COPD Flashcards

1
Q

Summarise COPD

A

Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow limitation that is not fully reversible.

Suspected in patients with a history of smoking, occupational and environmental risk factors, or a personal or family history of chronic lung disease.

Presents with progressive shortness of breath, wheeze, cough, and sputum production, including haemoptysis.

Diagnostic tests include pulmonary function tests, chest x-ray, chest computed tomography scan, oximetry, and arterial blood gas analysis.

Patients should be encouraged to stop smoking or occupational exposure and be vaccinated against viral influenza and Streptococcus pneumoniae.

Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids.

Long-term oxygen therapy improves survival in severe COPD

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2
Q

Define COPD

A

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases. It is primarily caused by cigarette smoking. Although COPD affects the lungs, it also has significant systemic consequences. Exacerbations and comorbidities are important contributors to the overall condition and prognosis in individual patients.

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3
Q

Describe the epidemiology of COPD

A

COPD is more common in older people, especially those aged 65 years and older. The Burden of Obstructive Lung Disease (BOLD) Initiative estimates a worldwide population prevalence of COPD for stages II or higher as equivalent to 10.1 ± 4.8% overall with 11.8 ± 7.9% for men and 8.5 ± 5.8% for women.[5] Its associated mortality in women has more than doubled over the past 20 years and now matches that in men. The number of COPD cases in the US has increased by 41% since 1982, and COPD affects 1% to 3% of white women and 4% to 6% of white men. COPD is now projected to be the third leading cause of death in the world by 2020.[1][6] This is because of the expanding epidemic of smoking and ageing of the world population and reduced mortality from other causes of death such as cardiovascular disease.[1][7] A systematic review and meta-analysis has shown that the prevalence of COPD in adult offspring of people with COPD is greater than population-based estimates.[8] A retrospective study conducted in the UK between 1990 and 1997 estimated COPD prevalence to be 2% in men and 1% in women

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4
Q

Describe the aetiology of COPD

A

Tobacco smoking is by far the main risk factor for COPD. It is responsible for 40% to 70% of COPD cases and exerts its effect by causing an inflammatory response, cilia dysfunction, and oxidative injury. Air pollution and occupational exposure are other common aetiologies. Oxidative stress and an imbalance in proteinases and antiproteinases are also important factors in the pathogenesis of COPD, especially in patients with alpha-1 antitrypsin deficiency, who have panacinar emphysema that usually presents at an early age

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5
Q

What is the hallmark feature of COPD

A

The hallmark of COPD is chronic inflammation that affects central airways, peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature. The main components of these changes are narrowing and remodelling of airways, increased number of goblet cells, enlargement of mucus-secreting glands of the central airways, and, finally, subsequent vascular bed changes leading to pulmonary hypertension. This is thought to lead to the pathological changes that define the clinical presentation.

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6
Q

Describe the host response in COPD

A

Evidence suggests that the host response to inhaled stimuli generates the inflammatory reaction responsible for the changes in the airways, alveoli, and pulmonary blood vessels. Activated macrophages, neutrophils, and leukocytes are the core cells in this process. In contrast to asthma, eosinophils play no role in COPD, except for occasional acute exacerbations. However, a patient-level meta-analysis found that patients with COPD with lower blood eosinophil counts have more pneumonia events than do those with higher counts.[

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7
Q

Describe the two subtypes of COPD

A

In emphysema, which is a subtype of COPD, the final outcome of the inflammatory responses is elastin breakdown and subsequent loss of alveolar integrity.[11] In chronic bronchitis, another phenotype of COPD, these inflammatory changes lead to ciliary dysfunction and increased goblet cell size and number, which leads to the excessive mucus secretion. These changes are responsible for decreased airflow, hypersecretion, and chronic cough. In both conditions, changes are progressive and usually not reversible.

