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23 spring: pharm > Test 1: lecture 10-13 > Flashcards

Test 1: lecture 10-13 Flashcards

1
Q

flight or fight is —

A

sympathetic

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2
Q

rest and digest is —

A

parasympathetic

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3
Q

sympathetic has — preganglionic nerves and — post ganglionic nerves

A

short
long

sympathetic= flight or fight

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4
Q

parasympathetic has — preganglionic nerves and — post ganglionic nerves

A

long
short

parasympathetic= rest and digest

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5
Q

— come from cranial and sacral

A

parasympathic
(rest and digest)

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6
Q

— comes from thorasic and lumbar

A

sympathetic = flight and fight

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7
Q

— is dilated pupil

A

mydriasis
happens with SYM

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8
Q

— is constrict pupils

A

miosis

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9
Q

adrenergic can also be called

A

SYMP
epi
adrenaline
norepinephrine
neoadrenaline
catecholamine

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10
Q

cholinergic responses are also called

A

PARA
acetylcholine (ACh)

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11
Q

what type of nerves release ACh

A

all PARA
all somatic
all preganglionic SYMP

only SYMP to sweat glands

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12
Q

what type of sympathetic neuron releases ACh

A

all preganglinic neurons

but only post ganglionic are the nerves to sweat glands

all other symp release NE after post ganglion

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13
Q

what kind of neurotransmitter does PARA release

A

ACh at pre and post

unlike symp which release ACh at pre and NE at post, exception is sweat glands where ACh released at both

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14
Q

epinephrine is the same as —

A

adrenaline

catecholamines

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15
Q

— is the starting chemical for catecholamines

A

L-tyrosine

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16
Q

how to get from L-tyrosine to epi

A
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17
Q

what is the rate timing step in the synthesis of epi?

A

tyrosine hydroxylase

enzyme that takes L-tyrosine and turns it into dopa

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18
Q

— acts as negative feed back inhibitor of the enzyme tyrosine hydroxylase

A

norepinephrine (NE)

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19
Q
A

tyrosine hydroxylase and DOPA decarboxylase are both found in the cytoplasm

dopamine gets into vesicle by VMAT(vesicular monoamine transporter)

dopamine β hydroxylase is found inside the vesicle

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20
Q

where does dopamine turn into NE in neuron

A

dopamine gets into vesicle by VMAT(vesicular monoamine transporter)

then interacts with dopamine β hydroxylase to form NE

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21
Q

EPI is made in — cells in the adrenal medulla

A

chromaffin cells

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22
Q

how does EPI form in adrenal gland

A

inside chromaffin cell

Tyrosine( tyrosine hydroxylase)→DOPA
DOPA(DOPA decarboxylase)→ Dopamine
dopamine moves through VMAT into vesicle
dopamine (dopamineβ hydroxylase) → NE
NE leaks out of vesicle
NE (PNMT) →epi
epi moves through VMAT back into vesicle
vesicle released= will be full of EPI and small amounts of NE

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23
Q

PNMT

A

Phenylethanolamine-N-methyl transferase

NE(PNMT) → EPI

happens in cytoplasm of chromaffin cells of the adrenal medulla

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24
Q

chromaffin cell vesicles contain

A

80% epi and 20% NE

(some of the NE do not move back out of vesicle and get released at the same time)

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25
Q

NE and EPI released by acetylcholine (ACh)-mediated —

A

Ca2+-dependent exocytosis

from chromaffin cells in the adrenal medulla

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26
Q

where is PNMT found

A

found in chromaffin cells of the adrenal medulla

not found in nerve terminals- nerves can’t make EPI, only get to NE stage

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27
Q

No active reuptake of — into adrenal gland …. unlike in — reuptake in neurons

A

EPI

NE

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28
Q

why does the adrenal gland act as a modified sympathetic ganglion

A

preganglionic releases ACh
but chromaffin cell releases NE and EPI directly into blood supply

no post ganglion

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29
Q

Stimulation of preganglionic fibers release ACh directly onto chromaffin cells which then release — directly into the blood stream

A

EPI/NE

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30
Q

what happens to NE released into post synaptic cleft

A

can bind to postsynaptic receptor on other nerve

can bind to ⍺2 presynaptic autoreceptor: cause negative feedback

can be pulled through plasma membrane transporters back into synapse

from there NE can either move through VMAT back into vesicles or it can be broken down by MAO (monoamine oxidase)

any left over NE in the terminal will get eaten by COMT

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31
Q

NE in the cytoplasm of 1st nerve can

A

move through VMAT back into vesicle

can be broken down by MAO (monoamine oxidase)

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32
Q

— is a receptor on the presynaptic membrane side that pulls NE back into cytoplasm of 1st nerve

A

plasma membrane transporter

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33
Q

two ways catecholamines are metabolized

A

MAO (monoamine oxidase)
* degrades cytoplasmic NE
* MAO found in outer member of mitochondria

COMT (Catechol-o-methyl transferase)
* found in synaptic cleft and liver
* will break catecholamines (EPI, NE) into metabolites that are then excreted in the urine

