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Pharmacology > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

0
Q

amino acid NT (2)

A

Gamma-aminobutyric acid or GABA
Glycine
Glutamate
Aspartate

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1
Q

amine neurotransmitters? (6)

A 
Ach
5-HT
DA
Histamine
NE
Epinephrine
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2
Q

Soluble gases NT (2)

A

nitric oxide

carbon monoxide

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3
Q

NT from adrenal medulla with inh effect

A

Epinephrine

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4
Q

source of Ach

A

Acetyl CoA + Choline

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5
Q

source of epinephrine

A

tyrosine produced from the liver from phenylalanine

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6
Q

source of norepinephrine

A

tyrosine found in pons, reticular formxn, locus cereleus, thalamus, mid-brain

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7
Q

source of dopamine

A

tyrosine

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8
Q

source of serotonin

A

tyrptophan

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9
Q

source of histamine

A

histidine

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10
Q

source of glutamate

A

by reductive amination of Kreb’s cycle intermediate alpha-ketoglutarate

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11
Q

source of aspartate

A

acidic amines

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12
Q

source of GABA

A

decarboxylation of glutamate by glutamate decarboxylase by GABAnergic neuron

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13
Q

simple aa having amino group and a carboxyl group attached to a carbon atom

A

Glycine

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17
Q

Ach site of synthesis

A

cholinergic nerve endings

cholinergic pathways of brainstem

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18
Q

epi site of synthesis

A

adrenal medulla and some cns cells

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19
Q

norepi site of synthesis

A

from inside axoplasm of adrenergic nerve ending

completed inside secretory vesicles

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20
Q

dopamine site of synthesis

A 
cns, concentrated in basal ganglia and dopamine pathways
eg. 
nigostriatal
mesocorticolimbic
tuberohypophyseal pathways
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21
Q

serotonin site of synthesis

A

cns, gut (chromaffin cells), platelets, retina

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22
Q

aspartate site of synthesis

A

spinal cord

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23
Q

glycine site of synthesis

A

spinal cord

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24
Q

GABA site of synthesis

A

CNS

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25
Q

histamine site of synthesis

A

hypothalamus

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26
Q

glutamate site of synthesis

A

brain, spinal cord eg hippocampus

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29
Q

glycine postsynaptic receptor fxn

A

makes postsynaptic membrane more permeable to Cl- ion

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30
Q

aspartate postsynaptic receptor

A

spinal cord

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31
Q

GABA postsynaptic receptor

A

GABA-A increases Cl- conductance
GABA-B is metabotropic works with G protein
GABA transaminase catalyzes
GABA-C found exclusively in the retina

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33
Q

fate of glycine

A

deactivated in synapse by simple process of reabsorption by active transport back into the presynaptic membrane

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34
Q

receptor that mediates platelet aggregation and smooth muscle contraction

A

5HT2A

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35
Q

glutamate postsynaptic receptors

A

ionotropic

metabotropic

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36
Q

three types of ionotropic receptors

A

NMDA
AMPA
kainate receptors

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38
Q

fate of GABA

A

metabolized by transamination to succinate in the Citric acid cycle

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41
Q

form an excitatory/ inhibitory pair in the ventral spinal cord

A

Aspartate

Glycine

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42
Q

inactivates serotonin to form 5-hydroxyindoleacetic acid

A

MAO

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43
Q

glycine function

A

inh transmitter to Renshaw cells

found in the ventral spinal cord

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44
Q

enzyme that breaks down histamine

A

diamine oxidase

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45
Q

fate of glutamate

A

cleared from the brain ECF by Na+ uptake system in neurons and ganglia

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47
Q

Function of GABA

A

anxiety disorders
GABA-A causes hyperpolarization (inh)
anxiolytic drugs like BENZODIAZEPINE cause increase in Cl- entry into the cell and cause soothing effects
GABA-B causes increase conductance of K+ into the cell

