RESP - COPD

Question 1

What is COPD?

Answer 1

• Group of disorders characterised by airway inflammation and airflow limitation that is not fully reversible
• A progressive condition associated with an abnormal inflammatory response to noxious stimuli
• Fully reversible asthma is NOT COPD

Question 2

Pathogenesis of COPD

Answer 2

Noxious agent -> inflammation ->

1. Small airway disease
   - airway inflammation
   - airway remodelling

and/or

2. Parenchymal destruction
   - Loss of alveolar attachments
   - Loss of elastic recoil

-> airflow limitation

• Inflammation in the airways, lung parenchyma and pulmonary vessels
• Neutrophils, macrophages, CD 8 cells
• Proteinase - antiproteinase imbalance
• Oxidative stress

Question 3

(4) changes in lung parenchyma in COPD

Answer 3

1. Alveolar wall destruction
2. Loss of elasticity
3. Destruction of pulmonary capillary bed
4. Increased inflammatory cells; macrophages, CD8+ lymphocytes

Question 4

Describe emphysema

• mechanism
• cells prominent
• (3) different patterns

Answer 4

• Mechanism: protease/antiprotease imbalance (proteases digest elastin and other structural proteins in alveolar wall; antiproteases protect against attack)
• Macrophages and T lymphocytes prominent

Different patterns in emphysema:

1. Centriacinar (radiates from terminal bronchiole)
2. Panacinar (more generalized)
3. Bullae

Question 5

Risk factors for COPD

Answer 5

• Smoking
• Occupational exposure to irritants
• Alpha-1 antitrypsin deficiency
• Bronchial hyper-responsiveness
• Passive smoking
• Air pollution (indoor and outdoor, esp biomass fuels)
• Recurrent RTIs in childhood
• Genetic predisposition

Question 6

When should you consider the COPD diagnosis?

Answer 6

–any past or current smoker
–chronic cough
–productive cough
–dyspnoea
–history of exposure to other risk factors

Question 7

How do you diagnose COPD?

Answer 7

•Spirometry is the best measure of airflow obstruction
•Measures time course of exhaled volume or flow
•FER = forced expiratory ratio
•FER = FEV1/FVC or FEV1/VC
–using the larger of FVC or VC
•FER less than 0.7 -> airflow obstruction
–this cut-off varies slightly with age

Question 8

What is the cut off for airflow obstruction on spirometry?

Answer 8

Forced Expiratory Ratio (FEV1/FVC) LESS THAN 0.7

The cut off varies slightly with age

Question 9

Compare COPD vs. Asthma

• timeline
• onset of symptoms
• smoking Hx
• airflow limitation reversible or irreversible

Answer 9

COPD:

• progressive
• late onset of symptoms
• moderate heavy smoking Hx
• airflow limitation not completely reversible

Asthma:

• variable course
• onset at young age
• no a/w smoking Hx
• airflow limitation substantially or completely reversible

NOTE: there is however overlap of respiratory symptoms b/w COPD & Asthma

Question 10

Discuss the pathology of asthma

• inflammation?
• parts of airways affected
• involvement of lung parenchyma
• fibrosis?

Answer 10

• Inflammation (largely eosinophilic) affects ALL the airways (large and small) and doesn’t involve lung parenchyma
• Fibrosis is NOT a feature (sub-epithelial fibrosis may be present but is minimal compared with that seen in COPD)

Question 11

Discuss the pathology of COPD

• inflammation?
• parts of airways affected
• involvement of lung parenchyma
• fibrosis?
• mucus?

Answer 11

• Neutrophilic inflammation
• In contrast with asthma, most of pathologic changes are in peripheral airways where there is also fibrosis leading to obliterative bronchiolitis
• Mucus hypersecretion is more prominent than in asthma

Question 12

(4) cells involved in asthma

Answer 12

1. Epithelial cells
2. Mast cells
3. CD4+ cells (Th2)
4. Eosinophils

Question 13

(4) cells involved in COPD

Answer 13

1. Epithelial cells
2. Alveolar macrophage
3. CD8+ cells (Th1)
4. Neutrophil

Question 14

(2) main differences of inflammation consequences in asthma vs. COPD

Answer 14

Asthma:

1. Bronchoconstriction
2. Airway hyperresponsiveness

COPD:

1. Small airway narrowing
2. Alveolar destruction

Question 15

List the GOLD classification of COPD severity

Answer 15

Stage I: Mild
FER less than 0.70
FEV1 > 80% predicted

Stage II: Moderate
FER less than 0.70
FEV1: 50-80% predicted

Stage III: Severe
FER less than 0.70
FEV1: 30-50% predicted

Stage IV: Very severe
FER less than 0.70
FEV1 less than 30% predicted OR
FEV1 less than 50% predicted + chronic respiratory failure

NOTE: Stages only differ by the % of FEV1 predicted. All stages have FER less than 0.70

Question 16

List the treatments for different GOLD classification of COPD severity

Answer 16

Stage 1-4:

• Active reduction of RF
• Influenza vaccination
• Add short acting bronchodilator PRN

Stage 2-4:

• Regular Rx with 1 or more long acting bronchodilators when needed
• Rehabilitation

Stage 3-4:
- Inhaled glucocorticoids if repeated exacerbations

Stage 4:

• Long term oxygen if chronic respiratory failure
• Consider surgical treatments

Question 17

What are the goals of therapy of COPD?

