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COPD Flashcards

1
Q

COPD

A

chronic obstructive pulmonary disease

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2
Q

COPD definition

A

COPD is characterised by progressive airflow obstruction, which is not fully reversible and does not change markedly over several months

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3
Q

COPD Epidemiology: Risk of COPD and age?

A
  • risk increases with age
  • > 60 years
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4
Q

COPD Epidemiology: FEV1 decline?

A
  • decline in FEV1 of about 30 ml/year after the age of 30, but smoking accelerates this decline
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5
Q

Globally COPD is the —- cause of death (2010)

A

3rd

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6
Q

How many are affected globally by copd?

A

3.3 million (5.8%)

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7
Q

In the UK how many people are diagnosed with COPD?

A

1.2 million

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8
Q

How many GP visits a year in the UK for COPD?

A

1.4 million

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9
Q

How many acute hospital admissions due to COPD?

A

1/8

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10
Q

How many deaths per year in the UK due to COPD?

A

30,000 deaths per year
5th leading cause of death

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11
Q

Economic burden in UK of COPD:

A
  • total cost: 1.9bn
  • of the 5 costliest drugs to the NHS, all are respiratory inhalers
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12
Q

COPD is —% of all respiratory disease cost?

A

29%

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13
Q

How much more likely are you to die from COPD if you are in the most deprived 10% of the population?

A

10%

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14
Q

Aetiology: 90% of COPD cases

A

patients who smoke

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15
Q

What is one of the potential causes of corpulmonarae?

A

right heart failure secondary to lung disease, generally COPD

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16
Q

Aetiology of COPD:

A
  • number of pack years indicates risk of COPD
  • cigar and pipe smoking increases risk of COPD to a lesser extent than cigarette smoking
  • passive smoking also increases risk of developing COPD
  • only 15-20% of those who smoke develop COPD
  • occupational exposure to dust, coal mining
  • air pollution: COPD is more common in urban areas compared to rural areas
  • 1-2% of cases are due to alpha - 1 antitrypsin deficiency
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17
Q

How to calculate pack years?

A

20 cigarettes a pack (standard)
Number of packs a day * years

Or if not standard
(cigarettes a day/pack size)*years

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18
Q
A

Decline in lung function with age and smoking

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19
Q

Which inherited condition can cause COPD?

A

Alpha-1 antitrypsin deficiency

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20
Q

Chronic bronchitis due to smoking:

  • symptoms
  • is
A

sputum production for at least 3 months/year for at least 2 consecutive years

Patients are usually breathless

essentially inflammation of the airways

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21
Q

Emphysema

A

destruction of alveoli distal to terminal bronchioles resulting in loss of elastic supporting tissue

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22
Q

Why does emphysema reduced TLCO?

A
  • reduction in transfer factor as the interstitium is destroyed
  • surface area where oxygen diffuses reduced
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23
Q

Are chronic bronchitis and emphysema used interchangeably

A

yes

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24
Q

COPD patients generally have both chronic bronchitis and emphysema

True or False?

A

False
Generally one or the other phenotype is predominant

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25
Q

What imaging done for emphysema?

A

Chest X-ray/ CT

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26
Q

In COPD why might you be hypoxic:

A
  • hypoventilation = type 1 respiratory failure
  • emphysema = diffusion impairment
  • V/Q mismatch, areas of the lungs in COPD are not being ventilated and hence not perfused

Multiple mechanisms that can affect and cause type 1 respiratory failure in COPD patients

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27
Q

What does alpha-1 antitrypsin do?

