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ESA 5 - Pharmacology > Pharmacology of Airway Control > Flashcards

Pharmacology of Airway Control Flashcards

1
Q

Describe the pathophysiology of asthma

A

Th2-driven and eosinophilic inflammation leads to;

  • Mucosal oedema
  • Bronchoconstriction
  • Mucus plugging
  • Airway remodelling
  • Smooth muscle dysfunction
  • Bronchial hyperresponsiveness (airway remodelling also contributes to this)
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2
Q

What airway remodelling occurs in asthma?

A
  • Mucous gland hyperplasia
  • Subepithelial fibrosis
  • Epithelium desquamation
  • Airway wall thickening
  • Increased smooth muscle mass
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3
Q

In what ways is smooth muscle dysfunction in asthma?

A
  • Increased contraction and mass
  • Increased cytokines and chemokines
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4
Q

What part of the asthma pathophysiology do ß2 antagonists act on?

A

The smooth muscle dysfunction

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5
Q

What part of the asthma pathophysiology do steroids act on?

A

Inflammation

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6
Q

In what respects is asthma a heterogenous disease?

A
  • Pathologically
  • Symptom pattern and triggers of exacerbations
  • Response to treatment
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7
Q

What is meant by ‘good’ asthma control?

A
  • Minimal symptoms during day and night
  • Minimal need for reliever medication
  • No exacerbations
  • No limitation of physical activity
  • Normal lung function
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8
Q

What constitutes normal lung function in asthma?

A

FEV1 and/or PEF >80% predicted

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9
Q

What should be aimed for regarding asthma control?

A

Early control, with stepping up or down as required

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10
Q

What should be considered before initiating a new drug therapy for asthma?

A
  • Check compliance with existing therapies
  • Check inhaler technique
  • Eliminate trigger factors
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11
Q

What are the steps in asthma management?

A
  1. Short acting ß2 agonists as required
  2. Regular preventer
  3. a. Initial add on therapies - b. Additional add on therapies
  4. High dose therapies
  5. Continuous or frequent use of oral steroids
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12
Q

When should moving up a step on asthma management be considered?

A

If using three doses a week or more

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13
Q

Give two examples of short acting ß-agonists

A
  • Salbutamol
  • Terbutaline
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14
Q

How do short-acting ß2 agonists reduce the symptoms of asthma?

A

Through reversal of bronchoconstriction

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15
Q

When might short acting ß2-agonists be used preventatively?

A

On exercise

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16
Q

On what basis should short acting ß2-agonists be used?

A

Only on an as-required basis

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17
Q

What happens if short-acting ß2-agonists are used regularly?

A

They reduce asthma control

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18
Q

What is the mechanism of action of short acting ß2 agonists?

A
  • Predominant action is on airway smooth muscle, preventing contracting
  • Potentially inhibit mast cell degranulation if only used intermittently
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19
Q

How does regular use of ß2 agonists reduce asthma control?

A

Causes mast cell degranulation in response to allergens to increase

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20
Q

What are the classes of inhaled ß2 agonists?

A
  • Fast onset, short action
  • Fast onset, long action
  • Slow onset, long action
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21
Q

Give two examples of fast onset, short action ß2 agonists

A
  • Terbutaline
  • Salbutamol
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22
Q

What are fast onset, short duration ß2 agonists used for?

A

Reliever medication

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23
Q

Give three examples of fast onset, long duration ß2 agonists

A
  • Formoterol (12 hours)
  • Olodaterol (24 hours)
  • Indacaterol (24 hours)
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24
Q

Give two examples of slow onset, long duration ß2 agonists

A
  • Salmetarol (12 hours)
  • Vilanterol (24 hours)
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25
Q

What are the side effects of ß2 agonists?

A

Adrenergic activity, including tachycardia, palpitations, tremor

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26
Q

What kind of drugs are used in regular preventer therapy in step 2 of asthma management?

A

Inhaled corticosteroids

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27
Q

When should a regular preventer therapy be started in asthma?

A
  • Using ß2 agonists 3 or more times a week
  • Symptoms 3 or more times a week
  • Waking 1 or more time a week
  • Exacerbations requiring steroids in the last 2 years
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28
Q

What point in the asthma pathogenesis does corticosteroids act?

A

The initial inflammation

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29
Q

What are the advantages of the use of inhaled corticosteroids in asthma treatment?

A
  • Improve symptoms
  • Improve lung function
  • Reduce exacerbations
  • Prevent death
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30
Q

What is the result of the lipophilic substiuents on the D-ring of inhaled corticosteroids?

A
  • A very high affinity for the GCS receptor
  • Increased uptake and dwell time in tissue on local application
  • Rapid inactivation by hepatic biotransformation following systemic absorption
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31
Q

How do inhaled drugs reach the systemic circulation?

