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Respiratory 2 > COPD > Flashcards

COPD Flashcards

1
Q

COPD

A

Chronic obstructive pulmonary disease - characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible - preventable and treatable.

COPD is an umbrella term for emphysema and chronic bronchitis.

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2
Q

Emphysema

A

Damage or destruction of the alveoli resulting in alveolar enlargment.

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3
Q

How are the alveoli affected in emphysema?

A

The alveoli enlarge, and lose their elasticity.

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4
Q

What aspect of breathing people with emphysema have difficulty with?

A

Exhaling

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5
Q

What is the difference between emphysema and chronic bronchitis?

A

Chronic bronchitis has clinical features such as a productive cough where as emphysema is based on structural changes to the lung.

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6
Q

What is FEV1/FEV ratio is a sign of COPD?

A

0.7

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7
Q

How does smoking cause COPD?

A

When the alveoli is exposed chemical irritants in cigarettes it cause inflammation of the alveolar wall.
The inflammatory reaction attracts immune cells which release inflammatory mediators such as leukotrienes, IL and TNF and proteases such as ELASTASES and COLLAGENASES.

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8
Q

What is the significance of the elastases and collagenases being released?

A

The cause break down of the collagen and elastin in the alveolar wall. This causes the alveoli to lose their elasticity and collapse.

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9
Q

How does lose of elastin affect septa?

A

Septa are the thin alveolar walls, breakdown of the septa causes alveoli to merge to form much larger air spaces, this decreases the surface area available for gas exchange. Affecting Co2 and O2 levels.

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10
Q

Acinus

A

Endings of the lung airway where the clusters of alveoli are located.

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11
Q

Centriacinar emphysema affects where?

A

The proximal alveolar of the acinus - typically in the upper lobes of the lungs.

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12
Q

Panacinar emphysema affect where?

A

Where the entire acinus is affected, specifically in the lower half of the lungs

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13
Q

What genetic condition is panacinar emphysema often associated with?

A

Alpha 1 antitrypsin deficiency (A1AT deficiency)

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14
Q

What is alpha 1 antitrypsin?

A

A protease inhibitor of elastase

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15
Q

How does cigarette smoke affect AIAT?

A

Cigarette smoke decreases Alpha 1 antitrypsin activity.

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16
Q

Paraseptal emphysema affects where?

A

The distal alveoli of the acinus, classicly affects the periphery of the lobes of the lungs, near the interlobular septa.

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17
Q

What is the big clinical risk with paraseptal emphysema?

A

The lung wall can rupture leading to a pneumothorax.

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18
Q

What are the symptoms of emphysema?

A 
Dyspnea
Slow exhalation through pursed lips
Hypoxemia
Cough with small amount of sputum
Barrel shaped chest
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19
Q

Dyspnea

A

Shortness of breath

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20
Q

What blood pressure complication occurs as a result of emphysema?

A

Pulmonary hypertension

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21
Q

Cor pulmonale

A

Enlargement of the right side of the heart due to pulmonary hypertension, leads to right sided heart failure.

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22
Q

Treatment of COPD?

A

Reduce risk factors - stopping smoking
Supplemental oxygen
Medication: Bronchodilators, ICS, antibiotics

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23
Q

Overview of emphysema

A

Irritants in cigarette smoke lead to break down of elastin in alveolar walls. This leads to air trapping and poor gas exchange - which eventually leads to hypoxemia.

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24
Q

Chronic bronchitis

A

Inflammation of the bronchial tubes, said to be chronic because it results in a productive cough present for 3 months a year for 2 years.

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25
Q

What are the risk factors of chronic bronchitis?

A

Smoking
Air pollutants (S2 and NO2)
Family history
Exposure to dust and silica

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26
Q

What type of epithelium lines the airways?

A

Ciliated pseudostratified columnar epithelium.

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27
Q

How does smoking cause chronic bronchitis?

A

Smoke causes hypertrophy and hyperplasia of the mucinous glands of the main bronchi and the goblet cells in the bronchioles.
> this increases mucus production
Smoking also makes the cilia shorter and less mobile making it hard to move mucus out of the lungs.

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28
Q

Why is the increased production in bronchioles such a problem?

A

As the bronchioles are smaller, it is easy for an increase in mucus production to lead to airway obstruction.

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29
Q

How are chronic bronchitis and emphysema diagnosed differently?

