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MD2 Respiratory > COPD > Flashcards

COPD Flashcards

1
Q

Define COPD

A

Group of disorders (including chronic bronchitis, emphysema and asthma) characterised by airway inflammation and airflow limitation that is not reversible
Condition is progressive and associated with an abnormal inflammatory response to noxious stimuli

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2
Q

Epidemiology of COPD

A

3rd leading cause of disease burden
4th leading cause of death in Australian men, 6th in women
Mortality 10x higher in Indigenous Australians
Continues to have a growing rate

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3
Q

Pathogenesis of COPD

A

Noxious agent causes an inflammatory response
Small airway disease is caused by airway inflammation and remodelling
Parenchymal destruction is caused by loss of alveolar attachments and elastic recoil, as well as destruction of the pulmonary capillary bed
Changes result in airflow limitation

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4
Q

Describe the inflammatory processes involved in the pathogenesis of COPD

A

Inflammatory infiltrate consisting of neutrophils, macrophages and CD8 cells
Proteinase-antiproteinase imbalance
Oxidative stress

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5
Q

Describe the pathogenesis of emphysema

A

Protease/antiprotease imbalance, with prominent macrophage and CD8 cell infiltrate

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6
Q

Describe the 3 different patterns of emphysema

A

Centriacinar (radiates from terminal bronchiole)
Panacinar
Bullae

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7
Q

Risk factors for COPD

A 
Cigarette smoking
Air pollution (indoor air pollution from use of biomass fuels is a significant risk factor in India and China)
Occupational exposure to irritants
a1-antitrypsin deficiency
Bronchial hyper-responsiveness
Recurrent RTIs in childhood
Genetic predisposition
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8
Q

How is COPD diagnosed?

A

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

FER

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9
Q

Distinguish between COPD and asthma in terms of its course, onset, relationship to smoking and reversibility

A

COPD: progressive course, later onset of symptoms, usually moderately heavy smoking history, airflow limitation not completely reversible
Asthma: variable course, onset at young age, no association with smoking, airflow limitation substantially or completely reversible

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10
Q

Describe the histopathology of asthma

A

Inflammation (largely eosinophilic and CD4 cells) affects ALL airways and does not involve lung parenchyma
Fibrosis is NOT a feature (may be sub-epithelial fibrosis but minimal compared with COPD)

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11
Q

Describe the histopathology of COPD

A

Neutrophilic inflammation
Most pathological changes in peripheral airays
Fibrosis leading to obliterative bronchiolitis
Mucus hypersecretion is more prominent than in asthma

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12
Q

GOLD classification of COPD severity

A

Stage I (mild): FEV1/FVC

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13
Q

Describe the COPD-X plan for management of COPD

A 
Confirm diagnosis and assess severity
Optimise lung function
Prevent deterioration
Develop support network and self-management plan
eXacerbation - manage appropriately
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14
Q

List 5 non-pharmacologic and 3 pharmacologic smoking cessation strategies

A

Non-pharmacologic: willpower alone, doctor’s advice, self-help materials, intensive counselling, smoking cessation courses
Pharmacologic: nicotine replacement therapy, bupropion (Zyban), varenicline (Champix)

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15
Q

What options are available for B2-agonist therapy for COPD?

A 
Salbutamol (Ventolin, Airomir)
Terbutaline (Bricanyl)
Salmeterol (Serevent)
Eformoterol (Oxis, Foradile)
Indacaterol (Onbreez)
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16
Q

When are short-acting vs long-acting B2-agonists indicated?

A

Short-acting PRN

Long-acting regularly (to reduce exacerbations, improve QOL, before exercise)

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17
Q

What is the effect of B2-agonists on QOL?

A

Lower QOL with higher doses

SEs include tremor and tachycardia

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18
Q

List 2 anticholinergics used in the treatment of COPD

A

Tiotropium (Spiriva)

Ipratropium (Atrovent)

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19
Q

Are short-acting or long-acting anticholinergics typically used to manage COPD?

A

Longer: more convenient, less dyspnoea, improve exercise, reduce exacerbations and mortality

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20
Q

Common SE of inhaled anticholinergics

A

Dry mouth

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21
Q

When are inhaled corticosteroids indicated in the management of COPD?

A

Indicated for neutrophilic inflammation steroid-resistant COPD, i.e. severe COPD (FEV1

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22
Q

What dose of inhaled corticosteroids is used for the management of severe COPD?

A

Higher doses than in asthma

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23
Q

What combination therapies are available for COPD?

A

Seretide (fluticasone and salmeterol)

Symbicort (budesonide and formoterol)

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24
Q

When are combination therapies recommended in COPD and what is their effect on disease management?

A

In moderate to severe COPD (FEV1

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25
Q

What is pulmonary rehabilitation?

A

A course incorporating fitness improvement and education
Runs over 6-8 weeks with twice weekly visits and exercise maintenance at home
Usually supervised by physiotherapists

26
Q

What is the effect of pulmonary rehabilitation on COPD management? What are some of the limitations?

A

Improves exercise capacity and QOL
May reduce exacerbations and hospitalisations
BUT patients need to be well motivated, and there is variable availability and cost to patients

27
Q

Why are theophyllines rarely used in Australia?

A

Significant SEs including nausea, dysrhythmias and seizures
Drug interactions
Requires monitoring of blood levels

28
Q

How might theophyllines be used effectively for the management of COPD?

A

Low dose theophylline may have anti-inflammatory and immunomodulatory effects with fewer SEs

29
Q

What vaccines are recommended for COPD patients? When are they given and what are their effects on disease management?

A

Influenza (yearly): reduces mortality, hospital admissions and exacerbations
Pneumococcal (given twice 5 years apart): evidence lacking

30
Q

How is home oxygen therapy given for COPD patients?

