Pathophysiology and Pharmacology in COPD – A case report
Question
Task:
Background to Clinical Scenario:
Robert is a 51 year old man who lives with his wife in regional Victoria. He has been admitted to your ward from the Intensive Care Unit (ICU), where he had a 3 day stay for an acute exacerbation of COPD, caused by community acquired pneumonia. He required several days of non-invasive ventilation whilst in ICU. Robert tells you his wife (Jill) was very frightened when he was admitted to ICU, and he doesn’t want ‘to put her through that anymore’. He would like some help to understand and manage his COPD. Robert said he was diagnosed with COPD about 18 months ago by his GP, but admits he was sick for ‘a while’ before that. He is a current smoker, and has smoked for about 40 years. He has unsuccessfully attempted to quit on more than 5 occasions. Robert worked for many years on his chicken farm, but now finds he becomes breathless very easily and Robert and Jill have had to hire a farm helper. Robert’s medications include:
Salbutamol 2 – 4 puffs PRN
Budesonide/Efomoterol fumarate dehydrate 2 puffs daily
Metoprolol 25mg daily
Aspirin SR 100 mg daily
Pathophysiology 1.1: Describe the pathophysiology of COPD. Include in your answer the two disease processes contained in the umbrella term ‘ COPD’ and how they develop.
Robert has been diagnosed with a severe exacerbation of COPD, caused by Community-Acquired Pneumonia.
1.2 Explain the term ‘acute exacerbation of COPD’. What factors put patients like Robert at high risk for exacerbations of COPD? What else may contribute to an exacerbation of COPD?
1.3 Describe the pathophysiology of pneumonia
Include in your answer the differences between Community Acquired, Hospital Acquired and Health Care Associated Pneumonia.
Pharmacology: The Respiratory Physician who reviewed Robert in ICU suggested some changes to his current inhaler regime. The physician suggested that Robert cease his Budesonide/Efomoterol fumarate dehydrate, and commence on Tiotropium 2 puffs daily.
2.1 For each of the three inhalers (Salbutamol, Budesonide/Efomoterol fumarate dehydrate and Tiotropium), describe the Mechanism of action in COPD Contraindications and Adverse Reactions Nursing Considerations and Patient Education Points Include in your answer why the respiratory physician might have changed Robert’s medication regime.
CRICOS Provider No. 00103D NURBN 2012 Semester 1, 2018 Clinical Scenario Assignment Page 3 of 3
Robert was diagnosed with Community-Acquired Pneumonia, and Streptococcus pneumoniae was cultured from his sputum.
2.2 Identify three antibiotics that could be used to treat Streptococcus pneumoniae in Robert’s case. For each antibiotic, describe the Mechanism of action Contraindications and Adverse Reactions Nursing Considerations and Patient Education Points
Psychosocial issues 3.1 Discuss three evidence-based interventions to help Robert manage his COPD.
Answer
1. Pathophysiology
1.1 Pathophysiology of COPD
Chronic obstructive pulmonary disease (COPD) is a progressive disorder with emphysema (alveolar destruction) and bronchial fibrosis in variable proportions. Inhalational particles such as allergens and chronic bacterial infections generate inflammatory response resulting COPD (A. Bhat and Panzica, 2015). The inflammatory cells are responsible for COPD are a type of white blood cells which include macrophages and neutrophil granulocytes. People having COPD due to smoking have Tc1 lymphocyte involvement. These inflammatory factors produce chemotactic factor in cell.
The factors which are responsible for lung damage are-
1) Due to tobacco smoke, free radicals are generated which results in oxidative stress
2) Discharge of inflammatory cells
3) Proteases damage the connective tissue of lungs
The term umbrella characterizes the chief persistent disorders of lungs e.g emphysema and chronic bronchitis.
Emphysema- it is a disorder of lungs which is responsible for shortness of breath because of over-inflation of air-sacs present in lungs (Sharafkhaneh, Hanania and Kim, 2008). It comes under umbrella term COPD because in emphysema cessation of airflow occurs due to inappropriate exchange of air on person breathing because air sacs are present in lungs. It develops due to cigarette smoking, air pollution, deficiency of an enzyme known as alpha-1-antitrypsin.
Chronic Bronchitis (CB) - it is explained as the generation of persistent cough and release of sputum from last 3 months to 2 consecutive years. It is comes under the umbrella term of COPD because in CB inflammation and lots of mucus get accumulated in bronchi. It is developing because of smoke inhalation, infections occur due to microorganism, and activation of inflammatory cell of mucin gene transcription which oversecrete the mucus by goblet cells and hence restrict airflow pathway (Kim and Criner, 2013).
