Impact Of Mucolytic Agents On COPD Exacerbations Discussion Paper

Pathophysiology Of COPD

Discuss about the Impact Of Mucolytic Agents On COPD Exacerbations.

Chronic Obstructive Pulmonary disease (COPD) is a form of obstructive lung disease where there is a change in the normal structure of central airways, peripheral bronchioles and lung parenchyma. Among other factors such as genetics, air pollution and occupational factors, it primarily results from cigarette smoking which acts as the noxious stimuli. It produces an inflammatory response involving neutrophils, granulocytes, macrophages and to some extent T Lymphocytes (CD8+). These immune cells (polymorphonuclear leukocyte and macrophage) release elastases which cause lung destruction, elastases are insufficiently inhibited by protease inhibitors (Mitchell, 2015).

Elastases (Human leukocyte elastase) and an increase in oxidative stress caused by free radicals of Cigarette are usually the primary offender that usually cause the cascade of events that lead about lung destruction, narrowing and inflammation of the airways. This results in an inability to breathe out fully and increased total volume of air in lungs (hyperinflation) which causes shortness of breath. It is usually accompanied by airway hyperresponsiveness to irritants. There is usually a worsening of symptoms during exacerbations as there is a worsened gas transfer and increased inflammation.  Impact Of Mucolytic Agents On COPD Exacerbations Discussion Paper

The overall effect is usually a decreased oxygen levels in blood with an increased concentration of carbon(IV)oxide caused by improper ventilation. The decreased O₂ levels after some time causes narrowing of arteries in lungs and breakdown of capillaries thus leading to increased blood pressure in pulmonary arteries (Kawut & Poor,2014).

Chronic bronchitis is usually associated with production of large amounts of sputum as a result of mucous gland hyperplasia which is its histologic hallmark. There are usually structural changes which include ciliary abnormalities, atrophy, metaplasia and bronchial wall thickening. Inflammation and secretions accompanied with it causes obstruction. These changes and an additive effect of loss of alveolar attachment results in limitation of ventilation.

Emphysema is an irreversible enlargement of air spaces distal to terminal bronchioles, this causes a decrease in surface area for gaseous exchange. There is also a decrease in elastic recoil and airway narrowing as a result of loss of alveolar supporting structures. Inability to oxygenate properly is as a result of destruction of alveolar septae. A V/Q mismatch is also experienced as there is limited perfusion in a well-ventilated lung. The overall resultant effect is usually muscle wasting and weight loss (Sohal, 2016).

This is usually some sudden worsening of COPD symptoms characterized by a significant increase in both shortness of breath and intensity of coughing. It is typically caused by an infection by either bacteria or virus, in most cases this lasts for several days. The infection causes a change in sputum appearance to green yellow. In some cases, it might also be caused by toxins especially environmental pollutants. Symptoms of exacerbation include increased coughing, significant chest congestion, shortness of breath that is associated with wheezing. This sudden worsening of COPD symptoms might cause rupturing of the airways hence leading to pneumothorax (Zhou & Li, 2015).

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Disease Processes Contained In COPD

In Robert’s case, he developed an exacerbation due to infection by a community acquired pneumonia, the exacerbation lasted for about 3days. He was put under non-invasive ventilation to aid in breathing as it is usually associated with significant decrease in ability to ventilate properly. He was at a high risk of developing exacerbation or rather having the COPD itself since he has been smoking for the past 40 years or might have refused to follow a drug therapy after being diagnosed of COPD, this include improper use of inhalers or failure to take the prescribed drugs. The infection then worsened the situation making hence developing an exacerbation. Other factors that may cause this include exposure to certain allergens (such as wood, pollen) and air pollution.

To some extent, exacerbations can be prevented by smoking cessation, immunization to certain pathogens such as pneumococcal vaccinations, maintain a good diet and avoiding contact with people already infected with certain pathogens. In Robert’s case, he should follow these measures to reduce the chances of this event happening again. He should also follow the right regimen of medication to ensure that there is proper management of the COPD symptoms. Although there is no known cure, these measures will significantly improve his life.

