Psychopharmacology for Psychiatry Flashcards

1
Q

What are the 4 main psychiatric treatments?

A
  • chemical (drugs + immunotherapies)
  • electrical stimulation (ECT)
  • structural rearrangement (psychosurgery/deep brain stimulation)
  • talking therapies (CBT)
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2
Q

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

A

each drug has a unique structure, easy to allocate data.

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3
Q

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

A

no use in clinical decision making

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4
Q

What is the advantage of classifying psychiatric drugs based on the disease that they treat?

A

easy for doctors to choose drugs as they make diagnosises

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5
Q

What is the disadvantages of classifying psychiatric drugs based on the disease that they treat?

A
  • many psychiatric drugs are used in several disorders
  • most disorders have multiple symptoms and may not all be treated with one drug
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6
Q

What is classifying psychiatric drugs based on their pharmacology?

A

neuroscience based nomenclature (NbN)

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7
Q

What are the 4 different drug targets?

A
  • receptors
  • neurotransmitter reuptake sites
  • ion channels
  • enzymes
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8
Q

What are some examples of drugs that block enzyme activity?

A
  • monoamine oxidase inhibitors (depression)
  • acetylcholinesterase inhibitors (dementia)
  • lithium (bipolar)
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9
Q

What does lithium block?

A

glycogen synthase kinase - for mood stability

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10
Q

What are some examples of receptors which drugs (antagonists) block?

A
  • dopamine receptors
  • serotonin receptors
  • histamine receptors
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11
Q

What are dopamine receptor blockers used to treat?

A

schizophrenia

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12
Q

What are serotonin receptor subtype antagonists used to treat?

A

depression

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13
Q

What are histamine receptor antagonists used to treat?

A

sleep

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14
Q

What are some examples of drug agonists?

A
  • benzodiazepines
  • guanfacine
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15
Q

What do benzodiazepines do?

A
  • enhance GABA
  • help with sleep
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16
Q

What does guanfacine do?

A
  • enhance noradrenaline
  • helps with ADHD
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17
Q

What do reuptake site blockers do?

A
  • block reuptake sites
  • increase neurotransmitter concentration in the synapse
  • enhance post-synaptic receptor activity
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18
Q

What are some examples of reuptake blockers?

A
  • citalopram
  • desipramine
  • methylphenidate
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19
Q

What does citalopram do?

A
  • enhances serotonin
  • serotonin reuptake inhibitor (SRI)
  • treats depression and anxiety
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20
Q

What does desipramine do?

A
  • noradrenaline reuptake inhibitor (NRI)
  • enhances noradrenaline
  • treats depression
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21
Q

What does methylphenidate do?

A
  • dopamine reuptake inhibitor (DRI)
  • enhances dopamine
  • treats ADHD
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22
Q

Which drugs swap reuptake site direction to enhance release?

A
  • amfetamine (for ADHD)
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23
Q

What do drugs that target Ion Channels do?

A

block channels to reduce neuronal excitability

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24
Q

What are some examples of drugs that block sodium channels?

A
  • sodium valproate
  • carbamazepine
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25
Q

What do sodium valproate and carbamazepine treat?

A

epilepsy and mood stabilisation

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26
Q

What are some examples of calcium channel blockers?

A
  • gabapentin
  • pregabalin
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27
Q

What do gabapentin and pregabalin treat?

A

epilepsy anxiety

28
Q

How would you describe fast acting neurotransmitters?

A

on-off switch

29
Q

What is an example of an excitatory fast acting neurotransmitters?

A

Glutamate
80% of all neurons
pyramidal cells

30
Q

What is an example of an inhibitory fast acting neurotransmitters?

A

GABA
15% of interneurons

31
Q

What do fast-acting neurons tend to be involved in?

A
  • memory
  • movement
  • vision
32
Q

How would you describe slow acting neurons?

A

modulators

33
Q

How common are slow-acting neurons?

A

5% of all neurons

34
Q

What are some examples of slow acting neurotransmitters?

A
  • dopamine
  • serotonin
  • noradrenaline
  • acetylcholine
  • endorphins
35
Q

What do fast-acting neurotransmitters tend to be involved in?

A
  • emotions
  • drive
  • valence of memory
36
Q

What is epilepsy caused by?

A

excess glutamate

37
Q

What drug can be used to treat excess glutamate in epilepsy?

A

perampanel - glutamate blocker

38
Q

What is alcoholism caused by?

A

excess glutamate

39
Q

What drugs can be used to treat excess glutamate in alcoholism?

A
  • acamprosate
  • ketamine
    (glutamate blockers)
40
Q

What is thought to cause anxiety?

A

GABA deficiency

41
Q

What drug can be used to treat a GABA deficiency?

A

benzodiazapine - GABA enhancer

42
Q

What is thought to be caused by a 5-HT deficiency?

A

depression and anxiety

43
Q

What can be used to treat a 5-HT deficiency?

A

SRIs
MAOIs
(serotonin enhancers)

44
Q

What is thought to be caused by excess dopamine?

A

psychosis

45
Q

What can be used to treat excess dopamine?

A

dopamine receptor blockers

46
Q

What can be caused by excess noradrenaline?

A

nightmares

47
Q

What can be used to treat excessive noradrenaline?

A

prazosin - noradrenaline blocker

48
Q

What is caused by a acetylcholine deficiency?

A

impaired memory/dementia

49
Q

What is the treatment for a deficiency in acetylcholine?

A

acetylcholine esterase enzyme blockers

50
Q

What do most drugs for depression act on?

A

the 5-HT systems

51
Q

What is the difference between partial and full agonists?

A

partial agonists have a lower maximum efficacy than full agonists

52
Q

What are the advantages of using a partial agonist over a full agonist?

A
  • improved safety (especially in overdose)
  • combats hyperactivity while still maintaining the necessary amount of the neurotransmitter
  • in states of high neurotransmitter or excess agonist medicine can act as an antagonist
53
Q

What are inverse agonists?

A

drugs that have the the opposite effects to agonists but don’t block receptors like an antagonist

54
Q

What is allosteric modulation?

A

When drugs work on different sites on the target proteins compared to the endogenous neurotransmitter

55
Q

What is an orthosteric site?

A

the site that the desired substrate binds to

56
Q

What is an allosteric site?

A

a different binding site of the substance, but on the same protein complex

57
Q

What happens when GABA binds to the GABA receptor?

A
  • enhances Cl ion conductance
  • inhibits neurons
  • calms the brain
58
Q

What happens when benzodiazepines, barbituates, alcohol and neurosteroids bind to the allosteric point on the GABA receptor?

A
  • enhances the action of GABA
  • sedation
  • sleep, reduced anxiety, anti-epilepsy
59
Q

What is the selectivity of haloperidol?

A
  • highly selective for the dopamine receptor
  • adverse effects are due to dopamine receptor block
60
Q

What is the selectivity of clozapine?

A
  • non-selective
  • lots of adverse effects due to off-target effects
    (eg; sedation, weight gain, metabolic syndrome)
61
Q

What is the selectivity of amitriptyline?

A

low, also binds to histamine and acetylcholine receptors causing adverse effects

62
Q

What is the selectivity of citalopram?

A
  • selective SRI
  • adverse effects are solely due to increased serotonin
63
Q

What do agonist drugs do?

A

Stimulate/ enhance receptors

64
Q

What does the partial agonist buprenorphine treat?

A

Heroin addiction

65
Q

What does the partial agonist aripiprazole treat?

A
  • dopamine receptor partial agonist
  • treats psychosis along
  • better treatment than haloperidol
66
Q

What is varenicline used to treat?

A

Nicotine addiction