Randhawa Psychopharmacology Lecture Flashcards
(192 cards)
1
Q
what does pharmacokinetics describe
A
how an organism affects the drug
person–> drug
2
Q
what does pharmacodynamics describe
A
how a drug affects the organism
drug–> person
3
Q
what determines the effect of a drug on a person
A
4
Q
what 5 factors determine HOW MUCH drug is delivered to its target
A
Liberation
Absorption
Distribution
Metabolism
Elimination
5
Q
what 4 CYP enzymes/system commonly affect psychiatric medications
A
1A2
2D6
2C19
3A
6
Q
which CYP enzyme is related to cigarette smoking
A
1A2
7
Q
what CYP enzyme is affected by fluoxetine and paroxetine
A
2D6
8
Q
which CYP enzyme is inhibited by grapefruit juice
A
3A4
9
Q
what 4 factors can affect individual variability in terms of drug response
A
Genetics
Age
Disease
Environment
10
Q
where are the primary dopamine projections
A
from the ventral tegmental area and substantia migra (midbrain)
11
Q
where are the primary noradrenergic projections
A
from the locus ceruleus
12
Q
in which disease is there a substantial loss of locus ceruleus cells
A
alzheimers
13
Q
where do the serotonergic projections originate
A
raphe nucleus
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
15
Q
upon which channel do gabapentin/pregabalin act
A
the voltage gated calcium channel (which controls neurotransmitter release at the synapse)
16
Q
what are SNARE proteins and why do we care about them in psychiatry
A
are altered in SCZ and bipolar d/o
17
Q
does lithium affect CYP?
A
no
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
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
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
21
Q
name two examples of post synaptic ionotropic receptors
A
GABA and glutamate receptors
22
Q
what are metabotropic receptors
A
work through second messenger systems–> most MONOAMINE receptors are metabotropic
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
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
25
what is the role of the alpha subunit of the G protein
activates phospholipase C (PLC)--> acts on phosphatidylinositol biphosphate (PIP2)--> activated PLC CLEAVES PIP2 into diacylglycerol (DAG) and inositol triphosphate (IP3)
26
how does lithium interact with G protein coupled receptors
inhibits the activation of G proteins
27
what do IP3 and DAG do
IP3 binds to receptors on endoplasmic reticulum and causes release of calcium into the cell
DAG binds to and activates protein kinase C (PKC)
28
what drugs are known to act on protein kinase C (PKC)
lithium and tamoxifen both inhibit PKC--> robust ANTI MANIC effect
29
what are bryostatins
PKC *activators* and are being investigated as treatments for dementia
30
what happens to IP3 once it has bound to endoplasmic reticulum causing release of calcium into the cell
gets broken down into inositol, then rebuilt into PIP2 (to start the process of cell signalling over again)
31
how does lithium impact IP3
lithium prevents breakdown of IP3 into inositol--> so that inositol cannot be recycled back into PIP2
32
how do protein kinase A levels differ in normal controls, people w bipolar and people w depression
elevated levels in bipolar
lower levels in depression
33
what is the TAAR1 receptor
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
34
how does amphetamine interact with the TAAR1 receptor
binds to the intracellular TAAR1 receptor and increases release of dopamine into the synaptic cleft --> reversing the dopamine transporter
35
what is the impact of blockade of the TAAR1 receptor
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
36
what powers the SERT receptor
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
37
what are the 3 major classes of monoamine transporter family receptors
SERT--> serotonin transporter
DAT--> dopamine transporter
NAT--> norepinephrine transporter
38
which of the serotonin receptors are INHIBITORY
5-HT1 and 5-HT5
39
which of the serotonin transporters are EXCITATORY
all the rest other than 5HT1 and 5HT5 lol--> so excitatory are 5HT2, 5HT3, 5HT4, 5HT6 and 5HT7
40
which of the serotonin transporters is ionotropic
5HT3
all the others are metabotropic/G protein coupled
41
which serotonin receptors do we want to STIMULATE to produce an antidepressant effect
POST-synaptic 5-HT1A, 5-HT2B and 5-HT4
42
which serotonin receptors do we want to BLOCK to enhance antidepressant effect
PRE-synaptic 5-HT1A, 5-HT2A, 5-HT2C, 5-HT3, 5-HT6 and 5-HT7
43
where are 5-HT1A receptors pre-synaptic? where are they post-synaptic?
