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Respiratory > COPD - Full summary > Flashcards

COPD - Full summary Flashcards

1
Q

What does COPD stand for?

A

Chronic Obstructive Pulmonary Disease

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2
Q

How is COPD characterised?

A

By inflammation of the airways (Chronic bronchitis) and destruction of the alveolar wall with dilation of the airspace (Emphysema)

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3
Q

What is the common age range for COPD diagnosis?

A

Between the ages of 40 and 60

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4
Q

How is chronic bronchitis defined?

A

Having a productive cough for >3 months each year for ≥2 years
It is caused by an inflammatory process, leading to increased mucus production

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5
Q

How does emphysema occur in COPD?

A

The body usually contains a balance of elastases that breaks down elastin in the alveolar wall, and anti-elastases which inhibit it

In emphysema, an inflammatory response favours the action of elastases due to an increase in neutrophil elastases, leading to increased destruction of the elastin in alveolar walls

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6
Q

What is emphysema?

A

Breakdown of the alveolar wall causing a decrease in elastic recoil of the lungs, meaning the airways can collapse upon expiration, therefore trapping air in the alveoli. This also destroys the diffusion surface, leading to hypoxaemia and CO2 retention

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7
Q

What are some clinical features of emphysema?

A

Reduced breath sounds on auscultation
Reduced diffusing capacity of the lungs for carbon monoxide (DLCO)
Black holes on chest X-rays or high resolution CT (HRCT)

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8
Q

What are the most common causes of COPD?

A

Inhalation of tobacco smoke, cannabis smoke or occupational pollutants such as dust or silica

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9
Q

What could be a common cause of COPD in someone under 45?

A

An alpha-1 anti-trypsin deficiency

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10
Q

Is alpha-1 anti-trypsin deficiency an autosomal dominant or recessive condition?

A

Autosomal dominant

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11
Q

What occurs in alpha-1 anti-trypsin deficiency, causing COPD?

A

A1AT is synthesised by the liver and inhibitors the action of neutrophil elastase
In A1AT deficiency, the protein isn’t exported out of the liver, and so is deficiency in the lungs
This allows the accumulation of elastases in the lungs, therefore damaging lung walls
Accumulation of the protein in the liver can also cause liver cirrhosis

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12
Q

What are the main symptoms of COPD?

A

Exertion shortness of breath (dyspnoea)
Chronic productive cough

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13
Q

What are some less common signs and symptoms of COPD?

A

Wheezing
Chest tightness
Sitting up, pursed lips breathing
Active expiration
Increased AP chest diameter
Hyper-ressonance upon percussion
Expiratory wheeze upon auscultation
Cyanosis
Cor pulmonale

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14
Q

How is dyspnoea classified?

A
  • mMRC grade 0 - Only breathless with strenuous exercise
  • mMRC grade 1 - Short of breath when hurrying or walking up a slight hill
  • mMRC grade 2 - I walk slower than people of the same age and have to stop for breath when walking my own pace
  • mMRC grade 3 - I stop for breath after walking about 100m or after a few minutes of waling
  • mMRC grade 4 - I am too breathless to leave the house or i am breathless when dressing or undressing
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15
Q

What are some red flag signs that should be taken for X-ray?

A
  • Haemoptysis
  • Unexplained persistent cough for more than 3 weeks
  • Change in cough
  • Dypnoea
  • Chest/shoulder pain
  • Weight loss
  • Chest signs
  • Hoarseness
  • New finger clubbing
  • Fatigue in a smoker aged over 50
  • Cervical and/or persistent supraclavicular lymphadenopathy
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16
Q

What is cor pulmonale?

A

Right sided heart failure caused by pulmonary hypertension

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17
Q

How does cor pulmonale occur?

A

Chronic hypoxaemia causes vasoconstriction of the pulmonary vessels, as low levels of O2 leads to vasoconstriction
This vasoconstriction increases pulmonary blood pressure, leading to pulmonary hypertension
This increases after load of the right side of the heart, leading eventually to right sided heart failure

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18
Q

How does cor pulmonale present?

A

Jugular venous distension
Peripheral oedema
Hepatomegaly due to congestion

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19
Q

What is the main diagnostic tool for COPD?

A

Pulmonary Function Testing (PFT)

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20
Q

What is meant by FVC?

A

Forced vital capacity - the maximum amount of air that a person can breath out after a maximum inspiration

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21
Q

What is meant by FEV1?

A

Forced Expiratory Volume in 1 second - The maximum amount of air a person can breath out in the 1st second of FVC

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22
Q

What is meant by FER?

A

Forced Expiratory Ratio

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23
Q

How is the FER calculated?

