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Respiratory > COPD > Flashcards

COPD Flashcards

1
Q

Define chronic bronchitis.

A

Clinical diagnosis characterised by excessive secretions of bronchial mucosa and productive cough for >3months in 2 consecutive years.

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2
Q

What is COPD?

A

Chronic airflow obstruction due to chronic bronchitis or emphysema. Usually progressive, +/- accompaniment by airway hyperreactivity (may be partially reversible).

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3
Q

What is the typical FEV1 of COPD?

A

FEV1 will be less than 80% of expected.

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4
Q

What is emphysema?

A

Pathologic diagnosis denoting abnormal, permanently enlarged air spaces distal to the terminal bronchiole, with destruction of their walls without obvious fibrosis.

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5
Q

What are the major causes of COPD? Other RFx?

A

-Inhalational injury (smoking)
-a1-antitrypsin deficiency
RFx:
-Occupational exposure
-Bronchial hyperreactivity
-Passive smoking
-Air pollution

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6
Q

What is the common presentation of COPD?

A

Patients present with progressively worsening dyspnoea (exertion -> rest).
Vary in appearance: blue bloater (chronic bronchitis, overweight, oedematous,cyanotic) OR pink puffer (emphysema, thin ruddy cheeks).
Consider Dx in anyone with chronic or productive cough, dyspnoea, RFx.

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7
Q

How do ABGs apppear throughout the course of COPD?

A

Early: Initially normal in early phase
Advanced: hypoxemia and hypercapnia. Often with a chronic compensated respiratory acidosis due to CO2 retention.

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8
Q

What is the 50-50 club?

A

PaO2 near 50
PaCO2 near 50
Near normal pH

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9
Q

What are the spirometric patterns of obstructive lung disease?

A

Obstructive diseases have:

  • larger lung volumes (TLC normal or increased)
  • decreased FER (to
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10
Q

What is the spirometric pattern of restrictive lung disease?

A

Lower lung volumes (decreased TLC and VC)

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11
Q

What are the underlying principles of COPD management?

A

Relieving airway obstruction and correcting life threatening gas exchange abnormalities.

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12
Q

What is the Rx (inc non pharmacologic) of COPD?

A
  • Smoking cessation
  • Drug therapy: short term exacerbations and long term (FEV1 Bronchodilators
  • > Corticosteroids
  • > Antibiotics (if infection suspected)
  • Oxygen therapy
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13
Q

How should bronchodilators be used in COPD?

A
  • B-adrenergic agonists initially:
  • > SABA: (ventolin = Salbutamol);
  • > add LABA (serevent = salmeterol) if indicated by mod-severe disease.
  • Antimuscarinic agent:
  • > e.g (spiriva = Tiotropium; atrovent = ipratropium)
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14
Q

Do anti-muscarinics improve decline in FEV1?

A

Anti-muscarinic agents e.g. tiotropium improve patient’s function and quality of life but decline in FEV1 is unaffected.

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15
Q

Describe corticosteroid therapy in COPD.

A

In symptomatic patients with mod-severe COPD –> trial prednisolone 30mg for 2/52.

Measure lung function before and after; improvement FEV1>15% –> replace prednisolone with inhaled beclomethasone 40ug bd.

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16
Q

Does the combination of LABA and inhaled corticosteroid improve mortality?

A

No. Protects against a decline in lung function but does not improve mortality.

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17
Q

How should antibiotics be used in COPD?

A

Shortens exacerbations –> always give acutely.

e.g. amoxicillin, co-amoxyclav

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18
Q

Does oxygen use improve mortality? Under what conditions?

A

Yes. Substantial improvement only when administered 19h daily at flow rate 1-3L/min with 28% O2 mask.

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19
Q

What are the signs of acute respiratory failure?

A

Tachypnoea (resp >40 breaths/min); inability to speak due to dyspnoea; accessory muscle use with fatigue; confusion; restlesness/agitation/lethargy; rising PCO2 and hypoxia.

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20
Q

How is acute respiratory failure treated?

A

Endotracheal intubation with ventilatory support (to correct gas exchange disorders).

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21
Q

What are the complications of mechanical ventilation?

A

Difficulty in extubation, ventilator-associated pneumonia, pneumothorax, ARDS.

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22
Q

What are the long term complications of COPD from hypoxia?

A
  • Pulmonary hypertension
  • Secondary erythrocytosis
  • Exercise limitation
  • Impaired mental functioning
23
Q

Which interventions have been shown to improve mortality and interrupt natural history of COPD?

A

Smoking cessation
Supplemental oxygen therapy (if chronic hypoxemia)
Lung volume reduction surgery

24
Q

When does home oxygen therapy provide benefit?

A

Patients with resting hypoxemia:

PaO2 <88%

25
Q

What is the most likely examination finding in COPD?

Diffuse expiratory wheeze, clubbing, bibasal inspiratory crackles + increased JVP, inspiratory stridor, S3.

A

Diffuse expiratory wheeze.
COPD OBSTRUCTIVE! Most airflow limitation in small airways of LRT –> expiratory wheeze.
Inspiratory stridor = upper airway
Clubbing not generally COPD feature (look for other process e.g. bronchogenic carcinoma)
Crackles, increased JVP and S3 indicate CCF.

26
Q

Why does nocturnal hypoxia occur in COPD patients?

