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YA - Interactive seminars/University lectures > RESP - COPD > Flashcards

RESP - COPD Flashcards

1
Q

What is COPD?

A
  • 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
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2
Q

Pathogenesis of COPD

A

Noxious agent -> inflammation ->

  1. Small airway disease
    - airway inflammation
    - airway remodelling

and/or

  1. 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
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3
Q

(4) changes in lung parenchyma in COPD

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

Describe emphysema

  • mechanism
  • cells prominent
  • (3) different patterns
A
  • 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
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5
Q

Risk factors for COPD

A
  • 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
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6
Q

When should you consider the COPD diagnosis?

A 
–any past or current smoker
–chronic cough
–productive cough
–dyspnoea
–history of exposure to other risk factors
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7
Q

How do you diagnose COPD?

A

•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

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8
Q

What is the cut off for airflow obstruction on spirometry?

A

Forced Expiratory Ratio (FEV1/FVC) LESS THAN 0.7

The cut off varies slightly with age

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9
Q

Compare COPD vs. Asthma

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

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

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10
Q

Discuss the pathology of asthma

  • inflammation?
  • parts of airways affected
  • involvement of lung parenchyma
  • fibrosis?
A
  • 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)
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11
Q

Discuss the pathology of COPD

  • inflammation?
  • parts of airways affected
  • involvement of lung parenchyma
  • fibrosis?
  • mucus?
A
  • 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
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12
Q

(4) cells involved in asthma

A
  1. Epithelial cells
  2. Mast cells
  3. CD4+ cells (Th2)
  4. Eosinophils
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13
Q

(4) cells involved in COPD

A
  1. Epithelial cells
  2. Alveolar macrophage
  3. CD8+ cells (Th1)
  4. Neutrophil
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14
Q

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

A

Asthma:

  1. Bronchoconstriction
  2. Airway hyperresponsiveness

COPD:

  1. Small airway narrowing
  2. Alveolar destruction
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15
Q

List the GOLD classification of COPD severity

A

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

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16
Q

List the treatments for different GOLD classification of COPD severity

A

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
17
Q

What are the goals of therapy of COPD?

A

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

18
Q

Describe the Management of COPD; COPD-X plan

A 
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
19
Q

Discuss the smoking cessation strategies

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

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

20
Q

Describe beta2 agonists in COPD

  • examples
  • types
  • SE
A 
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

21
Q

Describe anticholinergics in COPD

  • examples
  • types
  • SE
A

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 %
22
Q

Describe inhaled corticosteroids in COPD

  • doses compared to asthma
  • who does it benefit
A
  • Neutrophilic inflammation-steroid “resistant”
  • Higher doses than in asthma
  • Studies show benefit in severe COPD (FEV1 less than 50 %) with frequent exacerbations
23
Q

What are the combination therapies in COPD?

A

•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

24
Q

Describe theophyllines in COPD

  • effects
  • SE
A
  • 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
25
Q

What are the (2) vaccines recommended in COPD?

  • effects
  • SE
  • frequency
A

•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

26
Q

Describe home oxygen therapy in COPD

  • how is it delivered
  • indication
  • effects
A

•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

27
Q

Describe portable oxygen in COPD

  • how is it delivered
  • indication
  • effects
A

•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!

28
Q

Comment on the following treatments for COPD

  • chronic antibiotics
  • mucolytics
  • non-invasive ventilation
  • lung volume reduction surgery
A

•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
29
Q

Define the exacerbation of COPD

A

“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.”

30
Q

(6) causes of acute COPD exacerbation

A

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
31
Q

COPD exacerbation features

  • (3) Anthonisen Criteria
  • Antibiotics
  • CXR
A

•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
32
Q

(6) Management of exacerbation of COPD

A

•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)

33
Q

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

A

–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

34
Q

How (9) do we prevent exacerbations of COPD?

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

YA - Interactive seminars/University lectures (87 decks)

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