pre-synaptic--> brainstem
post-synaptic--> limbic system, hippocampus, cortex
44
which are the most widespread 5HT receptors
5-HT1A
45
how do 5HT1A receptors act in the raphe nucleus
are presynaptic autoreceptors and down regulate serotonergic neurones --> elsewhere they are post synaptic
46
which serotonin receptors are targets of the triptans
5HT1B
--> 5HT1B receptors are both autoreceptors and heteroreceptors
47
name two drugs that are AGONISTS at the 5HT1A receptor
buspirone (presynaptic)
vortioxetine
48
activation of the 5HT1A receptor causes what to happen
stimulates dopamine release
49
name 7 drugs that are partial agonists at the 5HT1A receptor
buspirone (post synaptic)
trazodone
vilazodone
aripiprazole
brexpiprazole
lurasidone
cannabidiol
50
name two drugs that are ANTAGONISTS at the 5HT1A receptor
pindolol
risperidone
51
which serotonin receptor is responsible for the psychedelic effects of LSD
5HT2A
52
how are 5HT2A receptors affected by atypical antipsychotics
INHIBITED POTENTLY by atypical antipsychotic medications
(atypicals have more affinity for 5HT2A than for D2)
53
what is the result of blockade of 5HT2A receptors
blockade INHIBITS DOPAMINE release in the prefrontal cortex
also restores locus seruleus firing in SSRI treated patients
blockade also IMPROVES SLOW WAVE SLEEP
54
name 3 meds that are antagonists at the 5HT2A receptor
trazodone
mirtazapine
atypical antipsychotics
55
what are some functions associated with the 5HT2A receptor
smooth muscle contraction in the GI tract
platelet aggregation
psychedelic effect of LSD
atypical antipsychotics
56
what happens when you STIMULATE the 5HT3 receptor
stimulation causes N/V
57
which receptor is targeted by ondansetron
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
58
how is the 5HT3 receptor related to antidepressant response
bloackade may enhance antidepressant response
59
where is the 5HT3 receptor found
nervous system and GI tract
60
name 5 drugs that BLOCK the 5HT3 receptor
ondansetron
mirtazapine
clozapine
olanzapine
quetiapine
61
which serotonin receptor is involved primarily in gastric motility
5HT4
62
where does metoclopramide act
on the 5HT4 receptor--> primarily a prokinetic that is used to enhance gastric motility
63
what makes a TCA either a tertiary or a secondary amine?
either three carbons or two carbons on the nitrogen
tertiary amines (3 carbons) are methylated to secondary amines
64
which TCA uniquely has a curvilinear dose response
nortriptyline
65
name the two secondary amines we use as antidepressants
desipramine
nortriptyline
(the rest are tertiary amines)
66
how do tertiary amines and secondary amines differ in terms of their effects
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)
67
list foods to avoid if taking an MAOi
all cheese
tap beer
dry sausages
chicken livers
pickled fish
caviar
pickled herring
marmite
soy sauce
tofu
miso soup
fava beans
sauerkraut
68
why do you have to avoid the foods you have to avoid if taking an MAOi
69
which MAOis inhibit both MAO-A and MAO-B
phenelzine (more hepatotoxic)
tranylcypromine (les heptatotoxic, more stimulating)
70
are dietary restrictions required for moclobemide
no--> is a reversible inhibitor of MAO-A only
71
in which disorder is selegeline used
parkinsons
72
are dietary restrictions required with selegiline
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
73
which receptor mediates the anticholinergic side effects of SSRIs
the muscarinic receptor
--urinary retention, constipation, blurry vision, dry mouth
74
which receptor mediates the antihistamine side effects of SSRIs
H1 receptor
--weight gain, sedation
75
which receptor mediates the adrenergic effects of SSRis
alpha-1 receptor
--postural hypotension, dizziness
76
what side effects are common to MOST SSRIS
nausea, dyspepsie, dry mouth, headaches, sleep disturabance
weight gain = uncommon but not rare
sexual dysfunction is common and may persist
77
what are side effects somewhat unique to venlafaxine
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
in which patients is buproprion contraindicated and why
contraindicated in bulimia, EtOH withdrawal, benzo withdrawa due to higher risk of seizures
79
how does mirtazapines MOA differ from other antidepressants
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
does mirtazapine have higher or lower risk of restless leg syndrome than SSRIs
higher risk of restless legs in mirtazapine
81
side effects of mirtazapine
most common = sedation and weight gain
1.5% risk of neutropenia
2% risk liver enzyme elevation
15% risk of cholesterol elevation
82
which antidepressant has highest affinity for norepinephrine receptor
desipramine (duloxetine, atomoxetine are close behind)
83
which antidepressant has the lowest affinity for NET
trazodone
84
which antidepressant has the highest affinity for SERT
paroxetine
85
which antidepressant has the lowest affinity for SERT
buproprion (well actually, mirtazapine doesnt even act there?)
