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Respiratory > 2. COPD > Flashcards

2. COPD Flashcards

1
Q

Is COPD restrictive or obstructive?

A

Obstructive
- Lung volume is fine but not able to blow air in/out

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2
Q

Define COPD.

A

Chronic Obstructive Pulmonary Disease.

Non-reversible long-term progressive deterioration + limitation in air flow through the lungs, caused by damage to lung tissue (almost always due to smoking).

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3
Q

Which 2 categories can COPD be sub-divided into?

A
  1. Chronic bronchitis.
  2. Emphysema.
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4
Q

Define chronic bronchitis.

A

A persistent cough with sputum for 3/12 (3 months) for 2 or more consecutive years

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5
Q

Explain chronic bronchitis.

A
  1. Exposure to irritants and chemicals e.g. smoke
  2. Leads to hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree
  3. Increased mucus
  4. Airway obstruction = fibrosis/thickening of airways
  5. Neutrophil and macrophage involvement
  6. Bronchi become inflamed
  7. ALSO: ulceration of the epithelial layer -> heals as squamous epithelium instead of columnar cells = squamous metaplasia
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6
Q

What can happen over time in a patient with chronic bronchitis?

A

The patient might become hypercapnic, hypoxic and have progressive right sided cardiac failure (cor pulmonale) due to pulmonary vasoconstriction. There is fibrosis and tissue destruction.

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7
Q

Why does someone with chronic bronchitis develop cor pulmonale?

A

There is pulmonary vasoconstriction in the lungs in an attempt to shunt blood to better ventilated alveoli -> pulmonary hypertension -> RHF -> cor pulmonale.

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8
Q

Give 5 signs of chronic bronchitis.

A
  1. Chronic productive cough.
    - Purulent sputum
  2. Wheeze and crackles - dyspnoea
  3. Hypoxic and hypercapnic.
  4. Cyanosis (hypoxaemia)
  5. Vasoconstriction -> pulmonary hypertension -> cor pulmonale.
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9
Q

What is the effect of chronic bronchitis on lung function?

A
  • Reduced FEV1/FVC ratio.
  • Reduced PEFR.
  • Increased TLCO.
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10
Q

Define emphysema.

A

Histologically, it’s enlarged air spaces distal to terminal
bronchioles, with destruction of alveolar walls, resulting in the loss of elastic recoil in the alveoli (based on structural changes).

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11
Q

Explain emphysema.

A
  1. Irritants and chemicals trigger inflammatory mediators to release matrix destructive enzymes
  2. Elastin destruction
  3. Dilation + destruction of alveoli / lung tissue distal to the terminal bronchioles
  4. Loss of elastic recoil (normally keeps the airway open during expiration)
  5. Limits expiratory airflow -> leads to air trapping
  6. Premature closure of airways limits expiratory flow while the loss of alveoli decreases capacity for gas transfer
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12
Q

Give 5 signs of emphysema.

A
  1. Pursed lip breathing.
  2. SOB.
  3. Barrel chest.
  4. Weight loss.
  5. CO2 retention.
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13
Q

Which disease is predominant in each of pink puffers and blue bloaters?

A

Pink puffers = predominantly emphysema
Blue boaters = predominantly chronic bronchitis

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14
Q

What are the features of a pink puffer?

A

Increased alveolar ventilation
Nearly normal PaO2 + normal/low PaCO2
May progress to Type 1 respiratory failure

Symptoms:
- Weight loss
- SOB but NO cyanosed
- Barrel chest
- Pursed lip breathing
- CO2 retention

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15
Q

What are the features of a blue bloater?

A

Decreased alveolar ventilation
Low PaO2 and high PaCO2
Rely on hypoxic drive as respiratory centres are insensitive to CO2

Symptoms:
- Chronic productive cough with phlegm
- Cor pulmonale
- Hypoxia + hypercapnia
- Wheeze + crackles
- Cyanosis but NO SOB
-> Can cause secondary polycythemia
-> May develop pulmonary hypertension (reactive pulmonary
vasoconstriction)

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16
Q

Give 2 causes of COPD.

