Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Unit 2 > Autonomics IV-VI > Flashcards

Autonomics IV-VI Flashcards

1
Q

How is NE removed from the synapse?

A

Primarily reuptake, extraneuronal uptake followed by metabolism, dissemination into blood

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

Synthesis of NE

A

Tyrosine -> DOPA -> Dopamine -> NE -> E

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

Alpha 1 receptor mechanism

A

Simulatory G-protein increases phosphotidyl inositol hydrolysis

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

Alpha 2 receptor mechanism

A

inhibitory G-protein decreases cAMP

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

B1, 2, 3 receptor mechanism

A

Stimulatory G-protein increases cAMP; B1 also activates voltage-sensitive Ca2+ channels in heart

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

D1 receptor mechanism

A

stimulatory G-protein increases cAMP

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

Enzymes involved with NE, Epi metabolism. Location?

A

Monoamine oxidase (MAO) - mitochondrial surface, Catechol-O-methyltransferase (COMT) - cytoplasm of many cells, notably liver

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

Beta 1 receptor, prominent effector organs and response

A

Heart - Increased HR and force of contraction; Kidney - Renin secretion

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

Beta 2 receptor, prominent effector organs and response

A

Arterioles in skeletal muscle/coronaries - dilation; Bronchial Muscle - Relaxation; Uterus - Relaxation; “Several sites” - Increased metab.

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

Beta 3 receptor, prominent effector organs and response

A

Adipose tissue (lipocytes) - lipolysis, thermogenesis

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

Alpha 1 receptor, prominent effector organs and response

A

Arterioles in skin, mucosa, viscera, kidney - Constriction; Veins - Constriction; Uterus and Spleen - Constriction

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

Alpha 2 receptor, prominent effector organs and response

A

Presynaptic nerve endings - Inhibit NE release and ACh release (gut); Postsynaptic nerves in CNS - Decreased Peripheral Sympathetic Tone

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

D1 receptor, prominent effector organs and response

A

Renal, mesenteric and cerebral arterioles - dilation

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

How does autoregulation work in the sympathetic NS?

A

Alpha2 receptors on presynaptic nerves regulate NE release.

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

Describe heteroreceptor control. What substance does this process regulate?

A

Gut relaxation. Activation of Alpha 2 receptors by Sympathetic NS NE on parasympathetic neurons decrease release of ACh which relaxes gut.

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

Describe the dose-dependent effects of Epinephrine on skeletal muscle blood vessels

A

Skeletal muscle vessels have Alpha 1 and Beta 2. Beta 2 dominant a physiological (low) concentrations and therefore you get vasodilation. At therapeutic levels, Alpha 1 effects predominate and vessels constrict.

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

What receptors do Phenylephrine activate?

A

Alpha 1

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

What receptors do Clonidine activate?

A

Alpha 2

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

What receptors do Norepinephrine activate?

A

Alpha 1, Beta 1, Alpha 2

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

What receptors do Epinephrine activate?

A

Alpha 1, Beta 1, Beta 2, Alpha 2

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

What receptors do Isoproterenol activate?

A

B1, B2

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

What receptors do Dopamine activate?

A

DA, A1, B1

23
Q

What are the four main agonists for B1?

A

ISO > Epi >= NE > DA

24
Q

Four main agonists for B2?

A

ISO > Epi&raquo_space; NE&raquo_space; DA

25
Q

Four main agonists for A1?

A

Epi >= NE > DA&raquo_space; ISO

26
Q

Four main agonists for A2?

A

Clonidine > Epi >= NE&raquo_space; ISO

27
Q

Two Indirect adrenergic agonists

A

Tyramine and amphetamine

28
Q

Effects of low, medium and high doses of Dopamine

A

Low: Direct action of DA on D1 receptors - vasodilation at renal, mesenteric and cerebral arteries resulting in lower BP and increased urine output; Medium: Same as low with some direction action on B1 receptors in heart - increase hr; High: More of above and some direct activation of A1 resulting in vasoconstriction (including renal because A1 dominates D1)

29
Q

How does fenoldopam work and what is it used for?

