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8. Psychopharmacology > Randhawa Psychopharmacology Lecture > Flashcards

Randhawa Psychopharmacology Lecture Flashcards

1
Q

what does pharmacokinetics describe

A

how an organism affects the drug

person–> drug

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2
Q

what does pharmacodynamics describe

A

how a drug affects the organism

drug–> person

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3
Q

what determines the effect of a drug on a person

A
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4
Q

what 5 factors determine HOW MUCH drug is delivered to its target

A

Liberation
Absorption
Distribution
Metabolism
Elimination

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5
Q

what 4 CYP enzymes/system commonly affect psychiatric medications

A

1A2

2D6

2C19

3A

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6
Q

which CYP enzyme is related to cigarette smoking

A

1A2

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7
Q

what CYP enzyme is affected by fluoxetine and paroxetine

A

2D6

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8
Q

which CYP enzyme is inhibited by grapefruit juice

A

3A4

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9
Q

what 4 factors can affect individual variability in terms of drug response

A

Genetics
Age
Disease
Environment

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10
Q

where are the primary dopamine projections

A

from the ventral tegmental area and substantia migra (midbrain)

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11
Q

where are the primary noradrenergic projections

A

from the locus ceruleus

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12
Q

in which disease is there a substantial loss of locus ceruleus cells

A

alzheimers

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13
Q

where do the serotonergic projections originate

A

raphe nucleus

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14
Q

how do TCAs and SSRIs differ with regard to their effect on voltage gated sodium channels

A

TCAs block the voltage gated sodium channel in nerves/neurons–> SSRIs do not

this makes TCAs more toxic in overdose but may underlie their efficacy in neuropathic pain
*venlafaxine also blocks this channel

*the voltage gated sodium channel is responsible for generation of the action potential along the neuron/cell… it is the influx of sodium that generates the action potential

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15
Q

upon which channel do gabapentin/pregabalin act

A

the voltage gated calcium channel (which controls neurotransmitter release at the synapse)

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16
Q

what are SNARE proteins and why do we care about them in psychiatry

A

are altered in SCZ and bipolar d/o

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17
Q

does lithium affect CYP?

A

no

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18
Q

what happens when the action potential reaches the synapse in the neuron

A

influx of calcium through the voltage gated calcium channels (VGCC)–> activation of synaptotagmins–> activates SNARE proteins on the cells membrane and synaptic vesicles–> causes vesicles to merge with cell membrane

*SNARE proteins are altered in SCZ and bipolar

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19
Q

how do botulinum and tetanus toxins work to impair cell signalling?

A

they cleave the SNARE proteins and prevent vesicles from being able to release neurotransmitter

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20
Q

what are ionotropic receptors

A

post synaptic receptirs that are ion channels–> a binding of a ligand to the receptor changes the receptors permeability to particular ions–> typically have multiple subunits

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21
Q

name two examples of post synaptic ionotropic receptors

A

GABA and glutamate receptors

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22
Q

what are metabotropic receptors

A

work through second messenger systems–> most MONOAMINE receptors are metabotropic

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23
Q

what the role of presynaptic autoreceptors and heteroreceptors

A

decrease the chance that a synapse will fire–> by opening potassium or chloride channels to hyperpolarize the cell and decrease the likelihood that an incoming signal/action potential will reach threshold

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24
Q

how do G protein coupled receptors work

A

G proterins have 3 subunits (alpha, beta, gamma)–> when ilgand binds the G protein breaks apart and separates from the receptor

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25
Q

what is the role of the alpha subunit of the G protein

A

activates phospholipase C (PLC)–> acts on phosphatidylinositol biphosphate (PIP2)–> activated PLC CLEAVES PIP2 into diacylglycerol (DAG) and inositol triphosphate (IP3)

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26
Q

how does lithium interact with G protein coupled receptors

A

inhibits the activation of G proteins

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27
Q

what do IP3 and DAG do

A

IP3 binds to receptors on endoplasmic reticulum and causes release of calcium into the cell

DAG binds to and activates protein kinase C (PKC)

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28
Q

what drugs are known to act on protein kinase C (PKC)