1.2 Acute exacerbation of COPD
An acute exacerbation of COPD is explained as incidents described by damaged respiratory symptoms of person which is away from regular day-to-day changes and hence result in alteration in medication (Garvey and Ortiz, 2012).
In patients like Robert exacerbations of COPD get high by various factors-
1) As continuous smoking and especially in older age causes lung destruction which leads to high risk of acute exacerbation.
2) Streptococcus pneumonia virus worsens the condition of COPD and leads to acute exacerbation of COPD.
3) Working in chicken farm, there may be presence of influenza virus which also increases the chances of exacerbation of COPD.
Acute exacerbation is life-threatening and leads to negatively affect the treatment of disease. It is started by infection of microorganisms or pollutants. It retards the quality of life, accelerates death rate, and increases lung function damage specifically among hospitalized patients. In acute exacerbation, air entrapment and lung hyperinflation becomes negligible which leads to poor expiratory air flow and accelerate dyspnoea.
1.3 Pathophysiology of pneumonia
It is defined as an inflammatory condition that affects the small air sacs known as alveoli which are present on lungs which leads to abnormal high body temperature and shortness of breath. It is mainly produced by toxic agent like bacteria, viruses and rarely caused by fungi, parasites, certain medications and due to autoimmune diseases.
The pathophysiology is mostly the same, regardless of causative agent.
In this, microorganism invades into the lung with inhalation although microorganism can enter into the lung through the systemic circulation also if any other body part is infected. Mostly, microorganism resides in upper respiratory tract and breath into the alveoli in continuous manner. On reaching in the alveoli, microorganism moves between the gaps and between the adjacent alveoli through linked pores. Due to this, immune system gets activated. It triggers the leukocytes for attacking microorganism to the lungs. The helpful microorganism (neutrophils) invades harmful microorganism and also releases cytokines (Cilloniz and Ignacio, 2016). Hence as a result, cytokines result boost up the immune system which leads to abnormal rise in body temperature, restlessness, chills. Lung damage occur due to attack of microorganism on it and due to production of cytokine in response to immune system, fluid gets leaked into the alveoli which results in impaired oxygen transportation. In addition to damage to lungs, if there is attack of viral organism, it can affect other organs of body also. On bacterial attack, it mostly travel from the lungs to the surrounding blood vessels which result in ill health like septic shock which leads to hypotension results in multiple damage of body parts including brain, kidney, heart.
Community-acquired pneumonia- it is acquired in community. The main difference between community-acquired pneumonia and hospital acquired pneumonia (HAP) is that persons having HAP resides in hospital from long term or recently admitted in hospital. CAP involves less multidrug-resistant bacteria (W. Pletz and G. Rohde, 2016).
Health care–associated pneumonia (HCAP) - It is an infection associated with current exposure to the healthcare system which includes hospitals, nursing home, and dialysis centre.
Hospital-acquired pneumonia- It is acquired in hospital. It is due to the presence of pathogen in the hospital or it may be acquired due to the other patient’s illness. It mostly occurs after the admission of 2-3 days in hospital. It consists of higher risk of multi-drug resistant bacteria.
2. Pharmacology
2.1 Salbutamol
M.O.A- It causes bronchodilatation through ?2 adrenergic receptors stimulation. These receptor are mainly present in bronchial smooth muscle of lungs. Activation of ?2 receptors causes increased in cAMP formation in bronchial muscle cells which results in relaxation of these smooth muscles cells and reduction of airway blockage by decreasing intracellular ionic calcium concentrations. When cAMP level gets increased then it also retards production of many bronchoconstrictor factors e.g allergic histamine, leukotriene from the mast cells in the airways (Ullmann and Caggiano, 2015).
Contraindication- it is contraindicated in persons having hypersensitive reaction like urticaria, angioedema, in patients having cardiac tachyarrhythmias.
Adverse effect- Tremor in skeletal muscle specially in hands, nervousness, headache, tachycardia, palpitation, muscle cramp, hypokalemia, chest discomfort are adverse effect of salbutamol.
Nursing consideration and patient education points-
1) In the patients who suffer from cardiovascular abnormalities, it should be used carefully.
2) If patient is using both tablets and inhaler at one time, monitor the patient for toxicity.
3) If patient is doing exercise, tell him to take inhaler before 15 minutes to workout to avoid exercise-provoked bronchospasm.
4) The patient should know about the danger of paradoxical bronchospam. If it happens patient should cease the administration of drug immediately.
5) Patient should know how to use inhaler properly. Nurses should properly educate the patient about it.
