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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
what is brain alterations found by fMRI in depression
atypical activity = frontal, cingulate, insular cortices, amygdala, thalamus, striatum
26
name neurochemical factors, and neuroendocrine factors for depression
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
what is brain alterations found by MRI in bipolar
less grey matter vol, small prefrontal, hippocampus
28
what is brain alterations found by fMRI in bipolar
atypical activation in frontal, medial temporal, basal ganglia
29
what neurochemical levels can cause mania
low serotonin, high norepinephrine
30
give triggers for mania
increased responsiveness to reward, reaction to antidepressant, disrupted circadian rhythm, reasons, stress, exposure to high expressed emotion families
31
name 2 types of monoamine NT
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
how do MAOI drug work
MAO breakdown NT, MAOI inhibits action so more NT in neuron for release
33
why are MAOI not as commonly used
side effect cheese and red wine contain tyramine, increase BP and usually broken down in liver but is prevented by MAOI
34
give efficacy of MAOI
50% show improvement
35
what are tricyclic antidepressants
contains 3 ring chain, blocks reuptake of NE/serotonin prozac safer than MAOIs
36
give efficacy of tricyclic antidepressant
60-65% shows improvements
37
what is lithium
only drug for bipolar interfere with 2nd messengers system, not fully sure how work, mood stabiliser (dampen down mania cycle w/ depression)
38
outline monoamine theory of depression
antidepressants act on monoamines,so depression due to deficit of ma NT (modulates emotive, cognitive region of amygdala, orbital and medial prefrontal cortex
39
provide evidence of monoamine hypothesis
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
give contradictory evidence for monamine hypothesis
monoamine agonists not effective treatment, other NT plays a role
41
outline neuroplasticity theory of depression
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
explain rTMS
repetitive transcranial magnetic stimulation non invasive repetitive mag pulse in cortex
43
outline ECT (electroconvulsive therapy)
passing current through head
44
outline stepped care-model
emphasising treating tailored to specific symptom
45
give an overview for Becks cognitive triad
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
name some biases of thinking (cognitive models)
arbitrary inference, selective abstraction, overgeneralisation, magnification, minimization, personalisation, all-or-none thinking
47
outline arbitrary inference
jump to conclusion when evidence is lacking or to contrary of conclusions
48
outline selective abstraction
abstracting detail out of context, missing significance of whole situation
49
outline overgeneralisation
unjustified generalisation on basis of single events
50
outline personalisation
interpreting events in term of personal meaning to individual rather than objectives
51
outline learned helplessness (Seligman)
experiencing uncontrollable and unavoidable negative life events causes cognitive set making individual feel helpless, lethargic, depressed
52
application of learned helplessness - battered woman syndrome
pattern of repeated partner abuse results in symptoms of depression, and passivity
53
outline research for learned helplessness
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
outline Seligmans attributional model
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
for Seligmans attributional theory, outline global/stable for internal
global stable - lack intelligence global unstable - i am exhausted specific stable - i lack maths abilities specific unstable - i am fed up with maths
56
for Seligmans attributional model, outline global, stable for external
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
explain hopelessness theory
exhibiting expectation that positive outcome won't occur and neg outcomes will, individual has no responses available that will change it
58
explain rumination theory
repetitive dwelling driven by metacognitive belief that ruminations necessary in order to resolve depression, and are associated with overgeneral autobiographical memory
59
compare antidepressants, CBT
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
give overview of CBT
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
give overview of reattributional training
interpreting difficulties in more hopeful, constructive way not in negative, global, stable previous way
62
give overview of MCBT
reduces risk of relapse from negative mood reactivating patterns of negative or depressogenic thinking, self-devaluation, and hopelessness
63

PSY1003 SEMESTER 2 (10 decks)

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