Pathogenesis of COPD
Discuss about the Nursing for Chronic Obstructive Pulmonary Disease
Chronic Obstructive Pulmonary Disease (COPD) is manifested by airflow limitation which is persistent and rarely reversible. It is related to chronic inflammatory response in the lungs and airways due to some gases or particles particularly from smoking. Presence of these smoke particles in the lungs trigger inflammatory response which leads to increased macrophage and neutrophil infiltration into the lungs. Cytokines, chemokines and elastases are released by these immune cells and this eventually damage the parenchyma with time (Wells, & Dransfield, 2013).
Besides inflammation, there are two other processes involved in the pathogenesis of COPD. One is the imbalance between proteases and antiproteases and the other is imbalance between oxidants and antioxidants in the lungs. The first, that is, protease-antiprotease imbalance has been associated with pathogenesis of emphysema. Emphysema is a disease of alveoli whereby the fibers that forms the walls of alveoli becomes destroyed. The destructions render them less elastic and unable to function during exhalation. Proteases like elastase and matrix metalloproteinase (MMPs) released by the inflammatory cells breaks down the connective tissue of alveolar walls and the septae. This loss of the elasticity leads to reduced rates of expiratory flow, air trapping and collapsing of the airway.
Inflammation from smoke exposure also leads to fibrosis of bronchiolar walls, hypersecretion of mucus, airway edema and bronchoconstriction. This generally may be referred to chronic bronchitis. In chronic bronchitis, the epithelium of the central airways and also the mucus-producing glands are inflamed. This is associated with mucus production, reduced mucociliary clearance and increased permeability of the airspace epithelial barrier. Goblet cells hyperplasia, mucous gland enlargement and mucociliary dysfunction causes excessive mucus production in larger airways and build up reducing the airway lumen. Despite the fact that these changes occur in the larger airway, it is evident that the increased airway resistance is majorly in the small airways(≤2mm) (Kim, & Criner,2013). Fibrosis and smooth muscle hypertrophy likely occur together with increased mucus production and also cellular infiltration in the peripheral airways.
Acute exacerbations of COPD is when there an abrupt worsening of the symptoms of COPD that is, shortness of breath, amount and color of sputum which likely last for many days. Acute exacerbations of chronic bronchitis (AECB) is another term for Acute exacerbation of COPD. This condition may be caused by an infection with microorganisms such as bacteria or viruses or even by pollutants of the environment. Basically most of the causes is due to infections either by bacteria or viruses or both. During exacerbation, there is an increased airway inflammation which leads to increase in hyperinflation, reduce in air flow during exhalation and also decreased gas exchange. (Ko, Chan,Hui, Goddard, Shaw, Reid & Yang,2016)
Exacerbation of COPD
Robert is diagnosed with exacerbation of COPD due to community acquired pneumonia which can be due to infections with bacteria, fungi, viruses and parasite with little contact with the healthcare system (Vestbo, Hurd, Agustí, Jones, Vogelmeier, Anzueto & Stockley, 2013). Factors that can put patient like Robert at high risk for exacerbation of COPD may include; obstruction of airway part and lung disease. When the bronchus is obstructed for example by mucus, the lung cannot eliminate fluid and hence this can lead to pneumonia which in turn cause exacerbations. Underlying lung diseases such as emphysema and habits such as smoking as in for Robert’s case also lead to more frequent and even more severe bouts of pneumonia.
Other factors that can cause exacerbations may include severe allergy or heavy air pollution. Weather changes, too much activity, lack of enough sleep, undergoing stress or anxiety also triggers exacerbations. In some cases, however, the exact cause is unknown.
- Pathophysiology of pneumonia and the differences between Community Acquired, Hospital Acquired and Health Care Associated Pneumonia.
Pneumonia is a lung condition whereby the lung parenchyma becomes inflamed due to infection. It can be caused by bacteria, viruses or fungi. The pathogen enters the lungs either through the throat, nose, blood or airborne droplets. It then invades the spaces between the alveoli and cells. Immune response is activated and the macrophages and neutrophils inactivates the microorganism resulting in chills, fever and fatigue. The alveoli are then filled by fluid, pathogen and neutrophils leading to consolidation which can be seen on chest x-ray.
Sometimes one get pneumonia after being admitted to a hospital or health facility for treatment due to another infection. This is referred to hospital-acquired pneumonia(HAP). If the infection is acquired outside a hospital setting for example due to contact with an infected one is diagnosed with community-acquired pneumonia (CAP) (Marti& Esperatti,2016).). Whereas, pneumonia resulting from aspiration of a foreign objects or stomach contents into the respiratory tract is known as aspiration pneumonia.