6) If patient is using the steroid inhaler also, then he/she should use bronchodilator first and after that wait for 5 minutes for using steroid.
7) Between puffs of inhaler there should be gap between 2 minutes.
8) To avoid the dry mouth after inhalation, nurses should teach the patient to wash the mouth with water after using each inhalation.
9) The patient should be informed about noxious taste of salbutamol..
Budesonide-
M.O.A- it retards the activity of broad area of inflammatory cells which includes eosinophils, T lymphocytes, macrophages, mast cells, neutrophils (Iborra, 2014).
Contraindication- it is contraindicated in nasal ulcers and in presence of infections. In the initiative medical care of status asthmatics budesonide is contraindicated. The patients who suffers from hypersensitivity of budesonide, it is contraindicated in these patients.
Adverse effect- ankle edema, hirsutism, nausea, rhinitis, arthralgia.
Nursing consideration and patient education points-
1) Nurses should check patient history like nasal infections, nasal surgery etc.
2) Nurses should teach the patients that they do not cut, crush or chew capsule, it should be swallowed completely.
3) Nurses should motivate the patient to compete the drug therapy of 8 weeks.
4) Nurses should monitor the patients for adverse effect of drug like acne, hirsutism, buffalo hump. If this effect occurs then dosage regimen should be decreases.
5) Nurses should teach the patient if they forget to take a capsule a day, then on the next day take the drug at regular time.
6) Nurses should advise the patient to not to take grapefruit juice with this drug.
7) Nurses should aware the side effect of drug to the patients like dizziness, headache, and nausea.
8) If patient feel chest pain, ankle swelling, respiratory infection during the treatment of this drug, he/she should immediately reported.
Tiotropium-
M.O.A- it is a quaternary ammonium compound which is badly absorbed across cell membranes which leads to reducing its effect to the airways after inhalation. There are three types of muscarinic receptors in human airways i.e. M1, M2 and M3. M1 and M3 trigger the release of acetylcholine from vagal nerve endings and hence results in bronchoconstriction.. Tiotropium antagonize the two receptor and results in potent bronchodilation (Halpin, 2016).
Contraindication- it is not used for remedial therapy for acute COPD. If after its administration, hypersensitive reactions like urticaria, swelling of lips, toungue, throat, itching occurs then its therapy should be stop immediately. Tiotropium powder should not be used in eyes because dryness of eyes can be occurring by using it which leads to irritation in eyes. In elderly males having prostatic hypertrophy- urinary retention can occur.
Adverse effect- dry mouth, throat infection, urinary retention, palpitation, increased risk of heart attacks, constipation, acute angle closure glaucoma.
Nursing consideration and patient education points-
1) Do not take the capsule by mouth. Take them only by oral inhalation by Handi Haler device.
2) Use only one capsule at a time.
3) The drug should not be administered for acute bronchospasm although it should be used be used for maintenance remedy of COPD.
4) Nurses should monitor the patient for hypersensitive reactions like angioedema and paradoxical bronchospasm.
5) This medicine should be used in same manner as prescribed by doctor for patient.
Respiratory physician might have changed Robert’s medication regime because the role of inhaled corticosteroid in the management of COPD is still uncertain (Qureshi and Sharafkhaneh, 2014).
2.2
Levofloxacin-
M.O.A- it inhibits the enzyme bacterial DNA gyrase. This enzymes nicks double stranded DNA due to which negative supercoiling occur nicked end get resealed. In gram positive bacteria it inhibits the enzyme topoisomerase IV which nicks and separates daughter DNA strand after DNA replication (J. Aldred and J.kerns, 2014).
Contraindication-
It is contraindicated in patients with known hypersensitivity to levofloxacin
Cardiovascular collapse, hypotension, angioedema may occur.
Adverse drug effect-
Hepatotoxicity, peripheral neuropathy, prolongation of QT interval, blood glucose disturbances, hypersensitive reaction, tendon rupture, crystalluria, photosensitivity.
Nursing consideration and patient education points-
1) Nurses should administer the patient for previous sensitivity reaction like rashes, urticaria.
2) Nurses should examine the patient for possible drug induced adverse reaction.
3) Nurses should monitor the patient for hypersensitivity and thrombophlebitis in routine manner.
4) Nurses should advise the patient to take lots of fluid while taking drug
5) Nurses should teach the patient to report if any joint pain, sore throat, itching, occurs.
6) Patients should be advised to use sunscreen or avoid sun exposure to prevent photosensitivity.
Ceftriaxone
M.O.A-
It is bactericidal in nature and inhibits bacterial cell wall synthesis (Leyenaar, 2014).
