S3M1 Pharmacology Azid Adrenergic Drugs

Front 1

What receptors does the alpha-beta agonist epinephrine bind?

Back 1

a12
B123

Front 2

What receptors does the alpha-beta agonist norepinephrine bind?

Back 2

a12
B1

Front 3

This is a alpha-beta agonist drug that Only binds to a12 and B1.

Back 3

Norepinephrine
(Dopamine)

Front 4

This is a pure alpha-1 agonist used to treat hypertension.

Back 4

Phenylephrine

Front 5

This is a pure alpha 2 agonist.

Back 5

Clonidine and Apraclonidine

Front 6

This is a B123 agonist.

Back 6

Isoproterenol

Front 7

This is a pure B-1 agonist.

Back 7

Dobutamine

Front 8

This is a pure B-2 agonist.

Back 8

Albuterol and Salmetrol

Front 9

Dopamine binds...

Back 9

D1,D2

Front 10

What is the effect of a-1 receptor on the pancreas?

Back 10

severe decrease in insulin secretion

Front 11

Explain the PNS effect on the bladder.

Back 11

M3 receptors contract the detrussor and the pressure on the internal sphincter causes it to involuntarilly relax (no receptor needed).
PEE is initiated

Front 12

Explain the SNS effect on the bladder.

Back 12

B-2 receptors on the detrussor cause relaxation
a-1 receptors contract trigone and internal sphincter

-Hold it in!

Front 13

Catecholamines are produced by what AA? What is the first enzyme (comitted step)?

Back 13

Catecholamines are produced with tyrosine and are carried inside the synaptic terminal and converted into dopa by Tyrosine hydroxylase.

Front 14

What is the G protein for each adrenergic receptor?
a-1
a-2
B-1
B-2

Back 14

a-1 Gq
a-2 Gi
B-1 Gs
B-2 Gs

Remember Qiss "Kiss"

Front 15

Which adrenergic receptors are Gq and what do they do?

Back 15

Gq= alpha 1
Increase Phospholipase which increases IP3/DAG and raises intracellular Ca

Usually causes constriction

Front 16

Which adrenergic receptors are Gi and what do they do?

Back 16

a-2=Gi

Gi decrease cAMP, which decreases Ca channels and increases K channels

Front 17

Which adrenergic receptors are Gs and what do they do?

Back 17

B1,B2,B3 are all Gs
Gs increases cAMP, which will actually inactivate MLCK and inhibits smooth muscle contraction.

Front 18

What characteristic of catecholamines makes the degradable by MAO and COMT?

Back 18

The two OH's on the benzene ring.

Front 19

Place the three catecholamines in order of highest to lowest affinities by B receptors.

Back 19

Highest=Isoproterenol, Epinephrine, Norepinephrine

The larger the amine group, the higher the affinity for B receptors.

Front 20

Place the three catecholamines in order of highest to lowest affinities by A adrenoceptors.

Back 20

Highest=Epi
Nore
Isoproterenol

Front 21

-Phenylephrine is a...

-Clonidine is a...

Back 21

Alpha agonist a1>>>>a2

Alpha agonist a2>>>>a1

Front 22

Nore binds to all the adrenergic receptors except:

Back 22

B2,B3

Front 23

Isoproterenol binds...

Back 23

B1=B2=B3

Front 24

Dobutamine binds...

Back 24

B1>B2

Front 25

Albuterol binds...

Back 25

B2>>>B1

Albuterol is a powerful asthma drug

Front 26

Renin secretion is increased via which receptor?

Back 26

Renin is stimulated via B1 receptor.
Renin will activate the RAA axis and increase BP

Front 27

This drug acts in the following ways:
SA node: increase in heart rate
AV node: increase in automaticity and conduction, decrease in refractoriness
Atria and Ventricles: increase in automaticity, conduction and contractility

Back 27

Epinephrine

Epinephrine mostly affects B-1 receptors(80%) and B2 (20%)

Front 28

How would epinephrine affects blood vessels on cutaneous, GI and renal vessels vs. Sk. muscle and liver vessels?

Back 28

Epi binds a-1 receptors in skin, GI and Kidney to cause massive vasocontriction.

Epi binds B-2 in skeletal muscle and the liver and causes vasodilation.

Front 29

In the adrenal medulla, what stimulates the production of Epi from Nore?

Back 29

Glucocorticoids made by the adrenal cortex flow into the medulla and stimulate methyl transferase, which converts Nore-->Epi

Front 30

Describe epi effects on BP in both low doses and high doses.

Back 30

In low doses, there is a decrease in BP due to B2 vasodilation that predominates.

At high doses, systolic BP increases b/c increase CO while diastolic BP usually decreases (again via B-2 vasodilation.

-MAP is slightly elevated

Front 31

Epi causes bronchial smooth muscle relaxation and increased mucociliary clearance by binding...

Back 31

B2

Front 32

How does epi affect the GI?
Smooth muscle?
Peristalsis?
Sphincters?

Back 32

Relaxation of smooth muscle via a-2 that reduce Ach release
while B-2 directly relaxes smooth muscle.
-EPI also decreases peristalsis and contracts sphincters via a-1

Front 33

How does Epi affect the GU system?

Back 33

Epi relaxes kidneys and detrussor muscles while contracting trigone and internal sphincter.

Front 34

Epi causes contraction of the radial muscle, and a decrease in intraocular pressure and causes vasocontriction via ________ receptors.

Back 34

alpha 2

Front 35

Epi causes tremor in skeletal muscle by activating _______ receptors. Explain the mechanism.

Back 35

B-2
causes an increase in cell Ca and increased K uptake(also due to B-2)

Front 36

Explain briefly how Epi affects metabolism.
-Liver
lipolysis

Back 36

-Stimulates glycogenolysis and gluconeogenesis via B2 receptors.
-Increased lipolysis via B3 receptor

Breakdown of TAG-->30% increase in O2 consumption

Front 37

Epi affects mast cells and platelets...

Back 37

Epi inhibits degranulation (B2) which inhibits release of inflammatory mediators.

Stimulation of platelet aggregation(a-2 non innervated receptors)

Front 38

Which is the fastest route for epinephrine absorption:
-oral
SC
IM

Back 38

IM is the fastest and oral bioavailability is 0 b/c it is destroyed by MAO in enterocytes.

Front 39

Contraindications for EPI are:

Back 39

hypertension
Angina
Heart disease
Shock
Diabetes