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Psychopharmacology > Final: Antidepressants > Flashcards

Final: Antidepressants Flashcards

1
Q

Diagnosis of depression

A

5 symptoms for two weeks

main ones: depressed mood, loss of interest/pleasure

Sleeping Difficulties Change in Activity Level Change in Appetite Loss of Energy Negative Self-Concept Difficulty Concentrating Indecisiveness Thoughts of Death Suicidal Ideation

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2
Q

highest heritability mood disorder

A

bipolar

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3
Q

What explains identical twins not both having same disorder?

A

Epigenetics: different interpretations of fixed template (genetic code) different read outs dependent upon the variable conditions under which template is interrogated.

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4
Q

Experiment: mama rat and the agouti gene

A

Makes rat obese and yellow with cancer/diabetes

BUT, diet high in methyl groups silence expression in offspring

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5
Q

Methylation

A

reduce gene expression

Packs DNA closer together

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6
Q

Acetylation

A

unravels DNA so increases expression

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7
Q

Chromatin

A

DNA + Histone proteins that the DNA winds around

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8
Q

Epigenetics

A

environmental factors that determine if genes expressed

i.e. Diet, drugs, stressors, parental neglect

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9
Q

HPA axis

A

elevated cortisol

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10
Q

Hypothalamic-Pituitary-Thyroid Axis

A

Reduced thyroid hormones

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11
Q

Hypothalamic-Pituitary-Gonadal Axis

A

Reduced estrogen/testosterone

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12
Q

Pineal Gland

A

Elevated melatonin during daytime

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13
Q

HPA axis in detail

A

Hypothalamus: CRH

Pituitary: ACTH

Adrenal: Glucocorticoid (Cortisol)

Negative feedback back to hypothalamus, pituitary and adrenal, activates hippocampus, which also inhibits hypothalamus

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14
Q

Corticotropin Releasing Hormone (CRH)

A

41-Amino Acid Peptide

Hormone Regulating ACTH Release from Anterior Pituitary

Neurotransmitter Released in Anxiety Circuits Within Brain

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15
Q

Baseline cortisol in depression

A

Cortisol should be high in morning, low at night

But elevated in depression, and levels off (flat rhythm)

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16
Q

Dexamethasone Suppression Test Reveals Impaired Negative Feedback

A

DEX: synthetic control

MDD/early life stress can’t suppress cortisol, thought that early life stress leads to abnormal axis functioning which brings on elevated cortisol levels and disorder vulnerability.

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17
Q

Depression and REM sleep

A

rem is active sleep

Depression = REM early. More REM early in the night than later.

REM pattern is intermittent

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18
Q

Depression and sleep patterns

A

Poor Sleep Difficulty Getting to Sleep Increased Awakening Decreased Sleep Time
Decreased REM Latency Increased Early REM Decreased Late REM

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19
Q

Evidence for the monoamine theory of depression

A

1) Respirine depletes monoamines/induces depression
2) 5-HIAA levels in CSF reported low in some dpressed patients
3) Failure to suppress cortisol release may be related to deficiency of hypothalamic monoamines (NE)
4) Short alleles for serotonin linked to depression
5) Antidepressants increase synaptic monoamines

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20
Q

Reserpine

A

depletes monoamines

Inhibits vesiclularization of monoamines

Free monoamines degraded by MAO

Depletes brain of monoamines

precipitates depression

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21
Q

5-HIAA

A

last metabolite in serotonin degradation

low = more likely to be depressed

serotonin –MAO–> intermediate –aldehyde dehydrogenase–> 5-HIAA

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22
Q

Long and short alleles for SERT genes

A

Short allele + 3+ life stressors = increase risk of depression

did not hold up in metanalysis

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23
Q

Monoamine oxidase inhibitors

A

reduce breakdown of monoamines

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24
Q

Tricyclic antidepressants

A

Reduce reuptake of monoamines

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25
Q

Selective monoamine reuptake inhibitors

A

reduced selective reuptake of 5-HT, NE

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26
Q

How do antidepressants work?

A

Treatment –> increase monoamines –> 2-4 weeks later effects start happening (not sure the mechanisms, not sure how, we got theories)

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27
Q

Depression does ____ to BDNF and friends?

A

Lower BDNF

Raise Glucocorticoid levels

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28
Q

Antidepressants do what to BDNF?

A

Increase BDNF and 5-HT and NE

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29
Q

What does BDNF do?

A

Stimulates dendrite growth

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30
Q

How do antidepressants stimulate dendrite growth?