A

lithium and tamoxifen both inhibit PKC–> robust ANTI MANIC effect

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29
Q

what are bryostatins

A

PKC activators and are being investigated as treatments for dementia

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30
Q

what happens to IP3 once it has bound to endoplasmic reticulum causing release of calcium into the cell

A

gets broken down into inositol, then rebuilt into PIP2 (to start the process of cell signalling over again)

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31
Q

how does lithium impact IP3

A

lithium prevents breakdown of IP3 into inositol–> so that inositol cannot be recycled back into PIP2

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32
Q

how do protein kinase A levels differ in normal controls, people w bipolar and people w depression

A

elevated levels in bipolar

lower levels in depression

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33
Q

what is the TAAR1 receptor

A

an intracellular receptor in the presynaptic terminal

activity depends on the ligand either being transported into the cell or diffusing across the cell membrane

has high affinity for AMPHETAMINES and TRACE AMINES–> regulates transmission in dopamine, norpinephrine and serotonin neurons

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34
Q

how does amphetamine interact with the TAAR1 receptor

A

binds to the intracellular TAAR1 receptor and increases release of dopamine into the synaptic cleft –> reversing the dopamine transporter

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35
Q

what is the impact of blockade of the TAAR1 receptor

A

leads to a hyper-dopaminergic state, increasing firing rates of dopaminergic neurons–> seems particularly mediated by D2 receptors

TAAR1 agonists on the other hand downregulate dopamine activity and promote glutamatergic activity
–> agonists have been shown to reduce response to amphetamines and are being investigated for treatment of stimulant addiction as well as other addiciton related behaviours i.e eating disorder

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36
Q

what powers the SERT receptor

A

the gradient of sodium and chloride ions–> these are transported along w serotonin (one each for serotonin and norepinephrine, and 2 Na+ and 1 Cl- for dopamine)

for SERT to return to normal position, needs export of K+ from the cell

Na+ binds first–> conformational change–> allows serotonin to bind–> Cl- binds and results in transport of serotonin into the cell

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37
Q

what are the 3 major classes of monoamine transporter family receptors

A

SERT–> serotonin transporter

DAT–> dopamine transporter

NAT–> norepinephrine transporter

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38
Q

which of the serotonin receptors are INHIBITORY

A

5-HT1 and 5-HT5

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39
Q

which of the serotonin transporters are EXCITATORY

A

all the rest other than 5HT1 and 5HT5 lol–> so excitatory are 5HT2, 5HT3, 5HT4, 5HT6 and 5HT7

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40
Q

which of the serotonin transporters is ionotropic

A

5HT3

all the others are metabotropic/G protein coupled

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41
Q

which serotonin receptors do we want to STIMULATE to produce an antidepressant effect

A

POST-synaptic 5-HT1A, 5-HT2B and 5-HT4

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42
Q

which serotonin receptors do we want to BLOCK to enhance antidepressant effect

A

PRE-synaptic 5-HT1A, 5-HT2A, 5-HT2C, 5-HT3, 5-HT6 and 5-HT7

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43
Q

where are 5-HT1A receptors pre-synaptic? where are they post-synaptic?

A

pre-synaptic–> brainstem

post-synaptic–> limbic system, hippocampus, cortex

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44
Q

which are the most widespread 5HT receptors

A

5-HT1A

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45
Q

how do 5HT1A receptors act in the raphe nucleus

A

are presynaptic autoreceptors and down regulate serotonergic neurones –> elsewhere they are post synaptic

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46
Q

which serotonin receptors are targets of the triptans

A

5HT1B

–> 5HT1B receptors are both autoreceptors and heteroreceptors

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47
Q

name two drugs that are AGONISTS at the 5HT1A receptor

A

buspirone (presynaptic)

vortioxetine

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48
Q

activation of the 5HT1A receptor causes what to happen

A

stimulates dopamine release

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49
Q

name 7 drugs that are partial agonists at the 5HT1A receptor

A

buspirone (post synaptic)

trazodone

vilazodone

aripiprazole

brexpiprazole

lurasidone

cannabidiol

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50
Q

name two drugs that are ANTAGONISTS at the 5HT1A receptor

A

pindolol

risperidone

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51
Q

which serotonin receptor is responsible for the psychedelic effects of LSD

A

5HT2A

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52
Q

how are 5HT2A receptors affected by atypical antipsychotics

A

INHIBITED POTENTLY by atypical antipsychotic medications

(atypicals have more affinity for 5HT2A than for D2)

