COPD: Aetiologies, Symptoms, Aids to Diagnosis and Management Flashcards
1
Q
What is the definition of COPD?
A
COPD is characterized by progressive airflow obstruction which is not fully reversible and does not change markedly over several months.
2
Q
How does COPD prevalence change with age?
A
COPD increases with age, particularly in individuals over the age of 60 years.
3
Q
What is the rate of decline in FEV1 after the age of 30, and how does smoking affect this decline?
A
After the age of 30, there is a decline in FEV1 of about 30 ml/year. Smoking accelerates this decline.
4
Q
What is the primary cause of COPD?
A
Cigarette smoking is the primary cause of COPD in approximately 90% of cases.
5
Q
How is the risk of developing COPD associated with smoking?
A
The risk of developing COPD is associated with the number of pack years of smoking. Higher pack years indicate a greater risk.
6
Q
Does cigar and pipe smoking increase the risk of COPD?
A
Yes, cigar and pipe smoking increase the risk of COPD, although to a lesser extent than cigarette smoking.
7
Q
Does passive smoking contribute to the development of COPD?
A
Yes, passive smoking (exposure to second-hand smoke) also increases the risk of developing COPD.
8
Q
What percentage of smokers develop COPD?
A
Only 15-25% of individuals who smoke develop COPD.
9
Q
Besides smoking, what other factors can contribute to COPD?
A
Occupational exposure to dusts (e.g., coal mining), air pollution (more common in urban areas), lower socioeconomic status, and α-1 antitrypsin deficiency (1-2% of cases) can also contribute to COPD.
10
Q
What is the definition of chronic bronchitis?
A
Chronic bronchitis is characterized by sputum production for at least 3 months per year for at least 2 consecutive years.
11
Q
What is emphysema?
A
Emphysema is a condition characterized by the destruction of alveoli distal to the terminal bronchiole, resulting in the loss of elastic supporting tissue.
12
Q
How does emphysema affect gas exchange?
A
Emphysema affects gas exchange by destroying the interstitium. This destruction leads to a reduction in the transfer factor (TLCO), which is responsible for the efficient exchange of gases.
13
Q
How does α-1 antitrypsin contribute to lung protection?
A
In healthy lungs, α-1 antitrypsin protects the lung from neutrophil elastase, maintaining a balance that prevents damage to healthy lung tissue.
14
Q
How does cigarette smoking affect the lung’s defense mechanism?
A
Cigarette smoking activates neutrophils in the lungs, leading to an increased release of proteases that overwhelm α-1 antitrypsin, causing damage to the lung tissue.
15
Q
What is the impact of neutrophil invasion and proteases in the lungs?
A
Neutrophils invading the bronchial mucosa release proteases such as elastase and collagenase, which damage alveolar sacs. This damage can lead to the formation of large bullae and contribute to the development of emphysema.
16
Q
How does chronic bronchitis affect the airways?
A
In chronic bronchitis, there is inflammation of the airways along with structural changes. There is an increase in goblet cells and hypertrophy of goblet cells, leading to the production of viscous mucus that is difficult to clear.
17
Q
What are the consequences of mucus accumulation in chronic bronchitis?
A
The thick mucus acts as a culture medium for infective organisms and impairs the host defense mechanisms. This can lead to recurrent respiratory tract infections and further inflammation of the lungs, causing a decline in lung function.
18
Q
How does COPD affect airway resistance and lung function?
A
In COPD, there is an increased airway resistance and loss of elastic recoil of the lungs. Airways tend to collapse on expiration, resulting in air trapping and hyperinflation. This increased work of breathing can lead to the use of accessory muscles and the adoption of pursed-lip breathing.
19
Q
What are the consequences of end-stage COPD?
A
In end-stage COPD, patients may develop right heart failure (cor pulmonale) due to the increased pulmonary vascular resistance. They may also develop pulmonary hypertension, which further complicates the cardiopulmonary status.
20
Q
How is COPD diagnosed?
A
A diagnosis of COPD should be suspected in any individual over the age of 35 years who presents with symptoms of breathlessness and has a history of cigarette smoking. Confirmation is made by spirometry, which shows an FEV1/FVC ratio of less than 70% predicted post administration of a short-acting bronchodilator.
21
Q
What is a common symptom of COPD?
