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Y3M - Respiratory > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD?

A

Airflow limitation that is not fully reversible

Usually both progressive and associated with an abnormal inflammatory response of lungs to noxious particles or gases.

It’s an overarching diagnosis of emphysema, small airways disease and chronic bronchitis associated with airflow limitation and destruction of lung parenchyma.

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2
Q

Resultants of the COPD.

A

Hyperinflation of the lungs

Ventilation/perfusion mismatch

Increased work of breathing

Breathlessness

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3
Q

Co-morbidities of COPD.

A

Ischaemic heart disease

Hypertension

Diabetes

Heart failure

Cancer

Bronchiectasis

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4
Q

Causes and risk factors of COPD.

A

Long term exposure to toxic particles and gases.

Over 90% of cases are due to cigarette smoking.

Can also be inhalation of smoke from biomass heating fuels, and cooking in poorly ventilated areas.

Urbanisation, air pollution, socioeconomic class and occupation may also play a role.

Alpha-antitrypsin deficiency.

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5
Q

Structural changes in COPD.

A

Emphysema

Small airway disease

Increased mucus-producing goblet cells in bronchial mucosa (hyperplasia)

Inflammation (both acute and chronic)

Neutrophils, CD8 predominant lymphocytes, macrophages

Scarring

Fibrosis

Destruction of alveolar walls (emphysema)

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6
Q

Definition of emphysema

A

Abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, accompanied with destruction of their walls.

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7
Q

Classifications of emphysema.

A

Centri-acinar emphysema

Pan-acinar emphysema

Irregular emphysema

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8
Q

What is centri-acinar emphysema?

A

Distension and damage of lung tissue that is concentrated around the respiratory bronchioles.

More distal alveolar ducts and alveoli are usually well-preserved.

This is the most common form.

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9
Q

What is pan-acinar emphysema?

A

Distension and destruction affecting the whole acinus, in severe cases the lung is just a collection of bullae.

Severe airflow limitation and mismatch occur.

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10
Q

What is pan-acinar emphysema associated with?

A

Alpha-antitrypsin deficiency

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11
Q

What is irregular emphysema?

A

Scarring and damage that affect the lung parenchyma patchily and independent of acinar structure.

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12
Q

What does emphysema lead to?

A

Loss of lung elastic recoil and increase in TLC.

Hyperinflation and in severe cases barrel chest.

Loss of alveoli leading to decreased capacity for gas transfer.

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13
Q

Explain pathogenesis of COPD regarding smoking.

A

Increase in neutrophil granulocytes. The granulocytes can release elastases and proteases. An imbalance in protease to antiprotease activity leads to emphysema.

Mucuous gland hypertrophy in larger airways is thought to be a direct response to persistent irritation due to the inhalation of cigarette smoke.

The smoke has an adverse effect on surfactant, favouring over-distension of lungs.

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14
Q

Pathogenesis of COPD in regards to infection.

A

A common precipitating cause of acute exacerbations of COPD.

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15
Q

How can acute exacerbations of COPD due to infection be prevented?

A

Prompt use of antibiotics

Routine vaccinations against influenza and pneumococci

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16
Q

Explain alpha1-antitrypsin deficiency.

A

It is a proteinase inhibitor produced in the liver and then secreted into the blood.

It diffuses into the lungs and will inhibit proteolytic enzymes such as neutrophil elastase which can otherwise destroy the aleolar wall connective tissue.

If there is deficiency the alpha1-antitrypsin will accumulate in the liver and not reach the lungs. This leads to emphysema as well as liver disease.

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17
Q

Symptoms of COPD

A

Productive cough with white or clear sputum

Wheeze

Breathlessness

More prone to LRTI

Hypertension

Osteoporosis

Depression

Weight loss

Reduced muscle mass

General weakness

Right heart failure

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18
Q

Signs in mild COPD

A

Might be no signs

Quiet wheeze

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19
Q

Signs in severe COPD.

A

Tachypnoeic

Prolonged expiration

Use of accessory muscles

Intercostal indrawing on inspiration

Pursed lip breathing on expiration

Cricosternal distance reduced

Poor chest expansion

Hyperinflation

Loss of normal cardiac and liver dullness

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20
Q

Features of patients with COPD that remain responsive to CO2.

A

Usually dyspnoeic and rarely cyanosed.

Heart failure and oedema are rare

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21
Q

Features of patients with COPD who are unresponsive to CO2.

A

Oedematous

Cyanosed

Not breathless

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22
Q

Features of patients with COPD who are hypercapnic.