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8
Q

What is the physiological definition of COPD

A

Increased airway resistance is the physiological definition of COPD. Decreased elastic recoil, fibrotic changes in lung parenchyma, and luminal obstruction of airways by secretions all contribute to increased airways resistance. Expiratory flow limitation promotes hyperinflation. This finding, in addition to destruction of lung parenchyma, predisposes COPD patients to hypoxia, particularly during activity. Progressive hypoxia causes vascular smooth muscle thickening with subsequent pulmonary hypertension, which is a late development conveying a poor prognosis.

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9
Q

Describe one typical case history for COPD

A

A 66-year-old man with a smoking history of one pack per day for the past 47 years presents with progressive shortness of breath and chronic cough, productive of yellowish sputum, for the past 2 years. On examination he appears cachectic and in moderate respiratory distress, especially after walking to the examination room, and has pursed-lip breathing. His neck veins are mildly distended. Lung examination reveals a barrel chest and poor air entry bilaterally, with moderate inspiratory and expiratory wheezing. Heart and abdominal examination are within normal limits. Lower extremities exhibit scant pitting oedema.

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10
Q

Describe a second typical case history for COPD

A

A 56-year-old woman with a history of smoking presents to her primary care physician with shortness of breath and cough for several days. Her symptoms began 3 days ago with rhinorrhoea. She reports a chronic morning cough productive of white sputum, which has increased over the past 2 days. She has had similar episodes each winter for the past 4 years. She has smoked 1 to 2 packs of cigarettes per day for 40 years and continues to smoke. She denies haemoptysis, chills, or weight loss and has not received any relief from over-the-counter cough preparations.

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11
Q

Describe some other typical presentations for COPD

A

Other presentations include weight loss, haemoptysis, cyanosis, and morning headaches secondary to hypercapnia. Physical examination may demonstrate hypoxia, use of accessory muscles, paradoxical rib movements, distant heart sounds, lower-extremity oedema and hepatomegaly secondary to cor pulmonale, and asterixis secondary to hypercapnia. Patients may also present with signs and symptoms of COPD complications. These include severe shortness of breath, severely decreased air entry, and chest pain secondary to an acute COPD exacerbation or spontaneous pneumothorax.[2][3] Patients with COPD often have other comorbidities, including cardiovascular disease,[4] skeletal muscle dysfunction, metabolic syndrome and diabetes, osteoporosis, depression, lung cancer, gastro-oesophageal reflux disease, bronchiectasis, and obstructive sleep apnoea

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12
Q

Describe an approach to the history in patients with COPD

A

COPD has an insidious onset and usually presents in older people. A history of productive cough, wheezing, and shortness of breath, particularly with exercise, is typical. Patients may complain of fatigue as a result of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia and hypercapnia. The patient’s smoking history, occupational exposures, and any family history of lung disease should be determined.

Patients with COPD may also present with acute, severe shortness of breath, fever, and chest pain during acute infectious exacerbation. See our topic on Acute exacerbation of chronic obstructive pulmonary disease for further information.

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13
Q

Describe the physical examination in COPD

A

Examination may show tachypnoea, respiratory distress, use of accessory muscles, and intercostal retraction. Barrel chest is a common observation. There may be hyper-resonance on percussion, and distant breath sounds and poor air movement on auscultation. Wheezing, coarse crackles, clubbing, and cyanosis, as well as signs of right-sided heart failure (distended neck veins, loud P2, hepatomegaly, hepatojugular reflux, and lower-extremity oedema), may be present. Occasionally patients may exhibit asterixis - loss of postural control in the outstretched arms (commonly known as a flap) caused by hypercapnia. This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of respiratory failure.

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14
Q

Describe the initial tests in COPD

A

Spirometry is the first test for diagnosis of COPD and for monitoring disease progress. Patients with COPD have a distinctive pattern seen on spirometry, with a reduced FEV1 and FEV1/FVC ratio. The presence of airflow limitation is defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria as a post-bronchodilator FEV1/FVC <0.70.[1] In cases where FVC may be hard to measure, forced expiratory volume at 6 seconds (FEV6) can be used.[21] Chest x-ray (CXR) is rarely diagnostic but can help to exclude other diagnoses. Pulse oximetry screens for hypoxia.

