Chronic Obstructive Pulmonary Disease

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Сhrоniс Оbstruсtivе Рulmоnаry Disеаsе (COPD)

Сhrоniс Оbstruсtivе Рulmоnаry Disеаsе (COPD)

Part 1: Pathophysiology Template related to the Study

COPD is an extra-pulmonary disease state. Its indications include reduced progressive flow of airway that is preventable and curable but not completely irreversibly (Kon, Hansel, & Barnes, 2009).


Through smoking, over 400 chemicals and gases are inhaled. Of the 400, about 43 are known to be mutagens, carcinogen, and noxious inflammatory irritants. Genetically, those who lack Alpha-1 antitrypsin have a risk of the disease. In terms of race, Caucasians are at a higher risk than Asians and Blacks due to higher occurrence of Alpha-1 antitrypsin. Age is also associated to it with regards to the structural changes in the respiratory muscles, lungs and thoracic cage (Allen, 2010).


An accumulation of lymphocytes, neutophils, and macrophages is caused by inhaled irritants. The three later become chemoattractants that lead to mast and globlet hyperplasia, which further causes hypersecretion of mucus. This reduces the dimension of the airway and enhances hardship in the removal of secretions that makes the ciliary defense mechanism weak (Durstine & Moore, 2009).


Some of the common symptoms of COPD include sputum production, wheezing, and chronic persistent cough. When the state worsens, the patient faces dyspnoea on exertion and at rest. Swollen alveolar together with enhanced air trapping leads to a flattened diaphragm, and a barrel shaped chest; hence difficulty in abdominal breathing. This leads the patient to settle on pused-lip breathing, tripod positioning, and use of accessory muscles (McCance & Huether, 2013).


Acute respiratory distress syndrome may occur due to infective exacerbation. As a result of hypersecretion of gastric juices and enhanced arterial carbon dioxide, gastric ulcer may take place. Additionally, just as Ellen’s case, pulmonary vessel resistance, blood viscosity, and hypertension may be increased due to hypoxia induced polycythaemia (Wells, DiPiro, & Schwinghammer, 2014).


This is quite difficult although the main predictors include FEV₁ and age.


The use of smoking history, physical examination, history of exposure to environmental pollution is helpful in diagnosis of COPD. COPD can be confirmed with pulmonary function test by use of spirometry that stages COPD and a forced expiratory volume in one second/forced vital capacity of less than 70 percent. Additionally, low levels of the disease can be indicated by AAT screening. Hyperinflated lungs and flattened diaphragm can be shown by chest radiography, which can as well rule out cor-pulmonale (Green, 2007).

Treatment and prevention

Anxiety and depression can be relieved through behavioural and cognitive therapy. Enhancement of bronchodilation and prevention of bronchoconstriction can be done by a beta-adrenoreceptor agonist, salbutamol and an anticholinergic, ipratropium. Additionally, An oral corticosteroid, prednisone controls inflammation. Prevention of COPD can be through having yearly flu vaccine, cessation of smoking, and avoiding crowded environments in winter (Martin, 2011).

Part 2: Questions related to case study

Question 1

The functional and structural changes faced by Mrs. White are a result of a huge history of smoking. It is through smoking that she inhaled noxious substances and irritants that led to the inflammation of the airway epithelium. This was done by initiating a buildup of inflammatory cells that include lymphocytes, neutrophils, as well as macrophages. When these cells were activated, they ended up being chemoattractants and initiated the release of inflammatory mediators and oxidants (Allen, 2010).

The inflammatory substances tend to activate a hyperproduction of mucus as well as hyperplasia of globlet and mucus glands. The sticky mucus creates a platform for bacteria to implant and impair a defensive ciliary mechanism by hindering clearance of mucus. As a result, the bronchial wall becomes inflamed due to oedema and infiltrated inflammatory cells. This eventually leads to narrowing of the airway and bronchospasm (Kon, Hansel, & Barnes, 2009).

Later, the airway collapses early in expiration. This contributes to trapping of gas in the distal section of the lungs causing reduction in FEV₁ as well as FVC ; hence increased total lung capacity. Additionally, the airway dimension is reduced by persistent remodeling in response to injury as a result of scar tissue accumulation, peri-bronchial fibrosis, and excessive epithelial cells lining the airway. Later, chances of getting emphesema and bronchitis become obvious because of parenchymal damage linked to loss of lung tissue elasticity. For purposes of protecting the damage of lung protein by proteolytic enzymes such as metalloprotease and elastaste, the liver secretes an antiprotease AAT that is found in the lungs. On the other hand, smoking releases cytokines that eventually leads to outnumbering of AAT by proteolytic enzymes. Eventually, the loss of elastin in alveolar and bronchial walls is caused by the mismatch of protease to antiprotease (Martin R. , 2010).

As a result of elastic recoil loss, there is reduction in the volume of air that can be expired passively. The alveolar hyperinflates then progressively forms larger air segments within the lungs known as the bullae and the entrapment of air spaces neighboring the pleura called blebs. Eventually, pressure is exerted on the diaphragm with the increase in total lung capacity which makes it flat. At this particular stage, Mrs. White ends up breathing from partially inflated lungs with poor abdominal breathing. As a chest breather, she depends on muscles such as scalene and sternocleidomastoid (Durstine & Moore, 2009).

