Copd Flashcards

1
Q

What is copd

A

COPD is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking

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2
Q

What does copd encompass

A

COPD is an umbrella term encompassing:
• Emphysema
• Chronic Bronchitis
• Patients may have features of either or both

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3
Q

What is emphysema

A

• Emphysema is a pathological process in which there is destruction of the terminal bronchioles and distal
airspaces.
• This leads to loss of the alveolar surface area and therefore the impairment of gas exchange.

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4
Q

What can happen when emphysema progresss

A
  • The process often progresses to the development of larger redundant airspaces within the lung called bullae.
  • Emphysema causes the destruction of the supporting tissue surrounding the small airways, which therefore close / collapse during expiration when the pressure outside the airways rises. This results in airflow obstruction particularly affecting the small airways.
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5
Q

What can happen to the elastic tisue in emphysema and what can that lead to

A
In addition, the loss of
elastic tissue in the
lung causes the lungs
to hyperinflate
because the lungs are
unable to resist the
natural tendency of
the rib cage to
expand outwards.
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6
Q

What is chronic bronchitis

A

• Chronic bronchitis refers to chronic mucus hypersecretion that frequently occurs in smokers.
• Mucus hypersecretion is caused by inflammation in the large airways (usually due to cigarette smoke) leading to proliferation of mucus producing cells in the respiratory
epithelium - airway remodelling
• The result is a chronic productive cough and frequent respiratory infections. In COPD, this frequently persists even after smoking has stopped.
• Chronic bronchitis results in airflow
obstruction due to remodelling and
narrowing of the airways.

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7
Q

What can cause copd

A
  • Smoking (Most)
  • Alpha-1-antitrypsin deficiency (about 1%)
  • Occupational exposure e.g. coal dust
  • Pollution
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8
Q

Do all smokers get copd?

A
• Approximately 15% of
smokers will develop
COPD
• Why not all? Probably
genetically determined
factors
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9
Q

What are the symptoms of copd

A
  • Cough and sputum production are frequently the first symptoms of COPD but many patients do not present until they are breathless
  • Breathlessness is often progressive
  • Exacerbations are associated with increased breathlessness (compared to baseline) and increased cough and sputum production – may be infective - Acute flare up
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10
Q

What is the Mac dyspnoea score

A

Grade of breathlessness related to activities:
1 Not troubled by breathlessness except on strenuous exercise
2 Short of breath when hurrying or walking up a slight hill
3 Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace
4 Stops for breath after walking about 100m or after a few minutes on level ground
5 Too breathless to leave the house, or breathless when dressing or
undressing

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11
Q

What are the signs of copd

A

• Sometimes no signs
• The “purse lip” breathing often seen in patients with COPD is a protective manoeuvre that increases the pressure within the airways. This causes a reduction or a delay in the
closure of the airways
• Tachypnoea
• Using accessory muscles - eg leaning over, sitting forwards
• Patients may havewheeze or quiet
breath sounds onauscultation
• In more advancedcases – cyanosis and CO2 retention, right heart failure (cor pulmonale) with oedema
- hyperinflation

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12
Q

What does hyperinflation cause in copd

A

Hyperinflation is an important cause of breathlessness in COPD because th diaphragm and other respiratory muscles have to work much
harder to ventilate the lungs

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13
Q

How might a patient with copd present

A

• Patients with COPD may have a mixture of
respiratory symptoms and signs, and are
usually smokers or ex-smokers
• It is important to quantify breathlessness in
patients with respiratory disease – MRC
dyspnoea score

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14
Q

How is the measurement of airflow obstruction carries out and why is it important

A

Spiromety - essential for the diagnosis

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15
Q

As well as confirming the diagnosis, what else is spirometers important for?

A

As well as confirming the diagnosis of COPD, spirometry gives a measure of the severity of airflow obstruction
• Simple staging systems are used to categorise the severity of COPD according to the reduction in FEV1
The NICE guidelines suggest the following:
● Mild airflow obstruction - FEV1 50–80% predicted
● Moderate airflow obstruction - FEV1 30–49% predicted
● Severe airflow obstruction - FEV1 <30% predicted

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16
Q

What does the diagnosis of copd rely on

A

• The diagnosis of COPD relies on the combination of suggestive symptoms and signs together with the presence of airflow obstruction on spirometry (FEV1 <80% predicted and FEV1/FVC ratio <70%)
The following features are suggestive of COPD:
● Smoker or ex-smoker
● Older patient (>40 years old) and onset of symptoms in later life
● Chronic productive cough
● Breathlessness that is usually persistent and progressive

17
Q

Descrbe differences between asthma and copd

A

Ss

18
Q

What are other investigation s

A

• The Chest X-Ray is not diagnostic in COPD but is
mandatory to exclude other diagnoses
• High-resolution computed tomography (HRCT) scanning provides a detailed assessment of the degree of macroscopic alveolar destruction in emphysema. This may be helpful if surgical intervention is contemplated or if the diagnosis is in doubt, but is not required for routine assessment of COPD.
• Arterial Blood Gas to assess for respiratory failure
• Alpha-1-antitrypsin blood test for younger patients

19
Q

Describe teh epidemiology

A
• COPD is common and a leading cause of
morbidity and mortality
• There is a huge burden (financial and
resources) on the NHS as a result of
COPD
20
Q

What is the copd care bundle

A
Improve mortality outcomes 
‘COPD Care Bundle’ - MDT approach 
• SMOKING CESSATION 
• Pulmonary Rehabilitation 
• Bronchodilators 
• Antimuscarinics 
• Steroids 
• Mucolytics 
• Diet – supplements / dietician review 
• Supportive e.g. flu vaccine Also consider: 
• LONG TERM OXYGEN THERAPY if appropriate 
• LUNG VOLUME REDUCTION if appropriate
21
Q