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53
Q

what is the result of blockade of 5HT2A receptors

A

blockade INHIBITS DOPAMINE release in the prefrontal cortex

also restores locus seruleus firing in SSRI treated patients

blockade also IMPROVES SLOW WAVE SLEEP

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54
Q

name 3 meds that are antagonists at the 5HT2A receptor

A

trazodone

mirtazapine

atypical antipsychotics

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55
Q

what are some functions associated with the 5HT2A receptor

A

smooth muscle contraction in the GI tract

platelet aggregation

psychedelic effect of LSD

atypical antipsychotics

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56
Q

what happens when you STIMULATE the 5HT3 receptor

A

stimulation causes N/V

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57
Q

which receptor is targeted by ondansetron

A

5HT3–> ondansetrono blocks 5HT3 which is how it has its anti nausea/vomiting effects

has also shown some efficacy in OCD and negative symptoms of schizophrenia

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58
Q

how is the 5HT3 receptor related to antidepressant response

A

bloackade may enhance antidepressant response

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59
Q

where is the 5HT3 receptor found

A

nervous system and GI tract

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60
Q

name 5 drugs that BLOCK the 5HT3 receptor

A

ondansetron

mirtazapine

clozapine

olanzapine

quetiapine

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61
Q

which serotonin receptor is involved primarily in gastric motility

A

5HT4

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62
Q

where does metoclopramide act

A

on the 5HT4 receptor–> primarily a prokinetic that is used to enhance gastric motility

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63
Q

what makes a TCA either a tertiary or a secondary amine?

A

either three carbons or two carbons on the nitrogen

tertiary amines (3 carbons) are methylated to secondary amines

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64
Q

which TCA uniquely has a curvilinear dose response

A

nortriptyline

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65
Q

name the two secondary amines we use as antidepressants

A

desipramine

nortriptyline

(the rest are tertiary amines)

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66
Q

how do tertiary amines and secondary amines differ in terms of their effects

A

tertiary amines have SIMILAR affinity for BOTH 5HT and NE

secondary amines have HIGHER AFFINITY for NE than for 5HT

(both types of amines are quite similar in the DAT affinity, which is the lowest of the affinities)

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67
Q

list foods to avoid if taking an MAOi

A

all cheese

tap beer

dry sausages

chicken livers

pickled fish

caviar

pickled herring

marmite

soy sauce

tofu

miso soup

fava beans

sauerkraut

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68
Q

why do you have to avoid the foods you have to avoid if taking an MAOi

A
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69
Q

which MAOis inhibit both MAO-A and MAO-B

A

phenelzine (more hepatotoxic)

tranylcypromine (les heptatotoxic, more stimulating)

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70
Q

are dietary restrictions required for moclobemide

A

no–> is a reversible inhibitor of MAO-A only

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71
Q

in which disorder is selegeline used

A

parkinsons

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72
Q

are dietary restrictions required with selegiline

A

it is an IRREVERSIBLE inhibitor of MAO-B–> normally NO dietary restrictions are required but at higher doses is may also inhibit MAO-A and have an antidepressant effect and in this case, would need dietary restriction

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73
Q

which receptor mediates the anticholinergic side effects of SSRIs

A

the muscarinic receptor

–urinary retention, constipation, blurry vision, dry mouth

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74
Q

which receptor mediates the antihistamine side effects of SSRIs

A

H1 receptor

–weight gain, sedation

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75
Q

which receptor mediates the adrenergic effects of SSRis

A

alpha-1 receptor

–postural hypotension, dizziness

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76
Q

what side effects are common to MOST SSRIS

A

nausea, dyspepsie, dry mouth, headaches, sleep disturabance

weight gain = uncommon but not rare

sexual dysfunction is common and may persist

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77
Q

what are side effects somewhat unique to venlafaxine

A

may cause ELEVATIONS IN CHOLESTEROL

causes HYPERTENSION in a dose dependent fashion (13% of people taking over 300mg)

