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M2 Psychiatry > 6. Anxiety, Depression, Mania PHARM > Flashcards

6. Anxiety, Depression, Mania PHARM Flashcards

1
Q

Big picture: drugs for depression target what kind of system?

A

monoamine neurotransmission

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2
Q

how long do antidepressants take to exert their effects?

A

6-8 weeks

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3
Q

in what % of pts are antidepressants effective?

A

only 60-70%

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4
Q

what is a monoamine?

A

close relative of ammonia (NH3), only one of the H ias been replaced by a different group

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5
Q

what are the 3 endogenous monoamines?

A

serotonin, norepi, dopamine

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6
Q

are depressed people actually deficient in monoamines?

A

it was originally thought that they were, but it turns out that they are not.

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7
Q

what is the current leading theory about why giving monoamines works for depression?

A

that they change brain structure and neural connectivity/neurogenesis.

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8
Q

what are some ways to structure the antidepressant meds?

A
  • by age (old/new depending on whether before or after prozac/Fluoxetine - 1986)
  • by structure (mono/secondary/tertiary amines)
  • by function (reuptake inhibitor, MAOI)
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9
Q

do we have more effective drugs now than we did in the 50s?

A

No more effective, possibly fewer side effects/less lethal w OD

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10
Q

why is there so much cross-reactivity with monoamines?

A

the receptors are all very similar. (histamine, muscarinic, adenosine, serotonin, dopamine….)

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11
Q

serotonin: should associate nerves that carry it with what anatomical structure?

A

raphe nucleus

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12
Q

serotonin is involved in what types of emotions?

A

fear, depression, anxiety, cognition, memory

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13
Q

pts on monoamines that target the serotonin system may have issues with what?

A

incr fear/anxiety, problems with memory

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14
Q

SSRI: prototypical drug?

A

citalopram

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15
Q

what are the side effects of SSRIs

A

GI issues, sexual interest, sleep problems, night sweats, hyponatremia, mania

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16
Q

SSRIs: black box warning is what?

A

can incr suicidal ideation in teens to 25 yrs. but doesn’t increase actual suicide completion. better to give SSRI than to let depr go unchecked.

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17
Q

Citalopram: interactions?

A

weak 2D6, MAOI, TCA, NSAIDS, thioridazine

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18
Q

Citalopram: heart effects?

A

QT prolongation. may not be enough to be a problem, but if pt is borderline anyway may be problem. can cause Torsades arrythmia.

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19
Q

citalopram: give to possibly bipolar pt?

A

no, can induce mania

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20
Q

which SSRIs cause QT prolongation? (2)

A

citalopram, escitalopram.

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21
Q

Excitalopram: what kind of drug?

A

SSRI

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22
Q

fluoxetine: what kind of drug

A

SSRI

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23
Q

paroxetine: what kind of drug?

A

SSRI

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24
Q

fluvoxamine: what kind of drug?

A

SSRI

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25
Q

chlomipramine: what kind of drug?

A

TCA, but works only on serotonin.

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26
Q

SNRI: what do they do?

A

same as SSRI but for norepi.

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27
Q

Norepinephrine-containing neurons are predominantly in what anatomical struct

A

locus coeruleus

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28
Q

compared to serotonin, how does NE affect the amygdala? hippocampus?

A

less affect on amygdala, less on hippocampus??

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29
Q

what is the prototypical SNRI

A

venlafaxine

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30
Q

venlafaxine: side effects?

A

GI, sexual, sleep, sweating, hyponatremia, mania

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31
Q

venlafaxine: black box?

A

yes, suicidal ideation up to 25 yrs

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32
Q

venlafaxine: interactions?

A

weak 2D6, MAOI, TCA, NSAIDS

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33
Q

venlafaxine: only antidepressant that will affect what?

A

BP (elevate diastolic by 8 mmHg)

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34
Q

venlafaxine: what are the discontinuation sx’s?

