Pharm: Test 2: 2. Adrenomimetics

Front 1

1. For alpha receptors, what activates it more, Epi or NE?

Back 1

a. E>or equal to NE

Front 2

2. For B1 receptors, which activates more, E or NE?

Back 2

a. EQUAL!

Front 3

3. For B2 receptors, what activates more epi or NE?

Back 3

a. E>>>>>NE

Front 4

4. What 2 things inactivate Epi and NE?

Back 4

a. MAO and COMT

Front 5

What is Depivefrin

Back 5

a. Prodrug converted into epinephrine
b. Topical, ophthalmic agent
c. Direct acting adrenomimetic

Front 6

6. What are the 5 alpha 1 selective agonists and method of delivery

Back 6

a. Phenylephrine (Neo-Synephrine, Sudafed PE)
b. Metaraminol (Aramine): Paraenteral
c. Xylometazoline (Chlorohist-LA, Inspire, Neo-Synephrine II Long Acting, Otrivin):nasal
d. Oxymetazoline (Afrin, Neo-Synephrine 12 Hours, etc.) – also activate a2 :Nasal
e. Midodrine (ProAmatine): oral

Front 7

7. What are the 2 alpha 2 selective agonists? How are they given?

Back 7

a. Brimonidine (Alphagan)
b. Apraclonidine (lopidine)
c. Both topical for the eye

Front 8

8. What is isoprotenernol and how is it administered?

Back 8

a. Non-selective B agonis
b. Parenteral

Front 9

9. What is dobutamine and how is it administered?

Back 9

a. (+) isomer – b1 agonist, a1 antagonist
b. (-) isomer – a1 agonist
c. Pareneteral

Front 10

11. What are the direct acting adrenomimetics for B2 selective agonists? 4

Back 10

a. Albuterol (Proventil, Ventolin, etc.)
b. Metaproterenol (Alupent)
c. Pirbuterol (Maxair)
d. Terbutaline (Brethine, etc.)

Front 11

12. What are the 3 drugs used as nasal decongestants?

Back 11

a. Phenylephrine
b. Xylometazoline
c. Oxymetazoline

Front 12

13. How are the 3 nasal decongestant drugs applied?

Back 12

a. Topically

Front 13

14. How does phenyephrine work on the body for nasal congestion?

Back 13

a. Phenylephrine
i. Activate alpha 1 receptors
1. Vasoconstriction
a. End result: shrink swollen mucosa

Front 14

15. What is the difference in duration between the 3 decongestant drugs?

Back 14

a. Phenylephrine: short duration of action
b. Xylometazoline and Oxymetazoline: long duration of action

Front 15

16. What is the problem with chronic use of the nasal decongestants?

Back 15

a. Chronic use will cause rebound nasal congestion
b. Can occur within a week of using the drug
c. Chronic use causes down regulation of the alpha 1 receptor
i. But you still are using the drug so you still get an open nasal passage
1. Yet the second you take it away, the receptors are down regulated so you get rebound nasal congestion!

Front 16

17. Chronic use of alpha agnosists summary

Back 16

a. Chronic activation of the a1 receptor on the nasal mucosa causes down regulation of the receptor
b. When the drug is stopped, there is insufficient endogenous NE to activate the few receptors that remain
c. This causes rebound nasal congestion

Front 17

18. When you have anaphylaxis, what is the Mast cell response?

Back 17

a. Release histamine, bradykinin, leuktrienes

Front 18

19. When you have anaphylaxis, it is possible to get angioedema, how does epi act on this?

Back 18

a. a1 – constrict capillary beds. This counteracts the dilation & increased vascular permeability of capillaries

Front 19

20. when you have anaphylaxis, you can have bronchoconstriction, what does epi do to treat?

Back 19

a. b2 – bronchodilation

Front 20

21. when you have anaphylaxis, you can have pruritus or urticaria, what does Epi do to treat it?

Back 20

a. b – suppress release of mediators from mast cells

Front 21

22. when you have anaphylaxis, you can have hypotension, how does epi treat this?

Back 21

a. a1, b1 – raise BP

Front 22

23. Why is NE not the drug of choice for anaphylaxis?

Back 22

a. NE doesn’t bind to B2 receptors, so it doesn’t treat bronchoconstriction

Front 23

24. What are 2 drugs that are used in hypotension, how do they work?

Back 23

a. NE and PE
i. Activate alpha 1 receptors
1. Vasoconstriction
a. Increase BP

Front 24

25. What are 3 drugs that can be used to treat shock?

Back 24

a. Dopamine
b. Dobutamine (gets heart squeezing, use for Cardiogenic Shock)
c. NE (used for Hypovolemic shock)

Front 25

26. What is the difference between hypotension and shock?

Back 25

a. Shock is extreme hypotension, and you are not perfusing organs

Front 26

27. Where is the major location of dopamine receptors? What effect does this have

Back 26

a. Renal vasculature
b. Causes vasodilation to increase renal blood flow (to help preserve kidneys)

Front 27

28. What are 2 other locations dopamine acts (other than renal) and what is the effect?

Back 27

a. Middle dose of dopamine effects B1 receptors
i. Leads to increase CO and BP
b. High dose of dopamine effects a1 receptor
i. Increase PVR and BP