A
Breathlessness on exertion (dyspnea) is a common symptom of COPD. It tends to progressively worsen over time.
22
Q
What is a characteristic symptom of chronic bronchitis?
A
A chronic productive cough is a characteristic symptom of chronic bronchitis, which is a form of COPD.
23
Q
What are some other symptoms associated with COPD?
A
Other symptoms of COPD include frequent lower respiratory tract infections, progressive weight loss (in some cases), peripheral (ankle) edema (seen in end-stage COPD suggesting cor pulmonale), and red flag symptoms such as hemoptysis, chest pain, and night sweats.
24
Q
Can clinical examination be normal in mild COPD?
A
Yes, clinical examination may be normal in mild COPD.
25
What is a common sign of COPD?
Tachypnea (raised respiratory rate) is a common sign of COPD.
26
What is a potential tremor associated with COPD?
Tremor can occur if a person is overusing a β-2 agonist inhaler.
27
What are some respiratory-related signs of COPD?
Pursed-lip breathing and the use of accessory muscles can be observed in individuals with COPD. Hyperinflation of the chest and a barrel-shaped chest (increased anteroposterior diameter of the thoracic cage) are also common signs.
28
What respiratory sound may be heard in COPD?
Wheezing is often present in individuals with COPD.
29
What are signs of right heart failure (cor pulmonale)?
Signs of cor pulmonale may include a raised jugular venous pressure (JVP) and ankle edema.
30
What are some signs of CO2 retention in COPD?
Signs of CO2 retention may include a CO2 retention flap (flapping tremor of the outstretched hands), bounding pulse, irritability, and confusion.
31
What can be a consequence of advanced COPD?
Advanced COPD can lead to the development of type 2 respiratory failure.
32
What spirometry findings indicate obstruction in COPD?
In COPD, spirometry will show reduced FEV1 (forced expiratory volume in 1 second) and an FEV1/FVC (forced vital capacity) ratio less than 70%.
33
What is the criterion for reversibility to a bronchodilator in COPD?
There is no significant reversibility to a bronchodilator in COPD if, 20 minutes after inhaling 200 mcg of salbutamol, the FEV1 does not increase by at least 15% of the baseline value or by more than 200 ml. In asthma, there is typically reversibility.
34
What changes in lung volumes are observed in COPD?
In COPD, there is an increase in total lung capacity (TLC) and residual volume (RV) due to air trapping.
35
How is the transfer factor or diffusing capacity affected in COPD?
The transfer factor or diffusing capacity (TLCO/DLCO) is reduced in COPD.
36
What do the abbreviations TLC and RV stand for?
TLC stands for total lung capacity, which is the maximum volume of air the lungs can hold, and RV stands for residual volume, which is the volume of air remaining in the lungs after maximal expiration.
37
Why is it important to determine the extent of breathlessness in COPD?
The extent of breathlessness correlates with the severity of COPD. Determining baseline measurements of breathlessness helps assess prognosis and the impact of treatment.
38
What is the mMRC Dyspnoea Scale?
The mMRC Dyspnoea Scale is a tool used to assess the severity of breathlessness in COPD. It ranges from 0 to 4, with higher numbers indicating greater levels of dyspnea.
39
What are the different levels of dyspnea on the mMRC Dyspnoea Scale?
The levels on the mMRC Dyspnoea Scale are as follows:
0: Dyspnea with strenuous exercise.
1: Dyspnea when hurrying or walking up a slight hill.
2: Walks slower than others of the same age due to dyspnea or has to stop for breath when walking at own pace.
3: Stops for breath after walking 100 yards or after a few minutes.
4: Too dyspneic to leave the house or breathless when dressing.
Severity of COPD:
40
How does the GOLD guideline define the severity of COPD?
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines the severity of COPD as mild, moderate, severe, and very severe based on spirometry values when the FEV1/FVC ratio is less than 70%.
41
What are the different severity categories of COPD according to GOLD?
According to GOLD, the severity categories of COPD are as follows:
Mild: FEV1 ≥ 80%
Moderate: FEV1 50-79%
Severe: FEV1 30-49%
Very Severe: FEV1 ≤ 30%
42
What can be observed on a chest X-ray (CXR) in COPD?
A CXR in COPD may show signs of hyperinflation, such as flat diaphragms and increased anterior rib space.
