Adrenergic Agonists- T2 Flashcards Preview

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Flashcards in Adrenergic Agonists- T2 Deck (22):
1

define asthma

increased inflammation and contractile responsiveness of bronchial smooth muscle in response to allergens, pollutants, exercise and upper respiratory infections.

2

4 structure examples given of beta2 adrenergic agonists

albuterol, metaproterenol, terbutaline, and formoterol.

3

beta2 adrenergic agonists are suppled as ____ mixtures of R and S forms of the drug

racemic

4

Levalbuterol is which isomer?

R

5

which isomer is more efficacious and why is the other not as good

R. S tends to hang around longer making it more susceptible to metabolism and has a longer half life.

6

beta2 adrenoceptors predominate as the primary adrenergic receptor producing __

relaxation of bronchial smooth muscle.

7

activation of M3--> ___ --> ---

increase Ca (PLC)--> increase bronchoconstriction

8

activation of B2--> ___ --> ___ --> ____

increase cAMP--> PKA --> decrease Ca

9

is beta2 selectivity absolute?

no, if you take enough, you can activate beta1.

10

what size particle is optimal for bronchial tree deposition

2-5 micrometers

11

systemic effects of beta agonists

skeletal muscle tremors, weakness, tachycardia, CNS excitation.

12

genetic studies have revealed that polymorphism in ____ may modify asthmatic disease or response

beta2 receptor

13

polymorphism is __ and mutation is ___

polymorph: greater than 1% and mutation is less than 1%

14

differences in ___ lead to differences in the ___

receptors, patients response to the drug

15

these polymorphisms change how the receptors react-

the beta receptors couple to cAMP production though a Gs, this cAMP buildup through PKA in the bronchioles is going to cause bronchiodilation, this is going to be caused by removal of Ca, ig we have a polymorph then the receptor doesn't couple well to the G protein system so we reduce the ability for the receptor to cause bronchodilation.

16

polymorphisms in what two cases cause patients to be poor responders to beta agonists? and what would you use instead

Thr164 and ile164. would want to use a muscarinic antagonists instead.

17

Thr164--> ile polymorphism results in

poor coupling of the receptors to adenylyl cyclase activation

18

Arg16-->Gly polymorphism results in

more rapid down regulation of the receptor

19

Gln27-->Glu polymorph shows

greater resistance to down regulation than the Arg16 receptor

20

Gly16_Gln27_ile164:

poor adenylyl cyclase coupling vs Thr164

21

Gly16_Gln27_Thr164:

rapid receptor downregulation vs Arg16

22

Arg16_Glu27_ile164:

resistant to receptor downregulation vs Gln27