Chronic Obstructive Pulmonary Disease (COPD) Flashcards

1
Q

What is COPD?

A

A chronic, slowly progressive disorder characterised by airflow obstruction that does not change markedly over several months. Most of the lung function impairment is fixed, although some reversibility can be produce by bronchodilator (or other) therapy.

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2
Q

What is important to note about the definition of COPD?

A

Defined by airflow obstruction.

NO mention of symptoms, chronic bronchitis, emphysema or smoking.

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3
Q

What causes airway obstruction in COPD?

A

Small-airway narrowing and can be worsened by inflammation and mucus (increased no. of goblet cells). Also get thickening of airway walls, loss of elasticity and disrupted alveolar attachments. Lymphoid follicles in severe disease.

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4
Q

What do the vast majority of people in COPD have?

A

Chronic bronchitis and emphysema.

Some only have emphysema and this is due to a genetic component - alpha 1-antitrypsin deficiency.

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5
Q

What is the prevalence of COPD like in the UK?

A

1.2 mil diagnosed
50% of total no of COPD patients diagnosed
Total prevalence approx. 1.5-2 mil.

Male predominance and increasing prevalence.

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6
Q

Why can COPD be called a disease of social deprivation?

A

Affects those in social deprivation as they are more likely to smoke/lower education.

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7
Q

COPD is the —th most common cause of death in the UK.

A

6th
(5th most common WW).
By 2030, will be third leading cause of death.

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8
Q

What burden does COPD have on the NHS?

A

Responsible for 1.5% of all acute hospital admissions (164, 000 admissions, 1, 300, 000 bed days).

10% acute admissions due to COPD.
15% of COPD patients admitted per year.
86% are exclusively primary care.
On average each COPD patient visits GP 6-7 per year.

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9
Q

How does COPD affect the patient?

A

Ranges depending on severity of COPD. May cause difficulty climbing stairs, gardening, housework, dressing and sleep disturbance.

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10
Q

What is the majority of COPD attributable to?

A

85% COPD attributable to smoking.

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11
Q

What are some other less common causes of COPD?

A

Chronic asthma
Passive smoking
Maternal smoking (reduces FEV1 and increases resp illness)
Air pollution (prevalence of COPD increased with air pollution)
Occupation - jobs exposing to dusts, vapours and fumes (e.g. coal mining, hard rock mining, tunnel working, concrete manufacturing, construction, farming, foundry working, plastics, textiles, rubber, leather…).
a1-antitrypsin deficiency.

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12
Q

What is the role of a1-antitrypsin?

A

Produced in the liver, circulates in the blood and particularly important in the lungs. When you breathe in cig smoke you kill off neutrophils, neutrophils release a lot of prolytic enzymes which can cause COPD. a1-AT neutralises neutrophil enzymes and protects the lungs.

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13
Q

What is a1-antitrypsin deficiency?

A

75 different variants (normal genotype 86% UK - PiMM and troublesome genotype PiZZ (10-20% MM).
PiZZ accounts for 0.03% of population (not all COPD).
People with this develop COPD at a very young age.
E.g.
Non-smokers with this develop dyspnoea @ 51 yrs, and die @ 67 yrs.
Smokers with this develop dyspnoea @ 32 yrs and die @ 48 yrs.

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14
Q

How many smokers develop clinically significant COPD? Subclinical airflow obstruction? Never develop any significant airflow obstruction?

A

Cig smoking is clearly the single most important identifiable aetiological factor in COPD.
Only 20% of smokers develop clinically significant COPD.
30% significant but subclinical airflow obstruction.
50% never develop significant airflow obstruction.

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15
Q

How much COPD develop in non-smokers?

A

Asthma, a1-AT deficiency.

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16
Q

Tobacco consumption is important in assessing a COPD patient, how is this measured?

A

Pack years
= 1 pack a day for a year.
Typically people develop COPD once they’ve smoked 20 ack years.

17
Q

What is rate of decline of FEV1 like in smokers compared to non smokers?

A

Nonsmoker about 30ml/yr.

Smoker about 50ml/yr (some 80).

18
Q

What is the typical COPD patient like?

A

Patient 40+ years, smoker/exsmoker, SoB on exertion, cough.

19
Q

What would be your differentials from hearing ‘patient 40+, smoker/ex-smoker, SoB on exertion, cough’?

A
COPD
Asthma
Lung cancer
LVF
Fibrosing alveolitis 
Bronchiectasis
Rarities - TB, recurrent pulmonary emboli.
20
Q

What is it important to check about the patients symptoms if you suspect COPD?

A

Exclude other possible diagnoses (heart failure, Ca).
None of the features of variable airflow obstruction of asthma.
Symptoms are insidious, gradually worsening over the years.

21
Q

What is SoB like in patients with COPD?

A

Gradual onset, little variation.
Will get increasingly worse, so may start with SoB with hills, stairs, loads, hurrying, then to walking on flat with contemporaries, gardening, to then having difficulties doing housework then dressing and washing to finally having SoB at rest.