A
  1. Cigarette smoking
  2. Exposure to pollutants at work (mining, building, chemical, outdoor air pollution, )
  3. Alpha-1 antitrypsin deficiency (early onset COPD)
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17
Q

What generally causes early-onset COPD?

A

Alpha-1 antitrypsin deficiency

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18
Q

What is alpha1-antitrypsin?

A

A protease inhibitor - inactivated by cigarette smoke

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19
Q

Explain how cigarette smoke causes COPD.

A

Cigarette smoke:
1. Causes mucus gland hypertrophy in the larger airways
2. Leads to an increase in neutrophils, macrophages and lymphocytes in the airways and walls of the bronchi and bronchioles
3. These cells release inflammatory mediators (elastases, proteases, IL-1,-8 & TNF-alpha)
4. Actions of inflammatory mediators:
- Attract inflammatory cells (further amplify the process)
- Induce structural changes
- Break down connective tissue (protease-antiprotease imbalance) in the lung, resulting in emphysema

  1. Inactivates the major protease inhibitor, alpha-1 antitrypsin
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20
Q

What type of T lymphocyte is involved in COPD?

A

CD8+.

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21
Q

What are the main cells responsible for inflammation in COPD?

A

Neutrophils and macrophages.

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22
Q

In short-term COPD, what provides the inspiratory drive?

A

In the short term, the rise in CO2 leads to stimulation of respiration.

CO2 excretion is less affected by V/Q mismatch and many patients have low-normal PaCO2 values due to increasing alveolar ventilation in an attempt to correct their hypoxia (pink puffers).

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23
Q

In long-term COPD, what provides the inspiratory drive?

A

Hypoxia.
CO2 is permanently high as not able to blow it off, so body becomes desensitised.

Such patients appear less breathless and because of renal hypoxia, they start to retain fluid and increase erythrocyte production (leading eventually to polycthaemia) - they become bloated and cyanosed (blue) and have a typical blue bloater appearance.

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24
Q

Give 3 risk factors of COPD.

A
  1. Smoking
  2. Pollutant exposure
  3. Frequent lower respiratory infections in childhood
  4. Age
25
Q

What is the characteristic symptom of COPD?

A

Productive cough with white or clear sputum, wheeze and breathlessness, usually following many years of a smoker’s cough

26
Q

Give 5 main symptoms of COPD.

A
  1. Breathlessness/dyspnoea.
  2. Wheeze.
  3. Chronic cough.
  4. Sputum production.
  5. Recurrent respiratory infections.
27
Q

Give other (later, systemic) symptoms of COPD.

A
  1. Presence of frequent, infective exacerbations + better periods
  2. Chest ‘tightness’
  3. Pursed lip breathing, bent over

Systemic:
1. Hypertension
2. Osteoporosis
3. Depression
4. Weight loss
5. Reduced muscle mass with general weakness

On examination:
1. Breathless at rest
2. Prolonged expiration
3. Poor chest expansion
4. Hyper-inflated lungs (barrel chest)

Advanced:
1. Fluid retentions + peripheral oedema secondary to heart failure

28
Q

What scale might be used to assess breathlessness?

A

MRC dyspnoea scale; scored from 1-5.
5 statements that describe the entire range of respiratory disability from none to almost complete incapacity.

29
Q

Describe the MRC Dyspnoea Scale.

A

MRC (Medical Research Council) Dyspnoea Scale:
This is a 5 point scale that NICE recommend for assessing the impact of their breathlessness.

Grades:
Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

30
Q

Give 3 complications of COPD.

A
  1. Acute exacerbations ± infection
  2. Polycythaemia
  3. Hypercapnic Respiratory failure
  4. Cor pulmonale
    - right heart failure, caused by pulmonary hypertension as a result of chronic hypoxic pulmonary vasoconstriction
  5. Pneumothorax
  6. Lung carcinoma
  7. Osteoporosis
    - due to chronic steroid use, smoking, lack of bone-strength exercise and vitamin D deficiency
31
Q

Give 3 differential diagnoses of COPD.

