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BMS1052 > CONTROL AND DRUGS > Flashcards

CONTROL AND DRUGS Flashcards

1
Q

What are the main transmitters of the ANS?

A
  • Ach

- Noradrenaline (norepinephrine)

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2
Q

Where is Ach released in SNS?

A
  • At preganglionic synapse
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3
Q

Where is Ach released in PNS?

A

At preganglionic synapse aswell!!

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4
Q

Where is Ach released in somatic efferent?

A
  • At NMJ
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5
Q

Is Ach released at the adrenal medulla?

A

YES!

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6
Q

What is the neurotransmitter for the ganglia regardelss of whether it is in SNS or PNS?

A
  • Acetylcholine!!
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7
Q

Are sweat glands from the PNS or SNS and what is the neurotransmitter released at the end?

A
  • Sympathetic nervous system by sympathetic cholinergic nerves
  • Neurotransmitter is Ach (release this instead of noradrenaline)
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8
Q

What is a co transmitter and what is it involved in?

A
  • Stored with the main transmitter (like Ach), released at the same time and have their own receptors that they interact with.
  • Involved in moderating
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9
Q

What are examples of cotransmitters?

A
  • ATP
  • NO (cotype role in parsympathetics)
  • NPY (SNS)
  • Vasoactive Intestinal Peptide (VIP) in PNS
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10
Q

Do nerves release Ach or Noradrenaline as the main neurotransmitter?

A

NO! Some don’t release EITHER!

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11
Q

What are nerves called that don’t release Ach nor NA called and what is an example?

A
  • Non Adrenergic Non Cholinergic

- e.g. Nitric oxide (NO) main CO- neurotransmitter released from PNS nerves for erection

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12
Q

Where are Ach and NA synthesised?

A

In the nerve terminal

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13
Q

Uptake of precursor is an a…..

A

active transport system

- Enzymes then convert precursor into Active neurotransmitter

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14
Q

What would happen if a neurotransmitter stayed in a terminal for too long?

A
  • Enzymes would break it down (degradation products)
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15
Q

How do we solve the issue of neurotransmitters being broken down if in terminal for too long?

A
  • Store it with co-transmitters in vesicles
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16
Q

Where is Ach broken down?

A
  • In the neuro effector junction
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17
Q

Where is NA broken down?

A
  • Reuptake in the nerve terminals
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18
Q

Which transmitter is NOT stored within vesicles?

A
  • Nitric Oxide (NO)
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19
Q

Which transmitters ARE stored within vesicles?

A
  • Ach
  • NA (noradrenaline)
  • ATP
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20
Q

What effect does the PNS have on our body?

A
  • Constricts pupils
  • Constricts bronchioles
  • Lowers heart rate
  • NO EFFECT ON BLOOD VESSELS
  • INCREASES MOTILITY
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21
Q

Does the PNS have an effect on blood vessels?

A
  • NO!!
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22
Q

What effect does the SNS have on the body?

A
  • Dilate pupils
  • Bronchdilation
  • Increased heart rate
  • CONSTRICT blood vessels to increase blood pressure( (small amount of dilation from muscles)
  • decrease in motility
  • increase in sweating (Ach)
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23
Q

What is bronchodilation caused by?

A
  • Release of adrenaline from adrenal medulla
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24
Q

What are the RECEPTORS of the ANS for Acetylcholine?

A
  • Nicotinic

- Muscarinic

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25
Q

What are the RECEPTORS of the ANS for NA?

A
  • Alpha

- Beta

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26
Q

Can receptors be in a tissue even if they don’t have nerve supply?

A
  • YES!
    e. g1. Ach receptors present in blood vessels (even though there are no nerves to the receptors)
    e. g.2. NA–> Receptrors in bronchial smooth muscle even though no nerves supplying them
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27
Q

Where are the nicotinic receptors located?

A
  • At the ganglia and muscle
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28
Q

What is miosis in the context of ANS?

A
  • Pupil constriction
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29
Q

Can autonomic receptors also exist in other parts of the body not associated with the ANS?

A
  • YES!! There is Ach in the CNS (brain)
  • so have to take into account how drugs will affect receptors in BOTH CNS and ANS (because it will hit receptors in both)
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30
Q

What does a muscarinic receptor mediate?

A
  • Response of Ach (PARASYMPATHETIC affects of Ach)
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31
Q

Where are muscarinic receptors located?

A
  • On the tissue (so PNS)
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32
Q

What actions are caused by muscarinic receptors (end organ) in the PNS?

A
  • Miosis
  • Increased Gi motility
  • Bronchoconstriciton
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33
Q

What are the actions caused by nicotinic receptors ?

A
  • Stimulation of the post ganlgionic parasympathetci nerve fibres
  • Stimulation of the post ganglionic sympathetic nerve fibres
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34
Q

Do muscarinic receptors mediate the actions of sympathetic cholinergic nerves as an acception?

A
  • YES! For example in sweating. They do an this is an acception because muscarinics are usually for the parasympathetics
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35
Q

Why are adrenoreceptors classified into alpha and beta?

