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FunMed Pharmacology > Pharmacology of the ANS > Flashcards

Pharmacology of the ANS Flashcards

1
Q

What do both parasympathetic and sympathetic system both use

A
  • Acetylcholine and nicotinic receptors between pre and post synaptic neurones
  • Excitatory
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2
Q

what does the parasympathetic post ganglionic neurone use

A
  • Acetylcholine and muscarinic receptors on target organs

- Excitatory or inhibitory

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3
Q

Sympathetic post-ganglionic neurones use:

A

• Noradrenaline and α or β adrenoreceptors
• Sweat glands - acetylcholine and muscarinic receptors
• Kidney - dopamine and dopamine receptors
• Adrenaline and noradrenaline secreted by adrenal gland
• Excitatory and inhibitor
- they use noradrenaline at post ganglionic synapse except for sweat glands which use ACh

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4
Q

what does ganglionic transmission use

A

Ach

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5
Q

what does NANC stand for

A

NON adrenergic and non cholinergic

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6
Q

what does NANC

A 
- it is cotransmitters with ACh or noradrenaline 
o	Nitric oxide
o	Vasoactive intestinal peptide 
o	Neuropeptide Y 
o	5-hydroxtryptamine 
o	ATP
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7
Q

where is NANC

A
  • widely distributed in peripheral tissues
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8
Q

describe acetylcholine

A
  • Choline + acetyl CoA using choline transferase = acetylcholine
  • Packaged into vesicles
  • Broken down into choline and acetate by acetylcholinesterase
  • Choline then transferred back into pre-synaptic terminal fro recycling
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9
Q

what do Parasympathomimeticdo

A
  • These mimick the parasympathetic activation
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10
Q

what is a parasympathetic agonist

A
  • Produce similar response to acetylcholine
  • Can be substances that activate the muscarinic receptors
  • Prevent normal ACh breakdown so more endogenous neurotransmitter
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11
Q

what activates a nicotinic receptor

A
  • Selectively activated by alkaloid nicotine
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12
Q

what activates a muscarinic receptor

A
  • Selectively activated by alkaloid muscarinic such as fly agaric
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13
Q

what are the nicotinic agnostic

A

Nictotine

  • for ganglionic and CNS
  • Smoking cessation

Suxamethonium

  • for neuromuscular junction
  • Short term neuromuscular block – depolarising blockade
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14
Q

what are the nitoctirnic antagonist

A

Hexamethonium –
• for ganglionic nicotinic receptors
• 1st effective antihypertensive treatment – it casues vascodilation, activates the sympathetic system to cause vascodilation

Pancuronium
• for neuromuscular junction receptors
• Longer neuromuscular block – prevents sodium from entering, cuases long term blockage
• Used in lethal injections

Tubocurarine
• Causes skeletal muscle relaxation / paralysis

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15
Q

what is the structure of the nicotinic receptor

A 
	Found in ganglions 
	2 alpha subunits and 3 beta subunits
	Different subtypes have different affinities for nicotine (more in ganglionic and CNS than neuromuscular) 
	Alpha 3 – autonomic ganglia
	Alpha 1 – neuromuscular junction
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16
Q

what is the nicotinic receptor in the ganglia

A

alpha 3

17
Q

what is the nicotinic receptor in the neurmuscular junction

A

alpha 1

18
Q

where are the muscarinic receptors found

A

 Found on postganglionic parasympathetic fibres

19
Q

what are the 5 types of muscarinic receptors

A
  • M1 – excitatory – increases gastic acid secretion
  • M2 – inhibitory – decreases heart rate and force
  • M3 – excitatory – increase GI motility, bladder contraction, bronchiocontriction, constricts pupil
  • M4&5 – CNS
20
Q

what are the muscarinic agonists

A 
carbachol
•	Work at both nicotinic and muscarinic
Bethanechol
•	Selective for muscarinic receptors
•	Not hydrolysed by cholinesterase so has long duration of action
•	Increases bladder and gastrointestinal contraction
Pilocarpine
•	Selective for muscarinic receptors
•	Eye drops for glaucoma
21
Q

what are the antagonist for muscarinic receptor non selective for muscarine receptors