In addition to airflow limitation, the GOLD guidelines recognise the importance of exacerbations in affecting the natural course of COPD, and place emphasis on assessment of symptoms, risk factors for exacerbations, and comorbidities.

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15
Q

Describe how acute exacerbation of COPD are monitored according to the GOLD guidelines

A

In addition to airflow limitation, the GOLD guidelines recognise the importance of exacerbations in affecting the natural course of COPD, and place emphasis on assessment of symptoms, risk factors for exacerbations, and comorbidities.[1]

The Modified British Medical Research Council (mMRC) questionnaire or the COPD Assessment Test (CAT) are recommended to assess symptoms. These can be found in the GOLD guidelines.[1]

The number of previously treated exacerbations (2 or more per year) is the best predictor of having another exacerbation. In addition to previous exacerbations, airflow limitation <50% is predictive of exacerbations.

The GOLD guideline uses a combined COPD assessment approach to group patients according to symptoms and previous history of exacerbations. Symptoms are assessed using the mMRC or CAT scale.

Group A: low risk (0-1 exacerbation per year, not requiring hospitalisation) and fewer symptoms (mMRC 0-1 or CAT <10)
Group B: low risk (0-1 exacerbation per year, not requiring hospitalisation) and more symptoms (mMRC≥ 2 or CAT≥ 10)
Group C: high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and fewer symptoms (mMRC 0-1 or CAT <10)
Group D: high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and more symptoms (mMRC≥ 2 or CAT≥ 10).

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16
Q

Describe some other important tests in COPD

A

Detailed pulmonary function tests performed in specialist pulmonary function laboratories can measure diffusing capacity of the lung for carbon monoxide (DLCO), flow volume loops, and inspiratory capacity. They are not used routinely but can be helpful in resolving diagnostic uncertainties and for preoperative assessment.[1]

In young patients (<45 years) with a family history or with rapidly progressing disease and lower lobe changes on imaging tests, alpha-1 antitrypsin level should be checked. The World Health Organization recommends that all patients with a diagnosis of COPD should be screened once, especially in areas with high prevalence of alpha-1 antitrypsin deficiency.[22] This may aid in family screening and counselling.

Computed tomography scans show anatomical changes, but their usefulness in diagnosis is confined to patients considered for surgery and for ruling out other pathologies.[1]

Pulse oximetry should be used to assess all patients with clinical signs of respiratory failure or right heart failure. If peripheral arterial oxygen saturation is less than 92%, then arterial or capillary blood gases should be measured.

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17
Q

What is associated with an increased risk of death in patients with COPD

A

Obstructive sleep apnoea is associated with increased risk of death and hospitalisation in patients with COPD

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18
Q

Describe how exercise testing may also be useful in COPD

A

Exercise testing can be useful in patients with a disproportional degree of dyspnoea.[24] It can be performed on a cycle or treadmill ergometer, or by a simple timed walking test (e.g., 6 minutes, or duration <6 minutes).[25] Exercise testing is also of use in selecting patients for rehabilitation. Respiratory muscle function may also be tested if dyspnoea or hypercapnia are disproportionately increased with respect to FEV1, as well as in patients with poor nutrition and those with corticosteroid myopathy.[26]

In patients with frequent exacerbations, severe airflow limitation, and/or exacerbations requiring mechanical ventilation, sputum should be sent for culture

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19
Q

Describe the key diagnostic factors of COPD

A

presence of risk factors (e.g., smoking)
The main risk factor is smoking. Other key risk factors include advancing age and genetic factors.

cough
Usually the initial symptom of COPD.

Frequently a morning cough, but becomes constant as disease progresses.

Usually productive, and sputum quality may change with exacerbations or superimposed infection.

shortness of breath
Initially with exercise but may progress to shortness of breath even at rest.

Patients may have difficulty speaking in full sentences.

20
Q

Describe some key diagnostic features of COPD that you may see on examination

A

barrel chest
The anteroposterior diameter of the chest is increased.

