Pharma 6.2 Pharmacology of Airway Control Flashcards Preview

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Flashcards in Pharma 6.2 Pharmacology of Airway Control Deck (17)
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1
Q

Describe the pathophysiology of asthma

A

Can be divided into immediate and late phase.

Immediate phase - allergen causes interaction of mast cells with IgE. Results in release of histamine and bronchospasm.

Late phase - Leukocytes enter area. Results in exacerbation of bronchospasming, thickening of basement membrane, oedema, and mucus production. Epithelial damage leads to increased exposure of the sensory irritant receptors, vicious cycle.

2
Q

What receptors do asthma drugs act on in the airways? What are the effects?

A

beta 2 receptors - bronchodilation, reduced histamine release, increased mucociliary clearance

M3 receptors

3
Q

Explain the 5 step asthma control

A
  • Step 1: Inhaled short-acting β2-agonist when required
  • Step 2: Addition of inhaled steroids (200-800mg a day)
  • Step 3: Addition of inhaled long acting β2-agonist (LABA)
  • Step 4: Increase inhaled steroid levels or addition of fourth drug (i.e. leukotriene receptor antagonist, theophylline, or oral β2-agonist tablet)
  • Step 5: Addition of oral steroid tablet or Anti-IgE therapy

Once asthma controlled, stepping down is recommended.

4
Q

Explain how bronchodilators work.

A
  • Bind to beta 2 receptors
  • Results in increased cAMP and reduction of intracellular calcium, which reduces muscle contractions.
  • Also increases calcium activated potassium currents, hyperpolarising muscle cells further
5
Q

Name the bronchodilators

A
6
Q

What are the ADRs of bronchodilators?

A

Systemic adrenergic effects - tachycardia, palpitations, tremors

Which is why they are preferentially given inhaled not orally

7
Q

What is the main DDI of bronchodilators?

A

beta antagonists e.g propanolol

8
Q

How do corticosteroids exert their anti-inflammatory effects?

A

Transactivation - Suppress gene transcription in inflammatory cells

Transrepression - Represses the inflammatory responses seen

Induces apoptosis in inflammatory cells and reduces number of mast cells in respiratory mucosa. Corticosteroids work better with eosinophilic asthma

9
Q

What are the 2 types of asthma?

A

eosinophilic and non eosinophilic

10
Q

Why might a combined inhaler be preferable to non combined? What is a combined inhaler?

A

Combined inhaler - contains LABA and glucocorticoids e.g. symbicort.

Ease of use, good compliance, cheaper, safer

11
Q

How do leukotriene receptor antagonists work?

A

LTC released from mast cells and eosinophils to induce bronchoconstriction, mucus secretion, oedema and inflammation. LRA therefore inhibits.

12
Q

How do anticholinergics work?

A

Muscarinic receptor antagonists. Bind to and block M3 receptors preventing bronchoconstriction and mucus secretion

13
Q

When would anticholinergic be used?

A

Used to augment beta 2 agonists or where beta 2 agonist action is contraindicated e.g. IHD

14
Q

Give 2 examples of methylanthines

A

theophylline and aminophylline

15
Q

How do methylanthines work?

A

antagonising adenosine receptors.

16
Q

Why is methylanthines not used more often?

A

ADRs too high and narrow therapeutic window

17
Q

What are the ADRs of methylanthines?

A

psychomotor agitation and tachycardia.