A

D1 selective agonist that increases blood flow to renal, mesentery, and cerebral arteries. Used in hypertensive emergencies

30
Q

What would be the results of giving NE injection?

A

A1 increases peripheral resistance B1 increase HR. Because baroreceptors detect increase in BP, their action results in an overall decrease in HR with a slight increase in BP.

31
Q

What would be the results of giving Epinephrine injection?

A

Peripheral resistance decrease due to B2 activation although there is an increase in HR due to B1 activity. Net slight increase in BP with increase in PP.

32
Q

What would be the results of an Isoproterenol injection?

A

Isoproterenol is strictly a beta agonist. B1 increases HR while B2 causes massive decrease due to vasodilation. PP increases with a slight decrease in BP.

33
Q

Describe the physiological process of sweating

A

Sympathetic fibers travel to eccrine sweat glands and release ACh onto (probably) M3 receptors on the secretory cells

34
Q

Uses of Epinephrine

A

Control hemorrhage (A1 vasocon), Nasal Decongestion (A1 vasocon decrease swollen mucosa), Allergic/Anaphylactic Shock (A1 Vasoconstriction, B2 bronchodilation, decrease histamine release), Hypotension, (A1 vasocon)

35
Q

In shock, why would you want to administer alpha blockers and dopamine?

A

To perfuse organs. Shock results in sympathetic vasoconstriction to raise BP. By giving alpha blocker you facilitate vasodilation and by giving dopamine you cause vasodilation of the kidney, mesentery and cerebral arteries

36
Q

What does Ergonovine treat?

A

Post partum bleeding (Alpha agonist)

37
Q

What does Ergotamine treat?

A

Acute migraine (A agonist)

38
Q

What does bromocriptine treat?

A

Hyperprolactenemia and Parkinsonism

39
Q

Use of Alpha2 agonists

A

Central control of BP in NTS by acting on regulatory A2 receptors in the midbrain. Therefore BP decreases

40
Q

Clonidine uses

A

HTN, prevent withdrawal from opioids and alcohol

41
Q

B1 agonists and their uses

A

Epinephrine, Isoproterenol, - Cardiac Arrest, A-V block, CHF Dobutamine - candidate for treadmill stress test

42
Q

B2 agonists and their uses

A

Smooth muscle relaxation - tx of bronchial asthma - terbutaline and albuterol b/c they are B2 selective, Uterine smooth muscle relaxation

43
Q

What are amphetamines used for?

A

Narcolepsy, hyperkinesis (ADHD)

44
Q

First generation Beta blocker

A

classic nonselective B1 and B2 blocker; Propanolol

45
Q

Second generation beta blockers

A

B1 selective, metoprolol, atenolol

46
Q

Third generation beta blockers

A

Nonselective B blocker with additional actions (A1 receptor antagonism), Labetalol Tx: hypertension, lower TPR with little tachycardia

47
Q

Conditions treated with Beta blockers

A

HTN, Arrhythmias, Angina Pectoris, Glaucoma, Migraine, Stage Fright, HF

48
Q

What Beta blockers should you use for CHF? Why?

A

ONLY SECOND OR THIRD GENERATION; Second generation slows down heart, third generation slows down heart and has A1 antagonism so the heart pumps against less peripheral resistance. If you use first generation, you will slow the heart down but there will be unopposed A1 action causing massive vasoconstriction!

49
Q

Nonselective Alpha blockers

A

Phentolamine, Phenoxybenzamine

50
Q

A1 selective blockers

A

Prazosin, Terazosin

51
Q

Major application of Alpha blockers

A

HTN

52
Q

Mechanism explaining less tachycardia with Prazosin compared to nonselective Alpha blockers

A

NSABs block A1 on effector organ and autoregulator A2s. NE goes to B1 receptor causing tachycardia. A1SBs disallow for NE to bind to A1 but can still bind autoregulator A2s. This decreases overall NE in synaptic cleft and thus resulting in less NE binding to B1. Less tachycardia!

53
Q

Uses for Alpha blockers

A

Hypertension, Raynauds, Frostbite, Pheochromocytoma, Shock, BPH

Pharmacology Unit 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions