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Pharmacology > Airway Control > Flashcards

Airway Control Flashcards

1
Q

What do the T-helper cells 2 cause?

A

Secrete interleukins causing

  • mucosal oedema
  • bronchoconstriction
  • mucus plugging
  • airway remodelling
  • bronchial hyperresponsiveness
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2
Q

What changes in airway remodelling?

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

How can asthma vary between individuals?

A

Pathologically - eg eosinophils vs neutrophil if inflammation
By symptom patterns
Triggers of exacerbation
How it responds to treatment

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4
Q

Which β2 agonists have a fast onset but are short acting?

A

Inhaled terbutaline

Inhaled salbutamol

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5
Q

Which β2 agonists have fast onset and long acting?

A

Inhaled formoterol

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6
Q

Which β2 agonists have a slow onset and short acting

A

Oral salbutamol
Oral terbutaline
Oral formoterol

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7
Q

Which β2 agonists are slow onset and long duration?

A

Inhaled salmeterol

Oral bambuterol

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8
Q

What are short-acting β2 agonists used for?

A

Symptom relief though reversal of bronchoconstriction

Prevention of bronchoconstriction eg on exercise

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9
Q

Why should short-acting β2 agonists only be used when required?

A

If used regularly, can reduce control of asthma

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10
Q

Mechanism of action of short-acting β2 agonists?

A

β adrenoceptors are coupled to Gs proteins
Activate adenylyl cyclase to convert ATP to cAMP
Increased cAMP activates PKA which phosphorylates L-type calcium channels, increasing calcium entry into cells
Leads to smooth muscle relaxation and inhibition of of agonist-induced contraction

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11
Q

What drives inflammation in asthma?

A

T-helper cell 2 which secrete interleukins

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12
Q

How do beta-2 agonists reduce bronchoconstriction?

A

Beta-adrenoceptors coupled to Gs proteins
Activate adenylyl cyclase to convert ATP to cAMP
Increased cAMP activates PKA which
-reduces intracellular Ca2+ concentration
-inhibits MCLK leading to dephosphorylation of myosin
= smooth muscle relaxation

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13
Q

How can beta-2 agonists potentially make asthma worse?

A

Regular use can increase mash cell degranulation in response to allergens

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14
Q

Side effects of short acting beta-2 agonists?

A

Tachycardia
Palpitations
Tremor

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15
Q

When are long-acting beta-2 agonists used?

A

In step 3 as an add-on therapy

  • must check patient compliance
  • check inhaler technique
  • eliminate triggering factors
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16
Q

What is the first choice for a long-acting beta-2 agonist?

A

Formoterol or salmeterol

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17
Q

What is the onset time and duration of action for beta-2 agonists?

A

Formoterol works in 1-3 minutes
Salmeterol works in 10-20 minutes

Work for 12 hours

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18
Q

Benefits of long-acting β2 agonists?

A

Reduce asthma exacerbations
Improve symptoms
Improve lung function

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19
Q

What must long-acting β2 agonists be prescribed with?

A

An inhaled steroid as they do not have anti-inflammatory properties of their own

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20
Q

What are the different combination inhalers with a long-acting β2 agonist and steroid?

A 
Budesonide/formoterol
Beclomethasone/formoterol
Fluticasone/formoterol
Fluticasone/salmeterol
Fluticasone furoate/vilanterol
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21
Q

Why are combined inhalers useful?

A

Better compliance and easy to use
Only one prescription
Cheaper than two inhalers

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22
Q

When are inhaled corticosteroids introduced?

A

Using β2 agonist 3 or more times a week
Have symptoms 3 or more times a week
Waking once or more a week
Exacerbation requiring oral steroids in last two years

23
Q

Mechanism of action of inhaled corticosteroids?

A

Suppress gene transcription in a wide range of pro-inflammatory structural cells
This reduces infiltration of the lung by eosinophils and other cells that execute the exaggerated immune response
Increase expression of β2 receptors
Increase anti-inflammatory ILs which induce apoptosis in many inflammatory cells and reduce the number of mast cells in respiratory mucosa

Overall, reduce inflammation

24
Q

Benefits of inhaled corticosteroids?

A

Improve symptoms
Improve lung function
Reduce exacerbations
Prevent death

25
Q

When are optimum effects seen with inhaled corticosteroids?

A

Weeks/months after surgery

26
Q

What proportion of inhaled corticosteroids are delivered to the lungs?

A

10-50%

27
Q

What can reduce the amount of corticosteroid reaching the target site when inhaled?

A

Deposited in upper airway

Swallowed

28
Q

What is given for an acute exacerbation of asthma?

A

Oral steroids - 40mg prednisolone

29
Q

ADRs of inhaled corticosteroids?

