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The Patient 20300 > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD

A

Chronic obstructive pulmonary disease is a treatable (but not curable) and largely preventable lung disease

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2
Q

How is the obstruction to airflow characterised in COPD?

A

COPD is characterised by airflow obstruction that is not fully reversible. The airflow obstruction does not change markedly over several months and is usually progressive in the long term. This is in contrast to asthma symptoms.

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3
Q

What causes airflow obstruction in COPD?

A

The airflow obstruction is present because of a combination of airway and parenchymal damage and is associated with an abnormal inflammatory response of the lungs, mainly to noxious particles, especially cigarette smoke. The damage is the result of chronic inflammation that differs from that seen in asthma and which is usually the result of tobacco smoke.

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4
Q

What other names are used for COPD

A

Chronic bronchitis, COAD or emphysema

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5
Q

How do we diagnose COPD?

A

There is no single diagnostic test for COPD. Making a diagnosis relies on clinical judgement based on a combination of history, physical examination and confirmation of the presence of airflow obstruction using spirometry

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6
Q

What are the symptoms of COPD

A 
A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with one or more of the following symptoms:
•	exertional breathlessness
•	chronic cough
•	regular sputum production
•	frequent winter 'bronchitis'
•	wheeze
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7
Q

What supplementary symptoms are sometimes seen alongside the common ones

A
  • weight loss
  • effort intolerance
  • waking at night
  • ankle swelling
  • fatigue
  • occupational hazards
  • chest pain
  • haemoptysis (blood in mucus from coughing)
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8
Q

What are the systemic features of COPD

A 
Cachexia - loss of fat free mass (due to lack of movement)
skeletal muscle wasting
osteoporosis
depression
increased likelihood of developing CVD
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9
Q

What clinical tests do we use to diagnose COPD

A

FEV1/FVC ratio

Airflow obstruction is defined as a reduced FEV1/FVC ratio (where FEV1 is forced expired volume in 1 second and FVC is forced vital capacity), such that FEV1/FVC is less than 0.7.
If FEV1 is ≥ 80% predicted normal a diagnosis of COPD should only be made in the presence of respiratory symptoms, for example breathlessness or cough.

All patients should also receive:
• Spirometry
• a chest radiograph to exclude other pathologies
• a full blood count to identify anaemia or polycythaemia
• Body mass index (BMI) calculated.

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10
Q

What impact does the introduction of a bronchodilator have on COPD patients

A

In comparison to asthma, reversability i.e. FEV1% increasing following a broncholdilator, is only modest in COPD whereas in asthma we expect an increase in lung capacity of ~ 400ml

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11
Q

What are the treatment aims for COPD

A
  • Stop smoking
  • Improve symptoms
  • Prevent acute infective exacerbations
  • Reduce rate of disease progression
  • Maintain nutritional intake, BMI > 20
  • Increase QoL
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12
Q

Which drug classes are used in COPD

A 
BROCHODILATORS
-b2 adreoceptor agonists
-antimuscarinics
-methylxanthines
ANTI-INFLAMMATORY AGENTS
corticosteroids
OXYGEN
VACCINATION
ANTIBIOTICS
MUCOLYTIC
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13
Q

How do bronchodilators work in COPD

A

Much the same as in asthma
-Continuous bronchodilation important
Short-acting ß2 agonists (SABA) e.g. salbutamol
• Onset 15mins, duration 4-6h
• Most commonly used bronchodilator in COPD
Long-acting ß2 agonists (LABAs) e.g. salmeterol, Formoterol and indacaterol, olodaterol
• Duration 12h
LABA/SABA - Modest increase in FEV1, but symptoms reduced, exercise capacity increase, health status improved.
Relax airway smooth muscle by stimulating B2 receptors, increasing cAMP, reducing bronchoconstriction

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14
Q

How do we use antimuscarinics in COPD

A

As a first line therapy (in contrast to asthma)
Block the bronchoconstrictor effects of acetylcholine on M3 muscarinic receptors. Reduce vagal airway tone & reflex bronchoconstriction
• Short-acting: Ipratropium (SAMA)
• Long-acting: Tiotropium (LAMA)
Use alone or add to ß2 agonists if inadequate relief (improve breathing)
[glycopyrronium, tiotropium, umeclidinium …]

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15
Q

What are the anticholinergic side effects

A

Anticholinergic side effects – dry mouth, blurred vision, urinary retention, constipation, hypotension …

Cant see, cant pee, cant spit, cant shit

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16
Q

How do we use methylxanthines in COPD

A

See Asthma
• strengthen diaphragm
• increase mucociliary clearance
• improve CNS response to hypoxaemia
Use as add-in therapy if there is inadequate control with short- and long-acting bronchodilators
Caution: elderly, interactions, ADRS, smoking

17
Q

Which methyxanthines do we use

A 
Oral
Theophylline or aminophylline
IV 
Aminophylline: Loading dose (if no previous use) then continuous infusion
Monitor levels
18
Q

What interactions do we need to be aware of with the methylxanthines

A

Interactions are very important
• Cigarette smoke (inducer of cyp enxymes, increases clearance we need to increase the dose)
• Antibiotics used for chest infections (macrolysed/cyprofloxacin inhibit cyp enzymes which lead to increased levels of theophylline. We need to decrease the dose to avoid toxicity)

19
Q

When do we use corticosteroids

A

Use for patients with
• FEV1 <50% predicted in patients who remain breathless or have exacerbations despite using short acting bronchodilators as required
• Patients that remain breathless on LABA, LAMA regardless of FEV1% (i.e. even if it is >50%)
None licensed for use alone in COPD