The major difference between HAP and CAP is that people with HAP live in long term care facilities or have recently been in a hospital. HAP may be more serious since the bacteria causing it may have developed resistance and also the people getting in are already sick. Aspiration pneumonia on the other hand is more certain if something interferes with normal gag reflex, for example, problem with swallowing or a brain trauma or even excessive alcohol intake or drugs (DiBardino & Wunderink,2015).
Mechanism of action, Contraindications and Adverse Reactions, Nursing Considerations and Patient education points
Salbutamol:
Salbutamol is a highly selective beta 2-adrenergic receptor stimulating drug that has a bronchodilator effect. It is used for relieving bronchospasm in emphysema, chronic bronchitis and other airway resistance diseases.
Salbutamol works by stimulating beta 2 adrenergic receptors, predominant receptors in bronchial smooth muscles. These triggers activation of enzyme adenyl cyclase which forms adenosine mono-phosphate(AMP) from adenosine tri-phosphate(ATP). Increase of cyclic AMP causes the bronchial smooth muscle to relax and makes the airway resistance decrease by lowering intracellular ionic calcium concentrations (Gordon,& Panos,2010). The drug relaxes the smooth muscles of the airways. This increase in the cyclic AMP also inhibits bronchoconstrictor mediators from being released. These mediators include histamine, leukotriene from mast cells in the airway.
Salbutamol is contraindicated in pregnancy. Studies from animals have shown teratogenic effects on the fetus. It should be administered only if the potential risk outweighs the potential risk of the fetus. It is also contraindicated in persons with a history of allergic or hypersensitivity reactions. It should also not be administered to patients with pre-existing cardiac tachyarrhythmia.
The most common adverse reactions of salbutamol are palpitations, fine tremors, anxiety, hypertension. Others include headache, cramps, dry mouth, tachycardia, arrhythmia, flushing of the skin sleep disturbances and rarely myocardial ischemia.
The nurse should assess cardio respiratory function of the client and also determine previous history of the medication and thereafter monitor for allergic reactions. The nurse should also consider instructing the patient on dosage and not to overdose. She should also teach the client to use the inhaler and advise spacing and also to report any allergic reactions. Budesonide
Budesonide is an anti-inflammatory corticosteroid that portrays potent weak mineralocorticoid activity and potent glucocorticoid activity. The precise mechanism of actions is unknown but corticosteroids have been illustrated to have a variety of inhibitory actions against many cell types such as neutrophils, macrophages and mediators such as histamine, leukotrienes involved in inflammation. So this anti-inflammatory response is like to be contributing to the efficacy in the concern disease.
This drug is contraindicated if the patient is allergic to it or to corticosteroids. It is also contraindicated in conditions such as tuberculosis involving the lungs, Cushing’s syndrome, osteoporosis, herpes simplex infection, cataracts, inactive tuberculosis and even oropharynx candidiasis. Its common side effects include; nausea, heartburn, stomach pain, indigestion, headache, thinning of skin, cough, easy bruising, runny nose, skin rash, myalgia and changes in menstrual periods for women. Others but rare include vision problems, unusual hair growth, slow wound healing and mood changes such as depressions or agitation.
Budesonide:
Nursing considerations for budesonide include assessing the patient past medical history and physical examination like blood pressure, auscultation, adventitious sounds. Also to advise the patient to rinse mouth after each use. The should also monitor the patient for acne, bruising, hirsutism which could indicate need to decrease dosage.
Finally, the nurse should teach the patient not to use more than prescribed dose and teach also about the side effects expected. She should advise the patient on when to report and not to stop the drug if immediate actions are no achieved since the medications may take sometimes before its effect is seen.
Tiotropium is anticholinergic bronchodilator which is long acting an is used to manage chronic obstructive pulmonary disease. It is a muscarinic receptor antagonist i.e. antimuscuranic agent. When applied topically it acts particularly on the m3 muscarinic receptors which are found the airways. This leads to relaxation of the smooth muscles hence producing a bronchodilatory effect(Gordon & Panos,2010).
It is contraindicated in allergic reactions involving anticholinergics and ipratropium. Also contraindicated in conditions such as closed angle glaucoma, urinary bladder blockage, enlarged prostate and even chronic kidney disease stage 3-5. Safety and efficacy in children is also not established. Adverse effects associated with tiotropium include pain when urinating or burning, dry mouth, vomiting, stomach upset or constipation, sore throat and even muscle pain
The nurse should closely monitor the patient for any adverse reactions. She or he should asses for respiratory status before administration and during the peak of medication. Patient teaching involves information the patient that the drug is long acting and not for immediate relief. Also to caution the client not to let powder get into eyes. Finally, to advise the patient to report immediately any reactions of all medications.