A

Emphysema has a pathlogical diagnosis (CT scan).

Chronic bronchitis has a clinical diagnosis - history productive cough (3 months a year for 2 years).

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30
Q

Why do people with chronic bronchitis cough so much?

A

Due to the increased mucus production and decreased functioning of cilia, patients relying on coughing to get rid of their mucus plugs.

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31
Q

What are the symptoms of bronchitis?

A

Wheezing due to airway obstruction
Crackles
Hypoxemia
Hypercapnia

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32
Q

Activation of B2 receptors =

A

Bronchodilation by noradrenaline (sympathetic nervous system).

33
Q

Activation of muscarinic receptors =

A

Bronchoconstriction and mucus production by acetylcholine (parasympathetic nervous system).

34
Q

Hypercapnia

A

Increase CO2 concentration in the blood.

35
Q

Where are B2 receptors and muscarinic receptors located in the airway?

A

B2 distal airway (terminal bronchioles)

Muscarinic proximal main and lobar bronchi

36
Q

What causes the hypoxemia and hypercapnia in COPD?

A

There is increased partial pressure of CO2 in the alveoli and decreased partial pressure of oxygen. This makes it harder for CO2 to exit the blood and hard for oxygen to enter it.
> can lead to cyanosis

37
Q

What are some of the systemic manifestations of COPD?

A

Weight loss
Osteoporosis
Depression and fatigue

38
Q

How is a diagnosis of COPD made?

A

Taking a history

Spirometrty - FEV1/FEV ratio of less than 0.7

39
Q

Why are spirometry readings useful in COPD?

A

Aids diagnosis and evaluation of severity, therefore guiding treatment and prognosis.

40
Q

What are the treatments of advanced COPD?

A 
Pulmonary rehabilitation
Long term oxygen therapy
Non-invasive ventilation
Surgery
Palliation
41
Q

Use of azithromyocin

A

Azithromoycin is used clinically for its anti-inflammatory effects in patients with cystic fibrosis and in lung transplantation patients with chronic rejection. Azithromoycin reduced the frequency of exacerbations of COPD.

42
Q

What is the difference between type 1 and type 2 respiratory failure?

A

Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels. Type II respiratory failure involves low oxygen, with high carbon dioxide levels.

43
Q

NICE Guidelines on COPD Treatment:

A

Support stopping smoking.
Pneumococcal and influenza vaccines.
Pulmonary rehabilitation.

Offer above treatments first - then offer SABA and SAMA. Then progress to LABA and LAMA.

The progress to including ICS (inhaled corticosteroids).

44
Q

Pulmonary rehabilitation

A

Pulmonary rehabilitation is a supervised program that includes exercise training, health education, and breathing techniques for people who have certain lung conditions or lung problems due to other conditions.

45
Q

What NANC nerves in the lung do?

A

Non-noradrenergic, non-cholinergic transmitter (NANC), relaxes airway smooth muscle through release of NO and VIP.

46
Q

B2 receptors

A

Present in the bronchioles - acted upon by noradrenaline. Causes airway smooth muscle relaxation.

47
Q

How does salbutamol work?

A

B2 agonist causing airway smooth muscle relaxation.

48
Q

Ipratropium Bromide is what?

A

SAMA - short acting muscarinic antagonist.

- blocks all muscarinic receptors.

49
Q

Formeterol is what?

A

LABA

50
Q

Vilanterol is what?

A

LABA

51
Q

Why are corticosteroids use to treat asthma?

A

To reduce inflmaation in the lung - mainly used to reduce exacerbations of COPD.

52
Q

What are Budesonide and Fluticasone?

A

Inhaled corticosteroids used to treat asthma.

53
Q

Roflumilast

A

Used to treat severe COPD <0.5 with chronic bronchitis.

54
Q

Carbocysteine

A

Mucolytic

55
Q

Mechanism of Roflumilast:

A

Roflumilast (and its active metabolite, roflumilast N-oxide) increases cyclic adenosine-3′, 5′-monophosphate (cAMP) in lung cells by inhibiting PDE4. Increased cAMP activates PKA, which inactivates transcription factors involved in inflammation.

INHIBITS PDE4 INVOLVED IN INFLAMMATION.

56
Q

When should antibiotics be used in COPD?

A

During exacerbations especially if the person is systemically unwell.

57
Q

How is an exacerbation of COPD diagnosed?

