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RANZCP exam preparation > Psychopharmacology- Depression and bipolar > Flashcards

Psychopharmacology- Depression and bipolar Flashcards

1
Q

Public perceptions of mental illness

A 
Emotional weakness
Bad parenting
Victims fault
Incurable
Sinful behaviour
Biological
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2
Q

Vegetative sx

A

Sleep
Appetite
Weight
Sex drive

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3
Q

Cognitive sx

A 
attention span
frustration
tolerance
memory
negative distortions
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4
Q

impulse control features

A

suicide and homicide

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5
Q

behavioural and physical sx

A 
motivation
pleasure
interests
fatigueability
headaches
stomach aches
muscle tension
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6
Q

Brief psychoed for depression

A

Medical illness, not character defect
Recovery is the rule
Treatments are effective, many options
Aim is complete symptom remission, not just getting better and staying wel
Risk of recurrence is 50% after 1, 70% after 2 and 90% after 3.
Should be alert to early warning signs and seek treatment.

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7
Q

How many % of those with affective disorder exhibit non-fatal suicidal behaviours

A

20-40%

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8
Q

Depression and the rules of 7

A

1/7 with recurrent depressive episode commits suicide
70% suicides have depressive illness
70% suicide see GP within 6 weeks
Suicide 7th leading cause of death

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9
Q

Causes of mortality in depression

A

suicides
fatal accidents due to poor concentration/attention
due to illness sequelae-alcohol etc

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10
Q

morbidity in depression

A 
suicide attempts
accidents
illness
job loss
failed advance in school/career
substances
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11
Q

societal costs depression

A 
dysfunctional families
absenteeism
decreased productivity
job related injuries
quality control in workforce
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12
Q

how long does untreated depression last

A

6-24 months

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13
Q

3 R’s improvement in treated depression

A

Response- 50% reduction (Hamilton depression rating scale)
Remission
recovery- remission for 6-12 mo

(relapse and recurrence)

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14
Q

predicting relapse in depression

A 
multiple
severe
long duration
bipoolar/psychotic
incomplete recovery
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15
Q

followup of depressed patients after 1 year clinical treatment

A

40% no diagnosis
40% diagnosis
20% partial

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16
Q

response rate to every antidepressant

A

67% respond

33% fail to respond

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17
Q

Apathetic responders (partial remission)

A

Reduction in depressed mood
Continuing anhedonia, lack of motivation, decreased libido, lack of interest, no zest
cognitive slowing
dec concentration

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18
Q

Anxious responders

A

Reduced depressed mood
anxiety
worry, insomnia, somatic

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19
Q

implications of partial response in patients who do not attain remission

A 
milder form
inadequate early treatment
?underlying PD or dysthymia
increased relapse rates
functional impairment
increased suicide rates
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20
Q

Monoamine hypothesis depression

A

deficiency of NE and serotonin +(DA)

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21
Q

mechanism of TCA

A

inhibit reuptake pump of NE, 5HT

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22
Q

Amino acid precursor for NE, conversion steps

A

Tyrosine-> converted by tyrosine hydroxylase->DOPA-> DOPA decarboxylase-> DA-> dopamine beta-hydroxylase-> NE

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23
Q

NE destroyed by which enzymes

A

MAO in presynaptic neurons

COMT outside presynaptic terminal

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24
Q

Types of NE receptors

A

B1, B2

A1, A 2 (autoreceptors)

25
Q

Location and function of most nonadrenergic neurons

A

Locus coerulus
determine whether attention is being focused on external environment or internal

Cognition, mood, emotions, movements, blood pressure, energy, psychomotor agitation/retardation

26
Q

Dopamine receptors in pharmacology

A

Dopamine 1,2,3,4

27
Q

NE deficiency syndrome

A 
Impaired attention
Poor concentration
Deficiency in working memory
Slowness of information processing
Depressed mood
Psychomotor retardation
Fatigue
28
Q

AA converted to 5HT

A

tryptophan-> try hydroxylase->5 hydroxytryptophan-> aromatic AA decarboxylase into 5HT

29
Q

Serotonin receptor subtyeps

A
  1. presynaptic 1A- autoreceptors-> reduce
  2. 1D-> terminal autoreceptor- inhibit release
  3. a2 heteroreceptors-presynaptic, inhibit release when occupied by 5HT (cortex)
  4. Axodendritic interactions a1 on cell bodies, enhance serotonin release when occupied with NE (brainstem)
  5. 2A-> projections to basal ganglia-> movements, obsessions and compulsions. Raphe to limbic-> eating and appetite, anxiety Brainstem-> sleep
    2C, 3 (CTZ vomiting), appetite GIT motility-> postsynaptic, sexual functions
30
Q

Serotonin deficiency syndrom

A 
Depressed mood
Anxiety
Panic
Phobia
Anxiety
Obsessions and compulsions
Food craving, bulimia
31
Q

Why doesn’t the monoamine hypothesis fit

A

Immediate increase in MA, however delayed response

32
Q

Neurotransmitter receptor hypothesis for depression

A

depletion of MA causes compensatory up regulation of NT receptors
?abnormality in gene expression