A
  • The swallowed fraction travels to GI tract and gets absorbed in the gut. It then travels to the liver, where some is inactivated in the ‘first pass’, and some active drug remains which then enters the systemic circulation
  • Some is deposited in the lungs, and absorbed from the lungs into the systemic circulation
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32
Q

Give an example of an inhaled corticosteroid which is absorbed through the gut and lungs

A

Beclomethasone

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33
Q

Give two examples of inhaled corticosteroids that undergo extensive first pass metabolism

A
  • Budesonide
  • Fluticasone
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34
Q

Why is it important to consider lung absorption with inhaled corticosteroids?

A

Because lung absorption is still relavent, and high doses of all inhaled corticosteroids have the potenital to produce systemic side effects

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35
Q

Which patients have a better response to inhaled corticosteroids?

A

Patients with eosinophilic asthma have a better response than non-eosionophilic patients

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36
Q

What should be done before initiating a new drug therapy in asthma?

A
  • Re-check patients medication compliance
  • Check inhaler technique
  • Eliminate trigger factors
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37
Q

What is the first choice of add on therapy in stage 3 of asthma management?

A

Long acting ß2 agonists, e.g. formoterol, salmeterol

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38
Q

When should a long-acting ß2 agonist be added to asthma therapy?

A

When a patient is not controlled on 400mcg/day inhaled corticosteroids

39
Q

What is the usual dosage of formorerol?

A

12μg bd

40
Q

How long is the onset of action of formoterol?

A

1-3 minutes

41
Q

What is the duration of action of formoterol?

A

12 hours

42
Q

What are the molecular properties of formoterol?

A

Moderately lipophilic

43
Q

What is the usual dosage of salmeterol?

A

50μg bd

44
Q

How long is the onset of action of salmeterol?

A

10-20 mins

45
Q

What is the duration of action of salmeterol?

A

12 hours

46
Q

What are the molecular properties of salmeterol?

A

Highly lipophilic

47
Q

What are the advantages of long-acting ß2 agonists?

A
  • Reduce asthma exacerbations
  • Improve asthma symptoms
  • Improve lung function
48
Q

What must long-acting ß2 agonists always be prescribed in conjunction with?

A

An inhaled steroid, as they are not anti-inflammatory on their own

49
Q

Give five examples of combined inhalers containing both an inhaled corticosteroid and a long-acting ß2 agonist, and how often they should be administered?

A
  • Budesonide/formoterol, twice daily
  • Beclomethasone/formoterol, twice daily
  • Fluticasone/formoterol, twice daily
  • Fluticasone/salmeterol, twice daily
  • Fluticasone furoate/vilanterol, once daily
50
Q

What are the advantages of combining a long acting ß2 agonist and an inhaled corticosteroid in one inhaler?

A
  • Ease of use
  • Improved compliance
  • 1 versus 2 prescriptions to worry about
  • Potentially cheaper than 2 individual inhalers
  • Safer
51
Q

Give 4 examples of alternative drug classes used in step 3/step 4 add ons for the management of asthma

A
  • High dose inhaled corticosteroid
  • Leukotriene receptor antagonists
  • Methylxanthines
  • Long acting anticholinergics
52
Q

Give two examples of leukotriene receptor antagonists

A
  • Montelukast
  • Zafirlukast
53
Q

How to leukotriene receptor antagonists help with asthma?

A

LTC4 release by mast cells and eosionophils can induce bronchoconstriction, mucus secretion, and mucosal oedema, and promote inflammatory cell recruitment. LRAs block the effect of cysteinyl leukotrienes in the airways at the CysLT1 receptor.

54
Q

How effective are leukotriene receptor antagonists?

A

They have some anti-asthma activity, but only useful in about 15% of patients as an add on therapy

55
Q

What are the side effects of leukotriene receptor antagonists?

A
  • Angiodema
  • Dry mouth
  • Anaphylaxis
  • Arthralgia
  • Fever
  • Gastric disturbances
  • Nightmares

Rarely a problem in clinical practice

56
Q

What are the important drug interactions with leukotriene receptor antagonists?

A

None

57
Q

Give two examples of methylxanthines?

A
  • Theophylline
  • Aminophylline
58
Q

What is the mechanism of action of methylxanthines?

A
  • Antagonise adenosine receptors
  • Inhibit phosphodiesterase, and increase cAMP
59
Q

What are the problems with methylxanthines?

A
  • Often poorly efficacious
  • Narrow therapeutic window
  • Frequent side effects
  • Potentially life-threatening toxic complications
  • Important drug interactions
60
Q

What are the side effects of methylxanthines?

A
  • Nausea
  • Headache
  • Reflux
61
Q

What are the potentially life threatening toxic complications possible with methylxanthines?

