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Pharmacology ANS > ANS: Presynaptic Drugs > Flashcards

ANS: Presynaptic Drugs Flashcards

1
Q

Mecamylamine MOA

A

Noncompetitive antagonist of Nn receptors (no effect on Nm)

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2
Q

Mecamylamine therapeutic use

A

Antihypertensive, tobacco smoking cessation

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3
Q

Mecamylamine blocks…

A

Both PNS and SNA postganglionic

Reveals dominant ANS division

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4
Q

Side effects Mecamylamine

A
  • tachycardia
  • mydriasis
  • cycloplegia
  • constipation
  • urinary retention
  • dry mouth
  • increased BT
  • peripheral pooling in veins
  • vasodilation
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5
Q

Vesamicol

A
  • experimental
  • inhibit ACh storage
  • fusion of empty vesicles with PM
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6
Q

OnabotulinumtoxinA MOA

A
  • Inhibit Ach release
  • inactivate SNAP-25
  • temporary state of cholinergic denervation
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7
Q

SNAP-25

A

Required for docking of vesicle (ACh) with presynaptic membrane

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8
Q

Drug action of OnabotulinumtoxinA

A
  • flaccid paralysis of skeletal muscle

- inactivate sweat gland

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9
Q

Restoration of function from OnabotulinumtoxinA

A
  • requires sprouting of new nerve terminals

- 3-4 months

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10
Q

Therapeutic uses of OnabotulinumtoxinA

A
  • cosmetic
  • muscle spasms/dystonias
  • axillary hyperhidrosis,
    Overactive bladder
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11
Q

Side effects of OnabotulinumtoxinA

A
  • dysphagia (BOXED warning)
  • breathing difficulties (BOXED warning)
  • muscle weakness (ptosis)
  • pain
  • allergic reaction rare
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12
Q

Muscarine

A
  • Prototype agonist of muscarinic receptors

- mushroom

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13
Q

Atropine

A

Prototype antagonist

  • belladona (deadly nightshade)
  • blocks all subtypes equally
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14
Q

What are the two drugs that affect M cholinergic receptors?

A

Muscarine, atropine

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15
Q

What are the drugs that affect N receptors

A
  • nicotine
  • mecamylamine
  • d-tubocurarine
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16
Q

All muscarinic receptors have ______ response. All nicotinic have _______ response

A

GPCR

Ligand gated ion channels

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17
Q

Which drugs affect the Nn receptor

A

Nicotine

Mecamylamine

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18
Q

Which drugs affect the Nm receptor?

A

Nicotine

D-tubocurarine

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19
Q

Nicotine in Nn

A
  • prototype agonist (high affinity)

- causes receptor desensitization

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20
Q

Mecamylamine of Nn

A

Prototype antagonist

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21
Q

Nn structure

A

2a, 3b

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22
Q

Nm structure

A

2a, b, y, d

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23
Q

Nicotine Nm

A 
Prototype agonist (low affinity)
- desensitization, skeletal muscle paralysis
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24
Q

D-tubocurarine Nm

A
  • Prototype antagonist
  • (Curare)
  • Non-depolarizing (competitive) Nm blockade
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25
Q

Termination of cholinergic transmission

A
  • AChE rapidly terminates by hydrolysis of transmitter

- allows for next depolarization and prevent lateral diffusion

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26
Q

Inhibition of AChE

A
  • accumulation of Ach in synapse

- increased receptor stimulation and desensitization

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27
Q

BuChE

A
  • plasma, glial cells, liver
  • drug metabolizing enzyme
  • deficient in some
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28
Q

Succinylcholine-induced apnea is prolonged in those deficient in what?

A

BuChE

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29
Q

Where is NE formed?

A

Adrenergic postganglionic neurons

30
Q

Where is DA formed?

A

Basal ganglia & renal vasculature

31
Q

Where is Epi formed?

A

Adrenal medulla

32
Q

Formation of catecholamines

A

Tyrosine —> DOPA —> DA —> NE —> Epi

33
Q

What is the rate limiting step of synthesis of catecholamines?

A

Tyrosine —> DOPA
Tyrosine hydroxylase
- regulated by stress

34
Q

What is the synthesis of Epi increased by?

A

PNMT

35
Q

What dose vesicular storage protect DA, NE, and Epi from?

