Management of COPD Flashcards

1
Q

What causes COPD & which part of the lungs is mainly effected?

A

It is caused by exposure to noxious gases/particles.

It mainly affects the peripheral airways & lung parenchyma.

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2
Q

What part of the respiratory tract is more prone to colonisation of bacteria in COPD patients?

A

The lower respiratory tract (LRT).

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3
Q

CD8 lymphocytes, neutrophils, oxidants & proteases can lead to what 3 things in COPD?

A
  1. Increased mucus
  2. Abnormal tissue repair
  3. Alveolar wall destruction
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4
Q

What are the symptoms of COPD?

A
  1. Chronic cough
  2. Breathlessness
  3. Arterial hypoxemia
  4. Pulmonary hypertension
  5. Systemic effects
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5
Q

What is the FEV1/FVC ratio of a COPD patient using a spirometer?

A

FEV1/FVC <0.7

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6
Q

What does the mMRC dyspnoea scale measure?

A

It is a questionnare used to measure breathlessness in patients.
Ranges from grade I (normal) - grade V(severe)

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7
Q

What are some non-pharmacological treatments of COPD?

A
  1. Smoking cessation
  2. Vaccinations
  3. Pulmonary rehabilitation
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8
Q

What are some examples of B2 agonists and what is their duration of action?

A

SABA: salbutamol, terbutaline
- 3-5h duration

LABA: salmeterol, formoterol
- 8-12h duration

Ultra LABA: vilanterol, indacaterol
- 24h

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9
Q

What are the side effects of using B2 agonists?

A
  1. Tremor
  2. Headaches
  3. Tachycardia
  4. Hypokalaemia
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10
Q

What is the mechanism of action of B2 agonists?

A
  1. B2 agonist binds & forms structural changes
  2. Alpha subunit of receptor dissociates & allows cAMP levels to increase
  3. cAMP binds to PKA, causing bronchodilation
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11
Q

What can chronic use of B2 agonists lead to?

A

Desensitisation of the receptors & a higher tolerance in patients.
This can also decrease cAMP levels.

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12
Q

What are some examples of musarinic agonists?

A

SAMA: ipratropium
- <15min onset

LAMA: tiotropium
- Selective for M3 receptors

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13
Q

What is the mechanism of action of xanthines?

A

E.G. aminophylline, theophylline

  • They decrease cytokines/apoptosis/neutrophils = reducing inflammation
  • Bronchodilation is hence enhanced.
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14
Q

How is theophylline given & how is it eliminated?

A

It is given IV, and it eliminated via CYP450.
It also has a narrow therapeutic index.
Side effects can include: vomiting, hypokalaemia, insomnia, nervousness.

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15
Q

What is the mechanism of action of theophylline?

A

It inhibits phosphodiester enzymes, so CAMP levels are increased (+ cGMP)
This leads to bronchodilation & also antagonise adenosine receptors.
It can also cause seizures.

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16
Q

What is the mechanism of action of oral phosphodiesterase 4 inhibitors (PDE4)?

A

E.G. Roflumilast

  • They inhibit cAMP hydrolysis into AMP
  • cAMP increases = bronchodilation
17
Q

Why arent ICS’s used in COPD patients?

A

They have a limited response in COPD patients.

It can also cause pneumonia for them.

18
Q

What do mucolytics do?

A

E.G. carbocisteine, acetylcysteine

- They loosen sputum making it easier to cough out

19
Q

What antibiotic can be used to optimise therapy for COPD & for those who are having acute exacerbations?

A

Azithromycin 250mg TDS for a week.

20
Q

What are the 3 types of oxygen therapies?

A
  1. LTOT - long term O2 therapy
    - Used at home for chronic hypoxia
    - Patient would have O2 levels <92%
  2. Ambulatory O2
    - Used for patients who are active
    - Portable O2 cylinders used
  3. SBOT - short burst O2 therapy
21
Q

What can you do to manage exacerbations?

A
  1. Increase the dose of their bronchodilator

2. Give antibiotic or oral corticosteroid, e.g. prednisolone 30mg (for symptom relief)

22
Q

What can be given during in hospital treatment?

A
  1. IV aminophylline
  2. Doxapram
  3. Invasive ventilation