SWEATING and SEXUAL SEs are COMMON

78
Q

in which patients is buproprion contraindicated and why

A

contraindicated in bulimia, EtOH withdrawal, benzo withdrawa due to higher risk of seizures

79
Q

how does mirtazapines MOA differ from other antidepressants

A

instead of working thru reuptake inhibition, mirtazapine acts PRE-SYNAPTICALLY by BLOCKING ALPHA-2 receptors, stimulating neurons to RELEASE larger amounts of neurotransmitter

post synaptically, it BLOCKS 5HT2 and 5HT3–> may serve to limit side effects and may also be antidepressant itself

80
Q

does mirtazapine have higher or lower risk of restless leg syndrome than SSRIs

A

higher risk of restless legs in mirtazapine

81
Q

side effects of mirtazapine

A

most common = sedation and weight gain

1.5% risk of neutropenia
2% risk liver enzyme elevation
15% risk of cholesterol elevation

82
Q

which antidepressant has highest affinity for norepinephrine receptor

A

desipramine (duloxetine, atomoxetine are close behind)

83
Q

which antidepressant has the lowest affinity for NET

A

trazodone

84
Q

which antidepressant has the highest affinity for SERT

A

paroxetine

85
Q

which antidepressant has the lowest affinity for SERT

A

buproprion (well actually, mirtazapine doesnt even act there?)

86
Q

which antidperessants are likely to have the most histaminergic side effects

A

mirtazapine, amitriltyline

87
Q

what is the most anticholinergic antidepressant

A

amitriptyline

followed by paroxetine and desipramine

then fluoxetine

88
Q

which antidepressant is least likely to cause weight gain with ongoing treatment

A

buproprion

(fluoxetine is also less likely to cause weight gain, but more likely than buproprion)

89
Q

which antidepressant is most likely to cause weight gain with ongoing treatment

A

paroxetine and mirtazapine

90
Q

how is vortioxetine marketed in terms of MOA

A

as a “serotonin modulator and stimulator”

91
Q

why does vortioxetine have fewer GI side effects

A

because has 5HT3 BLOCKADE

92
Q

which receptors does vortioxeitne work on

A
93
Q

how does vilazodone work

A

SERT inhibitor + 5HT1A partial agonist at PREsynaptic receptors

FEW sexual SEs and NO weight gain but ++ diarrhea and nausea

94
Q

what are SERT, NET, DAT

A

the monoamine TRANSPORTERS that get sertraline, norepinephrine and dopamine into and out of the cell where they can then act on their respective RECEPTORS (i.e 5HT1, D2)

95
Q

levomilnacipran is similar to which other antidepressants

A

the other SNRIs

96
Q

how does levomilnacipran differ from other SNRIs

A

has a more “balanced” effect between serotonin and norepinephrine reuptake inhibition

i.e for ratio of serotonin:norepinephrine reuptake inhibition:
venlafaxine has 10:1 ratio
duloxetine have 15:1 ratio
levomilacipran has 1:2 ratio
**FAVORS NOREPINEPHRINE REUPTAKE INHIBITION

97
Q

what receptors does psilocybin act on

A

5HT1A, 2A and 2C

98
Q

what receptors does LSD act on

A

5HT1A, 2A and 2C but is a partial agonist at some of these

also acts on D1, D2 and D4 receptors

99
Q

are the dopamine receptors ionotropic or metabotropic

A

all metabotropic

100
Q

what are the subtypes of the dopamine receptor

A

D1-like (D1 and D5)–> excitatory

D2-like (D2, D3, D4)–> inhibitory

*not much is known about the role of these subtypes

101
Q

what is the predominant dopamine autoreceptor

A

D2

102
Q

which dopamine receptor plays a role in the action of psychostimulants

A

D1

103
Q

how are typical antipsychotics divided?

