COPD Flashcards

1
Q

Definition of COPD

A

-Persistent airflow limitation that is usually progressive
-Associated with enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases
-Exacerbations and comorbidities contribute to severity

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2
Q

Why is COPD underrecognized?

A

-Disease with insidious onset
-Often treated as asthma
-Smokers don’t seek treatment
-Can present late with more advanced disease

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3
Q

Prevalence of COPD

A

-Prevalence increasing as living longer
-More prevalent in older individuals
-2%/ 1.2 million

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4
Q

Describe the triad of pathological changes in COPD

A

-Bronchial gland enlargement
-Bronchiolitis
-Emphysema

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5
Q

What is chronic bronchitis?

A

-Hyperplasia of goblet cells
=Increased inflammatory
=Mucus hypersecretion

-Cough productive of sputum on most days for 3 months over 2 consecutive years

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6
Q

Definition of emphysema

A

-Condition of the lung characterised by abnormal, permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis

=Loss of elastic recoil
=Airflow limitation and gas trapping

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7
Q

Types of emphysema

A

-Centrilobular
=Central part of lobule destroyed
=Upper lobe predominance
=Common type in smokers
=Associated with bullous disease

-Panlobular
=End lobule destroyed
=Lower lobes
=Genetic (alpha-1 antitrypsin deficiency)

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8
Q

Histological changes in emphysema

A

-Loss of attachments
-Fibrosis inflammation

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9
Q

Exposure risk factors for COPD

A

-Cigarette smoke
-Occupational dust and chemicals
-Environmental tobacco smoke (ETS)
-Indoor and outdoor air pollution
-Infections (recurrent in children)
-Socio-economic status

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10
Q

Host risk factors for COPD

A

-Alpha-1 antitrypsin deficiency
-Airway hyper-responsiveness
-Poor lung growth
-Age

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11
Q

Describe Alpha-1 antitrypsin deficiency

A

-Alpha 1 proteinase deficiency
-1/5000 live births UK
-A1-AT aggregates in liver (liver disease in some cases in childhood)
-Emphysema <50 years of age (often 4th decade)
=Panlobular predominantly basal emphysema
-Smoking is cofactor
-Fam history

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12
Q

Pathogenesis of COPD

A

-Cigarette smoke (biomass particles/ particulates)
-Host factors/ amplifying mechanisms
=Lung inflammation
=Activation of alveolar macrophages and epithelial cells
=Neutrophil and CD8+ activation
=Small airway narrowing, alveolar destruction

=Oxidative stress (reactive oxygen species)
=Proteinases (destruction of lungs)

=COPD pathology

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13
Q

History taking in COPD

A

-Onset, variability and progression of symptoms such as:
=Breathlessness — assess severity using the Medical Research Council (MRC) dyspnoea scale.
=Cough and sputum production — ask about haemoptysis and consider other causes.
=Peripheral oedema — consider cor pulmonale.
=Weight loss – consider other causes.

-Exposure to risk factors including:
=Smoking — if the person is a current smoker document pack-years smoked (number of cigarette smoked per day divided by 20 multiplied by number of years smoked).
=Occupational or environmental exposures.

-Impact of symptoms on daily life and occupation:
=Impact of COPD on wellbeing and daily life can be assessed using the COPD Assessment test (CAT)

-Previous exacerbations or hospitalization.

-Past medical history and comorbidities including:
=Anxiety and depression.
=Cardiovascular disease and metabolic syndrome.
=Lung or liver disease.
=Osteoporosis.
=Asthma.

-Family history including:
=Lung or liver disease – consider underlying causes such as alpha-1-antitrypsin deficiency.

-Severity in FEV1% pred
-LTOT
-Previous exacerbations/ hospital admissions +/- NIV
-Any previous discussions/decisions around escalation of
care/resuscitation/anticipatory care planning. Care requirements/ability to manage ADLs/PADLs.
Smoking/vaping status. Usual treatment including any recent steroids/antibiotics

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14
Q

Symptoms of COPD

A

Suspect COPD in people aged over 35 years with a risk factor (such as smoking, occupational or environmental exposure) and one or more of the following symptoms:
-Breathlessness — typically persistent, progressive over time, and worse on exertion.
-Chronic/recurrent cough (may be intermittent and unproductive)
-Regular sputum production (increase could suggest infective exacerbation)
-Frequent lower respiratory tract infections.
-Wheeze.

