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Mrs Ellen White, a 68 year old woman, is brought to the emergency department by her husband. She presents with worsening dyspnoea, cough and increasing sputum production over the past three days.
On examination Mrs White is severely dyspnoeic, centrally cyanosed and exhibits pursed-lip breathing. She is alert and oriented but very anxious. Mrs White is using accessory muscles and on auscultation has decreased breath sounds, prolonged expiration and an expiratory wheeze.
Observations on admission
Temperature: 38.2° C
Pulse: 96 beats/minute
Respiration rate: 28 breaths/minute
Oxygen saturation: 91%
Mrs White began smoking when she was 17 and smoked between 20 and 25 cigarettes a day until 10 years ago when she was diagnosed with pulmonary emphysema. Mrs White lives with her husband and is experiencing more difficulty with her usual activities due to increasing breathlessness. The medications that she has been taking are tiotropium bromide (Spiriva®) inhaler once daily and salbutamol inhaler every 4-6 hours when required.
Results of tests and investigations
Pulmonary function tests
FVC: 1.8L (75% of predicted)
FEV1: 1.0L (55.5% of predicted)
FEV1/FVC: 55% (Normal >70%)
TLC: 4.5L (109% of predicted)
The chest X-ray shows a flattened diaphragm and lung hyperinflation with a translucent appearance of the lungs and no cardiac enlargement. The AP (anterior-posterior) diameter of the chest is increased. These changes are suggestive of COPD.
pH: 7.30 (7.35-7.45)
PaO2: 45 mmHg (80-100 mmHg)
PaCO2: 51 mmHg (35-45 mmHg)
Bicarbonate: 36 mmHg (21-28 mmHg)
Sputum culture and sensitivity
Mrs White was diagnosed with an acute exacerbation of chronic obstructive pulmonary disease resulting from a respiratory infection.
Oxygen: 2L/minute via nasal prongs.
Salbutamol: 400 micrograms and ipratropium 80 micrograms via metered dose inhaler and spacer 4th hourly prn.
Prednisolone: 40 mg orally daily for one week.
Doxycycline: 100mg orally daily.
Mrs White is transferred to a medical ward.
Part 1 - Pathophysiology template
Complete a pathophysiology template related to the case study.
Part 2 - Questions related to the case study
1. Explain how two of Mrs White’s clinical manifestations are related to the structural and functional changes of her chronic obstructive pulmonary disease.
2. Select two drugs that have been used to treat Mrs White’s chronic obstructive pulmonary disease. Discuss the rationales for the administration of these drugs. Relate your discussion to the pathophysiological process.
COPD or chronic obstructive pulmonary disease is a type of obstructive lung infection exemplified by steady poor airflow. It deteriorates eventually. COPD occurs as constant and considerable inflammatory response to inhaled irritants (MacNee & Rennard, 2009). Frequent bacterial infection may involve in inflammatory condition. Poor airflow in COPD is the result of lung tissue destruction that is also termed as emphysema. COPD that is connected with small airways is identified as obstructive bronchitis.
Cigarette smoking is considered as the main cause of COPD and the other associated factors are air pollution and genetic factors. The probability of COPD development increases with total smoking exposure (Cazzola, 2009). Poor ventilation of cooking fires, biomass fuels lead to air pollution and also considered as one of the most important causes of COPD. Other risk factors may include asthma, a constant airway complication and smoking raises the chance of COPD especially.
Small airways damage causes the formation of big air pouches that is medically known as bullae. This formation changes lungs tissue. These problems are referred to as bullous emphysema. Inflammatory cells for example: neutrophil granulocytes, macrophages and few white blood cells are associated with COPD (Anzueto, 2009). In addition smokers pose eosinophil, TC1and lymphocyte association. Narrowing down of airways takes place due to scar formation and inflammation. This is somewhat responsible for inability to breathe out completely. Decrease in highest airflow occurs while breathing out. This is because chest pressure compresses airways during this incidence.
Chest pressure compression gives rise to air from previous left over breath in lungs when next breath is started. This causes increase in total air volume inside lungs. This method is identified as hyperinflation or air trapping. Normal alveolar ventilation is the amount of air volume that reaches to the alveoli and accessible for gaseous exchange with blood per unit volume (Morris, 2009). But in COPD, individual has lesser oxygen levels and elevated levels of carbon dioxide levels in blood; this takes place from deprived gaseous exchange due to airway obstruction, decreased ventilation from hyperinflation and lessened want for breathe.
