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8. Respiratory > COPD (Chronic Obstructive Pulmonary Disease) > Flashcards

COPD (Chronic Obstructive Pulmonary Disease) Flashcards

1
Q

Define COPD.

A

A chronic disease of progressive airway obstruction, which is irreversible and does not change markedly over several months

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2
Q

List 3 causes of COPD.

A

Smoking
Environmental pollution
Alpha 1 anti-trypsin deficiency

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3
Q

How does smoking cause COPD?

i.e.

Describe the effect of cigarette smoking on the lungs. (6)

A
  1. Reduced cilia motility/destruction of cilia
    a. Causes reduced mucous clearance
    b. Leads to increased frequency of infection and damaged lungs
  2. Airway inflammation
  3. Mucous gland and Goblet cell hypertrophy
    a. Causes increased mucous production
    b. Leads to increased frequency of infection and clear sputum production
  4. Increased protease activity and decreased production of anti-proteases
  5. Oxidative stress caused by inflammatory cells
  6. Squamous metaplasia
    a. Causes increased risk of lung cancer
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4
Q

Briefly list the 6 effects of smoking on the lungs.

A
  1. Reduced cilia motility/cilia destruction
  2. Airway inflammation
  3. Mucous gland/Goblet cell hypertrophy
  4. Increased protease activity and decreased production of anti-proteases
  5. Oxidative stress
  6. Squamous metaplasia
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5
Q

Which mutation is found in an alpha 1 anti-trypsin deficiency?

A

Normal alleles: M

Alleles causing disease: SS and ZZ

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6
Q

How does an alpha 1 anti-trypsin deficiency cause COPD? (2)

A
  1. Normally, alpha 1 anti-trypsin is a serine proteinase inhibitor which inhibits destructive enzymes in the lung
  2. Deficiency of anti-trypsin is unable to counter-balance proteinases in the lung
    a. Therefore lung destruction occurs
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7
Q

What are the 2 main aspects of COPD pathophysiology?

Define them.

A

Chronic bronchitis:
“Production of sputum on most days for at least 3 months, over at least 2 years”

Emphysema:
“Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles”

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8
Q

Describe the pathophysiology of chronic bronchitis. (5)

A
  1. Infiltration of bronchiole wall with:
    a. Neutrophil
    b. T lymphocytes
    c. Macrophages
  2. Release of inflammatory mediators from inflammatory cells
  3. Loss of interstitial support
    a. This causes increased risk of airway collapse
  4. Increased mucous production, caused by:
    a. Increased numbers of epithelial goblet cells
    b. Mucous gland hyperplasia
  5. Squamous metaplasia
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9
Q

List 8 inflammatory mediators which are involved in chronic bronchitis.

HINT: there are 4 categories.

A

Chemokines, e.g.

  • TNF
  • IL-8

From neutrophils, e.g.

  • Neutrophil elastase
  • Proteinase 3
  • Cathepsin G

From macrophages, e.g.

  • Elastase
  • MMPs

Reactive oxygen species

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10
Q

What are the 2 types of chronic bronchitis?

A

Bronchitis
-Affects larger airways (4+mm diameter)

Bronchiolitis
-Affects smaller airways (2-3mm)

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11
Q

What are the main features of bronchitis? (1)

What are the main features of bronchiolitis? (2)

A

BRONCHITIS:
Chronic inflammation leads to scarring and thickening of the airways

BRONCHIOLITIS:

  • Narrowing of bronchioles due to mucous plugs
  • Further narrowing due to inflammation and fibrosis
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12
Q

What are the 3 types of emphysema?

A

Centri-acinar
Pan-acinar
Paraseptal

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13
Q

Where are the 3 types of emphysema found?

A

Centri-acinar: around respiratory bronchioles (most often in upper lobes)

Pan-acinar: throughout whole acinus

Paraseptal: along the edges of the septum between acini

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14
Q

What are the features of pan-acinar emphysema? (2)

What are the features of paraseptal emphysema? (2)

A

Pan-acinar emphysema:

  • Uniformly enlarged from the terminal bronchiole
  • May form large bullae

Paraseptal emphysema:

  • May form bullae
  • Appears as lines around the septa
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15
Q

Describe the pathophysiology of emphysema. (2)

A
  1. Loss of surface area for gas exchange
  2. Loss of elastic recoil in bronchioles
    a. This causes airway collapse on expiration
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16
Q

Describe the pathophysiology of COPD. (5)

A
  1. Airway inflammation
  2. Loss of elasticity of the alveoli and small bronchioles (caused by: emphysema)
    a. This causes loss of alveolar attachments
    b. This causes airway collapse on expiration
  3. Small airway collapse on expiration
    a. This causes air trapping and hyperinflation
    b. This causes increased work of breathing
    c. This causes breathlessness
  4. Goblet cell metaplasia
    a. This causes increased mucous production
    b. This causes mucous plugging of small airways
  5. Smooth muscle hypertrophy and peri-bronchial fibrosis
    a. This causes thickening of the bronchiole wall
17
Q

How would you diagnose COPD? (4)

A
  1. Smokers or ex-smokers
  2. Above 35 yo
  3. Clinical history of:
    - Breathlessness on exertion
    - Chronic cough
    - Regular sputum production
    - Frequent winter “bronchitis”
    - Wheeze
  4. Spirometry:
    - Obstructive pattern, i.e. FEV1/FVC <70%
18
Q

Describe how to classify COPD severity. (4)

A

Stage 1: mild
-Predicted FEV1: 80+%

Stage 2: moderate
-Predicted FEV1: 50-80%

Stage 3: severe
-Predicted FEV1: 30-50%

Stage 4: very severe
-Predicted FEV 1: <30%
OR
-Predicted FEV 1: <50% WITH respiratory failure

19
Q

What investigations can be done for COPD? (3)

What is seen on each?

