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Stage 2: Supporting Life > Pharmacology of Asthma > Flashcards

Pharmacology of Asthma Flashcards

1
Q

What are the goals of asthma treatment?

A

1) Reducing impairment → reducing symptoms, maintaining normal activities and achieving near normal pulmonary function
2) Minimising risks associated with the disease e.g. asthma exacerbations which puts patients in hospital and adverse effects of medication e.g. steroids

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2
Q

What are the two classifications of pharmacological treatment for asthma?

A

1) Reliever - short term benefit

2) Controller - long term

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3
Q

How are asthmatic airways blocked?

A

Blockage with e.g. eosinophils or narrowing by inflammation

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4
Q

What is the first step in asthma treatment?

A

As needed reliever inhaler (blue) → SABA

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5
Q

Describe use of only as needed SABAs

A
  • SABAs are highly effective for relief of asthma symptoms
  • However there is insufficient evidence about the safety of treating asthma with SABA alone
  • This option should reserved fr patients with infrequent symptoms (less than twice a month) of short duration, with no night waking due to asthma and with no risk factors for exacerbations
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6
Q

What is step 2 of asthma treatment?

A

Low dose controller (ICS to control inflammation first line) + as needed SABA

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7
Q

What is step 3 of asthma treatment?

A

One or two controllers (ICS/LABA) + as needed SABA

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8
Q

What is step 4 of asthma treatment?

A

Two or more controllers _ as needed SABA

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9
Q

Why is increasing the dose of medication past step 4 not a good idea?

A

Bc after this, even if you increases the dose a lot, it might make no difference and just have really bad side effects

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10
Q

What is step 5 of asthma treatment?

A

Higher level care and/or add on treatment

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11
Q

Why are bronchodilators quick relief?

A

Bc they relax smooth muscle

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12
Q

What are the two types of bronchodilators?

A

1) Selective beta 2 adrenoreceptor agonists (short and long acting)
2) Anticholinergic/muscarinic receptor antagonists (short and long acting)

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13
Q

How are bronchodilators given?

A

Inhaled (but SBAA can be given IV in intensive care)

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14
Q

What is an example of a short acting selective beta 2 adrenoreceptor agonists (SABA)?

A

Salbutamol → works within half an hour but effect is gone after 4h

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15
Q

What are some examples of long acting selective beta 2 adrenoreceptor agonists (LABA)?

A

Formoterol, salmeterol → last up to 12h

Vilanterol → lasts up to 24h (72h)

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16
Q

What is an example of a short acting anticholinergic/muscarinic receptor antagonist?

A

Ipratropium (bromide)

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17
Q

What are 2 examples of long acting anticholinergic/muscarinic receptor antagonist?

A

Tiotropium, umeclidinum

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18
Q

How do SABAs (salbutamol) work?

A

1) Salbutamol stimulates beta-2 adrenergic receptors (the prominent receptors in bronchial smooth muscle)
2) Stimulation of beta-2 receptors leads to activation of adenyl cyclase leading formation of cyclic AMP from ATP
3) High levels of cyclic AMP relaxes bronchial smooth muscle and also inhibits the release fo bronchoconstrictor mediators e.g. histamine and leukotrienes from mast cells in the airway

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19
Q

What happens to salbutamol in the body?

A

1) After inhalation, salbutamol reaches the lungs directly and acts within 3-5 minutes with a peak at 15-20 minutes
2) After oral administration, ~50% of salbutamol is absorbed from the gut with a slower onset of action, reaching a peak at ~2 hours after intake

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20
Q

What is the overall duration of action of salbutamol?

A

4-6 hours → buys time to get to hospital/GP, doesn’t treat asthma

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21
Q

How do anti-cholinergic/muscarinic receptor antagonists work?

A

Block effects of ACh released from cholinergic parasympathetic nerve fibres to smooth muscle and mucus glands → prevents airway smooth muscle contraction and mucus hypersecretion
(Less effective than BAAs at relaxing smooth muscle)

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22
Q

What are side effects of anti-cholinergic/muscarinic receptor antagonists?

A

Unusual but can include dry mouth, palpitations (bc anti-cholinergic), headache, dizziness, blurred vision → if it doesn’t help after two weeks, stop

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23
Q

What are the effects of tiotropium?

A

Increases FEV1 and reduces the risk of severe exacerbations

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24
Q

How does tiotropium work?

A

It attenuates IL-13-induced goblet cell metaplasia and potentially reduces mucus hypersecretion

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25
Q

Why does asthma required anti-inflammatory therapies in most patients?

A

Bc it is an inflammatory condition

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26
Q

What is the cornerstone of asthma management?

A

Inhaled corticosteroids (ICS) - brown inhaler

27
Q

What are the effects of ICS therapy?

A

1) Reduces asthma symptoms
2) Increases lung function
3) Improve QoL
4) Reduces the risk of exacerbations, hospitalisations and death

28
Q

How do corticosteroids work?

A

They suppress Th2/type 2 airways inflammation → reduces the infiltration and activation of eosinophils, Th2 cells and other inflammatory cells

29
Q

What do patients with elevated blood eosinophil levels experience?

