Brainscape's Knowledge GenomeTM

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


See full index

Neuro Exam #1 > ANS pharmacology > Flashcards

ANS pharmacology Flashcards

1
Q

locations of nicotinic receptors

A

NMJ, autonomic ganglia, brain

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

location of M1 muscarinic receptors

A

CNS, gastric parietal, sympathetic postganglionic cells

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

differences between nicotinic and muscarinic receptors, including difference in signal transduction mechanisms

A

nicotinic are ligand-gated ion channels, muscarinic are G protein coupled receptors.

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

state the significance of presynaptic versus postsynaptic cholinergic receptors

A

drugs that act postsynaptically are more selective than drugs that act presynaptically. because drugs that act presynaptically affect all synapses for that particular neurotransmitter

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

list the 3 categories of acetylcholinesterase inhibitors and the relation between the nature of the inhibitor interaction with AChE adn its duration of action-clinical utility

A

1) reversible, short acting (edrophonium) 2) reversible, intermediate-to-long acting (neostigmine-physostigmine) 3) irreversible, very long acting (isofluorophate-Nerve Gas)

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

action of cholinergic agonists

A

PNS stimulation

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

antimuscarinic agents/parasympatholytics

A

cholinergic antagonists that act at parasympathetic end organs

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

neuromuscular blockers

A

cholinergic antagonists that act at the neuromuscular junction (NMJ)

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

monoamine oxidase inhibitors

A

indirect-acting adrenergic agonists that increase storage and release of norepinephrine/epinephrine

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

sympatholytic action

A

just means inhibition of some aspect of synthesis-storage-release of NE

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

ACh synthesis and storage

A

Choline is taken up by active transport system that is dependent on Na+ and blocked by hemicholinium. Rate-limiting step. Synthesis occurs in the cytoplasm of the terminal and is catalyzed by choline acetyl transferase (ChAT). ACh is then stored within vesicles by a second transporter.

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

hemicholinium

A

enzyme that blocks uptake of choline

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

vesamicol

A

enzyme that inhibits ACh vesicle storage

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

How is ACh release modulated?

A

NE interacts with presynaptic alpha2-adrenergic heteroreceptors.

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

How is ACh action terminated?

A

hydrolysis catalyzed by acetylcholinesterase (AChE)

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

Pathway for interaction of ACh with acetylcholinesterase

A

Ac: esteratic site attracts acetyl group (CH3-COO) of acetylcholine. Cat: catalytic site where acetyl group is covalently bound to the serine [Ser-OH] of acetylcholinesterase while the choline group is released. Acetyl-serine-enzyme bond is hydrolyzed rapidly.

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

choline esters, examples, and pharmacokinetics

A

direct-acting muscarinic receptor agonists, including acetylcholine and bethanechol. low lipid solubility, poor oral absorption and distribution into CNS.

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

acetylcholine applications

A

not used, rapidly hydrolyzed by AChE

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

bethanechol and applications

A

synthetic analog of acetylcholine. can be modified structurally to produce selectivity for muscarinic receptors (by adding methyl group) and/or resistance to AChE (replace acetyl group with carbamyl group).

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

parasympathamomimetic alkaloids, examples mechanism, pharmacokinetics.

A

direct acting-muscarinic receptor agonists. pilocarpine. lipid soluble so well absorbed and can distribute into CNS.

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

pilocarpine (salagen)

A

muscarinic agonist

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

nicotine, class, mechanism.

A

direct-acting nicotinic neuronal (ganglionic) receptor agonists. stimulates both PNS and SNS. mechanism is dose dependent, agonist at low doses (impt - causes vasoconstriction via epinephrine released from adrenal gland activating SNS). At larger or prolonged doses it causes depolarization blockade and thus antagonism.

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

edrophonium

A

indirect-acting, reversible, short acting cholinesterase inhibitor. bond is readly reversible/not ionic so short acting.

