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Medical Pharmacology > Overview of Neurotransmission > Flashcards

Overview of Neurotransmission Flashcards

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USMLE® Step 1 flashcards
1
Q

what is an agonist that directly interacts with Nn receptors

A

nicotine

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2
Q

what is a partial agonist that directly interacts with Nn receptors

A

varenecline (chantix)

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3
Q

what is an antagonist that directly interacts with Nn receptors

A

mecamylamine

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4
Q

action of succinylcholine

A

a noncompetitive, depolarizing Nm blocker (cannot reach Emax)

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5
Q

action of CURare derivatives

A

nondepolarizing Nm blocker (competitive) (can still reach Emax)

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6
Q

example of CURare derivative

A

roCURonium (zemuron )

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7
Q

what are 5 targets for neurotransmitters?

A
  1. synthesis
  2. storage
  3. release
  4. termination of action
  5. receptor (direct)
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8
Q

4 indirect targets of NT

A

synthesis, storage, release, termination of action

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9
Q

direct target of NT

A

receptors

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10
Q

role of adrenal medulla in sympathetic activation

A

releases 80% epinephrine and 20% norepi in response to ACh stimulation

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11
Q

receptor type on sweat glands

A

Muscarinic receptors (M3) on erector pili and sweat glands, even though anatomically sympathetic (but postgang fibers release ACh)

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12
Q

what receptors are associated with the enteric nervous system

A

oral and aboral

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13
Q

what are oral receptors for

A

control peristalsis of GI via Gq GPCR

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14
Q

what are aboral receptors for

A

activate relaxation of GI via Gs GPCR

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15
Q

what activates oral receptors

A

ACh and other substances and Gq (peristalsis)

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16
Q

what activates aboral receptors

A

norepi and other substances and Gs (relaxation)

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17
Q

how does alteration of ACh, norepi serotonin and others with drugs impact ENS?

A

impacts oral and aboral receptors to either increase peristalsis (diarrhea!!) or cause GI slowing

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18
Q

what is NANC

A

nonadrenergic noncholinergic neurons

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19
Q

what are the NANC “players”

A

nitric oxide, vasoactive intestinal peptide, calcitonin gene related peptide, adenosine, CCK, endogenous opioids, tachykinins

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20
Q

what do NANC do

A
  1. penile erection
  2. peristalsis GI
  3. relaxation of vascular smooth muscle
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21
Q

action of sympathetic activation on blood vessels

A

a1 receptors are innervated, but B2 receptors are NOT innervated…therefore, GPCR a1 causes primary vasoconstriction then slight relaxation as the adrenal medulla releases epinephrine to activate (noninnervated) B2

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22
Q

action of sympathetic activation on lungs

A

B2 receptors (not innervated) are activated by epinephrine release by adrenal medulla, causing bronchodilation

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23
Q

what activates epi and norepi release from adrenal medulla?

A

ACh on Nn

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24
Q

sympathetic actions

A
  1. mydriasis (dilation)
  2. reduced saliva flow (a1)
  3. increased SV and HR (B1)
  4. vasoconstriction
  5. reduced peristalsis and secretion
  6. increased glucogenolysis
  7. inhibition of gladder contraction
  8. epinephrine release
  9. B2 bronchodilation
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25
Q

parasympathetic actions

A
  1. miosis (constriction) and accommodation
  2. stimulated saliva flow
  3. decreased HR (vagus)
  4. bronchoconstriction (vagus)
  5. peristalsis and secretion (vagus)
  6. stimulate bile release (vagus)
  7. bladder contraction
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26
Q

which effector organ is innervated by the sympathetic nervous system but is activated when postgang sympathetic nerve releases ACh?

