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PCTH 325 > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

What can the peripheral nervous system be broken down into?

A
  1. Afferent (sensory)
  2. Efferent (motor)
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2
Q

What can efferent nervous system be broken down into?

A
  1. Somatic (conscious)
  2. Autonomic (unconscious)
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3
Q

What are the two branches of autonomic (ANS) and what are their functions?

A

SNS - fight or flight

PSNS - rest and digest

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4
Q

What does dominant tone mean?

A

Either SNS or PSNS dominates in certain organs

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5
Q

What receptors are used in the PSNS?

A
  1. Cholinergic
  2. Muscarinic
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6
Q

What receptors are used in the SNS?

A

Adrenergic

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7
Q

Where does PSNS originate from?

A

cranio-sacral

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8
Q

Where does SNS originate from?

A

thoraco-lumbar

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9
Q

True or false (and why):
Most drugs target ganglia

A

False. Most drugs target the post ganglionic receptors for selective effect

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10
Q

Both SNS and PNS have (blank) in their preganglionic and postganglionic fibres

A

ganglion

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11
Q

This NT is released onto the ganglia in both SNS and PSNS:

A

Ach

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12
Q

What are the receptors at the ganglia

A

Nicotinic receptors

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13
Q

How Acetylcholine stored and synthesized?

A

Synthesized from Acetyl CoA and Choline

Stored in synaptic vesicles

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14
Q

What do post-ganglionic neurons of the SNS release?

A

Norepinephrine (NE)

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15
Q

What does the adrenal medulla release?(include percentages)

A

20% NE and 80% Epi

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16
Q

What do postganglionic parasympathetic nerves release?

A

Ach

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17
Q

Key NT synthesized from: (and what they are called as a group)

A

From tyrosine
Called Catecholamines

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18
Q

Receptor distribution: Cholinergic

A

Nicotinic

Muscarinic (5 subdivisions)
M1, M3, M5
M2, M4

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19
Q

Receptor distribution: Adrenergic

A

Alpha: a1, a2

Beta: B1, B2, B3

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20
Q

M1, M3, M5 receptors

A

PSNS: muscarinic
G-protein coupled (GQ)
Excitation - when agonist binds = increase activity

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21
Q

M2, M4 receptors

A

PSNS (muscarinic)
G-protein coupled (Gi)
Inhibitory - when bound to receptor = decrease activity

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22
Q

Effect of muscarinic receptors on:
1. Heart
2. lungs
3. sphincters (specifically which ones)
4. walls (specifically what walls)

A
  1. heart = M2, decreased rate/contraction (rest)
  2. lungs = bronchoconstriction
  3. sphincters = M3, relaxation of GI and bladder sphincters
  4. walls =M3, contraction of GI tract and bladder walls
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23
Q

PSNS effect on secretion (specific what secretion)?

A

Increased

salivary, respiratory, tears

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24
Q

Two main paths to stimulate M receptors?

A
  1. Direct
  2. Indirect
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25
Q

What is direct stimulation of M receptor?

A

Using an agonist

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26
Q

What is indirect stimulation of M receptor?

A

acetylcholinesterase inhibitors increase the concentration of acetylcholine

Reversible or Irreversible

27
Q

What are the three types of chemical reaction that can occur when cholinesterase is bound?

A

acetylation, carbamylation, phosphorylation

28
Q

What is the result of the following when cholinesterase is bound?
1. acetylation
2. carbamylation
3. phosphorylation

A
  1. acetylation = What happens normally in our body, rapidly recover the cholinesterase
  2. carbamylation = slower recovery but is still reversible
  3. phosphorylation = irreversibly bound - no recovery
29
Q

Excessive cholinergic response affect which systems (5)

A

Secretions
lung
heart
GI mobility
Urinary tract

30
Q

Excessive cholinergic response specific symptoms:
1. secretions
2. lungs
3. heart
4. GI motility
5. Urinary tract

A
  1. secretions = increased drooling, tearing, clogged airways
  2. lungs = Bronchoconstriction (difficulty breathing)
  3. heart = Reduced heart rate (decreased endurance)
  4. GI motility = Increased (nausea, vomiting, diarrhea)
  5. Urinary tract = contraction of bladder, relaxation of sphincters (urination)
31
Q

Parasympatholytics (aka):