A

worse for discontinuation than other abtidepressants. bad headache, double vision, can yield ER visit even if miss for 2 days.

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35
Q

desvenlafaxine: what category?

A

SNRI

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36
Q

duloxetine: what category?

A

SNRI

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37
Q

nortryptiline: what category?

A

TCA/SNRI

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38
Q

with tertiary amines, is cross reactivity higher or lower than that of monoamines?

A

higher

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39
Q

imipramine: what kind of drug?

A

tertiary amine (TCA/SNRI)

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40
Q

amitryptyline: what kind of drug?

A

tertiary amine (TCA/SNRI)

41
Q

desipramine: what kind of drug?

A

tertiary amine (TCA/SNRI)

42
Q

imipramine, when metabolized, becomes what in the body?

A

part tertiary amine, part secondary amine.

43
Q

what was the first antidepressant?

A

imipramine

44
Q

how do secondary amines compare to tertiary amines?

A

fewer side effects, also different predominant action. tertiary amine tends to block serotonin reuptake, but secondary amine tends to block NE reuptake more.

45
Q

what is the prototypical TCA?

A

nortriptyline

46
Q

nortriptyline: side effects

A

weight gain, sedation, hypotension, arrythmia, sexual, sweating

47
Q

nortriptyline: interactions

A

MAOI, tramadol, 2D6, cimetidine

48
Q

nortriptyline: lethality how?

A

if OD, blocks cardiac Na channels and is a Class 1a antiarrythmic. lethal dose is only about 20 pills.

49
Q

nortriptyline: how does the lethality factor into decision about prescribing?

A

don’t want to prescribe to a very depressed person who may OD. or give only a week at a time perhaps.

50
Q

what is the protorypical dopamine reuptake inhibitor (NDRI)?

A

bupropion

51
Q

NDRI stands for what

A

norepinephrine-dopamine reuptake inhibitor

52
Q

bupropion has what structure

A

monoamine

53
Q

why can buproprion be taken for ADD?

A

works a little like amphetamines: works in the ventral tegmental area. projects to frontal lobe. improves exec function, focus.

54
Q

bupropion: side effects

A

insomnia, tremors, risk of seizures. Can get jittery. Can help with energy, cognitive sharpness. Doesn’t tend to cause sexual side effects, weight gain.

55
Q

bupropion: why avoid giving with eating disorders?

A

both decr the threshold level for seizure activity.

56
Q

for a patient who could potentially become manic, what would be the best antidepressant?

A

bupropion: least likely to cause mania.

57
Q

how do MAOIs work?

A

knock out MAO, which destroys the monoamine in the presynaptic terminal. (same for serotonin, norei, dopamine). thereby increases amt of avail monoamine.

58
Q

what’s a washout period?

A

need to take about 2 wks between antidepressant classes to avoid interaction. can be lethal.

59
Q

what are the 2 MAOIs we should know?

A

phenelzine, tranylcypromine

60
Q

Phenelzine: developed as what kind of drug? tends to have what effect on energy

A

TB, tends to be sedating.

61
Q

tranylcypromine: developed as what kind of drug? tends to have what effect on energy

A

dev as amphetamine, tends to be stimulating.

62
Q

why are MAOIs not used as much as other antidepressants?

A

risk of serotonin syndrome and hypertensive crisis from high amounts of monoamines in your body.

63
Q

what is serotonin syndrome?

A

fever, muscle jerks, confusion, arrythmias

64
Q

how would MAOIs cause hypertensive crisis?

A

eat tyramine (cheese, pickles, etc) while on an MAOI -> too much monoamine -> metabolized into norepi and dopamine -> HTN

65
Q

what do patients have to do who are on MAOIs?

A

follow a low tyrosine diet

66
Q

with MAOIs, what do you need to NOT prescribe?

A

SSRIs, SNRIs, TCAs, tramadol, meperidine, dextromethorphan, amphetamines

67
Q

Mirtazapine: mechanism?