A
  • in healthy lungs, protein alpha 1 antitrypsin produced and secreted by liver circulates in lungs.
  • Alpha 1 antitrypsin protects the lungs from neutrophil elastase, maintains a balance so that healthy lung tissue is not damaged
  • elastase will hydrolyse elastin in lung tissue
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28
Q

COPD Pathophysiology: Emphysema:

A
  • cigarette smoking activates neutrophils in the lungs: neutrophils secreted proteases (elastase, collagenase)
  • the proteases are more than alpha 1 antitrypsin.
  • neutrophils invade the bronchial mucosa, secrete more proteases, which damage the alveolar sacs leading to a large bullae and therefore emphysema
  • reduces surface area for gas exchange
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29
Q

COPD Pathophysiology: Chronic bronchitis:

A
  • patients with chronic bronchitis develop inflammation of the airways with fixed structural changed
  • increase number of goblet cells and hypertrophy of goblet cells, hence lungs produce more viscous mucus which is hard to clear.
  • mucus acts as a culture medium for infective organisms
  • damage to cilia ( due to smoking) affects the host defence mechanisms leads to recurrent respiratory tract infections
  • recurrent infections lead to further inflammation of lungs and decreased lung function
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30
Q

pathophysiology of COPD

A
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31
Q

COPD results in increased

A
  • airway resistance and loss of elastic recoil of the lungs
  • airways collapse on inspiration
  • causes air trapping and hyperinflation
  • increases work of breathing: use of accessory muscles of breathing, pursed lip breathing
  • end stage of COPD:
    • right heart failure (cor pulmonale)
    • pulmonary hypertension
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32
Q
A

emphysematous lung

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33
Q

COPD risk factors

A
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34
Q

Diagnosis of COPD

A
  • should be suspected in any individual over the age of 35 years, who presents with symptoms of breathlessness and has a history of cigarette smoking
  • spirometry shows FEV1/FVC ratio of less than 70% predicted post administration of a short-acting bronchodilator confirms the diagnosis of COPD
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35
Q

Diagram of COPD

A
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36
Q

Signs of COPD (11):

A
  • clinical examination may be normal in mild
    COPD
  • tachypnoea with raised respiratory rate
  • tremor (over use of beta-2 agonist inhaler)
  • pursed-lip breathing and use of accessory
    muscles
  • barrel chest (increased AP diameter of
    thoracic cage)
  • hyperinflation
  • wheeze
  • signs of cor pulmonale: raised JVP and
    ankle oedema
  • cyanosis
  • signs of CO2 retention: CO2 retention flap,
    bounding pulse, irritability and confusion
  • development of type 2 respiratory failure
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37
Q

Symptoms of COPD (5)(3):

A
  • breathlessness on exertion (dyspnoea),
    progressively getting worse
  • chronic productive cough
  • frequent lower respiratory tract infections
  • progressive weight loss
  • peripheral ankle oedema (end stage COPD suggesting cor pulmonale)
  • Red Flag symptoms: haemoptysis, chest pain, night sweats
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38
Q

In COPD spirometry will show:

1 = Increased FVC > 70%
2 = Reduced FVC < 70%
3 = Increased FEV1 > 70%
4 = FEV1/FVC of > 70%
5 = FEV1/FVC of < 70%

39
Q

Spirometry of COPD will show:

A
  • reduced FEV1
  • FEV1/FVC < 70%
  • no reversibility to bronchodilator 20 minutes after 200mcg inhaled salbutamol with the FEV1 increasing by at least 15% of baseline or by more than 200 ml
40
Q

Lung Function test in COPD will:

A
  • increase in TLC (total lung capacity) and RV (residual volume) due to air trapping
    -reduced transfer factor/diffusing capacity (TLCO/DLCO)
41
Q

Which of these statements about COPD is true?

1 = is an irreversible obstructive airways
disease
2 = is a restrictive lung disease
3 = is associated with increased eosinophil
count
4 = is associated with atopy
5 = does not usually run in families

42
Q

How do we assess breathlessness?

A
  • mMRC dyspnoea scale (modified medical research council)

0 = dyspnoea with strenuous exercise
1 = dyspnoea when hurrying or walking up a slight hill
2 = walks slower than others of same age because of dyspnoea or has to stop for breath when walking at own pace
3 = stops for breath after walking 100 yards or after a few minutes
4 = too dyspnoeic to leave house or breathless when dressing

43
Q

How do we measure the severity of COPD?

