Chronic Obstructive Pulmonary Disease Flashcards

1
Q

What is COPD?

A

Non-reversible obstruction of the airways, caused by damage to the lung tissue, which is almost always due to smoking.

Note that obstruction cannot be significantly reversed by the use of bronchodilators such as salbutamol. This distinguishes the disease from asthma whereby obstruction is significantly reversible.

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2
Q

Why are COPD patients prone to infections?

A

Non-reversible obstruction –> reduced ventilation of the lung –> increases risk of infection.

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3
Q

How do patients with COPD present?

A
  • Long term smoker
  • Chronic SOB
  • Cough
  • Productive sputum
  • Wheeze
  • Recurrent respiratory infections, especially in the winter
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4
Q

What differentials must you always consider?

A
  • Lung cancer
  • Lung fibrosis (ILD)
  • Heart failure
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5
Q

What signs/symptoms takes you away from COPD diagnosis?

A

COPD does not cause clubbing.

It is unusual for COPD to cause haemoptysis or chest pain.

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6
Q

What scale is used to measure a COPD patient’s breathlessness?

A

MRC Dyspnea Scale

Grade 1 - Breathless on strenuous exercise

Grade 2 - Breathless whilst walking up a hill

Grade 3 - Breathless that slows walking on a flat surface

Grade 4 - Stop to catch their breath after walking 100m on the flat

Grade 5 - Unable to leave the house because of their breathlessness

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7
Q

How do you diagnose patients with COPD?

A

Diagnosis depends on the patient’s clinical symptoms and spirometry.

Clinical presentation

  • Long term smoker
  • Chronic SOB
  • Wheeze
  • Cough
  • Productive sputum
  • Recurrent respiratory infections, particularly in the winter

Spirometry

  • Spirometry will show an obstructive picture.
  • FEV1/FVC < 0.7 (FEV1 will be reduced significantly, FVC less so).

Note that this obstruction is not reversible with the use of bronchodilators e.g. salbutamol. If there is a large amount of reversibility, consider asthma diagnosis

Other investigations to consider that will help with diagnosis and management of the patient.

  • Chest X ray to exclude other pathologies like cancer.
  • FBC: patients with COPD tend to have polycythemia
  • BMI: as a baseline to assess weight loss (which is the case in cancer or severe COPD) or weight gain (which can be due to excessive steroid use)/
  • Sputum culture - to assess for chronic infections such as pseudomonas.
  • ECG and echocardiogram - to assess heart function
  • CT thorax - to consider alternative diagnosis such as cancer or lung fibrosis
  • Serum alpha 1 anti-trypsin = to assess for alpha 1 anti-trypsin deficiency which is associated with more severe disease and earlier onset of pathology.
  • Transfer factor for carbon monoxide (TLCO) –> decreased in COPD. May be increased in other conditions such as asthma.
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8
Q

How can you grade the severity of the obstruction in COPD patients?

A

Severity of obstruction can be graded using FEV1 scale.

Stage 1 : FEV1 > 80%
Stage 2: FEV1 : 50-79%
Stage 3: FEV1 : 30-49%
Stage 4: < 30%

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9
Q

What is the long-term management of COPD patients?

A

NICE GUIDELINES

It is important to advise patients against smoking as smoking will exacerbate the patient’s symptoms –> offer nicotine replacement therapy, varenicline or bupropion

It is important that COPD patients are vaccinated with pneumococcal vaccine and the annual flu vaccine.

Step 1 Management:
- SABA (e.g. salbutamol, or tetrabutaline) or SAMA (ipratroprium bromide)

Step 2:
If the patient does not have asthmatic features or are steroid responsive, then give the patient a combined inhaler (LABA+ LAMA).

Examples of combined LABA+LAMA inhaler

  • Anoro Ellipta
  • Ultibro Breezhaler
  • DuaKlir Genuair

If they have asthmatic or steroid responsive features, they should have a combined LABA+ICS inhaler.

  • Examples of combined LABA + ICS therapy
    > Foster
    > Symbicort
    > Seretide

If these LABA+ICS doesn’t work, then it can stepped up to a combination inhaler including LABA, LAMA and ICS.

> Examples of combination inhalers containing LABA, LAMA and ICS

  • -> Trimbo
  • -> Trelegy Ellipta

In more severe cases, additional treatment options are:

  • Nebulisers (salbutamol and/or ipratropium)
  • Oral theophylline
    > Reduce dose, if a macrolide or fluoroquinolone antibiotic is also being used e.g. azithromycin.
  • Oral mucolytic therapy to break down mucus e.g. carbocisteine
  • Long-term prophylactic therapy - antibiotics (azithromycin) –> consider if the patient has had 2 or more exacerbations that required steroid treatment and 1 admission to the emergency department.
    > Before starting azithromycin, carry out an ECG to rule our long QT syndrome and carry out LFTs.
  • Long-term oxygen therapy at home
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10
Q

Who is long term oxygen therapy used for?

A

Patients with severe COPD that is causing problems such as:

1) Hypoxia
2) Cyanosis
3) Polycythemia
4) Heart failure due to pulmonary hypertension (Cor pulmonale)
> Raised JVP
> Peripheral oedema
5) FEV1 < 30%

Note that smoking is contraindicated in patients treated with long-term oxygen therapy as it’s a fire hazard.

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11
Q

What is an exacerbation of COPD?

What are exacerbations of COPD often due to?

What are the most common bacterial pathogens causing infective exacerbations?

What are the most common viral pathogens causing infective exacerbations?

