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BMS1052_ > Drugs affecting peripheral neurotransmission > Flashcards

Drugs affecting peripheral neurotransmission Flashcards

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1
Q

where are the cell bodies for symp and parasym located?

A

both system has their cell bodies in the central nervous system
thoraco-lumbar region –> symp
cranial and sacral region –> parasymp

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2
Q

Sympathetic system (SNS) -pre and post synaptic neuron

A

short pre-ganglionic and long post-ganglionic

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3
Q

Parasympathetic system (PNS)

A

long pre-ganglionic neurons and short post ganglionic neuron

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4
Q

Transmitters of the ANS

A
  • sympathetic pre-ganglionic neurons release Ach and post ganglionic neurons release Noradrenaline
  • The presynaptic neurons release Ach to the adrenal medulla and adrenal medulla can release adrenaline and noradrenaline released in the circulation not tissue
  • Parasympathetic system pre and post synaptic neuron release Ach
  • the somatic neurons release Ach at target tissue
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5
Q

Sweat glands

A

sweat gland is part of the sympathetic NS –> sweat glands is part of the sympathetic –> cholinergic–>use Ach as neurotransmitter

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6
Q

co-transmitters in ANS

A

stored with and release with the main transmitter - have their own receptor - modulate activity
e.g. (ATP + NA) and (NO + ACh)

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7
Q

Does all part of the ANS use acetylcholine OR noradrenaline as the main neurotransmitter?

A

NO, in parts of the ANS the main transmitter is neither
acetylcholine OR noradrenaline…= NANC system (Non Adrenergic Non Cholinergic) e.g. nitric oxide (NO) involvement in erection - ) involvement in erection
ACh
sweat glans is part of the sympathetic cholinergic
stored with and release with the main transmitter - parasymp

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8
Q

Summary of the process of neurotransmission

A

1-start with the uptake of transmitter precursor entering the nerve terminal via an active transport
2-precursor is activated by metabolized enzyme
to form the neurotransmitter
3-neurotransmitter is stored within the storage system
4-action potential arrives at axon terminal- causes influx of calcium and release of the neurotransmitter
6-intract with receptors on effector organs
final step = determination of the action of the transmitter either by
- inactivation of the transmitter
- by metabolism
- taken back by the neural tissue by active uptake
- or it might be taken up by non-neuronal tissue

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9
Q

response of the neurotransmitter depend on the

A
  • response dependent on
  • tissue type
  • neurotransmitter release and the receptor type
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10
Q

effect of sympathetic NS

A

pupil dilation - contraction of radial muscle
Broncho-dilation -no direct intervention -adrenaline released can effect the lung
-increase in heart rate and force of contraction
- vasoconstriction
- increase in blood pressure and vasodilation
- decrease in GI motility
- sweating

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11
Q

Parasympathetic NS

A 
pupil constriction
bronchoconstriction
decrease in heart rate
no effect and change on blood vessles 
increase gasto-intestinal
motility
stimulate exocrine secretion
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12
Q

Receptors of the ANS

A 
ACH - choline receptor
 - nicotinic
 - muscarinic
Noradrenaline - adrenoreceptor
alpha and beta 
both systems can have some effect- most effect by most dominant system
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13
Q

ANS Receptors in other part of the body

A

•Tissues may have receptors for both ACh & NA
Receptors may be present even if the nerves aren’t: e.g
- NA receptor in bronchial smooth muscle
- ACH receptor in blood vessels
- no physiological role - can be activated by drugs
autonomic receptors” may exist in other parts of the
body not associated with the ANS eg brain….

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14
Q

Nicotinic receptors

A

found on
- skeletal muscle –> contraction of muscle
- parasympathetic and sympathetic ganglion
found on the post -symp ganglion

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15
Q

Muscarinic Receptors

A
  • Neuroeffector tissues of parasympathetic NS

-

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16
Q

 What effects are seen when peripheral muscarinic receptors are stimulated?

A
  • misosis (pupil constriction )
  • stimulated saliva flow
  • decreased heart rate
  • bronchoconstriction
  • stimulates peristalsis and secretion
  • stimulate bile release
  • bladder constriction
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17
Q

Adrenoceptors

A

classification based on rank order of potency of:
noradrenaline(NA), adrenaline (adr) & isoprenaline (iso)
classification based on rank order of potency of:
—Alpha: noradrenaline(NA)> adrenaline (adr) >isoprenaline (iso)
—-Beta: isoprenaline > adrenaline ≥ noradrenaline

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18
Q

What effects are seen when peripheral adrenoceptors are stimulated?

