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Clinical Pharmacology, Therapeutics & Intro to Prescribing > Lecture 18- Respiratory pharmacology > Flashcards

Lecture 18- Respiratory pharmacology Flashcards

1
Q

Asthma pathophysiology

A
  • Chronic inflammatory airway disease often caused by exposure to allergens or other environment exposure
  • Causes intermittent airway obstruction and hyper-reactivity in small airways
    • Non allergic around 30-40%
  • Reversible
  • A heterogeneous disease (don’t know everything about asthma)
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2
Q

What does good Asthma control look like:

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)
  • Aim is for early control with stepping up OR down as required
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3
Q

what does uncontrolled asthma look like

A
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4
Q

Before stepping up or down asthma treatment check…

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

Chronic asthma management 2 slightly different guidelines

A

BTS vs NICE

BTS

  • low dose ICS (preventrer) + SABA prn
  • add on LABA
  • then consider increasing ICS and adding LTRA

NICE

  • low dose ICS + SABA prn
  • option 1: add on ICS/LABA
  • or option 2: add on LTRA

Can step up and step down therapy

  • LTRA cheaper than LABA
  • Most end up on LABA anyway
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6
Q

name some Steroids- inhaled corticosteroids (ICS) used to treat athma (as preventer)

A
  • Beclomethasone
  • Budesonide
  • Fluticasone
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7
Q

uses of ICS in asthma

A
  • First line treatment
  • Regular preventer when reliver alone not sufficient
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8
Q

Pharmacokinetics steroids

A
  • Poor bioavailability
    • Due to lipophilic side chain added
    • Slow dissolution in aqueous bronchial fluid
    • High affinity for glucocorticoid receptor
      • Local effect
  • Most IC are substrate of CYP450 3A4
    • If steroids absorbed po transported from stomach to liver via hepatic portal system (almost complete first pass metabolism)
      • But at high doses all ICS potential to produce systemic side effects
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9
Q

MOA of ICS

A
  • Pass through plasma membrane, activate cytoplasmic receptors, activated receptor then passes in to nucleus to modify transcription
  • Reduces mucosal inflammation, widens airways, reduces mucus
  • Reduces symptoms, exacerbations and prevents death
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10
Q

Adverse drug response ICS

A
  • If taken correctly very few significant ADRS
  • Local immunosuppressive action e.g. candidiasis, horse voice (in pharynx)
    • Wash mouth out after
  • Pneumonia risk at high doses
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11
Q

Drug-drug interactions ICS

A

CYP450 3A4 inhibitors e.g. budesonide

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12
Q

name some drugs under B agonists

A

SABA and LABAs

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13
Q

SABA uses

*

A
  • ‘reliever’
  • Symptom relief through reversal of bronchoconstriction
  • Only to be use prn (when required)
  • May be used prior to exercise to prevent bronchoconstriction
    • When used regularly can reduce asthma control – tolerance?
    • Seen as a quick fix esp in young adults
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14
Q

uses of LABA taken with ICS

A

Add on therapy to ICS and prn SABA

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15
Q

Mode of action B agonists

A
  • Bind to B2 receptors (GPCR)
  • Increase cAMP
  • Increase PKA
  • Cause airway smooth muscle to relax
  • Also increase mucus clearance by action of cilia
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16
Q

Adverse drug response B agonists

*

A
  • Adrenergic- fight or flight effects
    • Tachycardia
    • Palpitations
    • Anxiety
    • Tremor
    • Increase glycogenolyis (liver)
    • Increased renin (kidney
    • Supraventricular tachycardia
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17
Q

Contraindication B agonist

A
  • Should only be prescribed alongside ICS
    • Alone can mask airways inflammation in near fatal and fatal attacks (LABA now always prescribed mixed with ICS)
  • CVD- tachycardia may provide angina
18
Q

Drug-drug interactions B agonist

A

B-blockers may reduce effects of B2 agonists

19
Q

Additional asthma controller therapies:

A
  1. leukotriene receptor antagonist (LTRA) e.g. Montelukast (PO)
  2. Long acting muscarinic antaognist (LAMA) e.g. tiotropium
  3. theophylline
20
Q

Uses of LTRA

A
  • Alternative to LABA in NICE guidelines
  • Only useful in 15% of asthmatics- most end up moving up to LABA
21
Q

