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brs (phase 1b) > (psych) psychopharmacology > Flashcards

(psych) psychopharmacology Flashcards

1
Q

what types of treatment are available in psychiatric medicine?

A

chemicals (drugs/medicines)

electrical stimulation

structural rearrangement (surgery & orthopaedics)

talking therapies

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2
Q

how are chemicals used in psychiatric medicine?

A

drugs for psychosis

drugs to treat depression

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3
Q

how is electrical stimulation used in psychiatric medicine?

A

electroconvulsive therapy for depression

neurostimulation for pain stimulation

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4
Q

how is structural rearrangement used in psychiatric medicine?

A

psychosurgery

deep brain stimulation for sever depression

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5
Q

how are talking therapies used in psychiatric medicine?

A

cognitive behaviour therapy (CBT)

exposure for phobias

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6
Q

what is the advantage of classifying psychiatric drugs based on chemical structure?

A

each drug has a unique structure = extremely precise way of classifying drugs

easy to allocate data

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7
Q

what is the disadvantage of classifying psychiatric drugs based on chemical structure?

A

no use in clinical decision making as most of the time, clinicians do not know chemical structure of every drug

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8
Q

what is the advantage of classifying psychiatric drugs based on the illnesses they treat?

(e.g. antidepressants, antipsychotics, anxiolytics, hypnotics)

A

easier for doctors and clinicians to choose a drug to treat the condition

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9
Q

what do hypnotic drugs do?

A

drugs that induce sleep and are used to treat insomnia

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10
Q

what are the disadvantages of classifying psychiatric drugs based on the illnesses they treat?

(e.g. antidepressants, antipsychotics, anxiolytics, hypnotics)

A

many psychiatric medicines (e.g. antidepressants, antipsychotics etc) work in several disorders and not just the ones they have been named after

most psychiatric conditions have multiple symptoms and a single medicine may not treat all of them

can be discerning for the patient to find out they have been prescribed e.g. ‘an antipsychotic’ for depression

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11
Q

how are psychiatric drugs classified based on their pharmacology?

A

using neuroscience-based nomenclature (NbN)

= an app with core pharmacology used to classify psychiatric medicines

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12
Q

what is NbN?

A

neuroscience-based nomenclature

= an app that contains the core pharmacology used to classify psychiatric medicines

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13
Q

what is the problem with classifying drugs as antipsychotics and antidepressants etc - and how is this overcome?

A

can be discerning for the patient to find out they have been prescribed e.g. ‘an antipsychotic’ for depression

so instead classify drugs based on target neurotransmitters (e.g. dopamine blocker, serotonin enhancer)

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14
Q

how are drugs classified based on target neurotransmitters?

A

antipsychotics = dopamine blockers

antidepressants = serotonin enhancer

hypnotic = GABA enhancer

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15
Q

what are antipsychotics also known as?

A

dopamine blockers

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16
Q

what are antidepressants also known as?

A

serotonin enhancers

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17
Q

what are hypnotics also known as?

A

GABA enhancers

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18
Q

which structures do psychiatric drugs (like all drugs) target?

A

transport proteins (i.e. neurotransmitter re-uptake sites)

enzymes

receptors

ion-channels

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19
Q

where are the targets for psychiatric drugs mostly found?

A

in the brain

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20
Q

what causes adverse/side effects when taking psychiatric drugs?

A

when other sites elsewhere in the body are structurally similar to the desired target site, drug can binds to secondary sites and cause side effects

(if unwanted = adverse effects)

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21
Q

which structure, besides the brain, is commonly affected by psychiatric drugs?

A

liver enzymes

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22
Q

in neuronal transmission, why are reuptake proteins important?

A

enable the neurotransmitter in the synaptic cleft to be taken back up into the pre-synaptic terminal and then recycled

= prevents continuous activation of the post-synaptic neurone

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23
Q

which is the only neurotransmitter that is not taken back up into the pre-synaptic nerve terminal?

A

acetylcholine

(Ach is hydrolysed in the synaptic cleft and one of the resultant products, choline, is taken back up into the pre-synaptic neurone)

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24
Q

which two main receptors can a neurotransmitter act on?

A

post-synaptic membrane receptor (main target)

autoreceptors (on the pre-synaptic neurone)

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25
Q

what is the impact of a neurotransmitter acting on an autoreceptor?

A

autoreceptors are usually inhibitory

= inhibit Ca2+ influx into pre-synaptic nerve terminal so there is reduced neuronal firing and reduced release of neurotransmitter into the synaptic cleft

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26
Q

what is an autoreceptor?

A

type of receptor located on the membranes of presynaptic nerve cell

part of a negative feedback loop

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27
Q

which enzyme inhibitors are used for anxiety and depression treatment?

A

monoamine oxidase inhibitors (MAOIs)

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28
Q

how do monoamine oxidase inhibitors work in treating anxiety and depression?