Pneumonia typically starts as an upper respiratory tract infection that progresses slowly downwards and eventually gets to the alveoli. Causes of pneumonia can be extrinsic or intrinsic, extrinsic is from irritants whereas intrinsic factors are related to the host. In relation to this, bacteria may find itself in lung parenchyma and depending on its virulence and immunity of the patient, may cause an infection. During an infection there is an active migration of neutrophils into air spaces which kill microbes by release of cytokines that cause immune system activation. This usually results in inflammation and lung damage. This manifests as clinical symptoms where one has fever, chills and fatigue. The infection usually fills the lung alveoli with fluid hence affecting the normal oxygenation (Kamo & Tasaka, 2015)

Community-acquired pneumonia (CAP) is defined as pneumonia acquired outside of hospital or healthcare facilities. Clinical diagnosis is based on a group of signs and symptoms related to lower respiratory tract infection with presence of fever >100ºF (>38ºC), cough, expectoration, chest pain, dyspnea, and signs of invasion of the alveolar space. However, older patients in particular are often afebrile and may present with confusion and worsening of underlying diseases. (Marti & Esperatti, 2016).

Acute Exacerbation Of COPD

Hospital acquired pneumonia is lower respiratory tract infection that is acquired 48-72hrs after admission. Its distinguishing factor is that it is caused by bacteria and not a virus. This is usually seen in people attaining mechanical ventilation since the ventilatory tubes are a great harbor of bacteria (Kalil & Metersky, 2016)

Health Care Associated Pneumonia is where patients come from the community but frequent hospitals hence they are susceptible to acquiring infection. Risk factors include attending clinics, residence in a nursing home and receiving outpatient intravenous care for approximately 30 days (Karabo?a & Uzun,2015).

It acts by stimulating β₂ adrenergic receptors on bronchial smooth muscle, this leads to activation of adenyl cyclase to cAMP from ATP. High levels of cAMP relax bronchial smooth muscle, reduces air way resistance and inhibits release of bronchoconstrictor substances such as histamine. Salbutamol acts from trachea to the terminal bronchioles, hence it is effective in management of COPD cases (Malerba & Montuschi, 2015).

It is contraindicated in persons with some history of a hypersensitivity reaction to it or any of its constituents. It is also contraindicated in patients with an existing history of cardiac arrhythmias.

Salbutamol is usually well tolerated. In some patients, they may present with skeletal muscle tremors and nervousness. In a few it may cause chest discomfort, palpitations, headache, muscle cramps, difficulty in micturition and paradoxical bronchospasms.

One has to be aware of the side effects as mentioned above since it is normal to have these negative responses after taking the medication. This drug should also be used with caution in some patients with certain heart problems, hypertension or seizure disorders.

Nursing assessment should include taking of vital measurements such as heart rate and blood pressure. Lung sounds should also be monitored prior to taking the medication. It is very vital to also check for paradoxical bronchospasm which is the opposite intended effect of this drug.

The patient which in our case is Robert should be properly educated on how to this medication, this include important points on when and how frequent to use it. Salbutamol which comes as an inhaler, he should know how to maintain and store the drug. This ensures a proper treatment process.

MOA

It is an anti-inflammatory corticosteroid that decreases inflammation by limiting the migration of polymorphonuclear leukocytes and reducing the permeability of capillaries. It also increases the synthesis of surfactant, inhibits prostaglandin and also reduces the proinflammatory cytokines. This greatly reduces inflammation hence effective in COPD cases as it involves bronchitis (O’Byrne & FitzGerald, 2018)

Pathophysiology Of Pneumonia

It is contraindicated in patients with hypersensitivity to it and also as a primary treatment of acute episodes of asthma where intensive care is usually required.

Primary adverse effects include headache, acne, nausea and respiratory infection. Others include back pain, abdominal pain, vomiting and fatigue. To some lesser extent there might also be GI irritation, pharyngitis and migraine.

Nursing Considerations and Patient Education Points

The patient should be monitored closely especially if they have any liver disease and lab tests such as periodic serum potassium should be taken regularly.

The patient should notify the physician if they experience any significant side effects such as rashes, edema, fever and itching. One should not breast feed when undertaking this medication and he should avoid people with certain infections such as chicken pox.

