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PSYCH 473 > Depression > Flashcards

Depression Flashcards

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1
Q

What are depressive disorders?

A

the presence of sad, empty, or irritable mood, accompanied by somatic and cognitive changes that significantly affect the individual’s capacity to function

largest economic burden of illness

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2
Q

What is disruptive mood dysregulation disorder?

A

children (6-18)

chronic and severe irritability and angry outburst out of proportion to situation and developmental level of child

prevalence 2-5%, higher in males and school-age than females and adolescents

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3
Q

What is persistent depressive disorder (dysthymia)?

A

persistent depressed mood (most of the day, most days) for at least 2 years without remission (<2 months)

presence of hypo- or hyperphagia, insomnia or hypersomnia, fatigue, etc.

prevalence of 1.5-2%

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4
Q

What are premenstrual dysphoric disorder?

A

affective lability, irritability, anger, depression or anxiety in the week preceding menses

symptoms leading to clinical distress or interference with normal occupational and social functioning

prevalence 1.8 - 5.8% of women

heritability of 30-80%

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5
Q

What is the DSM-5 criteria for major depressive disorder?

A

five or more symptoms during the same 2 week period that marks a change from prior functioning

these occur most of each day, most days

symptoms cause clinically significant distress or interfere with normal social or occupational functioning

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6
Q

What are the symptoms for major depressive disorder outlined in the DSM-5?

A

depressed mood, (feelings of sadness, hopelessness) or irritable mood in children/adolescents (subjective/objective)

marked decrease in interest or enjoyment of daily activities (subjective/objective)

significant weight loss/gain or increased/decreased appetite (outside of dieting)

insomnia or hypersomnia

psychomotor agitation or retardation (observable by others)

fatigue or loss of energy

feeling of worthlessness, inappropriate guilt

diminished ability to think or concentrate, indecisiveness

recurrent thought of death, suicidal ideation, suicide attempt or planning

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7
Q

What are correlates of MDD?

A

lifestyle, sociodemographic, and other factors that correlate with risk of MDD

women, homemakers, unemployed/disabled, never married, previously married

less than 12 years of education

living in or near poverty

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8
Q

What are common comorbidities of MDD?

A

medical or psychiatric conditions found at increased rates i populations with MDD

72.1% with MDD meet criteria for another DSM-5 disorder

anxiety disorder, substance use disorder, impulse control disorder

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9
Q

What are medical comorbidities of MDD?

A

cardiovascular disease (congestive heart failure, myocardial infarct, and stroke)

diabetes

cancer

dementia

many risks are bidirectional: stroke or diabetes increases risk of MDD, and MDD increases risk of stroke or diabetes

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10
Q

What is the incidence and progression of MDD?

A

onset typically after puberty

incidence peaks in 20s

MDD is episodic in most people with spontaneous recovery starting at 3 months to 1 year (in 4/5 patients)

remission is any 2 month period symptom-free

length of remission and severity of the previous episode impact risk of recurrence

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11
Q

What are the temperamental risk factors for MDD?

A

neuroticism (negative affectivity)

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12
Q

What are the environmental risk factors for MDD?

A

adverse childhood experiences (abuse, neglect, trauma)

stressful life events

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13
Q

What are the genetic risk factors for MDD?

A

2-4 fold increased risk in first-degree family members

up to 40% heritability

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14
Q

What are the functional consequences of MDD?

A

impact highly variable

increased pain and physical illness

decreased social and occupational functioning: depression is the leading cause of disability in Canada

decreased cognitive functioning

elevated risk of suicide

can lead to incapacity, muteness, or catatonia

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15
Q

What is the cognitive affective bias (CAB) in depression?

A

interaction of emotional and cognitive processes

highly relevant to cognition in depression

depressed patients are more likely to remember negative emotion information, interpret ambiguous social signals negatively

correlated with increased risk of relapse

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16
Q

What is the psychodynamic perspective on depression?

A

focus on loss as an initiator

Freud: depression represents inward projection of anger following actual or threatened loss (person, object, or personal failure)

self-focus/self-examination, fixation on subject of loss or failure

excess rumination without reconciliation

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17
Q

What is the learning perspective on depression?

A

depression arises from insufficient reinforcement or reciprocal interactions

partner or peers alter interactions with a depression-prone person further reducing opportunities for positive interactions

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18
Q

What is the cognitive perspective on depression?

A

depression resulting from a negative view of self, environment, or the future

negative attention bias / pessimistic world view leads to depression

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19
Q

What is the learned helplessness perspective on depression?

A

depression results from a perceived inability to control their environment or change for the better

cyclic or self-reinforcing - depressive behaviors lead to further helplessness

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20
Q

What factors cause an individual to develop affective bias?