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49
Q

Function of NE

A

controls attention and arousal

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51
Q

increased dopamine conc causes

A

schizophrenia

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52
Q

dec dopamine conc seen in

A

Parkinsons dse

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53
Q

serotonin function

A 
mood control
sleep
pain feeling
temp
BP
hormonal activity
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54
Q

histamine function

A 
arousal
pain threshold
BP
blood flow control
gut secretion
allergic rxn- itch sensation
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55
Q

glutamate function

A

long term potentiation involved in memory and learning by causing Ca2+ influx

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58
Q

most common NT fate

A

reuptake mechanism

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59
Q

pathway for negative symptoms

A

mesocortical- projects from ventral tegmentum to the cerebral cortex

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61
Q

pathway for positive symptoms

A

mesolimbic- projects from dopaminergic cell bodies in the ventral tegmentum to the limbic system

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62
Q

STEPS model

A 
safety
tolerability
efficacy
price
simplicity
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63
Q

pathway for movement regulation- dopamine suppresses Ach activity

A

nigrostriatal

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64
Q

blocking dopamine in this pathway will predispose your patient to hyperprolactinemia

A

tuberoinfundibular

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65
Q

in schizophrenia there is inc in dopamine transmission between ___ and dec transmission in _____

A

inc: subs nigra to the caudate nucleus- putamen (neostriatum)
dec: mesolimbic forebrain and tuberoinfundibular system

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66
Q

serotonergic stimulation inc or dec dopamine relase?

A

decrease

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67
Q

inversely correlated with aggitation and arousal

lower in acute and paranoid and higher in chronic patients

A

CSF 5 -HIAA

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68
Q

CSF GABA is lower in ____ and is higher in ____

A

young drug-free schizophrenic patients

patients with negative symptoms

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69
Q

Phenycylidine (Angel Dust) induced psychosis

A

blockade of NMDA action or glutamate receptors

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70
Q

CSF NE is elevated at ____ and is decreased at ____

A

drug-free patients

neuroleptic treated patients

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71
Q

classification of antipsychotics

A

a. Typical / first gen: DRAs

b. Atypical / second gen: SDAs

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72
Q

antipsychotics: PHENOTHIAZINE

A

aliphatic: chlorpromazine
piperidine: thioridazine, mesoridazine
piperazine: trifluoperazine, fluphenazine, perphenazine

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73
Q

antipsychotics: non-phenothiazines

A

thioxanthenes: thioxanthenes, chlorprothixene
butyrophenone: haloperidol, loxapine
diphenylbutylpiperidone: pimozide
dihydroindolone: molindone
dibenzazepine: clozapine
benzisoxazole: risperidone
thienobenzodiazepine: olanzapine
dibenzothiazepine: quetiapine

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74
Q

D2 receptor antagonists AE with high potency

A

extrapyramidal symptoms

FLUPHENAZINE
HALOPERIDOL
PIMOZIDE

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75
Q

low potency antipsychotics tend to interact with nondopaminergic receptors - AE

A

cardiotoxic, anticholinergic effects like sedation, hypotension

CHLOPROMAZINE
THIORIDAZINE

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76
Q

risperidone drug forms

A

regular tab
IM depot
rapidly dissolving tab

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77
Q

functions more like a typical antipsychotic at doses greater than 6 mg

A

Risperidone (RISPERIDAL)

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78
Q

AE of Risperidone

A

weight gain and sedation

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79
Q

Olanzapine forms

A

regular tab
immediate release IM
rapidly dissolving tab

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80
Q

AE of Olanzapine (ZYPREXIA)

A

weight of 30-50 lbs
hypertriglyceredemia, hypercholesterolemia, hyperglycemia (even without weight gain)
hyperprolactenemia(<Risperidone)
transaminitis (2%)

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81
Q

Quetapine (SEROQUEL) forms

A

regular tab

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82
Q

AE of Quetapine (SEROQUEL)

A 
transaminitis (6%)
weight gain (<Olanzapine)
orthostatic hypotension
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83
Q

Ziprasidone forms

A

regular tab

IM release form

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84
Q

AE of Ziprasidone (GEODON)

A

cvs toxicities
QT prolongation
hyperprolactinemia (<Risperidone)
no associated weight gain!

