Psychopharmacology for Psychiatry Flashcards

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1
Q

What are the 3 classifications of medicines in psychiatry?

A

WHO chemical
Diagnostic
New NbN system - neuroscience based nomenclature

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2
Q

What are the 4 types of treatment in medicine?

Give examples in psychiatry for each:

A

Chemical - drugs / medicines (+immunotherapy) e.g. anti-depressants

Electrical stimulation e.g. ECT for depression

Structural rearrangement - surgery and orthopedics e.g. psychosurgery / deep brain stimulation for severe depression

Talking (psycho) therapies e.g. CBT

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3
Q

How are psychiatric drugs classified by the WHO classification system?

What are the pros and cons of this system?

A

Based on chemical structure

Pro = each drug has a unique structure = easy to allocate data

Con = no use in clinical decision making

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4
Q

How are psychiatric drugs classified based on diagnostics (i.e. what illness they treat)?

What are the pros and cons of this system?

A

E.g. anti-depressants, anti-psychotics, anxiolytics, anti-hypnotics

Pros = easy for doctors to choose a drug as doctors make diagnoses

Cons = many psychiatric medicines work in several disorders, and most psychiatric disorders have multiple symptoms and a single medicine might not treat them all

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5
Q

How are psychiatric drugs classified based on NbN?

A

NbN = Neuroscience based Nomenclature

The core pharmacology is used to classify medicines i.e. based on their target neurotransmitters

e.g. instead of antipsychotic, dopamine blocker
instead of antidepressant, serotonin enhancer
instead of hypnotic, GABA enhancer

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6
Q

What are the 4 possible systems on which medicines in psychiatry can act on?

A
  1. Receptors
  2. Neurotransmitter reuptake sites
  3. Ion channels
  4. Enzymes
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7
Q

Why do these medicines have side effects?

A

Because the target sites are found in the brain and around the body

When the drug acts on the target sites around the body outside the brain, it may cause side effects

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8
Q

What are some examples of drug treatments that block enzyme activity?

What are they used to treat?

A

MAOIs = block breakdown of serotonin and noradrenaline - anxiety and depression

Acetylcholinesterase inhibitors = block breakdown of ACh - dementia

Lithium = blocks glycogen synthase - mood stability (stabilises neurones)

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9
Q

What are some examples of drug treatments that are receptor blockers (antagonists)?

What are they used to treat?

A

Dopamine receptor blockers - SZ

Serotonin receptor subtype antagonists - depression

Histamine receptor antagonists - sleep

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10
Q

What are some examples of drug treatments that simulate receptors / enhancers (agonists)?

What are they used to treat?

A

Benzodiazepines = enhance GABA - sleep / reduce epilepsy

Guanfacine = enhance noradrenaline - ADHD

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11
Q

What are some examples of drug treatments that block reuptake sites?

What are they used to treat?

A

Citalopram (SSRI)= enhance serotonin - depression and anxiety

Desipramine (NRI) = enhance noradrenaline - depression

Methylphenidate (DRI) = enhance dopamine - ADHD

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12
Q

What are some examples of drug treatments that switch the reuptake site direction to enhance release of NTs?

What are they used to treat?

A

Amphetamines = enhance dopamine - ADHD

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13
Q

What are some examples of drug treatments that act to block ion channels?

What are they used to treat?

A

Sodium channel blocks = reduce no. of neurons firing
Sodium valproate - epilepsy and mood stabilisation
Carbamazepine - epilepsy and mood stabilisation

Calcium channel blocks = reduces excitability in the brain
Gabapentin and Pregabalin - epilepsy, anxiety

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14
Q

What are 2 types of neurotransmitters (NTs)?

A

Fast-acting (on-off switch)

Slow-acting (modulators)

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15
Q

What are fast-acting NTs?

A

Amino acid NTs

Excitatory = glutamate = present in >80% of all neurons
Inhibitory = GABA = make up 15% of the brain's neurons called interneurons

Balance of these two = responsible for memory, movement, vision etc.

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16
Q

What are slow-acting NTs?

A

Make up about 5% of all neurons

e.g. dopamine, serotonin, noradrenaline, acetylcholine, endorphins, other peptides etc.

Responsible for emotions, drives, valence to memories

17
Q

What can an excess of glutamate cause?

What is the treatment for this?

A

Epilepsy
Alcoholism

Perampanel - blocker
Acamprosate - blocker
Ketamine - blocker

18
Q

What can GABA deficiency cause?

What is the treatment for this?

A

Anxiety

Benzodiazepines - GABA enhancer

19
Q

What can serotonin deficiency cause?

What is the treatment for this?

A

Depression
Anxiety

SSRIs and MAOIs - serotonin enhancers

20
Q

What can dopamine excess cause?

What is the treatment for this?

A

Psychosis

Dopamine receptor blockers

21
Q

What can noradrenaline excess cause?

What is the treatment for this?

A

Nightmares
PTSD

Prazosin - blocker

22
Q

What can acetylcholine deficiency cause?

What is the treatment for this?

A

Impaired memory
Dementia

Acetylcholinesterase enzyme blockers

23
Q

What are multimodal drugs?

A

Drugs that act on multiple NT systems

e.g. Vilazodone for depression - SSRI and serotonin receptor agonist

24
Q

What is a partial agonist?

Why might a partial agonist be used over a full agonist?

A

Lower max efficacy that full agonist (i.e. partial efficacy compared to full agonist)
Partial agonists can act as an antagonist if there is excess NT, or act as an agonist if there is a deficit of the NT

Improved safety - especially in overdose
Reduces side effects - i.e. not all receptors are completely blocked, which can lead to adverse effects

25
Q

What is an inverse agonist?

How are inverse agonists different to antagonists?

A

Have an effect that is opposite to agonists - i.e. whilst agonists enhance the effect, inverse agonists diminish the effects

Antagonists do not have a diminishing effect on the receptor activity or NT release, they simply occupy the target site

26
Q

What are receptor subtypes?

A

Proteins rearrange differently to form slightly different structures
Have different effects / functions

e.g. 7 serotonin receptor subtypes

27
Q

What is allosteric modulation?

A

Some drugs act on the same site as the natural (endogenous) neurotransmitter

Others work on different sites on the target proteins - called allosteric sites

28
Q

Explain allosteric modulation in GABA?

A

GABA-A receptor is an ion-channel linked receptor

GABA binds to the GABA receptor = orthosteric site

This binding enhances chloride ion conductance = inhibits neurons = decrease neuron firing to calm the brain

Benzodiazepines, barbiturates, alcohol, neurosteroids

All act at allosteric sites on the same protein complex

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

29
Q

What does drug selectivity relate to?

A

Number of adverse effects due to off target effects