A

into high potency and low potency based on affinity for the D2 receptor

104
Q

what is the tradeoff in terms of effects/side effects between high potency and low potency antipsychotics

A

high potency–> more likely to lead to EPS but also less likely to have cholinergic, adrenergic and histaminic side effects

low potency–> less likely to lead to EPS but more likely to have cholinergic (dry mouth etc), histaminic (sedation) side effects

105
Q

what do pyramidal tracts regulate

A

voluntary body control (lateral and anterior corticospinal)

106
Q

what do extramyramidal tracts regulate

A

fine motor control, balance, posture

107
Q

how do you treat acute dystonia

A

with benzodiazapines or anticholinergics

108
Q

how do you treat akathisia

A

beta blockers or benzos

may be necessary to change antipsychotic

109
Q

who is more likely to develop acute dystonia

A

young males who are neuroleptic naive

more likely with high potency antipsychotics

110
Q

who is more likely to develop akathisia

A

elderly females

increased risk with caffeine and with high potency antipsychotics

111
Q

how do you manage parkinsonism

A

lower antipsychotic dose, using antiparkinsonian med or change to a different medication

112
Q

what is a distinguishing feature of tardive dyskinesia

A

DISAPPEARS during sleep

113
Q

what % of those with TD will have spontaneous remission after 5 years

A

about 20%

114
Q

what are risk factors for TD

A

increased age

female

affective disorder

diabetes

115
Q

which have higher rates of obesity, typical or atypical antipsychotics

A

atypical

116
Q

which 2 atypical antipsychotics have higher affinity for D2 than 5HT2A

A

quetiapine and abilify

–> the rest of the atypicals all have higher affinity for 5HT2A than D2, whereas the typicals are all D2 focused

117
Q

why do the atypicals cause more weight gain

A

affinity for H1 receptor

118
Q

how does lurasidone act at the 5HT1A receptor

A

partial agonist

119
Q

what type of receptor profile does lurasidone have

A

high specificity for serotonergic and dopaminergic receptors with only minimal activity at adrenergic receptors

120
Q

what is particular about asenapine’s receptor activity

A

20x potency at the 5HT2 receptors compared to D2 receptors

favorable metabolic profile

121
Q

how do abilify and brexpiprazole act at the D2 receptor

A

are PARTIAL AGONISTS–> provide “dopamine stabilization” by inhibiting dopaminergic neurons at high dopamine concentrations, and stimulating them when there are low dopamine concentrations

122
Q

why might you favor brexpiprazole over abilify

A

generally better tolerated–> lower rates of fatigue, akathesia, tremor

123
Q

what is the primary inhibitory neurotransmitter of the CNS

A

GABA

124
Q

what type of receptor is the GABA-A receptor

A

ligand-gated chloride channel

causing HYPERpolarization when it is activated

5 subunits–> 2 alpha, 2 beta, 1 gamma

125
Q

what type of receptor is the GABA-B receptor

A

metabotropic inhibitory receptor

(GHB = agonist here)

126
Q

how do benzos act at the GABA receptor

A

allosteric modulator–> increase efficiency of the main binding site and thus increase GABA binding to the receptor

127
Q

which benzo is the most likely to be abused

A

alprazolam–combines high potency w a short half life

next is diazepam–> has rapid onset as is highly lipophilic

128
Q

how quickly does tolerance develop to benzos

A

after 1-3 of daily admin

129
Q

zopiclone and eszopiclone are approved for what indicattion

A

sleep onset and maintenance

trials show efficacy up to SIX MONTHS

130
Q

what is zolpidem approved for

A

ONLY for sleep ONSET by the FDA, but for both onset and maintenance by health canada

131
Q

what is a possible side effect of zoplidem which may lead you to avoid it in certain people

A

PARASOMNIAS (including NREM sleep behaviour disorders) have been reports–> contraindicated in hx of parasomnias

avoid alcohol while using zolpidem

132
Q

is there an association between benzo use and dementia?

A

a 2016 prospective cohort study that followed over 3000 people over 7 years did NOT find an association between benzo exposure and dementia

a 2019 meta analysis = mayyyybe small relative risk?

