Obstructive Lung Disease - Pharmacology Flashcards Preview

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Flashcards in Obstructive Lung Disease - Pharmacology Deck (16):

What's the biggest pathophysiologic process to target in both asthma and COPD?

Airway resistance- with bronchodilators.


Is pulmonary HTN a process that occurs in asthma?

Nope, this is a feature of COPD.


Should you confuse vascular smooth muscle with the smooth muscle of bronchioles?

No, you shouldn't. They don't respond to the same signals - eg. NO won't relax bronchiole smooth muscle.


3 classes of bronchodilators?
What mechanism do they all share?

Leukotriene inhibitors.
Muscarinic antagonists. (ipratropium, etc.)
Beta-2 agonists.

These all increase intracellular cAMP in smooth muscle cells. (or cGMP?)


Why is it nice to have an inhaled drug have a high potency?

So you don't need to use as many puffs on the inhaler. (which limits compliance)


In cardiology, beta agonists lose effectiveness with time as receptors are internalized/degraded. Dose this happen with drugs like albuterol?

No, at the doses used, tachyphylaxis does not occur.


In COPD, is there a preference toward what sort of bronchodilator is used?

Yes. Muscarinic antagonists seem to work better than beta-agonists in COPD.
(recall that methylxanthines are avoided if possible due to side effects)


Most common cause of aerosol medication failure?

Poor inhaler technique.
Spacers are nice.


How is theophylline useful?
(MoA is unclear, but what are some effects?)

As an adjunct in COPD.
(phosphodiesterase inhibitor -> increased cAMP. Weak bronchodilator. Increases drive to breathe, muscle function, and decreases PVR... kind of a like a breathing inotrope.)


For what disease are leukotriene inhibitors used?
What effect do they have?
(some examples?)

They're used for asthma - but only 30% of pts respond.
They cause bronchodilation and inhibit mucus secretion.
(zileuton - inhibits synthesis. montelukast, zafirlukaset - antagonists)
(These don't work in COPD, which fits in with the narrative of asthma being more mediated by inflammation.)


Proposed MoA of glucocorticoids? (very simplified version)

Drug binds glucocorticoid receptor, forms active dimer, binds DNA... has trans-activator and trans-repressor properties.
(The lecture slides state a gross oversimplification that trans-repressor activity is good, and trans-activator activity is bad.)


Evidence for benefit of inhaled steroids in COPD is controversial.



Dual therapy is useful.



5 goals of asthma therapy?

Control chronic symptoms (esp. nighttime symptoms).
Maintain normal activity levels.
Maintain (near) normal PFTs.
Prevent exacerbations.
Limit adverse medication effections.


What are the major factors determining which treatment modality is used for asthma?

Nighttime symptom frequency.
Daytime symptom frequency.


What's the only "drug" that improves mortality in COPD?

Home O2.