86
which antidperessants are likely to have the most histaminergic side effects
mirtazapine, amitriltyline
87
what is the most anticholinergic antidepressant
amitriptyline
followed by paroxetine and desipramine
then fluoxetine
88
which antidepressant is least likely to cause weight gain with ongoing treatment
buproprion
(fluoxetine is also less likely to cause weight gain, but more likely than buproprion)
89
which antidepressant is most likely to cause weight gain with ongoing treatment
paroxetine and mirtazapine
90
how is vortioxetine marketed in terms of MOA
as a "serotonin modulator and stimulator"
91
why does vortioxetine have fewer GI side effects
because has 5HT3 BLOCKADE
92
which receptors does vortioxeitne work on
93
how does vilazodone work
SERT inhibitor + 5HT1A partial agonist at PREsynaptic receptors
FEW sexual SEs and NO weight gain but ++ diarrhea and nausea
94
what are SERT, NET, DAT
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
levomilnacipran is similar to which other antidepressants
the other SNRIs
96
how does levomilnacipran differ from other SNRIs
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
what receptors does psilocybin act on
5HT1A, 2A and 2C
98
what receptors does LSD act on
5HT1A, 2A and 2C but is a partial agonist at some of these
also acts on D1, D2 and D4 receptors
99
are the dopamine receptors ionotropic or metabotropic
all metabotropic
100
what are the subtypes of the dopamine receptor
D1-like (D1 and D5)--> excitatory
D2-like (D2, D3, D4)--> inhibitory
*not much is known about the role of these subtypes
101
what is the predominant dopamine autoreceptor
D2
102
which dopamine receptor plays a role in the action of psychostimulants
D1
103
how are typical antipsychotics divided?