A

Low due to poor systemic absorption and metabolised pre-systemically

Spacers also reduce effects such as croaky voice, sore throat and thrush

30
Q

Which patients have a better response to inhaled corticosteroids?

A

This with eosinophilic asthma rather than non-eosinophilic

31
Q

What is used in step 1 asthma treatment?

A

Mild intermittent asthma

-β2 short acting agonist prn

32
Q

What is used in step 2 management of asthma?

A

Regular preventer therapy

-add inhaled steroids 200-800mcg a day

33
Q

What is done in step 3 in management of asthma?

A

Add inhaled long-acting β2 agonist

  • if needed, increase dose of inhaled steroid to 800mcg a day
  • if no response, stop LABA and increase dose of inhaled steroid to 800mcg a day. If not enough, trial other therapies eg leukotriene receptor antagonist or SR theophylline
34
Q

What happens in step 4 asthma management?

A

Persistent, poor control
Consider trials of
-increasing inhaled steroid to 2000mcg/day
-addition of fourth drug eg leukotriene receptor antagonist, SR theophylline, β2 agonist tablet

35
Q

What is done in step 5 management of asthma?

A

Continuous/frequent use of oral steroids

  • use daily steroid tablet at the lowest dose providing adequate control
  • maintain high dose of inhaled steroid at 2000mcg/day
  • consider other treatments to minimise use of steroid tablet
  • refer for specialist care
36
Q

Name some leukotriene receptor antagonists

A

Montelukast

Zafirlukast

37
Q

How do leukotriene receptor antagonists work?

A

LTC4 is released by mast cells and eosinophils
Can induce bronchoconstriction, mucus secretion, mucosal oedema and promote inflammatory cell recruitment

LRAs block the effect of cysteinyl leukotrienes in the airways at CysLT1 receptors

38
Q

Side effects of leukotriene receptor antagonists?

A 
Angioedema
Dry mouth
Anaphylaxis
Fever
Gastric disturbances
39
Q

Name some methylxanthines

A

Theophylline

Aminophylline

40
Q

Mechanism of action of methylxanthines?

A

Antagonise adenosine receptors

Inhibit phosphodiesterase leading to increase in cAMP (but unlikely to be relevant in vivo)

41
Q

Problems with methylxanthines?

A

Poorly efficacious
Narrow therapeutic window
Frequent ADRs - some potentially life threatening
DDIs

42
Q

ADRs of methylxanthines?

A

Nausea, headache, reflux

Arrhythmias and fits

43
Q

DDIs with methylxanthines?

A

Get increased levels with CYP450 inhibitors such as erythromycin and ciprofloxacin

44
Q

Name some long-acting anti-cholinergics

A

Tiotropium bromide

45
Q

What is tiotropium bromide used for?

A

COPD and asthma
Used once a day to reduce exacerbations
Can improve lung function and symptoms

46
Q

Side effects of long-acting cholinergics?

A

Dry mouth
Urinary retention
Glaucoma

47
Q

How does anti-IgE work?

A

Prevents IgE binding to high affinity IgE receptor

Therefore, cannot bind to IgE already bound to receptor, so cannot cross-link IgE and activate mast cells

48
Q

What is the ideal size of particles for inhaled drugs and why? What happens if they are too big or too small?

A

1-5 micron particles - settle in small airways
Too big, deposited in mouth and oropharynx
Too small, inhaled to alveoli without being deposited in lungs

49
Q

What happens once asthma is controlled?

A

Stepping down of therapy to ensure patients are not receiving a higher dose than is necessary

50
Q

What are the criteria for severe acute asthma?

A 
Any one of these features 
Unable to complete sentences
Pulse at or above 110 bpm
Resp rate at or above 25 bpm
Peak flow 33-50% of best or predicted 
Plus any one of some life-threatening features
51
Q

What are the life threatening features for severe acute asthma?

A 
Low PEF
Low oxygen sats (below 92)
High CO2 >4.5kPa
Silent chest
Cyanosis
Feeble respiratory effort
Hypotension, bradycardia, arrhythmia
Exhaustion, confusion, coma
52
Q

When is mechanical ventilation required in a severe acute asthma attack?

A

If PaCO2 rises above 6kPa

53
Q

Treatment of severe acute asthma?

A

High flow oxygen - need to keep O2 94-98%
Nebulised salbutamol
Oral prednisolone - 40mg/day for 10-14 days
If not responding, nebuliser ipratropium bromide
If no improvement, IV aminophylline

54
Q

What is ipratropium bromide?

A

An anti-cholinergic

  • bronchodilation develops more slowly than adrenergic agonists
  • response may last up to 6 hours

Pharmacology (23 decks)

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