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Pharmacology > Autonomic Nervous System > Flashcards

Autonomic Nervous System Flashcards

1
Q

ANS Pharmacology

A

The study of drugs that act on receptors and neurotransmitters in the ANS to alter nervous system function.

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2
Q

Drugs acting on the ANS are important in the treatment of which diseases?

A
  • eye
  • cardiovascular system
  • respiratory tract
  • GI and urinary tract
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3
Q

What are the 2 branches of the Nervous System?

A
  1. Central (brain and spinal cord)

2. Peripheral (Somatic and autonomic)

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4
Q

Describe the Peripheral Nervous System.

A 
Efferent Neurons (Motor) and Afferent Neurons (Sensory)
-Efferent Nervous system divided into somatic (conscious) and autonomic (unconscious)
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5
Q

What are the 3 divisions of the ANS?

A
  1. parasympathetic
  2. sympathetic
  3. enteric- collection of neurons that regulates the GI tract
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6
Q

How do ANS fibers interact with their target neurons (3 steps)?

A
  1. cell body of the first neuron resides in brain/spinal cord (pre-ganglionic neuron)
  2. pre-ganglionic neuron synapses w/ post ganglionic neuron in a ganglia (autonomic ganglion)
  3. ganglionic neuron innervates the target organ (cardiac muscles, smooth muscles, exocrine glands)
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7
Q

In what 3 ways do the PNS and SNS differ in their organization?

A
  1. Preganglionics in different regions of CNS
  2. Different location of ganglia
  3. Different lengths of preganglionic fibres
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8
Q

SNS v PNS: From what region of the CNS do the preganglionics originate?

A

PNS-cranial and sacral SC region

SNS-thoracic and lumbar SC region

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9
Q

SNS v PNS: Where is the ganglia located?

A

PNS-close to target tissue

SNS-close to spinal cord in a chain

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10
Q

SNS v PNS:What length is the pre-ganglionic fibre?

A

PNS-long

SNS-short

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11
Q

How do SNS and PNS affect the heart?

A

SNS= increased rate and contractility

PNS=decreased rate

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12
Q

How do SNS and PNS affect the intestine?

A

SNS=decreased motility

PNS=increased motility

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13
Q

How do SNS and PNS affect the pupil?

A

SNS=dilate

PNS=constrict

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14
Q

How do SNS and PNS affect the respiratory system?

A

SNS=bronchodilation

PNS=bronchoconstriction

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15
Q

How do SNS and PNS affect the LUTS?

A

SNS= stimulates ejaculation/voiding

PNS=stimulates erection/voiding

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16
Q

Explain PNS neurotransmission?

A
  • Releases Ach at autonomic ganglion, neuronal nicotinic R
  • releases Ach at post ganglionic neuron, muscarinic R
  • affects cardiac and smooth muscle, gland cells, nerve terminals
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17
Q

Draw out diagram of SNS transmission-include neurotransmitters and receptors.

A

See ANSI lecture

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18
Q

Explain ANS regulation in the eye

A

PNS: Ach causes sphinctor pupillae to contract-Miosis
SNS: Noradrenaline cause dilator pupillae to contract-Mydriasis

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19
Q

Explain organ level integration of the ANS.

A

See ANSII

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20
Q

Cholinergic Agonists

A

-drugs that mimic the action of Ach at cholinergic R and increase PNS responses

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21
Q

Cholinergic Antagonists

A

-drugs that inhibit the action of Ach at cholinergic R and decreases PNS response

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22
Q

Cholinergic Receptors (2)

A
  1. muscarinic-high affinity for muscarine, low affinity for nicotine
  2. nicotinic-high affinity for nicotine, low for muscarine
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23
Q

Acetyl cholinesterase

A

-breaks down Ach in the synaptic cleft, choline is recycle back to axon terminal

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24
Q

Draw the pathway for cholinergic neurotransmission.

A

See ANSII

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25
Q

Vesamicol

A

Inhibits Ach uptake into synaptic vesicles

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26
Q

Botulinum toxin

A

Inhibits vesicular release of Ach

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27
Q

Describe the Muscarinic Receptor Subtypes (3)

A

M1: CNS, ANS
M2: acts on heart, decreased heart rate
M3: smooth muscle contraction, exocrine gland-increased secretion

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28
Q

Describe the Nicotinic R Subtypes (2)

A 
Nn: 
Autonomic ganglia- stimulate both SNS and PNS
Adrenal Medulla-releases Adr/NA
Nm: 
skeletal muscle contraction
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29
Q

Muscarinic Agonists

A

-activate muscarinic R directly

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30
Q

What is a non-selective muscarinic agonist?

A

ACh

-dont see long duration of action due to ACh esterase

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31
Q

What is a selective muscarinic agonist (2)?

A
  • muscarine

- pilocarpine

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32
Q

What is a synthetic analogue of Ach?

A

-bethanechol

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33
Q

What are uses of direct muscarinic antagonists?