Contraindications-
Hypersensitivity, crystalline material was observed in lungs and kidney, prolongation of prothrombin time.
Adverse effect-
Pain after i.m injection, diarrhoea, hypersensitivity reactions like urticaria, asthma, nephrotoxicity.
Nursing consideration and patient education points-
1) Patient should monitor for renal and hepatic function.
2) If hypoprothrombinemia occur, then vitamin K should be given.
3) Patient should be assess for thrombophlebitis.
4) Patient should advise to take the dug with food.
5) Nurses should teach to the patient that they have to avoid alcohol while taking the medication and afterward 3 days on completion of course.
Vancomycin-
M.O.A- it is a glycopeptides antibiotic. It acts by preventing the synthesis of bacterial cell wall. It attached to the peptidoglycan units by terminal dipeptide D-ala-D-ala sequence and hence avoid its cross-linking to form the cell wall of bacteria (Kalil, 2010).
Contraindication-
Rapid i.v injection has caused chills, fever, urticaria and intense flushing known as Red man syndrome.
Adverse effect-
Systemic toxicity, skin allergy, fall in B.P, kidney damage.
Nursing consideration and patient education points-
1) Nurses should assess renal function.
2) If red man syndrome occurs during administration of drug, then give antihistamine to patient.
3) Nurses should avoid extravasations during therapy because necrosis can be occur due to it.
4) Patient should be taught if symptom of superinfection, sore throat, fever occur then he/she should be consult to doctor.
Psychosocial issues
1) Inhaled bronchodilators- ?2 agonists which are short-acting inhalation and anticholinergic drugs treat the COPD. Salbutamol act by triggering the release of cAMP (J, 2001).
2) Formoterol which is long acting ?2 inhalation also recommended for treatment of acute exacerbation of COPD in cumulative manner (Qureshi and Sharafkhaneh, 2014).
3) Antibiotics- there are evidence which supports the need of antibiotics in exacerbation of COPD when there are also signs of bacterial infection. Antibiotics decrease the danger of short-term mortality by 77%.
References-
A. Bhat, T. and Panzica, L. (2015). Immune Dysfunction in Patients with Chronic Obstructive Pulmonary Disease. Annals of the American Thoracic Society.
Cilloniz, C. and Ignacio, M. (2016). Microbial Etiology of Pneumonia: Epidemiology, Diagnosis and Resistance Patterns. International Journal of Molecular Sciences.
Garvey, C. and Ortiz, G. (2012). Exacerbations of Chronic Obstructive Pulmonary Disease. The open nursing journal.
Halpin, D. (2016). Effect of tiotropium on COPD exacerbations: A systematic review. Respiratory Medicine.
Iborra, M. (2014). Long-term safety and efficacy of budesonide in the treatment of ulcerative colitis. Clinical And Experimental Gastroenterology.
J. Aldred, K. and J.kerns, R. (2014). Mechanism of Quinolone Action and Resistance. ACS.
J, M. (2001). Safety of formoterol Turbuhaler at cumulative dose of 90 microg in patients with acute bronchial obstruction. Eur Respir J.
Kalil, A. (2010). Treatment of hospital-acquired pneumonia with linezolid or vancomycin: a systematic review and meta-analysis. BMJ.
Kim, V. and Criner, G. (2013). Chronic Bronchitis and Chronic Obstructive Pulmonary Disease. American Journal of Respiratory and Critical Care Medicine.
Leyenaar, J. (2014). Comparative Effectiveness of Ceftriaxone in Combination with a Macrolide Compared with Ceftriaxone Alone for Pediatric Patients Hospitalized with Community Acquired Pneumonia.
Overington, J. (2014). Implementing clinical guidelines for chronic obstructive pulmonary disease: barriers and solutions. Journal Of Throacic disease.
Qureshi, H. and Sharafkhaneh, A. (2014). Chronic obstructive pulmonary disease exacerbations: latest evidence and clinical implications. Therapeutic Advances in Chronic Disease.
Sharafkhaneh, A., Hanania, N. and Kim, V. (2008). Pathogenesis of Emphysema. American Thoracic Society.
Ullmann, N. and Caggiano, S. (2015). Salbutamol and around. Italian Journal of Pediatrics.
Van Rensburg, D. (2010). Efficacy and Safety of Nemonoxacin versus Levofloxacin for Community-Acquired Pneumonia. Antimicrobial agents and chemotherapy.
W. Pletz, M. and G. Rohde, G. (2016). Advances in the prevention, management, and treatment of community-acquired pneumonia. F1000 Research.