Front 28

29. Why does standing on your head cardiovert SVT (supraventricular tachycardia)

Back 28

a. Blood flows to baroreceptor want to decrease the heart flow
i. So you INCREASE VAGAL outflow (PNS)

Front 29

30. If you have AV block what do you want to give to treat? (2)

Back 29

a. Want to activate B1 receptors
b. Give Epi or isoproterenol

Front 30

31. What are the 4 short acting Asthma/COPD drugs?

Back 30

a. albuterol
b. metaproterenol
c. pirbuterol
d. terbutaline

Front 31

32. What are the 3 long acting Asthma/COPD drugs

Back 31

a. salmeterol
b. formoterol
c. arformoterol

Front 32

33. How does albuterol help treat asthma?

Back 32

a. Activate B2 receptor, bronchodilation, open airways

Front 33

34. What is the advantage of giving albuterol vs. epinephrine/isoproterenol to treat asthma?

Back 33

a. Less B1 side effects

Front 34

35. What drug do you give to prevent premature labor? How does it work

Back 34

a. Terbutaline
b. Activation of B2 receptors to cause uterine smooth muscle relaxation
c. End result: stop uterine contractions

Front 35

36. What drug can be used to dilate the pupil? What is the mechanism?

Back 35

a. PE (phenyephrine)
b. Will activate alpha 1 receptor to contract iris radial smooth muscle
c. End result: Pupil dilation without cycloplegia

Front 36

37. What in the F is cycloplegia?

Back 36

a. Paralysis of the ciliary muscle

Front 37

38. What is the adverse effect from alpha adrenergic activation (blood vessels)

Back 37

a. Reduce peripheral blood flow
b. Marked elevation of BP, increased Cardiac work and precipitate cardiac ischemia, MI and failure
i. Due to increasing afterload

Front 38

39. What is the adverse effect from alpha adrenergic activation at the infusion site?

Back 38

a. Can have excessive contraction of blood vessels at infusion site
b. Causing ischemia and necrosis

Front 39

40. What is the adverse effect from beta adrenergic activation?

Back 39

a. Increased heart rate
i. Causing: Palpitations, tachycardia,
cardiac arrhythmias
ii. Increase force of contraction
1. Leading to increased workload
a. Causing angina

Front 40

41. What adverse effect of B activation can be seen in the liver?

Back 40

a. B2 receptor activation on liver stimulates glycogenolysis

Front 41

42. What adverse effect can B activation have on skeletal muscle (negative)

Back 41

a. Tremor

Front 42

43. What are the contraindicaitons for direct acting adrenomimetics? 3

Back 42

a. Cardiovascular disease
b. Hyperthyroidism
c. Diabetes

Front 43

44. What is tyramine? Is it a drug? How does it work?

Back 43

a. Indirect acting adrenomimetics
b. Not a drug
c. Promotes the release of NE from the sympathetic nerve terminal

Front 44

45. What metabolizes tyramine?

Back 44

a. MAO

Front 45

46. If tyramine is not metabolized in the liver, what can happen?

Back 45

a. It gets into the blood stream
b. Finds a NE transporter
c. Gets into sympathetic nerve terminal and displaces NE from the terminal
d. This ends up activating a1 and B receptors!

Front 46

47. What may happen if a person is taking a drug that inhibits the activity of MAO (i.e., MAO inhibitor) and eats a lot of cheese and drinks a lot of beer?

Back 46

a. Hypertensive crisis!

Front 47

48. What are the mixed acting adrenomimetics?

Back 47

a. Ephedrine (generic)
b. Pseudoephedrine (Sudafed, generic, etc.)

Front 48

49. How does Ephedrine work? What kind of adrenomimetic is it?

Back 48

a. Mixed acting adrenomimetic
i. Releases NE from nerve terminals
ii. Activates a and b receptors
b. Crosses the blood brain barrier
i. Mild stimulant

Front 49

50. What are the approved uses of Ephedrine? 3

Back 49

a. Asthma, COPD
b. Nasal congestion

Front 50

51. How would ephedrine be useful for treating nasal congestion?

Back 50

a. Want to activate alpha 1
i. Ephedrine causes increase release of NE
1. This activates the a1 receptors in blood vessels of the nasal mucosa (note that the ephedrine itself also activates these a1 receptors)
a. Leads to decreased nasal congestion

Front 51

52. How would ephedrine be useful for treating asthma?

Back 51

a. Ephedrine
i. Activates B2 receptors on bronchiole smooth muscle
1. Bronchodilation

Front 52

53. Ephedrine is seldom used to treat asthma. Why?

Back 52

a. Side effects

Front 53

54. What are the side effects of ephedrine? 2 areas, multiple effects

Back 53

a. Cardiovascular
i. Excessive stimulation of the heart (b1)
ii. Use of ephedra or ephedrine alkaloids has been temporally linked to stroke, MI, and sudden death
b. CNS
i. Insomnia
ii. Nervousness
iii. Anxiety

Front 54

55. How does pseudoephedrine work? How is it different than ephedrine? What is its use? Delivery method?

Back 54

a. Directly activates a, and to a lesser extent, b receptors
b. Releases NE from the nerve terminal
c. Has less CNS effects than ephedrine
d. Used as a nasal decongestant
i. Oral