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

neostigmine, physostigmine

A

indirect-acting, reversible, intermediate-to-long acting cholinesterase inhibitor. transfers a carbamyl group to anionic site on AChE, thereby inhibiting acetylcholinesterase. IMPT: physostigmine is distributed to CNS but neostigmine is not.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
isofluorophate - nerve gas
indirect acting, irreversible cholinesterase inhibitor. covalently transfers a phosphate group to AChe, thereby inhibiting AChe.
26
location of M2 muscarinic receptors
cardiac cells
27
location of M3 muscarinic receptors
smooth muscle organs and glands
28
alkaloids mechanism and examples
high affinity and specificity antimuscarinic agents. atropine and scopolamine.
29
propantheline and glycopyrrolate, (ipratropium?)
semisynthetic-synthetic antimuscarinic agents with greater effect on GI activity. Quaternary ammonium compounds so low lipid solubility and poor oral absorption and excreted unchanged in urine.
30
benztropine, oxybutynin, tolterodine
semisynthetic-synthetic antimuscarinic agents with greater effect on CNS. Tertiary amines so well absorbed from GI and conjunctival membranes and eliminated by a combination of hepatic metabolism and renal excretion.
31
how do anti-nicotinic ganglionic blocking agents work? applications?
block neurotransmission in autonomic ganglia so affect predominant tone. since predominat tone is largely sympathetic for arteries/veins, blockage leads to vasodilation/hypotension/reduced cardiac output. not used anymore.
32
biosynthesis of norepinephrine
tyrosine is natural precursor and taken up by active transporter --> converted to dihydroxyphenylalanine (DOPA) by tyrosine hydroxylase. DOPA converted to dopamine by L-aromatic amino acid decarboxylase (l-AAD) in cytosol --> dopamine is taken up into catecholamine storage vesicle by vesicular amine pump and converted to norepinephrine by dopamine beta-hydroxylase (DbetaH) --> (only in adrenal gland and certain CNS neurons) NE converted to epinephrine by phenylethanolamine n-methyl transferase.
33
metyrosine
enzyme that inhibits conversion of tyrosine to DOPA
34
alpha-methyl dopa/carbidopa
enzymes that inhibit conversion of DOPA to dopamine
35
what is the common structural property of catecholamine neurotransmitters
they all have the phenylethylamine nucleus and catechol hydroxyl (OH) groups in common.
36
what defines neurotransmitter group of monoamines or "biogenic" amines?
catecholamines + indoleamine 5-hydroxytryptamine (serotonin)
37
norepinephrine storage and release
the vesicle membrane for NE contains an active pump called VMAT.
38
NE transporter
This is the pump located on the presynaptic membrane that removes released NE from the synapse.
39
monoamine oxidase
enzyme on mitochondria that degrades NE
40
bretylium
enzyme that prevents release of catecholamines
41
How is NE terminated following synaptic action?
most impt mechanism is reuptake by NET (norepinephrine transporter).
42
What are some drugs that inhibit reuptake of NE?
cocaine, TCAs
43
action of amphetamines, pseudoephedrine
these are phenylethylamine drugs that indirectly release NE by reversing the NET transporter.
44
a1-receptor activation
Gq protein that activates phospholipase C --> release of IP3 (releases intracellular stores of Ca++) and DAG (activates protein kinase C)
45
a2-receptor activation
Gi protein that inhibits adenylyl cyclase activity --> decreases cAMP levels or opens K+ channels. Effect is to decrease Ca++ movement.
46
b1 and b2 receptor activation
Gs protein that stimulates adenylyl cyclase --> increased cAMP synthesis --> which activates protein kinase A. Thus increases Ca++ movement.
47
what is the most common mechanism of indirect acting adrenergic agonists?
increasing storage and release of NE
48
how is the ability of adrenergic agonists to enter the CNS determined?
lack of hydroxyl groups on phenyl ring increases drug's lipophilicity.
49
How do you increase the oral effectiveness of adrenergic agonists?
non-catechols (no hydroxyl group) are resistant to first pass metabolism because they are not substrates for catechol-O-methyl transferase in the liver. Drugs with a methyl group are protected from degradation from MAO in the liver.
50
general pharmacokinetics of catecholamine neurotransmitters (NE and E)
not effective orally, don't enter brain well, and have short duration of action.
51
sympatholytic action
interference with adrenergic function in the PRESYNAPTIC neuron. Little clinical utility.
52
reserpine mechanism
inhibits catecholamine storage. It does this by inhibiting VMAT.
53
bretylium, guanethidine
inhibit catecholamine release
54
metyrosine mechanism and use
inhibits tyrosine hydroxylase. pheochromocytoma.
55
disulfiram mechanism
inhibits dopamine b-hydroxylase
56
alpha-methyldopa
inhibits DOPA decarboxylase. metabolized to alpha-methylnorepinephrine which is an agonist at alpha2 receptors in the CNS; used as an antihypertensive agent.
57
carbidopa mechanism and uses
inhibits L-DOPA decarboxylase so prevents metabolism of levodopa to dopamine. used as an adjunct to levodopa therapy for PD.
58
phentolamine / phenoxybenzamine
alpha adrenergic receptor antagonists. phentolamine is a non-selective (a1 and a2) reversible antagonists. phenoxybenzamine is an irreversible non-selective antagonist.
59
Prazosin / terazosin / doxazosin
highly selective, reversible alpha adrenergic receptor antagonists.
