dums powerpoint Flashcards

1
Q

dopamine hypothesis

A

dopamine mediates salience of external events + internal representations

dopamine dysregulation causes psychosis:
- subcortical dopamine hyperactivity causes positive symptoms
- frontal dopamine hypOactivity causes negative symptoms

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2
Q

function of nigrostriatal, tuberoinfundibular + mesocorticolimbic pathways in brain

A

nigrostriatal = extrapyramidal motor system

tuberoinfundibular = inhibits prolactin release

mesocorticolimbic = reward system + executive function

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3
Q

structural + neurochemical changes in schizophrenia

A

enlarged ventricles
reduced frontal cortex volume

dopamine dysregulation

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4
Q

r the positive or negative symptoms of schizophrenia treated by antipsychotics

A

positive

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5
Q

what type of antipsychotics cause extrapyramidal side effects?

A

typical - haloperidol, chlorpromazine

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6
Q

antipsychotic side effect dystonia

A

involuntary movement of head/vaace, commonly young men

soon after treatment

Mx = IM anticholinergic

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7
Q

what are some of the things monitored in patients taking antipsychotics?

A

fasting blood glucose - impaired glucose tolerance
prolactin
ECG - QT prolongation
FBC - agranulocytosis when taking clozapine

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8
Q

why do you get raised prolactin when taking antipsychotics?

A

due to inhibition of dopaminergic tuberoinfundibular pathway

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9
Q

do patients on clozapine need to let doctors know when they cut down or begin smoking?

A

yes
- smoking increases levels of clozapine in the body so if patient starts smoking increased levels of drug may be harmful

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10
Q

which antipsychotic has the best side effect profile

A

aripiprazole

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11
Q

a patient is being started on anti-psychotics + wants to avoid weight gain + T2DM risk, what drug should be avoided?

A

olanzapine
- assoc with most weight gain + T2DM risk

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12
Q

which antipsychotic do you give in patients with parkinsons?

A

***NONE !!!!!

give lorazepam

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13
Q

only absolute contraindication to ECT

A

raised ICP

(not used in personality disrders)

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14
Q

what part of brain mediates emotions of anxiety?

A

cingulate cortex

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15
Q

benzodiazepines

A

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

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16
Q

reversal of benzodiazepine side effects

A

IV flumazenil

17
Q

criteria for generalised anxiety disorder (GAD)

A

6 months of disproportionate anxiety about everyday issues

CBT +/- SSRI

18
Q

obsessions + compulsions

A

obsessions = unwanted, disturbing, intrusive thoughts/images/impulses

compulsions = repetitive acts that neutralise obsession + reduce distress

19
Q

difference between PTSD + acute stress disorder

A

> 1month post trauma = PTSD

<1 month = acute stress diorder

20
Q

PTSD features + Mx

A

> 4wks
re-experiencing
avoidance
emotional numbing

hyperarousal - hypervigilance, exagerated startle, sleep problems, difficulty concentrating

trauma focused CBT
EMDR
venlafaxine

21
Q

key symptoms of depression

A

low mood
fatigue
anhedonia - reduced ability to experience pleasure

22
Q

monoamine hypothesis

A

monoamines = serotonin (5-HT), dopamine, noradenaline

medications which increase monoamine activity reduce depressive symptoms

depression thought to be related to monoamine deficiency

23
Q

use of antidepressants in anxiety disorderss

A

in combo with psycotherapy
SSRI first line

consider
- tricyclics -> panic disorder
- venlafaxine -> generalised anxiety disorder
- moclobemide -> social anxiety

24
Q

how long should antidepressants be continued for?

A

6 months into recovery

25
when is ECT used?
if life threatening or rapid response needed
26
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
27
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)
28
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
29
treatment of delirium tremens
long acting BZD -> chlordiazepoxide or diazepam
30
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
31
frontotemporal dementia key bits
rarer younger patients personality change + social conduct problems relatively preserved memory + visuospatial skills gradual onset progressive non fluent aphasia