133
Q

how does lemborexant work

A

is a dual orexin receptor ANTAGONIST–> slightly more specific for OX2 receptor

take before bed

should only be taken when at least 7 hours avail for sleep

134
Q

why is vyvanse “harder” to abuse

A

because it is a prodrug that is enzymatically activated by the body–> less likely to snort

135
Q

what is solriamfetol

A

approved for the treatment of daytime sleepiness in patients with narcolepsy or sleep apnea

most common SEs are anxiety and decreased appetite (+ headaches, nausea)

136
Q

what type of receptors are opioid receptors

A

inhibitory G coupled receptors

3 main types: mu, delta, kappa

137
Q

what type of receptors are the cannabinoid receptors

A

G protein coupled receptors

CB1 and CB2–> may be the MOST PREVALENT G coupled receptors in the brain

138
Q

where are CB1 receptors expressed

A

brain
lungs
liver
kidneys

139
Q

where are CB2 receptors expressed

A

immune system

140
Q

what effect do cannabinoids have when they bind to the CB1 receptor

A

decrease the release of GABA

141
Q

how is lithium excreted

A

entirely by the kidneys

142
Q

what is the mechanism of action of lithium

A

multiple mechanisms are likely

  1. modulation of neurotransmission–> reduction of glutamatergic activity
  2. modulation of second messenger systems–> protein kinase A and C, inositol depletion
143
Q

list common side effects of lithium

A

nausea

lethargy

fine tremor

weight gain

144
Q

what makes lithium induced tremor worse

A

caffeine, higher doses of lithium

145
Q

list symptoms of lithium toxicity

A

COARSE tremor

ataxia

hyper reflexia

twitches

can also get: hypothyroidism (5% of patients), cardiac changes (t wave flattening or inversion), cardiac conduction disturabnces

146
Q

are men or women more likely to be affected by lithium induced hypothyroidism

A

9x more likely in women

147
Q

what direct impact may lithium have on the kidneys

A

about 5-10% of those on long term lithium therapy develop INTERSTITIAL FIBROSIS that reduces kidney function–> usually mild tho

148
Q

what % of patients on lithium develop polyuria and polydipsia

A

35-40%–> usually is mild

but may persist for months after stopping lithium

some patients go on to develop diabetes insipidus

149
Q

why does lithium cause polyuria and polydipsia

A

inhibits ADH

150
Q

what skin conditions are seen in lithium

A

acne exacerbation

psoriasis

151
Q

what are the concerns with lithium in pregnancy

A

teratogen–> increased risk of ebsteins anomaly from 0.05%-0.1%

despite this, is often mood stabilizer of choice in pregnancy (although preferably avoided in first trimester)

monitor therapeutic levels closely

check weekly after 36 weeks

152
Q

what do. you need to monitor when someone is on lithium

A

kidney and thyroid function

153
Q

where do pregabalin/gabapentin act (on what receptors)

A

bind to the voltage gated CALCIUM channels (VGCC)

INHIBIT the channels

*have NO affinity for GABA receptors

154
Q

what is the most common side effect of pregabalin

A

dizziness

then somnolence, edema, weight gain, dry mouth, weakness, blurry vision

155
Q

what are some serious side effects that can occur with carbamazepine

A

can cause APLASTIC ANEMIA or AGRANULOCYTOSIS (2 per 1 million)

can cause leukopenia in 5% of patients

common SEs = nausea, dizziness, ataxia, nystagmus, double vision

156
Q

on which receptors does carbamazepine work? what does it do to those receptors?