A

blocks presynaptic alpha2 receptors, NaSSA – noradrenergic and specific serotonergic antidepressant
(basically SSRI and SNRI)

68
Q

nefazodone: mechanism?

A

SARI. dual reuptake inhibitor but different mech from others

69
Q

trazodone: mechanism?

A

SARI. dual reuptake inhibitor but different mech from others

70
Q

Mirtazapine: side effects

A

sedating! weight gain! but low sexual side effects

71
Q

Benzodiazepines: what are they used for?

A

anti anxiety

72
Q

where to benzos exert their action? (receptor)

A

GABA

73
Q

benzos: class leader?

A

diazepam

74
Q

though benzos are mostly anti-anxiety, what other effects do they have?

A

sedative
seizure control
muscle relaxant
anterograde amnesia (basically forget unpleasant experiences)

75
Q

GABA is the most abundant inh or excit receptor in the brain?

A

inh.

76
Q

describe the general structure of a GABA receptor. which ones to benzos work on?

A

GABA receptors like lego pieces: each receptor can be a different combination of different subunits. Benzos only work on those that have alpha1, alpha2, alpha 3 and alpha5. which is about 30% of the brain.

77
Q

does the benzo have a direct effect on the receptor?

A

Benzo binding doesn’t do anything. It sensitizes the receptor so that when endogenous GABA binds, it binds more frequently and for longer. Positive Allosteric Modulator

78
Q

what ion flows through the GABA receptor?

A

Cl-

79
Q

what is the effect of increase GABA receptor permeability to Cl-?

A

drives down the resting membrane potential. (hyperpolarizes). Takes a lot more input to fire the neuron. So less anxiety because you’re firing the neuron less freq. seizure benefit.

80
Q

diazepam: half life?

A

LONG, 20-50 h

81
Q

diazepam: side effects

A

sedation, depression, amnesia, ataxia, dependence, withdrawal

82
Q

diazepam: interactions

A

CNS depressants, cimetidine

83
Q

diazepam: where cleared?

A

hepatic (liver)

84
Q

diazepam: what reverses its effects?

A

flumazenil, by driving resting potential back up.

85
Q

diazepam: metabolites?

A

there are active metabolites that also have long half-lives, which can last for days.

86
Q

diazepam: problem with cirrohosis

A

hepatically cleared, so if liver damage, metabolites will build up.

87
Q

chlordiazepoxide: what category?

A

benzodiazepine/GABA (anti anxiety)

88
Q

clonazepam: what category?

A

benzodiazepine/GABA (anti anxiety)

89
Q

lorazepam: what category?

A

benzodiazepine/GABA (anti anxiety)

90
Q

alprazolam: what category?

A

benzodiazepine/GABA (anti anxiety)

91
Q

what benzodiazepine is the only one that is renally cleard?

A

lorazepam

92
Q

which benzodiazepine has the shortest half life?

A

alprazolam. have to take several times a day. psychiatrists don’t like. psychologically reinforcing.

93
Q

which benzodiazepine is the most addictive?

A

alprazolam.

94
Q

what is zolpidem?

A

GABA α1-selective BZD agonist

95
Q

what is the result of zolpidem’s affinity for GABA a1 receptors?

A

Only work on receptors that have GABA alpha1 subunits. Good for inducing sleep, don’t do anything for muscle relaxation, seizures, don’t help with anxiety. Sleep and memory. Problems with amibien: can sleepwalk, sleep-eat.

96
Q

busprione: what does it do?

A

5Ht-1a partial agonist, given for generalized anxiety disorder and augmentation treatment for major depressive disorder

97
Q

busprione: side effects

A

dizziness, headache, sedation, restlessness. No sexual SE, No dependence, No withdrawal

98
Q

busprione: interactions?

A

MAOI

99
Q

busprione: how long to work?

A

4+ weeks

M2 Psychiatry (24 decks)

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