-Weight loss, anorexia and fatigue — common in severe COPD but other causes must be considered.
-Waking at night with breathlessness.
-Ankle swelling – consider cor pulmonale.
-Chest pain – uncommon in COPD, consider other causes.
-Haemoptysis – uncommon in COPD, consider other causes.
-Reduced exercise tolerance.
-Acute confusion?
-Right sided HF with peripheral oedema

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15
Q

Symptoms of acute exacerbation of COPD

A

-Commonly reported symptoms include:
=Increased breathlessness.
=Increased cough.
=Increased sputum production and change in sputum colour.

-Other reported symptoms may include:
=Increased wheeze and chest tightness.
=Upper respiratory tract symptoms (for example cold or sore throat).
=Reduced exercise tolerance.
=Ankle swelling.
=Increased fatigue.
=Acute confusion.

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16
Q

Conditions in past medical history

A

-Asthma
-Allergies
-Sinusitis
-Nasal polyps
-Respiratory infections in childhood

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17
Q

Inspection findings in clinical examination

A

-Resting RR >20 breaths/minute
-Use of accessory muscles of respiration
-Pursed lip breathing (emphysematous)
-Chest wall abnormalities reflecting pulmonary hyperinflation
=Horizontal ribs, barrel shaped, protruding abdomen
-Flattening of hemi-diaphragm associated with paradoxical indrawing of:
=Lower rib cage on inspiration, reduced cardiac and liver dullness, widening of xiphisternal angle, decreased crico-sternal distance
-Central cyanosis, signs of CO2 retention
-Peripheral oedema
-Weight loss/ loss of muscle tone
-Raised jugular venous pressure and/or peripheral oedema (may indicate cor pulmonale).
-Cachexia
-Flapping tremor

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18
Q

Palpation and percussion findings in clinical examination

A

-Often unhelpful in COPD
-Decreased cricosternal distance
-Detection of the apex beat may be difficult due to pulmonary overinflation
-Lower sternum resonant percussion (gas trapping)
-Loss of lover dullness

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19
Q

Auscultation findings in clinical examination

A

-Reduced breath sounds
-Wheezing during quiet breathing (scattered bilateral)
-Respiratory crackles occur vary with coughing but not diagnostic (infection)

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20
Q

4 components of COPD management

A
  1. Assess and monitor disease
  2. Reduce risk factors
  3. Manage stable COPD
    =Education
    =Pharmacologic
    =Non-pharmacologic
  4. Manage exacerbations
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21
Q

Diagnosis of COPD

A

-Symptoms
-Exposure to risk factors
-Spirometry
=Post-bronchodilator and baseline FEV1
=FEV1/FVC<0.7 confirms airflow limitation

NICE recommend considering a diagnosis of COPD in patients over 35 years of age who are smokers or ex-smokers and have symptoms such as exertional breathlessness, chronic cough or regular sputum production.

The following investigations are recommended in patients with suspected COPD:
=post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
=chest x-ray: hyperinflation, bullae (can mimic pneumothorax), flat hemidiaphragm. Also important to exclude lung cancer
=full blood count: exclude secondary polycythaemia
=body mass index (BMI) calculation
=Spirometry: Measure post-bronchodilator spirometry to confirm the diagnosis of COPD — do not routinely perform reversibility testing as part of diagnostic work up.

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22
Q

Additional investigations for COPD

A

-Sputum culture – if sputum is purulent and persistent (to identify organisms).
-Serial home peak flow measurements – to exclude asthma if diagnosis is in doubt.
-ABG
-Bloods: FBC, US, CRP, LFT
-ECG and serum natriuretic peptides – if cardiac disease or pulmonary hypertension are suspected.
=Echocardiogram may also be indicated.
-CT thorax – if symptoms seem disproportionate to spirometry measurements; another diagnosis (such as fibrosis or bronchiectasis) is suspected, or an abnormality on chest x-ray requires further investigation.
-Serum alpha-1-antitrypsin.
=Consider alpha-1-antitrypsin deficiency in people with early onset of symptoms, minimal smoking history or a positive family history.
=Referral to a specialist for management and screening of family members is required if alpha-1-antitrypsin deficiency is identified.