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34
Q

how does Gprotein cycle work

A
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35
Q

how to measure drug affinity

A

saturation binding isotherm

Kd= concentration of drug that fills 50% of the receptors

lower the Kd= higher affinity

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36
Q

The lower the Kd the — the ligand affinity

A

higher

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37
Q

Described by the agonists intrinsic activity (IA) which is the maximal amount of system stimulation achievable in the presence of saturating concentrations of the agonist

A

efficacy

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38
Q

Described by the EC50: the concentration of drug that results in 50% of its maximal stimulation

A

potency

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39
Q

which one is more potent?
what is the ranked order

A

A is more potent (takes less A to get to 50% activation)

rank order: A>B

EC50 of A= 0.01 nM
EC50 of B= 1 nM

smaller the EC50 the more potent the agonist

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40
Q

what is the intrinsic activity (IA) of each line and what does it mean

A

this is comparing potency and efficacy of different agonists

both A and B get to top= 100%= IA=1 full agonist (all the receptors are bound and working at full capacity)

C does not make it to the top, IA= 0.6= partial agonist

A and B are more efficacious than C (intrinsic activity is 1 for A+B, less then 1 for C)

A and B are also more potent then C (EC50 is smaller= more potent, takes less drug to get to 50% total)

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41
Q

A and B are more — than C

A

potent (EC50 smaller= increased binding)

efficacious (shorter= 0-1 → IA higher, agonist at max saturation has reached max stimulation)

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42
Q

rank order of catacholamines for ⍺ receptors

A

EPI ≥ NE > DA ⫸ ISO

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43
Q

rank order for β adrenergic receptors

A
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44
Q

what type of adrenergic receptors in the heart?

A

there are only β

increase HR, increased conduction velocity and decreased refractory period and increased contracility are all by β1 receptors

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45
Q

in skeletal muscle ⍺ receptors cause — and β receptors cause

A

contriction

β2: dilation

46
Q

EPI has HIGHER affinity for — receptors than — receptors

A

β2
⍺

47
Q

low dose epi will do what to vascular smooth muscle?

A

has lower Kd/ higher affinity for β2 receptors

will bind those first → relaxation

48
Q

what happens with high dose EPI on vascular smooth muscle

A

1st fills β2 then will spill over to ⍺1

if there are more ⍺1 then will cause contraction

49
Q

in the GI tract effect of ⍺ and β

A

same direction

both cause smooth muscle relaxation

50
Q

in the heart effect of ⍺ and β

A

no ⍺

β only → increase HR, contractility and conduction velocity

51
Q

in the blood vessel effect of ⍺ and β

A

⍺ and β opposite direction

⍺: constriction
β: dilation

52
Q

in the urinary bladder (trigor and sphincter) effect of ⍺ and β

A

only ⍺ : contraction
no β

53
Q

under basal conditions there is a continous release of NE onto vessels keeping them partillary contracted due to binding and activiation of — on the vascular smooth muscle cell

A

⍺1 receptors

54
Q

for blood vessel:
Adding — causes vasodilation because there is already norepinephrine-mediated vasoconstrictive tone on vessels

A

α1 receptor antagonist

blood vessels always have small amount of NE causing slight contraction, if you decrease NE release or release ⍺1 antagonist, will cause vasodilation

55
Q

GI tract is under — — tone which causes —. If you block this signal it will cause —

A

parasympathetic cholinergic

movement
constipation

cholinergic (receptor that responds to ACh- all PARA are under ACh control)

sweat glands are under SYM cholinergic control

all other SYM are controlled by NE/adrenergic receptors

56
Q

arterioles is under — — tone which causes —. If you block this signal it will cause —

A

sympathetic adrenergic

vasoconstriction

vasodilation (increased flow) hypotension

57
Q

heart is under — — tone which causes —. If you block this signal it will cause —

A

parasympathetic cholinergic

bradycardia
tachycardia

58
Q

sweat glands are under — — tone which causes —. If you block this signal it will cause —

A

sympathetic cholinergic

hidrosis- sweating

anhidrosis- not sweating

59
Q

if you give βblocker to healthy person what will happen to resting heart rate

A

nothing

NE binds to β1 adrenergic receptors to cause increased HR

if you block β1 receptor, HR will stay the same

heart controlled by PARA (Ach) → keeping HR down, under normal conditions very little SYM/NE tone on heart, therefore trying to block with B1 does not have a significant change

an antagonist needs an agonist present to block to change physiology

60
Q

What would happen to resting heart rate if you gave a muscarinic ACh receptor blocker ?