A

Two of the following three features must be present:
• Increased breathlessness
• Increased sputum production
• Increased sputum purulence

58
Q

What is an exacerbation of COPD?

A

A sustained acute worsening of the person’s
symptoms from their usual stable state, which
goes beyond their normal day-to-day variations.

59
Q

In what cases would you prescribe antibiotics for COPD?

A

Clinical assessment – change in phlegm required: colour > volume and thickness.

60
Q

Corticosteroids used to improve patients feeling of wellness - does not have any affect on mortality.

A

Corticosteroids used to improve patients feeling of wellness - does not have any affect on mortality.

61
Q

What is the rationale behind giving oxygen to COPD patients?

A

To prevent Type 2 (hypercapnic) respiratory failure.

62
Q

What are the two different types of respiratory failure?

A

Type 1 Respiratory failure - gas exchange failure which is manifested by hypoxemia.
Type 2 Respiratory failure - Ventilatory failure manifested by hypercapnia.

63
Q

What is the most common mechanism that leads to type 2 respiratory failure?

A

Alveolar hypoventilation.

64
Q

Which form of ventilation is normally preferred?

A

Non-invasive ventilation.

65
Q

What are the goals of chronic COPD?

A
  1. Reduce symptoms and improve patients health status.
  2. Prevent disease progression.
  3. Prevent and treat exacerbations.
  4. Reduce mortality.
66
Q

List of non-pharmacological chronic COPD treatments:

A
  • Smoking cessation
  • Influenza and pneumococcal vaccination
  • Pulmonary rehabilitation
  • Consider lung volume reduction surgery
  • Consider lung transplantation
  • Self-management
  • Chronic ventilation
67
Q

List of pharmacological chronic COPD treatments:

A
  • Short acting bronchodilators
  • Long acting bronchodilators (LABA and LAMA)
  • Inhaled corticosteroids (ICS)
  • Theophylline and roflumilast (anti-inflammatories).
  • Low-dose antibiotics
  • Long term oxygen therapy and ambulatory oxygen
68
Q

What is the normal pharmacological treatment plan for chronic COPD?

A

SABA - reliever.

Long acting bronchodilator with inhaled steroids.

69
Q

Prescribing an ICS achieves what?

A

Reduces the occurence of COPD exacerbations. So if a person does not experience exacerbations ICS treatment will likely not benefit them.

70
Q

What is a huge problem in COPD treatment?

A

Not using inhaler properly.

71
Q

What is the current NICE guidance on antibiotic treatment for people with COPD?

A

Azithromycin (usually 250mg x3/week)

  • provided to people who have 4 or more acute exacerbations a year.
  • Not provided to smokers - low dose antibiotics provide no benefit to people who smoke.
72
Q

Pulmonary rehabilitation (self management) involves what?

A
  • Supervised exercise and education/disease management programme.
  • Effective if subject is symptomatic with breathlessness.
  • Typically conducted in the community or home
  • Evidence for all types of training – endurance, interval or strength.
  • Highly cost effective but very under-utilised
73
Q

Lung volume reduction procedures:

A

Lung volume reduction is a treatment for emphysema. It aims to reduce the amount of air trapped in the lungs.
Removes non-functioning lung tissue and enables remaining tissue to have better function.

74
Q

What are the systemic affects of COPD?

A 
There may be a lot of other complications to consider in a person with COPD such as:
Stroke
Anxiety / Depression
Osteoporosis
Anaemia
PVD
IHD
CCF (congestive cardiac failure)
Pulmonary HTN / Cor Pulmonale
Muscle deconditioning and myopathy (steroid)
Weight loss
75
Q

What can trigger acute exacerbations of COPD?

A

Bacteria
Viruses
Pollutants

All of which lead to inflammation in COPD airways = bronchoconstriction, mucus leading to further reduced FEV1 ratio and worsening symptoms.

76
Q

How is non-infective COPD managed?

A

Oxygen
Salbutamol neb
30mg Prednisolone

77
Q

What are the side effects of prednisolone?

A

Cushings
Immunosuppression
Affects sugar levels esp in diabetics

78
Q

What is the management of an infective exacerbation of COPD?

A 
Oxygen - salbutamol neb - prednisolone.
1st Line - Amoxicillin / clarithromycin / doxycycline
2nd Line - If in 2/3 days no improvement use a different class of antibiotic.

Respiratory 2 (22 decks)

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