A

Increase adenylyl cyclase and cAMP

Then increase pKa, pCREB, and BDNF

Results in Dendritic Sprouting, Neurogenesis, Neuronal Remodeling

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31
Q

BDNF binds to

A

Trk B for proliferation, survival, plasticity, hippocampal function

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32
Q

Antidepressants in the rat hippocampus and BDNF

A

5-10 mg/kg amitriptyline/venlafaxine for 21 days

They increase BDNF in rat hippocampus

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33
Q

BDNF:
____ acetylation
____ methylation

A

increase acetylation
decreases methylation

reduces deacetylation

If you inhibit BDNF, get methylation (gene silencing)

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34
Q

Evidence of hippocampal atrophy and loss in MDD patients

A

Compared to controls, depression patients had smaller hippocampal volumes

Decreased hippocampal volume may be related to depression

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35
Q

PAPA test for depression reveals

A

Hippocampal Volume Linked to Severity of Depression and Maternal Support

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36
Q

Acute

A

achievement of REMISSION

6-12 weeks

(symptom free from illness)

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37
Q

Continuations

A

Prevention of RELAPSE

4-9 months

(no relapse = no return of depressive symptoms once remission occurs)

38
Q

Maintenance

A

Prevention of RECURRENCE

> 1 year

(another depressive episode after recovery has been attained)

39
Q

Response

A

improvement from the initial onset of your illness

40
Q

Remission

A

experience of being symptom free from illness

41
Q

Recovery

A

no symptoms for at least 4 months after onset of remission

42
Q

Relapse

A

full return of depressive symptoms once remission has occurred

43
Q

Recurrence

A

another depressive episode after recovery has been attained

44
Q

First line of treatment

A

SSRIs

45
Q

Treatments for affective disorders

A

Monoamine Oxidase Inhibitors (MAOI)
Tricyclic Antidepressants (TCA)
Selective Serotonin Reuptake Inhibitors (SSRIs)

Atypical Antidepressants
Ketamine

Psychotherapy

Electroconvulsive Therapy (ECT)

Trans-magnetic Stimulation (TMS)

46
Q

MAOI

A

first prescribed antidepressant (50’s)

Effective for atypical forms (overeat, oversleep, upset when criticized)

Inhibit degradation of NE and 5-HT

Risk of hypertensive crisis (food/drug interactions)
*risk reduce with newer MAOI’s selective for DA, but these have less effect

47
Q

MOIA: hypertensive crisis

A

Tyramine, an amino acid, found in food.

Acts like amphetamine. MAO breaks it down

MAOI: inhibits degradation of tyramine

Tyramine forces NE from axon terminals

Rapid increase in BP
Stroke or death possible

48
Q

MAOI-A

A

inhibit degradation of NE and serotonin

treats atypical depression

49
Q

MAOI-B

A

inhibits degradation of dopamine

treat’s Parkinson’s

high dose for treatment of depression

50
Q

Tricyclic Antidepressants (TCA)

A

used extensively prior to advent of SSRIs (50’s)

inhibit NE and 5-HT reuptake

side effects, risk of OD (confusion, mania, arrhythmia), some drug interactions with alcohol and MAOI

51
Q

Example of TCA?

A

Amitripyline (Elavil)
imipramine (tonfranil)

Know for 3 ring structure

52
Q

Side effects of TCA

A

Orthostatic hypotension; Dry mouth; Constipation; Blurred vision; Sedation or activation; Increased heart rate; Fatigue/weakness; Urinary hesitancy; Ataxia/Muscle tremors / twitches; Sexual impairment; Dizziness; Weight gain

53
Q

If antidepressants block [M] receptors, does it reduce heart rate?

A

NO

54
Q

Histamine receptor blocker

A

sedation

55
Q

[M] receptor blocker

A

dry mouth, blurred vision, constipation, increased heart rate, urinary retention

56
Q

Alpha 1 receptor block

A

postural hypotension

57
Q

Serotonin reuptake blocker

A

reduced libido, impotence, delayed ejaculation

58
Q

FDA approved use of antidepressants

A

Depressive disorders
Anxiety
Bulimia
(BAD)

59
Q

Off-label use of antidepressants

A

eating disorders, premenstrual dysphoric disorder, ADHD, substance abuse disorder, neuropathic pain

60
Q

SSRIs

A

Most popular treatment for depression and anxiety (1980’s)

inhibit reuptake of 5-HT primarily

fewer side-effects than MAOIs or TCAs

61
Q

Examples of SSRIs (inhibit serotonin reuptake)