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23
Q

Stratification of severity of COPD

A

-Mild FEV1>80% predicted
-Moderate 50%<FEV1<80% pred
-Severe 30%<FEV1<50% pred
-Very severe FEV1<30% pred

(post-bronchiodilator)

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24
Q

Diagnosis of asthma-COPD overlap group

A

-Post-bronchodilator FEV1
-Before and after nebulised salbutamol and/or nebulised ipratropium bromide

-Significant response: increase that is both greater than 200mls and 12% of the pre-drug value/ large increases in FEV1 (>400 mls)

=any previous, secure diagnosis of asthma or of atopy
=a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
=substantial variation in FEV1 over time (at least 400 ml)
=substantial diurnal variation in peak expiratory flow (at least 20%)

25
Q

COPD vs Asthma

A

COPD:
-Onset mid-life
-Slowly progressive symptoms
-Long smoking history
-Dyspnoea during exercise
-Largely irreversible airflow limitation

ASTHMA:
-Early life onset
-Symptoms vary day to day, night/ early morning
-Allergy
-Family history
-Largely reversible airflow limitation

26
Q

Assessment of COPD

A

-Current level of patient’s symptoms
-Severity of spirometry abnormality
-Frequency of exacerbations
-Presence of comorbidities

27
Q

Assessing symptoms

A

-Modified MRC (mMRC) questionnaire (2 or more high symptoms)
-CAT tool, self-assessment, out of 40, measure overall impact of life

28
Q

Modified MRC questionnaire dyspnoea scale

A

-Grade 1: only gets breathless with strenuous exercise
-Grade 2: short of breath when hurrying/ walking up slight hill
-Grade 3: Walks slower than people the same age as breathless/ stop for breath when walking on my own pace on the level
-Grade 4: Stop for breath after walking 100m/ after few minutes on the level
-Grade 5: Too breathless to leave house/ breathless undressing or dressing

29
Q

High risk exacerbation history

A

-2 or more exacerbations within last year
-1 or more hospitalisations with COPD exacerbation in last year

30
Q

ABCD risk stratification classification

A

-A: mMRC 0/1, CAT <10, 0/1 exacerbation last 12 months, no hospital (low risk less symptoms)

-B: mMRC 2 or more, CAT>10, 0/1 exacerbations, no hospital admission (low risk, more symptoms)

-C: stable period mMRC 0/1/ CAT <10 but 2 or more exacerbations or 1 or more hospitalised admission (high risk less symptoms)

-D: High risk high symptoms

31
Q

Additional investigations in COPD

A

-CXR: valuable to exclude alternative diagnosis and establish significant comorbidities

-Lung volumes and Diffusing Capacity: characterise severity (high residual volume, low diffusion capacity)

-Oximetry and ABG: sats and need for supplemental oxygen therapy, respiratory failure?

-A1-AT deficiency screening: Caucasian descent under 45 years/ strong family history of COPD

32
Q

Systemic effects/ comorbidities of COPD

A

-Ischaemic HD, congestive HF, Hypertension

-Lung infections and cancer

-Weight loss
-Muscle weakness

-Osteoporosis

-Depression

-Metabolic syndrome

-Diabetes

=SYSTEMIC INFLAMMATION

33
Q

Reducing risk factors

A

-Avoidance of risk factors
=Smoking cessation (nicotine, varenicline, bupropion)
=Reduction of indoor pollution
=Reduction of occupational exposure

-Influenza and pneumococcal vaccination

-Pulmonary rehab to those viewing themselves as functionally disabled MRC grade 3

34
Q

Therapeutic options for COPD management

A

-Bronchodilators
-Inhaled corticosteroids

35
Q

Describe bronchodilators

A

-Symptomatic management
-Prescribed as-needed/ regular basis
-Beta 2 agonists, anticholinergics/muscarinic (LAMA), theophylline or combination therapy (LAMA), corticosteroids (dual therapy only)
=Based on individual response (symptoms and side effects)
=a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
=for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’