A

Oxygen concentrator: 2-4L/min via nasal prongs for >16 hours/day

31
Q

When is home oxygen therapy recommended for COPD patients?

A

When at his/her best and stable, pO2 on air at rest

32
Q

What is the effect of home oxygen therapy on COPD management?

A

Improves mortality

No effect on symptoms (usually)

33
Q

What is the effect of portable oxygen therapy on COPD management?

A

Designed to improve symptoms and increase exercise (may be placebo effect!)

34
Q

What are the requirements for eligibility for portable oxygen?

A

No cigarettes for 3 months

SpO2

35
Q

What treatments are available for COPD?

A 
B2 agonists
Anticholinergics
Inhaled corticosteroids
Pulmonary rehabilitation
Theophyllines (not in Aus)
Vaccination
Home oxygen or portable oxygen
Chronic Abx (not used)
Mucolytics
NIV (unproven for chronic use)
Lung volume reduction surgery (may consider transplantation)
Other experimental devices (e.g. endobronchial valves)
36
Q

When are chronic Abx indicated?

A

Generally not recommended but recent studies show some benefit from low dose macrolides (may be due to antibacterial or immunomodulatory effects)

37
Q

Main AEs of macrolides

A

Deafness

Resistance

38
Q

What is the effect of lung volume reduction surgery on COPD management?

A

Improves symptoms and QOL

No clear survival advantage

39
Q

Describe COPD therapy through the stages

A

Stage I: reduce RFs (vax, smoking cessation), SABAs
Stage II: add LABAs and pulmonary rehabilitation
Stage III: add inhaled corticosteroids if repeated exacerbations
Stage IV: add long term oxygen if chronic respiratory failure, consider surgical treatments

40
Q

Define COPD exacerbation

A

An event in the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication

41
Q

List common causes of acute COPD exacerbation

A 
RTIs (bacterial, viral, URTI, bronchitis, pneumonia)
HF
Arrhythmias
Systemic infection, fever
Anaemia
Anxiety
Anything that increases metabolic rate
42
Q

What are the Anthonisen criteria?

A

Increased dyspnoea
Increased sputum production
Sputum becoming discoloured

43
Q

Abx given for acute COPD exacerbation

A

To cover strep and GNs if Anthonisen criteria met

+ cover for atypical bacteria if there is evidence of pneumonia on CXR

44
Q

How is a COPD exacerbation managed?

A

Supplemental O2 aiming to keep SpO2 >90% and/or PaO2 >60mmHg (do not give too quickly; consider the O2 concentration, flow rate and patient’s inspiratory flow rate)
Bronchodilators (B2 agonists, anticholinergics)
Corticosteroids (PO, rarely IV)
Abx (if evidence of infection)
Physical activity (to prevent deconditioning)
NIV (BiPAP, VPAP)

45
Q

Why should supplemental O2 be given slowly to a COPD patient?

A

High dose of O2 in COPD with chronic hypercapnoea may lead to a further rise in pCO2

46
Q

What is the Haldane effect?

A

O2 displacing CO2 from Hb

47
Q

Why might a high dose of O2 in COPD with chronic hypercapnoea lead to a further rise in pCO2?

A

Reduced ventilatory drive
Worsening V/Q mismatch due to high pO2 in parts of the lung overcoming hypoxic vasoconstriction
Haldane effect

48
Q

How many smokers are there worldwide? Where are numbers of smokers increasing the most?

A

1.1 billion (1.6 by 2025)

Numbers increasing in low and middle income countries

49
Q

What % of smokers have some degree of airflow limitation? How many develop disabling airflow limitation?

A

50%

15-20%

50
Q

When should COPD be considered?

A 
Any past or current smoker
Chronic cough
Productive cough
Dyspnoea
Hx of exposure to other risk factors
51
Q

What does spirometry measure?

A

Time course of exhaled volume or flow

52
Q

FER

A

Forced expiratory ratioi

FER = FEV1/FVC or FEV1/VC (using the larger of FVC or VC)

53
Q

What is the difference in lung volumes between COPD and normal patients?

A

Increased RV (gas trapping)
Reduced FVC
Reduced FEV1
Reduced FEV1/FVC?

54
Q

Describe the overlap of respiratory symptoms in COPD and asthma

A

May be impossible to differentiate between patients with asthma with some irreversible airflow obstruction, and between some patients with chronic bronchitis and emphysema who have partially reversible airflow obstruction

55
Q

Pathogenesis of asthma vs COPD

A

Asthma: allergens induce inflammatory response from epithelial cells and mast cells, leading to activation of CD4+ cells (TH2) and eosinophils, and resulting in bronchoconstriction and AHR which causes a reversible airflow limitation
COPD: irritants including cigarette smoke induce inflammatory response from alveolar macrophages and epithelial cells, leading to activation of CD8+ cells and neutrophils, and resulting in small airway narrowing and alveolar destruction which causes an irreversible airflow limitation

56
Q

Does FEV1 (as a % of value at age 25) improve with smoking cessation?

A

No; there is a normal age-related decline in FEV1, and smoking cessation SLOWS this decline

57
Q

What are the current treatment guidelines for COPD?

A

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

58
Q

What is the benefit of mucolytics in the management of COPD?

A

Small benefit

May help selected patients

59
Q

What is the benefit of NIV in the management of COPD?

A

Unproven for chronic use

Use only for selected patients

60
Q

How can COPD exacerbations be prevented?

A 
Smoking cessation
Vaccinations
Tiotropium (antimuscarinic)
LABAs
Theophylline
ICS
Combination of ICS and LABA (+Tio)
Pulmonary rehabilitation
Mucolytics

MD2 Respiratory (9 decks)

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