A 
Sertraline (Zoloft)
Floxetine (Prozac)
Citalopram (Celexa)
Paroxetine (Paxil)
Escitralopram (Lexapro)
62
Q

SSRIs Side-effects

A

Nausea, Diarrhea, Insomnia, Somnolence, Dry mouth, Tremor, Anxiety, Sweating, Sexual Dysfunction, Weight gain

63
Q

Atypical Reuptake Inhibitors

A

1990’s fewer sexual side effects

Selective Reuptake Inhibitors of NE, 5-HT, DA

Fewer Side-effects than MAOIs or TCAs

64
Q

What is…
venlafaxine (Effexor)
duloxetine (Cymbalta)

A

SNRI

serotonin-norepinephrine

atypical reuptake inhibitor

65
Q

What is…

atomoxetine (Strattera)

A

NSRI

NE reuptake

atypical reuptake inhibitor

66
Q

What is…

Bupropion (Wellbutrin, Zyban)

A

DSRI

dopamine reuptake

atypical reuptake inhibitor

67
Q

Ketamine

A 
Anesthetic Agent
Analgesic agent
Psychedelic drug
Predatory drug
Antidepressant agent (2010's)
68
Q

What are the antidepressant effects of ketamine?

A

symptom relief within an hour after intravenous infusion

effect persists for up to a week, sometimes longer

effective in some treatment resistant patients

Limited # of clinical studies to date: long-term effects unknown

off-label at specialty clinics: approved intranasal

Mechanism: increase BDNF

69
Q

model of animal depression: Porsolt forced swim test

A

more immobility, more depression

ketamine exerts antidepressant effects, reducing immobility

70
Q

Ketamine: How does it work?

A

increases BDNF in mouse hippocampus

Blocks ion channels of NMDA receptors

BDNF translation, synaptic protein synthesis

Rapid acting, can be mere hours

71
Q

Animal models of depression tested by

A

swim test, and hung by tail

72
Q

Why ketamine > SSRIs?

A

increases BDNF levels faster (30 min)

BDNF down when depression reduced, but traditional SSRIs take a while.

73
Q

Ketamine and dendrite sprouts

A 
stress = spine loss
ketamine = dendrite growth
74
Q

Ketamine cellular effect

A

block ion channels NMDA recpetors, sometimes AMPA too

This results in BDNF translation and protein synthesis

75
Q

Hamilton depression rating scale:

A

higher # = depression

Just 1 ketamine infusion helps symptoms

76
Q

Ketamine- dissociative

A

not connected to body, no hallucinations, more cognitive “like getting drunk w/out eating”

77
Q

Antidepressant vs. placebo: help patients after 6-8 weeks

A

20+ patients above placebo

P: 20-40%
AD: 40-60%

78
Q

Antidepressant vs. placebo: relapse after 1-2 years

A

prevent relapse in 27 more patients

P: 50%
AD: 23%

79
Q

Metanalysis: combine and analyze results from individual studies

A

Placebo for non-severe, saves time and money

80
Q

Factors in experimental bias

A

selective reporting, placebo effects, Biased study samples (homeless), failure of subjects to complete study (drop out), short follow up

81
Q

Davis

A

merit in concern
but, 33-11% AD>P

Depression so serious, try all we got

82
Q

Kirsh

A

It’s all a placebo

83
Q

Kramer

A

Antidepressants are they best and cure everything

84
Q

Drug Over persceiption

A

Less expensive/time then psychotherapy

money for corporations

reduced risks/side effects

85
Q

Psychotherapy pros and cons

A

Pros: often as effective as pharmacotherapy, combinations works well

cons: time consuming, expensive (partial coverage/limited visits)

86
Q

Amick on antidepressants vs. CBT

A

no difference between 2nd gen. antidepressants and CBT

87
Q

Electroconvulsive therapy

A

Treatment for severest cases of depression

Must induce seizure to be effective

Muscle relaxant, anesthetic, respirator

Administration 3x per week for 3 weeks

Improves 90% of cases with delusional depressants

Anterograde and Retrograde Amnesia (Ach decrease)

Most effective treatment, but for people with very severe depression.

88
Q

Transcranial Magnetic stimulations (TMS)

A

40-minute treatment

Two small electromagnetic coils

Aimed at the left prefrontal cortex

Too weak for the patient to feel

Does not trigger seizure

Not a cure
Can’t do if you have facial tattoos with metallic ink

89
Q

Kirsch

A

placebo

90
Q

ioannidis

A

metaanalysis, only severe

91
Q

Insel

A

in the middle on the issue

92
Q

Kramer

A

antidepressants for everyone

Psychopharmacology (16 decks)

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