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PSY1003 SEMESTER 2 > PSY1003 SEMESTER 2 - WEEK 8 > Flashcards

PSY1003 SEMESTER 2 - WEEK 8 Flashcards

1
Q

summarise clinical depression

A

longer than 2 weeks, cause struggle to keep job, maintain social contacts, eat, personal hygiene, sleep disturbance, thought of suicide

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2
Q

outline reactive depression, and the 2 subtypes

A

triggered by negative experience
SAD
peripartum depression

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3
Q

explain endogenous depression

A

no apparent negative life events

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4
Q

give incidence of unipolar affective disorder/depression

A

5 - 17%

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5
Q

give incidence of bipolar affective disorder

A

1%

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6
Q

what is bipolar type 1

A

experience bouts of depression, mania hypomania

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7
Q

what is bipolar type 2

A

only experience bouts of depression, and hypomania

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8
Q

what is hypomania

A

more mild mania, decrease need for sleep, high energy, positive affect, talktative, impulsive, confidence

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9
Q

what is mania

A

same feature as hypomania (more extreme), delusions of grandeur, overconfidence, impulsive, distractable, psychosis, overenthusiastic, hurtles between topic

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10
Q

give cognitive symptoms of depression

A

difficulty with concentration or making decisions

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11
Q

give behavioural symptoms of depression

A

social withdrawal and agitation
reduce appetite, sexual desire, slowed speech
inactivity, less energy

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12
Q

give somatic symptoms of depression

A

insomnia, hypersomnia, headaches, indigestion, constipation

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13
Q

give affective symptoms of depression

A

depressed mood, feeling worthlessness or guilt, loss of humour, anxiety, hopeless, miserable, dejected

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14
Q

give motivational symptoms of depression

A

loss in interest in daily normal life, lacking initiative, spontaneity

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15
Q

what is a major depressive episode

A

5+ symptoms during 2 weeks (includes feelings of worthlessness, suicidal ideation, impairment of daily functioning)

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16
Q

describe dsythymic disorder

A

form of depression for 2 year, depressed mood for more days than not, experiencing many beh/cog characteristic, less severe

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17
Q

explain cyclothymic disorder

A

mild bipolar, mood swings over many years, ranging from mild depression to euphoria and excitement

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18
Q

name 3 measures for depression

A

self report (PHQ)
Becks depression inventory
HADS- hospital anxiety, depression scale

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19
Q

give MZ, DZ concordance rate for unipolar/bipolar

A

unipolar = 39% MZ, 27% DZ
bipolar = 92% MZ, 24% DZ

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20
Q

explain environmental statistics for impact on depressive patient

A

84% depressed patients compared to 32% control patient experience severe stress in past year

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21
Q

explain heritaiblity

A

estimate of how much variation in some characteristic within some population is due to differences in heredity, ranges between 0-1

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22
Q

what is heritablity for bipolar disorder

A

0.85 = high

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23
Q

what is heritability for unipolar disorder

A

0.4 = moderate

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24
Q

what is brain alterations found by MRI in depression

A

reduced grey matter vol (prefrontal cortex, hippocampus, amygdala, cingulate cortex) involved in maintaining and achieving goals, emotional regulation, learning affective reactions

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25
Q

what is brain alterations found by fMRI in depression

A

atypical activity = frontal, cingulate, insular cortices, amygdala, thalamus, striatum

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26
Q

name neurochemical factors, and neuroendocrine factors for depression

A

neurochem = low serotonin, NE (cog, beh, motivational deficit) and low dop (reward system def, low motiv, initiative, pleasure)

neuroend = diff regulating cortisol (lacking IC, enlarged adrenal gland(

27
Q

what is brain alterations found by MRI in bipolar

A

less grey matter vol, small prefrontal, hippocampus

28
Q

what is brain alterations found by fMRI in bipolar

A

atypical activation in frontal, medial temporal, basal ganglia

29
Q

what neurochemical levels can cause mania

A

low serotonin, high norepinephrine

30
Q

give triggers for mania

A

increased responsiveness to reward, reaction to antidepressant, disrupted circadian rhythm, reasons, stress, exposure to high expressed emotion families

31
Q

name 2 types of monoamine NT

A

catecholamines (dopamine, NE, epinephrine)- dorsal projection into frontal, limbic system and whole brain
indolamines (serotonin)- serotonergic projection from raphe nucleus to frontal, limbic system

32
Q

how do MAOI drug work

A

MAO breakdown NT, MAOI inhibits action so more NT in neuron for release

33
Q

why are MAOI not as commonly used

A

side effect
cheese and red wine contain tyramine, increase BP and usually broken down in liver but is prevented by MAOI

