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Aneesha Flashcards BRS 2 > Psychopharmacology for psychiatry > Flashcards

Psychopharmacology for psychiatry Flashcards

1
Q

What 4 types of treatments are there in medicine (with psych examples)

A

Chemical: drugs/medicines (antidepressants, antipsychotics, anxiolytics)
Electrical stimulation: ECT for depression, neurostimulation for pain syndromes
Structural rearrangement: surgery and orthopaedics (psychosurgery/ deep brain stimulation for severe depression )
Talk therapy: CBT, exposure therapy for anxiety

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2
Q

What 3 methods can we use for drug classification?

A

Based on chemical structure
Based on the illness they treat
Neuroscience based nomenclature

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3
Q

Pros and cons of classifying drugs based on chemical structure

A

Pro: every single drug has a unique structure, so there’s specific identification and easy allocation of data

Con: no use in clinical decision making

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4
Q

Pros and cons of classifying drugs based on the illness they treat

A

Pro: easy for Drs to choose a drug as docs make diagnosis (e.g. antidepressants, anti-psychotics, anxiolytics, hypnotics)

Cons: Certain drugs treat many different mental conditions (e.g. antidepressants can be used to treat depression but also anxiety and OCD)
Mental conditions have many different symptoms, all of which cannot be treated by a single drug (e.g. depression is characterised by anhedonia, anergia, low mood, poor concentration, loss of appetite, loss of libido)

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5
Q

How does neuroscience based nomenclature work?

A

We classify drugs based on the neurotransmitter they target (e.g. instead of antidepressants, we say serotonin enhancers)

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6
Q

What are the 4 main drug targets?

A

Transport proteins
Ion channels
Receptors
Enzymes

((TIRE))

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7
Q

How do drugs that target receptors work?

A

Most of these are antagonists (blockers)
e.g. dopamine receptor antagonists for psychosis, serotonin receptor subtype antagonists for depression, histamine receptor antagonists for sleep

Some enhance receptor activity
e.g. benzodiazepines enhance GABA for sleep
guanfacine enhances noradrenaline for ADHD

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8
Q

How do drugs that target ion channels work?

A

Some drugs block ion channels and reduce neuronal excitability

Sodium channel blockers (e.g. carbamazepine, sodium valproate) for epilepsy and mood stabilisation

Calcium channel blockers (e.g. gabapentin, pregabalin) for epilepsy and anxiety

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9
Q

How do drugs that target enzymes work?

A

Generally block enzyme activity

e.g.
Monoamine oxidase inhibitors for anxiety and depression (prevent breakdown of serotonin)
Acetylcholinesterase inhibitors for dementia (Block ACh breakdown)
lithium blocks glycogen synthase kinase for mood stability (stabilises neurones)

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10
Q

How do drugs targeting reuptake sites function?

A

Many block re-uptake sites to increase neurotransmitter concentration in the synapse and enhance post synaptic receptor activity
Serotonin re-uptake transporters (citalopram): depression and anxiety
Dopamine reuptake inhibitors (methylphenidate): ADHD
Noradrenaline re-uptake inhibitors (desipramine): depression

Some drugs switch re-uptake site direction to enhance release
Amphetamines for ADHD

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11
Q

How does the 5-HT system stop itself from releasing too much 5-HT?

A

Serotonin released acts on presynaptic auto receptors to inhibit further NT release through negative feedback

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12
Q

How many post synaptic serotonin receptors are there in the brain?

A

14

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13
Q

What are the 2 main types of post synaptic serotonin receptor?

A

5-HT1A: inhibitory receptor which dampens activity in neurones to reduce depression and anxiety

5-HT2: psychedelic drugs act on this to produce hallucinogenic effects. May be involved in schizophrenia and is involved in eating and regulation of sleep

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14
Q

How can the effects of neurotransmitters be divided into 2 groups?

A

Fast acting
Slow acting

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15
Q

How can the effects of neurotransmitters be divided into 2 groups?

A

Fast acting
Slow acting

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16
Q

What is the function of fast acting neurotransmitters?

A

On-off switch

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17
Q

What is the function of slow acting neurotransmitters?

A

Modulators

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18
Q

Give 2 examples for fast acting neurotransmitters

A

Glutamate (major excitatory neurotransmitter)
GABA (major inhibitory neurostransmitter)

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19
Q

What type of neurones secrete glutamate and what percentage of all neurones do these make up?

A

Pyramidal cells
=>80%

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20
Q

What type of neurones secrete GABA and what percentage of all neurones do these make up?

A

Interneurons
15%

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21
Q

What is the balance of GABA and glutamate responsible for?

A

Contents of everything we do
e.g. memory, movement, vision

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22
Q

Give examples for slow acting neurotransmitters

A

Dopamine, serotonin, noradrenaline, enkephalins, endorphins and other peptides

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23
Q

What is the purpose of slow acting neurotransmitters through modulation?

A

Emotions, drive, valence of memory

24
Q

What percentage of neurotransmitters are slow acting neurotransmitters?

A

5%

25
Q

What conditions can excessive glutamate cause and what treatment can we give for each?

A

Epilepsy: perampanel (blocker)
Alcoholism: ketamine (blocker), acamprostate (blocker)

26
Q

What condition can a GABA deficiency cause and what treatment do we give?

