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Year 2 - BRS > 4.8 - Psychopharmacology for psychiatry > Flashcards

4.8 - Psychopharmacology for psychiatry Flashcards

1
Q

What are the four different types of treatments in medicine, with examples in psychiatry?

A
  • chemical - drugs/medicine(+ immunotherapy) e.g. drugs for psychosis or depression
  • electrical stimulation e.g. ECT for depression, neurostimulation for pain syndromes
  • structural rearrangement - surgery and orthopaedics e.g. psychosurgery/deep brain stimulation for severe depression
  • talking (psycho) therapies e.g. CBT or exposure to phobias
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2
Q

What are three ways that we can classify psychiatric drugs?

A
  • based on chemical structure
  • based on what illnesses they treat
  • based on their pharmacology (AKA neuroscience based nomenclature NbN)
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3
Q

Who uses the system of classifying drugs by chemical structure?

A

WHO uses this system

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4
Q

What is a pro and a con of classifying drugs by chemical structure?

A
  • pro - each drug has a unique structure –> specific identification and easy allocation of data
  • con - no use in clinical decision making
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5
Q

What are some examples of classifying drugs based on the illnesses they treat? (4)

A
  • antidepressant
  • antipsychotic
  • anxiolytic
  • hypnotic
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6
Q

What are some pros and cons of classifying drugs by the illnesses they treat?

A
  • pro - easy for doctors to choose a drug as doctors make diagnosis
  • con 1 - many psychiatric medicines work in several disorders e.g. antidepressants also treat anxiety and OCD, some antipsychotics used as add on treatment for depression
  • con 2 - most psychotic disorders have multiple symptoms and a single medicine may not treat them all e.g. in depression there is anhedonia, libido loss, low mood, anxiety, insomnia, appetite loss etc
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7
Q

How do we classify drugs based on their pharmacology (NbN)?

A
  • core pharmacology used to classify medicines
  • we classify drugs based on the neurotransmitters they target
  • e.g. instead of antipsychotic - dopamine blocker
  • e.g. instead of antidepressant - serotonin enhancer
  • e.g. instead of hypnotic/anxiolytic - GABA enhancer
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8
Q

What are the four targets that psychiatric drugs work on?

A
  1. receptors
  2. neurotransmitter reuptake sites (channel proteins)
  3. ion channels
  4. enzymes
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9
Q

How do drugs that target enzymes work?

A
  • generally drug treatments block enzyme activity
  • e.g. MAOIs for anxiety and depression (block breakdown of serotonin)
  • e.g. AChE inhibitors for dementia (block breakdown of ACh)
  • e.g. lithium blocks glycogen synthase kinase for mood stability (stabilises neurones)
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10
Q

How do drugs targeting receptors work?

A
  • most treatments are receptor blockers (antagonists)
    • e.g. dopamine receptor blocker for schizophrenia
    • e.g. serotonin receptor subtype antagonists for depression
    • e.g. histamine receptor antagonists for sleep
  • some stimulate receptors = enhancers (agonists)
    • e.g. BZs enhance GABA for sleep
    • e.g. guanfacine enhances NA for ADHD
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11
Q

What is a summary of what antagonists and agonists do?

A
  • antagonists block the endogenous agonist binding to the receptor
  • agonists mimic the endogenous agonist and stimulate the receptor
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12
Q

How do drugs targeting reuptake sites work?

A
  • most NTs are recovered and recycled via reuptake sites
  • many psychiatric drugs block these reuptake sites so increase NT concentration in synapse to enhance post-synaptic receptor activity
    • e.g. citalopram (SSRI) enhances serotonin for depression and anxiety
    • e.g. desipramine (NRI) enhances noradrenaline for depression
    • e.g. methylphenidate (DRI) enhances dopamine for ADHD
  • some switch the reuptake site direction to enhance release
    • e.g. amphetamine for ADHD increases dopamine
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13
Q

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

A

Serotonin release acts on presynaptic autoreceptors to inhibit further NT release through negative feedback

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14
Q

How many post-synaptic serotonin receptors are there in the brain and what are the two main ones?

A
  • 14
  • 5HT1A - inhibitory receptor which dampens activity in the neurons it is in to reduce anxiety and depression
  • 5HT2A - psychedelic drugs work on this to have hallucinogenic effects - might be involved in schizophrenia and is involved in eating and regulation of sleep
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15
Q

How do drugs targeting ion channels work?

A
  • some drugs block channels to reduce neuronal excitability
  • e.g. sodium valproate and carbamazepine block sodium channels - epilepsy and mood stabilisation
  • e.g. gabapentin and pregabalin block calcium channels - epilepsy and anxiety
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16
Q

How can neurotransmitters be divided into two types?

A
  • FAST acting (on-off switch)
  • slow acting (modulators) - about 5% of all neurons
17
Q

What are the two main fast-acting neurotransmitters and what action do they have?

A
  • glutamate - excitatory and make up >80% of all neurones (called pyramidal cells)
  • GABA - inhibitory and make up 15% of neurones (called inter-neurones)
18
Q

What is the balance of glutamate and GABA (fast NTs) responsible for?