34
Q

give efficacy of MAOI

A

50% show improvement

35
Q

what are tricyclic antidepressants

A

contains 3 ring chain, blocks reuptake of NE/serotonin
prozac
safer than MAOIs

36
Q

give efficacy of tricyclic antidepressant

A

60-65% shows improvements

37
Q

what is lithium

A

only drug for bipolar
interfere with 2nd messengers system, not fully sure how work, mood stabiliser (dampen down mania cycle w/ depression)

38
Q

outline monoamine theory of depression

A

antidepressants act on monoamines,so depression due to deficit of ma NT (modulates emotive, cognitive region of amygdala, orbital and medial prefrontal cortex

39
Q

provide evidence of monoamine hypothesis

A

evidence of more receptors in patient (compensates for low levels of transmission)
autopsy = more NE, serotonin receptor in depression suggesting less ma release, causes up-regulation (not enough NT so compensatory increase in receptors)

40
Q

give contradictory evidence for monamine hypothesis

A

monoamine agonists not effective treatment, other NT plays a role

41
Q

outline neuroplasticity theory of depression

A

due to less neuroplastic process = neuron loss
evidence as stress, depression associated with disrupted neuroplastic processes
antidepressants associated with enhanced neuroplastic processes (neurotrophin synthesis, synaptogenesis, adult hippocampal neurogenesis)

42
Q

explain rTMS

A

repetitive transcranial magnetic stimulation
non invasive repetitive mag pulse in cortex

43
Q

outline ECT (electroconvulsive therapy)

A

passing current through head

44
Q

outline stepped care-model

A

emphasising treating tailored to specific symptom

45
Q

give an overview for Becks cognitive triad

A

biased way of thinking, process info causes developing broad ranging negative schema influencing selection, encoding, categorisation and evaluation of stimuli and event
neg view of world, future, self
neg schema are stable, disposition, develop from adverse childhood experiences and reactivated by later stressful event

46
Q

name some biases of thinking (cognitive models)

A

arbitrary inference, selective abstraction, overgeneralisation, magnification, minimization, personalisation, all-or-none thinking

47
Q

outline arbitrary inference

A

jump to conclusion when evidence is lacking or to contrary of conclusions

48
Q

outline selective abstraction

A

abstracting detail out of context, missing significance of whole situation

49
Q

outline overgeneralisation

A

unjustified generalisation on basis of single events

50
Q

outline personalisation

A

interpreting events in term of personal meaning to individual rather than objectives

51
Q

outline learned helplessness (Seligman)

A

experiencing uncontrollable and unavoidable negative life events causes cognitive set making individual feel helpless, lethargic, depressed

52
Q

application of learned helplessness - battered woman syndrome

A

pattern of repeated partner abuse results in symptoms of depression, and passivity

53
Q

outline research for learned helplessness

A

dog in box with barrier, tone (sound) indicates shock
dog must jump over barrier to avoid shock
after dog had been in condition where they can’t escape shock, no longer jump to no shock zone

54
Q

outline Seligmans attributional model

A

attribute negative event, 3 dimensions (internal vs external, global vs specific, stable vs unstable)
patient learns to be helpless, possessing specific attributional style generates pessimistic thinking
attribute negative life events to internal, stable, global (to factors unlikely to change, not easily manipulated)

55
Q

for Seligmans attributional theory, outline global/stable for internal

A

global stable - lack intelligence
global unstable - i am exhausted
specific stable - i lack maths abilities
specific unstable - i am fed up with maths

56
Q

for Seligmans attributional model, outline global, stable for external

A

global stable- these tests are unfair
global unstable- its an unlucky day
specific stable- test is unfair
specific unstable- my maths test was number 13

57
Q

explain hopelessness theory

A

exhibiting expectation that positive outcome won’t occur and neg outcomes will, individual has no responses available that will change it

58
Q

explain rumination theory

A

repetitive dwelling driven by metacognitive belief that ruminations necessary in order to resolve depression, and are associated with overgeneral autobiographical memory

59
Q

compare antidepressants, CBT

A

similar efficacy long-term, small improvement in drugs short-term
CBT successfully adapted to bipolar alongside medication, aid medications compliance, mood monitors, anticipating stress, interpersonal functioning, problem solving

60
Q

give overview of CBT

A

identify negative belief, thought, and replace with rational and adaptive belief
monitor negative automatics thought that causes negative beliefs, and link between thought to situation, think through possible rational alternatives

61
Q

give overview of reattributional training

A

interpreting difficulties in more hopeful, constructive way not in negative, global, stable previous way

62
Q

give overview of MCBT

A

reduces risk of relapse from negative mood reactivating patterns of negative or depressogenic thinking, self-devaluation, and hopelessness

63
Q
A

PSY1003 SEMESTER 2 (10 decks)

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