Introduction to respiratory pharmacology + Anti-inflammatory medications: preventors Flashcards

1
Q

What is asthma? 3 characteristics?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Goals of treatment with asthma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the different classifications of asthma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the origins of asthma? (thing which sensitises people)

A

Exposure of antigetn (virus, allergens) to the dentrites. These are then given to the T helper cells. These CD4 cells often do not respond to this.

However, in an asthmatic the interlukens are released which activates the CD4 cell which, these then activate B lymphocytes and then activate eosinophils which produce this inflammatory response when the antigen is next exposed.

B cells = IgE response which bind to mast cells and eosinophils in bronchi. Re-encounter causes release of inflammatory cytokines and histamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What extra things (not histamine and cytokines) are released when an asthma exacerbation occurs?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are each of these responsible in asthma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the ‘slow-reacting’ substances of anaphylaxis’ in asthma? What affect do they have?

A

If we want to target this then we need to decrease C,D and E but also B4 because B4 is the chemoattractant.

This is done by knocking out the 5-lipooxygenase enzyme.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do prostacyclins and thromboxane A2 do in asthma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do you not want to completely knock out all of the prostaglandins?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain drug induced rhinitis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mechanism of a B2 agonist on asthma?

What is the second messenger?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why do you also need a muscarinic antagonist a long with B2 agonsit?

A

Essentially the beta 2 receptors work in the opposite direction to the muscurinic receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does theophylline work?

A

Increases the availability of cAMP as it is a PDE inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do muscarinic antagonists work?

A

Muscarinic antagonist will block the effects of acetylcholine therefor prevent bronchoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the anti-inflammatory compounds which can be used (aka preventors)?

A

Inhaled vs oral

17
Q

How does glucocorticoid work?

A

Will bind to the surface receptor which will chaperone it into the nucleus to alter cell function.

  • Highly effective at suppressing inflammatory cytokine production.
  • prevents phospholipid release and decrease eosinophil recruitment
18
Q

Glucocorticoid upregulates gene transcription of _________ inhibitors such as ________. This has the effect of….

A
19
Q
A
20
Q

Does glucocorticoids cause bronchodilation ?

A

NO: but over time decreases the airway responsiveness.

21
Q

Oral corticosteroids systemic effects?

A
22
Q

Some side effects of glucocorticoids?

A
23
Q

Explain the cushingoid effect and some other side effects of high dose oral corticosteroids?

How can you avoid this with respiratory diseases?

A

Inhaled reduce the systemic effects of oral corticosteroids.

24
Q

Main example of inhaled glucocorticoids?

A
25
Q

Enhancing the glucocorticoid effect while decreasing the mineralcorticoid effect will..

A

reduce the Na+ and H2O retention

26
Q

Inhaled glucocorticoid pharmacokinetics?
How many times per day?

What is it metabolised by? What does this mean?

A

Anything which makes it into the lung to the circulation is going to be broken down by the CYPs. This can cause problems because some people have very low action of CYP and some people have high CYP.

27
Q

What is inertial impaction and sedimentation and what does it refer to (percentage also).

A

Intertial impactation: bigger droplets cant corner quickly so hit sides.

Sedementation: tendency of a particle to settle in mucous and come to a rest.

28
Q

% of inhaled corticosteroid which makes it to lung?

% which makes it to systemic circulation?

where does the other stuff go?

A

High amounts of mucous will mean that a lot of the drug is swallowed. Most of the drug is broken down in the stomach, the other bits are broken down in the liver by CYPs.

Only 1% will make it to the systemic circulation.

29
Q

Adrenal crisis with inhaled corticosteroid?

Other risks? How can these be prevented?

A

Candidiasis: reduced if use spacer.

Dysphonia: hoarse voice due to laryngeal deposition of particles.

  • Rinse mouth after use (maybe with antifungal).
  • Use spacer
  • Reduce frequency depending on pulmonary function tests.
30
Q

Black box warning when switching a patient from oral corticosteroids to inhaled corticosteroids?

A
31
Q

Stepwise pharmacotherapy for asthma?

A

Step 1: Give the corticosteroids to reduce the inflammation because of the potential long term damage.

Monoclonal antibodies can be used to knock out interlukens 4 and 5.

32
Q

Stepwise pharmacotherapy for COPD?

When do you add corticosteroids?

A

Non-pharmacological are normally used first in COPD.

33
Q

Which disease would you use high dose inhaled corticosteroids? Which would you not?

A
34
Q

Treating a patient with COPD and asthma?

A
35
Q

What are cromolyns?

Mechanism of action?

Are they preventors or relievers?

A