A

Anxiety: benzodiazepines (GABA enhancer)

27
Q

What conditions can 5-HT deficiency cause and how do we treat them?

A

Depression and anxiety: SRIs and MAOIs (serotonin enhancers)

28
Q

What condition can excess dopamine cause and how do we treat it?

A

Psychosis: dopamine receptor blockers

29
Q

What condition can excess noradrenaline cause and how do we treat this?

A

Nightmares: prazosin (blocker)
used for PTSD

30
Q

What condition can acetylcholine deficiency cause and what treatment would you give?

A

Dementia: Acetylcholnesterase inhibitors

31
Q

What types of drugs treat depression?

A

MAOIs
Tricyclic antidepressants (TCAs)
SSRIs (selective serotonin reuptake inhibitors)
SNRIs (serotonin noradrenaline reuptake inhibitors)
NRIs (noradrenaline reuptake inhibitors)
DRIs (dopamine reuptake inhibitors)

32
Q

What are partial agonists?

A

Partial agonists are types of drugs that function similarly to full agonists but have lower maximal efficacy

33
Q

Why are partial agonists useful?

A

Safer than full agonists, especially in overdose
Can act as antagonists in states of excessive neurotransmitter/ high agonist, and agonists in states of reduced neurotransmitter.

34
Q

Give examples of partial agonists and name the full agonists they are used instead of.
What are they used for?

A

Buprenorphine is a safer alternative to heroin: used for pain and addiction

Varenicline is a safer alternative to nicotine: useful for replacement to smoking

35
Q

What partial agonist for dopamine can be used instead of haloperidol?

A

Aripiprazole

36
Q

What is the advantage of using aripiprazole instead of haloperidol in treating psychosis?

A

Aripiprazole acts as a partial agonist in dopamine deficient states but as an antagonists in states of dopamine excess

This is important as some dopamine activity is needed for normal motor function and haloperidol completely blocks dopamine activity and would therefore have negative side effects aside from its therapeutic effects

37
Q

What are inverse agonists?

A

Drugs which have the opposite effect to an agonist

38
Q

What is the function of inverse agonists to histamine?

A

Increase attention so can be used to target ADHD

39
Q

How many protein subtypes are involved in forming GABA-A receptor subtypes?

A

5

40
Q

What is the most common type of GABA-A receptor and where in the brain is it found?

A

alpha2beta2gamma1
cortex

41
Q

Where on neurones are alpha1 GABA-A receptor subtypes found?

A

Synaptic receptors

42
Q

Where on neurones are alpha2 GABA-A receptor subtypes found?

A

proximal segment of pyramidal cell

43
Q

Where on neurones are alpha5 GABA-A receptor subtypes found?

A

extra synaptic receptors

44
Q

What is the function of alpha1 GABA-A receptor subtypes?

A

Regulates inhibition from GABA inter-neurones onto pyramidal cells

45
Q

What is the function of alpha2 GABA-A receptor subtypes?

A

Control output of pyramidal cells
If we inhibit them we can prevent firing of pyramidal cell

46
Q

What is the function of alpha5 GABA-A receptor subtypes?

A
  • Dampen tonic activity in brain
  • Highly expressed in cingular cortex and hippocampus- emotional rich areas of brain
47
Q

What is an orthosteric receptor?

A

The receptor on the target protein which the natural (endogenous) neurotransmitter works on

48
Q

What is an allosteric receptor

A

A receptor on the target protein which is different to the one that the endogenous neurotransmitter acts on

49
Q

What type of receptor is the GABA-A receptor?

A

Ion-channel linked receptor

50
Q

How many orthosteric receptor sites are on the GABA receptor?

A

2

51
Q

What effect does GABA binding to orthosteric GABA receptor have?

A

Enhances Cl- conductance
Inhibits neurones
Calms brain

52
Q

Give examples for drugs/ chemicals that act on allosteric sites on the GABA-A receptor protein complex

What is their effect?

A

Benzodiazepines
Barbiturates
Alcohol
Neurosteroids

They enhance the action of GABA → sedation, sleep, reduce anxiety, anti-epilepsy

53
Q

What is the real world effect of highly selective vs minimally selective drugs?

A
  • Some drugs are very selective and only bind to few receptors, meaning they have minimal adverse affects
  • However some drugs can bind to multiple receptors and are therefore not selective. This means they can produce a lot of adverse affects
54
Q

Describe drug selectivity in relation to haloperidol and clozapine

A

They both are drugs used to treat schizophrenia

  • Haloperidol- D2 receptor antagonist but also has off target effects on alpha1 receptor
  • Clozapine- D2 receptor antagonist, 5HT1A partial agonist, 5HT2 antagonist but has off target effects on H1 receptor, M1-4 receptor and alpha-1 receptor causing side effects like sedation, weight gain and metabolic syndrome
55
Q

Describe drug selectivity in relation to amitryptiline and citalopram

A
  • These drugs treat depression as 5HT reuptake blockers
  • Amitriptyline- is a serotonin and noradrenaline uptake blocker but also a powerful H1 receptor, 5HT2 receptor and muscarinic M1-4 receptor blocker which gives side effects
  • Citalopram- very selective SSRI since it only works on serotonin transporter

Aneesha Flashcards BRS 2 (47 decks)

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