A

Degradation by MAO

36
Q

What are DA, NE and Epi transported into storage vesicles by?

A

VMAT-2

37
Q

What drug is an inhibitor of NE transmitter storage?

A

Reserpine

38
Q

MOA of reserpine

A
  • irreversible inhibitor of VMAT-2 (prevents uptake of DA and NE)
  • depletes catecholamines from all terminals
  • decreases CO & peripheral resistance —> lowers BP
39
Q

Therapeutic use of reserpine

A

Antihypertensive

Antipsychotic

40
Q

Side effects of reserpine

A
  • sedation
  • unopposed cholinergic effects (cramping, diarrhea)
  • psychotic depression (high doses)
  • orthostatic hypotension
41
Q

Release of catecholamines

A
  • AP, Ca2+ influx, exocytosis
42
Q

Negative feedback inhibition of catecholamines

A
  • NE stimulation of presynaptic a2 autoreceptors

- occurs via Gi mediated inhibition of Ca influx

43
Q

Which drug stimulates NE release?

A

Tyramine

44
Q

Which drug inhibits NE release?

A

Methyldopa

45
Q

Where is tyramine found?

A

Fermentation byproduct of tyrosine in protein rich foods

- aged cheese, beer/wine, soy/fish sauce, sauerkraut/kimchee, cured meats

46
Q

Why is there low oral bioavailability of tyramine?

A

GI/hepatic MAO

  • systemic abs can occur in patients taking MAOI (avoid taking)
47
Q

MOA of tyramine

A
  • displaces NE from vesicles

- causes non-vesicular release from nerve terminals by REVERSE transport through NET

48
Q

High systemic exposure of tyramine can cause what?

A 
Hypertensive crisis (abrupt NE release)
- dietary restrictions for those on MAOIs prevent this
49
Q

Where does methyldopa come from?

A

Prodrug converted to methyl-NE (mNE, active form) by DBH

50
Q

MOA of methyldopa

A

A2 receptor agonist

- reduces sympathetic outflow to periphery

51
Q

Therapeutic use of methyldopa

A

Gestational HTN

52
Q

Side effects of methyldopa

A
  • sedation
  • dry mouth
  • edema
  • autoimmune hemolytic anemia (Coomb’s test positive) with long term use
53
Q

Drug that affects termination of NE

A

Cocaine

54
Q

Synaptic NE termination

A
  • re-uptake via NET

- diffusion away from adrenergic receptors

55
Q

Termination of circulating NE and Epi

A
  • ENT in smooth muscle and glands

- metabolism (liver, kidney)

56
Q

Stimulant effects from cocaine are due to what?

A

Excess NE remaining in synapse

57
Q

3 metabolism mechanisms of catecholamines

A
  • MAO
  • COMT
  • VMA
58
Q

Where are MAO?

A

Mitochondrial

59
Q

Where are COMT?

A

Cytosolic (liver, kidney)

60
Q

What is the major metabolite excreted in urine?

A

VMA

61
Q

MAO

A
  • deaminates catecholamines, tyramine, histamine

- clear catecholamines in nerve terminals

62
Q

What are MAOIs used for ?

A

Depression

63
Q

COMT

A
  • o-mthylates catecholes

- clearence of circulating catecholamines

64
Q

What are COMT inhibitors used for?

A

Parkinson’s

65
Q

Significance of VMA

A

Clinical test of fractional metanephrines used to diagnose pheochromocytoma

66
Q

RLS of synthesis of Ach

A

Choline transported into pre-synaptic nerve ending by high affinity Na choline co-transporter

67
Q

Hemicholinium

A
  • Experimental
  • inhibit Ach synthesis
  • inhibit choline uptake
  • depletes Ach from nerve terminal
68
Q

Cocaine action

A

Inhibits NE re-uptake

69
Q

Therapeutic use of cocaine

A

Anesthetic/vasoconstrictor

70
Q

Action of amphetamine

A

Promote NE release/inhibits re-uptake

71
Q

Therapeutic use of amphetamine

A

ADHD

Narcolepsy

72
Q

Where does onabotulinumtoxin A come from?

A

Protein neurotoxin (protease) from C. Botulinum

Pharmacology ANS (3 decks)

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