Lecture - Pharmacology (Bronchodilators)

Question 1

I know he told you not to worry about the doses but what should you know?

Answer 1

You should know that eg with asthma - you hv sliding scale. You increase doses within reason and consider using more than one drug when appropriate

Like dont just hv really high doses of beta agonist - wont solve the problem, might need more than one drug

Question 2

Just tell me the names (spell them correctly) of the beta-2 agonists you are going to need to know?

Answer 2

SABA: salcutamol

LABA: salmeterol

Question 3

So tha SABAs are known as the ‘relievers’ - why do they have to be selective beta-2 agonists?

Answer 3

Because if they are non-selective, they can go around and bind to eg beta-1 in the heart or other organs

So salbutamol is a selective b2 agonist that 200 fold selects for b2 than b1

Question 4

How do B2 agonists work:

1. What are the effects of B2 agonists and on which tissues?
   - there are 3 things it has effects on (two actually but LABAs have effect on the third)
2. Why do you get variabilties in pateint responses to the B2 agonists?

Question 5

Salbutamol

1. So this is a SABA - do you use it in asthma or COPD?
2. How do you take it in to counteract bronchospasm?
3. How long is the onset and the how long is te effect?
4. So when should you tell your pateint to use it?
5. Why use the lowest dose possible?
   - why not use frequently if it is so good?
6. Is it used for nocturnal asthma?
7. What are some of the ADRs (red box!) that you should warn your pateint about?
8. What should you beware about using concomitantly with salbutamol?

Question 6

LABAs: Salmeterol

1. Okay, so why arent these used for rapid relief?
2. You couldnt use SABAs for nocturnal asthma, can you use them here?
3. What part of the molecule makes them longer lasting?
4. What is the onset of action, peak effect and bronchodilatory effect?
5. When should you take it?
6. Since these are so good, do you still need to use anti-inflammatories?
7. What can LABAs potentiate?

Question 7

Fixed dose combination inhaler:

1. What are the benefits of using LABA with steroids?
2. What is the adjunctive role?
3. What is an example of a LABA + corticosteroid combination?

Question 8

What is SMART therapy?

Question 9

Muscuranic receptor blockers:

1. What does parasym stimulation of M1,2,3,4 receptors lead to?
   - what sort of drugs can you use to antagonise this?
2. Why are there presynaptic M2 receptors located on the neurons that release Ach on the broncho SM?

Question 10

Muscuranic receptor blockers: Ipratropium

1. Say that drug out loud
2. What is the MOA?
3. How do you take it in?
4. Tell me about the onset and duration
5. What do you use it with to give an additivie effect?
6. What conditions is it used in?

Question 11

Vagal component differences in COPD vs asthma

-explain this

Question 12

ACh and eosinophils in airways sensitiation - what does this mean?

Question 13

What are the ADRs of ipratropium? Not in a red box but still

Question 14

Combination inhalers in COPD

1. What is used as a combinatio inhaler for reversible bronchospasm in COPD?
2. In repeat/severe exacerberations not controlled by LABAs - what do you use?

Question 15

Why do you need to give Mg2+ in acute severe asthma?

Question 16

Methylxanthines: Theophylline

1. How do you take it in?
2. . What is the primary and secondary effect?
   - aka MOA
3. What are its toxic effects?
4. What’s the one standout PK think you should know (it’s in red on slide 31)
5. On slide 34, it takes about the metabolism of it mainly through what CYPs?
   - so what things increase or decrewase the level of that? (red box!)

Question 17

Leukotriene pathway-modifying agents (LTRAs): Montelukast

1. How do you take them?
2. What is the MOA?
3. Only affects what? Sooooo what else do you give?
4. What is the evidence of the effectiveness of montelukast?
5. What about its adverse effects?
6. What are the long term risks?
7. Is it appropriate for actue asthma exacerberations?