A

block the breakdown of serotonin and noradrenaline so greater concentrations remain in the system to stimulate wellbeing and a better mood

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29
Q

which enzyme inhibitors are used for depression treatment?

A

acetylcholinesterase inhibitors

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30
Q

how do acetylcholinesterase inhibitors work in treating dementias?

A

block the breakdown of acetylcholine so more remains to make up for the acetylcholine deficit in dementia

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31
Q

which enzyme inhibitors are used for mood stability treatment?

A

glycogen synthase kinase inhibitors

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32
Q

how does lithium work for mood stability treatment?

A

lithium blocks glycogen synthase kinase for mood stability

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33
Q

what are agonists?

A

mimic the endogenous agonist and stimulate the receptors

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34
Q

what are antagonists?

A

block the endogenous agonist binding to the receptors

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35
Q

give examples of antagonists

A

dopamine receptor blockers (for schizophrenia)

histamine receptor blockers (for sleep)

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36
Q

give examples of agonists

A

benzodiazepines enhance GABA (for sleep)

guanfacine enhances noradrenaline (for ADHD)

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37
Q

why do some psychiatric drugs block reuptake sites?

A

to increase neurotransmitter concentration in the synapse to enhance post-synaptic receptor activity

(e.g. citalopram, desipramine, methylphenidate)

38
Q

how does citalopram work?

A

binds to and inhibits the serotonin re-uptake transporter to enhance serotonin in the CNS

to treat depression and anxiety

39
Q

how does desipramine work?

A

binds to and inhibits the noradrenaline re-uptake transporter to enhance noradrenaline in the CNS

to treat depression

40
Q

how does methylphenidate work?

A

binds to and inhibits the dopamine re-uptake transporter to enhance dopamine in the CNS

to treat ADHD

41
Q

how does amfetamine work?

A

bind to re-uptake transporters and switch the re-uptake site direction so release of neurotransmitter into the synaptic cleft is enhanced

42
Q

what is amfetamine used for?

A

to treat ADHD

43
Q

which drugs bind to reuptake proteins?

A

citalopram
desipramine
methylphenidate

amfetamine

44
Q

where does serotonin act in the CNS?

A

acts on auto-receptors to inhibit serotonin release (negative feedback)

acts on post-synaptic receptors (5HT1a) to dampen activity in the post-synaptic neurone, reducing anxiety and depression

45
Q

what is the effect of psychiatric drugs blocking ion channels?

A

reduces neuronal excitability

46
Q

which psychiatric drugs block sodium channels and why?

A

sodium valproate and carbamazepine

= reduce sodium influx into pre-synaptic neurones
= reduced stimulation of action potentials
= reduce neuronal excitability
= cannot recruit neurones in an epileptic focus so no seizures

to treat epilepsy and enable mood stabilisation

47
Q

which psychiatric drugs block calcium channels and why?

A

gabapentin and pregabalin

= reduced neuronal excitability

to treat epilepsy and anxiety

48
Q

what is the main excitatory neurotransmitter?

A

glutamate

approx 80% of all neurones

49
Q

what is the main inhibitory neurotransmitter?

A

GABA

approx 15% of all neurones

50
Q

what are the two types of neurotransmitter?

A

fast-acting (inhibitory or excitatory)

slow-acting (modulators e.g. dopamine, serotonin, noradrenaline, acetylcholine)

51
Q

give examples of fast-acting neurotransmitters

A

glutamate (excitatory)

GABA (inhibitory)

52
Q

give examples of slow-acting neurotransmitters

A

dopamine

serotonin

acetylcholine

noradrenaline

endorphins and other peptides

53
Q

what is the function of fast-acting neurotransmitters?

A

involved in memory, movement and vision

54
Q

what is the function of slow-acting neurotransmitters?

A

modulators

emotions, drives, valence of memory

55
Q

what happens to neurotransmitter levels in epilepsy?

A

excess glutamate

56
Q

how is epilepsy treated pharmacologically?

A

perampanel - glutamate (AMPA) receptor antagonist

57
Q

what happens to neurotransmitter levels in alcoholism?

A

excess glutamate

58
Q

how is alcoholism treated pharmacologically?

A

acamprosate

ketamine

= both glutamate (NMDA) receptor antagonists

59
Q

what happens to neurotransmitter levels in anxiety?

A

GABA deficiency

60
Q

how is anxiety treated pharmacologically?

A

benzodiazepines

= GABA enhancers

61
Q

what happens to neurotransmitter levels in depression/anxiety?

A

5HT (serotonin) deficiency

62
Q

how is depression(/anxiety) treated pharmacologically?

A

1) selective serotonin reuptake inhibitors (SSRIs)

= prevent serotonin reuptake back into the pre-synaptic neurone

OR

2) monoamine oxidase inhibitors

= block breakdown of serotonin and noradrenaline

63
Q

what happens to neurotransmitter levels in psychosis?