What si the importance of. Smoking cessation

A

• Smoking cessation is a key management step in COPD patients to prevent disease progression (and for all smokers to prevent diseases including respiratory, cardiovascular, cancer, stroke, etc.)
• It’s never too late to stop smoking
Stopping smiking - fev.1 wont decline as fast (see graph)

22
Q

What are save copd drug therapy

A

• Bronchodilators • Steroids – Inhaled • Antimuscarinics • Mucolytics • Methylxanthines

23
Q

What is the action of b3 agonists

A

ß-2- agonist (e.g. Salbutamol) Mechanism of Action: Ligand binds to receptor activating adenyl cyclase, increasing cAMP and activating Protein Kinase (PKA), leading to phosphorylation of downstream targets (Myosin light chain kinase - MLCK) leading to: relaxation of smooth muscle in airway → bronchodilation

24
Q

What are the adverse effects of b2 agonist

A
  • Tachycardia (atrial ß-2 receptors)
  • Tremor (skeletal ß-2 receptors)
  • Anxiety
  • Palpitations
  • Hypokalaemia (skeletal muscle uptake K+)
25
Q

What is the mechanism of action of anticholinergics

A
(e.g. Ipratropium)
• Atropine in use in the 1800s – extract from
plants such as deadly night shade 
• Ipratropium (Atrovent) 
• Tiotropium (Spiriva) 
• Synergistic with ß-2 agonists
Smooth muscle relaxation, dilation
26
Q

What are the adverse effects o annticholinergics

A

Ss

27
Q

What is the mechanism of action of methylxanthines

A

Methylxanthines Theophylline / Aminophylline
• Mode of Action
– Bronchodilatation
– Increase respiratory drive
– Anti-inflammatory effects
• Mechanism of action
– Inhibition of phosphodiesterases
• PDE’s break down cAMP so inhibition leads to an increase in cAMP → bronchodilation
• Toxicity – tachycardia / SVT, nausea, seizures – needs blood level monitoring - these are particularly toxic

28
Q

What are the side effects of long term steroids

A
  • Generally, if on less than 800mcg inhaled steroid/day, unlikely to get significant systemic effects If above this dose or oral steroids:
  • Thin skin
  • Bruising
  • Cataracts
  • Adrenal insufficiency
  • Osteoporosis
  • Diabetes
  • Increased weight (fluid retention)
  • Mental disturbance
  • GI symptoms
  • Proximal myopathy
29
Q

What are mucolytics

A

• e.g. carbocysteine
• Can help to reduce thickness of sputum
helping with airways clearance

30
Q

Give an verve’s o copd drug therapy

A
  • Bronchodilator therapy may provide symptomatic relief
  • Steroids can help reduce inflammatory pathways
  • Mucolytics can reduce sputum thickness
  • Drugs can help improve quality of life and reduce exacerbation frequency but do not provide cure or improve survival in COPD
  • Education on inhaler technique is essential as well as side effect counselling
31
Q

What is pulmonary rehabilitation

A

• Many patients with COPD avoid exercise and physical activity because of breathlessness
Deconditioning
• This may lead to a vicious cycle of increasing social isolation and inactivity leading to worsening of symptoms = Deconditioning
• Pulmonary Rehabilitation aims to break this cycle of Deconditioning
– a 6-12 week MDT (dietitians, clinicians, physiotherapists) programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease education

32
Q

What is one term oxygen therapy

A

• Extended periods of hypoxia cause renal and cardiac damage – can be prevented by LTOT
• Continuous oxygen therapy for most of the day – at least 16 hours/day for a survival benefit
• LTOT offered if pO 2 consistently below 7.3 kPa, or below 8 kPa with cor pulmonale
• Patients must be non-smokers and not retain high levels of CO
• Safety – Home Fire Risk Assessment
Oxygen does not help with breathlessness it is a treatment for hypoxia
Long term respiratory failure - persistently hypoxic so other organs could be affected by hypoxic damage

33
Q

What are surgical options

A
  • Lung Volume Reduction - The reduction of hyperinflation is the principal aim of surgical techniques in the treatment of appropriately selected COPD patients
  • Lung Transplant may be an option for younger patients
34
Q

Who are the MDT ppl involved

A

• Physicians • G.P.’s • Specialist nurses • Physiotherapists • Pharmacists • Occupational therapists • Dieticians • Sometimes surgeons
Stable COPD is managed by an experienced
MDT delivered as a “care bundle” with
non-pharmacological interventions, as well as
drugs, all aimed at improving quality of life

35
Q

Describe the cold exacerbation management

A
  • Aim for Sats 88-92% - controlled O 2 therapy
  • Nebulisers - bronchodilators
  • Steroids – oral (sometimes IV)
  • Antibiotics if infective features - raised CRP / WCC or purulent sputum
  • Consider IV aminophylline
  • Repeat ABG – if no better, consider Non-invasive ventilation or even ITU referral for invasive ventilation
36
Q

What is non invasive ventilation

A

Non Invasive Ventilation / BIPAP
Useful for acute exacerbations of COPD with Type II Respiratory Failure and mild acidosis (pH 7.25 - 7.35), co2 excess
Patients must be conscious to use it
• The provision of ventilatory support through the patient’s upper airway using a mask or similar device

37
Q

What are teh contraindications to NIV

A
• Untreated pneumothorax 
• Impaired conscious level (usually GCS <8) 
• Upper airway secretions +++ 
• Facial injury 
• Vomiting 
• Agitated 
• Life threatening hypoxia
Mask might not fit