22
Q

What is the cough like in COPD patients?

A
Long history of smokers cough. 
Clear or mucoid sputum. 
Early morning winter months. 
All day winter months. 
All day and all year. 
94% resolution if stop smoking.
23
Q

What would you think if there was haemopytsis?

A

Consider lung cancer, TB or bronchiectasis.

24
Q

What are some other symptoms that might come with COPD?

A

Wheeze, typically on exertion.
Weight loss (severe disease, TNFalpha).
Peripheral oedema - cor pulmonale, severe disease, resp failure.

25
Q

What could be expected in the PMH of a COPD patient?

A

Asthma as a child, adolescent.
Resp diseases.
Ischaemic heart disease.

26
Q

What might you expect in the D&A of a COPD patient?

A

List of current inhalers, doses (in micro).

Previous meds and effect on breathing (steroids).

27
Q

What would you expect in SH of a COPD patient?

A

Smoking history, age started, stopped, cig/day, pack years.

Occupation.

28
Q

What are the signs of COPD?

A

SoB walking into clinic, undressing - pursed lip breathing, accessory muscle.
Cyanosis
CO2 flap, tremor (beta-agonists).
Effects of steroids - tissue skin, bruising, Cushingoid.
Hyperexpanded (barrel chest), decreased expanision <3bf manubrium:larnyx.
Larnygeal descent
Paradoxical movement of ribs and abdomen.
Decreased cardiac dullness to percussion, decreased breath sounds (no crackles), prolonged expiration with wheeze, palpable liver).

29
Q

What are signs of cor pulmonale?

A

Elevated JVP, hepatomegaly, ascites, oedema.

30
Q

What investigations must you carry out?

A

Spirometry - if airway obstruction will have reduced FEV1 (<80% of predicted) and reduced FEV1/FVC ratio (<70%).
A normal FEV1 rules out diagnosis.
Full pulmonary function test (looking for emphysema)
- lung volumes - gas trapping:
increased residual volume, increased total lung capacity, RV/TLC >30%.

  • carbon monoxide gas transfer - decreased gas transfer - decreased TLCO, decreased KCO = tissue destruction.

Demonstrate fixed airflow obstruction by spirometry.

31
Q

How can severity of COPD be determined from spirometry?

A

> 80% - mild AFO = @ risk.
50-79% - moderate AFO = cough, SoB on moderate exertion.
30-49% - severe AFO = SoB on mild exertion, cough/sputum.
<30% - v severe AFO = SoBoE++, wheeze, cough, cor pulmonale.

32
Q

How do you demonstrate fixed airflow obstruction with spirometry?

A

Minimal bronchodilator reversibility
Baseline, 15 min post neb 2.5-5mg salbutamol
Baseline, 30 min post neb 2.5-5mg + 500microg ipratropium.

Minimal response to oral corticosteroids
30-40mg prednisolone daily for 2 weeks (0.6mg/kg)
Measure baseline and final FEV1

Increasing trend not to do trials of steroids.

33
Q

What is considered as significant reversibility? What would this suggest?

A

If chance in FEV1 is >200ml and change in FEV1 >15% baseline.

Suggests asthma/asthmatic component, as COPD has insignificant bronchodilator/steroid response, but does not predict benefit from long term use.

34
Q

What are some other useless investigations you might do?

A

CXR - hyperinflated lung fields (>10 posterior ribs), flattened diaphragms, lucent lung fields, bullae.
Bronchogenic carcinoma, interstitial disease, LVF can be picked up.

Blood gases can check for resp failure.
Full blood count to check for secondary polychythaemia.
ECG - right axis deviation, P pulmonale, T wave inversion V1-V4.
Sputum - MC&S (S pneumoniae, H influenzae, M catarrhalis).

35
Q

What are acute exacerbations of COPD usually precipitated by?

A

Viral/bacterial infection, but consider sedative drugs, pneumothorax, trauma.

36
Q

What happens in the acute exacerbations?

A

Increased coughing, sputum, sputum purulence, SoB, wheeze, oedema, drowsiness and confusion (hypoxia).

Unable to sleep.

Will be cyanosed, flapping tremor, pyrexial.

37
Q

If suspected AECOPD what do you do?

A

CXR, blood gases, FBC, U&E, sputum culture.

Management - neb bronchodilator, beta2 and anti-muscarinic, oxygen, IV/oral corticosteroid, antibiotic, diuretic IV aminophylline, resp stimulant, NIV.

38
Q

What are the most common bacterial organisms causing AECOPD?

A

H. influenzae (most common)
Strep pneumoniae
Moraxella catarrhalis

39
Q

How should AECOPD be managed?

A

Increased bronchodilator frequency, consider nebulising
Prednisolone 30mg 7-14d
Antibiotics if sputum purulent/signs of pneumonia (amoxicillin/clarithromycin/doxycycline)