Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > Depression/Anxiety > Flashcards

Depression/Anxiety Flashcards

1
Q

3 monoamines

A

dopamine
seratonin
norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

inhibitors of monoamine uptake: 4 examples

A

SSRI
SNRI
NDRI
TCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SSRI

A

selective serotonin reuptake inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SNRIs

A

serotonin and norepinpheinr reuptake inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NDRIs

A

norepinephrine and dopamine reuptake inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

TCA

A

tricyclic anti depressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MAOI stands for

A

monoamine oxidase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

NDRI example

A

duloxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

etiology of MDD: monoamine hypothesis

A

deficiency in the amount or function of 5HT/Serotonin, norepinephrine, and or dopamaine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

etiology of depression: neurotrophic hypothesis

A

deficiency in neurotrophic factors, especially BDNF (brain derived neurotrophic factor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

in depression or chronic stress, you’ll have a decrease in (2)

A

synapses

BDNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

increased dendritic arbors is associated with

A

increased bdnf

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

most proximal cause of depressive symptoms

A

neural apoptosis in hippocampus/pre frontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

stress mechanisms underlying neural apoptosis

A
  1. sustained high levels of cortisol which promotes neural apoptosis
  2. excessive glutamate levels which are high enough to be cytotoxic. leads to apoptosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what counteracts this neural apoptosis contributing to depressive symptoms?

A

monoamines and neurotrophic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

monoamines and their receptors counteract cytotoxic effects of stress. what do they promote?

A

genes which facilitate neurogenesis in hippocampus, producing an anti depressant response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

depression results in an imbalance of opposing signals.
too much _____ or _____
too little _____, _____, and or ______

A

too much glutamate or cortisol

or too little norepinephrine, serotonin, and or BDNF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

the way to counter depression is to reduce _______ or increase _______

A

reduce stress related signaling

increase monoamine NTs or BDNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

antidepressant strategy

A

increase synaptic concentrations of norepinephrine / serotonin in the hippocampus and prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

if an antidepressant strategy is increase synaptic concentrations of norepinephrine / serotonin in the hippocampus and prefrontal cortex, how can we go about doing that? (3)

A
  • inhibit reuptake of the monoamines once released from presynaptic neurons
  • prevent degradation of the monoamines once released
  • block pre synaptic forms of negative feedback regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

anti depressants may also work by mimicking the actions of

A

NE / serotonin and postsynaptic receptors (beta adrenergic or serotonin 1A receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

time course of response: anti depressants

A

initial response: 1-3 weeks

max response: 12 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

when can an anti depressant be considered failed?

A

after 1 month with no success

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

selecting an anti depressant is

A

patient specific. they’re nearly all the same efficacy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

early treatment management of the patient on anti depressant

A

assess for suicidal tendencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

SSRI drugs (6)

A 
fluoxetine
paroxetine
citalopram
escitalopram
sertraline
fluvoxamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

action of SSRI

A

selectively inhibiting the serotonin reuptake transporter SERT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

efficacy of SSRIs is attributed to

A

subsequent actions of elevated 5HT at 5HT1A receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

5HT 1A receptor activation

A

anti depressant response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

AEs of SSRIs are all serotonin mediated. They are (4)

A

nausea
agitation
insomnia
sexual dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AE of nausea from SSRI is due to which receptor activation

A

5HT3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

sexual dysfunction is due to activation of what receptor in SSRI use?

A

5HT2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

drug interactions with SSRIs can be due to

A

their inhibition of the metabolism of other drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

risk of overdose with SSRI is

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

SSRIs must not be combined with

A

MAOIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

SSRIs are potent inhibitors of

A

CYP 2D6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SSRIs inhibit which transporter

A

SERT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

which serotonin receptors are particularly problematic when stimulated re: adverse effects?

A

5HT2

5HT3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

which other SSRIs inhibit metabolism of other drugs the most?

A

fluoxetine

paroxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which SSRIs probduce active metabolites?

A

fluoxetine

sertraline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

stimulating 5HT14 in the wrong region of the brain

A

leads to undesired effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

by inhibiting CYP 1D6 AND 3A4, SSRIs can

A

increase plasma concentrations of many drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

which SSRI has the longest half life?