60
location of beta1 receptors
heart
61
location of beta2 receptors
lung, blood vessels
62
propranolol
nonselective reversible beta blocker
63
metoprolol,atenolol
cardioselective/b1 selective beta blocker, only at lower doses.
64
What is the effect of alpha-2 receptor activation in the CNS and SNS?
reduces SNS activity (counterintuitive). SNS: stimulates peripheral alpha2 receptors and reduces NE release. CNS: stimulation in brain stem reduces peripheral SNS activity.
65
How are most anti-adrenergics absorbed?
most are available via the oral route. significant 1st pass metabolism for some.
66
Why does nicotine act as a "depolarizing blocking agent" at toxic blood levels?
persistent depolarization desensitizes the nicotinic receptor.
67
Alkaloids
Naturally occurring agents with very high affinity and specificity for muscarinic receptors.
68
location of ACh muscarinic receptors
heart, lungs, GI/GU tract, eye, sweat glands,
69
location of alpha and beta adrenergic receptors
cardiac and smooth muscle, gland cells, nerve terminals
70
location of dopamine receptors
renal vascular smooth muscle
71
location of nicotinic ACh receptors
somatic/skeletal muscle, renal medulla, sympathetic ganglia
72
receptor and agonist responsible for smooth muscle contraction
A1, NE
73
action of NE on A1 receptors
smooth muscle contraction, mydriasis, vasoconstriction in the skin, mucosa and abdominal viscera, sphincter contraction of the GI tract and urinary bladder
74
Effect of E on A2 receptors
smooth muscle mixed effects, platelet activation
75
Effect of B1 receptor activation
positive chronotropic, dromotropic, and inotropic effects, increased amylase secretion
76
Effect of B2 agonism
smooth muscle relaxation (ex. bronchodilation)
77
Effect of B3 agonism
enhance lipolysis, promotes relaxation of detrusor muscle in the bladder.
78
heart regulation
effects largely mediated by B1 receptors
79
BP control
A1: vasoconstriction, B1: increased heart rate and increased force of contraction, B2: vasodilation, A2: decrease in SNS outflow decreases BP
80
respiratory tract regulation
relaxation and bronchodilation via B2 receptors. upper respiratory tract mucosal blood vessels: constriction via A1 receptors
81
what is an exception to the general rule that branches of autonomic system usually exert opposite effects
control of salivary glands: both branches stimulate secretion but alter saliva content in a different manner.
82
what is the treatment for glaucoma?
Muscarinic agonists (increase aqueous humor outflow) OR b1-2 antagonist (decrease aqueous humor production)
83
what is the treatment for urinary incontinence?
muscarinic agonists, which increase detrusor contraction
84
What is the treatment for paralytic ileus?
muscarinic agonists, which increase GI motility
85
what is the treatment for asthma?
***cholinergic antagonists, (bronchodilation) OR b2 agnosists (bronchodilation)
86
treatment for overactive bladder?
cholinergic antagonist (block detrusor)
87
treatment for diarrhea?
cholinergic antagonist (decrease GI motility)
88
treatment for hypotensive shock?
a1, b1 agonists (increase blood pressure)
89
what is the treatment for micturition disorders, BPH?
a1 agonists (open sphincter)
90
treatment for hypertension?
a1,b1 antagonists + a2 AGONIST
91
treatment for premature labor?
b2: uterine relaxation
92
treatment for ADHD
adrenergic agonists (increase vigilance/focus)
93
treatment for bradycardia?
cholinergic antagonists
94
treatment for cardiogenic shock?
b1 agonists (increase HR/contractility)
95
epinephrine
a1-b1-b2 agonist
96
norepinephrine
a1-b1 agonist
97
isoproterenol
b1-b2 agonist
98
albuterol
b2 agonist
99
phenylephrine
a1 agonist
100
pseudoephedrine
indirect adrenergic agonist
101
dobutamine
b1 agonist
102
dopamine
d1 indirect agonist
103
prazosin-doxazosin-terazosin
a1 antagonist
104
metoprolol-atenolol
b1 antagonist
105
propranolol
b1-b2 antagonist
106
labetalol-carvedilol
a1-b1-b2 antagonist
107
clonidine
a2 agonist
108
oxybutynin-tolterodine
cholinergic antagonist (M)
109
ipratropium-tiotropium
muscarinic antagonist
110
atracurium-rocuronium-succynilcholine
nicotinic antagonist
111
treatment for HTN/Angina/Arrhythmias/CHF
b1 antagonism
112
treatment for neurogenic shock?
...
113
optimal drug action for muscle relaxation in surgery?
cholinergic antagonists
114
optimal drug action for PD/anti-emetic?
cholinergic antagonists
115
optimal drug action for decongestion/relief of nasal congestion?
a1 agnoist (vasoconstriction)
116
activation of which PNS receptor subtype is most commonly associated with smooth muscle contraction?
a1
117
why does a2 agonism decrease BP?
Norepinephrine activation of α2 adrenergic receptors on cholinergic neurons in the GI tract will decrease acetylcholine release.
118
what is the effect of NE activation of a2 adrenergic receptors on adrenergic neurons in cardiac tissue?
decreases NE release
119
what is the effect of a2 receptor agonism?
CNS: reduces peripheral sympathetic nervous system activity SNS: preferentially stimulates peripheral a2 receptors and thus REDUCES NE release from sympathetic neurons.
120
Optimal drug to treat hypertension?
a1,b1 antagonist, or b1 antagonist.
121
Treatment for AD?
muscarinic agonists
122
Treatment for PD?
cholinergic antagonists
123
what do you use treat emesis/motion sickness?
cholinergic antagonists

Neuro Exam #1 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions