Pathophysiology Template and Emergency Department: Case Study

Pulmonary function tests

FVC:                 1.8L (75% of predicted)

FEV_1:                1.0L (55.5% of predicted)

FEV₁/FVC:        55% (Normal >70%)

TLC:                 4.5L (109% of predicted)

Chest X-ray

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.

Blood gases

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

Awaiting results.

Mrs White was diagnosed with an acute exacerbation of chronic obstructive pulmonary disease resulting from a respiratory infection.

Management

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.

Answers:

Part 1.

Definition

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.

Aetiology

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.

Pathogenesis

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.

Stimulus

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.

Clinical features

The basic clinical features of COPD include cough, breathing shortness and production of sputum.

Course and prognosis

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.

Diagnosis

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

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.

Prevention

COPD prevention includes mainly smoking cessation, improvement of indoor and outdoor air quality and improvement of occupational health.

Part 2

1. Mrs. White, a 68years old female, presents worsening dyspnoea, increasing production of sputum and cough. She is dyspnoeic, centrally cyanosed and shows pursed-lip breathing. Dyspnoea is said to be the feelings related with weakened breathing. It is considered as a common indication of deep exertion and becomes pathological when it takes place with unexpected conditions, for example: in Mrs. White’s case, COPD. To explain her structural and functional changes within the lungs, it can be said that her ventilator demand might increased because of hypoxemia that provokes the medulla area. However, Mrs. White has a proper oxygen saturation (91%) and almost normal/low carbon dioxide levels (45mm Hg), but still she experiences dyspnoea (YOZA, ARIYOSHI, HONDA, TANIGUCHI & SENJYU, 2009). Therefore, to intervene about her breathing difficulty focus can be put on other mechanisms. Upper airway mechanoreceptors can change the breathlessness perception. Airway dilation receptors also react with lung inflation. In case of Mrs. White it might have happened that the limitation of expiratory airflow caused hyperinflation during rest or activities which stimulated stretch receptors. The results of hyperinflation comprise mechanical restriction to enlarge tidal volume, increase in elastic recoil and compression of the diaphragm, especially the vertical muscle fibers (Ora, Jensen & OʼDonnell, 2010). The increased elastic recoil put an inspiratory load on diaphragm that has functional limitation because of undersized length of the muscle, resulting from hyperinflation.

Mrs. White is centrally cyanosed, which is thought because of an increased level of deoxygenated hemoglobin. Forcing deoxygenated blood in veins to the systemic circulation gives rise to the cyanosis condition. Associated features are dyspnoea, bluish discoloration of fingers, oral mucous membrane and toes. The hyper secretion of mucus is a severe condition which gives rise to neutrophil activation, epithelial injury and chemokines release (Jones et al., 2012). From the case study of Mrs. White, it is seen that she was a heavy smoker and this condition can be accepted as chronic exposure for Mrs. White to develop COPD. In such cases, during the exposure, continuous neutrophil activation takes place and stable secretion of proteases and inflammatory cytokines leads to hyper secretion of sputum. On the other hand, it is reported that neutrophils, which are involved in the airways and their products play important function in EGFR dependent hyper secretion of mucus.

2. Mrs. White has been recommended with Salbutamol and Prednisolone.

Salbutamol administration is useful because it belongs to bronchodilators class and specifically β2-adrenergic agonists (Drugbank.ca, 2015). Salbutamol administered during asthma, chronic bronchitis. It works by relaxing linings of the lung muscle in small airways wall inside lung. Salbutamol dilates airways and helps easier breathing. Salbutamol augments production of cAMP by the activation of adenylate cyclase and salbutamol actions are mediated by cAMP. Increased intracellular cAMP also increases cAMP dependent protein kinase A activity, which inhibits myosin phosphorylation and reduces intracellular calcium concentrations. Lower concentration of the intracellular calcium leads to smooth muscle relaxation and bronchodilation. This drug is commonly applied for bronchospasm, which brings about by chronic bronchitis, bronchial asthma and persistent brnchopumonary complications, for example: COPD. Except bronchodilation, salbutamol inhibits broncho-constricting agents release from mast cells. It slows down microvascular outflow and increases mucociliary clearance.

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.

References

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., & OʼDonnell, 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