Brainscape's Knowledge GenomeTM

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


See full index

MSII Pharmacology > Unit 2 - Autonomics IV > Flashcards

Unit 2 - Autonomics IV Flashcards

1
Q

explain synthesis of NE and E in adrenergic varicosity?

A

tyrosine (into cytoplasm) –> DOPA –> dopamine –> NE (vesicle) –> E (adrenal medulla)

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

is NE or E a neurotransmitter or a neurohormone?

A

NE is a neurotransmitter

E is a neurohormone

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

what is the receptor interaction and effector cell response of NE and E?

A

second messenger amplification

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

how do D1 (dopamine) exert its second messenger effect?

A

stimulatory GPCR increases cAMP (like beta1/2/3)

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

what is the adrenergic receptor excitation response?

A

constriction; Ca++ is made available to myofibrils and increases tension
-Ca++ from intracellular stores and/or transport from extracellular

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

what is the adrenergic receptor inhibition response?

A

relaxation; Ca++ is made unavailable to myofibrils and reduces tension
-Ca++ is taken into intracellular stores and/or pumped out

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

what is the adrenergic receptor metabolic response?

A

activation of AC

  • increased liver glycogenolysis
  • increase in plasma glucose and FFA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 3 ways specifically NE can “terminate” its action?

A
  1. neuronal reuptake (neuron-specific)
  2. effector cell uptake (non-specific and high capacity); extra-neuronal
  3. diffusion into capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the primary mechanism for terminating ACh? how is this different from NE?

A

enzymatic hydrolysis

-NE is reuptake

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

what and where is MAO?

A

monoamine oxidase on mitochondria surface

-metabolize NE, E, and other exogenous adrenergic drugs

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

what and where is COMT?

A

catechol-o-methyltransferase in cytoplasm of many cells, especially liver
-metabolize NE, E, and other exogenous adrenergic drugs

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

what are the major metabolites of NE/E that are measured in urine/plasma?

A

normetanephrine, metanephrine, VMA, MHPG

-for diagnostic purposes (increased plasma metanephrine indicates pheochromocytoma)

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

what does alpha-me-tyrosine do to modify chemical transmission?

A

decreases synthesis of NE (sympathetic) by decreasing pre-synaptic Ca++ influx

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

what does amphetamine do to modify chemical transmission?

A

increases release of NE (sympathetic)

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

what does isoproterenol do to modify chemical transmission?

A

combine with receptor to increase NE (sympathetic)

-increases post-synaptic Ca++ influx and second messengers

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

what does propranolol do to modify chemical transmission?

A

antagonist to beta-receptor sites to decrease NE (sympathetic)
-decreases post-synaptic Ca++ influx and second messengers

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

what does cocaine do to modify chemical transmission?

A

increases termination step such that synapse activity increases

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

what is the prominent effector organ and response to receptor activation of beta 1?

A

heart - increased heart rate and force of contraction

kidney - renin secretion

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

what is the prominent effector organ and response to receptor activation of beta 2?

A

arterioles (and arteries in skeletal muscle, coronary) - dilation
bronchial muscle - relaxation
pregnant uterus - N/A
several other sites - metabolic effects increase

20
Q

what is the prominent effector organ and response to receptor activation of beta 3?

A

adipose tissue (lipocytes) - lipolysis and thermogenesis increase

21
Q

what is the prominent effector organ and response to receptor activation of alpha 1?

A

arterioles in skin, mucosa, viscera, and kidney - constriction (resistance vessels)
veins - constriction
uterus and spleen - contraction

22
Q

what is the prominent effector organ and response to receptor activation of alpha 2?

A

presynaptic nerve endings - inhibit NE release and ACh release (gut)
postsynaptic in CNS - decreased peripheral sympathetic tone

23
Q

what is the prominent effector organ and response to receptor activation of D1?

A

renal, mesenteric, and cerebral arterioles - dilation

24
Q

what are the agonist/antagonist for a1?

A

agonist: phenylephrine
antagonist: prazosin

25
Q

what are the agonist/antagonist for a2?

A

agonist: clonidine
antagonist: yohimbine

26
Q

what are the agonist/antagonist for D1?

A

agonist: fenoldopam
antagonist: N/A

27
Q

what are the agonist/antagonist for B1?

A

agonist: dobutamine
antagonist: atenolol

28
Q

what are the agonist/antagonist for B2?

A

agonist: albuterol
antagonist: butoxamine

29
Q

what are the agonist/antagonist for B3?

A

N/A for both

30
Q

what are the agonist/antagonist for BOTH B1/2?

A

non-selective

agonist: isoproterenol
antagonist: propranolol

31
Q

explain presynaptic and postsynaptic autoreceptor regulation of NE release?

A

stimulation of presynaptic a2 receptors inhibits NE release from nerve terminal, while drugs that block postsynaptic a2 receptors enhance NE release

32
Q

how are organ responses to neurotransmitters/drugs determined?

A

by differences in receptor populations and receptor densities

33
Q

explain the adrenergic receptors on skeletal muscle vessels?

A

have both a1 and B2

  • low concentration: B2 (lower threshold, for physiologic response from sympathetic (adrenal) stimulation) –> relaxation and dilation
  • high concentration: a1 (higher threshold and “dominant constriction” only seen in high pharmacological EPI in lab or shock
34
Q

what is the guiding principle to therapeutic drugs?

A

selectivity to get max effects with minimum side effects

35
Q

for NE drugs, what does methylation at N seem to do?

A

NE (no methyl) is a1/2 (and less so B1)
E (1 methyl) is a1/2 and B2
isoproterenol (3 methyl) is B1/2 only (no a1 b/c too much methyl)

36
Q

what are the characteristic sympathomimetics for phenylephrine?

A

a1

37
Q

what are the characteristic sympathomimetics for clinidine

A

a2

38
Q

what are the characteristic sympathomimetics for NE?

A

a1, B1, (a2)

39
Q

what are the characteristic sympathomimetics for E?

A

a1, B1, B2, (+a2)

40
Q

what are the characteristic sympathomimetics for isoproterenol?

A

B1/2

41
Q

what are the characteristic sympathomimetics for dopamine

A

D1, a1, B1

42
Q

what are agonist potencies at adrenergic receptors for B1?

A

ISO > E >= NE > D

43
Q

what are agonist potencies at adrenergic receptors for B2?

A

ISO > E&raquo_space; NE&raquo_space; D

44
Q

what are agonist potencies at adrenergic receptors for a1?

A

E >= NE > D&raquo_space; ISO

45
Q

what are agonist potencies at adrenergic receptors for a2?

A

CLON > E >= NE&raquo_space; ISO

MSII Pharmacology (43 decks)

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