A

not clear which type of receptor Alpha or Beta is involved in each

  • Mydriasis
  • reduced saliva flow
  • increased SV and HR
  • Vasoconstriction
  • reduced peristalsis and secretion
  • glycogen –> glucose
  • inhibition of bladder contraction
  • adrenaline release
  • bronchodilation —> not involved
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19
Q

α-adrenoceptors

A

noradrenaline ≥ adrenaline > isoprenaline

excitatory more involved in contraction

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20
Q

β-adrenoceptors

A

isoprenaline > adrenaline ≥ noradrenaline
inhibitory(except in the heart)
Relaxation - dilation

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21
Q

receptor involved with

  • Mydriasis
  • increased SV and HR
  • Vasoconstriction
  • -inhibition of bladder contraction
A
  • Mydriasis –> Alpha
  • increased SV and HR –> Beta
  • Vasoconstriction –> Alpha
  • reduced peristalsis and secretion –> Beta
  • inhibition of bladder contraction –> Beta
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22
Q

Adrenoceptors

A

esponse of a tissue depends on:
 predominate subtype of receptor activated
 relative populations in the tissue
 relative potency of the agonist (eg NA vs adr)
α and β- adrenoceptors can coexist on different tissues, so the response seen depends on the relative abundance of the subtypes and how well the ligand activates each subtype.

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23
Q

Alpha vs Beta

A

Alpha receptor are sitting behind the sympathetic Nerve so they are the one that are going to be
targeted by NA and initate a response
Beta receptor - sit further away- they are most likley to be activated by the adrenaline released
from the medulla.

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24
Q

Synthesis & storage of acetylcholine

A

1-choline comes from diet enters the axon terminal by active transport through choline transporter
2-choline to acetylcholine by choline acetyl transferase
3- Acetylcholine into vesicle-associated transporter
Exocytosis of ACh
- AP arrives at Axon termina
- Influx of calcium
- fusion of the vesicel to the termina membrane
and release of Ach

