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

6. Anxiety, Depression, Mania PHARM Flashcards

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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close relative of ammonia (NH3), only one of the H ias been replaced by a different group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
chlomipramine: what kind of drug?
TCA, but works only on serotonin.
26
SNRI: what do they do?
same as SSRI but for norepi.
27
Norepinephrine-containing neurons are predominantly in what anatomical struct
locus coeruleus
28
compared to serotonin, how does NE affect the amygdala? hippocampus?
less affect on amygdala, less on hippocampus??
29
what is the prototypical SNRI
venlafaxine
30
venlafaxine: side effects?
GI, sexual, sleep, sweating, hyponatremia, mania
31
venlafaxine: black box?
yes, suicidal ideation up to 25 yrs
32
venlafaxine: interactions?
weak 2D6, MAOI, TCA, NSAIDS
33
venlafaxine: only antidepressant that will affect what?
BP (elevate diastolic by 8 mmHg)
34
venlafaxine: what are the discontinuation sx's?
worse for discontinuation than other abtidepressants. bad headache, double vision, can yield ER visit even if miss for 2 days.
35
desvenlafaxine: what category?
SNRI
36
duloxetine: what category?
SNRI
37
nortryptiline: what category?
TCA/SNRI
38
with tertiary amines, is cross reactivity higher or lower than that of monoamines?
higher
39
imipramine: what kind of drug?
tertiary amine (TCA/SNRI)
40
amitryptyline: what kind of drug?
tertiary amine (TCA/SNRI)
41
desipramine: what kind of drug?
tertiary amine (TCA/SNRI)
42
imipramine, when metabolized, becomes what in the body?
part tertiary amine, part secondary amine.
43
what was the first antidepressant?
imipramine
44
how do secondary amines compare to tertiary amines?
fewer side effects, also different predominant action. tertiary amine tends to block serotonin reuptake, but secondary amine tends to block NE reuptake more.
45
what is the prototypical TCA?
nortriptyline
46
nortriptyline: side effects
weight gain, sedation, hypotension, arrythmia, sexual, sweating
47
nortriptyline: interactions
MAOI, tramadol, 2D6, cimetidine
48
nortriptyline: lethality how?
if OD, blocks cardiac Na channels and is a Class 1a antiarrythmic. lethal dose is only about 20 pills.
49
nortriptyline: how does the lethality factor into decision about prescribing?
don't want to prescribe to a very depressed person who may OD. or give only a week at a time perhaps.
50
what is the protorypical dopamine reuptake inhibitor (NDRI)?
bupropion
51
NDRI stands for what
norepinephrine-dopamine reuptake inhibitor
52
bupropion has what structure
monoamine
53
why can buproprion be taken for ADD?
works a little like amphetamines: works in the ventral tegmental area. projects to frontal lobe. improves exec function, focus.
54
bupropion: side effects
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
bupropion: why avoid giving with eating disorders?
both decr the threshold level for seizure activity.
56
for a patient who could potentially become manic, what would be the best antidepressant?
bupropion: least likely to cause mania.
57
how do MAOIs work?
knock out MAO, which destroys the monoamine in the presynaptic terminal. (same for serotonin, norei, dopamine). thereby increases amt of avail monoamine.
58
what's a washout period?
need to take about 2 wks between antidepressant classes to avoid interaction. can be lethal.
59
what are the 2 MAOIs we should know?
phenelzine, tranylcypromine
60
Phenelzine: developed as what kind of drug? tends to have what effect on energy
TB, tends to be sedating.
61
tranylcypromine: developed as what kind of drug? tends to have what effect on energy
dev as amphetamine, tends to be stimulating.
62
why are MAOIs not used as much as other antidepressants?
risk of serotonin syndrome and hypertensive crisis from high amounts of monoamines in your body.
63
what is serotonin syndrome?
fever, muscle jerks, confusion, arrythmias
64
how would MAOIs cause hypertensive crisis?
eat tyramine (cheese, pickles, etc) while on an MAOI -> too much monoamine -> metabolized into norepi and dopamine -> HTN
65
what do patients have to do who are on MAOIs?
follow a low tyrosine diet
66
with MAOIs, what do you need to NOT prescribe?
SSRIs, SNRIs, TCAs, tramadol, meperidine, dextromethorphan, amphetamines
67
Mirtazapine: mechanism?
blocks presynaptic alpha2 receptors, NaSSA – noradrenergic and specific serotonergic antidepressant (basically SSRI and SNRI)
68
nefazodone: mechanism?
SARI. dual reuptake inhibitor but different mech from others
69
trazodone: mechanism?
SARI. dual reuptake inhibitor but different mech from others
70
Mirtazapine: side effects
sedating! weight gain! but low sexual side effects
71
Benzodiazepines: what are they used for?
anti anxiety
72
where to benzos exert their action? (receptor)
GABA
73
benzos: class leader?
diazepam
74
though benzos are mostly anti-anxiety, what other effects do they have?
sedative seizure control muscle relaxant anterograde amnesia (basically forget unpleasant experiences)
75
GABA is the most abundant inh or excit receptor in the brain?
inh.
76
describe the general structure of a GABA receptor. which ones to benzos work on?
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
does the benzo have a direct effect on the receptor?
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
what ion flows through the GABA receptor?
Cl-
79
what is the effect of increase GABA receptor permeability to Cl-?
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
diazepam: half life?
LONG, 20-50 h
81
diazepam: side effects
sedation, depression, amnesia, ataxia, dependence, withdrawal
82
diazepam: interactions
CNS depressants, cimetidine
83
diazepam: where cleared?
hepatic (liver)
84
diazepam: what reverses its effects?
flumazenil, by driving resting potential back up.
85
diazepam: metabolites?
there are active metabolites that also have long half-lives, which can last for days.
86
diazepam: problem with cirrohosis
hepatically cleared, so if liver damage, metabolites will build up.
87
chlordiazepoxide: what category?
benzodiazepine/GABA (anti anxiety)
88
clonazepam: what category?
benzodiazepine/GABA (anti anxiety)
89
lorazepam: what category?
benzodiazepine/GABA (anti anxiety)
90
alprazolam: what category?
benzodiazepine/GABA (anti anxiety)
91
what benzodiazepine is the only one that is renally cleard?
lorazepam
92
which benzodiazepine has the shortest half life?
alprazolam. have to take several times a day. psychiatrists don't like. psychologically reinforcing.
93
which benzodiazepine is the most addictive?
alprazolam.
94
what is zolpidem?
GABA α1-selective BZD agonist
95
what is the result of zolpidem's affinity for GABA a1 receptors?
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
busprione: what does it do?
5Ht-1a partial agonist, given for generalized anxiety disorder and augmentation treatment for major depressive disorder
97
busprione: side effects
dizziness, headache, sedation, restlessness. No sexual SE, No dependence, No withdrawal
98
busprione: interactions?
MAOI
99
busprione: how long to work?
4+ weeks

M2 Psychiatry (24 decks)

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