A

fluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

half life of fluoxetine’s metabolite’s half life?

A

3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

washout period

A

t1/2 of med’s active metabolites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

SSRIs have high Vd because

A

lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

SSRI with high protein binding, like fluoxetine, plus phenytoin

A

could cause phenytoin toxicity because they’d compete for protein binding and there would be more free phenytoin circulating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

anti depressant actions of SSRIs are similar in efficacy and time course to

A

TCAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

acute toxicity/cardiotoxicity in anti depressant use is seen more in/less in which drugs?

A

more often in MAO Is and TCAs

less often in SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

SSRI side effects

A

nausea
insomnia
sexual dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

sedation in antidepressants is seen more in/less in

A

more in TCAs

less in SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

SSRIs + MAOIs in comvination

A

risk for serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

serotonin syndrome s/s

A

tremor
hyperthermia
CV collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

paroxetine or fluoxetine in combination with TCAs

A

should not be combined.

these SSRIs inhibit CYP2D6 –> inc risk for TCA toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

which SSRIs are FDA approved for adolescents?

A

fluoxetine

escitalopram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

With regards to pregnancy, SSRIs are mainly

A

category C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

which SSRI do you want to avoid the most in pregnancy?

A

paroxetine - category D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

SSRIs may also treat (6)

A 
GAD
panic
social anxiety
OCD
premenstrual dysphoric syndrome
PTSD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

interactions between hydrocodone and fluoxetine or paroxetine

A

hydrocodone is a prodrug converted by CYP2D6 into hydromorphone, a much more potent opioid. fluoxetine or paroxetine will inhibit CYP2D6, which may decrease pain relief in those taking hydrocodone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

SNRIs (4)

A

duloxetine
venlafaxine
desvenlafaxine
milnacipran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

desvenlafaxine

A

active metabolite of venlafaxine, can be prescribed on its own

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

SNRIs inhibit which transporters?

A

SERT

NET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

the antidepressant effects of SNRIs are due to

A

activating 5HT1a receptors

activating beta adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

adverse effects of SNRIs are similar to SSRIs, plus

A

dose related elevation of bp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

risk of SSRI/SNRI overdose is

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

SNRIs cannot be used in combo with

A

MAOIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

why do you get elevated bp with SNRI?

A

activation of alpha adrenergic receptors in vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

SNRIs have a greater affinity for

A

SERT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Are SNRIs more efficacious than SSRIs or TCAs?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

inhibiting SERT and NET leads to

A

increases in serotonin and norepinephrine signaling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

bioavailability of SSRI and SNRIs

A

pretty good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

half life of SNRIs is ____ than SSRIs

A

shorter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

active metabolites / washout periods SNRIs

A

not a concern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

protein binding of SNRIs

A

varies between the drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

duloxetine protein binding as compared to other SNRIs

A

much higher, 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

if you’re concerned about drug:drug interactions but need to prescribe an anti depressant, what would be a good choice?

A

venlafaxine or milnacipran SNRIs because of low protein binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

SNRIs are mainly metabolized by _____ except for

A

CYP 2D6

except for desvenlafaxine

78
Q

metabolism of desvenlafaxine

A

phase II - conjugation

79
Q

SNRIs noradrenergic related adverse effects

A

inc bp
tachy
CNS activation

80
Q

like SSRIs, SNRIs may also be used to treat

A

anxiety disorders
fibromyalgia
neuropathic pain

81
Q

SNRIs are thought to help fibromyalgia and neurpathic pain, unlike SSRIs, because of

A

increased noradrenergic signaling

82
Q

TCA examples (5)

A 
amitryptaline
clomipramine
dose-in
imipramine
trimipramine
83
Q

why have TCAs fallen out of of favor (2)

A

not very well tolerated in regards to AE

risk for fatal cardiac arrhythmia with high doses

84
Q

TCA MoA

A

inhibit 5HT and NE uptake

85
Q

antidepressant effects of TCAs can be attributed to

A

effects on 5HT1a receptors and beta adrenergic receptors

86
Q

TCAs and active metabolites

A

they do have active metabolites that work at 5HT and norepinephrine receptors, but their affinity may defer. you can have varied response to TCAs depending on the active metabolites.