A

Peripheral vasodilation

Bounding pulse

Coarse flapping tremor of outstretched hand

In severe hypercapnia they may be confused and have progressive drowsiness.

Papilloedema might also occur.

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23
Q

Complications in late stages of COPD.

A

Respiratory failure

Pulmonary hypertension

Cor pulmonale

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24
Q

How is COPD diagnosed?

A

Based on clinical presentation, PMH, FH, social history (smoking)

This is then supported by spirometry.

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25
Q

How is dyspnoea assessed?

A

MRC dyspnoea scale

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26
Q

Explain the MRC dyspnoea scale.

A

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 100 metres 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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27
Q

Spirometry in support of COPD diagnosis.

A

Pre and post-bronchodilator spirometry

Obstructive pattern

FEV1/FVC ratio <70%

And reversibility should not be more than 15% on bronchodilators.

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28
Q

Other investigations in COPD

A

Transfer factor

CXR (often normal, can be hyperfinflation, large bullae, pruned blood vessels and flattened diaphgram)

HRCT scan

Hb levels and PCV (can be elevated in persistent hypoxaemia)

Blood gases

Sputum examination (S. pneumoniae, H. influenzae, Moraxella catarrhalis)

ECG often normal (tall P wave (pulmonary hypertension), right BBB, RV hypertrophy)

Echocardiography

Alpha1-antitrypsin levels

29
Q

Assessments of severity of COPD

A

FEV1

Smoking status

Low BMI

Heart disease

Severity and frequency of exacerbations

COPD assessment test

6 minute walk test

Co-morbidities

30
Q

Explain the COPD Assessment Test (CAT)

A
31
Q

How is the severity of airflow limitation assessed?

A

By GOLD score

32
Q

Types of management of COPD.

A

Smoking cessation (very essential)

Drug therapy

Oxygen therapy

Pulmonary rehabilitation

Vaccination

Surgery

33
Q

What vaccinations are offered in COPD?

A

Pneumococcal and yearly influenza vaccines

34
Q

Examples of drugs used in COPD.

A

Beta agonists

Antimuscarinic drugs

Theophyllines

Phosphodiesterase type 4 inhibitors

Corticosteroids

Antibiotics

Mucolytic agents

35
Q

Give examples of beta agonists used in COPD.

A

Salbutamol 200 microgram

LABAs can be used in more severe airway limitation.

36
Q

Give examples of antimuscarinic drugs used in COPD.

A

Tiotropium (LAMA) can improve lung fucntion, symptoms of dyspnoea and QOL.

However LAMAs do not prevent the decline in FEV1

37
Q

When are theophyllines used in COPD?

A

They are of little benefit so not often used.

38
Q

Give an examples of a phosphodiesterase type 4 inhibitor used in COPD.

A

Roflumilast.

They have anti-inflammatory properties.

39
Q

When is roflumilast used?

A

As an adjunct to bronchodilators for maintenance treatment in patients with an FEV1 of less than 50% and chronic bronchitis.

40
Q

When are corticosteroids used in COPD?

A

Inhaled are recommended in patients with frequent exacerbations, or a FEV1 of less than 50% of predicted.

High-dose inhaled steroid are not advised.

Oral steroids are prescribed in context of an acute exacerbation.

41
Q

When are antibiotics used in COPD?

A

Prompt antibiotic use should be done to shorten exacerbations and should always be used in acute episodes.

It can prevent further damage and hospital admissions.

42
Q

When should patients start antibiotic use?

A

As soon as their sputum turns yellow or green,

43
Q

How do mucolytic agents work?

A

Reduce sputum viscosity and can reduce the number of acute exacerbations.

44
Q

When might you give a long term azithromycin treatment for people with COPD?

A

Do not smoke and…

have optimised non-pharmacological management and inhaled therapies, relevant vaccinations and (if appropriate) have been referred for pulmonary rehabilitation.

and…

continue to have 1 or more of the following, particularly if they have significant daily sputum production:

frequent (typically 4 or more per year) exacerbations with sputum production

prolonged exacerbations with sputum production

exacerbations resulting in hospitalisation.

45
Q

What investigations need to be done before starting azithromycin treatment?

A

ECG to rule out prolonged QT interval

Liver function test

46
Q

Explain the non-pharmacological and inhaler-use treatment algorithm in COPD.

A
47
Q

In which patients should you consider giving long-term oxygen therapy?

A

Who do not smoke (< 3% carboxyhaemoglobin) and who:

have a partial pressure of oxygen in arterial blood (PaO2) below 7.3 kPa when stable or

have a PaO2 above 7.3 and below 8 kPa when stable, if they also have 1 or more of the following:

secondary polycythaemia

peripheral oedema

pulmonary hypertension

48
Q

Why is pulmonary rehab important in COPD?

