COPD Flashcards

1
Q

What is the definition of COPD?

A

Broad term for a few obstructive airway disorders:
Chronic bronchitis
Emphysema

Airflow obstruction is defined as a reduced FEV1/FVC ratio = <0.7

Airflow obstruction is present because of a combination of airway and parenchymal damage

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2
Q

What is the epidemiology of COPD?

A

1.5 million with 23,000 mortality/year in the UK
3rd leading cause of death by 2020 and increasing

More common in men but rising in women

Low socioeconomic status and low birth weight are predisposing factors

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3
Q

What is the aetiology of COPD?

A

Smoking is the main cause – 90-98% of all cases
Most commonly seen in ex smokers >35 yrs old

Unlikely to develop in someone with less than 10 pack years

Other causes are occupational:
Coal mining
Asbestos exposure

Genetic factors:
Alpha1-antitrypsin deficiency causes emphysema

Age related too – onset in 50s-60s

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4
Q

What is the pathophysiology of emphysema?

A

Destruction of lung parenchyma – alveoli and respiratory bronchioles

Confluent areas of destruction may cause macroscopic bullae (large blisters containing serous fluid)

Can be named according to location of damage

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5
Q

What is the pathophysiology of bronchitis?

A

Submucosal bronchial gland enlargement and goblet cell metaplasia and mucous hypersecretion

Inflamed bronchial glands

Airway epithelial squamous metaplasia

Cilliary dysfunction

Hypertrophy of smooth muscle and connective tissue

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6
Q

What are some other general features of the pathology of COPD?

A

Involvement of smaller airways is key:
- Loss of elasticity means the airways aren’t splinted open and so with increased intrathoracic pressure during expiration, they may collapse - limiting airflow

Pulmonary vasculature:

  • Thickening and endothelial cell destruction
  • Hypertrophy of vascular smooth muscle and collagen deposition lead to reduction in functioning of vessels
  • Pulmonary vasoconstriction due to hypoxia - pulmonary artery pressure rises – pulmonary hypertension - right heart failure

Inflammatory profile:

  • Different to asthma
  • Asthma – CD4 lymphocyte, eosinophils
  • COPD – CD8 lymphocytes, macrophages, neutrophils (may also have eosinophils)
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7
Q

How does COPD present?

A

SOB
Cough - often productive sputum (a spectrum of colours from mucoid/white to purulent/green, worse with infection, possible blood if Ca)

Wheeze
Poor expansion

Cyanosis
Use of respiratory muscles for respiration
Signs of CO2 retention i.e. confusion, flap

Nicotine/tar stained hands
Barrel chest
Pulmonary heart disease (cor pulmonale)

Asthmatic features:
Atopy, early onset symptoms, minimal smoking history, eosinophilia, bronchodilator reversibility

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8
Q

What is the MRC breathlessness scale?

A

Grading of breathlessness, used to assess functioning:

Grade 1 = not troubled by SOB, only on strenuous exercise

Grade 2 = SOB when hurrying on level or walking up slight incline

Grade 3 = walks slower than most on level ground, stops after a mile or so or after 15 mins walking at own pace

Grade 4 = stops for breath after 100yrds or a few mins on level ground

Grade 5 = too breathless to leave house, or breathless when undressing

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9
Q

How do you investigate COPD? What are the key findings?

A

Diagnosis = clinical judgement based on:

  • History
  • Physical examination
  • Confirmation of airway obstruction using spirometry
  • COPD assessment test (CAT) – questionnaire

Spirometry:

  • FVC<80% predicted
  • Low FEV1
  • FEV1/FVC <0.7
  • Increased residual volume

ABG:

  • Lower PaO2 - 88-92% are typical targets
  • Poor ventilation may also give high CO2 (T2 resp. failure)
  • Poor V/Q mismatch
  • Always note what FiO2 is (air? 2L? more?)

Other:

  • CXR, CT scan - possible: hyperinflation, flat hemidiaphragms, large pulmonary arteries, decreased peripheral vascular markings; pneumothoracies? infection? Ca?
  • ECG - right atrial and ventricular hypertrophy suggestive of cor pulomnale – large P waves
  • Blood α1 antitrypsin - possible deficiency (neutrophil enzyme elastase is then free to break down elastin in lungs, reducing elasticity and leading to COPD)
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10
Q

What are non-pharmacological managements for COPD?

A

Smoking cessation – the best thing to do, at any point in the illness

Encourage exercise at own level - walking

Nutritional support - either weight loss or gain might be required

Physiotherapy - breathing and coughing techniques

Possible need for OT/psychoT.

Recognising signs of exacerbations - hospital plan for when this is the case

Vaccination – pneumococcal and influenza - to prevent any respiratory infections

Follow up at least yearly, more regularly with severe disease +/- specialists

Fitness to fly assessments:

  • Enquiring whether the person is able to walk for 50 metres at a normal pace, or climb one flight of stairs, without significant breathlessness - If so, it is likely that the person will tolerate the normal aircraft environment
  • Also hypoxic challenge test
  • More guidelines re. specific questions pre-flying

Pulmonary rehabilitation

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11
Q

What is pulmonary rehabilitation for COPD?

A
  • Given when MRC score 3-5
  • 6-12 wks, 2-3 times/wk
  • Aerobic and resistance training
  • Education
  • Nutritional support
  • Psychological support
  • Repeat annually or if circumstances change
  • Improves - exercise capacity, QoL, SOB, Fewer hospitalisations

Not for patients that cannot walk or have unstable angina or a recent MI

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12
Q

What is the stepwise management for COPD?