A

Alveolar hypoventilation due to:

  • inhibition of accessory and intercostal muscles in REM
  • shallow breathing in REM reducing ventilation
  • increase in upper airway resistance due to decreased muscle tone
27
Q

What is nocturnal hypoxia?

A

PaO2 may drop as low as 19mmhg, esp in REM.

COPD patients already hypoxic –> much larger fall in O2 sat due to steepness of HbO2 dissociation curve

28
Q

What is contraindicated in patients with nocturnal hypoxia?

A

Sleeping tablets.

Will further depress respiration.

29
Q

How should acute COPD exacerbation be managed?

A
  • Oxygen therapy (watch PaCO2 levels)
  • Removal of retained secretions (cough, physio)
  • Respiratory support (e.g. CPAP)
  • Drugs: corticosteroids, B-agonists, antibiotics
30
Q

What are the signs of COPD?

A

Initially: nothing more than quiet wheeze

Advanced: tachypnoeic, prolonged expiratory phase, accesorry muscle use, intercostal indrawing on inspiration, poor chest expansion, lungs hyperinflated, loss of normal cardiac and liver dullness.a

31
Q

What are the signs of hypercapnia?

A

Peripheral vasodilation
Bounding pulse
Coarse flapping tremor (when PaCO2 >10kPa)
Severe: confusion and progressive drowsiness; +/- papilloedema (not diagonstic)

32
Q

What is cor pulmonale?

A

Heart disease secondary to disease of the lung.

Characterised by pulmonary HTN –> RVH –> RHF.

33
Q

What are the examination findings of cor pulmonale?

A
  • Patient is centrally cyanosed (due to lung disease);
  • when heart failure develops: increased breathlessness, ankle oedema.
  • Prominent parasternal heave due to RVH
  • Loud P2
  • RHF may lead to tricuspid incompetence with increased JVP, ascites and hepatomegaly.
34
Q

How is COPD diagnosed?

A

Usually clinical; GOLD criteria for classification.

Stage I - IV (mild - very severe) based on FEV1/FVC (80 / 50 / 30 /

35
Q

What investigations are required in COPD?

A

Lung function tests (show airflow limitation)
CXR: often normal, even in advanced disease. Classically: overinflation with low, flattened diaphragms, +/- bullae.
CT: can show emphyesematous bullae
ABGs: often normal at rest

36
Q

How is COPD prognosis estimated?

A 
BODE: 
Body mass index
Obstruction (degree of airflow obstruction)
Dyspnoe
Exercise capacity
BODE 0-2, mortality = 10%
BODE 7 - 10, mortality = 80% at 4 years
37
Q

Outline the pathogenesis of COPD.

A

Noxious agent triggers inflammation in airways, lung parenchyma and pul vessels causing:
i) Small Airway Disease: airway inflammation and remodelling
ii) Parenchymal destruction: loss of alveolar attachments and loss of elastic recoil.
Both precipitate airflow limitation.

38
Q

What is the mechanism of emphysema?

A
  • Protease /antiprotease imbalance (proteases digest elastin and other structural proteins in alveolar wall)
  • M0 and T lymphocytes prominent
39
Q

What are the different patterns in emphysema?

A
  • Centriacinar (radiates from terminal bronchiole)
  • Panacinar (more generalised)
  • Bullae
40
Q

What is FER?

A

Forced Expiratory Ratio.

=FEV1/FVC (or VC, whichever is larger).

41
Q

Clinical features distinguishing asthma from COPD?

A

Cf COPD, asthma has:

  • variable course
  • onset at young age
  • Not ass/w smoking
  • Airflow limitation substantially reversible
42
Q

Pathological features distinguishing COPD from asthma?

A

Cf COPD, asthma has:

  • mostly eosinophilic inflammation affecting ALL airways and doesn’t involve lung parenchyma
  • Fibrosis NOT a feature
43
Q

Pathology of COPD distinguishing from Asthma?

A

Cf asthma, COPD has:

  • Neutrophilic inflamm
  • Most pathology in peripheral airways, where there is also fibrosis => obliterative bronchiolitis
  • Mucus hypersecretion more prominent
44
Q

What is the management plan for COPD?

A

COPD-X

  • Confirm Diagnosis
  • Optimise lung function
  • Prevent deterioration
  • Develop support network and self management plan
  • eXacerbation - manage appropriately
45
Q

What is spiriva?

A

Tiotropium = anticholinergic

46
Q

What is atrovent

A

Ipratropium = anticholinergic

47
Q

Anticholinergic v beta agonist as bronchdilator?

A

Anticholinergics are:

  • Long acting, more convenient
  • less dyspnoea
  • better exercise
  • less exacerbation
48
Q

What is seretide?

A

Inhaled fluticasone and salmeterol.

49
Q

What is symbicort?

A

Inhaled budesonide and formoterol.

50
Q

What are the principles of pulmonary rehabilitation?

A
  • Improve fitness

- Education

51
Q

vaccines for COPD patients?

A
  • Fluvax (yearly)

- Pneumococcal vax (twice, 5years apart)

52
Q

When and how should home O2 be instituted in COPD therapy?

A

Oxygen concentrator 2-4L/min via nasal prongs >16h /day. Start when:
-PO2 on air at rest

53
Q

How is a COPD exacerbation defined?

A

Anthonisen criteria:

i) increased dyspnoea
ii) increased sputum production
iii) sputum become discoloured

Respiratory (17 decks)

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