Answer 17

–Control symptoms
–Improve lung function and health status
–Prevent exacerbations
–Reduce hospital admissions

Question 18

Describe the Management of COPD; COPD-X plan

Answer 18

C: Confirm diagnosis and assess severity
O: Optimise lung function
P: Prevent deterioration
D: Develop support network and self-management plan
X: eXacerbation – manage appropriately

Question 19

Discuss the smoking cessation strategies

• non pharmacologic
• pharmacologic

Answer 19

Non-pharm:
–Willpower alone
–Doctor’s advice
–Self-help materials
–Intensive counselling
–Smoking cessation courses

Pharm:
–Nicotine replacement therapy
–bupropion (Zyban)
–varenicline (Champix)

Question 20

Describe beta2 agonists in COPD

• examples
• types
• SE

Answer 20

E.g. 
–Ventolin, Airomir = salbutamol
–Bricanyl = terbutaline
–Serevent = salmeterol
–Oxis, Foradile = eformoterol
–Onbreez= indacaterol

•Short-acting for prn use
•Long-acting for regular use
–less symptoms, more exercise, better QOL
•Lower QOL with higher doses

•SE = tremor, tachycardia

Question 21

Describe anticholinergics in COPD

• examples
• types
• SE

Answer 21

E.g.
–Spiriva = tiotropium
–Atrovent = ipratropium

• Long-acting more convenient, and less dyspnoea, better exercise, less exacerbations (NTT = 14), less mortality
• SE = dry mouth in 14 %

Question 22

Describe inhaled corticosteroids in COPD

• doses compared to asthma
• who does it benefit

Answer 22

• Neutrophilic inflammation-steroid “resistant”
• Higher doses than in asthma
• Studies show benefit in severe COPD (FEV1 less than 50 %) with frequent exacerbations

Question 23

What are the combination therapies in COPD?

Answer 23

•Inhaled fluticasone and salmeterol (Seretide)
•Inhaled budesonide and formoterol (Symbicort)
•In moderate to severe COPD (FEV1 less than 60 %) may
–reduce exacerbations
–improve QOL
–Improve FEV1

Question 24

Describe theophyllines in COPD

• effects
• SE

Answer 24

• Rarely used in Australia
• Low dose theophylline may have anti-inflammatory and immunomodulatory effects with fewer side effects
• Significant SE: nausea, dysrhythmias, seizures
• Drug interactions
• Monitor blood levels

Question 25

What are the (2) vaccines recommended in COPD? - effects - SE - frequency

Answer 25

•Influenza vaccine –Reduces mortality, hospital admissions and exacerbations –Local side effects only –It is given yearly •Pneumococcal vaccine –More evidence needed about its use in COPD –It is given twice 5 years apart

Question 26

Describe home oxygen therapy in COPD - how is it delivered - indication - effects

Answer 26

•Oxygen concentrator: 2-4 L/min via nasal prongs for >16 hours/day IF –when at his/her best and stable –PO2 on air at rest less than 55 mmHg OR –PO2 less than 60 if evidence of hypoxic damage. i.e. cor pulmonale, pulmonary hypertension, polycythaemia –AND no cigarettes for 3 months •This oxygen improves mortality, and usually has no effect on symptoms

Question 27

Describe portable oxygen in COPD - how is it delivered - indication - effects

Answer 27

•This is designed to improve symptoms and increase exercise –No cigarettes for 3 months –SpO2 less than 88 % with exercise AND –Supplemental O2 prevents this desaturation –AND Exercise is improved •Recent trial suggested mainly placebo benefit!

Question 28

Comment on the following treatments for COPD - chronic antibiotics - mucolytics - non-invasive ventilation - lung volume reduction surgery

Answer 28

•Chronic antibiotics –Generally NOT recommended; –Some benefit from low dose macrolides in recent studies (selected patients? antibacterial or immunomodulatory effect?) - SE’s: deafness, resistance •Mucolytics –small benefit –may help selected patients •Non-invasive ventilation –unproven for chronic use, so only used for selected patients ``` •Lung volume reduction surgery –Improves symptoms –Improves quality of life –No clear survival advantage –Consider lung transplantation ```

Question 29

Define the exacerbation of COPD

Answer 29

“An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”

Question 30

(6) causes of acute COPD exacerbation

Answer 30

The cause is often unknown ``` •Respiratory infections –bacterial, viral –URTI, bronchitis, pneumonia •Heart failure, arrhythmia •Systemic infection, fever •Anaemia •Anxiety •Anything that increases metabolic rate ```

Question 31

COPD exacerbation features - (3) Anthonisen Criteria - Antibiotics - CXR

Answer 31

•Anthonisen criteria: –increased dyspnoea –increased sputum production –sputum becoming discoloured * Antibiotics to cover Strep and Gram negatives have been shown to be useful if all three criteria are present * CXR to look for pneumonia, and cover atypical bacteria if there is pneumonia

Question 32

(6) Management of exacerbation of COPD

Answer 32

•Supplemental O2 –Aim to keep SpO2 > 90% and/or PaO2 > 60 mmHg –Do not give high doses of O2 too quickly •Bronchodilators: anticholinergics and b2 agonists •Corticosteroids (oral, rarely intravenous): some benefit, but not great. must be balanced with side effects •Antibiotics: if there is evidence of infection •Physical activity: to prevent deconditioning •Non-invasive ventilation (BiPAP, CPAP)

Question 33

Why (3) would a high dose of O2 in COPD with chronic hypercapnia lead to a further rise in pCO2?

Answer 33

–Reduced ventilatory drive (hypoxic drive) –Worsening V/Q mismatch due to high PO2 in parts of the lung (the areas that were dysfunctional) overcoming hypoxic vasoconstriction –Haldane effect: O2 displacing CO2 from Hb

Question 34

How (9) do we prevent exacerbations of COPD?

Answer 34

* Smoking cessation * Vaccinations * Tiotropium (antimuscarinic) * Long-acting beta agonists * Theophylline * Inhaled corticosteroids (ICS) * Combination of ICS and LABA (+Tio) * Pulmonary rehabilitation * Mucolytics