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Question 1

dopamine hypothesis

Answer 1

dopamine mediates salience of external events + internal representations

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

Question 2

function of nigrostriatal, tuberoinfundibular + mesocorticolimbic pathways in brain

Answer 2

nigrostriatal = extrapyramidal motor system

tuberoinfundibular = inhibits prolactin release

mesocorticolimbic = reward system + executive function

Question 3

structural + neurochemical changes in schizophrenia

Answer 3

enlarged ventricles
reduced frontal cortex volume

dopamine dysregulation

Question 4

r the positive or negative symptoms of schizophrenia treated by antipsychotics

Answer 4

positive

Question 5

what type of antipsychotics cause extrapyramidal side effects?

Answer 5

typical - haloperidol, chlorpromazine

Question 6

antipsychotic side effect dystonia

Answer 6

involuntary movement of head/vaace, commonly young men

soon after treatment

Mx = IM anticholinergic

Question 7

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

Answer 7

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

Question 8

why do you get raised prolactin when taking antipsychotics?

Answer 8

due to inhibition of dopaminergic tuberoinfundibular pathway

Question 9

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

Answer 9

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

Question 10

which antipsychotic has the best side effect profile

Answer 10

aripiprazole

Question 11

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

Answer 11

olanzapine
- assoc with most weight gain + T2DM risk

Question 12

which antipsychotic do you give in patients with parkinsons?

Answer 12

***NONE !!!!!

give lorazepam

Question 13

only absolute contraindication to ECT

Answer 13

raised ICP

(not used in personality disrders)

Question 14

what part of brain mediates emotions of anxiety?

Answer 14

cingulate cortex

Question 15

benzodiazepines

Answer 15

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

Question 16

reversal of benzodiazepine side effects

Answer 16

IV flumazenil

Question 17

criteria for generalised anxiety disorder (GAD)

Answer 17

6 months of disproportionate anxiety about everyday issues

CBT +/- SSRI

Question 18

obsessions + compulsions

Answer 18

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

compulsions = repetitive acts that neutralise obsession + reduce distress

Question 19

difference between PTSD + acute stress disorder

Answer 19

> 1month post trauma = PTSD

<1 month = acute stress diorder

Question 20

PTSD features + Mx

Answer 20

> 4wks
re-experiencing
avoidance
emotional numbing

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

trauma focused CBT
EMDR
venlafaxine

Question 21

key symptoms of depression

Answer 21

low mood
fatigue
anhedonia - reduced ability to experience pleasure

Question 22

monoamine hypothesis

Answer 22

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

medications which increase monoamine activity reduce depressive symptoms

depression thought to be related to monoamine deficiency

Question 23

use of antidepressants in anxiety disorderss

Answer 23

in combo with psycotherapy
SSRI first line

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

Question 24

how long should antidepressants be continued for?

Answer 24

6 months into recovery

Question 25

when is ECT used?

Answer 25

if life threatening or rapid response needed

Question 26

which pathway in the brain do addictive drugs act on?

Answer 26

mesolimbic pathway
- ventral tegmental area (VTA) releases dopamine
- acts on nucleus accumbens (NA) to mediate pleasure/motivation

Question 27

mechanism of delirium tremens

Answer 27

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)

Question 28

time scale of delirium tremens

Answer 28

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

Question 29

treatment of delirium tremens

Answer 29

long acting BZD -> chlordiazepoxide or diazepam

Question 30

cholinesterase inhibitor vs mementine for alzheimers Mx

Answer 30

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

Question 31

frontotemporal dementia key bits

Answer 31

rarer
younger patients
personality change + social conduct problems
relatively preserved memory + visuospatial skills
gradual onset

progressive non fluent aphasia