Table of ContentsPART 1.........................................................................................................................................................1

Pathophysiological Template...................................................................................................................1

PART 2.........................................................................................................................................................2

Question 1...............................................................................................................................................2

Question 2...............................................................................................................................................3

Question 3...............................................................................................................................................5

References...................................................................................................................................................6

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PART 1

Pathophysiological TemplateThe primary risk factor for COPD is chronic tobacco smoking (Rennard &Vestbo2006). Lung

damage and inflammation in the large airways results in chronic bronchitis which is defined as a

cough with sputum production on most days for 3 months of a year, for 2 consecutive years

(Longmore, Murray,Wilkinson & Supraj,2004).In the airways of the lung, the hallmarks of

chronic bronchitis is hyperplasia and hypertrophy of the goblet cells and mucous glands of the

airway this results in more mucus in the airways, contributing to narrowing of the airways and

causing a cough with sputum. Lung damage and inflammation of the air sacs (alveoli) results in

emphysema defined as enlargement of the air spaces distal to the terminal bronchioles, with

destruction of their walls (Longmore et al, 2004) The destruction of air space walls reduces the

surface area available for the exchange of oxygen and carbon dioxide during breathing and the

elasticity of the lung itself, resulting in a loss of support for the airways.

The diagnosis of COPD should be considered in anyone who has dyspnea, chronic cough or

sputum production, history of regular tobacco smoking (Rabe, Hurd & Anzueto A, et al.(2007).

Cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur

due to respiratory failure. The diagnosis of COPD is confirmed by spirometry(Rabe et al.(2007)

a test that measures FEV1 and FVC, the diagnosis of COPD is made when the FEV1/FVC ratio

is <70 %.(Nathell, Malmberg,& Larsson,(2007). On chest x-ray, the classic signs of COPD are

hyperinflation, a flattened diaphragm, increased retrosternal airspace, and bullae (Torres M,

Moayedi, 2007).

Management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy

(often using inhalers). Some patients go on to require long-term oxygen therapy or lung

transplantation. ( Rabe et al,2007). Most COPD drugs work by keeping airways as wide open as

possible (Hall & Ahmed, 2007). Bronchodilators are medicines that relax smooth muscle around

the airways, increasing the calibre of the airways and improving air flow. They can reduce the

symptoms of shortness of breath, wheeze and exercise limitation (Liesker etal, 2002)

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Corticosteroids are used in tablet or inhaled form to treat and prevent acute exacerbations of

COPD

The factors that predict a poorer prognosis are; Low FEV1, poor exercise capacity, shortness of

breath, significantly underweight or overweight, complications like respiratory failure, continued

smoking, frequent acute exacerbations (Rabe et al, 2007).

COPD can be prevented by avoiding long-term inhalation of pollutants smokers who quit before

developing symptoms of COPD can often reduce the decline in their lung functions to nearly

normal levels within a few years of remaining smoke free (Lokke et al, 2007)

PART 2

Question 1Explain the pathogenesis that leads to the structural and functional changes resulting from

Mrs. White’s Chronic Obstructive Pulmonary Disease

COPD comprises a collection of different processes, including chronic or recurrent bronchitis,

emphysema, and airway responsiveness that contribute to the disease. The most important risk

factor is cigarette smoking, which can affect the lungs by a variety of mechanisms, (Rennard et

al, 1998). Other factors, including occupational or environmental exposures to dusts, gases,

vapors, biomass smoke, malnutrition, early life infections, recurrent respiratory infections

(Pauwels et al, 2001), Factors in addition to exposures, including both genetic (Silverman et al,

2001) and acquired conditions (Buist et al, 1994), also play a role and likely account for much of

the variable susceptibility of individuals to the effects of cigarette smoke and other exposures

and genetic predisposition

Chronic or recurrent bronchitis is a major component of COPD. It consists of bouts of increased

cough and sputum production that can occur frequently. The attacks may be related to an acute

bacterial or viral infection. The cough and sputum production that define chronic bronchitis

result from an innate immune response to inhaled toxic particles and gases in cigarette smoke. In

chronic bronchitis there is inflammation in the epithelium of the central airways and in the

Mucus-producing glands (Hogg, 2004) this airway inflammation is associated with increased

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mucus production, reduced mucociliary clearance, and increased permeability of the airspace

epithelial barrier.

