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pharmacology 2 > asthma > Flashcards

asthma Flashcards

1
Q

what is asthma?

A

an condition associated with: airway hyperresponsiveness reversible airflow limitation bronchial inflammation

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2
Q

what are the symptoms of asthma?

A

wheezing shortness of breath cough worse at night

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3
Q

what are the triggers for asthma?

A

intrinsic- emotion, diet, cold air/ exercise

extrinsic - exposure to allergens drugs (asiprin, beta blockers), pollutants (cigerette smoke, dust, fumes)

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4
Q

what are the long term aims of asthma treatment?

A

abolish symptoms maintain optimal lung function prevent permenant lung damage prevent death from acute attack avoid unnecessary side effects

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5
Q

what are the differences between reliever and preventer medication for asthma?

A

reliever - bronchodilator → relax smooth muscle / widens airway (works rapidly and directly to reverse bronchoconstriction)preventer - anti-inflammatory → stops response to allergen

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6
Q

name four types of bronchodilators used in asthma

A

beta 2 adrenergeric receptor agonists
theophylline
muscarinic receptor anatagonists
leukotriene receptor antagonists

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7
Q

give three examples of preventer medication used in asthma

A

beclometasone sodium cromoglicate montelukast

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8
Q

which target is most appropriate to treating asthma?

A

ß2 receptors as these are found in: lungs blood vessels muscle spindles

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9
Q

what does salbutamol have a similar structure to?

A

adrenaline

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10
Q

how can ß2 adrenergic receptor agonists be given?

A

inhaled or orally

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11
Q

name two short acting ß2 adrenergic receptor agonists and explain when they would be given

A

salbutamol

terbutaline*inhaled beefore exertion to reduce exercise induced asthma - duration of action 3-5hrs

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12
Q

name two long-acting ß2 adrenergic receptor agonists and explain when they would be given

A

salmeterol

formoterol* only used in patients taking inhaled steriods - can be taken 1-2 times daily - duration of actio 12hrs

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13
Q

what are the side effects of ß2 adrenergic receptor agonists? explain why these occur

A

tremor - ß2 receptors in muscles activated increased HR - stimulation of cells in SA node reduced K+ (hypokalaemia) - stimulation of sodium/potassium pump nervous tension/ headache - activation of ß2 receptors in CNS

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14
Q

how can the systemic effects of ß2 adrenergic receptor agonists be reduced?

A

by inhaling drug

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15
Q

when would a glucocorticosteroid be used in asthma?

A

as a preventer

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16
Q

name five glucovorticosteroids that are used via an inhaler to prevent asthma attacks

A 
beclomethasone diproprionate
budesonside
fluticasone propionate
prednisolone
hydrocortisone
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17
Q

why are the systemic effects of inhaled glucocorticosteroids reduced?

A

poor bioavailablity

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18
Q

what can glucocorticosteroids often be administered in combination with?

A

ß2 adrenergic receptor agonists

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19
Q

describe the activation of ß2 adrenoceptors

A

ß2 adrenergic receptor agonists bind to ß2 receptor causing a conformational change to the molecule. This change in shape converts ATP to cAMP which activates PKA and muscle relaxation

20
Q

describe the actions of glucocorticoids in asthma

A

reduces production of:
cytokines, spasmogens (LTC4, LTD4), leuocyte chemotaxins (LTB4, PAF)
therefore reduces:
bronchospasm, recruitment and activation of inflammatory cells

21
Q

explain the mechanism of action of glucocorticosteroids (GCs)

A

GCs are synthesised from cholesterol allowing them to cross cell membrane
when inside the cell GCs bind to steroid receptors
the drug-receptor complex forms a dimer which can cross into nucleus
in nucleus the dimer binds to specific DNA sequence inducing or supressing genes
protein production influenced
GCs inhibit transcription of COX-2 gene - reducing protein production and inflammation

22
Q

what are the side effects of glucocorticosteroids?

A

local immunosuppression - oral thrush local effects on vocal cords - dysphonia (hoarseness)

23
Q

what is prednisolone used forn and how does it work?