This suggests hyperinflation and air trapping secondary to incomplete expiration.

hyper-resonance on percussion
Caused by hyperinflation and air trapping secondary to incomplete expiration.

distant breath sounds on auscultation
Caused by barrel chest, hyperinflation, and air trapping.

poor air movement on auscultation
Secondary to loss of lung elasticity and lung tissue breakdown.

wheezing on auscultation
A common finding in exacerbations. The current accepted descriptive word for a continuous musical lung sound.

Is indicative of airway inflammation and resistance.

coarse crackles
A common finding in exacerbations. A discontinuous sound referring to mucus or sputum in airways.

Indicative of airway inflammation and mucus over-secretion.

21
Q

Describe some uncommon examination signs that you may see in patient’s with COPD

A

tachypnoea
An increased respiratory rate occurs to compensate for hypoxia and hypoventilation.

May involve use of accessory muscles.

asterixis
Loss of postural control in outstretched arms (commonly known as a flap) caused by hypercapnia.

This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of respiratory failure.

distended neck veins
Occurs secondary to increased intrathoracic pressure and cor pulmonale.

lower-extremity swelling
Suggests cor pulmonale and secondary pulmonary hypertension as a complication of advanced chronic lung disease.

fatigue
Occurs because of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia and hypercapnia.

headache
May occur due to vasodilation caused by hypercapnia.

cyanosis
loud P2
Sign of advanced COPD.

Indicates secondary pulmonary hypertension as a complication of cor pulmonale.

hepatojugular reflux
Sign of advanced COPD complicated by cor pulmonale.

hepatosplenomegaly
Sign of advanced COPD complicated by cor pulmonale.

clubbing
COPD itself does not cause clubbing, but if tobacco exposure in COPD patients leads to lung cancer and/or bronchiectasis, then clubbing may occur in COPD. Clubbing is usually not present until significant impairment of lung function has occurred.

22
Q

Describe some strong risk factors for COPD

A

cigarette smoking
Most important risk factor. It causes 40% to 70% of cases of COPD.[14]

Elicits an inflammatory response and causes cilia dysfunction and oxidative injury.

advanced age
The effect of age may be related to a longer period of cigarette smoking as well as the normal age-related loss of FEV1.

genetic factors
Airway responsiveness to inhaled insults depends on genetic factors. Alpha-1 antitrypsin deficiency is a genetic disorder, mostly encountered in people of northern European ancestry, which causes panacinar emphysema in lower lobes at a young age.

23
Q

Describe some weak risk factors for COPD

A

white ancestry
Despite high rates of smoking among black Americans and other racial and ethnic groups, COPD is more common in white people.

exposure to air pollution or occupational exposure
Chronic exposure to dust, traffic exhaust fumes, and sulphur dioxide increases risk of COPD.

developmentally abnormal lung
Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for COPD.

male sex
COPD is more common in men, but that is probably secondary to more smokers being male. However, there is a suggestion that women may be more susceptible than men to the effects of tobacco smoke.[15][16][17][18]

low socio-economic status
The risk for developing COPD is increased in people with lower socio-economic status.[19] However, this may reflect exposure to cigarette smoke, pollutants, or other factors.

24
Q

Describe spirometry in COPD

A

COPD is classified based on the patient’s FEV1 and its percentage of the predicted FEV1. In cases where FVC may be hard to measure, FEV6 (forced expiratory volume at 6 seconds) can be used

Result:
FEV1/FVC ratio <0.70; total absence of reversibility is neither required nor the most typical result

25
Q

Describe pulse oximetry in COPD

A

Checked as part of vital signs on acute presentation. A good pulse wave should be picked up by the device. In patients with chronic disease, an oxygen saturation of 88% to 90% may be acceptable.

If <92% arterial or capillary blood gases should be checked.

Result:
low oxygen saturation

26
Q

Describe ABG in COPD

A

Checked in patients who are acutely unwell, especially if they have an abnormal pulse oximetry reading. Should also be performed in stable patients with FEV1 <35% predicted or with clinical signs suggestive of respiratory failure, or if peripheral arterial oxygen saturation is <92%.

