council Australia, 2017).

While giving the medication, nurses should assess if Smith is improving or not. In case of no improvement, bronchodilator therapy is continued. Repeat doses of salbutamol every 20 minutes for first one hour (3 doses in total) or as sooner as required should be initiated. A muscarinic receptor antagonist (ipratropium bromide, 8 puffs through pMDI or 500 mcg nebule added to salbutamol) is added if response is still poor (National Asthma Council Australia, 2017). Oral prednisolone, a systemic corticosteroid (37.5-50 mg for 5 days) or intravenous hydrocortisone 100 mg every 6 hours is also given to lower down inflammation. Review of treatment in ASA is done within 1 week and a step up treatment done if no improvements have been recorded (National Asthma Council Australia, 2017). A step down therapy is done if good control has been achieved. Smith’s minimum effective doses for controlling the symptoms and ASA should be calculated. During this period, symptoms and peak expiratory flow rate is monitored and follow up visit scheduled. Drug dosage expiry dates should be checked as these can slow down the progress to a healthy patient life.

3.Modeof action of drugs

Ipratropium is an example of a short acting anti muscarinic. It has competitive binding properties to cholinergic receptors of bronchial smooth muscles, blocking acetylcholine and therefore preventing bronchoconstriction (FitzGerald et al., 2018). In effect, vasodilation and bronchodilation occurs. This is by their effect of inhibiting vagal stimulation.

Salbutamol, a short acting beta 2 adrenergic agonist acts via the G-protein coupled pathway. After G protein is stimulated, cAMP is activated in turn activating protein kinase A. subsequent activation of myosin light chain phosphatase and deactivation of myosin light chain kinase occurs enabling entry of calcium via gated ion channels mediating smooth muscle relaxation (Carotenuto, Perfetti, Calcagno, & Meriggi, 2018). This causes bronchodilation.

Hydrocortisone is a systemic corticosteroid, administered intravenously. It inhibits inflammatory pathway in asthma by blocking phospholipase A2 which is responsible for eicosanoids. Lipocortin-1, activated by hydrocortisone suppresses phospholipase A2. In effect, production of eosinophils and neutrophils is inhibited (Radojicic, Keenan, & Stewart, 2016)

Nursing implications for drug use

While giving Smith the drugs, the nurse in charge should be aware of their potential side effects, and how to monitor drug use. Salbutamol use should be monitored to ensure the correct dosage and route of administration (Carotenuto, Perfetti, Calcagno, & Meriggi, 2018). An under dose will mean that the drug will not be effective. An overdose may lead to side effects like headache, anxiety, tachycardia, hypotension and hypokalemia in prolonged use. Ipratropium bromide overdose may lead to dryness of mucous membranes, urinary retention (FitzGerald et al., 2018), while hydrocortisone overdose or prolonged use may lead to susceptibility to infections and weight gain (Radojicic, Keenan, & Stewart, 2016).

Monitoring of drug use can be done by taking liver and renal function tests to determine if the drugs like salbutamol are suitable for use. In case of poor renal function tests, dose adjustment should be made or alternative drug used. Nurses should know what to do in case of adverse effects, and the relevant authority to contact (National Asthma Council Australia, 2017). Other aspects of monitoring drug use is to ensure correct route, dosage, correct patient, correct drug and that the drug has not expired.

References

Carotenuto, M., Perfetti, L., Calcagno, M. G., & Meriggi, A. (2018). Comparison of Acute Bronchodilator Effects of Inhaled Ipratropium Bromide and Salbutamol in Adults with Bronchial Asthma. Journal of Allergy and Clinical Immunology, 141(2), AB209.

Chung, K. F. (2015). Targeting the interleukin pathway in the treatment of asthma. The Lancet, 386(9998), 1086-1096.

Craft, J.A., Gordon, C.J., Huether, S.E., McCance, K.L., Brashers, V.L. & Rote, N.E. (2015). Understanding pathophysiology – ANZ adaptation (2nd ed.). Chatswood, NSW: Elsevier Australia. Chapter 24 & 25.

FitzGerald, J. M., Buhl, R., Casale, T. B., El Azzi, G., Engel, M., Sigmund, R., & Halpin, D. M. G. (2018). Tiotropium Respimat® Reduces Episodes of Asthma Worsening in PrimoTinA-asthma®, Irrespective of Baseline Characteristics or Season. In B65. ASTHMA: PATHOPHYSIOLOGY AND CLINICAL TRIALS (pp. A3947-A3947). American Thoracic Society.

Johnson, R. A. (2017). A Quick Reference on Respiratory Acidosis. Veterinary Clinics: Small Animal Practice, 47(2), 185-189.

Kumar, V., Abbas, A., & Aster, J. (2013). Robbins Basic Pathology (9th ed., pp. 468-470). Canada: Elsevier Saunders.

Lougaris, V., Moratto, D., Baronio, M., Tampella, G., van der Meer, J. W., Badolato, R., … & Plebani, A. (2017). Early and late B-cell developmental impairment in nuclear factor kappa B, subunit 1–mutated common variable immunodeficiency disease. Journal of Allergy and Clinical Immunology, 139(1), 349-352.

Maslan, J., & Mims, J. W. (2014). What is asthma? Pathophysiology, demographics, and health care costs. Otolaryngologic Clinics of North America, 47(1), 13-22.

National Asthma Council Australia. (2017) Australian Asthma Handbook – Quick Reference Guide, Version 1.3. National Asthma Council Australia, Melbourne. Available from: https://www.asthmahandbook.org.au

Ojo, O. O., Basu, S., Jha, A., Ryu, M., Schwartz, J., Doeing, D., & Halayko, A. J. (2014). D29 MOLECULAR SIGNALS AND CELLULAR MECHANICS: FOCUS ON ASTHMA: S100a8/a9 is a Mediator of Asthma Pathophysiology: In an Acute Allergic Model of Asthma. American Journal of Respiratory and Critical Care Medicine, 189, 1.

Radojicic, D., Keenan, C. R., & Stewart, A. G. (2016). The Physiological Glucocorticoid (GC), Hydrocortisone, Limits Selected Actions of Synthetic GC in Human Airway Epithelium. In A40. EPITHELIAL REGULATION OF INFLAMMATION (pp. A1472-A1472). American Thoracic Society.

VENTILATOR, E. O. H. A. O. (2016). VARIBALE VENTILATION DECREASES AIRWAY RESPONSIVENESS IN ASTHMA. Respirology, 21(3), 3-213