all notse Flashcards
mitrazapine what class of drug?
NASSA
side effect of this drug?
weight gain
what does it prevent reuptake of?
5HT, NA (5N taru mitra) - varyingly inhibit
what class of drug is clomipramine?
TCA
what peptide transmitters are involved in aversive defensive systems?
NA/CRF
hippocampus - approach or defensive?
defensive
biosynthesis of serotonin?
try 5 - tryptophan -> 5 hydroxytryptophan -> serotonin
5HT2 receptors - where are they found?
everywhere basically
5HT1 ?
blood vessels/CNS - (a-f) alan
receptor effect of 5HT1?
inhibitory
effect of 5HT2?
excitory
an agonist of 5HT2?
LSD
Some biological functions of 5HT?
cooker - mood, apetite, sleep, anxiety, aggression, memory, learning, addiction
what can SSRIs be used to treat?
panic attacks, OCD, eating disorders, premature ejaculation, PTSD, chronic pain (knee), social anxiety disorder, DEPRESSION
how long does it take to increase synaptic 5HT?
hours
how long does it take to imove mood?
2-3 weeks
what does the increased concentration of extracellular 5HT stimulate?
5HT1a autoreceptors to inhibit firing
when do you get return to norma firing?
in chronic treatment
what sort of dose can you start an SSRI at?
ev therapeutic dose
side effects?
anxiety, sexual dysfunction, increased risk of suicude initial with young patients, dyspepsia, vomiting, diarrhoea, constipation.
which SSRIS inhibit CYP450?
fluoxetine and paroxetine
what drugs do SSRIs therefore have an interaction with>
drugs metabolised via the same pathway i.e. CYP450 pathway
sexual dysfunction in pathophysioogy?
can be dopamine blockade and/or 5HT2 activation
how can this be reversed?
5HT2 antagonists or 5HT1a partial agonists
TCA - block reptake of?
5HT and NA
titration?
require a bit more individualised dose titration
at higher doses, patients might need ECGs, what could be seen on ECG?
QT prolongation
adverse effects?
constipation, dry mouth, blurred vision, effects on cardiac function, postural hypotension.
CHAD. what does cholinergic and adrenergic blockade cause failure of?
peripheral orthostatic reflex
3 MAOIs?
Phenelzine, isocaroxazid, tranylcypromide
what does mono oxidase A metabolise?
5HT, NA, tyramine
MAO B, what does it metabolise?
DA, tyramine, phenylethylamine
which drug causes sympathy mimetic effects?
tranylcypromide
what are MAOIs used to treat?
atypical depression
what does MAO do in the gut?
inactivates tyrosine
how do patients on MAO inhbitors get hypertensive crisis ?
tyramine (in food like cheese) cause more NA to be released. under normal circumstances it would be broken down by MAO. increased levels of NA caused constriction of blood vessels
foods that contain tyrosine?
cheese, yoghurt, yeast extracts, broad beans, pickled herring, alcohol
can also cause high serotonin. symtptoms of high serotoin?
flushed, headache, increased BP
treatment? up hill ruri
chlorpremazine and phentolamine (prem, ph a)
what is akathisia?
inner restlesness
tremor, dystonia, akathisia and TD can occur which which anti depressant?
paroxetine
which hormone plays a key role in reward and motivation
dopamine
what is the main inhibitory neurone in developing brain
GABA
GABA actions in developing brain?
excitatory
GABA binding causes flow of which ions into post synaptic cell?
chlorine
do you get hyperpolarisation/depolarisation?
hyperpolarisation (cl-)
which ions flow into post synaptic cell from glutamate?
ca 2 +, causing depolarisation
two receptors that glutamate bind to?
NMDA and AMPA
which is faster?
AMPA
which one lets calcium through?
NMDA
GABA binding allows flow of either cl ions in to the cell or K ions out of the cell
yeah
antagonist of GABAa receptor?
flumazenil
agonists?
benzos, anaesthetics, ethanol, propofol
**GABA B agonists (GEE PROTEIN)
me and my back pack going to the show (baclofen, propofol)
Mood stabilisers? anti convulsants?
lamotrigine, valproate, carbamazepine
are they more effective at reducing manic episodes or depressive episodes?
manic
would you rather have type 1 BP or type 2?
type 1
ATYPICAL MOOD STABILISERS?
olanzepine, risperidone, quetiapine, ariprazole
other mood stabilisers?
lithium carbonate and nimodipine
what does lamotrigine do? Drug action)
blocks sodium channels
what overall effect does this have?
reduces cell firing
what also inhibit uptake of?___________
serotonin (MM)
Lithium. what does it do to BCL2? to 5HT auto receptors? inositol? GSK3?
increases apoptotic factor for BCL2, inhibition of 5HT autorecetors, depletion of inositol, inhibition GSK 3
what do you get in lithium overdose?
toxicity
there is a risk of inadvertent toxicity
y
what does lithium treatment require?
blood monitoring
anti psychotics show affinity for which receptor?
D2
in which circuit?
mesolimbic
movement disorders due to DA blockade in which pathway>
nigrostratial
hyperprolactinaemia?
tubero inffandibular
which part of the brain (in approach system) is involved in relative reward preference and rule learning?
OFC
periaqueductal grey matter - in approach or defence?
defence
average onset depression? bipolar?
27, 21
male to female ration depression, bipolar?
depression f2:1m , bipolar 1:1
in major depression what happens to cortisol?
increased
how would you test for this clinically?
increased cortisol in urine, saliva
what would the adrenal glands look like?
enlarged
in depression, TRH levels? TSH levels?
TRH up, TSH (pituitary) blunted
6 key regions implicated in mood disorders
orbital frontal cortex, hippocampus, ventromedial and prefrontal cortex, anterior cingulate nucleus, amygdala, DorsoLateral prefrontal cortex. down low
dense coactivation with AIC and ACC during almost all studies of emotion
y
there is dense connectivity with the anterior insular cortex and what?
anterior cingulate cortex
DO NOT use anti depressants to treat persistant sub threshold depressive symptoms or mild depression - risk benefit ratio is poor.
y
when do you consider anti depressants?
past history of moderate/severe depression, initial presentation of sub threshold depressive symptoms that have been present for a long period i.e. 2 years. also for sub threshold or mild depression that persists after other interventions
what is the typical treatment started for moderate or severe depression (top of page (yellow and red)
combination of anti depressant and high intensity pharmacological intervention