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neurology/psychiatry > Gibbs Mood > Flashcards

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
Q

the first antidepressant agent selected is effective __% of the time

A

50

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26
Q

disadvantages of TCAs?

A

toxic in overdose
ADEs bad: orthostatic hypotension, tachycardia, EEG changes, anticholinergic, seizure threshold lowered, weight gain

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27
Q

are TCAs stimulants?

A

no, they do not produce euphoria in healthy people

28
Q

__% of patients on TCAs improve

A

70%

29
Q

TCA drugs

A

imipramine
amoxapine
desipramine
amitriptyline
nortriptyline
doxepin
clomipramine
protriptyline
trimipramine

30
Q

mechanism of TCAs

A

-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
Q

TCA dosing? (generally speaking)

A

once daily dosing at bedtime (sedation)
because good oral absorption, long half life

32
Q

TCA is inactivated by ____ metabolism

A

hepatic

33
Q

why are TCAs not first line?

A

anticholinergic, cardiac side effects (because of blockade of other receptors)

34
Q

MAOI mechanism

A

increase neurotransmission by increasing NE, 5HT, DA levels in nerve terminal
inhibition of MAO is irreversible

35
Q

non selective MAOIs

A

phenelzine, tranylcypromine, isocarboxazid

36
Q

selective MAOIS

A

SELEGILINE
selective for MAO-B

37
Q

why does selegiline have reduced dietary restrictions

A

because it is more selective for MAO-B; avoids inhibition of MAO-A

38
Q

which MAOI has a transdermal patch

A

selegiline (EmSam)

39
Q

serious food interaction with MAOIs

A

they inactivate biogenic amines present in food (tyramine– aged cheese/cured meats, wine) and drugs (decongestants in OTC cold remedies)

40
Q

what happens with failure to avoid tyramine with MAOIs?

A

hypertensive crisis
must avoid (except not necessary with EmSam)

41
Q

most common side effects of MAOIs

A

orthostatic hypotension
insomnia
serotonin syndrome (overdose, combo w/ SSRI)
dry mouth, constipation, blurred vision, etc

42
Q

what is serotonin syndrome

A

a potential fatal drug interaction resulting in over-potentiation of serotonin effects that causes GI, CNS, CV, and psych symptoms

43
Q

what drugs are the SSRIs

A

fluoxetine
paroxetine
sertraline
fluvoxamine
citalopram
escitalopram

44
Q

which SSRI is most selective

A

citalopram

45
Q

escitalopram is the ____ of citalopram

A

active S-enantiomer

46
Q

what is the first line antidepressant for most patients

A

SSRIs (as effective as TCA but safer side effect profile)

47
Q

common SSRI side effects

A

GI disturbances, CNS excitation (insomnia, restlessness– except paroxetine which causes sedation), weight loss early on, weight gain later on, decreased libido/sexual dysfunction

48
Q

what is SSRI discontinuation syndrome

A

a withdrawal syndrome consisting of flu-like symptoms, GI effects, dizziness, paresthesia, mood/appetite, sleep changes

49
Q

how to mitigate SSRI discontinuation syndrome

A

gradually taper dose over several weeks

50
Q

which drug is NDRI

A

bupropion

51
Q

which drugs are SNRIs

A

venlafaxine
duloxetine
desvenlafaxine

52
Q

which drugs are 5HT/NE modulators

A

trazodone
nefazodone
mirtazipine

53
Q

mechanism of bupropion

A

norepinephrine/dopamine reuptake inhibition
weak blocker of DA uptake, even weaker blocker of NE uptake, virtually no effect on 5HT

54
Q

bupropion is also used for?

A

ADHD, smoking cessation

55
Q

bupropion side effects

A

generally well tolerated
nausea, restless, insomnia, anxiety
high risk of seizure activity at 450 mg/day
may precipitate psychotic episodes

56
Q

why is there lower incidence of sedation, hypotension, etc with bupropion

A

no muscarinic, alpha, or histaminic receptor effects

57
Q

SARIs

A

trazodone, nefazodone
serotonin antagonist and reuptake inhibitors
5HT2 antagonist and 5HT reuptake blocker

58
Q

trazodone place in therapy

A

very sedating, useful for patients with insomnia but not highly effective as antidepressant

59
Q

NSSA

A

mirtazapine
noradrenergic & specific serotoninergic antidepressant

60
Q

mirtazapine mechanism

A

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
Q

mirtazapine side effects

A

sedation (histamine blockade)
increased appetite, weight gain

62
Q

why does antagonism of 5HT2 receptors treat depression?

A

5HT2 receptors are excitatory
increase in 5HT2 receptor expression increases depression
decreasing 5HT2 receptor expression decreases depression

63
Q

what is the role of 5HT1 receptors in depression?

A

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
Q

strategies for treatment resistant depression

A

non pharm like ECT, light therapy, etc
pharm: lithium, thyroid supplement, stimulants, atypical antipsychotics, anticonvulsants, esketamine

65
Q

ketamine mechanism

A

non-competitive NMDA receptor antagonist
most commonly used anesthetic in the world

66
Q

esketamine role in treatment resistant depression

A

S(+) enantiomer of ketamine
FDA approved for treatment resistant depression, breakthrough therapy
also acts as partial DA reuptake inhibitor

67
Q

which atypical antipsychotics have FDA approval as adjunctive treatment for MDD in combo w/ current antidepressant therapy

A

aripiprazole, quetiapine

neurology/psychiatry (22 decks)

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