Psychopharmacology Flashcards
What is the WHO classification of drugs and benefits/downsides?
based on chemical structure
- pro: each drug has a unique structure, so easy to allocate data
- con: no use in clinical decision making
What are the pros and cons of classifying drugs based on the illnesses they treat?
- pros: easy for Drs to choose a drug as you make diagnoses
- con: many psychiatric medicines work in several disorders e.g. antidepressants also treat anxiety and OCD, and some antipsychotics are used as add ons for treatment of depression
- con: most psychiatric disorders have multiple symptoms and a single medicine might not treat them all e.g. depression symptoms include anxiety, insomnia, low mood etc…likely different neurotransmitter mechanisms
What is neuroscience based nomenclature (NbN)?
basing classification of drugs on core pharmacology
–> targets neurotransmitters e.g. dopamine blocker instead of antipsychotic, serotonin enhancer instead of antidepressant, and GABA enhancer instead of hypnotic
What are some examples of psych drugs that target enzymes?
generally drug treatments block enzyme activity:
e.g. monoamine oxidase inhibitors for anxiety and depression,
acetylcholinesterase inhibitors for dementias,
lithium blocks glycogen synthase kinase for mood stability
What are some examples of psych drugs that target receptors?
- most are receptor blockers (antagonists):
e.g. dopamine receptor blockers for schizophrenia,
serotonin receptor subtype antagonists for depression,
histamine receptor antagonists for sleep - some stimulate receptors (agonists):
e.g. benzodiazepines enhance GABA–> promote sleep or reduce epilepsy,
guanfacine enhances noradrenaline–> ADHD
What are some examples of psych drugs that target reuptake sites?
- many psychiatric drugs block reuptake sites–> inc. NT conc. in synapse to enhance post-synaptic receptor activity:
e.g. citalopram= serotonin reuptake inhibitor (SSRI)- enhances serotonin for depression and anxiety,
desipramine= noradrenaline reuptake inhibitor (NRI)- enhances noradrenaline for depression,
methylphenidate= dopamine reuptake inhibitor (DRI)- enhances dopamine for ADHD - some drugs switch activity of reuptake site–> causes release of NT:
e. g. amphetamine–> causes release of dopamine for ADHD
What is the 5HT1a receptor?
inhibitory receptor-
when we enhance serotonin–> inc. stimulation of receptor–> dampens down activity in neurones, reducing anxiety and depression
What is the 5HT2a receptor?
receptor that psychedelic drugs work on, involved in schizophrenia, eating and regulation of sleep
What are some examples of psych drugs that target ion channels?
- some drugs block channels, reducing neuronal excitability:
e.g. sodium valproate and carbamazepine- block sodium channels- for epilepsy and mood stabilisation in bipolar,
gabapentin and pregabalin- block calcium channels- for epilepsy and anxiety
How can we separate neurotransmitters into fast and slow acting?
fast acting (on-off switch):
- excitatory–> glutamate (>80% of all neurons in pyramidal cells, which regulate brain function)
- inhibitory–> GABA (15% in interneurons)
- content e.g. of memory, movement, vision etc…
slower acting (modulators):
about 5% of all neurons
- dopamine, serotonin, noradrenaline, acetylcholine
- endorphins and other peptides
- emotions, drives, valence of memory etc…
What are the benefits of partial agonists?
- partial agonists–> lower max efficacy than full agonists
- improved safety, esp. in overdose
- effect of partial agonist is determined by ongoing level of NTs, so if there is a lot of NT, partial agonist will act as an antagonist and block it
e. g. aripiprazole allows normal motor function- fewer side effects than haloperidol (drugs for psychosis)
What are inverse agonists?
- drugs that bind to the same receptor as an agonist, but induce an OPPOSITE response
- e.g. because GABA is an inhibitory NT, it decreases excitability–> so an alpha-5 inverse agonist can excite the brain (hippocampus) to improve memory by reducing GABA activity
What is allosteric modulation?
- some drugs act on same site as natural/endogenous NT (orthosteric site), whereas others work on different site (allosteric)
- e.g. GABA binds to GABA-A receptor (orthosteric site), enhancing chloride ion conductance and inhibiting neurons, calming the brain….whereas benzodiazepines barbiturates, alcohol, neurosteroids all act at allosteric sites on the same protein complex, also enhancing effect of GABA–> sedation
^work allosterically to make it more effective, but don’t act at same site