A

treats acute asthma attack short course - 7 days (high dose) continue with high dose inhaled steroid in chronic/severe asthma
works by: suppressing immune system activity and release of inflammatory mediators

24
Q

explain the danger of stopping glucocorticosteroids abruptly

A

results in acute adrenal insuffiency as patients ability to synthesise GCs has been suppressed → leads to patient being unable to maintain a stress response leading to addisonian crisis

25
Q

what are antimuscarinic receptor antagonists and what are they used for?

A 
short acting (reliever) - 3-5hrs	
used alonside high-dose inhaled glucocorticosteroids for severe asthma
26
Q

what is the mechanism of action for antimuscarinic receptor antagonists?

A

block muscarinic receptors → blocks action of endogenous acetylcholine
inhibits elevated mucus secretion

27
Q

given an example of an antimuscarinic receptor antagonists and explain its side effects

A

ipratropium - causes dry mouth and precipitates glaucoma

28
Q

what are cromoglicates and how do they work?

A

cromones inhibit release of chemicals from inflammatory cells(mast cells) → prevents bronchospasm reduces allergen induced responses and bronchospasm during/after exercise
stops mast cell degranulation

29
Q

name 2 cromoglicates

A

nedocromil sodium sodium cromoglicate

* stops mass cells releasing histamine and other chemicals - mainly used in children

30
Q

what do leukotrienes cause?

A

bronchoconstriction release of inflammatory cells increase in secretions in airways

31
Q

what do leukotriene receptors antagonists do?

A

relax airways and prevent inflammation

32
Q

give two examples of leukotriene receptor antagonists and explain side effects

A

montelukast
zafirlukast*
causes GI disturbance

33
Q

when is theophylline (aminophylline) used?

A

orally or IV in patients with persistant symptoms / severe acute asthma

34
Q

can theophylline be used with other drugs?

A

yes - ß agonists and/or steroids

35
Q

what are the drawbacks and side effects of theophylline?

A

drawbacks: narrow therapetic windowside effects: increased HR, palpitations, convulsions, headache

36
Q

explain the mechanism of action of theophylline

A

blocks phosphodiesterase enzyme (PDE) which breaksdown into 5’AMP - therefore more cAMP is available to stimulate smooth muscle relaxation

37
Q

what is omalizumab (xolair) used for and how it given?

A

an antibody (given subcutaneously) every 2-4 weeks reduces effect of allergen induced reactions used in adults with severe allergic asthma not controlled by ß agonists and glucocorticosteroids

38
Q

what are the side effects of omalizumab?

A

bruising pain on injection small risk of anaphylaxis

39
Q

what is the mechanism of action of omalizumab?

A

antibody inhibits binding of IgE to receptor surface of mast cell and basophils prevents release of pro-inflammatory mediators and reduces allergen induced airway reactions

40
Q

describe the treatment strategy for asthma from mild to severe

A

inhaled short acting ß2 agonists (as needed)
inhaled steroids
add inhaled long acting ß2 agonists and increase dose ofinhaled steroids
short and long acting ß2 agonists and inhaled steroids and another drug (eg. LTR antagonist)
continuous or frequent use of oral steriods (and immunosuppressants

41
Q

what can be substituted for inhaledß2 agonists in stage 1 of the asthma treatment strategy?

A

ipratropium
oral ß agonists
theophyllines

42
Q

describe what therapy would be given in acute asthma attack

A

bronchodilators given via nebuliser glucocorticosteroids given (oral prednislone, IV hydrocortisone) - route depends on severity oxygen therapy needed if O2 saturation reduced (
in poor response aminophylline injection (severe, acute attacks)

43
Q

what are the side effects of cromoglicates?

A

irritation of upper resp. tract

hypersensitivity reactions

44
Q

what are the actions of leukotriene antagonists?

A

act on cystrinyl-leukotriene receptors

prevent actions of LTC4, LTD4 (which are brochial spasmogens and stimulate mucus secretion)

45
Q

what are the side effects of leukotriene antagonists?

A

headache

GI disturbance

46
Q

when would antimuscarinic receptor antagonists be used?

A

in asthma where there is evidence of overactive Ach production

47
Q

describe the muscarinic system in normal airways and in some asthma airways

A

normal - Ach released from cholinergic nerves, few muscarinic receptors activated , smooth muscle relaxed airways open
asthma - Ach more active so more muscarinic receptors activated which causes contraction of smooth muscle

pharmacology 2 (11 decks)

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