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BRS Y2 > Pharmacology of Asthma > Flashcards

Pharmacology of Asthma Flashcards

1
Q

How is asthma generally diagnosed? When can this be a problem?

A

Via spirometry, can’t be done in children

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2
Q

What are the 2 components of an asthma attack?

A 
Acute phase (bronchoconstriction and breathlessness)
Late phase (inflammation exacerbates asthma)
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3
Q

What are some advantages of using nebulisers?

A

You can completely control the dose and concentration of the drugs you are giving
You can give multiple medications at a time
You can control what they breath and guarantee its all being delivered to them

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4
Q

What is the target of beta 2 agonists?

A

Beta 2 receptor

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5
Q

What is the location where beta 2 agonists work?

A

Bronchus

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6
Q

What is the effect of beta 2 agonists?

A

They decrease calcium entry and cause relaxation of smooth muscle

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7
Q

What hormone do beta 2 agonists mimic?

A

Adrenaline

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8
Q

What are the 2 main ways drugs for asthma can be administered?

A

Inhaled

Orally ingested

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9
Q

Out of inhaled and oral medicine, which is more effective?

A

Inhaled as it directly reaches the lung and doesn’t have to go into the blood and then the lungs

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10
Q

Why is local management always better?

A

The drug goes directly to the target so you have to give less and there is less chance of side effects

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11
Q

How much inhaled salbutamol actually reached the lungs and why?

A

20%
Most is swallowed
Some is exhaled
Some is absorbed into the blood

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12
Q

Why do spacers increase the amount of salbutamol that reaches the lungs?

A

By stopping loss of drug by exhalation

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13
Q

What is the target of flucatisone?

A

Glucocorticoid receptor

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14
Q

What is the location where flucatisone works?

A

Eosinophils mainly and other inflammatory cells like mast cells, dendritic cells, macrophages

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15
Q

What is the effect of flucatisone?

A

It reduces interleukin 5 production causing eosinophil apoptosis so eosinophilic inflammation is reduced.
Generally reduces no of inflammatory cells and the no of cytokines they produce

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16
Q

Why is it unideal to give children glucocorticoids chronically? How is it recommended to give them instead?

A

They are steroids so are really powerful and can stump growth. Try to only give them when needed in exacerbations

17
Q

Why is bioavailability of orally ingested drugs usually very low?

A

They are metabolised by the liver before they enter systemic circulation

18
Q

What is the target of montelukast?

A

Leukotriene receptors, its an antagonist of CysT1 on eosinophils

19
Q

Where is the location where montelukast works?

A

Bronchus

20
Q

What is the effect of montelukast?

A

Inhibition of leukotriene receptors C4, D4 and E4. This results in bronchodilation as they are powerful brochoconstriction
Also decreases the migration of eosinophils

21
Q

Why are oral pills useful for children in asthma management?

A

They have higher adherence- the parents can easily monitor and make sure the child takes them

22
Q

What is the target of NSAIDs?

A

Cyclooxygenase

23
Q

Why may NSAIDs be harmful for asthmatics?

A

The blockage of cyclooxygenase means arachidonic acid is forced down the other path to form leukotrienes which cause bronchoconstriction

24
Q

What is the oral bioavailability of fluticasone?

A

1 %

25
Q

What are systemic side effects of fluticasone?

A 
Growth retardation
Hyperglycaemia
Decreased bone mineral density
Immunosuppression
Effects on mood
26
Q

What are the local side effects of fluticasone?

A

Sore throat
Hoarse voice
Opportunistic oral infections

27
Q

Out of fluticasone and cortisol, which has the higher affinity for glucocorticoid receptors?

A

Fluticasone

28
Q

What is important to remember about the administration of montelukast?

A

It should be administered at least 2 hours before exercise

29
Q

How does salbutamol work?

A

It is an agonist of the beta 2 adrenergic receptor, upon binding it reduces calcium influx so the muscle cant constrict and causes bronchodilation

30
Q

What are the main side effects of salbutamol?

A 
Palpitations
Agitation
Tachycardia
Arrhythmia
Hypokalaemia (at higher doses)
31
Q

How long acting is salbutamol? What is its half life?

A

Its short acting, has a half life of 2.5-5hrs

32
Q

What is the selectivity of salbutamol like?

A

Not highly selective so cardiac side effects can be seen

33
Q

How does salbutamol cause hypokalemia?

A

Via affecting sodium potassium ATPase

34
Q

What drugs exacerbate side effects of salbutamol? Which side effect specifically do they exacerbate?

A

Corticosteroids, they increase the hypokaelmic effects of salbutamol

35
Q

Describe the pharmacology of mometasone

A

Same as fluticasone

36
Q

Describe the pharmacology of budesonide

A

Same as fluticasone, its oral bioavailability is higher (>10%) but it is less potent

BRS Y2 (85 decks)

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