In Robert’s case, his medication was changed since this drug has a side effect of causing respiratory infection. This will typically worsen his situation making the exacerbation escalate even further. In addition, Tiotropium is a long acting anti cholinergic agent hence longer duration of action. Though not used in exacerbations, hence it being administered after.

MOA

Long-acting ant muscarinic agent, often referred to as anticholinergic

Inhibits M3-receptors at smooth muscle, leading to bronchodilation

Adverse effects and Contraindications

Primary adverse effects include upper respiratory tract infection, dry mouth and sinusitis. Others include abdominal pain, chest pain, constipation and depression.

Should not be used with umeclidinium bromide since it causes pharmacodynamic synergism leading to toxicity.

Nursing Considerations and Patient Education Points

Drug should be withdrawn if angioedema occurs and anticholinergic effects should be monitored closely (urinary retention and tachycardia).

The patient should notify the physician if he experiences edema, constipation, blurred vision or urinary difficulties. He should not allow powdered medication to contact the eyes since it might cause blurred vision. He should also report if he experiences anything that might not feel normal.

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Cefotaxime

MOA

Binds to penicillin-binding proteins and inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell-wall death; resists degradation by beta-lactamase; proper dosing and appropriate route of administration are determined by condition of patient, severity of infection, and susceptibility of microorganism

Contraindications and Adverse Effects

Contraindicated in patients with a known hypersensitivity to it or other cephalosporins

AE’s include diarrhea, colitis, nausea, pain at injection site, rash, thrombocytopenia, fever and vomiting.

Nursing Considerations and Patient Education Points

There should be an assessment to determine hypersensitivity reactions to penicillin’s and cephalosporins before initiation of the treatment. Culture and sensitivity tests should also be carried out during treatment. In prolonged treatment, super infection with other organisms may occur hence this should also be closely monitored. In case there is diarrhea, it should be reported promptly.  Impact Of Mucolytic Agents On COPD Exacerbations Discussion Paper

MOA In COPD

MOA

Inhibits cell-wall biosynthesis; blocks glycopeptide polymerization by binding tightly to D-alanyl-D-alanine portion of cell wall precursor (Cercenado, 2017)

Contraindication and Adverse Effects

Should not be used concomitantly with anesthetic agents has it is associated with erythema. Since it is nephrotoxic, it should not be administered with other nephrotoxic drugs

AE’s include a bitter taste, nausea, vomiting, hypotension and erythematous rash on face and upper body.

Nursing Considerations and Patient Education Points

Blood pressure and heart rate should be monitored continuously. Lab tests such as urinalysis should be taken and hearing should also be accessed since it is ototoxic

The patients should notify physician if he experiences tinnitus and he should also adhere to the drug regimen.

MOA

L-stereoisomer of parent compound ofloxacin; D-isomer form is inactive

Inhibits DNA gyrase activity, which in turn promotes breakage of DNA strands

Good monotherapy with extended coverage against Pseudomonas spp, as well as excellent activity against pneumococcus

Giusti & Blasi, 2016)

Contraindication and Adverse Effects

It is contraindicated in people with myasthenia gravis, tendonitis, liver problems, slow heart beat and clostridium difficile infection.

AE’s include nausea, vomiting, diarrhea, edema, dyspnea, constipation and dizziness

Nursing Considerations and Patient Education Points

Treatment should be withheld if one experiences any devastating side effects and should be reported to the physician. The patient should take a lot of fluids while under this drug and excessive exposure to UV light should be avoided.

Evidence-based interventions to help Robert manage his COPD

Study shows that the use of inhaled short acting B₂ agonists during exacerbation leads to an improvement in FEV1 compared with anticholinergic bronchodilators which have safer side effects. Recent research illustrates that adding a second inhaled bronchodilating agent is beneficial after attainment of maximal dose of the initial agent. Evidence shows that use of methyl-xanthine is not beneficial as it does not improve FEV1. A meta-analysis also illustrates metered-dose inhaler and wet nebulizers as best method of administration (Vogelmeier & Criner, 2017).