into high potency and low potency based on affinity for the D2 receptor
104
what is the tradeoff in terms of effects/side effects between high potency and low potency antipsychotics
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
what do pyramidal tracts regulate
voluntary body control (lateral and anterior corticospinal)
106
what do extramyramidal tracts regulate
fine motor control, balance, posture
107
how do you treat acute dystonia
with benzodiazapines or anticholinergics
108
how do you treat akathisia
beta blockers or benzos
may be necessary to change antipsychotic
109
who is more likely to develop acute dystonia
young males who are neuroleptic naive
more likely with high potency antipsychotics
110
who is more likely to develop akathisia
elderly females
increased risk with caffeine and with high potency antipsychotics
111
how do you manage parkinsonism
lower antipsychotic dose, using antiparkinsonian med or change to a different medication
112
what is a distinguishing feature of tardive dyskinesia
DISAPPEARS during sleep
113
what % of those with TD will have spontaneous remission after 5 years
about 20%
114
what are risk factors for TD
increased age
female
affective disorder
diabetes
115
which have higher rates of obesity, typical or atypical antipsychotics
atypical
116
which 2 atypical antipsychotics have higher affinity for D2 than 5HT2A
quetiapine and abilify
--> the rest of the atypicals all have higher affinity for 5HT2A than D2, whereas the typicals are all D2 focused
117
why do the atypicals cause more weight gain
affinity for H1 receptor
118
how does lurasidone act at the 5HT1A receptor
partial agonist
119
what type of receptor profile does lurasidone have
high specificity for serotonergic and dopaminergic receptors with only minimal activity at adrenergic receptors
120
what is particular about asenapine's receptor activity
20x potency at the 5HT2 receptors compared to D2 receptors
favorable metabolic profile
121
how do abilify and brexpiprazole act at the D2 receptor
are PARTIAL AGONISTS--> provide "dopamine stabilization" by inhibiting dopaminergic neurons at high dopamine concentrations, and stimulating them when there are low dopamine concentrations
122
why might you favor brexpiprazole over abilify
generally better tolerated--> lower rates of fatigue, akathesia, tremor
123
what is the primary inhibitory neurotransmitter of the CNS
GABA
124
what type of receptor is the GABA-A receptor
ligand-gated chloride channel
causing HYPERpolarization when it is activated
5 subunits--> 2 alpha, 2 beta, 1 gamma
125
what type of receptor is the GABA-B receptor
metabotropic inhibitory receptor
(GHB = agonist here)
126
how do benzos act at the GABA receptor
allosteric modulator--> increase efficiency of the main binding site and thus increase GABA binding to the receptor
127
which benzo is the most likely to be abused
alprazolam--combines high potency w a short half life
next is diazepam--> has rapid onset as is highly lipophilic
128
how quickly does tolerance develop to benzos
after 1-3 of daily admin
129
zopiclone and eszopiclone are approved for what indicattion
sleep onset and maintenance
trials show efficacy up to SIX MONTHS
130
what is zolpidem approved for
ONLY for sleep ONSET by the FDA, but for both onset and maintenance by health canada
131
what is a possible side effect of zoplidem which may lead you to avoid it in certain people
PARASOMNIAS (including NREM sleep behaviour disorders) have been reports--> contraindicated in hx of parasomnias
avoid alcohol while using zolpidem
132
is there an association between benzo use and dementia?
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
how does lemborexant work
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
why is vyvanse "harder" to abuse
because it is a prodrug that is enzymatically activated by the body--> less likely to snort
135
what is solriamfetol
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
what type of receptors are opioid receptors
inhibitory G coupled receptors
3 main types: mu, delta, kappa
137
what type of receptors are the cannabinoid receptors
G protein coupled receptors
CB1 and CB2--> may be the MOST PREVALENT G coupled receptors in the brain
138
where are CB1 receptors expressed
brain
lungs
liver
kidneys
139
where are CB2 receptors expressed
immune system
140
what effect do cannabinoids have when they bind to the CB1 receptor
decrease the release of GABA
141
how is lithium excreted
entirely by the kidneys
142
what is the mechanism of action of lithium
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
list common side effects of lithium
nausea
lethargy
fine tremor
weight gain
144
what makes lithium induced tremor worse
caffeine, higher doses of lithium
145
list symptoms of lithium toxicity
COARSE tremor
ataxia
hyper reflexia
twitches
can also get: hypothyroidism (5% of patients), cardiac changes (t wave flattening or inversion), cardiac conduction disturabnces
146
are men or women more likely to be affected by lithium induced hypothyroidism
9x more likely in women
147
what direct impact may lithium have on the kidneys
about 5-10% of those on long term lithium therapy develop INTERSTITIAL FIBROSIS that reduces kidney function--> usually mild tho
148
what % of patients on lithium develop polyuria and polydipsia
35-40%--> usually is mild
but may persist for months after stopping lithium
some patients go on to develop diabetes insipidus
149
why does lithium cause polyuria and polydipsia
inhibits ADH
150
what skin conditions are seen in lithium
acne exacerbation
psoriasis
151
what are the concerns with lithium in pregnancy
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
what do. you need to monitor when someone is on lithium
kidney and thyroid function
153
where do pregabalin/gabapentin act (on what receptors)
bind to the voltage gated CALCIUM channels (VGCC)
INHIBIT the channels
*have NO affinity for GABA receptors
154
what is the most common side effect of pregabalin
dizziness
then somnolence, edema, weight gain, dry mouth, weakness, blurry vision
155
what are some serious side effects that can occur with carbamazepine
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
on which receptors does carbamazepine work? what does it do to those receptors?