A

stabilizes the INACTIVE STATE of voltage gated SODIUM channels

157
Q

how does carbamazepine act on the cyp 3A4 enzyme

A

causes autoinduction

takes 3-4 weeks to stabilize

158
Q

where (on what receptors) and how does valproic acid act

A

ENHANCES GABA transmission by inhibiting breakdown of GABA

blocks voltage gated SODIUM channels

(tends to inhibit the metabolism of other compounds like benzos, fluoxetine, lamotrigine)

159
Q

what are some rare but serious side effects of valproic acid

A

can cause rare but severe hepatitis or pancreatitis

*mild transaminitis is common and not reason to stop

(can also cause PCOS)

160
Q

where and how does lamotrigine act (receptor-wise)

A

INHIBITS GLUTAMATERGIC activity by blocking voltage gated SODIUM channels

161
Q

where and how does topiramate act

A

blocks voltage gated SODIUM and CALCIUM channels

decreases AMPA/kainate glutamatergic activity

acts as partial agonist on some GABA receptors

162
Q

are glutamate receptors in the brain metabotropic or ionotropic

A

can be both–> the ionotropic receptors are divided into NMDA and non-NMDA categories

(non-NMDA = kainate/AMPA receptors)

163
Q

why are NMDA receptors unique

A

are also voltage gated

at resting voltage, the channel is blocked by magnesium–> activation requires BOTH ligand binding and depolarization

require binding of BOTH GLUTAMATE and GLYCINE to activate

164
Q

how does alcohol interact with NMDA receptors

A

alcohol inhibits NMDA receptors

withdrawal seizures are thought to be related to over activity of up-regulated receptors

165
Q

name 5 medications that act through glutamate receptors

A

d-cycloserine

topiramate

memantine

riluzole

ketamine

166
Q

how does d-cycloserine act?

A

binds to the GLYCINE site on NMDA receptors–> potentiates glutamatergic action

167
Q

what is d-cycloserine used for

A

facilitates fear extinction

168
Q

how does topiramate act

A

BLOCKS the non-NMDA receptor (also blocks voltage gated sodium channel and facilitates GABA)

169
Q

what is topiramate used for

A

anticonvulsant

appetite suppression

170
Q

how does memantine act

A

blocks NMDA receptors

171
Q

what is memantine used for

A

dementia

172
Q

how does riluzole act

A

decreases glutamate release through blockade of calcium channels

173
Q

what is riluzole used for

A

ALS

174
Q

how does ketamine act

A

BLOCKS the NMDA receptor–> this in turn causes increased glutamate release and activation of AMPA receptors

175
Q

what is ketamine used for

A

anesthetic, and depression

176
Q

what is the response rate of repeated ketamine infusions for treating depression

A

response rate of 50% in patients who have not responded to other treatments

177
Q

how effective is IV infusion of ketamine on depression sx and how long does this last

A

rapid antidepressant effect

peaks within 24 hours and lasts 3-7 days

relapse usually occurs within 10 days but 20-30% of patients have sustained response for up to 30 days

178
Q

n-acetylcysteine has evidence in which disorders

A

obsessive skin picking

OCD

addiction

179
Q

how does n-acetylcysteine work

A

modulates glutamatergic activity basically

180
Q

what is a mnemonic for serotonin syndrome

A

HARMED

hyperthermia
autonomic instability
rigidity
myoclonus
encephalopathy
diaphoresis

181
Q

what is cyproheptadine

A

serotonin antagonist

can be used if serious serotonin syndrome

182
Q

what precipitates NMS

A

dopamine antagonists

183
Q

what precipitates serotonin syndrome

A

serotonergic agents

184
Q

how are reflexes affected in NMS vs serotonin syndrome

A

NMS–> hyporeflexia

serotonin syndrome–> hyperreflexia + clonus

185
Q

how are pupils affected in NMS vs serotonin syndrome

A

NMS–> normal pupils

serotonin syndrome–> dilated pupils

186
Q

which 4 antidepressant agents have more than 30% sexual dysfunction SE

A

fluoxetine

fluvoxamine

paroxetine

sertraline

187
Q

does ASA have drug interaction risk with lithium

A

while other NSAIDs yes, ASA does not seem to at low doses

188
Q

how do you perform an AIMS exam

A
189
Q

which antipsychotics are affected by diet

A

asenapine

lurasidone

ziprasidone

190
Q

which brain region is implicated in the fear response

A

amygdala

191
Q

which brain region is implicated in worry

A

cortico-thalamo-cortical loops

192
Q

what is varenicline’s MOA

A

partial agonist at alpha4 beta2 receptor

full agonist at alpha7 receptor

8. Psychopharmacology (21 decks)

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