Study shows that when you administer oxygen, it provides benefits such as pulmonary vasoconstriction and a decrease in both right heart strain and myocardial ischemia. This has made it become part of standard method of care as it is indicated that it also improves arterial oxygen tension without a significant effect on arterial carbon(IV)oxide tension or pH. Keeping its saturation at 90% through a mask is usually recommended (Yusen & Criner, 2018).

Analysis dictates that these agents improve symptoms of exacerbation, they also indicate that there is a significant reduction in number of exacerbation and days of illness when frequently used (Cazzola & Rogliani, 2017).

Contraindications And Adverse Effects

References

Cazzola, M., Rogliani, P., Calzetta, L., Hanania, N. A., & Matera, M. G. (2017). Impact of mucolytic agents on COPD exacerbations: a pair-wise and network meta-analysis. COPD: Journal of Chronic Obstructive Pulmonary Disease, 14(5), 552-563.

Cercenado, E. (2017). Antimicrobial spectrum of dalbavancin. Mechanism of action and in vitro activity against Gram-positive microorganisms. Enfermedades infecciosas y microbiologia clinica, 35, 9-14.

Giusti, M., Blasi, F., Iori, I., Mazzone, A., Sgambato, F., Politi, C., … & Bonizzoni, E. (2016). Prulifloxacin vs Levofloxacin for exacerbation of COPD after failure of other antibiotics. COPD: Journal of Chronic Obstructive Pulmonary Disease, 13(5), 555-560.

Jenkins, C., Calverley, P. M., Carter, K., Tetzlaff, K., de la Hoz, A., Anzueto, A., … & Wedzicha, J. A. (2018). Tiotropium/Olodaterol Versus Tiotropium in the Prevention of Exacerbations of Chronic Obstructive Pulmonary Disease: Impact of Adjusting for Baseline Characteristics. In A75. COPD: TARGETS, MODELS, AND CLINICAL STUDIES (pp. A2387-A2387). American Thoracic Society.

Kalil, A. C., Metersky, M. L., Klompas, M., Muscedere, J., Sweeney, D. A., Palmer, L. B., … & El Solh, A. A. (2016). Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases, 63(5), e61-e111.

Kamo, T., & Tasaka, S. (2015). Pathophysiology and diagnosis of severe pneumonia and acute respiratory distress syndrome. Japanese Journal of Chest Diseases, 74(5), 500-510.

Karabo?a, B., Uzun, R., & Cilli, A. (2015). Health-care associated pneumonia. Tuberkuloz ve toraks, 63(2), 86-93.

Kawut, S. M., Poor, H. D., Parikh, M. A., Hueper, K., Smith, B. M., Bluemke, D. A., … & Vogel-Claussen, J. (2014). Cor pulmonale parvus in chronic obstructive pulmonary disease and emphysema: the MESA COPD study. Journal of the American College of Cardiology, 64(19), 2000-2009.

Malerba, M., Montuschi, P., Radaeli, A., & Pirisi, M. (2015). Role of beta-blockers in patients with COPD: current perspective. Drug discovery today, 20(1), 129-135.

Marti, A. T., & Esperatti, E. M. (2016). Community-acquired pneumonia. In Respiratory infections (pp. 110-128). CRC Press.

Mitchell, J. (2015). Pathophysiology of COPD: Part 1. Practice Nursing, 26(4), 172-178.

O’Byrne, P., FitzGerald, M., Bateman, E. D., Barnes, P. J., Zhong, N., Keen, C., … & Reddel, H. K. (2018). Efficacy and Safety of As-needed Budesonide/Formoterol in Mild Asthma. In A34. ASTHMA CLINICAL STUDIES I (pp. A7655-A7655). American Thoracic Society.

Sohal, S. S. (2016). Endothelial to mesenchymal transition (EndMT): an active process in Chronic Obstructive Pulmonary Disease (COPD)?

Vogelmeier, C. F., Criner, G. J., Martinez, F. J., Anzueto, A., Barnes, P. J., Bourbeau, J., … & Frith, P. (2017). Global strategy for the diagnosis, management and prevention of chronic obstructive lung disease 2017 report. Respirology, 22(3), 575-601.  Impact Of Mucolytic Agents On COPD Exacerbations Discussion Paper