A
  1. Asthma
  2. Bronchiectasis
  3. Pulmonary embolism
  4. Congestive heart failure
  5. Pneumothorax
32
Q

List some features that would suggest it is more likely the patient has COPD than asthma.

A
  • Onset >35 YO
  • Smoking/pollution related
  • Chronic dyspnoea (instead of attacks)
  • Sputum production
  • Lack of diurnal FEV1 variation
33
Q

Differences between COPD and asthma?

A

COPD: non reversible, interval symptoms

34
Q

Give 3 symptoms of chronic disease that are generally NOT seen in COPD.

A
  1. Clubbing
  2. Haemoptysis
  3. Chest pain
35
Q

Investigations to diagnose COPD.

A

Based on a history of breathlessness and sputum production in a chronic smoker.

  1. Baseline blood tests: FBC, U&E, LFTs, CRP
    - FBC: polycythaemia or anaemia -> Polycythaemia (raised Hb) is a response to chronic hypoxia.
  2. Arterial blood gas (ABG):
    - During stable disease: PaCO2 >6.0 and bicarbonate >30 indicates that the patient is a “CO2-retainer”.
    - During exacerbations: check for respiratory acidosis (PaCO2 >6.0 and pH <7.35).
  3. Spirometry (lung function tests) - GOLD STANDARD
    1) FEV1/FVC < 70%
    2) FEV1 reduced (<80%)
    3) Transfer factor for carbon monoxide (TLCO) decreased
    4) TLC increased
  • FEV1 is also used to classify the severity of COPD
    = Stages 1 -> 4
  1. Chest X-ray: shows hyperinflation
    - Hyper inflated lungs
    - Flattened diaphragms and a long narrow heart shadow
    - Large central pulmonary arteries
    - Reduced peripheral lung/vascular markings
    - Bullae (air pockets)
    = excludes cancer
  2. CT thorax = to exlude alternativr diagnoses e.g fibrocis, cancer, bronchiectasis
  3. Sputum culture = to assess for chronic infections e.g. pseudomonas.
  4. ECG and echocardiogram = to assess heart function
36
Q

What would be the results of a lung function test in a COPD patient?

A

1) FEV1/FVC < 70%
2) FEV1 reduced (<80%)
3) Transfer factor for carbon monoxide (TLCO) decreased
4) TLC increased

37
Q

What might you see on CXR in a COPD patient?

A
  1. Hyperinflation of the lungs.
  2. Flat hemidiaphragms (flattened diaphragms).
  3. Large central pulmonary arteries.
  4. Decreased peripheral lung/vascular markings.
  5. Bullae (air pockets).
38
Q

What is TCLO and what does it tell you?

A

Transfer factor for carbon monoxide.

Low in COPD
High in asthma

39
Q

Management of COPD with asthmatic features.

A
  1. Conservative management (non-pharmacological)
    - Smoking cessation
    - Pulmonary rehabilitation
    - Annual influenza vaccine and one-off pneumococcal vaccine
    - Good diet to reduce weight and obesity
    - Personalised self-management plan
  2. 1st line - SAMA / SABA
    - SABA = short acting bronchodilators - beta-2 agonists e.g. salbutamol or terbutaline
    - SAMA = short acting antimuscarinics e.g ipratropium bromide
  3. 2nd line - LABA + ICS
    - LABA = long-acting beta-2 agonist e.g. salmeterol
    - ICS = inhaled corticosteroid e.g. beclamethasone
  4. 3rd line - LABA + LAMA + ICS (trial first for 2 weeks)
    - LAMA = long-acting antimuscarinics e.g. tiotropium bromide
40
Q

Management of COPD with no asthmatic features.