With time, the pulmonary vessels become thick as the inflammatory cells infiltrate blood vessels. There is loss of capillaries within alveoli and a ventilation perfusion mismatch since the perfusion of gases is impaired. Later, collagen gets deposited in pulmonary vessels enhancing the risk of pulmonary hypertension (Durstine & Moore, 2009).

Question 2

  1. Increasing Blood Pressure

At normalcy, the blood pressure is 60-90 and 90-120 millimeter mercury for diastolic and systolic respectively. In COPD, vessel constriction causes pulmonary hypertension in response to an atomic reduction of the pulmonary bed and hypoxia. This is because of an inflammatory induced remodeling. Additionally, hypoxia tends to induce blood viscosity, erythropoesis, and polycythaemia. This enhances vascular resistance leading to blood pressure. In severe cases, the pulmonary capillary is made thick by a deposition of collagen and inflammatory cells. Apart from that, increased pressure is exerted on the right side of the heart by the development of pulmonary hypertension; hence causing hypertrophy. However, Cor-pulmonale is not evident in Mrs. White at this stage but there exists a worrying and warning hypoxic sign like central cyanosis (Martin J. , 2011).

  1. Dyspnoea

This is led by an impediment of the airway as a result of bronchial cascade linked to a syndrome of bronchospasm, oedema, globlet cell hyperplasia and mucus plugging that captures air and reduces airway dimension. In addition, hyperinflation of the lungs is enhanced by destroyed and fibrotic alveolar attachments with blebs and bullae with loss of elastic recoil. This is to the extent that the pressure exerted on the diaphragm makes it flat-shaped and weakens its role functionally as a major muscle of respiration. This causes dyspnoea and enhanced work of breathing and Mrs. White settles on easing respiratory distress by sternocleidomastoid and scalene muscles, tachypnoea, pursed- lip breathing and tripod position as compensatory mechanisms to deter retained carbon dioxide (Kon, Hansel, & Barnes, 2009).

Question 3

  1. Salbutamol

Salbutamol is a short acting beta-adrenoreceptor agonist that works through selectively binding to beta adrenergic receptors in bronchial smooth muscles. This leads to bronchodilation; hence relieving bronchospasm, which is a pathophysiologic characteristic during an infective exacerbation of COPD. Through this, the diameter of the airway widens and the reversal of increase work of breathing, hypercapnia, wheezing, and ultimately the respiratory acidosis indicated in the blood gas results (Tainas, 2013).

The drug also potentiates drainage of mucus and slows down discharge of inflammatory mediators from mast cells. Delivery of the drug efficiently to the lungs is made possible by the spacer. Inhaled salbutamol has an onset of 5-15 minutes, a peak effect of ½ to 2 hours and a half life of 2-6 hours. The drug has side effects including nervousness, dry mouth, headache, tachycardia, palpitation, and throat irritation (Martin R. , 2010).

  1. Doxycycline

This is a bacteriostatic and broad-spectrum antibiotic belonging to the tetracycline family. It works by hindering protein synthesis through reversibly blocking the 30S subunit of ribosome. Therefore, it prevents access of transfer ribonucleic acid [tRNA] to messenger RNA [Mrna] complex (Allen, 2010).

As a result of its activity against both gram positive and gram negative bacteria, the drug has been temporarily prescribed to battle susceptible strains of bacteria such as Haemophilus influenza, Streptococcus pneumonia, Moraxella catarrhalis that are frequently isolated during infective exacerbation of COPD (Allen, 2010).

A more precise and sensitive antibiotic is to be prescribed at a time when sputum culture and sensitivity results are made available. The drug is given once daily. Some of the side effects are nausea, diarrhoea and epigastric burning.


Allen, T. (2010). Positive Options for Living with COPD: Self-Help and Treatment for Chronic Obstructive Pulmonary Disease. Chicago: Hunter House.

Durstine, L., & Moore, G. (2009). ACSM’s Exercise Management for Persons with Chronic Diseases and Disabilities-3rd Edition. New York: Human Kinetics.

Green, R. (2007). Natural Therapies for Emphysema and COPD: Relief and Healing for Chronic Pulmonary Disorders . Chicago: Healing Arts Press.

Kon, O. M., Hansel, T., & Barnes, P. (2009). Chronic Obstructive Pulmonary Disease (COPD) .
Oxford: Oxford University Press.

Martin, J. (2011). Live Your Life With COPD- 52 Weeks of Health, Happiness and Hope. New York: Infinity Publishing.

Martin, R. (2010). The Complete Guide to Understanding and Living with COPD: From A COPDer’s Perspective. London: CreateSpace Independent Publishing Platform.

McCance, K., & Huether, S. (2013). Pathophysiology: The Biologic Basis for Disease in Adults and Children. Chicago: Mosby.

Tainas, S. (2013). Understanding COPD and other Respiratory Diseases and Pulmonary Disorders. New York: Sage.

Wells, B., DiPiro, J., & Schwinghammer, T. (2014). Pharmacotherapy Handbook. New York: McGraw-Hill Medical.