A
  • Based on the rank order of potency (how well they caused a response) of NorAdrenaline, Adrenaline and isoprenaline
  • NA was best out of agonists (good at vasocnostriction)
  • BUT isoproline was best at bronchodilation, increasing HR etc.
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36
Q

What are alpha receptors classified as? (best to worst effect-chain of 3)

A
  • NA–> Adren–> Iso

NA is the best

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37
Q

What are beta receptors classified as? (best to worst potency-chain of 3)

A

Iso–> Adren–> NA
(Iso-dilating pupils)
(Iso is the best)

38
Q

What is myadriasis?

A
  • Dilation of pupils
  • Constriction of radial muscles to cause muscle dilation
  • alpha receptor response
39
Q

What effects are seen when peripheral adrenoreceptors are stimulated?

A
  • Affects both alpha and beta

- Dilation of the pupil of eye (all effects of SNS)

40
Q

What are the alpha adrenoreceptors known as?

A
  • Excitatory e.g. blood vessel constriction

- Causing muscle CONTRACTION

41
Q

What are the beta receptors known as?

A
  • INHIBITORY (except for increasing heart rate)
  • e.g. bronchodilartion
  • generally relaxing receptors
42
Q

Where do alpha receptors sit?

A
  • Under nerves

- when NA is released it hits alpha receptors to cause constriction

43
Q

What receptor is Adrenaline more likely to get to?

A
  • Beta receptors

- They are farther away (cause dilation type response)

44
Q

What does the response from the tissue depend on?

A
  • Relative proportions of the subtype receptors
  • Also depends on which is the most likely to be stimulated
  • Relative potency of agonist e.g. NA will go for alpha receptors more than beta receptors
  • adrenaline goes for alpha and beta
45
Q

Where can drugs act?

A
  • Receptors
  • Blocking uptake
  • Enzymes on junction and nerve to affect snyhtesis of NT
  • transmitter precursor effect
46
Q

What are protein targets for drug action?

A
  • Ion channels
  • Enzymes
  • Transport systems (carrier molecules)
  • Receptors (4 families of receptors)
47
Q

What are drugs called that mimic the actions of endogenous factors like Ach?

A
  • Parasympathomimetic

- Acts on same receptors as Ach

48
Q

What are drugs called that block the actions of endogenous factors called?

A
  • Parasympatholytic

- drugs can compete with their endogenous ligand

49
Q

Can Ach go out the same way choline came into the nerve terminal?

A

Yes but this is a very rare situation where the Ach builds up

50
Q

Which proteins are important in the release of Ach (exocytosis of it)?

A

SNAP and SNARE (RE=receptor) proteins

51
Q

What effect does Botulinum toxin have on a (SNAP and) SNARE protein?

A
  • It chops it up (cleves it)
52
Q

Is Ach a neurotransmitter at parasympathetic nerve endings? -

A

YES!

53
Q

What happens when no more Ach is released (depletion) ?

A
  • Symptoms can occur such as blurred vision
  • dry mouth (because parasympathetic secretions stop)
  • Fixed or dlated pupils (because can’t constrict pupil)
    Possibly constipation (due to Ach not being there to increase GI motility)
54
Q

What is a use of botox acting on the sympathetic cholinergic nerves?

A
  • Injecting it into sweat glands to control the amount of sweating (hyperhidrosis)
55
Q

How come Botox works for clinical use without killing you?

A

Because it is injected STRAIGHT INTO THE MUSCLES

  • effects on skeletal muscle
  • can be used for eye spasms(bleopharospasm) or cerebral palsy
56
Q

What is the enzyme that breaks Ach back down into Cholne and Acetetate?

A
  • Acetylcholinesterase
57
Q

What are examples of drugs that can interfere with Acetylcholinesterase?

A
  • Organophosphate insectisides
  • Sarrin-nerve gas
  • ( Sarrin is irreversible blocker of Acetytlcholinesterase , tears coming down, frothing at mouth)
58
Q

Which symptoms would be associated with poisining relating to blocking of Acetylcholinesterase (build up of Ach -anticholinesterases) ?

A
  • Increased bronchoconstriction
  • Increased salivation
  • Brachycardia (lowered heart rate)
  • Intestinal spasm
  • Miosis
59
Q

What are the symptoms of organophosphate insectisieds at the muscarinic receptors ?

A 
Dihorrhea 
Urination
Miosis
Bronchoconstriction
Brachycardia
Emesis (act of vomiting) 
Lacrimation
Lethargy
Salivation
60
Q

What occurs to the nicotinic receptors with injection of organophosphate insectisides?

A
  • They are stimulated particularly at NMJ

- also ganglion

61
Q

What occurs in the CNS with insectiside poisoning?

A
  • Anxiety, restlessness, lethargy, confusion, psychosis, coma, seizures
62
Q

Which 3 areas are affected with orgsnophosphate insectiside poisoning?