43
What can be seen on a high-resolution computed tomography (HRCT) scan in COPD?
HRCT scans may reveal the presence of bullae (large air-filled spaces) in the upper lobes of the lungs.
44
What can be assessed using pulse oximetry in COPD?
Pulse oximetry measures the oxygen saturation in the blood. In COPD, it may initially be normal in mild cases but can drop to less than 92% during exertion and eventually at rest as the condition worsens.
45
What does can arterial blood gas (ABG) analysis reveal in COPD?
ABG analysis can provide important information about respiratory function in COPD, including type 1 or type 2 respiratory failure, characterised by specific changes in oxygen, carbon dioxide, and pH levels. It can also show secondary polycythemia (increased red blood cell production) and measure the levels of α-1 antitrypsin (α-1 AT).
46
What cardiac investigations may be performed if cor pulmonale (right heart failure) is suspected in COPD?
Cardiac investigations that may be performed include an electrocardiogram (ECG) and an echocardiogram. These tests can assess for signs of right ventricular failure and pulmonary hypertension.
47
How can the quality of life in COPD be assessed?
Validated questionnaires are used to assess the overall function and quality of life in individuals with COPD. These questionnaires provide insights into the impact of the disease on various aspects of daily life.
48
What is the prognosis of COPD?
COPD is characterized by a progressive decline in lung function over time. The condition is largely irreversible, meaning that the lung damage cannot be fully reversed.
49
What are the potential complications of COPD?
COPD carries a risk of developing type 2 respiratory failure, which is characterized by hypoxia, hypercapnia, and acidosis. Additionally, individuals with COPD may develop cor pulmonale, which is right heart failure secondary to lung disease.
50
What lifestyle advice is important for managing COPD?
Lifestyle advice for COPD management includes smoking cessation, increasing physical activity levels, and improving nutrition.
51
What are the main pharmacological treatments for COPD?
The main pharmacological treatments for COPD include inhaled therapies, such as bronchodilators (short-acting and long-acting) and inhaled corticosteroids. Medications are used to manage exacerbations, and for individuals with severe COPD, long-term oxygen therapy (LTOT) and non-invasive ventilation (NIV) may be prescribed.
52
What are the surgical options for managing COPD?
Surgical options for COPD management include lung volume reduction surgery, which involves removing parts of the lung that are not adequately ventilating to improve overall lung ventilation. In severe cases, a lung transplant may be considered.
53
What non-pharmacological approaches are used in COPD management?
Non-pharmacological management of COPD includes pulmonary rehabilitation, which combines exercise training, education, and support. Counselling and psychosocial support can also be beneficial. In advanced cases, palliative care focuses on symptom management and improving quality of life.
54
What is Ipratropium bromide?
Ipratropium bromide, also known by the brand name Atrovent, is a muscarinic antagonist used in the management of COPD. It blocks M3 receptors in the smooth muscles of the airways.
55
How does Ipratropium bromide work?
By binding to M3 receptors, Ipratropium bromide inhibits a Gq type of receptor, decreasing calcium and bronchodilation. It also reduces mucus production and acts synergistically with short-acting beta-agonists (SABA).
56
How is Ipratropium bromide administered?
Ipratropium bromide is typically administered via inhalation as a daily maintenance therapy for COPD. It can also be administered via nebulization for acute exacerbations of asthma or COPD.
57
What are the systemic side effects of Ipratropium bromide?
The systemic side effects of Ipratropium bromide, which are minimal, are related to its anticholinergic properties. These include inhibition of the parasympathetic nervous system.
58
What is Tiotropium?
Tiotropium is a long-acting muscarinic antagonist (LAMA) used in the management of COPD and chronic asthma. It causes bronchodilation, reduces bronchospasm, and decreases mucus production.
59
What is the duration of action of Tiotropium?
Tiotropium has a prolonged duration of action due to its slow dissociation from muscarinic receptors. It typically has a duration of action of 12-24 hours.
60
How is Tiotropium administered?
Tiotropium is administered via inhalation using an inhaler device.
61
What are the common side effects of SAMA and LAMA medications?
The common side effects of SAMA and LAMA medications, which are due to their anticholinergic properties, include dry mouth, blurred vision, closed-angle glaucoma, urinary retention, cardiac arrhythmias, taste disturbance, dizziness, and epistaxis (nosebleeds).