A 
Atropine- opposite of carbachol 
•	Reduced bronchial secretions 
•	Pupil dilation
•	Treats bradycardia
•	Used in organophosphate poisoning – causes the neuromuscular junction to become depolarised
•	Can be given locally
•	M2 causes inhibitory
•	Problem – if you only want to open the eye up you don’t want to affect the heart but will do so anyway as it is non selective

Scopolamine
• GI Antispasmodic
• Motion sickness
• Can be given as a patch which can be absorbed across the skin

Ipratropium
• Inhaled for asthma (bronchodilator)

22
Q

what are the antagonists selective for muscarnic receptors

A

Pirenzepine / Telenzepine
• M1 selective antagonist
• Reduces gastric acid secretions
Gallamine
• M2 selective antagonist binds to M2 so M1 is more active causes tachycardia
• Causes tachycardia
Darifenacin / Solifenacin
• M3 selective antagonist
• Urinary incontinence – urge this is where they feel that they need to go but they don’t their bladder has just expanded more
• Used for people with Overactive bladder

23
Q

what do cholinestrase inhibitors do

A
  • Stimulate GI function - prokinetics
  • Cognitive enhancers – used in Alzheimer’s patients
  • Skeletal muscle activity
  • Neostigmine used for myasthenia gravis – this is so that the remaining nicotinic acetylcholine receptors have more of a chance of being activated/ works on both nicotinic and muscarinic receptors
24
Q

what does botulinum toxin do

A

Clostridium botulinum bacteria

  • Prevents acetylcholine release
  • Irreversible
  • Excessive sweating
  • Overactive bladder
  • Muscle spasm
  • No SNARE proteins to cause vesicles to move to the membranes so no acetylcholine is released
25
Q

what are sympathomimetrics

A

• Agents that produce a similar response as noradrenaline and adrenaline on the sympathetic nervous system

26
Q

what are the sympathomimetics

A

Monoamine – neurotransmitters
• Noradrenaline, adrenaline, dopamine, histamine, 5-hydroxytryptamine, melatonin
• Amine group connected to an aromatic ring
Catecholamine
• Noradrenaline, adrenaline, dopamine isoprenaline
• Catechol group (benzene + 2 hydroxyl) and amine side chain

27
Q

how is noradrenaline synthesised and broken down

A
  • Synthesised in the cell body and then transported down
  • Amino acid is tyrosine this si the starting point, this gets converted to L-dopa which is made into dopamine which is made into noradrenaline
  • After noradrenaline is released into the synaptic cleft it needs to be switched of, this happens by monoamine oxidase - Catechol-O-methyltransferase (COMT)
28
Q

what does the noradrenaline receptors do

A
  • Alpha 1 stimulation = vasoconstriction and inhibition of GI and bladder
  • Beta 1 stimulation = increase heart rate and force
  • Beta 2 stimulation = bronchodilation, vasodilation, inhibits GI and bladder
29
Q

what is the clinical use of noradrenaline receptors

A

o Alpha 1 antagonists for hypertension
o Beta 1 antagonists for angina and hypertension (beta blockers) - atenolol
o Beta 1 agonists for cardiac arrest and shock, increase cardiac contractility and heart rate and is used in cardiac arrest and shock
o Beta 2 agonists for asthma – salbutamol causes bronchodilation
- B3 solabegron - begin developed for overactive bladder and iBS

30
Q

what does a2 clonidine do

A 
o	Antihypertensive (inhibits noradrenaline release)
o	Analgesic and sedation used in combination with ketamine
31
Q

what does a1 do

A

prazosin, doxazosin, tramsulosin
• Anti-hypertensive- cause vascodilation
• Benign prostatic hyperplasia

32
Q

what is a non selective isoprenaline

A

Beta receptors agonists
• Non selective isoprenaline
• No longer used for asthma because of effects on heart
• Now only used to reverse overdose by β-blockers

33
Q

what are the beta receptor antagonists

A

Non selective
Propranolol
• Timolol used to decrease aqueous humour production
β1 atenolol
• Decreases heart rate and force of contractility used in angina, hypertension, cardiac dysrhythmias, tremor
β2 butoxamine
• Has no medical use

FunMed Pharmacology (5 decks)

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