A

Block PSNS response
AKA: anticholinergics or antimuscarinics

32
Q

Atropine

A

Prototypical anticholinergic

33
Q

What are uses for atropine? (4)

A

Intubation
Opthalmology
Asthma
Antidote

34
Q

How can atropine be used for the following?
1. Intubation
2. Opthalmology
3. Asthma
4. Antidote

A
  1. Intubation = Clear airways by drying up secretions
  2. Opthalmology = Dilate pupils to facilitate eye exams
  3. Asthma = Dilate bronchioles
  4. Antidote = Counteract poisoning by cholinesterase inhibitors
35
Q

Side effects of atropine

A

Mouth - dry mouth
Heart - tachycardia
Gut - constipation
Bladder - Difficulty urinating

36
Q

A1 receptor function

A

constriction of smooth muscle

37
Q

Locationof A1 receptors

A
  1. Sphincters: bladder, GI tract
  2. Blood vessels: vasoconstriction
38
Q

How do a1 receptors work?

A

G protein coupled

39
Q

A2 receptor function

A

inhibition of NE release

40
Q

Location of A2 receptors

A

presynaptic membrane

41
Q

How do a2 agonists work?

A

binding agonist to presynaptic a2 receptors inhibits release of NE

42
Q

Function of B1 receptor

A
  1. Heart stimulation (increased rate, atrioventricular conduction and contractility)
  2. Kidney (stimulate renin release = increase blood pressure)
43
Q

What 3 parts in the body are only innervated by the SNS?

A

liver kidney and uterus

44
Q

B2 receptor function

A

relaxation of smooth muscle

45
Q

Location of B2 receptor

A
  1. lungs - bronchodilation
  2. blood vessels in skeletal muscle - vasodilation
  3. GI tract, bladder, uterus WALLS- relaxation
46
Q

How does b2 receptor affect the liver?

A

beta 2 receptors mediate glucose release through:
1. gluconeogenesis
2. glycogenolysis (breakdown of glycogen to glucose)

47
Q

How does SNS affect the bladder?

A

B2 in bladder wall relaxes - no forcing of liquid out
A1 in sphincter contracts - stops fluid from leaving

prevents peeing from occuring

48
Q

Sympathomimetics

A

drugs that mimic the stimulation of the SNS

49
Q

How do sympathomimetics work?

A

by directly activating adrenergic receptors
by increasing the amount of NT in the synpase

50
Q

How to increase the amount of NT in synpase?

A
  1. increase NT release
  2. inhibit reuptake of NT
  3. inhibit metabolism of NT
51
Q

What is the mechanism to reuptake NT?

A

Reuptake pumps sit pre synpatically and remove Nt to stop them from binding to receptors

52
Q

What is the mechanism for metabolism of NT?

A

MAO (monoamine oxidase) - breaks down catecholamines like NE, serotonin, Dopamine

53
Q

Sympatholytics

A

drugs that reduce or block the sympathetic activity

54
Q

What is an example of a drug that directly blocks adrenergic receptors?

A

propanolol - a beta blocker/antagonist

55
Q

What is an example of a drug decreases the amount of NT that is released into synpase?

A

clonidine - a2 agonist

56
Q

What two muscles control the eye?

A
  1. Iris muscle (circular, radial muscle)
  2. Ciliary muscle
57
Q

What receptors control the circular muscle and what happens when it contracts?

A

M2, M3 receptors

contraction constricts pupil

58
Q

What receptors control the radial muscle and what happens when it contracts?

A

A1 receptor

contraction dilates pupil

59
Q

What does the ciliary muscle control?

A
  1. Shape of the lens and focuses image on retina
  2. Production of aqueous humor (AH)
60
Q

What is glaucoma caused by?

A

An increase in intraocular pressure (IOP)

61
Q

What causes an increase in IOP?

A

Build up of Aq humour due to decreased drainage/increased production

62
Q

PSNS treatment for glaucoma

A

M2 M3 receptor stimulation

contracts ciliary muscle, opens trabecular meshwork and canal of schlemm -> more drainage can occur

63
Q

SNS treatment for glaucoma

A
  1. B2 agonists to reduce Aq humor secretion
  2. A2 agonists to facilitate drainage/reduce production
64
Q

What other things in the eye does M receptor stimulation affect?

A

M receptor stimulation= contraction of ciliary muscle

causes lens to bulge - improves near vision but blurs far vision

PCTH 325 (19 decks)

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