PSY2003 SEMESTER 1 - WEEK 1

Question 1

what is a neuroleptic

Answer 1

antipsychotic

Question 2

how many people in population has sz, and when does it emerge

Answer 2

1% population
emerges late adolescence
alternate episode illness exacerb/partial-remission

Question 3

name positive symptoms for sz

Answer 3

1. prolonged visual, auditory hallucinations (short period = psychosis)
2. bouts of mania
3. delusions of grandeur
4. odd behaviour
5. paranoia
6. thought disorganisation

Question 4

name negative symptoms for sz

Answer 4

1. lacking drive and motivation
2. alogia
3. social withdrawal
4. negative affect
5. disconnect from emotions

Question 5

explain alogia

Answer 5

poverty of speech

Question 6

name cognitive symptoms for sz

Answer 6

1. poor performance on cog task of attention, WM
2. incoherent thoughts/cognitions

Question 7

name original perspective of sz

Answer 7

“splitting of psychic functions”
an integration breakdown between emotion, thought, action

Question 8

what was RD Lange antipsychiatry movement

Answer 8

sz is made up to alienate people and force them to conform to society
“Sanity, Madness and the Family” = communications between family cause sz in a child

Question 9

what did Freud believe about sz

Answer 9

paranoid delusions result from repressed sexual urge
commonly accepted belief in 1980

Question 10

explain genetic factors in sz

Answer 10

MZ only 45% so other factors like infections, autoimmune reactions, toxins, traumatic injury, exposure to stressors

Question 11

name concordance rates (MZ, DZ) for sz

Answer 11

MZ = 45%
DZ = 10%

Question 12

name a study into impact of bullying on sz

Answer 12

used CAPE (clinical measure for psychotic experience), recall of past experiences of severity of bullying. greater score correlated with severity/frequency of past bullying experiences

Question 13

name 2 antipsychots

Answer 13

chlopromazine, reserpine

Question 14

chlopromazine - where did it originate

Answer 14

originally anti histamine, anti-inflammatory calmed down ‘normal’ patient

Question 15

explain how chlopromazine works

Answer 15

blocks dopamine receptor = stop dopamine working
false transmitter (antagonist) bind to receptor but with no effect (stopping dopamine binding and then working)

Question 16

reserpine - where did it originate from

Answer 16

snake root plant, India used it for mental illness

Question 17

how does reserpine work

Answer 17

depletes vesicles, reduces amount of dopamine that is released (deplete brain of dopamine)

Question 18

name similarities of chlopromazine and reserpine

Answer 18

take 2-3week to work, PD side-effects (due to lost dopamine in nigrostriatal pathway)

Question 19

summarise dopamine hypothesis for sz

Answer 19

dopamine overactive in sz
drug reducing dopamine neurotranmission reduced symptom
drugs increasing dopamine neurotransmission produced symptom

Question 20

what recreational drug provides evidence for dopamine hypothesis

Answer 20

cocaine/amphetamine psychosis = blocks reuptake so more left in synapse

Question 21

explain efficacy of antipsychotic

Answer 21

efficacy correlate with its ability to bind to dopamine receptor = better binding work better
APART from haloperidol, v. effective but not as potent in binding

Question 22

explain structure of dopamine receptor

Answer 22

metabotropic, linked to G-protein, when NT bind subunit breaks into neuron and binds to ion channel or stimulates synthesis of 2nd messenger

Question 23

explain the “types/families” of dopamine receptor

Answer 23

2 families = D1 + D2 but 5 receptors (D1, 2, 3, 4, 5)

Question 24

what is relationship between ability of typical antipsychotic binding and clinical potency

Answer 24

positive correlation between ability of typical antipsychotic to bind to D2 receptors and clinical potency (effectiveness)
haloperidol binds better to D2 than D1

Question 25

how do D1 family (D1 and D5) dopamine receptor work

Answer 25

positively coupled to adenylate cyclase so increases adenylate cyclase activity (enzyme that hep send messages around cell)

Question 26

how do D2 family (D2, D3, D4) dopamine receptors work

Answer 26

negatively coupled to adenylate cyclase so reduces anylate cyclase activity

Question 27

name example of D2 family dopamine drug

Answer 27

newer atypical antipsychotic (clozapine) acts on D4

Question 28

what type of receptor do typical/atypical antipsychotic bind to

Answer 28

typical = D2
atypical can bind to other receptor

Question 29

name methods of testing dopamine hypothesis

Answer 29

PET, microdialysis, fMRI, post-mortems

Question 30

name issue of dopamine hypotheses

Answer 30

1. most antipsychotic occupy 60-80% D2 receptors but most effective ones (clozapine, quetiapine) only occupy 10-45%. suggest dop hypoth be extended to serotonin-dopamine hypothesis
2. global severity of pos symptom not correlate with occupancy of striatal D2 receptors by dopamine

Question 31

name issues with clozapine, quetiapine

Answer 31

occupies high level of D2 receptors but effects only last short time

Question 32

name what there is a tight correlation between in regards to clinical effect and receptor

Answer 32

btw clinical effects and D2 blocking action of antipsychotic, as well as elevated D2 receptors in Sz striatum

Question 33

outline Abi-Dargham influential study and her results

Answer 33

can only study IBZM (radioactive), not natural so groups would look same
so deplete natural dopamine, see how much green left
found in sz, large increase in green binding, D2 receptors significantly elevated

Question 34

for Abi-Dargham study, go into depth on variance of a-MPT effect on D2 receptor availability

Answer 34

larger in sz but with no age or gender effects

Question 35

for Abi-Dargham study, go into depth on previous medications

Answer 35

no statistical difference
increased occupancy of D2 receptors by dopamine present at onset of illness, not a consequence of previous drugs