Hypercapnia, hypoxia, and respiratory acidosis are signs of impending respiratory failure and possible need for intubation.

Result:
PaCO₂ >50 mmHg and/or PaO₂ of <60 mmHg suggests respiratory insufficiency

27
Q

Describe the CXR in COPD

A

Seldom diagnostic, but useful in ruling out other pathologies.

Increased anteroposterior ratio, flattened diaphragm, increased intercostal spaces, and hyperlucent lungs may be seen.

May also demonstrate complications of COPD, such as pneumonia and pneumothorax.

Result:
hyperinflation

28
Q

Describe the FBC in COPD

A

This test may be considered to assess severity of an exacerbation and may show polycythaemia (haematocrit >55%), anaemia, and leucocytosis

Result:
raised haematocrit, possible increased WBC count

29
Q

Describe the ECG in COPD

A

Risk factors for COPD are similar to those for ischaemic heart disease, so comorbidity is common.

Result:
signs of right ventricular hypertrophy, arrhythmia, ischaemia

30
Q

Describe how you may consider pulmonary function tests

A

Useful for resolving diagnostic uncertainties and preoperative assessment.[1] Requires specialist laboratory facilities.

Decreased diffusing capacity of the lung for carbon monoxide (DLCO) is supportive of emphysema over chronic bronchitis.

Result:
obstructive pattern, decreased DLCO

31
Q

Describe how you may consider a chest CT

A

Provides better visualisation of type and distribution of lung tissue damage and bulla formation than CXR.

In contrast to smoking-related COPD, alpha-1 antitrypsin deficiency mainly affects lower fields.

Useful in excluding other underlying pulmonary disease and for pre-operative assessment.

Result:
hyperinflation

32
Q

Describe how you may consider sputum culture in COPD

A

In patients with frequent exacerbations, severe airflow limitation, and/or exacerbations requiring mechanical ventilation, sputum should be sent for culture.

Result:
infecting organism

33
Q

Describe how you may consider alpha-1-anti-trypsin deficiency in COPD

A

Low level in patients with alpha-1 antitrypsin deficiency. Test is done if there is high suspicion for alpha-1 antitrypsin deficiency, such as a positive family history and atypical COPD cases (young patients and non-smokers). The World Health Organization recommends that all patients with a diagnosis of COPD should be screened once, especially in areas with high prevalence of alpha-1 antitrypsin deficiency.

Result:
should be normal in patients with COPD

34
Q

Describe how you may consider exercise testing in COPD

A

Can be of value in patients with a disproportional degree of dyspnoea compared with spirometry.[24] It can be performed on a cycle or treadmill ergometer, or by a simple timed walking test (e.g., 6 minutes, or duration <6 minutes).[25] Exercise testing is of use in selecting patients for rehabilitation.

Result:
poor exercise performance or exertional hypoxaemia is suggestive of advanced disease

35
Q

Describe how you may consider a sleep study in COPD

A

Obstructive sleep apnoea, a common finding in patients with COPD, is associated with increased risk of death and hospitalisation in patients with COPD.

Result:
elevated apnoea-hypopnoea index and/or nocturnal hypoxaemia

36
Q

Describe how you may consider testing respiratory muscle function in COPD

A

Respiratory muscle function may be tested if dyspnoea or hypercapnia are disproportionately increased with respect to FEV1, as well as in patients with poor nutrition and those with corticosteroid myopathy

Result:
reduced maximal inspiratory pressure

37
Q

Describe the signs/symptoms of asthma

A

Onset of asthma is usually in early life. A personal or family history of allergy, rhinitis, and eczema is often present. There is daily variability in symptoms, and patients have overt wheezing that usually rapidly responds to bronchodilators. Cough variant asthma mimics many features of COPD.

Investigations:
Pulmonary function tests (PFTs) show reversibility with bronchodilators and no decrease in diffusing capacity of the lung for carbon monoxide (DLCO). Sputum or blood eosinophilia is suggestive of asthma.