Since is diagnosed with Community Acquired Pneumonia and an inpatient from ICU, the following medications can be prescribed to treat streptococcus pneumoniae;
Moxifloxacin 400 mg IV or PO q24h or
Levofloxacin 750 mg IV or PO q24 h or
Combination of a beta-lactam (e.g. ceftriaxone
Moxifloxacin and levofloxacin are a broad spectrum antibiotic which are active against both gram positive and gram-negative bacteria. Works by inhibiting DNA gyrase, topoisomerase type ii and iv which are required to separate bacterial DNA, thus causing cell replication inhibition. Moxifloxacin is contraindicated in NSAIDS as may increase risk of CNS stimulation and convulsions and also in persons with history of hypersensitivity. Rare and serious side effects include irreversible peripheral neuropathy, hepatitis, tendonitis and photosensitivity. Levofloxacin is contraindicated in epilepsy and in history of quinolone-associated tendon rupture. The nurse should monitor the patient for any adverse reaction and stop the medication immediately if any and also discuss with the doctor any alternative. She should teach the patients about the drug, prescription and the side effects.
Tiotropium:
Beta-lactam antibiotics inhibits peptidoglycan layer of cell wall of bacteria. They are a broad-spectrum antibiotics and are bactericidal. Contraindicated in penicillin and cephalosporin allergy and also bacterial infections of brain and spinal cord. Side effects of this medication may include colitis, hypersensitivity, GI upset and even superinfection. Nursing consideration for this drug involve monitoring the patient reaction to the medication, and also performing physical assessment. The patient should be taught on the side effects dosage and even advised to report any reactions noticed as taught
First, Robert should be introduced to exercise training programs as this has been evident to be able to minimize and induce tolerance to the symptoms of COPD such dyspnea and tiredness (Cindy, Mackney, Jenkins, & Hill,2012). Secondly, Robert must be provided with psychosocial care. Since he already worried about his disease condition and also about his wife knowing the extend of it. This will help towards positive response towards medication. Lastly Robert has to be undertaken through some rehabilitation to help him quit smoking as this is going to worsen his conditions. It has been evident that in most cases those who undergoes rehabilitations are likely to benefit from it by obtaining the ease of quitting their addiction.
References
Cindy Ng, L. W., Mackney, J., Jenkins, S., & Hill, K. (2012). Does exercise training change physical activity in people with COPD? A systematic review and meta-analysis. Chronic respiratory disease, 9(1), 17-26.
DiBardino, D. M., & Wunderink, R. G. (2015). Aspiration pneumonia: a review of modern trends. Journal of critical care, 30(1), 40-48.
Fromer, L. (2011). Implementing chronic care for COPD: planned visits, care coordination, and patient empowerment for improved outcomes. International journal of chronic obstructive pulmonary disease, 6, 605.
Gordon, J., & Panos, R. J. (2010). Inhaled albuterol/salbutamol and ipratropium bromide and their combination in the treatment of chronic obstructive pulmonary disease. Expert opinion on drug metabolism & toxicology, 6(3), 381-392.
Ko, F. W., Chan, K. P., Hui, D. S., Goddard, J. R., Shaw, J. G., Reid, D. W., & Yang, I. A. (2016). Acute exacerbation of COPD. Respirology, 21(7), 1152-1165.
Kim, V., & Criner, G. J. (2013). Chronic bronchitis and chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine, 187(3), 228-237.
Kova?, V. B., Rise, J., & Moan, I. S. (2009). From intentions to quit to the actual quitting process: The case of smoking behavior in light of the TPB. Journal of Applied Biobehavioral Research, 14(4), 181-197.
Marti, A. T., & Esperatti, E. M. (2016). Community-acquired pneumonia. In Respiratory infections (pp. 110-128). CRC Press.
Wells, J. M., & Dransfield, M. T. (2013). Pathophysiology and clinical implications of pulmonary arterial enlargement in COPD. International journal of chronic obstructive pulmonary disease, 8, 509.
Tautermann, C. S., Kiechle, T., Seeliger, D., Diehl, S., Wex, E., Banholzer, R., … & Casarosa, P. (2013). Molecular basis for the long duration of action and kinetic selectivity of tiotropium for the muscarinic M3 receptor. Journal of medicinal chemistry, 56(21), 8746-8756.
van der Poll, T., & Opal, S. M. (2009). Pathogenesis, treatment, and prevention of pneumococcal pneumonia. The Lancet, 374(9700), 1543-1556.
Vestbo, J., Hurd, S. S., Agustí, A. G., Jones, P. W., Vogelmeier, C., Anzueto, A., … & Stockley, R. A. (2013). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. American journal of respiratory and critical care medicine, 187(4), 347-365.
Zakrisson, A. B., & Hägglund, D. (2010). The asthma/COPD nurses’ experience of educating patients with chronic obstructive pulmonary disease in primary health care. Scandinavian journal of caring sciences, 24(1), 147-155.
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