10- Adrenergic Pharmacology Flashcards

(94 cards)

1
Q

What are the 3 main NT’s of the adrenergic system?

A

Dopamine, Norepinephrine and Epinephrine

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

What AA is Dopamine, Norepinephrine and Epinephrine synthesized from?

A

Tyrosine

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

Give the general pathway from Tyr –> E

A

Tyr –> L-DOPA –> dopamine –> NE –> E

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

What are the systemic effects of SANS activation?

A

increase of rate/force of cardiac function, resistance (constriction of blood vessels and dilation of bronchioles), inhibition of the release of insulin, and breakdown of fat

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

What is the transporter that puts Dopamine into presynaptic vesicles?

A

VMAT

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

What causes the vesicle to exocytose?

A

Ca++ influx

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

When is dopamine turned into NE?

A

Once inside the synaptic vesicle

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

What is the name of the transporter on presynaptic cells that transports NE and Na back into the cell?

A

NET

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

What drug inhibits NET, thus increasing [NE] in the synapse?

A

COCAINE AWWWWWWWWWWWWW YUSSSSSSSS

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

What drug inhibits VMAT, thus preventing dopamine from entering vesicles?

A

Reserpine

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

What 2 enzymes degrade catecholamines?

A

MAO and COMT

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

Where are the 2 sources of catecholamines?

A

The two sources are either from synthesis de novo, or are molecules that are recycled via neuronal reuptake.

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

Which catecholamines does MAO A degrade?

A

degrades serotonin, norepinephrine, and dopamine

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

Which catecholamines does MAO B degrade?

A

degrades dopamine more quickly than A.

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

What type of G protein is alpha1 receptors?

A

Gq/Gi/Go

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

What are the systemic effects of alpha1 activation?

A

heavily involved in increasing blood pressure, and antagonists target the receptors for hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the tissue effects of alpha1 activation?

A

vascular smooth muscle contracton, GI contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which G protein is alpha2 receptors associated with?

A

Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the MOA of the Gi protein on alpha2 receptors?

A

decreases cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the effect of alpha2 stimulation on the pancreas?

A

decreased insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the effect of alpha2 stimulation on vascular smooth muscle?

A

vascular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of G protein are Beta1 receptors coupled with?

A

Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where are Beta1 receptors (typically)?

A

The heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the effect of beta1 stimulation?

A

Increased heart rate (chronotropy) and contractility (inotropy)?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What type of G protein are Beta2 receptors?
Gs
26
What are the effects of Gs activation? (think smooth muscle)
Smooth muscle relaxation, which included relaxation of the GI and vasodilation
27
What molecule binds to G-protein receptors when theyre overstimulated and down-regulates them?
BARK (Beta-Arrestin receptor Kinase)
28
Though Epi will bind to both alpha and beta proteins, which type does it bind a little stronger?
Beta
29
What are the systemic effects of Epi administration?
cardiac output and force, increases in blood pressure, relaxation of bronchial smooth muscle, and increase in concentration of glucose and fatty acids in blood
30
What type of adrenergic receptors does NE bind well to?
Beta 1 and alpha 1
31
What type of adrenergic receptors does NE not bind well to?
Beta 2
32
What are the systemic effects of NE administration?
Increases systemic blood pressure and stroke volume, but not heart rate. Used to treat distributive shock.
33
True or False: Dopamine does not cross the BBB.
True
34
What are the systemic effects of low [dopamine] infusion?
D1 receptors activate adenylyl cyclase, increase cAMP levels and vasodilation
35
What are the systemic effects of middle [dopamine] infusion?
positive inotrope due to B1 receptor activation
36
What are the systemic effects of high [dopamine] infusion and what is it used to treat?
alpha-1 receptor binding causes vasoconstriction, and is used in treatment of shock due to low cardiac output and compromised renal function from oliguria
37
α-methyltyrosine- MOA
inhibits catecholamine synthesis by inhibiting tyrosine hydroxylase
38
α-methyltyrosine- use
Hypertension with pheocytochroma
39
Reserpine- MOA
inhibits VMAT, so no D into vesicles
40
Reserpine- use
HTN
41
Tyramine- MOA
competes with NE in vesicles, especially if taken with MAOi's
42
Tyramine- use
found in the diet, normal
43
Guanethidine- MOA
dispaces NE in vesicles
44
Guanethidine- use
HTN
45
Amphetamine- MOA
displaces endogenous catecholamines, weak MAOi, blocks reuptake by NET
46
Amphetamine- use
depression/narcolepsy
47
Ephedrine/Pseudoephredine- MOA
Stimulation of Beta receptors
48
Ephedrine/Pseudoephredine- use
nasal/sinus congestion
49
Cocaine- MOA
blocks NET, no NE into presynaptic cell
50
Cocaine- use
can be used as an anasthetic
51
Tricyclics- MOA
inhibit NET and block serotonin reuptake
52
Tricyclics- use
depression
53
Phenelzine- MOA
nonselective irreversible MAOi
54
Phenelzine- use
depression
55
Selegiline- MOA
MAO-B inhibitor
56
Selegiline- use
Parkinsons
57
Methoxamine- MOA
alpha1 agonist
58
Methoxamine- use
shock
59
Phenylephrine- MOA
alpha1 agonist
60
Phenylephrine- use
Shock
61
Oxymetazoline- MOA
alpha1 agonist
62
Oxymetazoline- use
nasal congestion
63
Clonidine- MOA
alpha2 agonist, can cross BBB
64
Clonidine- use
HTN, especially in pregnancy
65
Guaficine- MOA
alpha2 agonist
66
Guaficine- use
HTN
67
Dexmedomidine- MOA
alpha 2 agonist
68
Dexmedomidine- use
sedative
69
Alpha-methyldopa- MOA
Alpha 2 agonist
70
Alpha-methyldopa- use
pregnancy related HTN
71
Isoproterenol- MOA
nonselective Beta agonist
72
Isoproterenol- use
bronchoconstriction
73
Dobutamine- MOA
beta1 agonist, increases cardiac output
74
Dobutamine- use
heart failure
75
Albuterol- MOA
beta2 agonist, short acting
76
Albuterol- use
asthma
77
Terbutaline/Salmetrol- MOA
beta2 agonist, long acting
78
Terbutaline/Salmetrol- use
asthma
79
Phenoxybenzamine/Phentolamine- MOA
nonselective irreversible alpha antagonist
80
Phenoxybenzamine/Phentolamine- use
Pheochromocytoma
81
Prazosin/Terazosin/Doxazosin- MOA
alpha1 antagonist
82
Prazosin/Terazosin/Doxazosin- use
HTN and BPH
83
Tamsulosin- MOA
alpha1 antagonist
84
Tamsulosin- use
BPH
85
Propanolol- MOA
nonselective beta blocker
86
Propanolol- use
HTN
87
Carvedilol- MOA
nonselective beta blocker
88
Carvedilol- use
HTN
89
Pindolol- MOA
partial agonist for beta1 and beta2
90
Pindolol- use
HTN pt's that have bradycardia or decreased cardiac reserve
91
Acebutolol- MOA
partial beta1 agonist
92
Acebutolol- use
HTN
93
Esmolol- MOA
beta1 antagonist
94
Esmolol- use
thyroid storm, very short acting so IV only.