MOA of LTRA

A
  • Inhibit leukotrienes released by mast cells/eosinophils by blocking CysLT1 receptor
  • Reducing bronchoconstriction
  • Reducing mucus
  • Reducing oedema
22
Q

Adverse drug response LTRA

A
  • Headache
  • GI disturbance
  • Dry mouth
  • hyperactivity
23
Q
A
24
Q

uses of LAMA e.g. tiotropium

A
  • Severe asthma and COPD
25
Q

Mode of action LAMA

A
  • Relatively antagonistic for M3 receptor (SAMA much less selective)
  • Block vagally mediated contraction of airway smooth muscle
26
Q

Adverse drug response LAMA

A
  • Infrequent
  • Anticholingeric effects
    • Dry mouth
    • Urinary retention
    • Dry eyes
27
Q

uses of theophylline

A
  • Chronic poorly controlled asthma
28
Q
A
29
Q

MOA theophylline

A
  • Adenosine receptor antagonist
  • Reduce bronchoconstriction
30
Q

Adverse drug response theophylline

A
  • Narrow therapeutic index
  • Life threatening complications inc arrhythmia – must measure [plasma]
31
Q

Drug-drug interactions theophylline

A

CYP450 inhibitors- will increase theophylline

32
Q

Self management plans

A
  • Important for all asthmatics
  • Written instruction on when and how to step up AND step down treatment
  • Better day to day management and reduced exacerbations
  • Think about who is involved
    • Adult
    • Child
    • Cognitively impaired
    • Carer
  • Should be reviewed following treatment for exacerbation and on discharge from hospital following acute attack
33
Q

define features of acute severe asthma

A
  • Unable to complete sentences
  • Peak flow 33-50% best or predicted
  • Respiratory rate ≥ 25/min
  • Heart rate ≥ 110/min

Plus any of the following considered life-threatening:

  • Peak flow < 33% best or predicted (if recordable)
  • Arterial oxygen saturation (SpO2) < 92%
  • Partial arterial pressure of oxygen (PaO2) < 8 kPa
  • Normal partial arterial pressure of carbon dioxide (PaCO2) (4.6–6.0 kPa)
  • Silent chest, Cyanosis, Poor respiratory effort, Arrhythmia, Exhaustion, Altered conscious level, Hypotension
34
Q

treatment of acute severe and life threatening asthma

A
  • Oxygen!!
    • Increase to 94-98%
  • High dose (nebulised) B2 agonist- continuous if necessary
    • Driven in with oxygen
  • Oral steroid (prednisolone) should be prescribed for minimum 5 days (IV if not oral- preferably oral)
    • Continuous IC alongside
  • Nebulised ipratropium bromide (ipratropium) – short acting muscarinic antagonist (SAMA) alongside b2 agonist if poor response alone
    • Ipratropium less selective for M3 receptors compared to tiotropium, M2 activity too
  • Consider IV aminophylline if life threatening/near fatal and no success with above
    • Caution with taking PO theophylline
35
Q

name a SAMA (short acting muscarinic antagonist

A

ipratropium bromide

Ipratropium is in a class of medications called bronchodilators. It works by relaxing and opening the air passages to the lungs to make breathing easier

36
Q

COPD management

A
37
Q

management of acute COPD exacerbations

A

In acute exacerbations – requiring hospitalisation

  • nebulised salbutamol and/or ipratropium should be prescribed
  • *If patient is hypercapnic or acidotic nebuliser should be driven by air and not oxygen**
  • Oral steroids
  • they can be less effective than in eosinophilic asthma due to reduced action on neutrophils
  • Antibiotics (narrow spectrum – less severe, broad spectrum – greater severity)
  • Review of chronic treatment and action plan
38
Q

inhaler selection and prescribing

A
39
Q

Inhaler options

A
  • Pressurised metered dose inhalers (pMDI)
  • Breath-actuated pMDI
  • Dry powder inhalers (DPI)
40
Q

Pressurised metered dose inhalers (pMDI)​

A
  • Inhalation and actuation of device
  • Slow breath in and hold
  • Can be used with a spacer to improve delivery
41
Q
  • Breath-actuated pMDI
A
  • Newer
  • Automatic actuation upon inspiration
42
Q
  • Dry powder inhalers (DPI)
A
  • Micro ionised drug plus carrier powder
  • Own inspiratory flow- fast deep inhalation (vs pressure metered dose inhalers)

Clinical Pharmacology, Therapeutics & Intro to Prescribing (39 decks)

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