dums powerpoint Flashcards
dopamine hypothesis
dopamine mediates salience of external events + internal representations
dopamine dysregulation causes psychosis:
- subcortical dopamine hyperactivity causes positive symptoms
- frontal dopamine hypOactivity causes negative symptoms
function of nigrostriatal, tuberoinfundibular + mesocorticolimbic pathways in brain
nigrostriatal = extrapyramidal motor system
tuberoinfundibular = inhibits prolactin release
mesocorticolimbic = reward system + executive function
structural + neurochemical changes in schizophrenia
enlarged ventricles
reduced frontal cortex volume
dopamine dysregulation
r the positive or negative symptoms of schizophrenia treated by antipsychotics
positive
what type of antipsychotics cause extrapyramidal side effects?
typical - haloperidol, chlorpromazine
antipsychotic side effect dystonia
involuntary movement of head/vaace, commonly young men
soon after treatment
Mx = IM anticholinergic
what are some of the things monitored in patients taking antipsychotics?
fasting blood glucose - impaired glucose tolerance
prolactin
ECG - QT prolongation
FBC - agranulocytosis when taking clozapine
why do you get raised prolactin when taking antipsychotics?
due to inhibition of dopaminergic tuberoinfundibular pathway
do patients on clozapine need to let doctors know when they cut down or begin smoking?
yes
- smoking increases levels of clozapine in the body so if patient starts smoking increased levels of drug may be harmful
which antipsychotic has the best side effect profile
aripiprazole
a patient is being started on anti-psychotics + wants to avoid weight gain + T2DM risk, what drug should be avoided?
olanzapine
- assoc with most weight gain + T2DM risk
which antipsychotic do you give in patients with parkinsons?
***NONE !!!!!
give lorazepam
only absolute contraindication to ECT
raised ICP
(not used in personality disrders)
what part of brain mediates emotions of anxiety?
cingulate cortex
benzodiazepines
GABA agonist (inhibitory)
short acting = lorazepam
long acting = diazepam
only use for rapid relief of severe symtpoms
avoid long term use (<4weeks) due to dependence
reversal of benzodiazepine side effects
IV flumazenil
criteria for generalised anxiety disorder (GAD)
6 months of disproportionate anxiety about everyday issues
CBT +/- SSRI
obsessions + compulsions
obsessions = unwanted, disturbing, intrusive thoughts/images/impulses
compulsions = repetitive acts that neutralise obsession + reduce distress
difference between PTSD + acute stress disorder
> 1month post trauma = PTSD
<1 month = acute stress diorder
PTSD features + Mx
> 4wks
re-experiencing
avoidance
emotional numbing
hyperarousal - hypervigilance, exagerated startle, sleep problems, difficulty concentrating
trauma focused CBT
EMDR
venlafaxine
key symptoms of depression
low mood
fatigue
anhedonia - reduced ability to experience pleasure
monoamine hypothesis
monoamines = serotonin (5-HT), dopamine, noradenaline
medications which increase monoamine activity reduce depressive symptoms
depression thought to be related to monoamine deficiency
use of antidepressants in anxiety disorderss
in combo with psycotherapy
SSRI first line
consider
- tricyclics -> panic disorder
- venlafaxine -> generalised anxiety disorder
- moclobemide -> social anxiety
how long should antidepressants be continued for?
6 months into recovery
when is ECT used?
if life threatening or rapid response needed
which pathway in the brain do addictive drugs act on?
mesolimbic pathway
- ventral tegmental area (VTA) releases dopamine
- acts on nucleus accumbens (NA) to mediate pleasure/motivation
mechanism of delirium tremens
Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
time scale of delirium tremens
symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety
peak incidence of seizures at 36 hours
peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia
treatment of delirium tremens
long acting BZD -> chlordiazepoxide or diazepam
cholinesterase inhibitor vs mementine for alzheimers Mx
chol inhibitor (rivastmine, donezapil, galantamine)
- inhibit acetylcholinesterase removal of Ach
- increases ACh neurotransmission
- used for mild-moderate
mementine
- glutamate receptor antagonist
- prevent excitotoxicity
- used for moderate-severe
frontotemporal dementia key bits
rarer
younger patients
personality change + social conduct problems
relatively preserved memory + visuospatial skills
gradual onset
progressive non fluent aphasia
