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Clinical Pharmacology > 9.2 Respiratory Pharmacology > Flashcards

9.2 Respiratory Pharmacology Flashcards

1
Q

what is asthma?

A

A Chronic inflammatory airway disease resulting in intermittent airway obstruction and hyper-reactivity. Primarily affects the small airways. Reversible both spontaneously and with drugs. a heterogeneous disease

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2
Q

Asthma is described as a heterogenous disease. What does this mean?

A

has both genetical and environment factors that influence its development

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3
Q

what evidence of asthma can be seen microscopically?

A

more eosinophils due to inflammatory nature

more macrophages and T cells

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4
Q

what are some of the macroscopic evidence of asthma?

A

tightening of smooth muscles in the airways
mucosal oedema
mucus plugging

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5
Q

what are the aims of asthma treatment?

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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6
Q

before adjusting asthma doses, what should be considered?

A

adherence
inhaler technique
eliminate/reduce trigger factors

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7
Q

what is uncontrolled asthma?

A

asthma that impacts a person’s lifestyle or restricts their usual activities
defined as:
- 3 days or more a week with symptoms
- 3 days or more a week with required use of SABA for symptom relief
- 1 or more night a week with awakening due to asthma

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8
Q

what are the symptoms associated with uncontrolled asthma?

A

coughing
shortness of breath
chest tightness

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9
Q

what are the different stages of pharmacological intervention for asthma?

A
  1. Short acting B2 agonist (salbutamol) and low dose ICS
  2. add inhaler LABA to low dose ICS
  3. increasing ICS to a medium dose or adding LTRA
  4. refer patient to specialist care
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10
Q

give some examples of inhaled corticosteroids

A

beclometasone
budesonide
fluticasone

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11
Q

what is the mechanism of action of inhaled corticosteroids?

A

Pass through plasma membrane, activate cytoplasmic receptors, activated receptor then passes in to nucleus to modify transcription.
gene activation results in increased number of B2 receptors, increased anti-inflammatory mediators and inhibition of the release of arachidonic acid
Gene repression causes a decrease in the inflammatory mediators interleukins, chemokines and cytokines

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12
Q

what is the action of inhaled corticosteroids?

A

Reduces mucosal inflammation, widens airways, reduces mucus

Reduces symptoms, exacerbations and prevents death

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13
Q

what are the adverse effects of inhaled corticosteroids?

A

can cause local immunosuppressive action - candidiasis
horse voice
pneumonia risk possible in COPD at high doses

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14
Q

how are inhaled corticosteroids modified to limit systemic side effects?

A

lipophilic side chain added

slow dissolution in aqueous bronchial fluid so less enters systemic circulation

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15
Q

give examples of fast short acting beta agonists?

A

salbutamol

terbutaline

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16
Q

give examples of fast long acting beta agonists?

A

formoterol

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17
Q

give examples of slow long acting beta agonists?

A

salmeterol

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18
Q

what is the function of SABAs?

A

symptom relief through reversal of bronchoconstriction

Used P.r.n. (as required)

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19
Q

what is the function of LABA?

A

Add on therapy to ICS and p.r.n SABA

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20
Q

what effects of beta agonists help relieve symptoms of asthmatics?

A

Bronchodilation
Also increase mucus clearance by action of cilia
Prevention of bronchoconstriction prior to exercise (SABA)

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21
Q

what are the adverse affects of Beta agonists?

A

Adrenergic - fight or flight effects (Tachycardia, palpitations, anxiety and tremor)
Increased Glycogenolysis (liver)
Increased renin (kidney)
SVT – (increased sinoatrial node activity -> increased HR, decreased refractory period at AVN)

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22
Q

why should LABAs only be prescribed alongside ICS?

A

alone can mask airway inflammation and near-fatal and fatal attacks
CVD – tachycardia may provoke angina

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23
Q

what are the advantages of combined fixed dose inhaler?

A

the combined inhaler includes both LABA and ICS.
Increases adherence
Decreased cost as only 1 inhaler
increased safety as the LABA comes with the ICS

24
Q

what are the drug interactions of beta agonists?

A

beta blockers may reduce effects of beta agonists

25
Q

what is the drug class of montelukast?

A

a leukotriene receptor antagonist

26
Q

what is the indication of montelukast?

A

in the nice guidelines, is the alternative to LABA addition in uncontrolled asthmatics already on SABA and low dose ICS

27
Q

what is the mechanism of action of montelukast?

A

Leukotrienes released by mast cells/eosinophils – increase bronchoconstriction, increase mucus, increase oedema
through CysLT1 – a GPCR
Leukotriene receptor antagonist (LTRA) block CysLT1

28
Q

what are the adverse drug reactions of montelukast?

A

headache
GI disturbance
dry mouth
hyperactivity

29
Q

what drug class is tiotropium?

A

LAMA

long acting muscarinic antagonist

30
Q

what are the indications of tiotropium?

A

severe asthma and COPD

31
Q

what is the mechanism of action of tiotropium?

A

relative selectivity for M3 receptors (SAMA much less selective)
block vagally mediated contraction of airway smooth muscle

32
Q

what are the ADRs of tiotropium?

A

infrequent - anticholinergic effects - dry mouth, urinary retention, dry eyes

33
Q

what are the indications of theophylline?

A

given p.o. for chronic poorly controlled asthma

34
Q

what drug class is theophylline?

