COPD Flashcards

1
Q

Is Airway obstuxn reversible or irreversible in COPD?

A

Airway obstruction is not reversible or
incompletely reversible by bronchodilators

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2
Q

Features of COPD:

A
  1. Chronic inflammation
  2. Bronchitis
  3. Small airways fibrosis
  4. Emphysema
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3
Q

Chronic inflammation involves:

A
  • incr. numbers of macrophages, neutrophils and T lymphocytes
  • the inflammatory mediators have not been as clearly defined as in asthma
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4
Q

Bronchitis is:

A

 Attacks of winter morning cough
 Progresses to chronic cough with intermittent
exacerbations
 Often initiated by an upper respiratory
infection

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5
Q

Emphysema includes:

A

 Destruction of alveoli and elastin fibres in the lung
 May be caused by proteases released during the inflammatory response
 Causes respiratory failure (b/c it’s a progressive dx)
 Destruction of alveoli impairs gas transfer

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6
Q

What are the principal of tx?

A
  1. Smoking cessation: Slows the progress of COPD
  2. Immunizations : Superimposed infections are potentially lethal
  3. Current licensed txs: (prevent exacerbations-just symptomatic relief)
     Do not reduce the progression of COPD
     Do not suppress inflammation
     Do not prevent development of emphysema
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7
Q

BRONCHODILATORS do what?

A

Are the main tx.

Provide Symptomatic relief in patients with a reversible component

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8
Q

2 classes of drugs that bronchodilate

A

Short-acting drugs
- Short-acting anti-muscarinic antagonists (SAMA)
- Short-acting beta agonists (SABA)

Long-acting drugs
- Long-acting anti-muscarinic antagonists (LAMA)
- Long-acting beta agonists (LABA)

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9
Q

Short- acting drugs:

A

 Short-acting anti-muscarinic antagonists (SAMA):
Ipratropium (-ium)
 Short-acting beta agonists (SABA): salbutamol
(-ol)

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10
Q

Long-acting drugs

A

 Long-acting anti-muscarinic antagonists (LAMA) :
Tiotropium (-ium)
 Long-acting beta agonists (LABA): salmeterol or
formoterol (LABA)

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11
Q

β2-ADRENOCEPTOR AGONISTS
MoA

A

Dilate the bronchi by a direct action on the β2-
adrenoceptors of smooth muscle
• Independent of spasmogen

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12
Q

β2 -ADRENOCEPTOR AGONISTS
Effects

A

Inhibit mediator release from mast cells
Inhibit TNF-α release from monocytes
Increase mucus clearance by action on cilia

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13
Q

RoA of β2 adrenoceptor agonists

A

Given by inhalation ( to minimise any AE & maximise delivery)

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14
Q

Short-acting β2 Adrenergic Agonists (SABA)
Exs. + duration of axn

A

Salbutamol (albuterol), metaproterenol, terbutaline
 Duration of action is 3–5 h

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15
Q

Long-acting β2 Adrenergic Agonists (LABA)
Exs. + Duration of axn

A

 Salmeterol and formoterol
 Duration of action is 8–12 h

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16
Q

AE of β2 Adrenergic Agonists

A

 Commonest adverse effect is tremor  Other unwanted effects
 Tachycardia (caution for those with CV disease)
 Cardiac dysrhythmia (caution for those with CV
disease)
 Anxiety
 Headache

High doses
 Hypokalemia
 Lactic acidosis

17
Q

CI in β2 Adrenergic Agonists

A

Pt. W/ angina.
just use an anti muscarinic

18
Q

Clinical uses of SABAS + LABAS

A

Acute asthma: SABAs
• Chronic asthma: LABAs (in combination with ICS)
• COPD

19
Q

MUSCARINIC RECEPTOR ANTAGONISTS
Exs.

A
  1. Ipratropium (Short-Acting Muscarinic Antagonist-SAMA)
  2. Tiotropium (Long-Acting Muscarinic Antagonist-LAMA)
20
Q

‘Ipratropium
- RoA
- when does it work best
- duration of axn

A

 Inhalational
 Maximum effect: approximately 30 min after inhalation
 Persists for 3–5 h

21
Q

Tiotropium (Long-Acting Muscarinic Antagonist-LAMA)
- RoA
- Duration of axn

A
  • inhalational
  • longer-acting (t1/2 = 35 hours)
  • more potent than ipratropium
22
Q

AE of Anti-muscarinics:

A

Well- tolerated.
Dry mouth Dry eyes
Raised intraocular pressure and blurred vision
- !(CI: Caution in glaucoma)
Metallic taste (in mouth) Constipation
Tachycardia - ! CI: Caution in CV disease
Urinary retention - ! (CI: Caution)
Cough/hoarse voice

23
Q

Clinical uses of anti-muscarinics

A

• Acute severe asthma: SAMAs may
augment bronchodilation of SABAs
• Chronic asthma: LAMAs can be trialled
if control is insufficient despite moderate-
dose inhaled corticosteroid and LABA
treatment. [SO IF LABA+ICS it work= use LAMA]
• COPD

PS don’t use SAMA w/ LAMA

24
Q

PRINCIPLES OF TREATMENT: CORTICOSTEROIDS (CS)

A

-Inhaled CS (ICS) attempt to temper
inflammation in COPD
- Not as effective as in asthma
- Do not halt lung function deterioration
- Decrease frequency of exacerbations and
improve quality of life

25
Q

CORTICOSTEROIDS how are the used?

A

-Use of oral steroids in patients with stable
COPD is discouraged
- ‘’ ICS may be used
-Not used as monotherapy

26
Q

Alternatives for COPD

A
  1. Theophylline
  2. Long-term oxygen therapy
27
Q

Theophylline
- RoA
- MoA

A

 Uncertain benefit (therefore not preferred)
 Brochodilator
 Respiratory stimulant effect may be useful for
patients who tend to retain CO2

28
Q

Long-term oxygen therapy
MoA

A

 Administered at home
 Prolongs life in patients with severe disease and hypoxaemia

29
Q

ACUTE COPD EXACERBATIONS tx

A
  1. Inhaled O2
  2. Broad-spectrum antibiotics if there is
    evidence of infection
  3. Inhaled bronchodilators for symptomatic
    improvement
  4. Oral prednisolone