Emphysema, another component of COPD, entails the destruction of alveoli (air sacs) in the

lungs, impairing their ability to bring oxygen into the body and eliminate carbon dioxide.

Emphysematous lung destruction reduces maximal expiratory airflow by decreasing the elastic

recoil force that drives air out of the lungs. There is a relationship between the degree of

emphysema and pack-yr of smoking, only about 40% of heavy smokers develop substantial lung

destruction from emphysema, and emphysema can be found in some individuals who have

normal lung function (Hogg, 2004)

The pathological hallmarks of COPD are destruction of the lung parenchyma, which

characterizes emphysema, inflammation of the peripheral airways, which characterizes

bronchiolitis, and inflammation of the central airways which characterizes chronic bronchitis.

The functional consequence of these abnormalities is expiratory airflow limitation. Emphysema

will contribute to the airflow limitation by reducing the elastic recoil of the lung through

parenchymal destruction, as well as by reducing the elastic load applied to the airways through

destruction of alveolar attachments. On the other hand, bronchiolitis will contribute to the

airflow limitation by narrowing and obliterating the lumen and by actively constricting the

airways. In summary, pathological changes in COPD can be found in central airways, peripheral

airways, lung parenchyma and pulmonary arteries

Question 2Explain how three of Mrs. White clinical manifestations are related to the structural and

functional changes of her chronic

COPD comprises a collection of different processes, including chronic or recurrent bronchitis,

emphysema, and airway responsiveness that contribute to the disease. The most important risk

factor is cigarette smoking, which can affect the lungs by a variety of mechanisms, (Rennard et

al, 1998), Other factors, including occupational or environmental exposures to dusts, gases,

vapors, biomass smoke, malnutrition, early life infections, recurrent respiratory infections

(Pauwels et al, 2001), Factors in addition to exposures, including both genetic[Silverman et al,

2001) and acquired conditions(Buist et al,1994), also play a role and likely account for much of

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the variable susceptibility of individuals to the effects of cigarette smoke and other exposures

and genetic predisposition

Chronic or recurrent bronchitis is a major component of COPD. It consists of bouts of increased

cough and sputum production that can occur frequently. The attacks may be related to an acute

bacterial or viral infection.

The cough and sputum production that define chronic bronchitis result from an innate immune

response to inhaled toxic particles and gases in cigarette smoke. In chronic bronchitis there is

inflammation in the epithelium of the central airways and in the Mucus-producing glands (Hogg,

2004) this airway inflammation is associated with increased mucus production, reduced

mucociliary clearance, and increased permeability of the airspace epithelial barrier.

Emphysema, another component of COPD, entails the destruction of alveoli (air sacs) in the

lungs, impairing their ability to bring oxygen into the body and eliminate carbon dioxide.

Emphysematous lung destruction reduces maximal expiratory airflow by decreasing the elastic

recoil force that drives air out of the lungs. There is a relationship between the degree of

emphysema and pack-yr of smoking, but not a strong one. Only about 40% of heavy smokers

develop substantial lung destruction from emphysema, and emphysema can be found in some

individuals who have normal lung function (Hogg, 2004)

The pathological hallmarks of COPD are destruction of the lung parenchyma, which

characterizes emphysema, inflammation of the peripheral airways, which characterizes

bronchiolitis, and inflammation of the central airways which characterizes chronic bronchitis.