A
  • Global Initiative for COPD (GOLD)

Mild: FEV1 ≥ 80%

Moderate: FEV1 50-79%

Severe: FEV1 30-49%

Very Severe: FEV1 ≤ 30%

44
Q
A

Copd
hyperinflation

45
Q
A

HRCT showing emphysematous bullae

46
Q

Investigations in COPD:

A
  • chest x ray to show hyperinflation and flat diaphragm and >6 anterior ribs
  • HRCT showing bullae in upper lobes of lungs
  • Pulse Oximetry:
    - may be normal in mild COPD
    - can drop to <92%, initially on exertion
    and then at rest as condition worsens
    - desaturation if 4% drop from baseline upon exertion
  • Arterial Blood Gases: (only acute hospital setting)
      - type 1 respiratory failure (hypoxia, normocapnia, normal pH)
  - type 2 respiratory failure 9hypoxia, hypercapnoea, acidosis)
  - secondary polycythaemia ( chronic hypoxemia causes EPO production increased, so increased RBCs)
  - alpha-1 antitrypsin level
  • cardiac investigations if cor pulmonale suspected: ECG, echocardiogram: right ventricular failure and pulmonary hypertension
47
Q

Assessing quality of life in COPD:

A
  • validated questionnaires to assess overall function and QOL
  • CAT: COPD Assessment Test
  • SGRQ: St Georges Respiratory Questionnaire
48
Q

Prognosis in COPD:

A
  • progressive decline in lung function
  • largely irreversible
  • risk of type 2 respiratory failure
  • may develop cor pulmonale
49
Q

Management of COPD: State the 4 categories:

A
  • Lifestyle Advice
  • Pharmacological Management
  • Surgical Management
  • Non-pharmacological Management
50
Q

Management of COPD: Lifestyle Advice:

A
  • smoking cessation
  • increase physical activity
  • improve nutrition
51
Q

Management of COPD: Pharmacological Management:

A
  • inhaled therapy: SABA, LABA, SAMA, LAMA, ICS
  • manage exacerbations
  • long term oxygen therapy
  • NIV for Type 2 Respiratory Failure
52
Q

Management of COPD: Surgical Management:

A
  • lung volume reduction surgery; removes parts of lung that are not ventilating, which improves ventilation to the rest of the lungs
  • lung transplant: mainly for young patients with alpha-1 antitrypsin
53
Q

Management of COPD: Non-Pharmacological:

A
  • pulmonary rehabilitation
  • counselling
  • palliative care
54
Q

Pharmacological management of COPD:

A
  • combination inhaled therapy: various combos, salbutamol SABA for symptom control
  • Methylxanthine (theophylline, aminophylline)
  • Carbocisteine (mucolytic) (symptom control)
55
Q

Core Drug: Why is ipratropium bromide (atrovent) not used as much anymore for COPD?

A
  • SAMA
  • use drugs that act for longer (LAMA eg: tiotropium)
56
Q

Core Drug: Ipratropium Bromide (atrovent) use in COPD:

  • drug class
  • how
  • onset of action
  • duration of action
  • route of administration
  • why?
  • with what?
  • side effects?
A
  • blocks M3 receptors in smooth muscle of airways
  • binds to M3 receptors, inhibits Gq receptor, which decrease calcium ion content inside cell, leading to bronchodilation
  • onset of action in 30mins
  • duration: 6 hours
  • via inhaler daily
  • nebulised for acute exacerbation
  • weaker bronchodilator effect than SABA
  • reduces mucus production
  • acts synergistically with SABA
  • Systemic side effects (anticholinergic) = inhibition of parasympathetic nervous system, minimal
57
Q

Core Drug: Tiotropium:

  • drug class?
  • used for
  • to treat
  • route of administration
  • duration of action
A
  • Long-acting Muscarinic Antagonist (LAMA)
  • COPD, chronic asthma
  • causes bronchodilation, reduces bronchospasm, decreases mucus production, slow dissociation from muscarinic receptors so prolonged duration of action
  • given via inhaler
  • duration: 12-24 hours
58
Q