A

A higher rate of exacerbations and lower asthma control

30
Q

What is an example of a long acting ICS?

A

Fluticasone furoate

31
Q

Describe fluticasone furoate (FF)

A
  • FF is an ICS with enhanced affinity for the glucocorticoid receptor (fast association and slow dissociation) → results in a longer duration of action and prolonger retention in the lung
  • This enables one-daily dosing → improves patient convenience and enhances adherence to treatment
32
Q

What combination of medication is currently the only available once daily inhaler?

A
  • FF/vilanterol → ICS/LABA combination inhaler licensed in asthma
33
Q

What medication might you take as well if the preventer inhaler (ICS) is not working v well?

A

Leukotriene receptor antagonist (LTRA)

34
Q

What is an example of an LTRA?

A

Montelukast

35
Q

What are leukotrienes?

A

A group of potent arachidonic acid-derived inflammatory mediators

36
Q

How do LTRAs work?

A
  • The CysLT1 receptor mediates the bronchoconstrictive and pro-inflammatory effects of cysteinyl-leukotrienes
  • Montelukast is a competitive antagonist of the CysLT1 receptor
37
Q

Describe LTRAs

A
  • Once daily oral administration → many patients prefer to take tablet than inhaler
  • Likely to work best in a subgroup of asthma patients with aspirin exacerbated respiratory disease (AERD) bc they have increased production of cysteinyl-leukotrienes
  • Side effects are rare but bad → headache, GI disturbances, nightmares
  • Only works in 10-20% of patients with severe asthma, can’t rely on it
38
Q

What is part of step 5 of asthma treatment?

A

Oral corticosteroids → excellent at controlling the inflammation fo asthma but at an expense

39
Q

What is an example of an oral corticosteroid?

A

Prednisolone

40
Q

How do oral corticosteroids work?

A

Get rids of eosinophils, relaxes smooth muscle and make salbutamol work better

41
Q

What are the side effects of OCS?

A

Obesity, osteoporosis, diabetes, cataracts, reflux, glaucoma, skin disease, psychiatric

42
Q

How do OCS lead to osteoporosis?

A

Inhibits osteoclasts so inhibits bone turnover

43
Q

How are OCS prescribed?

A

As short term relief → short course, 40mg for 5 days

44
Q

Which cytokine is largely involved in bronchoconstriction?

A

IL-13

45
Q

Why do you need steroids for asthma treatment?

A

Bc salbutamol does not get rid of eosinophils and inflammation

46
Q

What correlates with worse asthma and therefore what do biologics (MAbs) target?

A

More eosinophils → so target these by blocking IL-5

47
Q

In an ideal world what would we give all patients who need/use OCS?

A

MAbs

48
Q

What types of MAbs are used to treat asthma?

A

Anti IL-5

49
Q

How effect are anti IL-5 Mabs?

A

They reduce asthma exacerbations by >50%

50
Q

What are examples of anti IL-5 Mabs?

A

Mepolizumab, benralizumab, dupilumab (new, hoping will work for 20% of patients for who IL-5 targets doesn’t work

51
Q

What is the central effector cell in asthma?

A

Eosinophils

52
Q

What does IL-5 do?

A

IL-5 is critically involved in the synthesis, maturation, homing and activation of eosinophils

53
Q

What does mepolizumab target?

A

Serum IL-5

54
Q

What does benralizumab target?

A

IL-5 receptor

55
Q

How do anti IL-5 Mabs work?

A

Both lead to a significant reduction in eosinophils, asthma exacerbations and systemic steroid exposure

56
Q

What is benralizumab?

A

A humanised MAb that depletes blood eosinophils by specifically targeting IL-5a receptor on eosinophils and then recruits effector cells to APC

57
Q

What increases response to IL-5 MAb treatment?

A

The higher the blood eosinophil count

58
Q

What is another MAb used to treat asthma?

A

Anti-IgE MAb

59
Q

What is an example of an anti-IgE Mab?

A

Omalizumab

60
Q

How does omalizumab work?

A

1) Depletes IgE and disarms mast cells
2) This reduces allergen-induced mast cell activation, decreases expression of IgE high affinity receptors on mast cells and blocks effects of IgE on dendritic cells
3) This decreases exacerbation rates

61
Q

Describe omalizumab

A
  • Given by SC injection every 2-4 weeks, at a dose and frequency determined by body weight and serum IgE levels
  • It is licensed for patients with evidence of atopy to perennial allergens
  • It eliminates the seasonal peaks in asthma exacerbations
62
Q

What combination of factors is most associated with exacerbations?

A

The combination of virus, allergy and exposure to a relevant antigen

63
Q

What do anticholinergics offer?

A

Additional bronchodilation

64
Q

What are side effects of biologics?

A
  • Only available for 2-3 years in practice so don’t know long term effects
  • On day of injection → skin reaction, fatigue, headache
  • Slightly higher rate of pharyngitis and other infections

Stage 2: Supporting Life (30 decks)

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