62
Are systemic side effects common with SAMA and LAMA medications?
Systemic side effects are rare because these medications have minimal systemic absorption.
63
What are methylxanthines?
Methylxanthines are a class of medications that act as non-selective phosphodiesterase inhibitors and bronchodilators. Theophylline and aminophylline are examples of methylxanthines.
64
How are methylxanthines administered?
Theophylline is typically administered orally for chronic asthma or COPD management, while aminophylline can be administered intravenously for acute exacerbations of asthma and COPD.
65
What should be monitored when using methylxanthines?
Methylxanthines, such as theophylline, require monitoring of blood levels through regular blood tests due to their narrow therapeutic range. They are metabolized by the cytochrome P450 enzyme system and can interact with many drugs.
66
When are antibiotics prescribed for exacerbations of asthma or COPD?
Antibiotics may be prescribed for bacterial chest infections causing exacerbations of asthma or COPD. It is important to follow local prescribing guidelines and consider the sensitivity of organisms if required.
67
What factors should be considered when prescribing antibiotics?
When prescribing antibiotics, it is important to inquire about patient allergies, consider contraindications (e.g., pregnancy, renal failure), be aware of potential drug interactions, and inform patients about serious side effects. Consulting the British National Formulary (BNF) and seeking advice from a microbiologist can be helpful.
68
Which antibiotics are commonly used for asthma and COPD exacerbations caused by Streptococcus pneumoniae?
Amoxicillin and macrolides (such as clarithromycin) are commonly used antibiotics for asthma and COPD exacerbations caused by Streptococcus pneumoniae.
69
Which antibiotic is used for Staphylococcus aureus infections, including methicillin-resistant Staphylococcus aureus (MRSA)?
Vancomycin is used for Staphylococcus aureus infections, including MRSA.
70
What are the initial treatment options for acute exacerbation of COPD?
Initial treatment options include nebulized short-acting beta-agonist (SABA) such as salbutamol and short-acting muscarinic antagonist (SAMA) such as ipratropium bromide (Atrovent).
71
What is the role of systemic steroids in the management of acute exacerbation of COPD?
Systemic steroids, such as oral prednisolone, are commonly used to reduce inflammation and improve symptoms in acute exacerbation of COPD.
72
What is the target oxygen saturation (SpO2) range during acute exacerbation of COPD, and how is it achieved?
The target SpO2 range is 88-92%. Controlled oxygen therapy via a venturi mask achieves and maintains the desired oxygen saturation levels. Arterial blood gases (ABGs) may be checked to guide oxygen therapy.
73
What is the role of IV aminophylline in acute exacerbation of COPD?
IV aminophylline may be used as a bronchodilator in severe exacerbations of COPD that do not respond adequately to inhaled bronchodilators.
74
When are antibiotics prescribed in acute exacerbation of COPD?
Antibiotics are prescribed in acute exacerbation of COPD when there is evidence of a bacterial infection or clinical suspicion. The choice of antibiotics depends on the suspected pathogens and local guidelines.
75
What is non-invasive ventilation (NIV) used for in acute exacerbation of COPD?
Non-invasive ventilation (NIV) is used for type 2 respiratory failure in acute exacerbation of COPD to provide ventilatory support and improve oxygenation without the need for endotracheal intubation.
76
Is oxygen considered a drug and requires a prescription?
Yes, oxygen is considered a drug and must be prescribed by a healthcare professional.
77
When is oxygen indicated in Type 1 Respiratory failure?
Oxygen is indicated in Type 1 Respiratory failure when the partial pressure of oxygen (pO2) is less than 7.8 kPa. The goal is to maintain oxygen saturation between 94-98%.
78
What is the target oxygen saturation range in Type 2 respiratory failure?
In Type 2 respiratory failure, controlled oxygen therapy is used to maintain oxygen saturation between 88-92%.
79
What are the potential risks of inappropriate oxygen use?
Inappropriate use of oxygen can lead to iatrogenic Type 2 respiratory failure, carbon dioxide (CO2) retention, acidosis, and potentially death.
80
Is oxygen usually indicated for the treatment of breathlessness?
Oxygen is not typically indicated for the treatment of breathlessness in respiratory conditions, except in specific cases such as intractable breathlessness in the palliative care setting.
