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Clinical Pharmacology & Intro to Prescribing > Session 9: Respiratory Pharmacology > Flashcards

Session 9: Respiratory Pharmacology Flashcards

1
Q

What is asthma?

A

A chronic inflammatory airway disease with intermittent airway obstruction and hyper-reactivity of the small airways.

It is reversible both spontaneously and with drugs.

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2
Q

Aims of asthma control.

A

Minimal symptoms during both night and day.

Minimal need for medication

No exacerbations

No limitation of physical activity

Keep normal lung function

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3
Q

What should be checked before deciding to step up or step down medication of asthma?

A

Adherence

Inhaler technique

Eliminate trigger factors

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4
Q

Give examples of inhaled corticosteroids (ICS).

A

Beclometasone

Budesonide

Fluticasone

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5
Q

When are ICS used?

A

They are a regular preventer when reliever (SABA) is not sufficient on its own.

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6
Q

Briefly explain mechanism of ICS.

A

Pass through plasma membrane and activate cytoplasmic receptors.

The activated receptor then passes into the nucleus to modify transcription.

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7
Q

Action of ICS.

A

Reduces mucosal inflammation

Widens the airways

Reduces mucus production

Also reduces symptoms, exacerbations and prevents death.

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8
Q

ADRs of ICS.

A

Immunosuppressive action locally leading to candidiasis or hoarse voice.

Also a risk of pneumonia in COPD.

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9
Q

How are ADRs reduced in ICS?

A

If taken correctly

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10
Q

Pharmacokinetics of ICS.

A

It has a poor oral bioavailability but a lipophilic side chain is added.

There is slow dissolution in aqueous bronchial fluid and a high affinity for glucocorticoid receptors.

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11
Q

ICS are inhaled as the name suggest.

Why are they not taken orally?

A

Because they are transported from the stomach to the liver by the hepatic portal system but as they reach the liver they will almost complete first pass metabolism meaning none will end up in the systemic circulation.

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12
Q

ADRs of high doses of ICS.

A

Potential to produce systemic side effects

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13
Q

Give examples of types of beta 2 agonists.

A

SABA

LABA

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14
Q

Action of SABA.

A

Symptom relief through reversal of bronchoconstriction and are only used when needed.

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15
Q

When are LABAs used?

A

As an add on therapy to ICS and p.r.n. (when needed) SABA.

(When it’s not enough anymore)

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16
Q

Action of LABA.

A

Reversal of bronchoconstriction and also increase mucus clearance by action of cilia.

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17
Q

Give examples of SABAs.

A

Salbutamol

Terbutaline

Fast and short acting

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18
Q

Give examples of LABAs.

A

Fast and long acting - Formoterol (12h)

Slow and long acting - Salmeterol (12h), Vilanterol (24h)

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19
Q

Beta 2 - agonist ADRs.

A

Adrenergic fight or flight effects like tachycardia, palpitations, anxiety and tremors.

Can lead to SVT by higher activity of SAN, increased HR and decreased refractory period at AVN.

Also increased glycogenolysis and increased renin.

Muscle cramps.

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20
Q

Can LABAs be given on their own?

A

No. They need to be prescribed alongside of ICS because there is an increased risk of death when prescribed alone.

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21
Q

What may reduce the effects of b2 agonists.

A

Beta blockers

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22
Q

Difference between formoterol and salmeterol.

A

Formoterol is more potent and efficacious.

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23
Q

Why is LABA always given with ICS?

A

Because on its own it can mask airway inflammation and cause near-fatal or fatal attacks.

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24
Q

In order to prevent LABAs from being taken alone, what is done?

A

Combined inhaler.

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25
Q

Pros of a combined inhaler.

A

Ease of use

Adherence

Less prescriptions

But most of all safety

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26
Q

When LABAs + ICS + SABAs are not enough anymore, what are the next steps?

A

Increase ICS to medium dose.

LTRA (Leukotriene receptor antagonist)

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27
Q

Give an example of an LTRA.

A

Montelukast

28
Q

Explain the action of LTRAs.

A

LTC4 is released by mast cells and eosinophils.

This leads to increased bronchoconstriction, increased mucus production, oedema via CysLT1 - GPCR.

LTRAs will block CysLT1.

29
Q

ADRs of LTRA.

A

Headache

GI disturbance

Dry mouth

Hyperactivity

30
Q

If LTRAs and increased ICS dose is not enough.

What can be given?

A

Long acting muscarinic antagonists (LAMAs)

Methylxanthine

31
Q

When are LAMAs used?

A

In severe asthma and COPD.

32
Q

Mechanism of LAMAs.

A

Relative selectivity for M3 with an anticholinergic effects.

This is through inhibition of muscarinic receptors.

33
Q

Give examples of LAMAs.