A

Content of everything we do e.g. memory, movement, vision etc

19
Q

What neurotransmitters make up slow-acting neurotransmitters?

A
  • dopamine, serotonin, noradrenaline, acetylcholine
  • endorphins and other peptides
20
Q

What is the purpose of the slow-acting neurotransmitters (modulators)?

A
  • emotions
  • drives
  • valence of memory
21
Q

What conditions can excess glutamate cause and how can we treat these?

A
  • epilepsy –> Perampanel (blocker)
  • alcoholism –> Acamprosate / Ketamine (blockers)
22
Q

What condition can GABA deficiency cause and how can we treat this?

A

Anxiety –> benzodiazepines (GABA enhancer)

23
Q

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

A

Depression and anxiety –> SSRIs and MAOIs (serotonin enhancers)

24
Q

What condition can excess dopamine cause and how can we treat this?

A

Psychosis –> dopamine receptor blockers

25
Q

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

A

Nightmares –> Prazosin (blocker, used for PTSD)

26
Q

What conditions can ACh deficiency cause and how can we treat this?

A

Impaired memory/dementia –> AChE enzyme blockers

27
Q

What types of drugs treat depression? (8)

A
  • MAOI - monoamine oxidase inhibitors
  • TCA - tricyclic antidepressants
  • SSRIs - selective serotonin reuptake inhibitors
  • receptor antagonists
  • SNRIs - serotonin-noradrenaline reuptake inhibitors
  • NRIs - noradrenaline reuptake inhibitors
  • DRIs - dopamine reuptake inhibitors
  • melatonin agonist
28
Q

What are multimodal drugs for depression?

A
  • work on two different targets
  • e.g. Vilazodone - SSRI + 5HT1A agonist
  • e.g. Vortioxetine - SSRI + multiple other 5-HT receptor effects
29
Q

What are partial agonists?

A

Partial agonists are types of drugs which function similarly to agonist but have a lower max efficacy than full agonists

30
Q

Why are partial agonists useful?

A
  • improved safety - especially in overdose
  • in states of high NT or excess agonist, partial agonist medicine can act as an antagonist (and when there is a deficit of NT it can act as an agonist)
31
Q

What are some examples of partial agonists and what other drug they act like when being antagonists?

A
  • aripiprazole - haloperidol (psychosis)
  • buprenorphine - heroin (pain and addiction, safer alternative)
  • varenicline - nicotine (smoking replacement)
32
Q

Why is aripiprazole (partial agonist) better than haloperidol for psychosis?

A
  • aripiprazole acts like haloperidol (dopamine antagonist) when there is too much dopamine but as dopamine agonist when there is too little
  • important as we need some dopamine for normal motor function and haloperidol completely blocks dopamine activity so would have its own negative side effects
33
Q

What are inverse agonists?

A
  • opposite effects to agonists
  • not antagonists as they do not block receptor
  • e.g. inverse agonists for histamine increase attention –> treat ADHD?
34
Q

What receptor subtypes do GABA-A receptors have?

A
  • 5 separate proteins that make up a receptor in multiple different combinations
  • most common is alpha1beta2gamma2 found in cortex - different combinations found in different parts of the brain
35
Q

What are allosteric vs orthosteric receptors?

A
  • orthosteric - receptor on target protein where the natural (endogenous) neurotransmitter works on
  • allosteric - a different receptor/site on the target proteins
  • drugs act on orthosteric/allosteric site
36
Q

Describe how different things bind to orthosteric/allosteric sites on the GABA-A receptor.

A
  • GABA-A receptor is an ion channel-linked receptor
  • GABA binds to orthosteric GABA receptor sites –> enhances Cl- conductance –> inhibits neurons –> calms the brain
  • BZs, barbiturates, alcohol, neurosteroids act at allosteric sites on the same protein complex –> enhance the action of GABA –> sedation, sleep, reduce anxiety, anti-epilepsy
37
Q

What is drug selectivity?

A
  • some drugs are very selective and only bind to a few receptors = minimal adverse effects
  • however some drugs can bind to multiple receptors and are therefore not selective = many adverse effects
38
Q

Compare the drug selectivity of haloperidol and clozapine (dopamine receptor blockers for schizophrenia).

A
  • haloperidol - selective - D2 receptor antagonist but also off-target effects on alpha1 receptor
  • clozapine - not selective - D2 receptor antagonist, 5HT1A partial agonist, 5HT2 antagonist but has off-target effects on H1, M1-4 and alpha1 receptors causing side effects like sedation, weight gain and metabolic syndrome
39
Q

Compare the drug selectivity of amitriptyline and citalopram (5HT reuptake blockers for depression).

A
  • amitriptyline - SNRI but also powerful H1, 5HT2, alpha1 and muscarinic M1-4 receptor blockers = side effects
  • citalopram - very selective SSRI since it only works on serotonin transporter (adverse effects driven solely by increased serotonin)

Year 2 - BRS (84 decks)

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