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Applied Pharmacology for Nurses > 6 Treatments for Asthma > Flashcards

6 Treatments for Asthma Flashcards

1
Q

Treatments to be covered

A

Main (first line) drugs
glucocorticoids (steroids)
b2 adrenergic agonists

Others
 theophylline
 muscarinic receptor antagonists 
 cromoglicate
 leukotriene antagonists
 new biologics
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2
Q

Types of asthma

A 
Acute or chronic
Chronic
recurrent attacks of reversible airway obstruction of air flow
controlled with drugs
Acute severe asthma (status asthmaticus)
not easily reversed with drugs
can be fatal
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3
Q

Features of asthma

A 
Characterised by 
inflammation in the airways
hyper-reactivity of bronchioles
   e.g. to
irritant chemicals
cold air
stimulant drugs
Results in
bronchoconstriction 
mucus secretion
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4
Q

Airways calibre in asthma

A

Aim of drug treatment: to reduce inflammation, prevent bronchoconstriction and restore airways calibre to normal

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5
Q

Stimuli that trigger an attack

A 
exercise (cold air), respiratory infection, atmospheric pollutants 
intrinsic trigger (non-atopic)
allergens in sensitised people
pollen 
dust mite proteins 
animal dander
allergic trigger (atopic)
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6
Q

Development of asthma

A

When allergen first presents, B cells are activated (via T cell cascade) to make IgE, which recognises the antigen. Mast cells express a high-affinity receptor (FcεRI) for the Fc region of IgE. Very high affinity binding means that IgE is irreversibly bound, effectively coating the surface of Mast cells. Presentation of antigen to these Mast cells results in crosslinking of 2 IgE receptors, leading to degranulation.

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7
Q

Immediate/ early phase of attack

A 
Bronchospasm: bronchial muscle contracts
mast cells release spasmogens
histamine
leukotrienes (LTC4 and LTD4)
prostaglandin D2 
Mast cells release inflammatory mediators
interleukins (IL-4, IL-5, IL-13)
macrophage inflammatory protein-1a
tumour necrosis factor-a (TNF-a)
chemotaxins & chemokines attract leukocytes to area
sets stage for late phase
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8
Q

Late phase

A

Progressing inflammatory reaction
Th2 lymphocytes & eosinophils invade
Release cytokines, chemokine & toxic proteins

Agents from inflammatory cells cause
Damage to & loss of bronchial epithelium
smooth muscle cell hypertrophy & hyperplasia
hyper-reactivity to irritant stimuli

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9
Q

Bronchodilators

A

Dilate bronchioles and increase air flow to alveoli

Relax smooth muscle cells around walls of bronchioles

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10
Q

Types of bronchodilator

A

b2 adrenergic receptor agonists
theophylline
muscarinic receptor antagonists
leukotriene receptor antagonists

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11
Q

b2 adrenergic receptor agonists

A

Direct action on b2 adrenoceptors on bronchiole smooth muscle to relax muscle

Also
inhibit mediator release from mast cells & monocytes
may act on cilia to increase mucus clearance

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12
Q

b2 adrenergic receptor agonists

A 
Short acting
salbutamol, terbutaline
Max effect within 30 min, last 4-6 hours
Used “as needed” to control symptoms
Longer acting
salmeterol
duration of action 12 hours
twice daily dose in patients not controlled with glucocorticoids
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13
Q

Administration of b2 agonists

A

By inhalation
to target action in lung
& minimise systemic effects

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14
Q

Unwanted effects of b2 agonists

A

result from absorption into systemic circulation
most common is tremor
some tolerance to b2 agonists may develop - prevented by glucocorticoid

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15
Q

Theophylline

A

xanthine (constituent of coffee & tea)
mechanism still unclear
Phosphodiesterase (PDE) inhibitor

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16
Q

Theophylline use

A

second line drug (sustained-release tablet)
used with steroid when asthma response to b2 agonist inadequate
given i.v. in acute severe asthma

Unwanted effects
CNS: stimulant (tremor, sleep disturbance)
Cardiovascular (stimulate heart, vasodilation)
GI tract (anorexia, nausea, vomiting)

17
Q

Muscarinic receptor antagonists

A

main drug used – ipratropium
adjunct to b2 agonists and steroid when these are insufficient
max effect in 30 min, lasts 3-5 hours
given by aerosol inhalation
poorly absorbed into systemic circulation
Few unwanted effects
Safe, well tolerated

