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Pharmacology > Asthma treatments > Flashcards

Asthma treatments Flashcards

1
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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2
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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3
Q

Aim of drug treatment

A

to reduce inflammation, prevent bronchoconstriction and restore airways calibre to normal

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4
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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5
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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6
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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7
Q

IgE

A

Immunoglobulin E (IgE) is a type of antibody that is present in minute amounts in the body but plays a major role in allergic diseases. IgE binds to allergens and triggers the release of substances from mast cells that can cause inflammation. When IgE binds to mast cells, a cascade of allergic reaction can begin.

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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

beta2 adrenergic receptor agonists
theophylline
muscarinic receptor antagonists
leukotriene receptor antagonists

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11
Q

beta2 adrenergic receptor agonists

A

Direct action on beta2 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

beta2 adrenergic receptor agonists - short acting

A

Short acting
salbutamol, terbutaline
Max effect within 30 min, last 4-6 hours
Used “as needed” to control symptoms

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13
Q

beta2 adrenergic receptor agonists - longer acting

A

Longer acting
salmeterol
duration of action 12 hours
twice daily dose in patients not controlled with glucocorticoids

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14
Q

Administration of beta2 agonists

A

By inhalation
to target action in lung
& minimise systemic effects

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15
Q

Unwanted effects of beta2 agonists

A

result from absorption into systemic circulation
most common is tremor
some tolerance to beta2 agonists may develop - prevented by glucocorticoid

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16
Q

Theophylline

A

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

17
Q

PDE

A

Phosphodiesterase

18
Q

Theophylline uses

A

second line drug (sustained-release tablet)
used with steroid when asthma response to beta2 agonist inadequate
given i.v. in acute severe asthma

19
Q

Theophylline unwanted effects

A

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

20
Q

Muscarinic receptor antagonists

A

main drug used – ipratropium
adjunct to beta2 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

21
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

22
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

23
Q

Muscarinic system in asthma

A

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

24
Q

Leukotriene receptor antagonists

A

Examples
Montelucast (1x daily)
Zafirlukast (2x daily)
given orally
prevent exercise-induced and aspirin sensitive asthma
action additive with beta2 agonists
main use as add on for uncontrolled, mild-moderate asthma

25
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

26
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
27
Q

Actions of glucocorticoids

A

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

therefore reduce
bronchospasm
recruitment & activation of inflammatory cells

28
Q

Mechanism of glucocorticoid action

A

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

29
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

30
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’
31
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
32
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

33
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
34
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

35
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

36
Q

Unwanted effects of omalizumab

A

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

37
Q

Treatment of chronic asthma

A 
Mild asthmatic with rare attacks
Inhaled beta2 agonist when required
Mild asthma with more frequent attacks 
 glucocorticoid for prophylaxis
 beta2 agonist when needed for acute attack
Moderate to severe asthma
 drug combination preferred, usually
 beta2 agonist with glucocorticoid
 in combined inhaler
Other drugs added when this approach fails to control attacks

Pharmacology (13 decks)

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