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Psychopharmacology > Final: Antidepressants > Flashcards

Final: Antidepressants Flashcards

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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
Selective monoamine reuptake inhibitors
reduced selective reuptake of 5-HT, NE
26
How do antidepressants work?
Treatment --> increase monoamines --> 2-4 weeks later effects start happening (not sure the mechanisms, not sure how, we got theories)
27
Depression does ____ to BDNF and friends?
Lower BDNF | Raise Glucocorticoid levels
28
Antidepressants do what to BDNF?
Increase BDNF and 5-HT and NE
29
What does BDNF do?
Stimulates dendrite growth
30
How do antidepressants stimulate dendrite growth?
Increase adenylyl cyclase and cAMP Then increase pKa, pCREB, and BDNF Results in Dendritic Sprouting, Neurogenesis, Neuronal Remodeling
31
BDNF binds to
Trk B for proliferation, survival, plasticity, hippocampal function
32
Antidepressants in the rat hippocampus and BDNF
5-10 mg/kg amitriptyline/venlafaxine for 21 days They increase BDNF in rat hippocampus
33
BDNF: ____ acetylation ____ methylation
increase acetylation decreases methylation reduces deacetylation If you inhibit BDNF, get methylation (gene silencing)
34
Evidence of hippocampal atrophy and loss in MDD patients
Compared to controls, depression patients had smaller hippocampal volumes Decreased hippocampal volume may be related to depression
35
PAPA test for depression reveals
Hippocampal Volume Linked to Severity of Depression and Maternal Support
36
Acute
achievement of REMISSION 6-12 weeks (symptom free from illness)
37
Continuations
Prevention of RELAPSE 4-9 months (no relapse = no return of depressive symptoms once remission occurs)
38
Maintenance
Prevention of RECURRENCE >1 year (another depressive episode after recovery has been attained)
39
Response
improvement from the initial onset of your illness
40
Remission
experience of being symptom free from illness
41
Recovery
no symptoms for at least 4 months after onset of remission
42
Relapse
full return of depressive symptoms once remission has occurred
43
Recurrence
another depressive episode after recovery has been attained
44
First line of treatment
SSRIs
45
Treatments for affective disorders
Monoamine Oxidase Inhibitors (MAOI) Tricyclic Antidepressants (TCA) Selective Serotonin Reuptake Inhibitors (SSRIs) Atypical Antidepressants Ketamine Psychotherapy Electroconvulsive Therapy (ECT) Trans-magnetic Stimulation (TMS)
46
MAOI
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
MOIA: hypertensive crisis
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
MAOI-A
inhibit degradation of NE and serotonin treats atypical depression
49
MAOI-B
inhibits degradation of dopamine treat's Parkinson's high dose for treatment of depression
50
Tricyclic Antidepressants (TCA)
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
Example of TCA?
Amitripyline (Elavil) imipramine (tonfranil) Know for 3 ring structure
52
Side effects of TCA
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
If antidepressants block [M] receptors, does it reduce heart rate?
NO
54
Histamine receptor blocker
sedation
55
[M] receptor blocker
dry mouth, blurred vision, constipation, increased heart rate, urinary retention
56
Alpha 1 receptor block
postural hypotension
57
Serotonin reuptake blocker
reduced libido, impotence, delayed ejaculation
58
FDA approved use of antidepressants
Depressive disorders Anxiety Bulimia (BAD)
59
Off-label use of antidepressants
eating disorders, premenstrual dysphoric disorder, ADHD, substance abuse disorder, neuropathic pain
60
SSRIs
Most popular treatment for depression and anxiety (1980's) inhibit reuptake of 5-HT primarily fewer side-effects than MAOIs or TCAs
61
Examples of SSRIs (inhibit serotonin reuptake)
``` Sertraline (Zoloft) Floxetine (Prozac) Citalopram (Celexa) Paroxetine (Paxil) Escitralopram (Lexapro) ```
62
SSRIs Side-effects
Nausea, Diarrhea, Insomnia, Somnolence, Dry mouth, Tremor, Anxiety, Sweating, Sexual Dysfunction, Weight gain
63
Atypical Reuptake Inhibitors
1990's fewer sexual side effects Selective Reuptake Inhibitors of NE, 5-HT, DA Fewer Side-effects than MAOIs or TCAs
64
What is... venlafaxine (Effexor) duloxetine (Cymbalta)
SNRI serotonin-norepinephrine atypical reuptake inhibitor
65
What is... atomoxetine (Strattera)
NSRI NE reuptake atypical reuptake inhibitor
66
What is... Bupropion (Wellbutrin, Zyban)
DSRI dopamine reuptake atypical reuptake inhibitor
67
Ketamine
``` Anesthetic Agent Analgesic agent Psychedelic drug Predatory drug Antidepressant agent (2010's) ```
68
What are the antidepressant effects of ketamine?
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
model of animal depression: Porsolt forced swim test
more immobility, more depression ketamine exerts antidepressant effects, reducing immobility
70
Ketamine: How does it work?
increases BDNF in mouse hippocampus Blocks ion channels of NMDA receptors BDNF translation, synaptic protein synthesis Rapid acting, can be mere hours
71
Animal models of depression tested by
swim test, and hung by tail
72
Why ketamine > SSRIs?
increases BDNF levels faster (30 min) BDNF down when depression reduced, but traditional SSRIs take a while.
73
Ketamine and dendrite sprouts
``` stress = spine loss ketamine = dendrite growth ```
74
Ketamine cellular effect
block ion channels NMDA recpetors, sometimes AMPA too This results in BDNF translation and protein synthesis
75
Hamilton depression rating scale:
higher # = depression | Just 1 ketamine infusion helps symptoms
76
Ketamine- dissociative
not connected to body, no hallucinations, more cognitive "like getting drunk w/out eating"
77
Antidepressant vs. placebo: help patients after 6-8 weeks
20+ patients above placebo P: 20-40% AD: 40-60%
78
Antidepressant vs. placebo: relapse after 1-2 years
prevent relapse in 27 more patients P: 50% AD: 23%
79
Metanalysis: combine and analyze results from individual studies
Placebo for non-severe, saves time and money
80
Factors in experimental bias
selective reporting, placebo effects, Biased study samples (homeless), failure of subjects to complete study (drop out), short follow up
81
Davis
merit in concern but, 33-11% AD>P Depression so serious, try all we got
82
Kirsh
It's all a placebo
83
Kramer
Antidepressants are they best and cure everything
84
Drug Over persceiption
Less expensive/time then psychotherapy money for corporations reduced risks/side effects
85
Psychotherapy pros and cons
Pros: often as effective as pharmacotherapy, combinations works well cons: time consuming, expensive (partial coverage/limited visits)
86
Amick on antidepressants vs. CBT
no difference between 2nd gen. antidepressants and CBT
87
Electroconvulsive therapy
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
Transcranial Magnetic stimulations (TMS)
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
Kirsch
placebo
90
ioannidis
metaanalysis, only severe
91
Insel
in the middle on the issue
92
Kramer
antidepressants for everyone

Psychopharmacology (16 decks)

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