A

adenosine receptor antagonist

35
Q

what is the mechanism of action of theophylline?

A

blocks the adenosine receptor, preventing bronchoconstriction

36
Q

why is theophylline rarely used?

A

not as safe as other drugs used to treat asthma
Has a narrow therapeutic index, and can be potentially life-threatening in supratherapeutic doses. Complications include arrhythmia – must measure [plasma]. CYP450 inhibitors increase concentrations of theophylline and can cause supratherapeutic dosing

37
Q

what patients require a self management plan

A

all asthmatic patients

38
Q

what is an asthma self management plan?

A

Written instructions on when and how to step up AND down treatment
Help asthmatics have better day to day management and reduced exacerbations
Should be reviewed following
treatment for exacerbation and on discharge from hospital following acute attack

39
Q

what is an acute severe asthma attack?

A
  • Unable to complete sentences
  • Peak flow 33-50% best or predicted
  • Respiratory rate ≥ 25/min
  • Heart rate ≥ 110/min
40
Q

what is a life threatening asthma attack?

A

an acute severe asthma attack plus any of the following:
• 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

41
Q

what is the treatment for a life threatening asthma attack?

A
  • Oxygen! SPO2 level between 94-98%
  • High dose (nebulised) β2 agonist – continuous if necessary – oxygen driven
  • Oral steroids should be prescribed minimum 5 days, continue ICS alongside
  • Nebulised ipratropium bromide – short acting muscarinic antagonist (SAMA) alongside β2 agonist if poor response alone (ipratropium)
  • Consider i.v. aminophylline if life threatening/near fatal and no success with above – caution if taking p.o. theophylline
42
Q

what is the difference between tiotropium and ipratropium?

A

tiotropium is a long acting muscarinic antagonist with greater affinity for M3 receptors
ipratropium is a shot acting muscarinic antagonist with less selectivity for M3 receptors and therefore has some M2 activity aswell which can cause tachycardia

43
Q

what are the ADRs of prednisolone?

A 
CUSHINGOID
cataracts
ulcers
skin: straie, thinning, easy bruising 
hypertension, hyperglycaemia, hirsuitism
infections
necrosis (femoral head)
glycosuria
osteoporosis, obesity, 
immunosuppression
diabetes
44
Q

what are the 5 tasks of management of COPD?

A 
confirm diagnosis 
smoking cessation
breathlessness score
vaccination
medication
45
Q

what is the treatment of acute exacerbations of COPD requiring hospitalisation?

A
  • 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
46
Q

what should be considered when prescribing and selecting 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
re-assessed as part of regular medication review

47
Q

what are the 3 main inhaler options?

A

• Pressurised metered dose inhalers (pMDI)
inhalation and actuation of device. Slow breath in and hold. Can be used with a spacer to improve delivery
• Breath-actuated pMDI
automatic actuation – upon inspiration
• Dry powder inhalers (DPI)
micro ionised drug plus carrier powder. own inspiratory flow – fast deep inhalation

48
Q

why does the inhaled particle size matter when taking an inhaler?

A

too small – inhaled to alveoli and exhaled without being deposited
too big – deposited in the mouth and oropharynx

49
Q

what is the function of a spacer?

A

a spacer can be attached to pressurised metered dose inhalers. It helps reduce the amount of large particles of aerosol swallowed when taking the inhaler and therefore reduce the amount of systemic side effects.

50
Q

what factors dictate the particle size of deposition of the inhaled aerosol?

A

Inhaler, technique and drug formulation

51
Q

what can be used to help improve inhaler technique?

A

In-check dial - allows us to measure the inspiratory flow for different devices. allows us to see which type of inhaler would be most appropriate for the individual and show them how they should be inhaling.

52
Q

Why do ICS have relatively few systemic side effects at therapeutic doses?

A

as undergoes extensive first pass metabolism, so little enters systemic circulation
also has lipophillic side chain modification that slows the dissolution in the aqueous bronchial fluid, keeping the ICS within the lungs and preventing absorption.

53
Q

Why should a LABA only be prescribed with ICS?

A

As LABA alone can mask airway inflammation, resulting in near fatal and fatal attacks. Prescribing alongside a ICS will help reduce the inflammation and therefore the occurrence of the masking.

54
Q

In addition to reduction in inflammatory mediators, what other benefit do steroids afford to asthma patients?

A

reduces mucus
widens airways
decreases mortality though LABA masking inflammation

55
Q

Describe which drugs should be prescribed in a severe acute exacerbation of asthma. How do they work to alleviate symptoms?

A

Oxygen - increase sats to 94-98%. Increases the oxygen delivery and alleviates the increased respiratory drive.
high dose of nebulised B2 agonist - oxygen driven. bronchodilation and increased ciliary action
prednisolone for 5 days
continue ICS - reduce inflammation
nebulised ipratropium bromide - SAMA - block vagally mediated contraction of airway smooth muscle
i.v. aminophylline if life threatening and no success with above. Adenosine receptor antagonist that reduces the bronchoconstriction

56
Q

Describe which drugs should be prescribed in a severe acute hospital admission for COPD

A
  • nebulised salbutamol and/or ipratropium driven by air and not oxygen
  • Oral steroids
  • Antibiotics (narrow spectrum – less severe, broad spectrum – greater severity)
57
Q

What are the typical anticholinergic side effects associated with muscarinic antagonists?

A

dry mouth
urine retention
dry eyes

Clinical Pharmacology (26 decks)

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