A
  1. Conservative management (non-pharmacological)
    - Smoking cessation
    - Pulmonary rehabilitation
    - Annual influenza vaccine and one-off pneumococcal vaccine
    - Good diet to reduce weight and obesity
    - Personalised self-management plan
  2. 1st line - SAMA / SABA
    - SABA = short acting bronchodilators - beta-2 agonists e.g. salbutamol or terbutaline
    - SAMA = short acting antimuscarinics e.g ipratropium bromide
  3. 2nd line - LABA + LAMA
    - LABA = long-acting beta-2 agonist e.g. salmeterol
    - LAMA = long-acting muscarinic antagonist e.g. tiotropium
  4. 3rd line - LABA + LAMA + ICS (trial first for 2 weeks)
    - ICS = inhaled corticosteroid e.g. beclamethasone
41
Q

How would you conduct a steroid trial in COPD?
What information would it give you?

A

Patient given oral prednisolone for 2 wks.
If FEV1 rises by >15%, the COPD is steroid responsive - will benefit from long-term inhaled corticosteroids e.g. beclamethasone.

42
Q

What is first line for COPD?

A
  • Smoking cessation
  • Vaccinations
  • SABA OR SAMA
    = short acting B2 agonist e.g. salbutamol
    or
    = short acting anti muscarinic e.g. ipratropium bromide
43
Q

What is second line for COPD?

A

LAMA + LABA
- LABA = long-acting beta-2 agonist e.g. salmeterol
- LAMA = long-acting muscarinic antagonist e.g. tiotropium

44
Q

What is third line for COPD?

A

ICS (e.g. beclomethasone) + LABA (e.g. salmeterol) + LAMA (e.g. tiotroprium)

45
Q

What is second line for COPD with asthmatic features?

A

LABA + ICS

46
Q

What is third line for COPD with asthmatic features?

A

LABA + ICS + LAMA

47
Q

Give 1 side effect of using inhaled corticosteroids (ICS) in COPD treatment.

A

Pneumonia

48
Q

Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD.

A

Advantages:

  1. Improve Q.O.L.
  2. Improve lung function.
  3. Reduce the likelihood of exacerbations.

Disadvantages:
1. There is an increased risk of pneumonia.

49
Q

What are other treatments to give for severe COPD?

A
  1. Oral theophylline
    - For wheeze + cough
    - NICE only recommends this after SABA and LABAs treatment or to patients, who cannot tolerate inhaled therapy.
  2. Anti-mucolytic agents e.g. carbocisteine
    - Can help by reducing sputum viscosity
  3. Diuretics
    - Can be used to treat oedema
  4. Long term prophylactic antibiotics (e.g. azithromycin)
  5. Long term oxygen therapy at home
    - Used for severe COPD that is causing problems e.g. chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale).
50
Q

Shortness of breath can lead to exercise limitation. Give 3 potential consequences of this.

A
  1. Muscle wasting.
  2. Depression and anxiety.
  3. Disability.
51
Q

Define exacerbation.

A

An acute event characterised by worsening symptoms beyond normal day to day variation. It often leads to a change in medication.

52
Q

Give 5 potential consequences of exacerbations of COPD/asthma.

A
  1. Worsened symptoms.
  2. Decreased lung function.
  3. Negative impact on Q.O.L.
  4. Increased mortality.
  5. Huge economic cost.
53
Q

What is the likely cause for an exacerbation of COPD?

A

Viral infection e.g. RSV, influenza, parainfluenza, rhino and coronaviruses.

54
Q

What is the treatment for an exacerbation of COPD?

A
  1. Oxygen.
  2. Bronchodilators.
  3. Systemic steroids.
  4. Antibiotics if there is breathlessness and sputum production.
55
Q

What are the aims of treatment for exacerbations of COPD?

A
  1. Minimise the impact of the current exacerbation.
  2. Prevent subsequent exacerbations.
56
Q

Give 3 ways in which subsequent exacerbations be prevented.

A
  1. Smoking cessation.
  2. Vaccination.
  3. LABA/LAMA/ICS.
57
Q

What does a patients’ PaO2 have to be less than in order for them to qualify for home O2?

A

PaO2 < 7.3kPa when breathing room air.

58
Q

Describe the assessment process for home O2?

A
  1. Blood gas measurements are taken 3 weeks apart in a stable patient receiving bronchodilator therapy.
  2. The patient needs to have stopped smoking.
  3. The patient should have a PaO2 < 7.3kPa.

Respiratory (9 decks)

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