Brainscape's Knowledge GenomeTM

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


See full index

Daddy Pharm > Adrenergics > Flashcards

Adrenergics Flashcards

1
Q

Autonomic Adrenergic Transmission

A

SNS Postganglionic fibers release
norepinephrine (NE) (sometimes Epi and dopamine/DA)

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

Catecholamine Synthesis
dopamine neurons

A

1) adrenergic neurons uptake L-tyrosine (blood)
2) L-tyrosine→L-dopa
(tyrosine hydroxylase/TH)
3) L-dopa→dopamine
(dopa decarboxylase/DD/l-amino acid decarboxylase)

4) dopamine into storage granules (vesicles) via active transport carrier.
5) can be released from dopamine neurons.

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

the rate-limiting step in synthesis

A

L-tyrosine→L-dopa
(by tyrosine hydroxylase/TH)

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

Where is phenylethanolamine n-methyltransferase (PNMT) found?

A

cytoplasm

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

Catecholamine Synthesis
Norepi neurons

A

NE neurons:
1) dopamine β-hydroxylase (DBH) is in the vesicles.
2) dopamine→norepi
(DBH)

3) cytoplasmic norepi (reuptake/internal release from vesicles)
↓
epinephrine
(phenylethanolamine n-methyltransferase (PNMT)

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

Dopa decarboxylase
specificity
what can it convert?

A

fairly non-selective (broad substrate specificity)

L dopa→DA

5-hydroxytryptophan→5-hydroxytryptamine

αmethyldopa→αmethyldopamine

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

false transmitters

A

α-methylnorepinephrine

α-methyldopa

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

Dopa decarboxylase converts α-methyldopa to α-methyldopamine, which can be further converted to….

A

α-methylnorepinephrine (false transmitter)

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

acts in feedback loop on the enzymes TH and DD to decrease excessive production

A

Cytoplasmic NE

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

if there is excessive NE release, there is (more/less) NE in the cytoplasm, thus (more/less) feedback, and (more/less) rapid synthesis

A

excessive NE release
less NE in cytoplasm
less feedback
more rapid synthesis

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

main contributor to the NE pool

A

NE re-uptake

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

the NE pools

A

two cytoplasmic pools
(rapid & slow turnover)

cytoplasm (ie renal medulla chromaffin cells)

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

In the cytoplasm, NE acts to feedback on ___ production

A

DA

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

NE in the ________ is converted to EPI before packaging in vesicles

A

cytoplasm of the adrenal medulla chromaffin cells

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

In the chromaffin cells, both EPI and NE are stored and released in the ratio of ….

A

80% EPI, 20% NE
important d/t receptor specificity differences between EPI and NE

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

Epi vs NE
which has longer doA?

A

Epi

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

Catecholamine storage is mainly in ___

A

granular vesicles

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

making granular vesicles

A

in cell body & carried to terminal for filling

endocytosis (pinching off) of the nerve terminal membrane.

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

NE in the granules is in a complex with…

A

-ATP (4NE:1ATP)
-proteins (NTs & neuromodulators)
-DBH/dopamine β-hydroxylase
-DA

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

Neuropeptide Y

A

protein** stored with NE**
released with NE as a co-transmitter

potent local vasoconstrictor
increases fat deposition

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

Two cytoplasmic pools of NE

A

fast and slow turnover pools

fast:
used as transmitter
stored or released directly from cytoplasm

slow:
reserve pool
use when NE too low

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

Adrenergic enzyme inhibitors

A

experimental determination of the system mechanics

α-methyl-p-tyrosine
(inhibits TH, α-methyldopa, which inhibits DD)

Disulfiram (Antabuse)
(inhibits DBH)

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

post synaptic receptors

A

A1
A2 (also pre-synpatic)
B1
B2
B3

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

Presynaptic A2

A

control mechanism to prevent overrelease

sense too much/enough NT in synapse

once stimulated, shuts off further release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

prevents overstimulation of post synaptic neuron

A

presynaptic A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cholinergic vs adrenergic
cessation of action

A

cholinergic: destroy ACh by AChE

adrenergic: reuptake transporters (rapid acting; high affinity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

presynaptic A2r prevents the ___ dependent release of NT.

A

Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

T/F
NE reuptake is a slower process.

A

False
NE in synapse for very short time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MAO & COMT
location

A

MAO: mostly terminal; mitchondria external wall

COMT: ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

After NE is taken back up, it is subject to metabolism by ___ before its safely repackaged in vesicles.

A

MAO (outside wall of mitochondria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

T/F
MAO contributes to the 20% of NE that is not reuptaken by metabolizing it in the synapse.

A

False
COMT is in synapse
MAO is inside terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

NE
% reuptake
% lost (how?)