A
  1. stimulate tone in bladder after surgery
  2. increase gut motility
  3. glaucoma
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34
Q

How do muscarinic agonists work in the treatment of glaucoma?

A

Activate M3 receptors on the ciliary muscle to cause contraction and increase fluid drainage

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35
Q

What are the side effects of muscarinic agonists (5)?

A
  1. stimulate all muscarinic R
  2. GI disturbances (eg nausea and vomiting)
  3. miosis
  4. effects on heart rate (bradycardia)
  5. salivation and bronchoconstriction
    * overstimulation of the PNS
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36
Q

Muscarinic Antagonists

A

-bind to muscarinic R preventing Ach from binding

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37
Q

Give 2 examples of muscarinic antagonists.

A

Atropine-naturally occurring alkaloid

Ipratropium bromide-synthetic analogue

38
Q

3 Uses of Atropine

A
  1. Dilate eye pupil for ophthalmic exam
  2. treat bradycardia
  3. to reduce secretion during surgery
39
Q

What is the effect of muscarinic agonist on the eye?

A
  • ciliary muscles contract
  • refractive power of the lens increases, able to focus on near
  • miosis
40
Q

What is the effect of muscarinic antagonist on the eye?

A
  • block the PNS
  • make the lens thinner for far vision
  • mydriasis
41
Q

Uses of ipratropium bromide (Atrovent)

A
  • to reduce cholinergic bronchoconstriction
  • non-selective for all muscarinic subtypes (i.e. M1-M3)
  • used to treat asthma and COPD
42
Q

Name 2 nicotinic agonists?

A

Nicotine-selective

Non-selective-Ach

43
Q

What are the uses of nicotinic agonists?

A
  • to treat nicotine addiction

- patch, gum aerosol

44
Q

What are the side effects of nicotinic agonists?

A
  • CNS

- tremor, convulsions, coma

45
Q

Ganglionic Blockers

A
  • nicotinic R antagonist
  • block nicotinic nerve R at autonomic ganglia
  • not used
46
Q

Neuromuscular Blockers

A

-block nicotinic muscle receptors at the neuromuscular junction on skeletal muscles

47
Q

What are the 2 classes of neuromuscular blockers?

A
  1. Non-depolarizing (competitive) antagonists

2. Depolarizing (non-competitive) antagonists

48
Q

Non-depolarizing (competitive) nicotinic antagonists

A
  • binds in the place of Ach, doesn’t cause sodium influx

- can overcome blockade using acetylcholine esterase inhibitor

49
Q

Curare

A
  • Non-depolarizing (competitive) nicotinic antagonist
  • used to produce skeletal muscle paralysis during surgery and in ICU
  • side effects = paralysis
  • selective at the neuromuscular junction, doesn’t bind at the ganglion due to differences in structure
50
Q

Depolarizing (non-competitve) nicotinic antagonists

A
  • binds in the place of Ach and remains bounds
  • causes depolarization
  • receptor becomes desensitized
51
Q

Succinylcholine

A
  • Depolarizing (non-competitve) nicotinic antagonist
  • used to produce skeletal muscle paralysis during surgery and in ICU
  • takes time to wear off
52
Q

Cholinesterase Inhibitors

A

Enhance duration of action of Ach by prevent its metabolism in the synapse

53
Q

Reversible cholinesterase inhibitors

A
  • weakly bind Ach esterase

- neostigmine and physostigmine

54
Q

Uses of Reversible cholinesterase inhibitors (3)

A
  1. loss of tone in bladder and gut (increases gut and bladder motility)
  2. glaucoma (same as muscarinic agonists)
  3. myasthenia gravis
55
Q

What are side effects of reversible cholinesterase inhibitors?

A
  • same as for direct muscarinic agonists

- salivation, miosis, bronchocontriction, bradycardia

56
Q

Irreversible Cholinesterase Inhibitors

A

-covalent bond w/ Ach esterase

57
Q

Pralidoxime

A

-compound that can break down covalent bond of irreversible cholinesterase inhibitors

58
Q

Treatment for irreversible cholinesterase inhibitors

A
  • support respiration
  • decontamination
  • use muscarinic antagonist (atropine)
  • use pralidoxime
59
Q

Examples of irreversible cholinesterase inhibitors (2)

A
  • insecticides (parathion and malathion)

- nerve gases (sarin)

60
Q

Effects of irreversible cholinesterase inhibitors

A
  • effects at both muscarinic and nicotinic R
  • initial signs are muscarinic (bronchoconstriction, salivation, GI symptoms)
  • followed by central and peripheral nicotinic signs (e.g. persistent activation of skeletal muscle, paralysis)
61
Q

Adrenergic Agonists (sympathomimetics, adrenergics)

A

Mimic the action of epinephrine and norepinephrine at adrenergic R, increases SNS responses

62
Q

Adrenergic Antagonists (sympatholytics, antiadrenergics)

A

Inhibit the action of NA at adrenergic receptors and decrease SNS responses

63
Q

Localization of Adrenergic R

A
  • alpha1 and beta2 on smooth muscle
  • beta1 in heart
  • alpha1 and beta2 on blood platelets, adipose, endocrine tissue
  • alpha2 on presynaptic terminal of sympathetic neuron
64
Q

Draw the pathway for adrenergic neurotransmission

A

ANS III

65
Q

Cocaine

A

Inhibits NE reuptake

66
Q

Amphetamine

A

Stimulates release of NE

67
Q

What are the 3 ways that adrenergic agonists mimic the actions of NE?