87
Q

why aren’t TCAs as well tolerated as SSRIs/SNRIs?

A

they affect additional receptors unrelated to therapeutic efficacy

88
Q

what other receptors do TCAs antagonize, unrelated to therapeutic efficacy? (3)

A

muscarinic acetylcholine receptors
histamine H1 receptors
alpha1 adrenergic receptors

89
Q

TCA half lives

A

long

90
Q

TCA washout periods

A

important to pay attention to bc they do have active metabolites with long half lives

91
Q

TCa protein binding

A

high

92
Q

TCA lipophilicity

A

high

93
Q

metabolite half lives of TCAs as compared to just the half life of TCAs

A

longer

94
Q

washout period of TCA

A

long because of active metabolite half lives

95
Q

TCAs are metabolized by

A

CYP 2D6

96
Q

poor metabolizers of CYP 2D6 can have a _ fold difference in plasma conch

A

30 fold difference

97
Q

what actions are warranted to avoid toxicity when a pt who is a PM of CYP2D6 is taking a TCA?

A

plasma level monitoring

dose reduction

98
Q

a`

A
99
Q

AEs of TCAs r/t to antagonism of muscarinic receptors (4)

A

dry mouth
blurred vision
constipation
urinary retention

100
Q

AEs of TCA r/t antagonism of H1 histamine receptors? (2)

A

sedation

weight gain

101
Q

A Es of TCAs r/t antagonism of alpha1 adrenergic receptors (1)

A

postural hypotension

102
Q

potentially fatal A E of TCAs, particularly in overdose?

A

ventricular dyshythmias

103
Q

therapeutic index of TCA

A

narrow

104
Q

TCAs are only prescribed in 1 week intervals, why?

A

because they may be used for suicide in OD

105
Q

drug interactions and TCAs

A

likely to cause adverse effects bc they rely on CYPs

106
Q

TCAs potentiate the effects of (2)

A

alcohol

anesthetic

107
Q

TCAs interfere with the actions of _____ and may require _____

A

anti hypertensive drugs

may require dose adjustments up, as TCAs can cause hypertension

108
Q

efficacy and time course of TCAs as compared to SSRI and SNRI

A

identical

109
Q

at the present time, TCAs are used if

A

depression is unresponsive to more commonly used agents like SSRIs or SNRIs

110
Q

TCAs and chronic or neuropathic pain

A

efficacy

111
Q

first choice for patient with depression and chronic pain and what is your next choice if they don’t respond to it?

A

1st - SNRI

2nd - TCA

112
Q

acute TCA overdose s/s (3)

A

confusion
mania
cardiac dysrhythmias

113
Q

TCAs are likely to interact with drugs which

A

are metabolized by, inhibit, or induce CYPs

114
Q

(3) things that TCAs will interact with

A

alcohol
anesthetics
MAOIs

115
Q

monoamine receptor antagonists (2)

A

mirtazapine

trazodone

116
Q

monoamine receptor antagonist MoA

A

mirtazapine antagonizes 5HT2c and 5HT3 receptors, while also blocking a2 adrenergic receptors

117
Q

mirtazapine differs in its anti depressant response because it blocks __&__ instead of activating _______.

A

blocks 5HT2c and 5HT3 instead of activating 5HT1a.

118
Q

how do monoamine receptor antagonists, like mirtazapine, work? (2)

A

activation of 5HT2c and 5HT3 is actually depressive, so blocking them is anti depressive.

they also block a2 adrenergic receptors on NE and 5HT terminals, increasing the amount of NE and 5HT available for release to synaptic cleft.

119
Q

what non therapeutic receptors do monoamine receptor antagonists also bind to and block, and what is the effect?

A

histamine h1 receptors, resulting in sedation.

120
Q

MAOI for depression are

A

no longer preferred

121
Q

how do MAOIs work

A

irreversibly bind to monoamine oxidase and inhibit it, preventing metabolism/breakdown of NE, 5HT, and DA in the brain.