36
Q

Types of inhaler devices

A

-MDI (metered dose inhaler)
-DPI (dry powder inhaler)
-SMI (Soft mist inhaler)

=Depends on inspiratory capacity and hand to breath coordination

37
Q

Describe inhaled corticosteroids

A

-Improves symptoms, lung function, QOL, reduces frequency or exacerbations with FEV1<60% pred
-Associated with increased risk of pneumonia
-Withdrawal from treatment may lead to exacerbation

38
Q

Rationale for combining different classes of bronchodilators

A

-Targeting one bronchodilator pathway alone may not maximise bronchodilation
-Sympathetic activity more prominent during day/ parasympathetic at night

39
Q

GOLD therapy algorithm for ABCD classification

A

-A: bronchodilator (short acting)
-B: LAMA/LABA or both for persistent symptoms
-C: LAMA +LABA/ LABA +ICS
-D: LAMA+LABA+ICS

40
Q

Management of stable COPD when no asthmatic features/ features suggesting steroid responsiveness

A

-Add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)
=if already taking a SAMA, discontinue and switch to a SABA

41
Q

Management of stable COPD when asthmatic features/ features suggesting steroid responsiveness

A

-LABA + inhaled corticosteroid (ICS)
-if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
=if already taking a SAMA, discontinue and switch to a SABA
-NICE recommend the use of combined inhalers where possible

42
Q

Use of nebulizers in COPD

A

-Exacerbations in hospital short-term
-Chronic long-term nebulizer at home (severe)
=Ensure optimal treatment

43
Q

Non-pharmacological methods

A

-Pulmonary rehabilitation
=Improve exercise capacity
=PT
=Lifestyle modification solution
=Exercise programme
=Priority: high risk patients with high symptoms on high optimal bronchodilation

44
Q

What is an exacerbation?

A

-Event in natural course of the disease characterised by a change in the baseline symptoms beyond normal day-to-day variations
-Acute onset
-Warrant change in regular medication

45
Q

Triggers of COPD exacerbation

A

-Bacteria/ viruses/ pollutants
-Exaggerated inflammatory response
=Systemic inflammation
=Cardiovascular comorbidity

=Bronchoconstriction, oedema, mucus
=Expiratory flow limitation
=Dynamic hyperinflation

46
Q

Common causative agents of infective exacerbations

A

-Bacterial:
=H influenzae (most common)
=S Pneumoniae
=M Catarrhalis

-Viral (30%):
=Rhinovirus
=Influenza

47
Q

Criteria for admission with COPD exacerbation

A

-Severe breathlessness
-Acute confusion or impaired consciousness
-Cyanosis
-Oxygen saturation less than 90% on pulse oximetry.
-Social reasons e.g. inability to cope at home (or living alone)
-Significant comorbidity (such as cardiac disease or insulin-dependent diabetes)

48
Q

Management of COPD exacerbations

A

-Optimise bronchodilators
-Antibiotics
-Oral corticosteroids
-Treatment of Respiratory Failure
=Oxygen
=Ventilation

-Increase the frequency of bronchodilator use and consider giving via a nebuliser (salbutamol, ipratropium/muscarinic antagonist)
-Give prednisolone 30 mg daily for 5 days/ IV hydrocortisone
-It is common practice for all patients with an exacerbation of COPD to receive antibiotics. NICE do not support this approach. They recommend giving oral antibiotics ‘if sputum is purulent or there are clinical signs of pneumonia’
-The BNF recommends one of the following oral antibiotics first-line: amoxicillin or clarithromycin or doxycycline.
-The decision to give antibiotics will depend on several factors – sputum volume/purulence (and whether this
has changed), presence of pyrexia, new CXR changes, high WBC/CRP. Our local antimicrobial guidelines
suggest Doxycycline 200mg stat (day 1) then 100mg o.d. for a further 4 days, or Amoxicillin 500mg t.d.s. for 5
days, but it is also worth taking into account previous sputum results in terms of likely pathogens and their
sensitivities

-IV theophylline for pts not responding to nebulised bronchodilators?

