Psychopharmacology for psychiatry Flashcards
What are the types of treatments in medicine?
- Chemical – drugs/medicines (+ Immunotherapy)
e.g. drugs for psychosis e.g. drugs for depression - Electrical stimulation
e.g. ECT for depression e.g. neurostimulation for pain syndromes - Structural rearrangement - surgery & orthopaedics
e.g. psychosurgery/deep brain stimulation for severe depression - Talking (pycho) therapies
e.g Cognitive Behaviour Therapy (CBT) e.g. exposure for phobias
What are the different ways drugs can be classified?
- Based on chemical structure
- Based on what illnesses they treat
- Based on their pharmacology “how do the drugs works?”
What are the pros and cons of classifying drugs based on chemical structure?
Pro- each drug has a unique structure = a fact; easy to allocate data
Con- no use in clinical decision making
What are the pros and cons of classifying drugs based on what illnesses they treat?
Pros – easy for Drs to choose a drug as docs make diagnosis
Cons- many psychiatric medicines work in several disorders
- most psychiatric disorders have multiple symptoms and a single medicine might not treat them all
What systems are targeted by chemical treatments in psychiatry
Receptors
Neurotransmitter reuptake sites
Ion channels
Enzymes
How do enzyme targeting medicines work?
- general neuronal principles: enzymes are needed for re-uptake and breakdown for many neuronal processes
- THEREFORE, drug treatments target/ block enzyme activity
How do “receptor-targeting” medicines work?
- Most treatments are receptor blockers [antagonists]
- Some stimulate receptors = enhancers (agonists)
- It is easier to make a blocker than an agonist
- The brain doesn’t adapt as well to antagonists as it does agonists
How do “reuptake site- targeting medicines” work?
- Most neurotransmitters are recovered and recycled via reuptake sites (brain is extremely energy efficient- does not waste neurotransmitters)
- Many psychiatric drugs block these reuptake sites so increase neurotransmitter concentration in the synapse to enhance post-synaptic receptor activity
- Some switch the reuptake site direction to enhance release
Using the example of neurotransmitter 5-HT, explain how drugs can target re-uptake sites to treat depression?
Drug used= SSRIs (Selective serotonin reuptake inhibitors)
NORMAL MECHANISM:
- 5HT neurons released from the pre- synaptic neurons
- Bind to/ stimulate a range of different postsynaptic receptors (roughly 14 serotonin receptors; 14 diff genes coding for them)
- Serotonin (5HT) is taken back up to the pre synaptic terminals
DRUGS:
- Uptake is blocked by SSRIs
- some of the NTs act back on the releasing neurone (on atuoreceptors)- autorecptors inhibit the release of the NT “negative feedback loop”; prevents system going out of control
How do “ion channel- targeting medicines” work?
Some drugs block channels so reduce neuronal excitability
What are the the different types of neurotransmitters you can have (classified in terms of speed)?
- FAST acting (on-off switch)
* Excitatory – glutamate = > 80% of all neurons- pyramidal cells
* Inhibitory – GABA = 15% - inter-neurons content e.g. of memory, movement, vision etc. - SLOW acting (modulators) – about 5% of all neurons
* dopamine – serotonin – noradrenaline -acetylcholine
* endorphins and other peptides
* emotions, drives, valence of memory etc.
Which NTs are linked to which psychiatric disorders?
Excess of NT:
Glutamate - Epilepsy/ Alcoholism
GABA - Anxiety
5-HT - depression/ anxiety
Dopamine - Psychosis
Noradrenaline - Nightmares
Acetylcholine - Impaired memory/ Dementia
Drugs that treat depression?
- MAOI
- TCA
- SSRI
- Receptor antagonists
- SNRI
- NRI
- DRI
- Melatonin agonist
What is a partial agonist?
- Have a lower max efficacy than full agonists
- Have a plateau (which is less than that of a sole agonist)
- have different roles depending on the amount of neurotransmitter present:
- Improved safety – especially in overdose (reduces side effects)
- In states of high neurotransmitter or excess agonist medicine can act as an antagonist
What are inverse agonists?
- Opposite effect of agonists (switch the receptor in a different direction)
NOTE: NOT AN ANTAGONIST: - antagonists just blocks whatever is there
- an inverse agonist does something independent of the natural transmitter (makes it work- just in the opposite way)