A

(FEV1÷FVC) x 100

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24
Q

How is FVC, FEV1 and FER affected in COPD?

A

Both FVC and FEV1 are decreased, however, FEV1 is decreased by more, so FER decreases below around 70%

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25
Q

What is meant by reversibility testing?

A

A SABA is given to someone with a decreased FEV1 and FER
The test is then performed again
Reversibility is defined as >12% increase in FEV1 after a bronchodilator is given
COPD is non-reversible, Asthma is reversible

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26
Q

When would someone be screened for an alpha-1 anti-trypsin deficiency?

A

If they have suspected COPD and are <45 years old, have no risk factors of COPD such as smoking, have a family history of COPD or have unexplained liver disease

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27
Q

How would the diagnosis of COPD be confirmed in a secondary care setting?

A

Re-taking a thorough history
CT scanning
Echocardiography
Sputum cultures

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28
Q

What is included in COPD management?

A

Long term treatment and symptom management

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29
Q

What are some examples of long term management strategies for COPD?

A

Smoking cessation
Vaccinations
Oxygen therapy

30
Q

What are some pharmacological methods of smoking cessation?

A

Varenicline - Partial nACh agonist
NRTs - Patches, gum, sprays
Electronic cigarettes or vaporisers

31
Q

What are some important vaccinations in the management of COPD?

A

Annual influenza vaccine
23-valent pneumococcal polysaccharide vaccine (PPSV-23)

32
Q

When is oxygen therapy beneficial in COPD?

A

It is beneficial for those with an oxygen saturation below 88% (90% in right heart failure) or a PaO2 <55mmHg (60mmHg in right heart failure)

33
Q

What is the target oxygen saturation during oxygen therapy?

A

88-92%

34
Q

Why is the target for oxygen saturation not 100% in oxygen therapy?

A

In COPD, hypoxaemia is stimulating a respiratory drive, and so is keeping the person breathing to allow for the removal of CO2
This is caused by VQ mismatching

35
Q

How is COPD severity classified?

A

Using the GOLD classification:
GOLD 1 - Mild - FEV1 ≥80% predicted
GOLD 2 - Moderate - FEV 50-80% predicted
GOLD 3 - Severe - FEV1 30-50% predicted
GOLD 4 - Very severe - FEV <30% predicted

36
Q

When would someone with COPD be screened for an Alpha-1 Anti-Trypsin Deficiency?

A

If they were under 45, with no risk factors for COPD (e.g. smoking), had a family history of COPD or had unexplained liver disease

37
Q

How would a COPD diagnosis be confirmed in secondary care?

A

Re-taking of a thorough history
CT scanning
Echocardiography
Sputum cultures

38
Q

What are some long term management options for COPD?

A

Smoking cessation
Vaccinations
Oxygen

39
Q

What are some medicinal methods of smoking cessation?

A

Varenicline (Champix) - Partial nACh agonist (Most effective)
NRT - Patches, Gum, Sprays
Electronic cigarettes or vaporisers

40
Q

Which vaccinations is it important to keep up with in COPD?

A

Yearly influenza vaccine
23-valent pneumococcal polysaccharide vaccine (PPSV-23)

41
Q

Who should receive long term oxygen therapy?

A

Those with an oxygen saturation below 88% (90% in right sided heart failure) or a PaO2 <55mmHg (60mmHg in right sided heart failure)

42
Q

For how long is long term oxygen therapy carried out?

A

15 hours per day, meaning it can be harmful to some patients due to being housebound and static

43
Q

What is the aim oxygen saturation in those on long term oxygen therapy?

A

88-92%, as the hypoxaemia is stimulating a respiratory drive and so is keeping the person breathing to allow the removal of excess CO2

44
Q

What are the GOLD guidelines for COPD management based on mMRC and exacerbations?

A
45
Q

What occurs when ß-agonists bind to ß-receptors in the bronchial smooth wall?

A

Binding of ß-agonist activates the protein Gs
This activates adenylyl cyclase
This converts AMP to cAMP
cAMP activates Protein Kinase A (PKA)
This phosphorylates and activates myosin phosphatase, therefore facilitating smooth muscle relaxation
PKA also phosphorylates and inhibits myosin light chain kinase, therefore inhibiting contraction

46
Q

What is the function of phosphodiesterase in smooth muscle?

A

It breaks down cAMP into AMP, therefore preventing smooth muscle relaxation

47
Q

How do Methylxanthines and roflumilast work?

A

Methylxanthines are naturally occurring molecules, found in coffee, tea and chocolate containing beverages. They are all phosphodiesterase-4 (PDE4) inhibitors, so prevent the breakdown of cAMP

48
Q

What are some side effects of methylxanthines?