A

ACh keeps heart in bradycardia

if you block ACh will cause tachycardia

heart controlled by PARA cholinergic receptors keeping it in a resting state of bradycardia

61
Q

what is a adrenergic receptor

A

receptor that binds to NE

includes most sympathetics except sweat glands

62
Q

what is a cholinergic receptor

A

binds to ACh

includes all parasympathetics

also includes sympathetic control of sweat glands

also includes somatic control of skeletal muscles

63
Q

what is the baroreceptor(vagal reflex)

A

if blood pressure too high, baroreceptors in the aorta or the carotid will send signal to the brain

this will cause decrease in HR and vasodilation

64
Q

rank order of EPI vs NE in β1

A
65
Q

rank order of EPI vs NE in β2

A
66
Q

rank order of EPI vs NE in β3

A
67
Q

— = great nonselective β agonist (β1 and β2)

A

Isoproterenol

68
Q

Low doses of EPI → — effects predominate

A

β

spill over

69
Q

NE does not activate — very well

A

β2
EPI ⫸ NE

70
Q

↑ HR + force of contraction with ’no change’ in vascular resistance → —

A

increased blood pressure

71
Q

Vasodilation of blood vessels with ’no change’ in cardiac output will make —

A

decreased blood pressure

72
Q
A
73
Q

which catecholamine

A

NE

74
Q

which catecholamine

A

epi

75
Q

which catecholamine

A

ISO

76
Q

which catecholamine

A

dopamine

77
Q

if you give epi what will happen in general to a1, B1, B2, a2 receptors

A
78
Q

low dose NE will do what to the heart

A

Activate β1 in heart =↑HR ↑FC ↑CO

will cause vagal reflex that causes↶ of HR and CO

FC (force of contraction remains ACh, no effect on ventricles)

79
Q

low dose NE will do what to vasculature?

A

Activate α1 cause vasoconstriction → ↑ peripheral resistance

Low NE does not activate β2 well and is overwhelmed by α1 activation

80
Q

low dose NE will do what to vagal reflex

A

Initially a significant increase in Mean BP ( ↑ SP and DP)

Vagal Reflex → Bradycardia (decrease heart rate)

will have same effect as high dose epi

81
Q
A

low dose NE

82
Q
A

low dose NE

or high dose Epi or high dose DA
they have the same effect

83
Q

low dose EPI does what to heart

A

Activate β 1 in heart → ↑ in HR, FC, CO

84
Q

low dose EPI does what to vasculature

A

activates β2 causes vasodilation →↓ peripheral resistance

remember at low epi effect on B receptors predominate

85
Q

what happens to vagal reflex with low dose epi

A

No significant increase in Mean BP
No Vagal Reflex

86
Q
A

low dose epi

87
Q
A

low dose epi
iso

88
Q

high dose epi will look the same as —

A

high and low dose NE

this is because at high dose EPI, ⍺1 receptors will win causing vasoconstriction

89
Q

what happens to heart with high dose Epi

A

activates β1 in heart → increased HR, FC, CO

FC remains ACh no effect on ventricles

will have same effect as NE

90
Q

what happens to vasculature with high dose epi

A

Activate α1 causes vasoconstriction →. increased peripheral resistance

Activate β2 to try to cause vasodilation but activation of α1 ‘wins’

will have same effect as NE

91
Q

what happens to vagal reflex with high dose epi

A

Initially a significant increase in Mean BP ( ↑SP and DP)

Vagal Reflex → Bradycardia (decrease heart rate)

will have same effect as NE ( NE does not activate B2 well)

92
Q
A

high dose epi or low dose NE or high dose Dopamine

93
Q

iso will do what to the heart

A

activate β1 in heart → increased HR, FC and CO

94
Q

iso will do what to vasculature?

A

Activate β2 causes vasodilation →decreased peripheral resistance

95
Q

iso will do what to vagal reflex

A

Significant decrease in PR and increase in HR

No Vagal Reflex (Mean BP unchanged)

96
Q
A

low or high dose iso

97
Q
A

low or high dose iso

98
Q

DA has highest affinity for DA receptors but also has some affinity for — and even lower
affinity for — adrenergic receptors

A

α1 α2 β1

β2

99
Q

At LOW concs, Dopamine can activate — to some degree but does not activate — receptors at all

A

α1 α2 β1

β2

100
Q

At — concs, DA activates α1 α2 β1 but also now activates some β2 receptors

A

HIGH

101
Q

Effects of LOW vs HIGH Dopamine concentrations reminiscent of LOW vs HIGH —

A

epi

102
Q

low dose dopamine effect on heart

A

minimal activation of β1 in heart = increased HR, FC, CO

similar to low dose epi and iso

103
Q

low dose dopamine does what to vasculature

A

No activation of β2 receptors so no β2 -mediated vasodilation

Minimal activation of α1 receptors in vasculature- minimal vasoconstriction

Significant D1-mediated vasodilation of mesenteric (gut), renal, and coronary vascular beds decreasing peripheral resistance

104
Q

low dose dopamine does what to vagal reflex

A

no vagal reflex
mean BP unchanged

105
Q
A

low dose dopamine

106
Q

high dose dopamine will do what to heart

A

Significant activation β1 in heart = increased HR, FC, CO

107
Q

high dose dopamine will do what to vagal reflex

A

Vagal Reflex →Bradycardia (decrease heart rate)

108
Q
A

high dose dopamine, high dose epi, NE

109
Q
A
110
Q
A
111
Q
A
112
Q
A

23 spring: pharm (46 decks)

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