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Year 2- CNS > Applied Neuro- Pharmacology > Flashcards

Applied Neuro- Pharmacology Flashcards

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1
Q

Where does the synthesis and packaging of neurotransmitters usually occur?

A

Presynaptic terminals

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2
Q

Describe what happens when an action potential fires down the axon.

A

Causes presynaptic terminal to depolarise which opens voltage-gated calcium channels.

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3
Q

What happens when the calcium channels are opened in the process of synaptic transmission?

A

Calcium floods into cells, down electric and concentration gradients, triggering calcium-dependant exocytosis.

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4
Q

What happens during calcium-dependant exocytosis in synaptic transmission?

A

Neurotransmitter released into synaptic cleft and finds receptor.

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5
Q

What inhibits the release of further neurotransmitters?

A

Autoreceptors

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6
Q

How are neurotransmitters inactivated?

A

Through the process of uptake- brought back into the cell via a transporter and metabolised by cells, used to make more neurotransmitters which can be used in the cell.

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7
Q

What would happen if a drug blocked the voltage-gated sodium channels to reduce synaptic transmission?

A

No depolarisation, no opening of calcium channels hence no calcium-dependant exocytosis.

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8
Q

Name a drug in which it’s mechanism is to block these voltage-gated sodium channels.

A

Tetrodotoxin (from a pufferfish!)

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9
Q

Okay now give a clinical example of a drug which has the mechanism of blocking voltage-gated sodium channels.

A

Local anaesthetics e.g. lidocaine.

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10
Q

Another way to reduce synaptic transmission is by blocking the voltage-gated calcium channels.
Describe what would happen here.

A

No calcium flooding into cell, no calcium dependant exocytosis.

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11
Q

Which animal/creature can produce venom which can block voltage-gated calcium channels?

A

Black widow spider

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12
Q

As well as blocking voltage gated sodium/calcium channels, how else can we reduce synaptic transmission?

A

By blocking the release machinery

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13
Q

Name a drug which can be used to block the release machinery to reduce synaptic transmission.

A

Botulinum

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14
Q

Okay, so, all these drugs mentioned so far (local anaesthetics, venom from a black widow, botulinum) are non-specific.
What does this mean?

A

They inhibit all synapses if they are given systemically, which is not great :)

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15
Q

Botulinum can be given localised as what?

A

Botox injections to specific muscles.

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16
Q

When can local use of botulinum be useful?

A

Botox- improving muscle spasms or contractures in someone who has had a stroke/ cerebral palsy patients.

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17
Q

Another way to reduce synaptic transmission is by blocking postsynaptic receptors. How can this be achieved?

A

By using competitive antagonists.

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18
Q

RECAP- what is the efficacy and affinity of a competitive antagonist like?

A

High affinity
Low efficacy

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19
Q

Give an example of a competitive antagonist.

A

Beta blockers

->therefore, beta blockers have high affinity and low efficacy

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20
Q

What will beta blockers compete with to bind to beta adrenergic receptors?

A

Noradrenaline

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21
Q

Similarly, we could also block postsynaptic receptors with a non-competitive antagonist. What would this non-competitive antagonist do?

A

Bind to another site

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22
Q

Another way that we can reduce synaptic transmission is by activating these presynaptic inhibitory receptors.
What typically happens in this?

A

Voltage gated calcium channels become blocked preventing more neurotransmitters to be released via calcium-dependant exocytosis.

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23
Q

How could we potentiate synaptic transmission instead?

A

Increase the synthesis and packaging of the neurotransmitter

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24
Q

How could there be an increase in the packaging and synthesis of neurotransmitters?

A

Increasing availability of precursors.

-> this means there are more building blocks for the cells to make neurotransmitters.