A

Exacerbation of COPD is an acute worsening of the patient’s symptoms

  • SOB
  • wheeze
  • sputum production

Exacerbations are often due to viral or bacterial infections.

Most common bacterial

  • H. influenza
  • Strep pneumonia
  • M. Catarrhalis

Most common viral
- Human rhinovirus

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12
Q

When reading an ABG, what does raised bicarbonate indicate?

What can happen during an acute exacerbation?

A

Raised bicarbonate indicates that the patient has been chronically retaining CO2, so much so that the kidneys have responded by producing more bicarbonate to balance out acidic CO2 to maintain blood pH.

During an acute exacerbation, the patient’s CO2 levels may rise too quickly, faster than the kidney’s response to produce bicarbonate –> this would result in respiratory acidosis. The patient in this case would be acidotic despite having higher bicarbonate level than patients without COPD.

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13
Q

Define the two types of respiratory failure?

A

Type 1: normal pCO2, with low pO2 (only one is affected)

Type 2: Raised pCO2 with low pO2 (two are affected)

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14
Q

What investigations are carried out when a patient experiences an exacerbation of their COPD?

A
  • ABG
    > type of respiratory failure (type 1 vs 2)
    > pH (acidosis/ alkalosis/ compensation)
  • Chest X ray –> to look for pneumonia or other pathology
  • ECG –> to look for arrythmias or evidence of heart strain
  • FBC - to look for evidence of infection (raised WBC)
  • U&Es –> to check for electrolytes that may be affected by infection and medications
  • Sputum culture –> to see if there is significant infection going on.
  • Blood culture - if the patient is septic.
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15
Q

How do you deliver oxygen to COPD patients?

What are the different types of this delivery method?

Why oxygen saturation do you aim for? When is this not the case?

Why is it important to control oxygen saturation?

A

Venturi masks

Blue - 24% 
White - 28% 
Orange - 31%
Yellow - 35% 
Red - 40% 
Green - 60% 

88-92% saturation if a patient retains CO2 –> start with 88-92% before getting ABG results. If hypercapnic (if patient is CO2 retainer) then continue to aim for 88-92%.

> If the patient is normocapnic (i.e. is not a CO2 retainer), the aim for oxygen saturations > 94%.

It is important to control oxygen saturation because too much oxygen in COPD patients can depress their respiratory drive. Depression of their respiratory drive would cause their breathing to slow down, leading them to retain more CO2.

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16
Q

How do you manage a COPD exacerbation?

A

If the patient is well enough at home, typical treatments would include:

  • Prednisolone 30mg OD (7-14 days)
  • Regular inhalers or home nebulisers.
  • Antibiotics if there is evidence of infection

In hospital

  • Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h).
  • Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone).
  • Antibiotics if there is evidence of infection
  • Physiotherapy to get rid of the mucus

If the patient respond to first line treatment at the hospital, the following should be considered.

  • IV aminophyline
  • NIV (BiPAP or CPAP)
  • Intubation and ventilation, with admission to intensive care.
  • Doxapram - used when NIV or intubation and ventilation are contraindicated.
17
Q

What are examples of asthmatic features?

A
  • Previous diagnosis of asthma or atopy
  • Higher blood eosinophil count
  • Variation in FEV1 overtime (at least 400ml)
  • Diurnal variation in PEFR (at least 20%)
18
Q

What is the underlying pathophysiology for COPD?

Smoking has a multitude of effects on the respiratory tract, which explain for the underlying symptoms seen in COPD.

A
  • Bronchi
    o Hyperplasia of subendothelial cells and goblet cells  increased mucus production
  • Small Airways
    o Healing by fibrosis  stenosis of the airways  airway obstruction
  • Respiratory Bronchioles
    o Smoking causes recruitment of neutrophils which release elastases to break down the elastin in the alveolar walls.
    o Smoking also inhibits alpha 1 antitrypsin, to further promote the degradation of elastin.
    o Breakdown of the alveolar wall
     Removal of lung recoil  reduces expiration ability  FEV1 decline
     Reduce pulmonary surface area for diffusion of gases  hypoxia
  • Bronchi are affected first  cough and sputum production  earliest symptoms
  • If the patient continues to smoke, the smaller airways become affected  become increasingly breathless.
  • Death due to COPD is due to:
    o Bronchopneumonia
    o Respiratory and/or cardiac failure.
19
Q

What are the long-term complications of COPD?

A

COPD induces a number of changes to the pulmonary system including:

  • Emphysema causes loss of pulmonary arterioles and capillaries  pulmonary hypertension
  • Emphysema induces chronic hypoxia  increased erythropoietin production by the kidney  increased red blood cell production (erythrocytosis)  increases blood viscosity  induces pulmonary hypertension.
  • Emphysema causes hypoxia  pulmonary arterial vasoconstriction  increases TPR  pulmonary hypertension.

All of these changes lead to pulmonary hypertension, which in turn induces right ventricular hypertrophy. The heart eventually decompensates, resulting in RHF (cor pulmonale).

20
Q

How is an infective exacerbation of COPD different from that of pneumonia?

A
  • Site of infection for COPD  Airways  clear lung fields

- Site of infection in pneumonia  Alveoli  consolidation on CXR

21
Q

Compare the most common pathogen causing infective exacerbation of COPD vs pneumonia?

A
-	Infective exacerbation of COPD 
o	H Influenza
o	M Catarrhalis 
o	S pneumonia 
o	Viruses 
-	Pneumonia 
o	S pneumoniae 
o	H Influenza
o	Viruses 
o	Atypical Organisms