A

most psychological models address the onset, progression, or recurrence of depression but none address causal agents

some posit features of depression (e.g., excess rumination, negative bias) as causal agents

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21
Q

How are the neurobiological changes in depression assessed?

A

lesion-deficit studies

structural imaging: structural MRI, diffusion tensor imaging (DTI tractography)

functional imaging: functional MRI (fMRI), PET, SPECT

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22
Q

What are lesion-deficit studies?

A

one of the oldest “models” for functional specialization of the brain

has been very widely used historically to correlate changes in cognition, emotion, memory, personality, etc with specific structures of the brain

limited to observational studies (ethics)

23
Q

What structural differences in MDD are indicated by lesion studies?

A

develop depression after damage to the frontal lobe, temporal lobe, or basal ganglia

24
Q

What structures report decreased volume in depressed patients MRI?

A

hippocampus
anterior cingulate cortex (ACC)
caudate nucleus
putamen
orbitofrontal cortex

25
Q

What are the structural differences between MDD and neurological conditions?

A

conditions such as stroke, Alzheimer’s, Parkinson’s, and Huntington’s have high comorbidity with depression and have defined structural defects

high variability in structural differences

volumetric differences are worse in older patients

depression disproportionally affects younger patients

26
Q

What is positron emission tomography?

A

uses positron-emitting radiotracers to analyze brain metabolism

tissue uptake of FDG is proportional to glucose uptake and hence activity

27
Q

What is single photon emission computed tomography?

A

uses gamma-emitting radiotracers to analyze brain blood flow

tissue uptake of Tc-HMPAO is proportional to blood flow and hence activity

28
Q

What are the neuropsychological deficits of MDD found through functional imaging?

A

structural imaging fails to show consistent changes in MDD

functional imaging techniques allow investigation into changes in neural activity or connectivity

functional imaging can be correlated with specific tasks or emotional states

functional abnormalities may however affect connection regions

difficult to identify necessary and sufficient abnormalities

29
Q

What are the commonly observed areas of increased activity in depression?

A

frontal, orbital, parahippocampal cortices

ventrolateral prefrontal cortex

subgenual cingulate cortex

(amygdala), striatum, hypothalamus

30
Q

What are the commonly observed areas of decreased activity in depression?

A

dorsal medial prefrontal cortex

dorsal anterior cingulate cortex

posterior cingulate cortex

31
Q

What is the limbic-cortical dysregulation model of MDD?

A

depression results from dorsal hypoactivity (dmPFC, ACC) and ventral hyperactivity (frontal cortex, subgenual cingulate cortex, insula, hippocampus, hypothalamus)

32
Q

What structures are involved in the limbic-cortical dysregulation model?

A

lesion-deficit studies and functional imaging identified changes in limbic, paralimbic, striatal-palladial, and thalamic areas

subgenual cingulate cortex BA25 implicated as a key modulator of depressive circuits

anterior cingulate (BA24a) activity predicts treatment response to antidepressants

33
Q

What are the two major compartments of change in depression according to the limbic-cortical dysregulation model?

A

dorsal hypoactivity: dorsal anterior and posterior cingulate, inferior parietal and dorsolateral prefrontal cortex

ventral hyperactivity: subgenual cingulate, ventral frontal cortex, hippocampus, hypothalamus, and insula

34
Q

What is the monoamine hypothesis of depression?

A

depression is the result of a functional deficit of the neurotransmitters norepinephrine (NE) and/or serotonin (5-HT) at specific synapses in the CNS

35
Q

What are monoamines?

A

monoamines (biogenic amines) are a group of neurotransmitters / hormones that share a common single amino functional group

36
Q

What is serotonin?

A

derived from tryptophan in the brain (5-HT cannot pass the blood-brain barrier)

major neurotransmitter in the gut responsible for contraction

37
Q

What is the synthesis and catabolism of serotonin?

A

dietary L-tryptophan is transported into the brain where it is converted to 5-HT by tryptophan hydroxylase (the rate limiting enzyme)

5-HT is deaminated by monoamine oxidase to 5-hydroxyindoleacetic acid in the cytoplasm of serotonergic neurons

in contrast to the catecholamines, 5-HT breakdown occurs only through MAO

38
Q

What are the broad behavioral effects of serotonin?

A

5-HT is colloquially thought to contribute to happiness, mood, and spirituality

most antidepressants target serotonergic systems and improve mood

5HT receptors (5HT2A) are responsible for the effects of hallucinogenic drugs (e.g. LSD)

diverse effects on behavior make it difficult to ascribe an overall function to serotonergic systems: mood, emesis, migraine propagation, anxiety, attention/alertness

5-HT binding capacity has been suggested to correlate with tendency towards spirituality

39
Q

What is the bioavailability of tryptophan?