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25
where drugs targeting the Ach-choline receptor effect ?
Sympathetic system - preganglionic and post ganglionic interaction and interaction with medulla Parasymp system - will effect the transmission of neurotransmitter between the pre- and post synaptic neuron and the effector tissue and somatic system
26
BOTOX- botulinum toxin
cause of some form of food poisoning inhibits Ach Release | Interferes with exocytosis release of Ach - by preventing the fusion of the membranes
27
Symptoms of botulism
```  blurred or double vision  drooping eyelids  slurred speech  difficulty swallowing  dry mouth  progressive weakness with paralysis  fixed or dilated pupils  maybe constipation  facial weakness on both sides of the face  breathing difficulty that may lead to respiratory failure ```
28
If Botulinum toxin affects so many sites, can it | have a therapeutic use?i
injected directly to the target tissue | selectivity of action p- it's not getting into the circulation
29
Therapeutic uses of Botox
mostly related to effects on skeletal muscle neurotransmission e.g. - bleopharospasm – uncontrolled contractions of eyelid - relaxes those muscles and allows eyes to be kept open -cerebral palsy (not an approved use)- reduce muscles rigidity and uncontrollable spasms - not approved used
30
 hyperhidrosis
 hyperhidrosis – abnormal & excessive sweating - injected directly into the sweat gland to cause reduction in the amount of Ach released to stimulate sweating
31
Termination of the action of ACh
acetylcholinesterasecholine breaks down ACh to choline + acetate Choline which can be recycled Acetylcholinesterase results in enhanced neurotransmitter transmission at all site where Ach is released. Accounts for symptoms seen following poisoning with organophosphate which are Achestrase inhibitors
32
Symptoms of organophosphate poisoning
1- Stimulation of muscarinic receptors---DUMBBELLS 2-2. Stimulation of nicotinic receptors -  NMJ  Ganglion 3. CNS effects -  Anxiety; restlessness lethargy; confusion; pyschosis, coma; seizures
33
therapeutic use of anticholinesterases
``` myasthenia gravis (NMJ) - - autoimmune condition associated with decreased skeletal neuromuscular transmission of Ach Alzheimer’s disease (CNS)- given systematically ```
34
therapeutic use of anticholinesterases side effect
 Side-effects  diarrhoea, urination, miosis, bradycardia, bronchoconstriction emesis, lacrimation, (lethary), emesis….  Overtreatment  May lead to a cholinergic crisis with increased cholinergic effects....
35
Summary of the process of transmission of NA at sympathetic nerve terminals
1-L-tyrosine from diet 2- metabolized to dopamine 3-in the vesicle the final stage of NA synthesis occurs 4- vesicles contain : NA, DA and ATP 5- -AP and Ca influx 6- interacts with A or B depending on the location Termination - uptake to the axon terminal (1) - uptake by non-neural tissue (uptake 2)
36
How can drugs effect NA
Drugs can affect:  Synthesis  Storage  Release  Action  Inactivation •overlap between endogenous transmitters dopamine ⇒ noradrenaline ⇒ adrenaline Any drug effecting one of these hormone will also effect the others point of difference: receptor they interact with dopamine interact with dopamine receptors in the CNS ⇒ Maybe used for effects on the sympathetic NS effects ⇒ Maybe used for other effects – but their side effects maybe related to actions on the sympathetic NS
37
Drugs affecting NA release
can  Block release  Cause release
38
Drugs targeting NA release - direct blockers
= Noradrenergic neuron blocking drugs  Abolish response to nerve stimulation  interfere with sympathetic NS responses & reflexes reduces Mechanism of action? reduces Particularly with cardiovascular system - not very well understood - requires the uptake of these drugs into the nerve terminal - happens by same neuronal uptake NA uses. - once inside the nerve it interferes with the movement of AP in the nerve terminal and deplete the NA from the vesicles meaning there is less NA release to interact with the receptors Effect NA release from all site of the body
39
bretylium guanethidine
Noradrenergic neuron blocking drugs used for treatment of hypertension Bretylium inhibits norepinephrine release by depressing adrenergic nerve terminal excitability.
40
Drugs targeting NA release - releasers
eg amphetamine; ephedrine/pseudoephedrine (structurally related to NA weak direct action of NA receptors) Mechanism of action: = Indirectly acting sympathomimetics - NA released independently of AP - activation by indirect release of NA
41
Sympathomimetics
are substances that mimic or modify the actions of endogenous catecholamines of the sympathetic nervous system
42
Sympathomimetics modes of transmission
1- emphetamine ephedrine enter nerve terminal by uptake | 2-once inside they are taken up into vesicles by exchange with NA
43
Indirectly acting sympathomimetics
mostly used for their effects within the CNS - release of dopamine in the reward pathway system produce effect in the periphery which strongly resembles activation of symp NS - increase in Bp and HR
44
Pseudoephedrine
Pseudoephedrine  nasal decongestant ⇒ vasoconstriction of dilated nasal vessels via α-adrenoceptors ⇒ ↓ tissue swelling and nasal congestion
45
Amphetamine & related compounds
 ADD (ADHD) / recreational use (DA effects) |  Side-effects: tachycardia; hypertension…
46
Drugs affecting NA removal