A
  1. Muscarinic receptors (DUMMBELLS)
  2. Stimulation of nicotinic receptors
  3. CNS effects
63
Q

What is a therapeutic use of antiachetylcholineasterases?

A
  • In MYASTHENIA GRAVIS (antibodies attack nicotinic receptors at the NMJ)
  • AntiAchases try to increase amount of Ach to overcome the destroyed nicotninic receptors
  • Alzheimers disease
64
Q

What can be side effects of anticholinesterases?

A
  • DUMMBBELLS

- overtreatment can also result in too much Ach which results in cholinergic crisis

65
Q

What is the precursor for NA synthresis?

A
  • L-tyrosine (found in diet)
66
Q

What is the process of NA synthesis?

A
  • L-tyrosine gets converted to Dopamine (multistep pathway) which then goes to NA
    L-tyrosine–> Dopamine–>Storage vesicles–> NA
67
Q

What is the rate limiting step in formation of NA?

A
  • The first step with L-tyrosine
68
Q

Where can NA be taken up into?

A
  1. Reuptake into the nerve terminal (most important)

2. reuptake into other neuronal tissues (less important)

69
Q

How can drugs interfere with NA transmission?

A
  • Synthesis step
  • Storage (easier to target)
  • Release(easier to target)
  • Action
  • Inactivation
  • Used to target effects on the sympathetic nervous system
70
Q

What is the conversion pathway from dopamine to adrenaline?

A

-Dopamine–> Noradrenaline (NA)–> Adrenaline

71
Q

Which kinds of drugs affect NA release?

A
  • Those that DIRECTLY BLOCK release

- Those that CAUSE NA release (mimic the SNS)

72
Q

What are the drugs which block NA release known as?

A
  • Noradrenergic blocking drugs
  • (used to be used as antihypertensives-good at bringing down blood pressure-reducing heart rate
  • but not good because too many side effects
  • Block sympathetic nervous system responses
73
Q

What are the drugs that cause NA release?

A
  • Amphetamine (ephedrine/pseudoephedrine-cold and flu tablets)
  • compete with NA to be taken up into nerve terminal
  • When inside nerve terminal, it knocks NA out (goes out via reverse transporter) into neuroeffector junction
  • Indirectly acting sympathomimetics
74
Q

What does amphetamine affect the release of and what side effects can this proudce?

A
  • Affects dopamine release

- Side effects of increased blood pressure, HR and higher risk of stroke (because of dopmine–> NA)

75
Q

What are MAO-I inhibitors used as?

A
  • Interfere with NA metabolism

- Used mostly for effects in CNS (antidepressants)

76
Q

Can Ach be used clinically ?

A

No because it is broken down so rapidly

77
Q

What does activation or blockade of nicotinic receptors by drugs cause?

A
  • Affects ganglionic neurotransmission
  • Responses will be complicated as it will affect both parasympathetic and sympathetic nervous system (unpredictable effects)
  • So ganglion blockers are not useful
78
Q

Are ganglion blockers useful?

A

NO

79
Q

Is targeting muscarinic receptors the best?

A

YES! As these are just for the parasympathetic and oyu can go straight to the end organ

80
Q

What are muscarinic antagonists?

A
  • Drugs that stick at the receptor and them themselves don’t cause an effect (they would block the effects of the PNS)
  • Called parasympatholytics
81
Q

What are muscarinic agonists?

A
  • Drugs which stimulate muscarinic receptors and produce similar effects to PNS
  • Parasympathomimetic
82
Q

What are effects of antagonists (anti muscarinic)?

A
  • Opposite of DUMBBELLS
    e.g. Block miosis (so pupil dilation)
    Decrease slaviation
    Increase heart rate
    Decreased bronchioconstriction (so relaxed bronchial smooth muscle)
    Decreased GI motility and gastric acid secretion
    Decrease bladder constriction (urination) -decreased bladder emptying
    Inhibition of secretions (like saliva)
83
Q

Is it easier to design drugs for the nicotinic/muscarinic recepotrs or the alpha compared to beta receptors?

A

The nicotnic and muscarinic receptors are MUCH easier because they are easy to distinguish from one another (whereas alpha and beta much more similar so harder to target just one)

84
Q

Does an alpha or beta receptor cause mydriasis (dilation of pupils)?

A

Alpha receptor (SNS)

85
Q

Does alplha or beta receptor cause reduced saliva flow?

A
  • Alpha receptor
86
Q

Does alpha or beta receptor cause increased Stroke volume and heart rate?

A
  • Beta
87
Q

Does the alpha or beta receptor cause vasoconstriction?

A
  • Alpha
88
Q

Does the alpha or beta receptor cause reduced peristalsis and secretion?

A
  • Alpha AND Beta receptors
89
Q

Does the alpha or beta receptor cause glycogen to glucose conversion in liver?

A
  • Beta receptors
90
Q

Does the alpha or beta receptors cause inhibition of bladder contraction?

A
  • Beta
91
Q

Does the alpha or beta receptors cause adrenaline release?

A

Beta receptors

BMS1052 (14 decks)

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