Core Drug: Tiotropium: Adverse Effects of LAMA

A

Anticholinergic side effects
Inhibition of the parasympathetic nervous:
- system results in side effects
- dry mouth
- blurred vision
- closed-angle glaucoma
- urinary retention
- cardiac arrhythmias
- taste disturbance
- dizziness
- epistaxis

Systemic side effects are rare because little systemic absorption occurs

59
Q

Core Drug: Ipratropium Bromide: Adverse Effects on SAMA:

A

Anticholinergic side effects
Inhibition of the parasympathetic nervous:
- system results in side effects
- dry mouth
- blurred vision
- closed-angle glaucoma
- urinary retention
- cardiac arrhythmias
- taste disturbance
- dizziness
- epistaxis

Systemic side effects are rare because little systemic absorption occurs

60
Q

Three common combination of inhalers:

A
  • ICS/LABA
  • LAMA/LABA
  • ICS/LABA/LAMA
61
Q

Core Drug: Theophylline: can be used to treat which conditions?

A

Chronic asthma
COPD

62
Q

Antibiotic prescription in relation to COPD/asthma:

A
  • for bacterial chest infections causing exacerbations of asthma or COPD
  • check sensitivity of organisms
  • drug interactions
  • side effects of medications
  • contraindications for pregnancy or renal failure
  • check BNF
  • speak to microbiologist
63
Q

Antibiotics for asthma and copd exacerbations: Streptococcus pneumonia:

A
  • Core Drug: Beta lactam (cell wall) : amoxicillin, co-amoxiclav
  • Macrolides: Clarithromycin (inhibit 50s protein synthesis)
  • Tetracycline (inhibit 30s protein synthesis) Doxycycline
64
Q

Antibiotics for asthma and copd exacerbation: Staphylococcus aureus:

A
  • beta lactam fluclocacillin (cell wall)
  • core drug: peptidoglycans: vancomycin for MRSA (cell wall)
65
Q

Antibiotics for asthma and copd exacerbation: Haemophilus Influenza:

A
  • Tetracycline (inhibit 30s protein synthesis)
  • doxycycline
66
Q

Antibiotics for asthma and copd exacerbation: Pseudomonas aeruginosa:

A
  • Quinolones (inhibition of DNA Gyrases for supercoiling)
  • Aminoglycosides (inhibit 30s protein synthesis, bactericidal)
  • fluoroquinolone, gentamicin
67
Q

What does MRSA stand for?

A

Methicillin Resistant Staph Aureus

68
Q

Management of acute exacerbation of COPD:

A
  • nebulised SABA (salbutamol) + SAMA (ipratropium bromide)
  • systemic steroids
  • controlled oxygen via venturi
  • IV aminophylline
  • antibiotics
  • non-invasive ventilation (NIV) for type 2 respiratory failure
69
Q

A 48 year old man who has been smoking 20 cigarettes per day since the age of 18 is diagnosed with COPD. He is prescribed inhalers but continues to have breathlessness. What is the most important next step?

1 = advise to stop smoking and refer to SC clinic
2 = organise LTOT
3 = recommend daily peak flow monitoring
4 = refer for lung volume reduction surgery (LVRS)
5 = refer for pulmonary rehabilitation

SC = smoking cessation
LTOT = long term oxygen therapy

70
Q

When is oxygen prescribed?

A
  • indicated for type 1 respiratory failure to maintain the saturation between 94-98%
  • controlled oxygen for type 2 respiratory failure to maintain saturation between 88-92%
  • inappropriate use of oxygen can result in iatrogenic type 2 respiratory failure, CO2 retention, acidosis and death
  • not generally for treatment of breathlessness
  • can be used for intractable breathlessness in palliative care
71
Q

Oxygen is a drug. How can oxygen be delivered to a patient?

A
  • nasal cannula
  • simple face mask
  • re-breathe mask
  • controlled oxygen via venturi mask
  • CPAP
72
Q

Venturi mask table: match colours to O2 concentration

73
Q

Long term oxygen therapy for chronic hypoxemia

A
  • pO2 < 7.3kPa
  • COPD
  • pulmonary fibrosis
  • pulmonary hypotension
74
Q

A 67 year old man with severe COPD is admitted to hospital with an exacerbation of COPD. He is hypoxic and requires oxygen. What device should be used for delivering the oxygen?