A

tryptophan is dietary in source and availability of tryptophan can affect 5-HT production

the tryptophan transporter is a competitive amino-acid transporter, thus increased protein intake does not elevate tryptophan bioavailability in the brain

dietary restriction of tryptophan intake can dramatically alter 5-HT levels in the brain and induce depressive symptoms

40
Q

How does uptake inactive 5-HT signalling?

A

serotonin transporter (SERT or 5-HTT) regulates synaptic clearance of 5-HT

two polymorphisms of SERT-5-HTT were associated with increased risk of depression

SERT-5-HTT is the primary target of SSRI, SNRI, and TCA antidepressants

41
Q

How does catabolism by MAO inactive 5-HT signalling?

A

MAO breaks down 5-HT, NE, and DA in the brain and 5-HT in gut

primary target of MAOI antidepressants

42
Q

How is the raphe nuclei involved in depression?

A

serotonergic projections from the raphe nuclei project to many regions implicated in depression

limbic, frontal, temporal cortex (including BA25)

thalamus

basal ganglia

hippocampus

43
Q

What is the monoamine hypothesis?

A

depression is a result of a functional deficit of the neurotransmitters norepinephrine and serotonin (5-HT) at specific synapses in the CNS

44
Q

What is the pharmacology of the monoamine hypothesis?

A

first antidepressant was a monoamine oxidase inhibitor (MAOI), iproniazid, ad anti-tuberculosis drug (1952)

MAOI cause elevation of monoamines by inhibiting their breakdown

elevated monoamines leads to increases in monoaminergic neurotransmission (dopamine, norepinephrine, serotonin)

phenelzine was the most common MAOI in use clinically but discontinued due to the cheese effect

45
Q

What are some examples of MAO inhibitor drugs?

A

phenelzine

tranylcypromine

moclobemide

46
Q

What are MAO inhibitors?

A

increased presynaptic monoamine levels presumed to lead to enhanced monoamine release

MAOI such as phenelzine and tranylcypromine irreversibly inhibit both MAO-A and MAO-B

MAO-A and -B are present in the CNS

MAO-A is also found in the gut where it breaks down tyramine in food

47
Q

What is the cheese effect of MAOIs?

A

tyramine is degraded in the gut by MAO-A and thus not taken up systematically

tyramine-rich foods (cheese, red wine) lead to elevations in tyramine in the presence of MAOI (drug interaction)

tyramine acts to release NE from nerve terminals where (due to MAO inhibition) it persists

elevated NE symptoms range from headaches to hypertensive crisis (can be fatal)

MAO inhibitors are currently used as a last resort therapeutic

48
Q

What are examples of tricyclic antidepressant drugs?

A

imipramine

amitriptyline

desipramine

nortriptyline

49
Q

What are tricyclic antidepressants (TCA)?

A

developed in the 1950’s from chlorpromazine analogues

imipramine is an inhibitor of both norepinephrine transporters (NET) and 5-HT transporters (SERT)

impaired reuptake leads to elevated synaptic NE-5-HT

sustained NE/5-HT levels lead to prolonged and increased post-synaptic activity

side effects on muscarinic receptors (anti-cholinergic): dry mouth, constipation, urinary retention

poor safety margin - induces mania at higher doses

50
Q

What are examples of selective reuptake inhibitor drugs?

A

citalopram

fluoxetine (Prozac)

venlafaxine

51
Q

What are SSRIs?

A

selective serotonin reuptake inhibitors

second generation antidepressants - targeted drug design

fluoxetine (Prozac) most widely prescribed

selective inhibitors for SERT

5-HT accumulates in the synapse, enhancing post-synaptic activity

52
Q

What are SNRIs?

A

serotonin-norepinephrine reuptake inhibitors

second generation antidepressant - replaces TCA

first SNRI was venlafaxine

inhibits both SERT and NET

fewer side effects than TCAs, improved safety margin

53
Q

How do antidepressant effects compare to placebo effects?

A

antidepressants have an efficacy of approximately 60%

the placebo response in trials is typically ~75-82% of antidepressant effect

43% of AD trials show a significant benefit of drug over placebo - approximately half of trials go unpublished

AD have been suggested to function as active placebos: all have noticeable side effects, thus in AD trials most patients can guess their trial status, breaking blind

54
Q

What are the challenges to the monoamine hypothesis?

A

pharmacologic effects are very rapid (hours-days) but therapeutic effects are slow (weeks-months): monoamines normalize rapidly, but mood normalizes slowly

demonstrated efficacy of drugs that do not affect NA/5-HT reuptake: tianeptine, a selective serotonin reuptake enhancer is equally effective as SSRIs in clinical trials

cocaine (potent NA reuptake inhibitor) does not have antidepressant effects

inconsistent findings in antidepressant effects of amino acid precursors to NA/5-HT (e.g. tyrosine and tryptophan)

model was proposed retrospectively to explain the efficacy of MAOI and TCA class drugs

PSYCH 473 (14 decks)

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