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3.24 > Lecture 7: The pharmacology of COPD > Flashcards

Lecture 7: The pharmacology of COPD Flashcards

1
Q

Is COPD reversible with bronchodilator treatment?

A

No

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2
Q

What mediates COPD?

A

Neutrophil and macrophages

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3
Q

What mediates COPD?

A

Neutrophil and macrophages

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4
Q

Compare asthma patients and COPD patients

A
  • Inflamed airways narrowed by asthma
  • Collapsed airways and damaged alveoli with COPD
  • Exposure to triggers cause asthma attacks, periodically inflaming the lungs
  • Long term exposure to damaging substances cause chronic inflammation of the lungs
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5
Q

What is the main goal of managing COPD?

A

Improving health status, reducing symptoms, preserving lung function decline, preventing exacerbations, and reducing mortality

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6
Q

What are the characteristics of stage 0 (at risk) COPD?

A
  • Chronic symptoms (cough, sputum)
  • Exposure to risk factors
  • Normal spirometry
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7
Q

What is the recommended treatment for mild COPD?

A

Short-acting bronchodilator when needed

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8
Q

What are the characteristics of mild COPD?

A
  • FEV1/FVC < 70%
  • FEV1 < 80% predicted
  • With or without symptoms
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9
Q

What is the recommended therapy for moderate COPD?

A
  • Regular treatment with one or more bronchodilators
  • Rehabilitation
  • Inhaled Glucocorticosteroids if significant symptoms and lung function response
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10
Q

What are the charactersitics of moderate COPD?

A

FEV1 40 - 59%

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11
Q

What are the recommdended treatments for severe COPD?

A
  • Regular treatment with one or more bronchodilators
  • Inhaled glucorticosteroids if significant symptoms and lung function response or if repeated exacerbations.
  • Treatment of complications
  • Rehabilitation
  • Long-term oxygen therapy if respiratory failure.
  • Consider surgical treatments.
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12
Q

What are the characeristics of severe COPD?

A

FEV1 < 40%

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13
Q

What is the hallmark symptom of COPD?

A

Dyspnoea

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14
Q

Why do patients expiernece dyspnoea?

A

Dynamic hyperinflation as a result of increased lung volume

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15
Q

What does improvement in inspiratory capacity lead to?

A

reduced dyspnoea and improved exercise tolerance

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16
Q

How do beta 2 agonists act?

A

By binding to the β2AR

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17
Q

What are short acting beta 2 adrenoreceptor agonists?

A
  • Salbutamol
  • Piralbuterol
  • Levalbuterol
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18
Q

What are long acting beta 2 adrenoreceptor agonists?

A
  • Salmeterol
  • Formeterol
  • Arformeterol
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19
Q

Where are B2AR present?

A
  • vascular endothelium
  • ciliated cells
  • circulating inflammatory cells (such as eosinophils)
  • sub-mucosal glands.
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20
Q

What are the non bronchodilator effects of Beta 2 adrenoreceptor agonists?

A
  • attenuation of mast cell mediator release
  • reduction of plasma exudation
  • reduced activation of sensory nerves
  • enhancement of mucociliary transport
  • attenuation of neutrophil recruitment
  • inhibition of smooth muscle cell proliferation.
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21
Q

What is salbutamol used for in COPD?

A

Both in acute and chronic management of COPD

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22
Q

What is the onset of action of salbutamol?

A

3 minutes

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23
Q

When does salbutamol activity in COPD patinets peak?

A

After 2.5 hours

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24
Q

What is the duration of action of salbutamol?