A

1) Inhaled bronchodilators:
- For SOB + exercise limitation
- SABA - salbutamol - PRN OR
- SAMA - ipratropium bromide PRN
- Need to ensure appropriate delivery system (coordination, dexterity etc)

2a) If no improvement WITHOUT features of asthma or steroid responsiveness:
- LABA - salmeterol AND
- LAMA - tiotropium (often come as combined inhalers)
- Discontinue SAMA
- If no improvement, add 3/12 trial ICS and reassess for stopping/continuation

2b) If no improvement WITH features of asthma/steroid responsiveness:
- LABA + ICS (often come as combined inhalers)
- (+/- LAMA if still not improving = triple therapy; discontinue SAMA)

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13
Q

What other treatments can be prescribed by a specialist for people with COPD who require more than inhalers?

A

Home nebulisers:
- O2 vs air driven - if hypercapnic = air driven

Oral corticosteroids:
- Remember osteoporosis prophylaxis

Oral theophylline:

  • For those who have not benefitted from inhalers or who cannot use inhaled therapy
  • Plasma level monitoring and dose adjustment required
  • Reduce dose if macrolides or fluoroquinolones prescribed for an exacerbation

Oral mucolytic therapy:

  • Only if chronic productive cough
  • PO N-acetyl cystine

Oral prophylactic Abx:

  • Strict criteria, including >3 exacerbations requiring steroids in last year incl. 1 hospital admission
  • Macrolide e.g. azithromycin 500mg 3x/wk
  • Need ECG (QTc), LFTs, sputum MC+S, CT
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14
Q

What is long term oxygen oxygen therapy and the indications for it?

A

Long term oxygen therapy (LTOT):
2L via nasal cannula for at least 15hrs/day in really extreme cases

DO NOT START WITHOUT SPECIALIST SUPPORT:
May cause respiratory depression due to reduced hypercapnic drive for respiration

Indications:

  • Oxygen saturation less than or equal to 92% breathing air
  • Very severe airflow obstruction - FEV1 < 30% predicted
  • Cyanosis
  • Secondary polycythaemia
  • Peripheral oedema
  • Raised jugular venous pressure

Need counselling on fire/explosive risk - NO SMOKING

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15
Q

How do you grade acute exacerbations of COPD?

A

Acute exacerbation:

  • Worsening breathlessness
  • Increased sputum volume and purulence
  • (new) Cough
  • Wheeze
  • Fever
  • Upper respiratory tract infection in the past 5 days
  • Increased respiratory rate or heart rate increase 20% above baseline

Acute severe exacerbation:

  • Marked breathlessness and tachypnoea
  • Pursed-lip breathing and/or use of accessory muscles at rest
  • New-onset cyanosis (O2 <90% on oximetry) or peripheral oedema
  • Acute confusion or drowsiness
  • Marked reduction in activities of daily living

Need a full clinical assessment:

  • Vital signs, resp. examination, coping at home etc
  • Consider other possible Dx
  • Consider the need for hospital admission
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16
Q

How do you manage acute exacerbations of COPD?

A

At home:

  • Increase SABA to max dose; consider nebs
  • Prednisolone PO - 30mg OD 5/7 (non-infective ECOPD)
  • Abx - ONLY if purulent sputum e.g. amox 500mg TDS 5/7; doxycycline 200mg 1/7 then 100mg OD 4/7 (IECOPD)
  • Safetynet

If severe:

  • Hospital admission +/- ITU
  • Controlled O2 - carefully: follow local protocols/instructions on persons oxygen alert card if available; e.g. 24% Venturi at 2-3L/min; Aim for 88-92% in most instances; ABGs needed; possible NIV
  • Nebulised salbutamol
  • Steroids PO
  • Treat the cause – often a chest infection - IV abx etc
  • Aminophylline
17
Q

What are the GOLD stages?

A

Global initiative for chronic Obstructive Lung Disease

Grading ABCD based on: yearly exacerbations, breathlessness and severity of airflow limitation/FEV1%

A:

  • 1 or fewer exacerbations
  • Breathless on strenuous exercise
  • FEV1 >80% (GOLD 1/mild)

B:

  • 1 or fewer exacerbations
  • Has to stop when walking
  • FEV1 50-79% (GOLD 2/moderate)

C:

  • 2+ exacerbations or 1+ hospital admission
  • Breathless on strenuous exercise
  • FEV1 30-49% (GOLD 3/severe)

D:

  • 2+ exacerbations or 1+ hospital admission
  • Has to stop when walking
  • FEV1 <30% (GOLD 4/very severe)
18
Q

What are the features of alpha-1 antitrypsin deficiency?

A

Inherited condition caused by deficiency of a protease inhibitor (Pi) normally produced in the liver

  • Protects cells against neutrophil elastase over activation and degeneration of tissue
  • Autosomal recessive inheritance
  • 3 different allele variations on chromosome 14 M + normal, S = slow, Z = very slow
  • PiMM = normal; A1AT; PiSS = 50% normal levels; PiZZ = 10% normal levels - most likely to present

Mostly presents as a lower lobe emphysema in younger non-smokers
- Can be diagnosed prenatally on amniocentesis

GI effects:
- Cholestasis cirrhosis, HCC - and all the known sequalae of this (e.g. jaundice)

A1AT levels + genetic testing
Obstructive spirometry
Liver biopsy

Managed with non-smoking, bronchodilators and physio, IV A1AT protein concentrates, possible surgery or lung-liver transplant