A

Chest x-ray:

  • Hyperinflation
  • Reduced lung markings

Flow-volume loop:
-Church and steeple appearance

Volume-time plot:

  • Slow-rising curve
  • Reduced FEV1
20
Q

What are the 2 types of respiratory failure which might be seen in COPD?

A

Type 1 (pink puffers)
Features:
-Low pO2 and low/normal pCO2
-High respiratory drive

Type 2 (blue bloaters)
Features:
-Low pO2 and high pCO2
-Low respiratory drive THEREFORE DO NOT GIVE HIGH FLOW OXYGEN

21
Q

Describe the symptoms of type 1 respiratory failure. (6)

Type 1:

  • Low pO2
  • Low/normal pCO2
A 
Desaturation on exercise
Pursed lip breathing
Use of accessory muscles while breathing
In-drawing of intercostal muscles while breathing
Wheeze
Tachypnoea (RR 20+)
22
Q

Describe the symptoms of type 2 respiratory failure. (8)

Type 2:

  • Low pO2
  • High pCO2
A 
Cyanosis
Warm peripheries
Bounding pulse
Flapping tremor
Confusion/drowsiness
Right heart failure
Peripheral oedema
Raised JVP
23
Q

List the 7 types of drugs that can be given for COPD.

A

Inhaled beta 2 agonists

Inhaled anti-muscarinic drugs

Inhaled theophylline

Inhaled corticosteroids

Oxygen therapy

Mucolytic drugs

Nebulised therapy (bronchodilators/steroids)

24
Q

Give 2 examples of inhaled corticosteroids used in COPD.

A

Budesonide

Fluticasone

25
Q

Give 1 example of a mucolytic drug used in COPD.

A

Carbocysteine

26
Q

Apart from respiratory failure, what other complication can be caused by COPD?

List 2 features of this condition.

A

Cor pulmonale

FEATURES:
Right sided heart failure secondary to lung disease
Salt and water retention leading to peripheral oedema

27
Q

How is end-stage COPD treated? (2)

A

Non-invasive ventilation (continuous positive airway pressure)

Long term oxygen therapy

28
Q

What are the 3 criteria for long term, home oxygen therapy?

A

Non-smoker

pO2 <7.3

pO2 7.3-8.0 with any of the following:

  • Secondary polycytaemia
  • Nocturnal hypoxaemia
  • Peripheral oedema
  • Pulmonary hypertension
29
Q

How do you measure pack years for smoking?

A

Pack years = (number of packs per day) x years of smoking

NOTE: one pack is 20 cigarettes

30
Q

Summarise chronic COPD treatment. (10)

A

LIFESTYLE CHANGES:

  1. Smoking cessation
  2. Regular exercise

DRUG THERAPY:

  1. Inhaled beta 2 agonist
  2. Inhaled anti-muscarinic drugs (e.g. tiotropium, ipratropium bromide)
  3. Inhaled theophylline
  4. Inhaled corticosteroids
  5. Oxygen therapy
  6. Mucolytic drugs (e.g. carbocysteine)
  7. Nebulised therapy (e.g. bronchodilators, steroids)

RISK ASSESSMENT:
A-B: low risk of exacerbations
C-D: high risk of exacerbations

31
Q

How would you treat end-stage COPD? (3)

A

Non-invasive ventilation (continuous positive airway pressure)
Pulmonary rehabilitation
Long term oxygen therapy

32
Q

Which investigations would you do for an acute exacerbation of COPD? (6)

A

ABGs

CXR (to exclude infection, pneumothorax)

Bloods, e.g.

  • FBC
  • U&Es
  • CRP
  • Theophylline levels

ECG

Sputum cultures

Blood cultures (if pyrexial)

33
Q

How would you treat an acute exacerbation of COPD?

A
  1. Nebulised bronchodilators, e.g.
    a. Salbutamol
    b. Ipratropium
  2. Controlled oxygen therapy (start at 24-28%; aim for sats 88-92%)
  3. Steroids, including:
    a. IV hydrocortisone
    b. Oral prednisolone
  4. Antibiotics (if evidence of infection)
  5. IV theophylline (if no response to nebulisers/steroids)
  6. Non-invasive ventilation (if no response to theophylline)
  7. Intubation and ventilation (if no response to NIV)
34
Q

What is the empirical antibiotic therapy for non-severe infectious exacerbations of COPD?

For how long?

What route?

A

Oral amoxicillin, OR
Oral doxycycline, OR
Oral clarithromycin

Duration: 5 days

35
Q

What is the empirical antibiotic for severe infectious exacerbations of COPD?

For how long?

What route?

A

IV amoxicillin, OR
IV clarithromycin

Duration: 7 days

8. Respiratory (14 decks)

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