122
Q

MAOI effectiveness as compared to TCAs and SSRIs/SNRIs

A

as effective but more hazardous

123
Q

MAOIs will be considered for depression if

A

a patient is treatment resistant

124
Q

MAOIs are irreversible inhibitors of

A

MAO A and MAO B

125
Q

MAOI dietary restrictions

A

need to restrict tyramine

risk for HTN crisis

126
Q

seizure risk and MAOIs/SSRIs/SNRIs

A

seizure threshold is lowered

127
Q

adverse effects of MAOIs

A

CNS stimulation

orthostatic hypotension

128
Q

if you eat tyramine rich foods on an MAOI

A

htn crisis

129
Q

why is tyramine so dangerous on an MAOI?

A

inhibiting MOA in the liver makes tyramine able to enter the systemic circulation. when tyramine hits NE containing terminals in the CNS, it causes a massive dump of NE. this increases sympathetic tone to the point of htn crisis and possibly death.

130
Q

atypical antidepressant example

A

buproprion

131
Q

MoA of buprioprion

A

binds to and inhibits NET and DAT, increasing NE and DA signaling.
also functions as a partial agonist of nicotinic Act receptors, underlying its efficacy for smoking cessation.

132
Q

bupropion is a derivative of

A

amphetiamine

133
Q

most notable adverse effect of buproprion

A

seizure

134
Q

choosing an antidepressant is based on (6)

A 
cost
availability
adverse effects
drug interactions
pt history of response
pt preference
135
Q

choosing an anti depressant for an individual with depression who is also having insomnia

A

choose mirtazapine bc of sedating effects

avoid SSRI bc of excitatory effects

136
Q

if a patient is depressed and experiencing extreme fatigue, what would be a good choice?

A

buproprion

137
Q

if a patient is experiencing depression and decrease in libido, which would be 2 better anti depressant choices?

A

bupropion (atypical)

mirtazipine (monoamine receptor antagonist)

138
Q

most commonly prescribed first line agent in MDD

A

SSRI

139
Q

second or third line choices are

A

TCAs

MAOIs

140
Q

non pharmacological approaches may be preferred to

A

MAOIs

141
Q

patient teaching for antidepressants

A

3-4 week lag time exists between initiation of therapy and measurable therapeutic response

142
Q

if a pt doesn’t respond to a given antidepressant after a 12 week trial, what is the reasonable next step?

A

stopping and switching to another antidepressant, but you have to be mindful of washout periods in this instance

143
Q

if a partial response is observed on an SSRI or SNRI,

A

other drugs can be added concomitantly

144
Q

what is a typical maintenance treatment phase of antidepressants?

A

6-12 months

145
Q

when is lifelong treatment advisable? (2)

A

if a patient has experienced 2-3 separate episodes of major depression
if a patient is chronically depressed

146
Q

why don’t we withdraw antidepressants once remission occurs?

A

because they’re still at risk for relapse. the 6-12 month maintenance is recommended. you want to avoid episodes of MD because they get more severe as they come and treatment resistance becomes more likely with each episode.

147
Q

the most safe anti depressants in pregnancy (3)

A

fluoxetine (SSRI)
citalopram (SSRI)
TCAs

148
Q

antidepressants and breastfeeding

A

benefits of breastfeeding outweigh the risks of infant antidepressant exposure

149
Q

blackbox warning for antidepressants in children and young adults

A

increased risk in suicidality

150
Q

patients on antidepressants should be monitored

A

at least twice a year to assess if the drug is still needed or if the dose needs adjustment

151
Q

withdrawing of antidepressants

A

needs to be a slow, supervised taper over months or longer to minimize withdrawal symptoms like rebound anxiety/depression

152
Q

early warning signs of relapse and what you should do

A

insomnia
avoiding social engagement

adjust or restart treatment

153
Q

for those who are treatment resistant, what are non pharm treatment options? (3)

A

vagus nerve stimulation
ECT
transcranial magnetic stimulation

154
Q

new generation of anti depressants being introduced in clinical practice

A

NMDA receptor antagonist (ketamine)

155
Q

how does ketamine work?

A

rapidly increases glutamate levels in the brain by blocking NMDA receptors on gaba terminals.

156
Q

when you block glutamate signaling on a gaba terminal,

A

you reduce gaba release at the synapse. this increases glutamate signaling at the synapse, resulting in an increase of glutamate and brain neurotrophic signaling. this is all anti depressant.