18
Q

Actions of muscarinic antagonists

A

relax bronchial smooth muscle
bronchodilation
inhibit elevated mucus secretion in asthma
may increase clearance of bronchial secretions

same mechanism for each effect
block action of endogenous acetylcholine at muscarinic receptors

19
Q

Muscarinic system in airways

A

Low levels of Ach released from cholinergic nerves in airways
few muscarinic receptors activated
smooth muscle relaxed
airways open

20
Q

Muscarinic system in asthma

A

Evidence for increased Ach release
Muscarinic receptors activated
Smooth muscle contracted
Narrowed airways

21
Q

Leukotriene receptor antagonists

A

Examples
Montelucast (1x daily)
Zafirlukast (2x daily)
given orally
prevent exercise-induced and aspirin sensitive asthma
action additive with b2 agonists
main use as add on for uncontrolled, mild-moderate asthma

22
Q

Actions of leukotriene antagonists

A 
act at cysteinyl-leukotriene receptors
on bronchiole smooth muscle cells
prevent actions of LTC4, LTD4, which are
 bronchial spasmogens
 stimulate mucus secretion

Unwanted actions – few
Headache, GI disturbance

23
Q

Anti-inflamatory drugs

A 
glucocorticoids are main drugs
beclometasone diproprionate
budesonide
fluticasone propionate
occassionally prednisolone or hydrocortisone

usually given by inhalation
metered dose inhaler
localises effect in lung

full effect takes several days to develop

24
Q

Actions of glucocorticoids

A

reduce production of
cytokines
spasmogens (LTC4, LTD4)
leucocyte chemotaxins (LTB4, PAF)

therefore reduce
bronchospasm
recruitment & activation of inflammatory cells

25
Q

Mechanism of glucocorticoid action

A

Enter cells
bind to intracellular receptors in cytoplasm
GRa, GRb
receptor complex moves to nucleus
binds to DNA in nucleus
alters gene transcription
e.g. induction of lipocortin, repression of IL-3

26
Q

Clinical use of glucocorticoids

A

for patients requiring regular bronchodilators to control attacks
give inhaled steroid, with additional agent for severe asthma
e.g. budesonide + b2 agonist or theophylline
i.v. hydrocortisone + oral prednisolone for acute exacerbations
short course oral prednisolone if deterioration
prolonged oral predisolone needed for a few patients

27
Q

Unwanted effects of glucocorticoids

A 
Adverse effects uncommon with inhaled steroids
oropharyngeal thrush & dysphonia
minimised by using “spacer” devices
reduce oropharyngeal drug deposition
increase airways drug deposition
Oral/ regular large doses – serious effects
e.g. adrenal suppression
patients carry ‘steroid card’
28
Q

Cromoglicate

A 
Related drug - nedocromil sodium
Can reduce both early and late phase responses
Reduce bronchial hyper-reactivity
Effective in asthma caused by 
antigen, exercise, irritants
Not all asthmatics respond
unpredictable
children respond better than adults
29
Q

Cromoglicate mechanisms

A

Not fully understood
Mast cell stabiliser (but not main action)
may
reduce neuronal reflexes (desensitise to irritants)
inhibit release of T-cell cytokines
affect inflammatory cells and mediators
Unwanted effects – few
irritation of upper respiratory tract
hypersensitivity reactions reported, but rare

30
Q

Clinical use of cromoglicate

A 
Given by inhalation
by aerosol, nebulised solution or powder
Prophylactic use
to prevent both phases of attack
most effective in children
effects may take weeks to develop
31
Q

Biologic agents

A

A new development
omalizumab (Xolair)
recombinant DNA-derived humanized IgG1 monoclonal antibody

sub cutaneous injection every 2-3 weeks
absorbed slowly
peak plasma concentration in 7-8 days

32
Q

Omalizumab mechanism

A

binds to human IgE
inhibits binding of IgE to IgE receptor (Fc RI) on the surface of mast cells and basophils
inhibits IgE-mediated cascade of asthma

33
Q

Unwanted effects of omalizumab

A

Few, but can be severe
anaphylaxis – allergic reaction to protein
malignancies (slightly higher rate than normal)

34
Q

Treatment of chronic asthma

A 
Mild asthmatic with rare attacks
Inhaled b2 agonist when required
Mild asthma with more frequent attacks 
 glucocorticoid for prophylaxis
 b2 agonist when needed for acute attack
Moderate to severe asthma
 drug combination preferred, usually
 b2 agonist with glucocorticoid
 in combined inhaler
Other drugs added when this approach fails to control attacks

Applied Pharmacology for Nurses (14 decks)

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