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Y2 Pharmacology > Pharmacology of asthma > Flashcards

Pharmacology of asthma Flashcards

1
Q

what are the five options for drug treatment of asthma

A

salbutamol, fluticasone, mometasone, budesonide, montelukast

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2
Q

primary mechanism of action of salbutamol

A

Agonist at the β2 receptor on airway smooth muscle cells. Activation reduces Ca2+ entry and this prevents smooth muscle contraction

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3
Q

drug target of salbutamol

A

Beta 2 (β2) adrenergic receptor

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4
Q

main side effects of salbutamol

A

Palpitations/ agitation
Tachycardia/ Arrythmias
Hypokalaemia (at higher doses)

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5
Q

what class of drug does salbutamol belong to

A

SABA, short acting beta agonist
half life is 2.5-5h

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6
Q

why are cardiac effects seen with salbutamol use

A

bc beta 2 selectivity is not absolute
there are beta 1 receptors in the heart which also get activated

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7
Q

why does hypokalaemia occur with salbutamol use

A

can be caused via effect of sodium potassium ATPase
this effect can be exacerbated by co administration with corticosteroids

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8
Q

primary mechanism of action of fluticasone

A

Very powerful drugs. Multiple actions on many different cell types. Fluticasone directly decreases inflammatory cells such as eosinophils, monocytes, mast cells, macrophages, and dendritic cells. It reduces the number of these cells and also the number of cytokines they produce

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9
Q

drug target of fluticasone

A

glucocorticoid receptor

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10
Q

side effects of fluticasone

A

Local side effects:
Sore throat, hoarse voice, opportunistic oral infections

Systemic side effects:
Growth retardation in children
Hyperglycaemia
Decreased bone mineral density
Immunosuppression
Effects on mood
(Many others)

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11
Q

which has greater affinity to glucocorticoid receptor, cortisol or fluticasone and mometasone

A

fluticasone and mometasone both have higher affinity than cortisol

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12
Q

what is the oral bioavailability of fluticasone and mometasone and what does this then mean

A

less than 1% so systemic delivery via inhaled route is mainly through the pulmonary vasculature

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13
Q

mechanism of action of mometasone

A

Very powerful drugs. Multiple actions on many different cell types. Mometasone directly decreases inflammatory cells such as eosinophils, monocytes, mast cells, macrophages, and dendritic cells. It reduces the number of these cells and also the number of cytokines they produce

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14
Q

drug target of mometasone

A

glucocorticoid receptor

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15
Q

side effects of mometasone

A

Local side effects:
Sore throat, hoarse voice, opportunistic oral infections

Systemic side effects:
Growth retardation in children
Hyperglycaemia
Decreased bone mineral density
Immunosuppression
Effects on mood
(Many others)

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16
Q

mechanism of action of budesonide

A

Very powerful drugs. Multiple actions on many different cell types. Budesonide directly decreases inflammatory cells such as eosinophils, monocytes, mast cells, macrophages, and dendritic cells. It reduces the number of these cells and also the number of cytokines they produce

17
Q

drug target of budesonide

A

glucocorticoid receptor

18
Q

side effects of budesonide

A

Local side effects:
Hoarse voice, opportunistic oral infections

Systemic side effects:
Growth retardation in children
Hyperglycaemia
Decreased bone mineral density
Immunosuppression
Effects on mood
(Many others)

19
Q

what is the oral bioavailability of budesonide and what does this then mean

A

over 10%
so inhaled budesonide will still result in some systemic absorption through GIT

20
Q

which is least potent out of fluticasone, mometasone, budesonide

A

budesonide

21
Q

mechanism of action of montelukast

A

Antagonism of CysLT1 leukotriene receptor on eosinophils, mast cells and airway smooth muscle cells decreases eosinophil migration, broncho-constriction and inflammation induced oedema

22
Q

drug target of montelukast

A

CysLT1 leukotriene receptor

23
Q

side effects of montelukast

A

Mild side effects:
Diarrhoea
Fever
Headaches
Nausea or vomiting

Serious side effects:
Mood changes
Anaphylaxis

24
Q

what do you do for prophylaxis of exercise-induced bronchoconstriction in asthma patients

A

montelukast should be administered at least 2 hours before initiating exercise

25
Q

normally what are therapeutic objectives of asthma patients

A

Short term = Relief Relieve symptoms of breathlessness and expiratory wheeze during the acute asthma attack

Long term = Prevention
Dampen/prevent the late phase of the asthma attack
Reduce the risk of further asthma attacks.
Attempt to improve lung function

26
Q

why inhaled administration of salbutamol preferred over oral

A

bc of the local versus systemic effect each route has

27
Q

why is a nebulizer the best method for delivering salbutamol in an emergency situation

A

many drug solutions, can deliver combinations, minimal patient cooperation required, can deliver to all patient ages, conc and dose can be modified, normal breathing pattern

28
Q

evidence says only 20% of inhaled dose of salbutamol penetrates deep enough into lungs to influence lung function so what happens to the other 80%

A

various points on loss of drug
loss 1 = exhaled loss
loss 2 = absorption from lungs, it should remain in lungs to produce an effect
loss 3 = mucociliary clearance
loss 4 = some will go down to GIT instead of airways
loss 5 = some will be absorbed across mucous membrane in the oral cavity and pharynx

29
Q

how do you use a spacer and what is the benefit

A

load spacer with drug and after that you breathe in, without spacer you release the drug and immediately breathe in which is not easy to do
with the spacer you are more likely to inhale more of the drug

30
Q

how do viruses exacerbate asthma

A

viruses pollutants and allergens release mediators that activate eosinophils (IL5)
this recruits eosinophils which cause airway injury vie bronchoconstriction, airway edema, mucus hypersecretion, epitheliam damage and airway remodelling

31
Q

what is the vicious cycle in asthma

A

viruses cause eosinophil inflammation which causes epithelial damage which then makes you more susceptible to viruses

32
Q

why is there less than 1% of fluticasone that reaches plasma vie GIT when a significant portion of inhaled is actually swallowed

A

they are absorbed from the gut and go to the liver where there is first pass inactivation of the drug

33
Q

why is montelukast particularly useful for NSAID (non steroidal anti inflammatory drug) induced asthma

A

bc NSAIDs block the cyclooxygenase which is an enzyme that works on arachidonic acid
so instead the arachidonic acid makes leukotrienes via lipoxygenase and monetlukast acts on these leukotrienes

Y2 Pharmacology (8 decks)

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