A

excess dopamine

64
Q

how is psychosis treated pharmacologically?

A

dopamine receptor blockers

65
Q

what happens to neurotransmitter levels in nightmares?

A

excess noradrenaline

66
Q

how are nightmares treated pharmacologically?

A

prazosin

= blocks adrenoreceptors, preventing activation by adrenaline/noradrenaline

67
Q

what happens to neurotransmitter levels in dementia/impaired memory?

A

acetylcholine deficiency

68
Q

how is dementia/impaired memory treated pharmacologically?

A

acetylcholinesterase enzyme inhibitors

69
Q

what are multimodal drugs?

A

drugs that work on two different targets at the same time

70
Q

what classes of drugs act on 5HT systems to treat depression?

A

monoamine oxidase inhibitors (MAOIs)

tricyclic antidepressants (TCAs)

selective serotonin re-uptake inhibitors (SSRIs)

5HT receptor antagonists

serotonin-noradrenaline reuptake inhibitors (SNRIs)

melatonin agonist (?)

71
Q

what is an inverse agonist?

A

an inverse agonist is a drug that binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist

‘antagonises the effects of an agonist’

72
Q

give an example of an inverse agonist

A

inverse agonist for histamine receptor can increase attention in ADHD

73
Q

how is inverse antagonism used for ADHD treatment?

A

inverse agonist for histamine receptor can increase attention in ADHD

(histamine usually sedates so inverse agonist has the opposite effect)

74
Q

how can inverse antagonism be used to reverse alcohol’s amnestic effect?

A

amnestic effect of severe alcoholism could be reversed by giving a5IA

= improves functionality of hippocampus to improve memory again

75
Q

what are partial agonists?

A

ligands that bind to the agonist recognition site but trigger a response that is lower than that of a full agonist at the receptor

76
Q

why are partial agonists preferred in some cases?

A

improved safety (especially in overdose)

77
Q

how does a partial agonist act when there is excess neurotransmitter?

A

in excess neurotransmitter, partial agonist will have antagonising effects (blocking the receptor)

78
Q

what determines the effect of a partial agonist and how?

A

the ongoing levels of neurotransmitter present

79
Q

how does a partial agonist act when there is a deficit in neurotransmitter?

A

acts as an agonist (as required) to produce the desired outcome

80
Q

how many parts are there to a GABA receptor?

A

five different proteins make up the receptor

81
Q

what is an orthosteric site?

A

the sites for binding of the substrates or competitive inhibitors of enzymes and agonists or competitive antagonists of receptors

82
Q

what is an allosteric site?

A

sites to which binding will result in a conformational change (far from the orthosteric site)

83
Q

give an example of orthosteric site binding

A

the GABAa receptor is an ion-channel linked receptor

the neurotransmitter GABA binds to the GABA receptor’s orthosteric site

= enhanced chloride ion conductance
= inhibits neuronal excitability and activation
= calms the brain

84
Q

give an example of allosteric site binding

A

benzodiazepines, barbiturates, ethanol (alcohol), neurosteroids

= all act at allosteric sites (sites away from the orthosteric site) on the same protein complex

= enhance the action of GABA allosterically without interacting at the GABA orthosteric site directly

= sedation, sleep, reduced anxiety, anti-epilepsy

85
Q

what are the binding sites available on the GABA ion channel?

A

GABA

benzodiazepines

neurosteroids

ethanol

barbiturates

86
Q

which two dopamine receptor blockers are used to treat schizophrenia?

A

haloperidol and clozapine

= block dopamine neurotransmission

87
Q

how does haloperidol compare to clozapine in terms of drug selectivity?

A

haloperidol = very selective for the dopamine receptor (potent dopamine receptor blocker)

but some side effects

88
Q

how does clozapine compare to haloperiodol in terms of drug selectivity?

A

clozapine has a very low drug selectivity - binds to numerous receptors

= increased risk of off-target side effects
(weight gain, sedation, metabolic syndrome)

89
Q

which two serotonin reuptake inhibitors are used to treat depression?

A

amitriptyline and citalopram

= both block the serotonin transporter and prevent serotonin reuptake

90
Q

how does amitriptyline compare to citalopram in terms of drug selectivity?

A

binds to numerous transporters and receptors

= huge burden of side effects due to many off-target actions

91
Q

how does citalopram compare to amitriptyline in terms of drug selectivity?

A

much more selective as it binds only to the serotonin transporter

= not many side-effects unless due to excess serotonin

92
Q

what are the impacts of off-target effects in overdose?

A

can have a huge impact

= can lead to cardiac or brain toxicity (increased binding to undesired sites where can be very dangerous)

brs (phase 1b) (71 decks)

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