Acute Asthma Pharmacology 1 Flashcards

1
Q

What factors would lead to a diagnosis of severe asthma?

A
  1. Previous near fatal asthma
  2. Previous admission for asthma
  3. Requiring three or more classes of asthma medication
  4. Heavy use of B2 agonist
  5. Repeated attendances at A&E in the last year
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2
Q

Brief pathophys of asthma (4)

A
  • Airways tighten
  • Smooth muscle contraction
  • Associated inflammation
  • Thickening airway walls
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3
Q

What do we want to achieve from asthma treatment?

A
  1. Relaxation of smooth muscle

- increases airway diameter

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4
Q

How can we reduce the constriction of the bronchial wall smooth muscle?

A

Activation of the B2 adrenoreceptor.

  • G protein coupled receptor
  • increases cyclic AMP formation
  • enhances Ca2+ binding
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5
Q

What are adrenoreceptors?

A

Receptors in organs and tissues that are stimulated by the sympathetic nervous system.

Catecholamines will bind.

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6
Q

Examples of catecholamines

A

Adrenaline
Noradrenaline
Dopamine
Salbutamol

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7
Q

A1 Adrenoreceptor found (3)

A
  1. Acts on vascular smooth muscle.
  2. Pupil
  3. Pilomotor smooth muscle
    - attached to hair follicles
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8
Q

A1 Adrenoreceptor action

A
  • Vascular smooth muscle contraction.
  • Pupil dilation
  • Goosebumps
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9
Q

B1 adrenoreceptor found

A

Acts on heart

- stimulates rate and force

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10
Q

B2 adrenoreceptor found

A

Respiratory tissue

Somatic motor (voluntary muscle)

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11
Q

Roles of B2 adrenoreceptor

A

Bronchodilation

Tremors

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12
Q

Dopamine adrenoreceptors found…

A

Renal tissue

- relaxes arteries

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13
Q

Noradrenaline (4)

A
  • Predominantly alpha agonist.
  • Causes vasoconstriction.
  • Increases systolic and diastolic pressure.
  • Reflex bradycardia.
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14
Q

Isoprenaline (3)

A

B agonist.

Vasodilator.

Strongly increases cardiac force and rate.

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15
Q

Reasons why inhaled beta 2 agonist is not working

A

Patient has very severe asthma, cannot move air into their lungs.

Asthma resistant to drug.

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16
Q

Peripheral resistance

A

How shut down small vessels in legs and arms are

17
Q

Describe some corticosteroid induced changes in inflammatory cells?

A
  • Eosinophil numbers decrease.
  • Decrease of cytokine release from T-cells.
  • Mast cell numbers decrease.
  • Decrease cytokine release from macrophage
  • Decrease in numbers of dendritic cell
18
Q

Corticosteroid induced changes in structural cells

A
  • Decrease in cytokine mediator release from epithelial cells
  • Endothelial cells leak
  • Increase B2 receptor
  • Decreased mucus secretion
19
Q

How do corticosteroids act?

A
  1. Altering transcription of proteins.
  2. Has to go through cell wall.
  3. Binds to soluble glucocorticoid receptors in cytoplasm.
  4. Then transported into nucleus.
    - –> bind to nuclear receptor
    - –> affects transcription and translation
    - –> alters protein
    - –> causes effect
20
Q

Why is it important to give corticosteroids immediately when patient is admitted into hospital?

A

Corticosteroids take time to work!

Even IV hydrocortisone - C-max, top concentration , will still take 6 hrs to see effect

21
Q

State some examples of drugs commonly prescribed in asthma

A

Betamethasone
Dexamethasone
Pregnisolone

22
Q

Describe number of Beta 2 receptors throughout life

A

Babies under 1 y/o will have fewer b2 receptors.

B2 receptors are not evenly expressed throughout life.

23
Q

Describe Ipratropium bromide?

A
Parasympathetic antagonist (anti-cholingeric) 
- combined with beta-2-agonist, produces increased bronchodilation 

Deliver via a nebuliser

24
Q

If nebulised bronchodilator treatment has not helped what might we use?

A

IV magnesium sulphate.

DO NOT USE NEBULISED

25
Q

What are other IV options available is nebulised bronchodilator has not worked?

A

IV salbutamol
IV aminophylline
- v.toxic tho

26
Q

Describe the mechanism by which magnesium sulfate produces smooth muscle relaxation

A
  • Thought to enhance Ca2+ uptake in SR.
  • Mg co-factor regulating no. enzymatic and cellular activities in body.
  • Regulates adenyl cyclase, Na/K ATP-ase