Pharmacology of Asthma Flashcards

(36 cards)

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?

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?

25
What are systemic side effects of fluticasone?
``` Growth retardation Hyperglycaemia Decreased bone mineral density Immunosuppression Effects on mood ```
26
What are the local side effects of fluticasone?
Sore throat Hoarse voice Opportunistic oral infections
27
Out of fluticasone and cortisol, which has the higher affinity for glucocorticoid receptors?
Fluticasone
28
What is important to remember about the administration of montelukast?
It should be administered at least 2 hours before exercise
29
How does salbutamol work?
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
What are the main side effects of salbutamol?
``` Palpitations Agitation Tachycardia Arrhythmia Hypokalaemia (at higher doses) ```
31
How long acting is salbutamol? What is its half life?
Its short acting, has a half life of 2.5-5hrs
32
What is the selectivity of salbutamol like?
Not highly selective so cardiac side effects can be seen
33
How does salbutamol cause hypokalemia?
Via affecting sodium potassium ATPase
34
What drugs exacerbate side effects of salbutamol? Which side effect specifically do they exacerbate?
Corticosteroids, they increase the hypokaelmic effects of salbutamol
35
Describe the pharmacology of mometasone
Same as fluticasone
36
Describe the pharmacology of budesonide
Same as fluticasone, its oral bioavailability is higher (>10%) but it is less potent