1 = CPAP
2 = nasal cannula
3 = simple face mask
4 = re-breathe mask
5 = venturi device

75
Q

Discharge planning for COPD (11):

A
  • smoking cessation
  • appropriate inhaled therapy: ICS/LABA/LAMA and salbutamol for symptoms
  • check inhaler technique
  • oral theophylline
  • assess need for LTOT
  • assess need for home nebuliser
  • nutrition
  • pulmonary rehabilitation
  • psychological support
  • influenza and pneumococcal vaccination
  • palliative care
76
Q

What improves survival in COPD?

A
  • smoking cessation
  • LTOT
  • non-invasive ventilation
  • lung volume reduction surgery
  • reducing number of exacerbations
77
Q

What is classified as a frequent exacerbator in COPD cases?

A
  • If more than 2 exacerbations requiring oral corticosteroids and antibiotics or 1 hospital admission in a year is a frequent exacerbator
78
Q

The differences between asthma and COPD. Which of these statements is true ?

1 = COPD is common in people less than 30 years
2 = Asthma is a largely irreversible disease
3 = the predominant cell in COPD is the eosinophil
4 = COPD has a worse prognosis than asthma
5 = there are more deaths per day from asthma than from COPD

79
Q

Differences in the clinical features of asthma and copd slide

80
Q

Differences in the clinical features of asthma and copd table

81
Q

Which of these statements about COPD is true?

1 = is characterised by excellent prognosis
2 = is characterised by progressive loss of lung function
3 = can be described as an atopic condition
4 = can be described as a reversible airways condition
5 = is caused by damage to the pulmonary arteries

82
Q

Apnoea definition

A

cessation of breathing during sleep

83
Q

Central sleep apnoea

A
  • less common
  • absence of ventilatory drive
  • caused by brain stem injury
84
Q

Obstructive Sleep Apnoea/ Hypopnoea Syndrome

A
  • 3-7% men
    -2-5% women
  • recurrent episodes of upper airway collapse during sleep
  • can cause hypoxia and sleep fragmentation
85
Q

Symptoms of obstructive sleep apnoea Hypnopnea syndrome:

A
  • snoring
  • apnoeic episodes (stop breathing >10 seconds at a time)
  • excessive daytime sleepiness (raised epworth sleepiness score)
  • restless/disturbed sleep
  • nocturnal choking
  • morning headaches
  • unrefreshed on waking
  • nocturia
  • decreased cognition, concentration, memory, libido, irritability, change in mood
86
Q

Risk factors for obstructive sleep apnoea:

A
  • obesity with BMI >30
  • collar size >17 inches
  • enlarged tonsils/adenoids
  • enlarged tongue
  • long uvular
  • nasal pathology
  • retrognathia or micrognathia
  • acromegaly
  • hypothyroidism
  • Down Syndrome
87
Q

Anatomical changes in obstructive sleep apnoea

88
Q

3 worries of obstructive sleep apnoea:

A
  • increase in road traffic accidents
  • increased risk of developing hypertension
  • cardiovascular risk factor
89
Q

Investigations for obstructive sleep apnoea

A
  • overnight oximetry
  • full polysomnography
  • epworth sleepiness score
90
Q

Management of Obstructive Sleep Apnoea

A
  • weight loss
  • surgery: tonsillectomy, adenoidectomy
  • mild obstructive sleep apnoea: mandibular advancement device
  • Moderate or severe: continuous positive airway pressure CPAP
  • inform dvla: do not drive until treatment established
91
Q

The benefit of venturi masks:

A

Know exactly what piO2 is, unlike cannula which may vary slightly

92
Q

OSAHS stands

A

obstructive sleep apnoea hypopnea syndrom (under breathing)

93
Q

Symptoms of obstructive sleep apnoea syndrome:

A
  • snoring
  • apnoeic episodes (stop breathing >10 seconds at a time)
  • excessive daytime sleepiness (raised epworth sleepiness score)

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