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PHARM Exam 2 > Autonomic Neurotransmission > Flashcards

Autonomic Neurotransmission Flashcards

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

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

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?

A

Reserpine

25
Q

Use for reserpine

A

oral anti-HTN and antipsychotic

26
Q

Reserpine MAO

A

irreversible inhibitor of VMAT2, NTs not stored degraded by MAO, depletes catecholamines from nerve terminal, reduces SNS activity in CNS and peripheral nerves

27
Q

Reserpine Side Effects

A

sedation
unopposed cholinergic effects
psychotic depression

28
Q

Where is NE converted to Epi

A

cytosol of chromaffin cells

29
Q

How is epi transported back into vesicles?

A

VMAT2

30
Q

Release of Catecholamines

A

calcium influx –> exocytosis

negative feedback inhibition of NE release

31
Q

What receptors provide the negative feedback inhibition of NE release?

A

alpha-2 receptors

32
Q

What drug stimulates NE release?

A

Tyramine

33
Q

What type of foods is tyramine/tyrosine found in?

A

protein rich foods (cheese, fish, kimchee, meats)

34
Q

MOA of tyramine

A

displace NE from vesicle, causing non-vesicular release by reverse transport through NET

35
Q

What population would be most effected by ingesting tyramine rich foods?

A

patients taking MAO inhibitors

36
Q

What can result from an abrupt NE release?

A

hypertensive crisis

37
Q

What drug inhibits NE release?

A

Methyldopa

38
Q

What is methyldopa used for?

A

anti-HTN (safe during pregnancy)

39
Q

Methyldopa MOA

A

prodrug converted to methyl-NE, which is an alpha-2 selective adrenergic receptor agonist, which reduces “sympathetic outflow” to periphery

40
Q

Methyldopa Side Effects

A

sedation, dry mouth, PD, autoimmune hemolytic anemia (Coomb’s test)

41
Q

Adrenergic Receptor Subtypes

A

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
Q

Adrenergic Termination

A
  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
Q

What drug can inhibit the reuptake of NE?

A

cocaine

44
Q

How are catecholamines metabolized?

A
  1. MAO - mitochondria
  2. COMT - cystosolic
    VMA - excreted in urine
45
Q

Responsibility of MAO

A

clearing catecholamines in nerve terminals

46
Q

Example of why we would inhibit MAOs

A

elevate transmitter levels in neurons (SSRIs)

47
Q

Example of why we would inhibit COMT

A

treat Parkinsons

48
Q

What is VMA useful to diagnose?

A

diseases affecting SNS

49
Q

Botulinum toxin action and clinical use

A

Action: inhibit ACh release
Use: cosmetics, muscle paralysis

50
Q

Reserpine action & clinical use

A

Action: inhibit vesicular uptake of DA

Clinical Use: anti-HTN

51
Q

Cocaine Actions & Clinical Use

A

Actions: inhibit neuronal reuptake of NE
Use: local anesthetic, vasoconstrictor

52
Q

Tyramine action & clinical use

A

Action: promote NE release
Use: none, causes hypertensive crisis

53
Q

Methyldopa action and clinical use

A

Action: false transmitter/alpha-2 agonist
Use: anti-HTN safe during pregnancy

PHARM Exam 2 (4 decks)

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