A

80% reuptaken and survives MAO

20%
diffuses away, metab by MAO or COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Tyrosine hydroxylase
converts ___ to ___

A

L-tyrosine to L-dopa
(adds OH group)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

catecholamine nucleus

A

2 hydroxy groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

dopa decarboxylase
converts ___ to ___

A

L dopa to dopamine
(remove carbox acid group)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Dopamine B hydryxolase
converts ___ to ___

A

dopamine to L-norepi

adds OH group the B carbon (beta from amine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

phenylethanolamine n-methyltransferase (PNMT)

converts ___ to ___

A

L-Norepi to L-epi

(adds methyl group onto N)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The catecholamines

A

L-dopa
dopamine
L-Norepi
L-Epi

❌L-tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Adrenergics Release
neuron vs adrenal chromaffin cells

A

Ca inflow @ terminal
exocytosis of vesicles
synaptic release of NT

adrenal chromaffin cells:
same but NT released directly to blood stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

most important mechanism in stopping neurotransmitter action at the receptor sites

A

re-uptake pumps back into the cytoplasmic pool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

retrieved neurotransmitter is then taken up ____ concentration gradient back into vesicles

A

against

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Some of the released neurotransmitter in the synapse can act on presynaptic α2 autoreceptors to…

A

inhibit further release via feedback loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

catecholamine depletion

A

done by preventing reuptake

initial & transient increase in activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

pheochromocytoma

A

tumor of the adrenal medulla

increase in circulating catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

T/F
small amounts of neuronally released NT gets free to enter circulation but this isnt significant a amount.

A

True
rapidly destroyed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

The 2 principle enzymes responsible for the degradation of catacholamines

A

monoamine oxidase (MAO)
catechol-o-methyltransferase (COMT)

47
Q

MAO major forms

A

Type A: most active
metabolism of NE
(& DA, EPI, 5-HT/serotonin, tyramine)

Type B: less active
more selective for DA

48
Q

found in red wine

A

tyramine

49
Q

allows the liver the rapidly metab circulating catecholamines

A

has a lot of MAO and COMT

50
Q

can be assayed in blood to show adrenergic activity
(ie: adrenergic tumors)

A

VMA
MHPG

51
Q

MAO and COMT metabolizes NE into which compounds?

A

MAO
NE→DHMA & DHPG

COMT:
VMA & MHPG

52
Q

Which are found in blood?
DHPG
MHPG
DHMA
VMA

A

MHPG
VMA

53
Q

Adrenergic receptors
Characterized over 50 years ago based on

A

effects of NE, EPI and Isoproterenol (ISO) (Isuprel) - as α and β.

54
Q

α and β
Receptor types further broken down as

A

α1 α2
β1, β2, β3

55
Q

agonist comparative potencies

A

α1-agonist: NE > EPI > DA > ISO
α2-agonist: EPI > NE > DA > ISO

β1-agonist: ISO > EPI = NE > DA
β2-agonist: ISO > EPI > NE > DA
β3-agonist: ISO = NE > EPI > DA

56
Q

Selective antagonists

A

α: phenoxybenzamine
β: propranolol

(finalizes classical characterization of these receptors)

57
Q

T/F
Pre-junctional (α2) receptors are identical to post-junctional (α1)

A

False

58
Q

T/F
Clonidine has higher selectivity for A1 than A2.

A

False
more selective for A2 > A1

59
Q

Phenylephrine (Neo-Synephrine) is more potent at ___ than at __ receptors.

A

α1 > α2

60
Q

Selective A antagonists

A

α1: prazosin
α2: yohimbine

61
Q

A2 agonist post jxnl actvity

A

contraction of smooth muscles
platelet aggregation
etc

62
Q

α1 and α2 receptors
subgroups

A

α1 → α1A, α1B, α1D
(3 subgroups)

α2: 4 subgroups (so far)

63
Q

All α2 receptors have which moA?

A

inhibit adenyl cyclase by G protein interaction, causing a hyperpolarization

64
Q

α1 stimulation

A

increased ICF Ca release by activation of phospholipase C, (G protein mediated)

65
Q

A2r inhibit adenyl cyclase
&
A1r increases ICF Ca release

this is medicated thru _____

A

G proteins

66
Q

β receptors subclasses

A

β1 and β2

67
Q

β1 β2 β3
locations

A

1: mainly cardiac tissue

2: everywhere else

3: colon, bladder, adipose tissue

68
Q

β-receptor potencies

A

β1 receptor potency: NE >= EPI
β2 receptor potency: EPI > NE
β3 agonist potency: NE > EPI

69
Q

B Selective antagonists

A

β1- atenolol and metoprolol
β2– butoxamine

β3 selective antagonist is unknown at present

70
Q

B Selective agonists

A

β1- dobutamine
β2– albuterol

71
Q

B3 stimulation

A

lipolysis
relaxation of bladder detrusor muscle

72
Q

propranolol does not block the action of __ at __ .

A

isoproterenol @ β3

73
Q

All β receptors moA

A

via stimulatory G protein to stimulate adenyl cyclase.

74
Q

B agonism
cardiac fx

A

increased inotropy & chronotropy
controlled by increased Ca++ release

75
Q

B agonism
smooth muscle fx

A

increased cAMP → relaxation as membrane hyperpolarizes

76
Q

Tissue response is often a balance of

A

several effects

77
Q

Usually, the SNS postganglionic NT is norepi. Whats the exception?