A

Tiotropium

34
Q

ADRs of LAMAs.

A

Typical anticholinergic effects

Dry mouth

Urinary retention (M3)

Dry eyes etc…

35
Q

Give an example of a methylxanthine.

A

Theophylline

36
Q

Mechanism of methylxanthines.

A

Adenosine receptor antagonists.

37
Q

Why do methylxanthines need to be given with caution?

A

Because they have a narrow therapeutic index with potentially lif-threatening complications such as arrhythmias

38
Q

What will cause theophylline to increase in concentrations.

A

CYP450 inhibitors

39
Q

In case none of this work.

What is the specialist maintenance therapy?

A

Oral steroids such as prednisolone.

They’re given in post acute exacerbation or also in post acute COPD.

Anti IgE (monoclonal antibodies) and Anti Il-5 monoclonal antibodies can also be given.

40
Q

Explain a self management plan for asthmatic patients.

A

Individual for each patients and will differ.

There will be written instructions on when to use and when to either step up or step down.

41
Q

Who should be involved in the self-management plan?

A

Any adult (suffering with asthma, or parent of child with asthma)

Child

Cognitively impaired

Carer

42
Q

Give signs of acute severe asthma.

A

Inability to complete sentences

Peak flow low (33-50%)

RR over 25/min

HR > 110/min

43
Q

Life-threatening asthma.

A

Peak flow under 33%

O2 sat <92%

kPa <8

Silent chest

Cyanosis

Poor resp effort and lowered RR

Arrhythmia

Exhaustion

Altered conscious level

Drop in BP

44
Q

How to treat acute severe and life threatening asthma.

A

O2 (94%-98% is the aim)

High dose nebulised b2 agonist.

Oral steroids

45
Q

If O2, b2 nebuliser and steroids is not enough.

What could be given?

A

A short acting muscarinic antagonist (SAMA) nebulised.

46
Q

Give an example of a SAMA.

A

Ipratropium (with bromide)

47
Q

In life threatening asthma what can be given as well?

A

IV aminophylline if there is no success with above.

48
Q

Explain the 5 tasks of management in stable COPD.

A

1 - Confirm diagnosis of COPD. Exclude other diagnoses.

2 - Stop smoking

3 - Offer pulmonary rehabilitation and also encourage exercise.

4 - Offer vaccinations such as flu and pneumococcal.

5 - Consider medication.

49
Q

In acute exacerbation of COPD hospitalisation is required.

Explain what treatments are given.

A

Nebulised salbutamol and/or ipratropium.

These are given usually driven by air and not by oxygen.

Oral steroids can be given but usually not as effective.

Antibiotics

50
Q

Why are nebulisers in COPD driven by air and not oxygen?

A

Because the patient may be hypercapnic or acidotic

51
Q

Why are oral steroids not that effective in COPD compared to asthma?

A

Asthma = eosinophilic reaction where steroids act well.

COPD is a neutrophilic reaction where steroids don’t work as well.

52
Q

Explain the selection and prescribing of an inhaler.

A

Need to find an inhaler that the patient can use.

Should be assessed by an appropriately trained healthcare professional.

Dose needs to be titrated against clinical response of that individual.

Do a medication review in order to lower risk of re-admission.

53
Q

Give examples of inhalers.

A

Pressurised metered dose inhaler (pMDI)

Breath-actuated pMDI

Dry powder inhalers (DPI)

54
Q

Explain how a pMDI works.

A

Inhalation and actuation of device.

It is manual so you need to time your inhalation to pressing down the cannister.

You take a slow breath in and hold.

55
Q

How can you improve delivery of a pMDI?

A

Use a spacer.

56
Q

Explain how a breath-actuated pMDI works.

A

Automatic actuation so when you inspire the puff will come automatically.

57
Q

Explain how dry powder inhalers work.

A

Microionised drug plus carrier powder where own inspiratory flow is used.

This is a fast deep inhalation option.

58
Q

Why is inhaler, technique and drug formulation important to consider?

A

Because it dictates the particle size and the location of deposition of the drug.

59
Q

What happens if the patient inspires too slow.

A

Drug is deposited in mouth

60
Q

What happens if the patient inspires too fast?

A

Drug deposited in throat.

61
Q

Where will the drug be deposited if the inspiratory flow is optimal?

A

In the lungs

62
Q

What happens if the patient has too small of a dose?

A

It is inhaled into alveoli and exhaled without being deposited.

63
Q

What happens if the patient takes too big of a breath?

A

It is deposited in the mouth and oropharynx.

64
Q

What is used in order to educate patients and carers/parents/etc… about proper technique?

A

In-check DIAL device

65
Q
A

Clinical Pharmacology & Intro to Prescribing (24 decks)

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