A

adrenal medulla

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27
Q

describe somatic neuron

A

Ach Nm neuron (NMJ)

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28
Q

describe parasympathetic neuron

A

Ach releasing (long )preganglionic neuron at Nn, then Ach releasing (short) postganglionic fiber at Muscarinic receptor on target organ

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29
Q

describe sympathetic neuron

A

Ach releasing (short) preganglionic neuron at Nn, then norepi (mostly) releasing (long) postganglionic fiber at adrenergic receptor on target organ

except adrenal medulla, has Ach releasing neuron

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30
Q

how does SNS stimulate bronchodilation

A

works through Nn on adrenal medulla to release epi

relies on epi from adrenal medulla because B2 is not innervated

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31
Q

what is the autoreceptor

A

a2 – turns off further release of sympathetic outflow from the neuron

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32
Q

what is the M1 receptor

A

Gq receptor in head

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33
Q

M2 receptor

A

Gi receptor in heart, and autoreceptor

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34
Q

M3 receptor

A

Gq receptor everywhere else

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35
Q

a1 receptor

A

Gq coupled, increases Ca which acts on smooth muscle to contract (arterial smooth muscle, mydriasis)

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36
Q

a2 receptor

A

Gi coupled, autoreceptor, CNS, deactivates K (If) (funny current) channels (doesn’t bring back up to depolarizing)

on presynaptic terminal

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37
Q

B1 receptor

A

Gs on the heart and juxtaglomerular cells (macula densa) to increase renin

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38
Q

B2 receptor

A

Gs relaxation of smooth muscle, bronchioles, gravid uterus, vascular endothelium (epi>NE)

and skeletal muscle, increases glucose uptake and Na/K ATPase

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39
Q

what causes Reynaud’s syndrome

A

excessive a1 stimulation

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40
Q

B3 receptor

A

Gs lipolysis, thermogenesis, detrusor relaxation (step urination)

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41
Q

what causes contraction in gravid uterus

A

toward the end of pregnancy, increased number of a1 receptors in the gravid uterus cause it to contract

42
Q

how does Gs inhibit platelet activation

A

vasodilator activated phospholipid inside of the platelet is phosphorylated by Gs, which decreases likelihood of platelet being activated and aggregate

43
Q

what degrades cAMP

A

phosphodiesterase (PDE)

44
Q

how do some indirect agonists work

A

inhibit PDE so longer functioning of cAMP

45
Q

what is the SNS autoreceptor

A

a2

46
Q

what is the PSNS autoreceptor

A

M2 and M4

47
Q

presynaptic mechanism of regulation

A

a2 autoreceptor and M2 autoreceptors

48
Q

postsynaptic mechanism of regulation

A

receptor down and upregulation

49
Q

what occurs if receptor is constantly blocked

A

is upregulated

50
Q

what occurs if receptor is constantly activated

A

is downregulated and endocytosed via phosphorylation and activation of beta arrestin

51
Q

how to cause tolerance

A

constant exposure of drug to receptor causes downregulation of receptor.

52
Q

what causes withdrawal

A

a sudden stoppage of a drug that has caused downregulation of receptors, causes opposite effect of the drug bc fewer receptors and took away excess agonist

53
Q

what causes dependence

A

no longer have regular or normal function without an exogenous substance due to receptor downregulation and withdrawal

54
Q

steps of beta receptor desensitization

A
  1. initial exposure to agonist causes cAMP response
  2. continued exposure causes diminished response within a few minutes due to phosphorylation of receptor with subsequent beta arrestin binding
  3. internalization of bound receptor
  4. dephosphorylation by phosphatase
  5. return to cell membrane OR lysosomal degradation
55
Q

how are blood vessels controlled in PSNS

A

M3 receptors are NOT innervated aka no endogenous signal

therefore, a drug that increases ACh won’t impact this receptor because it can’t travel to it

56
Q

how are nicotinic receptors activated

A

2 ACh molecules

57
Q

where are M receptors found

A

organs innervated by PSNS and pili erector muscle and eccrine sweat glands

58
Q

what is the result of activation of Nn in the ganglia?

A

increased outflow of both SNS and PSNS

59
Q

what is the result of inhibition of acetylcholinesterase?

A

accumulation of ACh and increase of SNS and PSNS

60
Q

what controls BP

A

almost entirely SNS

61
Q

describe baroreceptor reflex arc

A

stimulation of a1 on vascular smooth muscle causes contraction and increased peripheral resistance, increasing BP. body responds by activating M2 on the heart which decreases HR.

62
Q

what do drugs that cause vasoconstriction usually cause?