A

Sweat glands
in symp: post ganglionic fiber is cholinergic (Ach; and not NE)

78
Q

radial vs. sphincter muscle

A

radial muscle: contract to pull iris open

sphincter muscle: around rim of pupil; contracts to close iris (miosis)

79
Q

parasympathetic effect on lens/vision

A
80
Q

sympathetic effect on lens/vision

A
81
Q

NE blocks the normal release of ___ by acting at ___.

A

NE
A2 (presyn)

also has post synaptic action

82
Q

Directly acting adrenergic agents

A

NE
phenylephrine
isoproterenol

83
Q

phenylephrine & isoproterenol
act on..

A

post synaptic A1 & B’s

84
Q

tyramine

A

indirect agent
triggers NE release
NE acts as normal

85
Q

Mixed action agents

A

Amphetamine
Ephedrine

indirect: triggers NE release
AND
direction: action @ post syn (less than NE)

86
Q

prolonged use of indirectly acting agents

A

catecholamine depletion d/t it stimulating NE release

tyramine
amphetamine
ephedrine

87
Q

Reuptake blocking agents

A

Cocaine
imipramine*
amitriptyline*

*TCAs

increases stimulation

88
Q

Inhibitors of NA storage

A

acts on & destroys vesicles
severe decrease in activity

89
Q

Why dont we use reserpine anymore

A

effects way too broad
affects adrenergic, cholinergic, etc

90
Q

Adrenergic receptor blockers

A

dont prevent release but occupy the post-synaptic receptor

phentolamine (A1 & 2)
Propanolol (B1 & 2)
Prazosin (A1)

91
Q

T/F
Adrenergic receptor blockers act by preventing release of NE.

A

False
dont prevent release but occupy the post-synaptic receptor

92
Q

False transmitter moA

A

release in place of normal NT

A-methyldopa
uptaken and converted into AmethylNE
released w/ NE
acts at post syn (<NE)

93
Q

Blocking NE release

A

prevents vesicle fusion with membrane

Clonidine (A2; blocks release)
Bretylium (doesnt let vesicle fuse with NT)
Guanethidine (releases NT intracellularly)

94
Q

Clonidine vs Reserpine

A

Reserpine destroys vesicle

Clonidine prevents its fusion with NT
(Bretylium & Guanethidine)

95
Q

Norepinephrine is the ___ isomer

A

L
“Levophed”

96
Q

Norepinephrine (Levophed) (l-isomer)
a & b

A

Potent vasoconstrictor and inotropic agent
L> d potency
More α than β activity

α: ↑ PVR, SBP, coronary flow
Some β1:
lower doses = cardiac stimulatory effects
larger doses = vasoconstrictive effects (α1) predominate cause of increased BP

97
Q

Like other catacholamines, NE increases cAMP in cells via _____, and decreases cAMP via _____.

A

increases: β stimulation

decreases: α stimulation

98
Q

Glycogenolysis
NE vs Epi

A

(inhibits insulin release & lipolysis)
Epi has more

99
Q

Levo
other fx

A

Reflexive vagal stimulation
(increased TPR & BP = ↓HR & ↑SV)

↓ Blood to abd organs & skeletal muscle

(coronary blood flow is increased indirectly due to alpha stimulation)

100
Q

Does Levop increase myocardial O2 consumption?

A

no

101
Q
A
102
Q

Does levo cross the BBB?

A

no

103
Q

When to use Levo

A

limited
mainly shock & severe hypoTN

104
Q

Epinephrine (Adrenalin)
routes

A

IV
inhalation(more selective compounds available)
opthalmic

105
Q

Epi
uses

A

cardiac stimulant and bronchodilator (anaphylactic shock)

w/ LAs & topical eye preps (prolong by vasoconstriction)

106
Q

Epi
receptor activity

A

Potent α & β agonist
(non-selective adrenergic agonist)

α1: arteriolar vasoconstriction
α2: ↓ NE release
β1: ↑ chrono & inotrope; ↓ mast hist. release
β2: arteriolar vasodilation, bronchial smooth muscle relaxation & increased glycogenolysis

107
Q

Epi
major therap. fx

A

Major therapeutic effects:
bronchodilation
cardiac stimulation
skeletal muscle vasodilation
glycogenolysis

108
Q

Epi
other fx

A

Smooth muscle:
depend on receptor density & hormonal fx

↓ IOP (wide-angle glaucoma) + brief mydriasis

Topical/local: constricts blood vessels (hemostasis)

109
Q

Epi
effect on SBP & DBP

A

SBP increased (increased inotropy)

DBP decreased (vasodilation)

110
Q

Epi
coronary effects
MDO2

A

coronary vasodilation

↑ myocardial O2 demand
has further local effect (via NO) to increased coronary vasodilation

111
Q

Epi
Increased risk of arrhythmias due to __ activity

A

β1

112
Q

___ doses of Epi will give mostly contstrictive effects

A

high

113
Q
A

Daddy Pharm (13 decks)

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