The functional consequence of these abnormalities is expiratory airflow limitation. Emphysema

will contribute to the airflow limitation by reducing the elastic recoil of the lung through

parenchymal destruction, as well as by reducing the elastic load applied to the airways through

destruction of alveolar attachments. On the other hand, bronchiolitis will contribute to the

airflow limitation by narrowing and obliterating the lumen and by actively constricting the

airways. In summary, pathological changes in COPD can be found in central airways, peripheral

airways, lung parenchyma and pulmonary arteries

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Question 3Select 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

Ipratropium

It is a short acting anticholinergic drug which relax airway, muscles by blocking the effect of

acetylcholine. Its side effects are in the periphery, causing, for example, pupillary dilation,

blurred vision, and dry mouth (Hall & Ahmed, 2007). It takes effect in 15 to 30 minutes, has its

peak action in 1 to 2 hours, and lasts 4 to 6 hours. It is given as a first step in counteracting the

sudden worsening of lung functions. All symptomatic patients are prescribed a short-acting

bronchodilator that they can use to recover from a bout of suddenly worsening dyspnea

(Restrepo, 2009).

Salbutamol

It is short-acting beta2 agonists, it stimulate the beta2-adrenergic neuroreceptors and cause

smooth muscles to relax; this widens airways. Muscle tremors and heart palpitations are the most

common side effects of beta2 agonists, but when the medicines are inhaled, the side effects are

usually mild; it is one of most commonly prescribed sympathetic bronchodilators.

Short-acting beta2 agonists are used as rescue medicines when a patient needs immediate relief

from sudden episodes of increased dyspnea. All symptomatic patients are prescribed a short-

acting bronchodilator that they can use to recover from a bout of suddenly worsening dyspnea

(Restrepo, 2009).The drug has a rapid onset of action, reaches peak activity at between 10 and 30

minutes, and remains effective for between four and six hours.

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ReferencesRennard, S. I, Vestbo, J.R, (2006). "COPD: the dangerous underestimate of 15%". The Lancet

367 (9518): 1216.doi:10.1016/S0140-6736(06)68516-4.)

Longmore, J. M.,& Murray, L., Wilkinson, I.,& Supraj, R.,& Rajagopalan (2004). Oxford handbook of clinical medicine. Oxford [Oxfordshire]: Oxford University Press. pp. 188–9. 

Rabe KF, Hurd S, Anzueto A, et al.(2007). "Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary". Am. J. Respir. Crit. Care Med. 176 (6): 532–55.

Nathell, L., Nathell, M.,& Malmberg, P.,& Larsson, K. (2007). "COPD diagnosis related to different guidelines and spirometry techniques". Respiratory research 8(1): 89. doi:10.1186/1465-9921-8-89. PMC 2217523. PMID 18053200.[1]

Torres, M., &Moayedi, S. (May 2007). "Evaluation of the acutely dyspneic elderly patient".Clin. Geriatr. Med. 23 (2): 307–25, vi. doi:10.1016/j.cger.2007.01.007.PMID 17462519.

Liesker, JJ,. Wijkstra, PJ. &Ten Hacken, NH., Koëter, GH., Postma, DS.,& Kerstjens HA (February 2002). "A systematic review of the effects of bronchodilators on exercise capacity in patients with COPD".Chest 121 (2): 597–608.doi:10.1378/chest.121.2.597.PMID 11834677.

Lokke, A., Lange, P., Scharling, H., et al. (2007) Developing COPD: A 25-year follow-up study of the general population. Thorax, 61(11), 935–39. Available online at http://thorax.bmj.com/cgi/reprint/61/11/935.

Buist AS, Vollmer WM(1994). Smoking and other risk factors. In: Murray JF, Nadel JA, eds. Textbook of Respiratory Medicine. Philadelphia: WB Saunders:1259-1287

Hogg JC. Pathophysiology of airflow limitation in chronic obstructive pulmonary disease. Lancet 2004;364:709–721.

Silverman EK, Chapman HA, Drazen JM, et al. (June 1998)."Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis". Am. J. Respir. Crit. Care Med. 157 (6 Pt 1): 1770–8

Restrepo, R. D. (2009). A stepwise approach to management of stable COPD with inhaled pharmacotherapy: A review. Respiratory Care,54(8), 1058–1081

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