A
  1. Direct acting
  2. Selective
  3. Indirect acting
68
Q

Direct Acting Adrenergic Agonists

A 
Non-selective
-bind to pre or post synaptic adrenergic Rs 
eg NE (alpha1, alpha2, beta1)
69
Q

Phenylephrine

A

-direct adrenergic alpha1 agonist

70
Q

What is phenylephrine used to treat (3)?

A
  1. Nasal congestion
    - constricts blood vessels in nasal mucosa
  2. to dilate pupils
    - activates alpha1 R on iris radial muscle
  3. combine w/ local anaesthetic
    - to constrict blood vessels and prolong nerve block
71
Q

What is a side effect of phenylephrine?

A

-can increase bp due to vasoconstriction

72
Q

SNS regulation of Vascular tone

A

NE acts on alpha1, causes vasoconstriction

  • circulating epinephrine for adrenal medulla causes vasodilation mediated by beta2R
  • ANSIII diagram
73
Q

Direct Alpha2 agonists

A
  • alpha2 R (autoreceptor) on pre-synaptic nerve terminal

- decreased NE release via inhibition of adenylate cyclase and cAMP signalling

74
Q

clonidine

A
  • direct alpha2 agonist
  • has CNS actions
  • used to treat hypertension by reducing SNS outflow from the brain to the periphery
  • side effects are sedation
75
Q

Direct beta1 agonists

A
  • acts in the heart
  • increased Ca influx
  • increased force of contraction cardiac muscle
  • dobutamine
76
Q

Direct beta2 agonists

A
  • beta2 in airway smooth muscle
  • decreased contraction of smooth muscle (bronchodilation)
  • salbutamol
77
Q

Direct Adrenergic Agonists (at multiple subtypes)

A

-adrenaline

78
Q

What is adrenaline used to treat? How?

A
  • anaphylaxis
  • activates alpha1 R in vascular smooth muscle and beta1 R in cardiac muscle to increase cardiac output, leading to increased BP
  • reduces mucous membrane congestion by activating alpha1
  • activates B2 in smooth muscle of respiratory system
79
Q

What are the 2 mechanisms of indirect adrenergic agonists?

A
  1. inhibition of reuptake (cocaine)

2. cause release of NE (amphetamine)

80
Q

Cocaine

A
  • indirect adrenergic agonist
  • blocks reuptake
  • useful as local anaesthetic in nasopharyngeal surgery (blocks sodium channels in nerves)
81
Q

What are the side effects of cocaine?

A
  • powerful CNS stimulant
  • increased HR, bp, force of contraction
  • arrhymias due to Ca influx into tissue
82
Q

Amphetamine/Ephedrine

A
  • indirect adrenergic agonist

- causes release of noradrenaline from sympathetic nerve terminals

83
Q

What is the mechanism of action of amphetamine?

A
  • amphetamine and NE taken up by same transporter
  • increases presence of cytosolic NE in the pre-synaptic nerve terminal, NE can’t be stored
  • Monoamine transporter works in reverse and moves NE into synapse
84
Q

What is amphetamine used to treat?

A
  • narcolepsy, ADHD

- appetite suppressant

85
Q

Tyramine and the Cheese Reaction

A
  • by product of tyrosine metabolism can be produced in protein rich foods
  • metabolized by MAO in liver
  • indirect agonist causing release of stored NE
  • inhibition of MAO produces increased tyramine levels and release of NE
  • patients taking MAO inhibitors (depression) must avoid tyramine rich food to prevent high bp
86
Q

Phentolamine

A
  • alpha adrenergic antagonist
  • non selective for alpha1 and 2
  • increased heart rate b/c NE can still act on beta2
87
Q

Prazosin

A
  • alpha adrenergic antagonist
  • selective for alpha1
  • used to treat high bp b/c doesn’t block alpha2 so NE can still feedback
88
Q

Propanolol

A
  • direct beta antagonist

- non selective

89
Q

Metropolol

A
  • direct beta antagonist

- cardioselective, beta1

90
Q

What are the uses of metropolol and propanolol?

A
  • high bp, angina, arrhythmias

- glaucoma, decrease aqueous humour secretion in the eye

91
Q

What are the side effects of metropolol and propanolol?

A
  • exercise tolerance

- asthma

92
Q

Beta AR blockers and glaucoma

A
  • aqueous humour is secreted by the ciliary epithelium
  • beta AR blockers act at Beta AR receptors on the epithelium and decrease aqueous humour secretion leading to a decreased pressure in the eye
  • used topically so non selectivity is ok

Pharmacology (9 decks)

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