81
When is long-term oxygen therapy (LTOT) indicated for chronic hypoxemia?
LTOT is indicated for individuals with a pO2 less than 7.3 kPa (or oxygen saturation below 88% at rest) in conditions such as COPD, pulmonary fibrosis, and pulmonary hypertension.
82
What is an important component of the discharge plan for COPD patients?
Smoking cessation should be emphasized as a crucial part of the discharge plan for COPD patients.
83
What inhaled therapy should be considered for COPD patients?
Appropriate inhaled therapy should be prescribed, such as ICS/LABA/LAMA combination. Salbutamol can be used for symptom relief.
84
What should be assessed regarding inhaler use?
Inhaler technique should be checked to ensure proper administration of medication.
85
What additional medication may be considered for COPD patients?
Oral theophylline may be prescribed as part of the treatment plan.
86
What other aspects should be addressed in the discharge plan?
Other components of the discharge plan may include assessing the need for long-term oxygen therapy (LTOT), home nebulizer use, nutritional support, referral for pulmonary rehabilitation, psychological support, and vaccinations (influenza, pneumococcal, and regular Covid vaccination).
87
What interventions can improve survival in COPD patients?
Smoking cessation, long-term oxygen therapy (LTOT), non-invasive ventilation (BiPAP), and lung volume reduction surgery can improve survival in COPD patients.
88
What is considered a frequent exacerbator of COPD?
A frequent exacerbator is defined as someone who experiences more than two exacerbations requiring oral corticosteroids and/or antibiotics, or one hospital admission for COPD per year.
89
How does reducing the number of exacerbations impact survival?
Reducing the number of exacerbations can help improve survival outcomes in COPD patients.
90
What are some clinical differences between asthma and COPD?
Asthma tends to present with wheezing in childhood, while COPD typically develops later in life, with symptoms usually starting after the age of 35.
Atopy (a genetic predisposition to allergic reactions) is commonly associated with asthma, whereas COPD is strongly associated with a significant smoking history.
Family history of asthma is more prevalent in asthma patients, while occupational exposures (such as exposure to dust, chemicals, or fumes) are more commonly associated with COPD.
Asthma symptoms often exhibit day-to-day variation, with diurnal variation in peak expiratory flow rate (PEFR) charts, while COPD symptoms are typically more constant.
Eosinophilia (an increase in eosinophils, a type of white blood cell) may be observed in asthma, but is generally not present in COPD.
Spirometry (lung function test) may appear normal in asthma, whereas COPD is characterized by persistent airflow obstruction on spirometry.
Asthma patients often show reversibility to short-acting beta-2 agonist bronchodilators, while this reversibility is limited in COPD.
Asthma patients may also show reversibility to steroid treatment, while the reversibility to steroids is generally limited in COPD.
91
What are the predominant cells observed in asthma and COPD?
In asthma, the predominant cells observed are eosinophils, which are involved in allergic and inflammatory responses. In COPD, the predominant cells observed are neutrophils, which play a role in chronic inflammation and tissue damage.
92
What is the characteristic spirometry finding in both asthma and COPD?
The characteristic spirometry finding in both asthma and COPD is a reduced FEV1/FVC ratio, with values below 70% indicating airflow obstruction. However, it is important to note that in asthma, there is often reversibility to bronchodilators, whereas in COPD, there is limited or no reversibility.
93
How does lung function differ in asthma and COPD?
In asthma, lung function may show increased total lung capacity (TLC) and residual volume (RV), indicating air trapping and hyperinflation. In contrast, COPD is characterized by a decrease in transfer factor for carbon monoxide (TLCO) and carbon monoxide transfer coefficient (KCO), which reflect impaired gas exchange. Additionally, COPD may also show an increase in TLC and RV due to air trapping.
94
What is the difference in lung structure between asthma and COPD?
In asthma, the lung structure is typically normal, but airway remodelling may be characterized by increased smooth muscle mass, mucus production, and thickening of the airway walls. In COPD, the lung structure is affected by the development of emphysema, which involves the destruction of alveoli and loss of elastic tissue, leading to airspace enlargement.
95
What is obstructive sleep apnoea (OSA)?