 Affect uptake  Affect NA metabolism NA uptake major pathway of NA removal in the periphery - so drugs that interfere with this will increase the amount of NA available to intract with the receptors lead to sympathomimetic actions
47
Drugs & NA uptake
Inhibitors of Uptake 1  eg cocaine; used for effects in CNS - causing excitement  enhance sympathetic transmission  ↑HR; ↑BP; (euphoria; excitement)
48
e.g. MAO-I
Monoamine Oxidase - main enzyme involved in metabolism of NA ⇒ increase releasable store of NA --> increase effects Uptake is the main removal process in the ANS Control the amount of NA and dopamine present in the Cytosol of Axon terminal Uptake is the main removal process in the ANS mainly used for their CNS effects ⇒ may cause side-effects related to ANS MAO more involved in termination of the action of NA and DP in CNS MAO inhibitors used for their action in CNS - maybe used as anti-depressant
49
MAO-B inhibitors
MAO-B inhibitors decrease the normal activity of an enzyme -- monoamine oxidase -- that breaks down dopamine after it completes its activity in the brain. These drugs allow available dopamine (made by remaining dopamine-producing cells or given via other medications) to function for a longer period of time
50
Advantage of targeting the receptor on tissue ?
Targeting receptors on the effector tissues is associated with fewer side effects than drugs that target the transmitter synthesis, storage, release or removal of the transmitter
51
Targeting nicotinic receptors
Activation or blockade of nicotinic receptors…..  will affect ganglionic neurotransmission ( in Smp + parasym ganglion)  responses complicated by affecting both the sympathetic and parasympathetic arms better to use drugs that have narrow effect
52
Receptor interaction
agonists (- Stimulate receptors ) ⇒ effects ≅ postganglionic nerve stim = parasympathomimetic - mimicking the action of parasymp NS -sympathomimetics antagonists - Block the action ⇒ effects ≅ postganglionic nerve inhibition = parasympatholytics sympatholytics
53
What effects will muscarinic AGONISTS cause?
``` drugs that will activate the muscarinic receptors in Smp + parasym ganglion pupil constriction stimulated saliva flow bronchoconstriction decrease in heart rate increase gasto-intestinal bladder contraction stimulate bile release ```
54
What effects will muscarinic ANTAGONISTS | cause?
pupil dilation inhibit secretions increase heart rate relax bronchial smooth muscle (bronchodilation) decrease gastric motility & gastric acid secretion decreased bladder emptying
55
Can ACh be used clinically?
no a really viable therapy of option - very rapidly broken down
56
Drugs targeting muscarinic receptors….eye
Agonists : cause pupil constriction and decrease intraocular pressure (used on glaucoma which is a condition with increased pressure in the eye . Antagonists: cause pupil dilation (e.f. eye examination )
57
Drugs targeting muscarinic receptors: Lungs
->asthma / COPD agonist - cause bronchoconstriction (no clinical need) Antagonist - cause bronchodilation e.g. chronic obstructive pulmonary disease  anaesthetic premedication (dry secretions) - musacrinic agonist = associated with exocrine secretion- primarily these secrestion can be stimulated in respiratory tract Agonist - cause secrestion Antagonist = inhibit secretion (eg. during surgery)
58
Drugs targeting muscarinic receptors ….GIT
GI motility muscarininc agonists will increase motility (may be useful to treat constipation) muscarinic antagonists will decrease motility (use to treat diarrhoea)
59
Drugs & adrenoceptors
effects we see depends on whether the drug effect the alpha or Beta receptors or both pupil dilation - contraction of radial muscle (alpha) Broncho-dilation -no direct intervention -adrenaline released can effect the lung -increase in heart rate and force of contraction (beta) - vasoconstriction (alpha) - increase in blood pressure and vasodilation - reduced peristalsis and secretion (alpha/beta) - decrease in GI motility - sweating - glycogen --> glucose (beta) - inhibition of bladder contraction (beta)
60
Therapeutic use of adrenaline?
 vasoconstriction (α) / vasodilatation (β)  increase HR & force of contraction (β)  bronchodilation (β) treatment for anaphylaxis- severe allergic reaction rapidly broken down has to be give via IM injcetion causes : decreased BP, HR bronchoconstriction Adrenaline opposes these symptoms
61
levophed
vasoconstriction (α) ⇒ increases BP used in life-theatening hypotension often used during of after CPR for rapid reponse it is given intravenously
62
Therapeutic uses of drugs targeting adrenoceptors?
we have much better drugs for agonist and antagonist that show better selectivity for alpha and beta receptors
63
Drugs targeting adrenoceptors - eyes
α- agonists cause pupil dilation - useful in eye examination and surgery - there's also a related effect on the blood vessels - drugs that activate alpha receptors cause vaso-constriction and produce decrease redning in the eye
64
Drugs targeting adrenoceptors – blood vessels
α-agonists - cause vasoconstriction  nasal decongestants and ocular decongestants α-antagonists - inhibit vasoconstriction  LOWER blood pressure (eg in hypertension)
65
Drugs targeting β-adrenoceptors – bronchi
β-agonists - cause bronchodilation useful in treatment of asthma main treatment for acute asthma attacks • β - antagonists - ??ult • β-antagonists are CONTRAINDICATED in asthmatics

BMS1052_ (18 decks)

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