38
Q

Describe the signs and symptoms of congestive heart failure

A

Usually a history of cardiovascular diseases is present. Patients report symptoms of orthopnoea, and fine bibasilar inspiratory crackles may be heard on auscultation.

Investigations:
B-type natriuretic peptide levels are usually elevated, and CXR reveals increased pulmonary vascular congestion. Echocardiogram may confirm the diagnosis.

39
Q

Describe the signs and symptoms of bronchiectasis

A

There may be a history of recurrent infection in childhood. Large volume of purulent sputum is usually present. Coarse crackles may be heard on auscultation. History of pertussis or tuberculosis is a clue to diagnosis.

Investigations:
Chest CT reveals bronchial dilation and bronchial wall thickening.

40
Q

Describe the signs and symptoms of TB

A

A history of fever, night sweats, weight loss, and chronic productive cough is usually present. Tuberculosis is more common in immigrants to non-endemic countries, and in people living in endemic countries.

Investigations:
The diagnosis requires microbiological confirmation. Infiltrates, fibrosis, or granuloma seen on CXR or chest CT may suggest tuberculosis. Patients usually have positive skin test for tuberculosis.

41
Q

Describe the signs and symptoms of bronchitis

A

Bronchiolitis may affect patients at younger ages. The patient may have a history of connective tissue disorders, especially rheumatoid arthritis, or fume exposure. Some cases are post-infectious.

Investigations:
PFTs in bronchiolitis can present with obstructive, restrictive, or mixed pattern. CXR shows hyperinflation. High-resolution chest CT may show diffuse, small, centrilobular nodular opacities, but is rarely done in children due to radiation risk.

42
Q

Describe the signs and symptoms of upper-airway dysfunction

A

Can affect patients of any age. History of prior trauma or intubation is very helpful. Lung examination is usually normal, but signs of upper airway restriction, such as wheezing and stridor, may be present. Patients may have voice hoarseness if vocal cords are involved.

Investigations:
The flow-volume curve in pulmonary function testing may reveal a characteristic expiratory or inspiratory plateau, or both. Diagnosis is confirmed by direct visualisation of the affected airway by endoscopy.

43
Q

Describe the signs and symptoms of chronic sinusitis/ postnasal drip

A

Chronic sinusitis/rhinitis is a very common cause of chronic cough. Patients may complain of sinus pressure, rhinorrhoea, non-productive cough, and/or headache.

Investigations:
CT of sinuses and/or empirical trial of antihistamines is commonly utilised to aid in diagnosis.

44
Q

Describe the signs and symptoms of GORD

A

CT of sinuses and/or empirical trial of antihistamines is commonly utilised to aid in diagnosis.

Investigations;
Diagnosis is usually based on response to empirical therapy with proton-pump inhibitors.

45
Q

Describe the signs and symptoms of an ACEi induced cough

A

ACE inhibitors can cause chronic cough; however, the cough is usually non-productive

Investigations:
Diagnosis is usually based on improvement of symptoms after empirical cessation of ACE inhibitor.

46
Q

Describe the signs and symptoms of lung cancer

A

Patients may have weight loss, night sweats, haemoptysis, and/or chest or back pain.

People with COPD are also at increased risk of lung cancer.

Investigations;
Radiography is important in the assessment for lung cancer. Bronchoscopy may be necessary to evaluate for endobronchial cancer if suspicion is high.

47
Q

Describe screening for COPD

A

There are no data to show conclusively that screening spirometry is effective in directing management decisions or in improving COPD outcomes in patients who are identified before the development of significant symptoms.[27] However, if COPD is diagnosed at an early stage and risk factors are eliminated, the rate of decline in lung function will dramatically decrease. Treatment is much more efficacious in the early stages of disease.[28]

Screening can be done by asking about smoking history and environmental or occupational exposure. In high-risk populations a screening spirometry should be obtained to document airway obstruction. Some experts advocate conducting screening spirometry in all patients with findings compatible with emphysema on chest x-ray or computed tomography of the chest. Significant pulmonary dysfunction may be present in asymptomatic smokers.