Obstructive sleep apnoea (OSA) is a sleep disorder characterized by recurrent episodes of partial or complete upper airway collapse during sleep. These episodes result in disrupted breathing patterns, with periods of reduced airflow (hypopnoea) or complete cessation of breathing (apnoea) lasting for more than 10 seconds. OSA leads to fragmented sleep and can cause hypoxia (low oxygen levels) in the body.
96
How common is obstructive sleep apnoea?
Obstructive sleep apnoea affects approximately 3-7% of men and 2-5% of women. It is a relatively common condition, and the prevalence increases with age.
97
What are the common symptoms of obstructive sleep apnoea?
Common symptoms of obstructive sleep apnoea include loud snoring, recurrent apnoeic episodes during sleep (witnessed by a bed partner), excessive daytime sleepiness, morning headaches, and difficulty concentrating. The Epworth Sleepiness Score is a questionnaire used to assess the severity of daytime sleepiness associated with sleep apnoea.
98
How does obstructive sleep apnoea affect sleep and oxygen levels?
Obstructive sleep apnoea disrupts normal sleep patterns as the airway repeatedly collapses and breathing is temporarily interrupted. These episodes can lead to frequent awakenings or arousals during sleep, resulting in fragmented and poor-quality sleep. Additionally, the recurrent apnoeic episodes can cause decreased oxygen levels (hypoxia) in the body, which can have various health implications if left untreated.
99
What are some common risk factors for obstructive sleep apnoea/hypopnea syndrome (OSAHS)?
Common risk factors for OSAHS include obesity, with a body mass index (BMI) greater than 30, a collar size larger than 17 inches (33 cm), enlarged tonsils and/or adenoids, an enlarged tongue, a long uvula, nasal pathology, retrognathia or micrognathia (abnormal positioning of the jaw), acromegaly (a hormonal disorder), hypothyroidism, and Down's syndrome. These factors can contribute to the narrowing or obstruction of the upper airway during sleep.
100
What are the typical symptoms of obstructive sleep apnoea/hypopnea syndrome?
The typical symptoms of OSAHS include loud snoring (often noticed by a bed partner), recurrent apnoeas (episodes of not breathing) during sleep, restless or disturbed sleep, nocturnal choking or gasping for breath, morning headaches, feeling unrefreshed upon waking, frequent urination during the night (nocturia), excessive daytime sleepiness, decreased cognition, concentration, memory, libido, irritability, mood changes, an increased risk of road traffic accidents, and an increased risk of developing hypertension. OSAHS is also considered a cardiovascular risk factor.
101
How does obstructive sleep apnoea affect daytime functioning?
Obstructive sleep apnoea can significantly impact daytime functioning due to the disrupted sleep patterns and poor-quality sleep it causes. Excessive daytime sleepiness is a common symptom, leading to decreased cognition, concentration, memory, and libido. Individuals with OSAHS may experience irritability, mood changes, and a general decrease in overall well-being. The increased risk of road traffic accidents is also a notable consequence of daytime sleepiness associated with OSAHS.
102
What are some common obstructive sleep apnoea/hypopnea syndrome (OSAHS) investigations?
Common investigations for OSAHS include overnight oximetry, which measures oxygen levels during sleep, full polysomnography, which involves monitoring various parameters during sleep such as brain activity, eye movements, muscle activity, and breathing patterns, and the Epworth Sleepiness Score, which is a questionnaire used to assess daytime sleepiness.
103
What are some management options for OSAHS?
Management options for OSAHS include weight loss, as obesity is a common risk factor, surgical interventions such as tonsillectomy or adenoidectomy, the use of a mandibular advancement device for mild OSAHS to help keep the airway open, and the use of continuous positive airway pressure (CPAP) therapy for moderate or severe OSAHS. CPAP involves wearing a mask during sleep that delivers a constant flow of air to keep the airway open. It is important to inform the DVLA (Driver and Vehicle Licensing Agency) and refrain from driving until treatment has been established.
104
What are some red flag symptoms in the context of OSAHS?
Red flag symptoms in the context of OSAHS suggest a serious underlying condition, such as cancer. These symptoms include haemoptysis (coughing up blood), persistent unexplained fever, persistent unexplained night sweats, unexplained weight loss, and stridor (a high-pitched wheezing sound during breathing). If any of these red flag symptoms are present, further investigation and evaluation are warranted to determine the underlying cause.