A

Nausea
Vomitting
Abdominal discomfort
Headaches
Dysarrhythmia
Seizures
Hypotension

49
Q

What are some examples of Short Acting ß-Agonists (SABAs)?

A

Salbutamol
Terbutaline

50
Q

What are some examples of Long Acting ß-Agonists (LABAs)?

A

Formoterol
Salmaterol

51
Q

What are some side effects of ß-agonists?

A

Fine tremor
Tachycardia
Cardiac dysarrhythmia
Hypokalaemia

52
Q

What happens when acetylcholine binds to M3 receptors in bronchial smooth muscle?

A

Binding activates Gq/11 protein
This activates phospholipase 3
This converts PIP2 (Phosphatidylinositol (4,5) biphosphate) into IP3 (Inositol (1,4,5) triphosphate)
IP3 activates IP3 receptors, which allows calcium release from the sarcoplasmic reticulum
Calcium movement into the cell wall via voltage gated Ca2+ channels also causes Ca2+ release by binding to Ryanodine receptors
Calcium then binds to calmodulin
This activates Myosin Light Chain Kinase (MLCK)
This phosphorylates myosin, causing contraction

53
Q

What is the effect of M1 ACh receptor stimulation?

A

It mediates fast neurotransmission by acetylcholine

54
Q

What is the effect of M2 ACh receptor stimulation?

A

It acts as an inhibitor auto receptor, which reduces acetylcholine levels

55
Q

Why should muscarinic antagonists be selective to M3 only?

A

If M3 is blocked, it will cause the desired effect of muscle relaxation
However, if M2 is also blocked, this increases the release of acetylcholine, which will cause smooth muscle constriction

56
Q

What is an example of a Short Acting Muscarinic Antagonist (SAMA)?

A

Ipratropium

57
Q

What are some examples of Long Acting Muscarinic Antagonists (LAMA)?

A

Tiotropium
Glycopyrronium
Aclidinium
Umeclidinium

58
Q

From which substance are all Muscarinic Antagonists derived?

A

Atropine - From Atropa belladonna (Deadly nightshade)

59
Q

What are some surgical management options for COPD?

A

Bullectomy
Lung volume reduction surgery
Endobrachial valves and coils
Lung transplant

60
Q

What is involved in a bullectomy?

A

The removal of bullae in the lungs, allowing the healthy lung around it to expand and receive more of the air, therefore decreasing the VQ mismatch of the lungs
This is carried out in patients with a bullae exceeding 50% of the volume of the thoracic cavity

61
Q

What is a bullae?

A

A large blister-like mass of alveolar wall breakdown, forming one large alveolus

62
Q

Where does cannabis smoking usually cause bullae formation?

A

Cannabis smoking is known to cause biapical bullae formation

63
Q

What is involved in lung volume reduction surgery?

A

Removal of sections of the lung that contain poor VQ mismatching due to emphysema, but they’re separated, so a bullae hasn’t formed. This allows airflow into areas of good VQ matching

64
Q

How do endobrachial valves work?

A

They are 1-way valves that are inserted into the bronchi of peripheral regions of VQ mismatching, thus preventing airflow into them, and allowing more air to reach the healthy sections of lung

65
Q

How do endobrachial coils work?

A

These are coils that are inserted into a central area of poor VQ matching, that drag in peripheral healthy lung, to bypass the central poorly perfused lung

66
Q

What is the only surgical option for those with pulmonary hypertension?

A

Lung transplant

67
Q

What is meant by a COPD exacerbation?

A

An acute worsening of respiration symptoms that result in additional therapy

68
Q

What are some common symptoms of a COPD exacerbation?

A

Increased shortness of breath
Worsening cough
Increased sputum volume
Production of purulent sputum

69
Q

What are some examples of causes of COPD exacerbation?

A

Respiratory tract infection
Heart failure
Pneumothorax
Pleural effusion
Pulmonary embolism
Pulmonary oedema
Cardiac arrhythmia
Medication such as ß-Blockers

70
Q

What are some tests that can show a COPD exacerbation?

A

Pulse oximetry
Chest X-ray
Arterial blood gas to show worsening hypercapnia

71
Q

How is an exacerbation of COPD usually treated?

A

Increased SABA dosage
Oral steroids for 5 days to improve lung function and oxygenation
Antibiotics if required
Possible supplemental oxygen via nasal cannula or venturi mask

72
Q

Why are Inhaled CorticoSteroids only used in those with very severe COPD?

A

They greatly increase the risk of pneumonia in COPD patients, so only in very severe COPD does the reward outweigh the risk of use

Respiratory (23 decks)

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