stabilizes the INACTIVE STATE of voltage gated SODIUM channels
157
how does carbamazepine act on the cyp 3A4 enzyme
causes autoinduction
takes 3-4 weeks to stabilize
158
where (on what receptors) and how does valproic acid act
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
what are some rare but serious side effects of valproic acid
can cause rare but severe hepatitis or pancreatitis
*mild transaminitis is common and not reason to stop
(can also cause PCOS)
160
where and how does lamotrigine act (receptor-wise)
INHIBITS GLUTAMATERGIC activity by blocking voltage gated SODIUM channels
161
where and how does topiramate act
blocks voltage gated SODIUM and CALCIUM channels
decreases AMPA/kainate glutamatergic activity
acts as partial agonist on some GABA receptors
162
are glutamate receptors in the brain metabotropic or ionotropic
can be both--> the ionotropic receptors are divided into NMDA and non-NMDA categories
(non-NMDA = kainate/AMPA receptors)
163
why are NMDA receptors unique
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
how does alcohol interact with NMDA receptors
alcohol inhibits NMDA receptors
withdrawal seizures are thought to be related to over activity of up-regulated receptors
165
name 5 medications that act through glutamate receptors
d-cycloserine
topiramate
memantine
riluzole
ketamine
166
how does d-cycloserine act?
binds to the GLYCINE site on NMDA receptors--> potentiates glutamatergic action
167
what is d-cycloserine used for
facilitates fear extinction
168
how does topiramate act
BLOCKS the non-NMDA receptor (also blocks voltage gated sodium channel and facilitates GABA)
169
what is topiramate used for
anticonvulsant
appetite suppression
170
how does memantine act
blocks NMDA receptors
171
what is memantine used for
dementia
172
how does riluzole act
decreases glutamate release through blockade of calcium channels
173
what is riluzole used for
ALS
174
how does ketamine act
BLOCKS the NMDA receptor--> this in turn causes increased glutamate release and activation of AMPA receptors
175
what is ketamine used for
anesthetic, and depression
176
what is the response rate of repeated ketamine infusions for treating depression
response rate of 50% in patients who have not responded to other treatments
177
how effective is IV infusion of ketamine on depression sx and how long does this last
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
n-acetylcysteine has evidence in which disorders
obsessive skin picking
OCD
addiction
179
how does n-acetylcysteine work
modulates glutamatergic activity basically
180
what is a mnemonic for serotonin syndrome
HARMED
hyperthermia
autonomic instability
rigidity
myoclonus
encephalopathy
diaphoresis
181
what is cyproheptadine
serotonin antagonist
can be used if serious serotonin syndrome
182
what precipitates NMS
dopamine antagonists
183
what precipitates serotonin syndrome
serotonergic agents
184
how are reflexes affected in NMS vs serotonin syndrome
NMS--> hyporeflexia
serotonin syndrome--> hyperreflexia + clonus
185
how are pupils affected in NMS vs serotonin syndrome
NMS--> normal pupils
serotonin syndrome--> dilated pupils
186
which 4 antidepressant agents have more than 30% sexual dysfunction SE
fluoxetine
fluvoxamine
paroxetine
sertraline
187
does ASA have drug interaction risk with lithium
while other NSAIDs yes, ASA does not seem to at low doses
188
how do you perform an AIMS exam
189
which antipsychotics are affected by diet
asenapine
lurasidone
ziprasidone
190
which brain region is implicated in the fear response
amygdala
191
which brain region is implicated in worry
cortico-thalamo-cortical loops
192
what is varenicline's MOA
partial agonist at alpha4 beta2 receptor
full agonist at alpha7 receptor
