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BRS YR2 > Pharmacology of Asthma > Flashcards

Pharmacology of Asthma Flashcards

1
Q

What is the primary mechanism of action of Salbutamol?

A

Agonist at the Beta 2 receptor on airway smooth muscle cells. Activation reduces Ca2+ entry, preventing smooth muscle contraction.

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2
Q

What is the drug target of Salbutamol?

A

Beta 2 adrenergic receptor

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3
Q

What are the main side effects of Salbutamol?

A
  • palpitations
  • agitation
  • tachycardia
  • arrhythmias
  • hypokalaemia (at higher doses)
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4
Q

What is the main classification of salbutamol?

A
  • SABA (short acting beta agonist)

- half life of 2.5-5 hours

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5
Q

How selective is salbutamol?

A
  • not absolute
  • cardiac (beta 1) effects can be seen
  • hypokalaemia caused by an effect on. Na/KATPase
    (effect worsened with corticosteroids)
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6
Q

What is the primary mechanism of action of Fluticasone?

A
  • powerful
  • multiple actions, on different cell types
  • directly decreases inflammatory cells (eosinophils, monocytes, mast cells, macrophages and dendritic cells) and the cytokines that they produce.
    (inhibits IL5)
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7
Q

What is the primary drug target of Fluticasone?

A

Glucocorticoid receptor (in eosinophils)

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8
Q

What are the local side effects of Fluticasone?

A
  • sore throat
  • hoarse voice
  • opportunistic oral infections
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9
Q

What are the systemic side effects of Fluticasone?

A
  • growth retardation in children
  • hyperglycaemia
  • decreased bone mineral density
  • Immunosuppression
  • effect on mood
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10
Q

Why is Fluticasone effective?

A

Has a higher affinity for the glucocorticoid receptor in comparison to cortisol

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11
Q

What is the mode of delivery of Fluticasone?

A

oral bioavailability <1%

systemic delivery via the inhaled route is through pulmonary vasculature

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12
Q

What is the primary mechanism of Mometasone?

A
  • powerful
  • multiple actions on different cell types
  • directly decreases inflammatory cells (eosinophils, monocytes, mast cells, macrophages, and dendritic cells) and the cytokines they produce.
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13
Q

What is the primary target of Mometasone?

A

Glucocorticoid receptor

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14
Q

What are the local side effects of Mometasone?

A
  • sore throat
  • hoarse voice
  • opportunistic oral infections
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15
Q

What are the systemic side effects of Mometasone?

A
  • growth retardation in children
  • hyperglycaemia
  • decreased bone mineral density
  • immunosuppression
  • effects on mood
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16
Q

Why is Mometasone effective?

A

greater affinity for the glucocorticoid receptor in comparison of cortisol.

17
Q

What is the mode of delivery of Mometasone?

A

oral bioavailability of <1%, due to excretion be the liver (therefore not a LT option, and WILL cause liver damage)
systemic delivery via inhalation is through pulmonary vasculature

18
Q

What is the primary mechanism of action of Budesonide?

A
  • powerful
  • multiple actions on different cell types
  • directly decreases inflammatory cells
    (eosinophils, monocytes, macrophages and dendritic cells) and the cytokines they produce.
19
Q

What is the primary drug target of Budesonide?

A

Glucocorticoid receptor

20
Q

What are the local side effects of Budesonide?

A
  • hoarse voice

- opportunistic oral infections

21
Q

What are the systemic side effects of Budesonide?

A
  • growth retardation in children
  • hyperglycaemia
  • decreased bone mineral density
  • immunosuppression
  • effects on mood
22
Q

How effective is Budesonide?

A

less potent than Fluticasone and Mometasone

23
Q

What is the mode of delivery of Budesonide?

A

oral bioavailability <10%

inhaled Budesonide results in systemic absorption through the GI tract

24
Q

What is the primary 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

25
Q

What is the primary drug target of Montelukast?

A

CysLT1 leukotriene receptor

26
Q

What are the mild side effects of Montelukast?

A
  • diarrhoea
  • fever
  • headaches
  • nausea
  • vomiting
27
Q

What are the serious side effects of Montelukast?

A
  • mood changes

- anaphylaxis

28
Q

When should Montelukast be administered to prevent exercise-induced bronchoconstriction?

A

at least 2 hours before initiating exercise

29
Q

When is an asthma case NOT considered urgent?

A
  • no previous history of hospitalisation
  • normal physical examinations
  • not unconscious or drowsy
  • able to speak
30
Q

What is the short term therapeutic objective when treating an asthma?

A

Relief

- reduce symptoms of breathlessness and expiratory wheeze during an acute attack

31
Q

What is the long term therapeutic objective when treating an asthma?

A

Prevention

  • dampen/prevent the late phase of an attack
  • reduce the risk of further attacks
  • attempt to improve asthma attacks
32
Q

What is the first line treatment for children <5 with suspected asthma?

A

offer SABA, reliever therapy

- symptom relief and all maintenance therapy

33
Q

Why is inhalation the preferred administration route of Salbutamol?

A
  • lower inhaled dose
  • direct delivery to tissues (instead of systemic)
  • fewer side effects
34
Q

What is the advantages of using inhalation to administrate drugs?

A
  • minimal patient co-operation required
  • all ages
  • normal breathing pattern
  • concentration and dose can be modified
  • can deliver combinations of different drugs
35
Q

Why is only 20% of inhaled salbutamol actually impacting the lungs?

A
  • poor inhalation technique
  • absorbed in the oesophagus, can cause a yeast infection due to inhaled steroids
  • absorbed in the blood and straight to the heart (quick access to the bloodstream)
36
Q

How do NSAIDs induce asthma?

A

prevents the conversion of arachidonic acid to prostaglandins (via cyclooxygenase) by inhibition cycloosygenase. Therefore increased luekotrines are produced leading to more inflammation and more bronchospasms.

BRS YR2 (70 decks)

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