A
  • Arrythmias
  • Fits
62
Q

What are the important drug interactions with methylxanthines?

A

Levels increased by cytochrome P450 inhibitors, e.g. erythromycin, ciprofloxacin

63
Q

What long-acting anticholinergic is used in asthma?

A

Tiotropium bromide

64
Q

How often is tiotropium bromide given?

A

Once daily

65
Q

What is the effect of tiotropium bromide?

A
  • Reduces exacerbations (does the same for COPD)
  • Small improvements in lung function and symptoms
66
Q

What does tiotropium bromide have relatively selectivity for?

A

M3 muscarinic receptors

67
Q

What are the side effects of tiotropium bromide?

A
  • Dry mouth
  • Urinary retention
  • Glaucoma
68
Q

What medications are used in step 5 of asthma management?

A
  • Oral steroids
  • Biological therapies
69
Q

What dose of oral steroids is given in asthma?

A

Usually need 10mg o.d. or more for maintenance therapy

70
Q

Give two examples of biological therapies used in asthma

A
  • Anti-IgE
  • Anti-IL5
71
Q

Give an example of an anti-IgE drug

A

Omalizumab

72
Q

What are the criteria for the use of anti-IgE therapy?

A

Strict criteria, e.g. atopy, IgE within strict range

73
Q

What are the advantages of anti-IgE therapy?

A
  • Potentially reduces exacerbation rates in patients not controlled on oral steroids
  • May allow oral steroid tapering
74
Q

How do anti-IgE drugs work to treat asthma?

A

Prevents IgE binding to high affinity IgE receptor

75
Q

What is the result of anti-IgE medications not being able to bind to IgE already bound to the receptor?

A

It cannot cross link IgE and activate mast cells

76
Q

Give two examples of anti-IL5 therapies

A
  • Mepolizumab
  • Reslizumab
77
Q

How do anti-IL5 therapies work in asthma?

A

They reduce peripheral blood and airway eosionophil numbers

78
Q

When is anti-IL5 therapy most effective?

A
  • In reducing the rate of severe asthma exacerbations
  • If >3 exacerbations/year with blood eos >0.3x109/L in the last year
79
Q

What should every asthmatic have?

A

A self management plan, with written instructions on when and how to step-up and step-down treatment

80
Q

What are the advantages of asthmatic self-management plans?

A

Leads to better outcomes in terms of day-to-day control, frequency, and severity of exacerbations

81
Q

When is stepping down recommended?

A

Once asthma is controleld

82
Q

Why is stepping down recommended once asthma is controlled?

A

Because if stepping down does not take place, patients may recieve a higher dose than is necessary

83
Q

What happens to 10 micron particles when they are deposited via inhaled devices?

A

They are deposited in the mouth and oropharyx

84
Q

What happens to 1-5 micron particles when they are delivered by an inhaler device?

A

They are the most effective, as they settle in small airways

85
Q

What happens to 0.5 micron particles when they are delivered via inhaler devices?

A

They are inhaled to alveoli, and exhaled without being deposited in the lungs

86
Q

What should be done when a patient is unable to use an inhaler device satisfactorily?

A

An alternative should be found

87
Q

Who should assess a patients ability to use their inhaler?

A

A competent healthcare professional

88
Q

What needs to be done to ensure optimum efficacy when using inhaler devices?

A

The medication needs to be titrated against clinical response

89
Q

What is the diagnostic criteria of severe asthma in adults?

A
  • Unable to complete sentences
  • Pulse > 110/min
  • Respiration >25/min
  • Peak flow 33-50% of best/predicted
90
Q

What features suggest that asthma is life threatening?

A
  • PEF <33%
  • sPO2 <92
  • PaO2 <8kPa
  • PaCO2 >4.5kPa
  • Silent chest
  • Cyanosis
  • Feeble respiratory effort
  • Hypotension
  • Bradycardia
  • Arrythmia
  • Exhaustion
  • Confusion
  • Coma
91
Q

How should severe acute asthma be treated?

A
  • High flow oxygen
  • Nebulised salbutamol
  • Oral prednisolone 40mg/day for 10-14 days
  • If moderate exacerbation not responding, or acute severe/life threatening, add neulised ipratropium bromide
  • Consider IV aminophylline if no improvement, and life threatening features not responding to treatment
92
Q

What oxygen saturations should be aimed for in the treatment of acute severe asthma?

A

94-98%

93
Q

What is ipratropium bromide?

A

A quaternary anti-cholinergic agent

94
Q

How does iprotrapium bromide differ to other adrenergic agonists?

A
  • Bronchodilation develops more slowly and less intense
  • Response may last up to 6 hours

ESA 5 - Pharmacology (28 decks)

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