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PHARM Exam 2 > Autonomic Neurotransmission > Flashcards

Autonomic Neurotransmission Flashcards

(53 cards)

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1
Q

Synthesis of ACh

A

acetyl CoA + choline + choline acetyl-transferase enzyme –> ACh

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2
Q

Storage of ACh

A

transported and stored in nerve terminal vesicles, uptake mediated by H_-ACh antiporter

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3
Q

Release of ACh

A

AP and depolarization of terminal

influx of Ca, initiate exocytosis

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4
Q

What would inhibit the release of ACh?

A

Onabotulinumtoxin A

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5
Q

Protein Botulinumtoxin is derived from

A

clostridium botulinum

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6
Q

Botulinumtoxin A MOA

A

inactivates synaptic vesicle protein required for vesicle docking
reversible state of cholinergic denervation

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7
Q

How is nerve function restored once being blocked by botulinumtoxin?

A

sprout new terminals, takes months

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8
Q

Action of Onabotulinumtoxin A

A

flaccid paralysis of skeletal muscle

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9
Q

Therapeutic uses of botulinumtoxin A

A

muscle spasms
cosmetic
OAB
axillary hyperhidrosis

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10
Q

Botulinumtoxin A Side Effects

A

distant spread from injection site, serious dysphagia, breathing difficulties, ptosis

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11
Q

What drug selectively stimulates muscarinic receptors?

A

Muscarine

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12
Q

What is muscarine derived from?

A

Amanita muscaria mushroom

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13
Q

What drug selectively blocks muscarinic receptors?

A

atropine

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14
Q

What is atropine derived from?

A

atropa belladonna, deadly nightshade

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15
Q

What kind of receptor is a muscarinic receptor?

A

G-protein-coupled receptors to induce change in cytosolic Ca or cAMP

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16
Q

What kind of receptor are nicotinic receptors?

A

ligand-gated ion channels, permeability to Na and K increases causing depolarization (EPSP)

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17
Q

What drug stimulates nicotinic neuronal receptor?

A

nicotine

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18
Q

What does persistent stimulation of the nicotinic neuronal receptor cause?

A

“Desensitization” (depolarizing blockade)

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19
Q

What drug blocks nicotinic neuronal receptors?

A

Mecamylamine

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20
Q

What drug competitively antagonizes nicotinic neuromuscular junction receptors?

A

d-Tubocurarine

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21
Q

Termination of Cholinergic Transmission

A
  1. AChE rapidly terminates transmission via hydrolysis
  2. Inactivation for next depolarization and prevent lateral diffusion
  3. Butyrylcholinesterase; functions as drug metabolizing enzyme active in plasma, glial cells, and liver
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22
Q

Adrenergic Transmission - Synthesis of Catecholamine NTs

Study These Flashcards
A
  1. NE formed in adrenergic postganglionic neurons
  2. DA formed in basal ganglia of CNS
  3. NE converted to Epi in adrenal medulla
  4. Tyrosine hydroxylase is rate limiting step
  5. Synthesis of epi is increased by GCs
23
Q

Vesicular Storage of Catecholamines

Study These Flashcards
A
  1. vesicles protect NE, Epi, DA from degradation by MAO

2. NTs actively transported into vesicles by vesicular membrane monoamine transporter-2 (VMAT2)

24
Q

What drug inhibits storage of NE, DA, or Epi into vesicles?

25
Use for reserpine
oral anti-HTN and antipsychotic
26
Reserpine MAO
irreversible inhibitor of VMAT2, NTs not stored degraded by MAO, depletes catecholamines from nerve terminal, reduces SNS activity in CNS and peripheral nerves
27
Reserpine Side Effects
sedation unopposed cholinergic effects psychotic depression
28
Where is NE converted to Epi
cytosol of chromaffin cells
29
How is epi transported back into vesicles?
VMAT2
30
Release of Catecholamines
calcium influx --> exocytosis | negative feedback inhibition of NE release
31
What receptors provide the negative feedback inhibition of NE release?
alpha-2 receptors
32
What drug stimulates NE release?
Tyramine
33
What type of foods is tyramine/tyrosine found in?
protein rich foods (cheese, fish, kimchee, meats)
34
MOA of tyramine
displace NE from vesicle, causing non-vesicular release by reverse transport through NET
35
What population would be most effected by ingesting tyramine rich foods?
patients taking MAO inhibitors
36
What can result from an abrupt NE release?
hypertensive crisis
37
What drug inhibits NE release?
Methyldopa
38
What is methyldopa used for?
anti-HTN (safe during pregnancy)
39
Methyldopa MOA
prodrug converted to methyl-NE, which is an alpha-2 selective adrenergic receptor agonist, which reduces "sympathetic outflow" to periphery
40
Methyldopa Side Effects
sedation, dry mouth, PD, autoimmune hemolytic anemia (Coomb's test)
41
Adrenergic Receptor Subtypes
alpha-1 (smooth muscle) - contraction (Gq) alpha-2 (nerves) - inhibitory (Gi) beta-1 (heart, kidney) - excitatory/contraction (Gs/cAMP) beta-2 (lung, skeletal muscle vasculature, uterus) - relaxation (Gs)
42
Adrenergic Termination
1. NE in synapse - reuptake via active NE transporter (NET) & diffusion away from adrenergic receptors 2. Circulating NE - ENT in vascular smooth muscle/glands 3. Inhibition of reuptake can occur (cocaine)
43
What drug can inhibit the reuptake of NE?
cocaine
44
How are catecholamines metabolized?
1. MAO - mitochondria 2. COMT - cystosolic VMA - excreted in urine
45
Responsibility of MAO
clearing catecholamines in nerve terminals
46
Example of why we would inhibit MAOs
elevate transmitter levels in neurons (SSRIs)
47
Example of why we would inhibit COMT
treat Parkinsons
48
What is VMA useful to diagnose?
diseases affecting SNS
49
Botulinum toxin action and clinical use
Action: inhibit ACh release Use: cosmetics, muscle paralysis
50
Reserpine action & clinical use
Action: inhibit vesicular uptake of DA | Clinical Use: anti-HTN
51
Cocaine Actions & Clinical Use
Actions: inhibit neuronal reuptake of NE Use: local anesthetic, vasoconstrictor
52
Tyramine action & clinical use
Action: promote NE release Use: none, causes hypertensive crisis
53
Methyldopa action and clinical use
Action: false transmitter/alpha-2 agonist Use: anti-HTN safe during pregnancy

PHARM Exam 2 (4 decks)

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