49
Q

Describe respiratory failure

A

-Type 1: PaO2<8.0 kPa, PaCO2 normal
=Hypoxic
=Ventilation perfusion mismatch

-Type 2 PaO2<8.0kPa, PaCO2>6.5kPa
=Hypercapnic
=Inadequate alveolar ventilation

50
Q

Factors associated with mortality in acute on chronic respiratory failure

A

-Age
-Acidosis H+ ion >55mmol/l (decompensated Type 2)
-Hypotension
-Uraemia

51
Q

Decompensated Type 2 Respiratory Failure treatment

A

-Non-invasive intermittent positive pressure ventilation (NIPPV)

-Typically used for COPD with respiratory acidosis pH 7.25-7.35
=The BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used

-Bilevel positive airway pressure (BiPaP) is typically used with initial settings:
=Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
=Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O

52
Q

Which patients should be offered long-term oxygen therapy?

A

Patients who receive LTOT should breathe supplementary oxygen for at least 15 hours a day. Oxygen concentrators are used to provide a fixed supply for LTOT

Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:
=secondary polycythaemia
=peripheral oedema
=pulmonary hypertension

53
Q

Indications for prophylactic azithromycin

A

NICE guidelines suggest a prescription of 250mg azithromycin three times per week if:
=The patient no longer smokes.
=Has optimised non-pharmacological management & inhaled therapies.
=Referred to pulmonary rehab (if appropriate).
=4 acute exacerbations in the last year (producing sputum), requiring hospital admission at least once

other prerequisites include a CT thorax (to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis)
LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

54
Q

Reasons to assess patient for long-term oxygen therapy

A

-Very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
-Cyanosis
-Polycythaemia
-Peripheral oedema
-Raised jugular venous pressure
-Oxygen saturations less than or equal to 92% on room air

NICE suggest that a structured risk assessment is carried out before offering LTOT, including:
the risks of falls from tripping over the equipment
the risks of burns and fires, and the increased risk of these for people who live in homes where someone smokes (including e-cigarettes)

55
Q

Describe oral theophylline role

A

-NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
-The dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed

56
Q

Role of standby medication

A

-Short course of oral corticosteroids and abx at home if:
=have had an exacerbation within the last year
=understand how to take the medication, and are aware of associated risks and benefits
=know to when to seek help and when to ask for replacements once medication has been used

57
Q

Role of phosphodiesterase-4 inhibitors

A

-Oral PDE-4 inhibitors such as roflumilast reduce the risk of COPD exacerbations in patients with severe COPD and a history of frequent COPD exacerbations
-NICE recommend if:
=the disease is severe, defined as a forced expiratory volume in 1 second (FEV1) after a bronchodilator of less than 50% of predicted normal, and
=the person has had 2 or more exacerbations in the previous 12 months despite triple inhaled therapy with a long-acting muscarinic antagonist, a long-acting beta-2 agonist and an inhaled corticosteroid

58
Q

Overview of cor pulmonale

A

Cor pulmonale is right heart failure secondary to lung disease, and is caused by pulmonary hypertension as a consequence of hypoxia.

-features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2 (second left intercostal space), hepatomegaly
-use a loop diuretic for oedema, consider long-term oxygen therapy
-ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE

59
Q

Differentials of COPD

A

-Asthma — COPD and asthma can be difficult to distinguish clinically and may co-exist.
=Consider asthma if the person has a family history, other atopic disease, or nocturnal or variable symptoms, is a non-smoker, or experienced onset of symptoms at younger than 35 years of age.

-Bronchiectasis — clinical features include copious sputum, frequent chest infections, a history of childhood pneumonia, and coarse lung crepitations.

-Heart failure — clinical features include breathlessness when lying flat, a history of ischaemic heart disease, and fine lung crepitations.

-Lung cancer — consider if the person has a persistent cough, haemoptysis, weight loss, or persistent hoarse voice.

-Interstitial lung disease (such as asbestosis, pneumoconiosis, fibrosing alveolitis, or sarcoidosis) — clinical features include a dry cough and fine lung crepitations.

-Anaemia — clinical features include fatigue, breathlessness, and palpitations.

-Tuberculosis (TB) — clinical features include persistent productive cough, which may be associated with breathlessness and haemoptysis. May co-exist with COPD.

-Cystic fibrosis.

-Upper airway obstruction (for example tracheal tumour).