157
Q

doses of ketamine for anti depression

A

much lower than doses taken recreationally

158
Q

ketamine’s antidepressant effect is

A

rapid

159
Q

obstacles to using ketamine as an antidepressant

A

abuse liability

potential for dissociative effects

160
Q

esketamine

A

intranasal ketamine

first FDA approved fast acting antidepressant

161
Q

therapeutic onset of esketamine

A

hours

162
Q

prescribed doses of esketamine can produce

A 
sedation
inattention
dissociation
abuse potential
suicidal behaviors
163
Q

to prevent abuse of esketamine, it is only available

A

at approved treatment centers. it cannot be taken home. patients go 2-3 times a week to get their treatment under supervision.

164
Q

brexanolone

what is it

A

new FDA Approved Drug for postpartum depression

allopregnanolone, a neuroactive metabolite of progesterone which typically drops right after delivery (this triggers depression/anxiety for some women). when given as a continuous IV over 60 hours immediately after delivery. goal is to reduce or prevent PPD.

165
Q

adverse effects of brexanolone

A 
sedation
headache
dizziness
dry mouth
hot flashes
LOC
166
Q

blackbox warning: brexanolone

A

for LOC

need to be supervised while on this med

167
Q

drugs used in anxiety disorders (5)

A 
SSRI
SNRI
benzodiazepines
buspirone
beta blockers
168
Q

types of anxiety disorders (5)

A 
GAD
OCD
panic disorder
PTSD
social anxiety disorder
169
Q

if acute relief is needed for anxiety, what is the drug of choice and for how long?

A

benzodiazepine

2-4 weeks

170
Q

if adequate acute response is not achieved in 2-4 weeks of benzodiazepine for anxiety, what will you try next?

A

SSRI or SNRI

171
Q

if SNRI or SSRI doesn’t provide an adequate for anxiety,

A

switch to another SSRI/SNRI

or switch to a different agent

172
Q

benzodiazepines bind to

A

gaba-A receptors

173
Q

benzos and barbiturates both

A

bind to and potentiate the effects of gaba

174
Q

if your benzodiazepine expresses an alpha 1 unit,

A

sedation

175
Q

if your benzodiazepine expresses an alpha 2 and 3 subunit,

A

decreased anxiety

176
Q

alpha 1 subunits

A

sedation

177
Q

alpha 2 and alpha 3 subunits

A

decrease anxiety

178
Q

other general effects from benzos (3)

A

anti convulsant activity
hypnosis
anterograde amnesia

179
Q

advantages of benzos for treating anxiety. (3)

A

rapid action
high therapeutic index
little or no induction of liver enzymes, so lower risk for drug interactions in terms of phase I metabolism

180
Q

disadvantages of benzos (4)

A

impairment of psychomotor performance
amnesia
dependence/withdrawal after long term treatment
rebound anxiety after short term treatment

181
Q

what to worry about after long term treatment of benzos

A

dependence

withdrawal

182
Q

what to worry about after short term benzo treatment

A

rebound anxiety

183
Q

pharmacokinetic considerations of benzos

A

long half lives

metabolites with long half lives

184
Q

desmethyldiazepam

A

active metabolite of multiple benzos which has a very long half life. It then is metabolized to oxazepam, which is also active.

185
Q

complicated metabolism of benzos

A

some have active metabolites who then have their own active metabolites. there are potentially many different wash out periods that we need to be aware of.

186
Q

if hepatic function is compromised in a patient who needs benzos

A

you’d want to select a benzo that only undergoes phase II metabolism. ie: lorazepam

187
Q

buspirone vs benzo

A

reduces symptoms of anxiety less effectively than benzos but has no risk of dependence

188
Q

MoA buspirone (2)

A

mysterious

likely blocks 5HT1a autoreceptors, increasing 5HT signaling in the brain
stimulates 5HT1a post synaptic receptors as a partial agonist

189
Q

Buspirone can be used as an adjunct

A

to SSRI/SNRIs if they’ve experienced only partial response. Its MoA allows an anti depressant effect as well.

190
Q

buspirone duration of onset

A

longer than benzos

similar to SSRIs

Pharm (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions