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Gibbs Mood Flashcards

1
Q

definition of clinical depression

A

persistent sadness that interferes with normal functioning; loss of interest, low self-esteem

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2
Q

what is reactive sadness

A

a transient emotional reaction to a minor event

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3
Q

depressive symptoms

A

SIG E CAPS
sleep patterns
interests gone
guilt
energy/fatigue
concentration/memory problems
appetite (inc or dec)
psychomotor changes: agitation
suicidal thoughts

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4
Q

how common is depression?

A

over 20% of women and 12% of men will suffer a major depressive episode in their lifetime

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5
Q

what are some risk factors for depression?

A

female (esp adolescence, postpartum, older)
prior depressive episodes
medical comorbidity
SUD
lack of social support
stress

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6
Q

DSM-V criteria for a major depressive episode

A

must have 5+ symptoms in 2 week period
must include depressed mood/anhedonia
must represent change from previous functioning
cause social or occupational impairment
not due to other cause

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7
Q

treatment phases of depression

A

acute, continuation, maintenance

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8
Q

what are the 5 Rs

A

response, remission, relapse, recovery, recurrence

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9
Q

goals of acute phase

A

reduce/eliminate symptoms (6-8 weeks)

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10
Q

goals of continuation phase

A

prevent relapse or return of symptoms (6-12 months)

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11
Q

goals of maintenance phase

A

protect susceptible patients against recurrence of future depressive episodes (potential for lifelong treatment)

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12
Q

(3) theories about the pathophysiology of depression

A

monoamine hypothesis
dysregulation hypothesis
neuroendocrine hypothesis

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13
Q

what is the monoamine hypothesis

A

decreased synaptic concentrations of monoamines results in depression

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14
Q

what is the dysregulation hypothesis

A

dysregulation of neurotransmitter release results in changes in pre and post synaptic receptors results in depression

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15
Q

what is the neuroendocrine hypothesis

A

dysregulation of thyroid and HPA axis results in depression

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16
Q

what is the role of stress in depression?

A

depressed patients have increased cortisol, CRH, ACTH, abnormal circadian rhythm of cortisol, failure to respond to dexamethasone challenge

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17
Q

what is the significance of thyroid hormone and depression?

A

when the thyroid gland doesn’t produce enough thyroid hormone (hypothyroidism) the body uses energy at a SLOWER pace. symptoms: fatigue, irritability, weight changes, sleep problems

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18
Q

GENERAL mechanisms of antidepressants

A

block the reuptake of NE, 5HT, and DA into nerve terminals (reuptake inhibitors)
block the metabolism of NE and 5HT in nerve terminals (MAOIs)

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19
Q

(4) general characteristics of antidepressant pharmacology

A

1) selective alleviation of depressive symptoms instead of CNS stimulant
2) neurotransmitter levels increase soon after administration, but symptom resolution is slow
3) stopping suddenly results in rapid return of symptoms
4) do not work for every9one! 30% are non-responders

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20
Q

therapeutic effects seen by week 1 of antidepressant

A

sleep, appetite, energy, anxiety

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21
Q

therapeutic effects seen by week 1-3 of antidepressant

A

activity, drive, concentration, memoryt

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22
Q

therapeutic effects seen by week 4-6 of antidepressant

A

mood, hopelessness

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23
Q

what is considered an adequate trial of an antidepressant

A

6-8 weeks

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24
Q

list of (6) antidepressant classes

A

TCA
MAOI
SSRI
SNRI
NDRI
5HT/NE modulators

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25
the first antidepressant agent selected is effective __% of the time
50
26
disadvantages of TCAs?
toxic in overdose ADEs bad: orthostatic hypotension, tachycardia, EEG changes, anticholinergic, seizure threshold lowered, weight gain
27
are TCAs stimulants?
no, they do not produce euphoria in healthy people
28
__% of patients on TCAs improve
70%
29
TCA drugs
imipramine amoxapine desipramine amitriptyline nortriptyline doxepin clomipramine protriptyline trimipramine
30
mechanism of TCAs
-block reuptake of monoamines (NE, 5HT) -increase neurotransmitter levels in synaptic cleft -bind to histamine, alpha 1 & 2, GABA-A, muscarinic receptors (side effects)
31
TCA dosing? (generally speaking)
once daily dosing at bedtime (sedation) because good oral absorption, long half life
32
TCA is inactivated by ____ metabolism
hepatic
33
why are TCAs not first line?
anticholinergic, cardiac side effects (because of blockade of other receptors)
34
MAOI mechanism
increase neurotransmission by increasing NE, 5HT, DA levels in nerve terminal inhibition of MAO is irreversible
35
non selective MAOIs
phenelzine, tranylcypromine, isocarboxazid
36
selective MAOIS
SELEGILINE selective for MAO-B
37
why does selegiline have reduced dietary restrictions
because it is more selective for MAO-B; avoids inhibition of MAO-A
38
which MAOI has a transdermal patch
selegiline (EmSam)
39
serious food interaction with MAOIs
they inactivate biogenic amines present in food (tyramine-- aged cheese/cured meats, wine) and drugs (decongestants in OTC cold remedies)
40
what happens with failure to avoid tyramine with MAOIs?
hypertensive crisis must avoid (except not necessary with EmSam)
41
most common side effects of MAOIs
orthostatic hypotension insomnia serotonin syndrome (overdose, combo w/ SSRI) dry mouth, constipation, blurred vision, etc
42
what is serotonin syndrome
a potential fatal drug interaction resulting in over-potentiation of serotonin effects that causes GI, CNS, CV, and psych symptoms
43
what drugs are the SSRIs
fluoxetine paroxetine sertraline fluvoxamine citalopram escitalopram
44
which SSRI is most selective
citalopram
45
escitalopram is the ____ of citalopram
active S-enantiomer
46
what is the first line antidepressant for most patients
SSRIs (as effective as TCA but safer side effect profile)
47
common SSRI side effects
GI disturbances, CNS excitation (insomnia, restlessness-- except paroxetine which causes sedation), weight loss early on, weight gain later on, decreased libido/sexual dysfunction
48
what is SSRI discontinuation syndrome
a withdrawal syndrome consisting of flu-like symptoms, GI effects, dizziness, paresthesia, mood/appetite, sleep changes
49
how to mitigate SSRI discontinuation syndrome
gradually taper dose over several weeks
50
which drug is NDRI
bupropion
51
which drugs are SNRIs
venlafaxine duloxetine desvenlafaxine
52
which drugs are 5HT/NE modulators
trazodone nefazodone mirtazipine
53
mechanism of bupropion
norepinephrine/dopamine reuptake inhibition weak blocker of DA uptake, even weaker blocker of NE uptake, virtually no effect on 5HT
54
bupropion is also used for?
ADHD, smoking cessation
55
bupropion side effects
generally well tolerated nausea, restless, insomnia, anxiety high risk of seizure activity at 450 mg/day may precipitate psychotic episodes
56
why is there lower incidence of sedation, hypotension, etc with bupropion
no muscarinic, alpha, or histaminic receptor effects
57
SARIs
trazodone, nefazodone serotonin antagonist and reuptake inhibitors 5HT2 antagonist and 5HT reuptake blocker
58
trazodone place in therapy
very sedating, useful for patients with insomnia but not highly effective as antidepressant
59
NSSA
mirtazapine noradrenergic & specific serotoninergic antidepressant
60
mirtazapine mechanism
serotonin & NE modulator blocks alpha2 autoreceptors resulting in increased NA release antagonizes 5HT2 receptor enhances activity at 5HT1 receptor blocks H1 and muscarinic receptors
61
mirtazapine side effects
sedation (histamine blockade) increased appetite, weight gain
62
why does antagonism of 5HT2 receptors treat depression?
5HT2 receptors are excitatory increase in 5HT2 receptor expression increases depression decreasing 5HT2 receptor expression decreases depression
63
what is the role of 5HT1 receptors in depression?
5HT1 are presynaptic inhibitory autoreceptors-- meaning they reduce 5HT release from serotonergic neurons (work against SSRIs) sustained activation: results in DESENSITIZATION so that effect decreases over time and this is why SSRIs take weeks to become fully effective
64
strategies for treatment resistant depression
non pharm like ECT, light therapy, etc pharm: lithium, thyroid supplement, stimulants, atypical antipsychotics, anticonvulsants, esketamine
65
ketamine mechanism
non-competitive NMDA receptor antagonist most commonly used anesthetic in the world
66
esketamine role in treatment resistant depression
S(+) enantiomer of ketamine FDA approved for treatment resistant depression, breakthrough therapy also acts as partial DA reuptake inhibitor
67
which atypical antipsychotics have FDA approval as adjunctive treatment for MDD in combo w/ current antidepressant therapy
aripiprazole, quetiapine

neurology/psychiatry (22 decks)

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