A

reflex decrease in HR

63
Q

what do drugs that cause vasodilation usually cause

A

reflex increase in HR

64
Q

what is mecamylamine used for

A

it is a Nn antagonist used in exams to test knowledge of reflex responses of HR to BP

65
Q

MOA mecamylamine

A

blocks Nn, the reflex pathway is blocked at the ganglia so no reflex change in HR can occur

66
Q

effect of PSNS on CNS

A

M1 receptors, help with memory/cognition, balances with dopamine for control of movement

67
Q

effect of PSNS on eye and ciliary muscle

A

M3 receptors for miosis (constriction) and lacrimation, and contract for accommodation (near vision)

68
Q

effect of PSNS on salivation

A

increased salivation (M3)

69
Q

effect of PSNS on bronchiolar smooth muscle

A

M3 - contraction (bronchoconstriction)

70
Q

effect PSNS on heart

A

M2 causes decreased rate

71
Q

effect of PSNS on blood vessels

A

M3 is not innervated on vasculature, but is stimulated by exogenous agonists’ increased NO release

72
Q

effect of PSNS on GI and sphincters

A

M3 receptors cause increased secretion and peristalsis

73
Q

effect of PSNS on bladder

A

contract detrusor muscle (urination) (M3), trigone and sphincter relax (M2)

74
Q

effect of PSNS on male GU

A

erection via NANC increased NO

M3

75
Q

effect of SNS on CNS

A

beta 2 provokes fear, anxiety, mood and learning

alpha 2 increases signal to noise ratio

76
Q

effect of SNS on the eye

A

alpha 1 causes mydriasis (dilation)

beta causes increased aqueous humor

77
Q

effect of SNS on salivary

A

alpha 1 decreases salivary

78
Q

effect of SNS on bronchiolar smooth muscle

A

beta 2 causes bronchodilation

79
Q

effect of SNS on the heart

A

beta 1 increases rate, force, conduction, and automaticity

80
Q

effect of SNS on blood vessels

A

alpha 1 causes contraction and increased blood pressure

beta 2 causes relaxation and decreased blood pressure via epi

81
Q

effect of SNS on GI and sphincters

A

alpha 1 causes decreased secretion, and decreased peristalsis, and decreased contraction

82
Q

effect of SNS on liver

A

alpha 1 and beta 2 cause glycogenolysis and gluconeogenesis

83
Q

effect of SNS on sweat glands

A

M3 receptors respond to promote sweating

84
Q

effect of SNS on kidney

A

beta 1 causes increased renin release from JGA

85
Q

effect of SNS on bladder

A

beta 3 causes detrusor to relax

alpha 1 causes trigone and sphincter to contract

86
Q

effect of SNS on male GU

A

alpha 1 causes ejaculation

87
Q

effect of SNS on uterus

A

alpha 1 causes gravid contraction

beta 2 causes gravid and nongravid relaxation

88
Q

effect of SNS on fat cells

A

beta 3 causes thermogenesiss, lipolysis, decreased leptin release

89
Q

effect of SNS on skeletal muscle

A

beta 2 causes K and glucose uptake

90
Q

MOA of nicotine

A

full agonist at nicotinic receptors, but at high doses is a depolarizing nicotinic antagonist (noncompetitive)

91
Q

initial action of nicotine

A

turns on Nn receptors, but doesn’t let go = depolarizing blockade (desensitization)

92
Q

why is vascular tone predominantly sympathetic

A

alpha 1 receptor gets the signal from neuron that releases norepi but M3 receptors on blood vessels don’t have innervation (no postganglionic fiber leads to M3) so see only sympathetic.

93
Q

dominant tone of arterioles

A

sympathetic (alpha 1 is innervated, M3 is not)

94
Q

dominant tone of veins

A

sympathetic

95
Q

dominant tone of heart

A

parasympathetic (M2)

96
Q

dominant tone of pupil

A

parasympathetic (M3)

97
Q

dominant tone of ciliary

A

parasympathetic (M3)

98
Q

dominant tone of GI

A

parasympathetic (M3)

99
Q

dominant tone of bladder

A

parasympathetic (M3)

100
Q

dominant tone of salivary

A

parasympathetic (M3)

101
Q

dominant tone of sweat

A

sympathetic (but have M3)

102
Q

what occurs with prolonged toxic levels of nicotine?

A

Nn receptor becomes refractory and effects will match “blockade” due to loss of dominant tone (opposite effect)

Medical Pharmacology (13 decks)

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