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Neuro > Applied Neuro-pharmacology > Flashcards

Applied Neuro-pharmacology Flashcards

1
Q

How do local anaesthetics work?

A

Block voltage gated Na+ channels

Blocks all synaptic transmission

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2
Q

How do spider toxins work?

A

Block voltage gated Ca2+ channels

Blocks transmitter release

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3
Q

How does botulinum toxin work?

A

Blocks the release machinery

Blocks transmitter release

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4
Q

How do receptor antagonists work?

A

Block postsynaptic receptors

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5
Q

What are some other ways to reduce synaptic transmission?

A

Activate presynaptic inhibitory receptors
Increase breakdown of transmitter
Increase uptake of transmitter
Inhibit synthesis and packaging of transmitter

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6
Q

How could precursors be useful in manipulating synaptic transmission?

A

Flooding cells with the appropriate precursors could increase synaptic transmission

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7
Q

What is the effect of benzodiazepines and barbiturates on GABA receptors?

A

Allosteric drugs which potentiate the effects of the endogenous transmitter

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8
Q

What is the effect of anticholinesterases?

A

Blocks breakdown of transmitter Ach

Increases transmission

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9
Q

What class of neurotansmitters do noradrenaline, dopamine and serotonin fall under?

A

Monoamines

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10
Q

List some examples of amino acid neurotransmitter.

A

Glutamate
GABA
Glycine

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11
Q

Give some examples of purines.

A

ATP

Adenosine

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12
Q

What are some examples of neuropeptides?

A

Endorphins
CCK
Substance P

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13
Q

What is the difference between analgesia and anaesthetic?

A

Analgesia is pain relief without loss of consciousness and without total loss of feeling or movement; anaesthesia is defined as the loss of physical sensation with or without loss of consciousness.

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14
Q

What are some unique characteristics of each neurotransmitter?

A

Anatomical distribution
Range of receptors it acts on
Range of functions in different regions

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15
Q

What is the anatomical distribution of dopamine in the brain?

A

Brain stem
Basal ganglia
Limbic system
Frontal cortex

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16
Q

What physiological functions are affected by dopamine?

A

Voluntary movement
Emotions/reward
Vomiting

17
Q

Impairment of which pathway is relevant to cognitive deficit in PD?

A

Mesocortical

18
Q

Which pathway plays a key role in reward and addiction?

A

Mesolimbic

19
Q

Impairment of which pathway leads to increased incidence of schizophrenia and hallucination in PD?

A

Mesolimbic

20
Q

What effect does PD have on DA in the brain?

A

Degeneration of DA cells in the substantia nigra

DA deficiency in basal ganglia

21
Q

What is the final product of dopamine metabolic breakdown?

A

Homovanillic acid

22
Q

What is levodopa?

A

DA precursor

Dopaminergic drug

23
Q

What does carbidopa do?

A

Peripheral AAAD inhibitor
Stops DOPA to dopamine
Reduces peripheral side effects of levodopa and allows greater proportion of the oral dose to reach the CNS

24
Q

What do MAO-B inhibitors do?

A

Stop DA to DOPAC

Prevents breakdown of dopamine

25
Q

What symptoms may dopaminergic drugs improve?

A

Some motor features of PD such as rigidity, bradykinesia and tremor

26
Q

What symptoms may dopaminergic drugs worsen or even cause?

A

Nausea
Vomiting
Psychosis
Impulsivity

27
Q

What symptoms may dopamine antagonists improve?

A

Nausea
Vomiting
Psychosis

28
Q

What kind of drug can worsen or even cause parkinsonism?

A

Dopamine antagonists

29
Q

What are the benefits of Domperidone as a DA antagonist antiemetic?

A

Does not cross BBB so will not worsen PD

30
Q

What adverse effect may dopaminergic drugs have on movement?

A

May cause dyskinesias like chorea

“Too much movement”

31
Q

What adverse effect may DA antagonists have on movement?

A

May cause parkinsonism

“Not enough movement”

32
Q

How do tricyclic antidepressants affect noradrenaline?

A

Prevent re-uptake

Neuro (29 decks)

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