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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
Location and function of most nonadrenergic neurons
Locus coerulus determine whether attention is being focused on external environment or internal Cognition, mood, emotions, movements, blood pressure, energy, psychomotor agitation/retardation
26
Dopamine receptors in pharmacology
Dopamine 1,2,3,4
27
NE deficiency syndrome
``` Impaired attention Poor concentration Deficiency in working memory Slowness of information processing Depressed mood Psychomotor retardation Fatigue ```
28
AA converted to 5HT
tryptophan-> try hydroxylase->5 hydroxytryptophan-> aromatic AA decarboxylase into 5HT
29
Serotonin receptor subtyeps
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
Serotonin deficiency syndrom
``` Depressed mood Anxiety Panic Phobia Anxiety Obsessions and compulsions Food craving, bulimia ```
31
Why doesn't the monoamine hypothesis fit
Immediate increase in MA, however delayed response
32
Neurotransmitter receptor hypothesis for depression
depletion of MA causes compensatory up regulation of NT receptors ?abnormality in gene expression
33
Monoamine hypothesis of gene expression
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
Neurokinin hypothesis of emotional dysfunction
antagonist to substance P may have depressant effects | Present in amygdala, may have role in regulating emotions
35
when is it rapid cycling
when it occurs more than 4 times/year
36
who described several categories along the bipolar spectrum
Hagop Akiskal
37
Bipolar 0.25
unstable mood, depressed with good response to antidepressant, may benefit from mood stabiliser
38
dichotomous view point in relation to schizphrenia and bipolar
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
bipolar 0.5
schizoaffective disorder
40
bipolar 1.5
hypomania without depression
41
bipolar 2.5
cyclothymic patients who develop MDD
42
bipolar 3
develop manic/hypomanic disorder on antidepressants (substance induced)
43
bipolar 3.5
mania induced by substances
44
bipolar 4
association of depressive episodes with pre-existing hyperthymic temperament. may respond well to mood stabiliser
45
bipolar 5
depression with mixed hypomania, requires mood stabiliser. | worse outcome- more mood episodes, more work impairment, likely FHx
46
bipolar 6
bipolarity in setting of dementia
47
Is it unipolar or bipolar depression- questions to ask
"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
What has been the paradigm shift in relation to prevalence of mood disorders
Many patients once considered to have MDD are now recognised as having bipolar illness along bipolar spectrum
49
Autoreceptor regulation for dopamine, serotonin and NE
Dopamine-> D2 Serotonin-> 5HT 1A, 5HT 1B/D NE-> a2
50
a1 and a2 regulation of serotonin
``` a1= accelerator for 5HT (raphe nucleus) a2= brake for 5HT (cortical) ```
51
Major dopamine projections
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
Major serotonin projections
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
Major NE projections
Locus C-> thalamus, cerebellum, basal forebrain, amygdala, hypothalamus
54
Link between stress, BDNF and brain atrophy in depression
++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
Vulnerability-stress model
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
explain the idea of mood-related sx of depression being characterised by their affective expression
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
Matching diagnostic sx for manic episode to hypothetically malfunctioning brain circuits
Motor agitation- striatum dec sleep/arousal- thalamus, hypothalamus, basal forebrain mood- amygdala risks, grandiosity, talkative/pressured speech, racing thoughts- PFC, NA
58
Neuroimaging in mood disorders- response to induced sadness vs happiness
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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