The basic clinical features of COPD include cough, breathing shortness and production of sputum.
It varies with disease stage, clinical phenotype and therapy responses. Heavier smokers, smokers with marked hyperinflation, diffusion abnormality, without atopy features and poor response to bronchodilators usually have worst prognosis (Suzuki et al., 2013). Cessation of smoking can alter the course and diagnosis of COPD.
COPD diagnosis includes spirometry measures, which measures the airflow obstruction and is commonly performed after the application of bronchodilator, which is a drug to open the airways (Chavez & Shokar, 2009). Chest X-ray and completed blood counts are also useful to eliminate complicated conditions during COPD diagnosis.
Treatment of COPD includes bronchodilators, exercise, corticosteroids and few antibiotics. The anticholinergics and beta2 agonists are effective in breathing complications and wheeze. Corticosteroids are generally administered in inhaled form and tablets forms are also used to treat acute exacerbations. Pulmonary rehabilitation is considered as a good exercise program, disease counseling and management benefit COPD affected individual.
COPD prevention includes mainly smoking cessation, improvement of indoor and outdoor air quality and improvement of occupational health.
Prednisolone is a glucocorticoid, a cortisol derivative that is applied to treat various auto-immune and inflammatory responses. Recommendation of this medication is significant for Mrs. White because in case of COPD scar tissue formation takes place inside the lungs. Corticoids inhibit inflammatory response and protect the lungs from the accumulation of collagen and formation of scar tissues. Prednisolone usually binds with the GR receptors or glucocorticoid receptors, irreversibly. Prednisolone can influence and activates the biochemical functions of most of the cells. Regulation of genetic expression (such as: inhibition of COX-2 gene transcription) leads to inflammation suppression and suppression of immune response. This is clinically useful.
Anzueto, A. (2009). The pathogenesis of acute infection in COPD. Breathe, 5(4), 311-315. doi:10.1183/18106838.0504.311
Cazzola, M. (2009). Acute exacerbations in COPD. Oxford: Clinical Pub.
Chavez, P., & Shokar, N. (2009). Diagnosis and Management of Chronic Obstructive Pulmonary Disease (COPD) in a Primary Care Clinic. COPD, 6(6), 446-451. doi:10.3109/15412550903341455
Drugbank.ca,. (2015). DrugBank: Salbutamol (DB01001). Retrieved 1 April 2015, from https://www.drugbank.ca/drugs/DB01001
Jones, B., Pepe, S., Sheeran, F., Donath, S., Hardy, P., & Shekerdemian, L. et al. (2012). Remote Ischaemic Preconditioning Fails to Protect Cyanosed Neonates Undergoing Cardiopulmonary Bypass: A Randomised Controlled Trial. Heart, Lung And Circulation, 21, S298. doi:10.1016/j.hlc.2012.05.731
MacNee, W., & Rennard, S. (2009). Chronic Obstructive Pulmonary Disease. Abingdon: HEALTH Press.
Morris, C. (2009). The impact of distractive auditory stimuli on indicators of health-related quality of life in patients with COPD.
Ora, J., Jensen, D., & OÊ¼Donnell, D. (2010). Exertional dyspnea in chronic obstructive pulmonary disease: mechanisms and treatment approaches. Current Opinion In Pulmonary Medicine, 16(2), 144-149. doi:10.1097/mcp.0b013e328334a728
Suzuki, M., Makita, H., Ito, Y., Nagai, K., Konno, S., & Nishimura, M. (2013). Clinical features and determinants of COPD exacerbation in the Hokkaido COPD cohort study. European Respiratory Journal, 43(5), 1289-1297. doi:10.1183/09031936.00110213
YOZA, Y., ARIYOSHI, K., HONDA, S., TANIGUCHI, H., & SENJYU, H. (2009). Development of an activity of daily living scale for patients with COPD: The Activity of Daily Living Dyspnoea scale.Respirology, 14(3), 429-435. doi:10.1111/j.1440-1843.2009.01479.x
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