A

4-6 hours

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25
What was the result of SABA after seven days?
- improved post bronchodilator lung function in patients with moderate to severe COPD. - Patients were also less dyspnoeic and more likely to comply with treatment.
26
What is an option for patients that are symptomatic despite regular SABA use?
Salmeterol and formoterol
27
Are Salmeterol and formoterol lipophilic or hydrophilic?
Lipophilic
28
Why is salmeterols onset of action slightly longer than formoterol?
Due to lipophilic properties that allow them to remain in the airway tissues in close vicinity to β2AR
29
What does the relative water solubility of formoterol allow it to do?
Enables it to diffuse rapidly to the β2AR and cause bronchodilation in between 1 to 3 minutes
30
What is the effect of long acting beta 2 agonists?
Effective over the medium and long term for patients with moderate to severe COPD with improved quality of life and reduced exacerbations, but did not significantly reduce mortality or serious adverse events.
31
What are the side effects of beta 2 adrenoreceptor agonists?
- Tachycardia, tremor (flight or flight!) - Hypokalemia (low potassium, stimulates the Na/K-pump) - Transiently decreases PO2 as they may increase perfusion to poorly ventilated areas supplemental oxygen helpful - LABAs not problematic in COPD (in contrast to Asthma- black box warning)
32
What does para sympathetic activity mediate?
- bronchial smooth muscle contraction - the release of mucus into the airway lumen through stimulation of muscarinic receptors
33
Where are M1 receptors found?
peribronchial ganglia
34
Where are M3 receptors found?
bronchial smooth muscle cells
35
Where are M2 receptors found?
post ganglionic para-sympathetic nerve
36
What do M2 receptors act as?
Auto receptors
37
What does agonist stimulation of M2 receptors result in?
Inhibition of further acetylecholine release. optimal inhibition achieved by selectively blocking M1 and M3 receptors
38
Name a short acting muscarinic antagonist
Ipratropium bromide
39
What does Ipratropium bromide do?
Blocks all muscarinic receptors without sub-type selectivity.
40
What is the onset of action of ipratropium bromide?
Minutes
41
When does Ipratropium bromide peak activity occur?
Between 1 and 2 hours
42
What is Ipratropium bromide duration of action?
Approximately 4 hours in the majority of patients
43
Name a long acting muscarinic antagonist
Tiotropium
44
What does tiotropium bind to?
M1, M3 receptors
45
What is the potency of tiotropium compared to ipatropium bromide
tiotropium is 10 times more potent
46
How does tiotropium have a long lasting effect?
Dissociates slowly from M1 and M3 receptors
47
How does tiotropium have kinetic activity?
Dissociates relatively rapidly from the M2 receptor
48
When does the onset of bronchodilation occur with tiotropium?
Within 30 minutes
49
When does tiotropium have its peak activity?
At 3 hours, sustained over more than 24 hours
50
What is the conclusion of tiiotropium?
Effects were superior to LABAs in terms of preventing exacerbations and disease related hospitalization.
51
What is a suitable drug fro patients with severe glaucoma?
LABA
52
What are the adverse effects of LAMAs?
largely those attributed to its anti-cholinergic activity - dry mouth - exacerbation of narrow angle glaucoma and myasthenia gravis (autoimmune neuromuscular disease-muscle weakness)
53
What did the cochrane review confirm about soft mist inhalers (respimat)?
- increased mortality risk associated with the soft mist inhaler (Respimat). - The Respimat device results in greater deposition in the lung than the Handihaler.
54
How are Ipratropium and tiotropium transported throughthe bronchial epithelium?
Actively transported using the OCTN2 transporter
55
Where are OCTN2 transporter present?
In the human heart
56
What is the inflammation in COPD dominated by?
Dominated by neautrophillic infiltration with an increased numbers of macrophages and CD8 T lymphocytes
57
Name inhaled corticosteroids
- Budesonide - Triamcinolone - Fluticasone - Mometasone - Flunisolide - Beclometasone - Ciclesonide
58
What is the effect of LABA/ICS combinations?
improve lung function and to reduce exacerbations in severe and very severe disease.
59
How do combination of ICS plus LABA act?
Synergistically
60
What does ICS regulate?
Regulate the coupling of β receptors to G proteins and enhancing cAMP activation
61
What does chronic LABA or SABA exposure lead to?
Reduced β receptor expression, as they are internalized and degraded
62
How is reduced β receptor expression reversed?
ICS reverse this effect through increased gene transcription and synthesis of these receptors
63
What is the mechanism of action of theophylline?
- Adenosine receptor antagonist/PDE inhibitor – airways bronchodilation - Inhibition of PDE4 on inflammatory cells, reduces cytokine and chemokine release - Enhancement of histone deacetylation, decreased inflammatory cell gene transcription
64
What are the symptoms of theophylline toxicity?
- anorexia - abdominal discomfort - anxiety - More severe toxicity: seizures and arrhythmias
65
What does oxygen administration reduce?
- reduces hematocrit, pulmonary artery pressures, dyspnea, and rapid eye movement related hypoxemia (low oxygen in blood) during sleep
66
What does comprehensive pulmonary rehabilitation program include?
exercise training, nutrition counseling, and education.
67
What is the best way to delay progression of COPD at all stages of the disease
Smoking cessation
68
What ar acute exacerbations of COPD defined by?
Increased cough, dyspnea, or increased sputum purulence from baseline
69
What are Common Causes of Acute Exacerbations of COPD?
- Tracheobronchial infection, Pneumonia (use of antibiotic to eliminate) - Air pollution - Pulmonary embolism (blood clots in pulmonary vessels) - Rib fractures/chest trauma, Pneumothorax (free air in pleural chest cavity-lung collapse) - Inappropriate use of sedatives, narcotics, beta-blocking agents - Right and/or left heart failure or arrhythmias
70
What patients are protease inhibitors helpful in?
Patients with emphysema caused by alpha 1 anti-trypsin deficiency- only small trials with moderate benefits
71
What are the side effects of protease inhibitors?
Anaphylaxis and low grade fever (especially in patients with IgA deficiency)
72
What is elastin?
Specific protease inhibitors
73
What are the functions of TNF-α?
- amplifies the inflammatory response, resulting in activation of epithelial cells, monocytes, macrophages, and neutrophils - induce emphysema through the release of proteinases, including NE and MMP-9, - stimulate mucus secretion, - induce apoptosis of skeletal muscle cells.
74
What is rofluminast?
Anti-inflammatory treatment i.e. phosphodiesterase (PDE) type 4 inhibitors

3.24 (28 decks)

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