A

Improves symptoms of fatigue and dyspnoea as well as exercise tolerance.

It’s a vicious cycle to more severe types of COPD if pulm rehab is not done.

49
Q

What can be given in alpha1-antitrypsin def?

A

Weekly or monthly infusion of alpa1-antitrypsin.

50
Q

Treatment of secondary polycythaemia in COPD.

A

Venesection if the PCV is >55%

51
Q

Treatment of sensation of dyspnoea in COPD.

A

Can be treated with short-acting sedation such as sublingual lorazepam or opiates. These might be a helpful palliative measure of intractable dyspnoea.

52
Q

How is air travel simulated in order to see if it is safe for a person with COPD?

A

Breathing 15% oxygen at sea level.

If saturation drops below 85% within 15 minutes the patient should be advised to contact their airline to request supplemental oxygen during their flight.

53
Q

Give examples of surgeries in COPD.

A

Surgical bullectomy

Single lung transplantation

Endobronchial valves

54
Q

Management algorithm in COPD

A
55
Q

Management of suspected acute exacerbation of COPD.

A

Investigations such as:

ABGs

CXR to exclude pneumothorax, and infection.

FBC, U&E, CRP

Theophylline levels if they are on it at home

ECG

Send sputum if it is purulent

Blood cultures if pyrexial

56
Q

Management of acute exacerbation of COPD.

A

Nebulised bronchodilators - salbutamol 5mg/4h and ipratropium 500mcg/6h (also do the CXR and ABGs)

Controlled O2 therapy if SaO2 <88% or PaO2 <7 kPa. Start at 24-28% aim sats at 88-92%. Adjust it according to ABGs.

Give steroids IV hydrocortisone 200mg and oral prednisolone 30mg od for 7-14 days.

Give antibiotics if there is evidence of infection. E.g. amoxicillin 500mg/8h or clarithromycin or doxycycline.

Physiotherapy to aid sputum expectoration.

If there is no response to nebulisers and steroids consider IV aminophylline.

If there is still no response…

Consider non-invasive positive pressure ventilation (NIPPV) if RR >30 or pH <7.35

Consider respiratory stimulant drug eg doxapram 1.5-4mg/min IV. This is used only if NIV is not available.

Consider intubation and ventilation if pH <7.26 and PaCO2 is rising despite NIV.

57
Q

When should NIV be used?

A

IF a patient has a persisten respiratory acidosis with a pH of <7.35

PaCO2 >6.5kPa

NIV reduces the need for intubation and lowers mortality.

58
Q

When should assisted ventilation with an endoctracheal tube be used?

A

If there is very severe respiratory failure.

Even then it is a difficult ethical problem due to the unlikelihood sometimes of reversibility.

59
Q

What predictive index is used in COPD?

A

BODE

60
Q

What does BODE involve?

A

BMI

Degree of airflow limitation

Dyspnoea

Exercise capacity

61
Q

What does a score of 0-2 on BODE mean for prognosis?

A

4 year mortality rate of 10%

62
Q

What does a score of 7-10 on BODE mean for prognosis of COPD?

A

80% 4 year mortality rate.

63
Q

Explain Pink puffers.

A

Increased alveolar ventilation and near normal PaO2 and normal or low PaCO2.

Breathless but not cyanosed.

64
Q

Explain blue bloaters.

A

Decreased alveolar ventilation

Low PaO2 and high PaCO2

Cyanosed but not breathless.

May go on to develop cor pulmonale.

Insensitive to CO2 and relay on hypoxic drive to maintain respiratory efforts.

This means that O2 should be given with care.

65
Q

Management of COPD according to FEV1.

A

SABA or SAMA

If FEV1 > 50% give LABA and LAMA

If FEV <50% give LABA + ICS and possibly LAMA

If all fails give all three regardless.

66
Q

Indications for specialist referral.

A

Uncertain diagnosis

Rapid decline in FEV1

Onset of cor pulmonale

Bullous lung disease

Assessment for oral corticosteroids, nebuliser therapy or LTOT

<10 pack years smkoing or COPD in patient <40y

Symptoms disproportionate to lung functions tests.

Frequent infections

67
Q

What does a CXR show in COPD?

A

Hyperinflation

Flattened hemidiaphragms

LArge central pulmonary arteries

Decreased peripheral vascular markings

Bullae

68
Q

What does a CT show in COPD?

A

Bronchial wall thickening

Scarring

Air space enlargement.

Y3M - Respiratory (21 decks)

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