33
Q

Monoamine hypothesis of gene expression

A

despite normal MA levels and receptors- deficiency in signal transduction to post-synaptic neuron
“pseudoamine deficiency”
BDNF-> normally sustains viability of neurons, when stressed, supressed-> apoptosis of vulnerable neurons in hippocampus-> depression

34
Q

Neurokinin hypothesis of emotional dysfunction

A

antagonist to substance P may have depressant effects

Present in amygdala, may have role in regulating emotions

35
Q

when is it rapid cycling

A

when it occurs more than 4 times/year

36
Q

who described several categories along the bipolar spectrum

A

Hagop Akiskal

37
Q

Bipolar 0.25

A

unstable mood, depressed with good response to antidepressant, may benefit from mood stabiliser

38
Q

dichotomous view point in relation to schizphrenia and bipolar

A

Krapelinian dichotomy- that they are two entities. Schizo- unremitting, poorer outcome.
If you have bipolar, do you have good outcome?
If you have schizophrenia, do you have poor outcome
Continuum disease model proposes both manifestations of complex set of disorders expressed on spectrum

39
Q

bipolar 0.5

A

schizoaffective disorder

40
Q

bipolar 1.5

A

hypomania without depression

41
Q

bipolar 2.5

A

cyclothymic patients who develop MDD

42
Q

bipolar 3

A

develop manic/hypomanic disorder on antidepressants (substance induced)

43
Q

bipolar 3.5

A

mania induced by substances

44
Q

bipolar 4

A

association of depressive episodes with pre-existing hyperthymic temperament. may respond well to mood stabiliser

45
Q

bipolar 5

A

depression with mixed hypomania, requires mood stabiliser.

worse outcome- more mood episodes, more work impairment, likely FHx

46
Q

bipolar 6

A

bipolarity in setting of dementia

47
Q

Is it unipolar or bipolar depression- questions to ask

A

“Who’s your daddy”
- fhx of mood disorder, psych hospitaliation, suicide, lithium/mood stabilisers/AP/ED, ECT

“Where’s your mumma?”
Need to get additional history

?Bipolar depression
-more time sleeping, overeating, co-morbid anxiety, motor retardation, mood lability, psychotic sx, suicidality.
Early age onset, hgih freq depressive sx, ++time spent ill, acute abatement or onset of sx
Response to AD- failure, rapid recovery, activating side effects, insomnia, agitation anxiety

48
Q

What has been the paradigm shift in relation to prevalence of mood disorders

A

Many patients once considered to have MDD are now recognised as having bipolar illness along bipolar spectrum

49
Q

Autoreceptor regulation for dopamine, serotonin and NE

A

Dopamine-> D2
Serotonin-> 5HT 1A, 5HT 1B/D
NE-> a2

50
Q

a1 and a2 regulation of serotonin

A 
a1= accelerator for 5HT (raphe nucleus)
a2= brake for 5HT (cortical)
51
Q

Major dopamine projections

A

VTA and SNg-> extend via hypothalamus, to PFC, basal forebrain, striatum, NAc
Movement, pleasure and reward, cognition, psychosis
May also have role in sleep via projections to thalamus

52
Q

Major serotonin projections

A

Ascending projections originate in brainstem-> thalamus, striatum, NA, basl forebrain, PFC, hypothalamus, amygdala
Regulate mood, anxiety, sleep
Descending down spinal cord-> pain, GIT, sexual function

53
Q

Major NE projections

A

Locus C-> thalamus, cerebellum, basal forebrain, amygdala, hypothalamus

54
Q

Link between stress, BDNF and brain atrophy in depression

A

++stress, reduced expression of BDGF, decrease in 5HT, increase then depletion of NE and DA
possible apoptosis of vulnerable neurons
These neurons normally regulate HPA-> when ++stress, atrophy, loss of inhibitory input to hypothalamus= overactivity of HPA.

55
Q

Vulnerability-stress model

A

Epigeneic changes
Environmental stressors creating molecular alterations in brain circuits
Vulnerable brain circuits that may break down into depression upon exposure to future stressor

56
Q

explain the idea of mood-related sx of depression being characterised by their affective expression

A

Positive affect reduced-> depressed mood, anhedonia, x happiness, loos of energy/enthusiasm, dec alertness, dec self-confidence-> DA dysfunction, NE dysfunction

Negative affect ++-> dep mood, guilt/disgust, fear/anxiety, hostility, irritability, loneliness

57
Q

Matching diagnostic sx for manic episode to hypothetically malfunctioning brain circuits

A

Motor agitation- striatum
dec sleep/arousal- thalamus, hypothalamus, basal forebrain
mood- amygdala
risks, grandiosity, talkative/pressured speech, racing thoughts- PFC, NA

58
Q

Neuroimaging in mood disorders- response to induced sadness vs happiness

A

DLPC in depression associated with cognitive sx, reduced activity
AMygdala- +activity in depression , over active to induce sadness, under active to induce happiness
OFC in manic pts-> fail to appropriately activate= problems with impulsivity associated with mania. Do not activate the ‘no-go’

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