17. Respiratory pharmacology Flashcards

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1
Q

what is asthma?

A

Chronic inflammatory airway disease
intermittent airway obstruction and hyper-reactivity small airways
reversible both spontaneously and with drugs
a heterogeneous disease

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2
Q

What are the 3 cardinal features of asthma?

A
  • Reversible airflow obstruction,
  • airway hyperresponsiveness,
  • and airway inflammation
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3
Q

aims of asthma control?

A
  • Minimal symptoms during the day and night
  • Minimal need for reliever medication
  • No exacerbations
  • No limitation of physical activity
  • Normal lung function (FEV1 and/or PEF >80% predicted or best)
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4
Q

What should you check before stepping up/down?

A
  • Adherence
  • Inhaler technique
  • Eliminate trigger factors
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5
Q

what are the steps in asthma management?

A
  1. low dose ICS + SABA
  2. add inhaled LABA
  3. consider increasing ICS to medium dose or adding LTRA, if no response to LABA consider stopping it
  4. refer to specialist care
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6
Q

Give examples of inhaled corticosteroids?

A
  • beclometasone
  • budesonide
  • fluticasone
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7
Q

How do ICS work?

A

Pass through plasma membrane, activate cytoplasmic receptors, activated receptor then passes in to nucleus to modify transcription

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8
Q

What are the effects of ICS?

A
  • Reduces mucosal inflammation, widens airways, reduces mucus
  • Reduces symptoms, exacerbations and prevents death
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9
Q

What genes are activated/repressed by ICS?

A

Activation: ↑β2 receptors, Anti-inflammatory mediators, also inhibit release of arachidonic acid

Repression: Inflammatory mediators: interleukins, chemokines, cytokines

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10
Q

What are the adverse effects of ICS?

A

• Can cause a local immunosuppressive action - candidiasis, horse voice

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11
Q

warnings, contraindications of ICS?

A

Pneumonia risk possible in COPD at high doses

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12
Q

DDIs of ICS?

A

very few if taken correctly

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13
Q

What is the purpose of the lipophilic side chains added to ICS?

A

slow dissolution in aqueous bronchial fluid - difficult to enter systemic circulation
high affinity for glucocorticoid receptor

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14
Q

Is there an issue of ICS are absorbed orally?

A

No:
• Poor oral bioavailability
• if absorbed: Transported from stomach to liver by hepatic portal system
• Almost complete first pass metabolism

High doses have potential to cause systemic side effects

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15
Q

Give examples of SABA.

A

Salbutamol, Terbutaline (both fast acting)

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16
Q

Give examples of LABA.

A
  • formoterol (fast acting - 12hrs)

- salmerterol (slow acting - 12hrs)

17
Q

What are the effects of β2 agonists?

A
  • bronchodilation

- also increase mucus clearance by action of cilia

18
Q

compare how SABA and LABA are prescribed?

A
  • SABA - Only to be used p.r.n (as required)

* LABA – Add on therapy to ICS and p.r.n SABA

19
Q

What are the adverse effects of β2 agonist?

A
  • Adrenergic - fight or flight effects Tachycardia, palpitations, anxiety and tremor
  • ↑Glycogenolysis (liver)
  • ↑renin (kidney)
  • SVT – (↑SAN activity → ↑HR, ↓refractory period at AVN)
20
Q

warnings, contraindications of B2 agonists?

A

CVD – tachycardia may provoke angina

21
Q

When should LABA be added?

A

When not controlled on ICS

22
Q

Can LABA be given without ICS, why?

A

No, never given alone
- alone can mask airway inflammation and near-fatal and fatal attacks

LABA should only be prescribed alongside ICS

23
Q

What is the rationale for combined inhaler?

A
  • Ease of use
  • Adherence
  • less prescriptions - administration, cost?
  • SAFETY - LABA comes with ICS
24
Q

DDIs of B2 agonist?

A

β-blockers may reduce effects of β2 agonists!

25
Q

Give an example of a leukotrine receptor antagonist.

A

montelukast (oral)

26
Q

How do leukotrienes cause symptoms in asthma?

A
  • LTC4 released by mast-cells/eosinophils
  • ↑bronchoconstriction, ↑mucus, ↑oedema
  • through CysLT1 receptor - GPCR
27
Q

How do LTRA work?

A

LTRA block CysLT1

- Useful in ~ 15% asthmatics most end up taking LABA

28
Q

WHat are some ADRs of LTRA?

A

Headache, GI disturbance, dry mouth, hyperactivity