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25
Use of an agonist could increase synaptic transmission. How so?
Receptors are activated all of time. However, this may be an issue as in normal physiology, receptors are only activated when an action potential coming down the presynaptic cell leading to the release of a neurotransmitter.
26
Therefore, what is a better way to increase synaptic transmission rather than with agonists?
Potentiating the effects of the transmitter on the receptor.
27
Give an example of a drug which potentiates the effects of a neurotransmitter on a receptor.
Benzodiazepines
28
Which neurotransmitter can benzodiazepines work on to potentiate the effects on receptors?
Potentiate effects of neurotransmitter GABA on the GABA-A receptors.
29
Another way that you can potentiate synaptic transmission is by blocking the breakdown of neurotransmitter. Which drug can do this?
Anti-cholinesterase's
30
What can anti-cholinesterase's be used to treat?
Myasthenia gravis
31
What do anti-cholinesterase's do?
Block the anticholinesterase enzyme that is responsible for breaking down acetylcholine into choline.
32
Potentiating synaptic transmission could also occur by blocking the uptake of the neurotransmitter. Given an example of a drug that uses this mechanism.
SSRI- a class of antidepressants
33
List the limited range of neurotransmitters in the body.
Acetylcholine Monoamines Amino acids Purines Neuropeptides Nitrous oxide ->more to be aware of these probs
34
Name some monoamines.
Noradrenaline Serotonin Dopamine
35
Name some purines which act as neurotransmitters.
ATP Adenosine
36
Name some neuropeptides which act as neurotransmitters
Endorphins CCK Substance P
37
Name some amino acids which act as neurotransmitters.
Glycine Glutamate GABA
38
Which is the most widely used excitatory neurotransmitter?
Glutamate
39
Which is the most widely used inhibitory neurotransmitter?
GABA
40
Name the four pathways on dopamine in the brain.
Mesocortical pathway Nigrostriatal pathway Tubero-infundibular pathway Mesolimbic pathway
41
What does the mesolimbic pathway have a role in?
Reward and addiction
42
What can overactivity of the mesolimbic pathway lead to?
Positive symptoms of schizophrenia- can lead to hallucinations
43
What can impairment of the neocortical pathway be responsible for?
Cognitive symptoms seen in Parkinson's Negative symptoms we see in schizophrenia
44
What does dopamine inhibit the release of?
Prolactin from the pituitary ->therefore, dopamine agonists can be used to inhibit
45
What is the area postrema in the medulla responsible for?
Control of vomiting
46
Which cells are degenerated in Parkinson's?
Dopaminergic cells in the substancia nigra.
47
How is dopamine synthesised in vivo?
Tyrosine is converted to DOPA by tyrosine hydroxylase. DOPA is converted to dopamine by decarboxylase.
48
Which of the following can cross the blood brain barrier: tyrosine, DOPA, dopamine
Tyrosine and DOPA can cross BBB
49
If you wanted to give a patient with Parkinson's dopamine, why couldn't you give it as an injection or an oral tablet?
Wouldn't cross the blood brain barrier and exert functions in the brain.
50
Although tyrosine can cross the BBB, why can't it be given to those with Parkinson's?
The enzyme which converts it to DOPA is lost through degeneration
51
Therefore, how can a Parkinson's patient be given dopamine?
Given DOPA in form L-DOPA, can cross BBB and be converted into dopamine.
52
DOPA can also be converted into dopamine in the periphery of the body. This can produce some side effects such as?
Vomiting Hypotension
53
There are five subtypes of metabotropic dopamine receptors, named D1-5. What can happen when dopamine binds to different dopamine receptors?
Variable effects as different dopamine receptors are present in different parts of the brain ->told we don't need to worry too much about the details of this
54
Dopamine can be metabolised in two different pathways. However, both pathways result in the same end product. What is this?
Homovanillic acid
55
Name the two enzymes which are key in the metabolism of dopamine.
MAO-B COMT ->In each pathway of the metabolism of dopamine, both MAO-B and COMT are used, but in a different order in each pathway.
56
What can be done to these enzymes if you wanted to increase the amount of dopamine?
Inhibit these enzymes to reduce the metabolic breakdown of dopamine.
57
What symptoms are present in those with Parkinson's?
Stiffness, slow movements, change in posture and tremor.
58
Which dopamine precursor can be given to increase levels of dopamine in someone with Parksinson's?
LDOPA (levodopa)
59
Which groups of DOPA agonists could be given to increase levels of dopamine?
Ergots Non-ergots Apomorphine
60
Ergot DOPA agonists are rarely used as have side effects such as?
Fibrosis of heart valves Retroperitoneal fibrosis
61
Non-ergots don't have these side effects and are commonly used in clinical practice. Name the types of non-ergots which are commonly used.
Ropinirole Pramipexole
62
Which DOPA agonist is given subcutaneously?
Apomorphine
63
How does dopamine help in Parkinson's?
Helps to reduce symptoms
64
List some of the enzyme inhibitor drugs for MAO-B.
Selegiline Rasagiline Safinamide
65
List some of the enzyme inhibitor drugs for COMT.
Entacapone Opicapone
66
List some of the peripheral AAAD inhibitors which can decrease the side effects of LDOPA.
Carbidopa Benserazide
67
If there are decreased peripheral LDOPA side effects, what does this mean?
Greater proportion of the oral dose can reach the CNS. ->because of this, LDOPA is only manufactured together with one of these peripheral AAAD inhibitor drugs
68
Dopaminergic drugs can also have some side effects. List some.
Nausea Vomiting Psychosis Impulsivity/abnormal activity
69
Which motor features of Parkinson's can dopaminergic drugs improve?
Limb rigidity Bradykinesia Tremor
70
Which features of Parkinson's are not helped by dopaminergic drugs?
Speech impairment Balance problems Gait difficulty Cognition
71
Dopamine antagonists may be given. What can these: 1. improve 2. worsen/cause
1. Improves nausea, vomiting, psychosis 2. worsen/cause parkinsonism (Parkinson's disease).
72
Which DOPA agonist doesn't cross the BBB and therefore helps to reduce vomiting/nausea while not increasing risks of Parkinson's?
Domperidone
73
What is a side effect of domperidone?
QT prolongation in ECG
74
Parkinsonism causes too little movement. Supplementing dopamine using dopaminergic drugs increases movement which can lead to???
Dyskinesias -> abnormal involuntary movements
75
What are GABA agonists use to treat?
They are anti-epilepsy drugs Have anti-anxiety properties
76
What can triptans (selective 5HT agonists) be used in the treatment of?
Migraines
77

Year 2- CNS (49 decks)

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