20
Q

When do we use oxygen

A

Improves hypoxia & reduces work of breathing
Used for acute exacerbations and for long term therapy if the patient has an FEV<30% and is symptomatic, or if the patient has polycythaemia or cor pulmonale. If the patients O2 saturation is less than 92% on air or is chronically breathless to the point that it affects daily life.
Long Term O2 Therapy (LTOT) (> 15 hours daily) prolongs life
Use 24 - 28% O2 (much lower than asthma, which is 40-60%) to prevent a reduction in respiratory drive (O2 is stimulus for breathing due to chronic retention of CO2 - danger! High O2 concentrations)

21
Q

How do we use vaccinations in the treatment of COPD

A 
Annual flu vaccine
Pneumococcal vaccine (one off)

This is because the development of a chest infection on the back of coming down with flu or pneumonia can be fatal

22
Q

How do we use antibiotics in the treatment of COPD

A 
For recurrent chest infections (prophylactically):
azithromycin 250mg tds if:
•	Non-smoker
•	Optimised inhaled therapies
•	Up to date vaccinations
•	Continue to have one or more symptoms
•	Baseline LFTs and ECG (QT interval)
•	Review in 3/12 and then 6/12 for benefit

Antibiotics are used in infective exacerbations. Choice dependent on:
• local policy
• lab sensitivity patterns
• previous Rx (resistance)

23
Q

How do we use mucolytics in the treatment of COPD

A

• Facilitate expectoration by reducing sputum viscosity - good for symptomatic relief
• Consider in pts with chronic productive cough
• Continue if improvement (stop after 4-week trial if no benefit)
E.g. Carbocisteine, Mecysteine

24
Q

How do we manage stable COPD

A

In people with stable COPD who remain breathless or have exacerbations despite using short-acting bronchodilators (salbutamol or ipatroprium) as required, offer the following as maintenance therapy:

  • If breathless and no asthmatic symptoms (wheeze, night waking, respose to triggers) offer LAMA+LABA (plus short acting saba)
  • If breathless with asthmatic symptoms offer LABA+ICS
  • If still breathless offer LAMA+LABA+ICS
25
Q

What do the following abbreviations stand for

LABA, LAMA, ICS, SABA, SAMA

A 
Long acting beta agonist
Long-acting muscarinic antagonists
Inhaled corticosteroid
Short acting beta agonist
Short acting muscarinic antagonist
26
Q

What are the monitoring requirements and lifestyle interventions needed to manage stable copd

A

Maintenance oral steroids are used at the lowest effective dose in patients that remain symptomatic – think ADRS, counselling and osteoporosis prophylaxis.
Assess need for oxygen (if FEV < 35% and breathless/hypoxic)
Stop smoking, encourage exercise, nutrition, flu and pneumococcal vaccine
Annual review

27
Q

How do we treat a non-infective acute exacerbation

A

Treat exacerbations very much like in asthma: nebulised salbutamol and ipratropium consider theophylline. The use of oxygen is however different to avoid a reduction in respiratory drive:
O2 saturations maintained – 88-92% (note asthma = 94-98%, hypercapnia)

28
Q

How do we treat a infective acute exacerbation of COPD

A

Antibiotics are used in infective exacerbations only. Choice dependent on:
• local policy
• lab sensitivity patterns
• previous Rx (resistance)
Increased susceptibility to chest infections due to lung degradation and steroid use
Pathogens:
Haemophilus influenzae
Streptococcus pneumoniae
1st choice – Amoxicillin 500mg tds or tetracycline (doxycycline 200mg stat then 100mg od) or clarithromycin 500mg bd -
2nd choice - broad spectrum cephalosporin or macrolide
Home 5d Hospital 7-14d

29
Q

What criteria do we need to check before administering antibiotics

A

Antibiotics if 2 or more of increased
• breathlessness
• sputum volume
• sputum purulence (how often and how much)
Home vs hospital management – depends on severity (reduce hospital admissions if possible)
Give oral Prednisolone 30mg for 7-14 days to reduce inflammation, symptom relief
Increase bronchodilator - nebulised

30
Q

What are the long term complications of COPD

A

Hypercapnia - Healthy adults take a breath when CO2 levels increase. A COPD patient is used to a high CO2 level and so adapts to take a breath when O2 levels drop. This is hypercapnia and many COPD patients are chronically hypoxic.
Chronic hypoxia can lead to cardiac complications. It can also lead to respirtory failure
Long-term corticosteroids lead to osteoporosis – offer prophylactic treatments

31
Q

What are the cardiac complications linked to COPD

A

Cor pulmonale
Right heart failure - 90% due to COPD due to pulmonary hypertension and thus blood flow resistance in the damaged pulmonary vasculature, hypoxia (secondary to hypercapnia) requiring an increase in oxygen demand, and polycythaemia (viscous blood harder to pump.
Symptoms: peripheral oedema, hepatomegaly, raised JVP
Rx:
• loop diuretics to reduce oedema
• O2 to reduce hypoxia

Polycythaemia
Chronically low o2
Increased number of RBCs in response to chronic hypoxia:
↓ O2 → ↑ RBC → ↑ haematocrit (number of rbcs in circulatory system)→ ↑ Blood viscosity
Prescribe O2 to ↓ hypoxia
Venesection – remove blood

The Patient 20300 (24 decks)

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