Psychopharmacology for Psychiatry Flashcards
What are the 3 classifications of medicines in psychiatry?
WHO chemical
Diagnostic
New NbN system - neuroscience based nomenclature
What are the 4 types of treatment in medicine?
Give examples in psychiatry for each:
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
How are psychiatric drugs classified by the WHO classification system?
What are the pros and cons of this system?
Based on chemical structure
Pro = each drug has a unique structure = easy to allocate data
Con = no use in clinical decision making
How are psychiatric drugs classified based on diagnostics (i.e. what illness they treat)?
What are the pros and cons of this system?
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
How are psychiatric drugs classified based on NbN?
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
What are the 4 possible systems on which medicines in psychiatry can act on?
- Receptors
- Neurotransmitter reuptake sites
- Ion channels
- Enzymes
Why do these medicines have side effects?
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
What are some examples of drug treatments that block enzyme activity?
What are they used to treat?
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)
What are some examples of drug treatments that are receptor blockers (antagonists)?
What are they used to treat?
Dopamine receptor blockers - SZ
Serotonin receptor subtype antagonists - depression
Histamine receptor antagonists - sleep
What are some examples of drug treatments that simulate receptors / enhancers (agonists)?
What are they used to treat?
Benzodiazepines = enhance GABA - sleep / reduce epilepsy
Guanfacine = enhance noradrenaline - ADHD
What are some examples of drug treatments that block reuptake sites?
What are they used to treat?
Citalopram (SSRI)= enhance serotonin - depression and anxiety
Desipramine (NRI) = enhance noradrenaline - depression
Methylphenidate (DRI) = enhance dopamine - ADHD
What are some examples of drug treatments that switch the reuptake site direction to enhance release of NTs?
What are they used to treat?
Amphetamines = enhance dopamine - ADHD
What are some examples of drug treatments that act to block ion channels?
What are they used to treat?
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
What are 2 types of neurotransmitters (NTs)?
Fast-acting (on-off switch)
Slow-acting (modulators)
What are fast-acting NTs?
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.
What are slow-acting NTs?
Make up about 5% of all neurons
e.g. dopamine, serotonin, noradrenaline, acetylcholine, endorphins, other peptides etc.
Responsible for emotions, drives, valence to memories
What can an excess of glutamate cause?
What is the treatment for this?
Epilepsy
Alcoholism
Perampanel - blocker
Acamprosate - blocker
Ketamine - blocker
What can GABA deficiency cause?
What is the treatment for this?
Anxiety
Benzodiazepines - GABA enhancer
What can serotonin deficiency cause?
What is the treatment for this?
Depression
Anxiety
SSRIs and MAOIs - serotonin enhancers
What can dopamine excess cause?
What is the treatment for this?
Psychosis
Dopamine receptor blockers
What can noradrenaline excess cause?
What is the treatment for this?
Nightmares
PTSD
Prazosin - blocker
What can acetylcholine deficiency cause?
What is the treatment for this?
Impaired memory
Dementia
Acetylcholinesterase enzyme blockers
What are multimodal drugs?
Drugs that act on multiple NT systems
e.g. Vilazodone for depression - SSRI and serotonin receptor agonist
What is a partial agonist?
Why might a partial agonist be used over a full agonist?
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
What is an inverse agonist?
How are inverse agonists different to antagonists?
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
What are receptor subtypes?
Proteins rearrange differently to form slightly different structures
Have different effects / functions
e.g. 7 serotonin receptor subtypes
What is allosteric modulation?
Some drugs act on the same site as the natural (endogenous) neurotransmitter
Others work on different sites on the target proteins - called allosteric sites
Explain allosteric modulation in GABA?
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
What does drug selectivity relate to?
Number of adverse effects due to off target effects