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85
Q

Ziprasidone intake

A

increased with food by 100%

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86
Q

newest antipsychotic

A

Aripiprazole (ABILIFY)

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87
Q

Aripiprazole (ABILIFY) forms

A

regular tab

immediate release IM

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88
Q

unique MoA of Aripiprazole

A

D2 partial agonist

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89
Q

Aripiprazole uses

A

psychosis
mood disorders
anxiety disorders

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90
Q

Aripripazole effects

A

low EPS
no QT prolongation
low sedation
not associated with weight gain

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91
Q

Aripripazole drug interactions

A

CYP2D6 (fluoxetine, paroxetine) 3A4 (carbamezipine, ketoconazole)
needs adjusted dosing> could cause intolerability due to akathisia or activation

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92
Q

Clozapine (CLOZARIL) forms

A

regular tab

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93
Q

reserved for treatment-resistant patients because of side effect profile

A

Clozapine (CLOZARIL)

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94
Q

AE of Clozapine

A

mostly associated with sedation, weight gain, transaminitis

agranulocytosis (0.5- 2%); requires weekly blood draws for 6 months then every 6 weeks for 6 months
-inc risk of seizure esp if LITHIUM is also taken

inc risk of hypertriglyceridemia, hypercholesterolemia, hyperglycemia, nonketotic hyperosmolar coma and death, with or without weight gain

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95
Q

baseline blood work for pre atypical antipsychotic tx

A

fasting lipid profile
fasting blood sugar
liver function tests

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96
Q

if patient has elevated total cholesterol and low HDL, avoid____

A

Olanzapine

Quietiapine

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97
Q

indications for antidepressants

A

unipolar or bipolar depression
organic mood disorders
schizoaffective disorder
anxiety disorders including OCD, panic, social phobia, PTSD, premenstrual dysphoric disorder, impulsivity

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98
Q

first MAOI originally used to treat TB

A

Iproniazid

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99
Q

initially as tx for schizophrenia
elevates mood and increase in energy in depressed individuals
sedating effect in non-depressed patients

A

Imipramine

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100
Q

first SSRI antidepressant developed with fewer SE

A

fluoxetine (PROZAC)

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101
Q

autoreceptors are typically located on the

A

presynaptic or axonal membrane

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102
Q

monoamine hypothesis states that

A

depression is the result of underactivity of monoamines, especially 5-HT

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103
Q

serotonin pathway in depression

A

reduced transmission from both caudal raphe nuclei and rostral raphe nuclei

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104
Q

NE pathway in depression

A

reduced transmission from both locus cereleus and caudal raphe nuclei

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105
Q

increase in NE in the frontal or prefrontal cortex

A

modulates SNRI

improves mood

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106
Q

increasing NE transmission to other areas

A

modulates attention

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107
Q

symptoms improve ____ weeks after a therapeutic dose is achieved

A

3-6

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108
Q

classification of antidepressants

A 
MAOI
TCAs
SSRIs
SNRIs
Novel antidepressants
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109
Q

metabolizes serotonin, NE, and dopamine

A

MAO A

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110
Q

metabolizes dopamine only

A

MAO B

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111
Q

MAOIs mechanism of action

A

irreversible binding to monoamine oxidase preventing inactivation of biogenic amines such as NE, Dopamine, Serotonin leading to increased synaptic levels

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112
Q

SE of MAOIs

A 
orthostatic hypotension
weight gain
dry mouth 
sedation
sexual dysfunction
sleep disturbance
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113
Q

can develop when MAOIs are taken with tyramine rich foods such as cheese or have sympathomimetic actions

A

hypertensive crisis

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114
Q

serotonin syndrome (ab pain, diarrhea, sweating, tachycardia, HTN, myoclonus, irritability, delirium) can lead to ________

A

hyperpyrexia
cardiovascular
shock
death

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115
Q

how to avoid Serotonin syndrome

A

wait 2 weeks before switching from SSRI and MAOI with exception of fluoxetine where there is need for 5 weeks because of the long half-life of the drug

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116
Q

MAO A converts monoamines into their corresponding carboxylic acid via

A

an aldehyde intermediate

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117
Q

MAO A regulates both the

A

free intraneuronal concentration

releasable stores of 5-HT and NE

118
Q

MAO A inhibitors (PHENELZINE) moa

A

bind to and inhibit MAO A preventing monoamine degradation resulting to greater stores available for release

119
Q

nonselective, irreversible, noncompetitive inh MAOIs

A

PHENELZINE

TRANYLCYPROMINE

120
Q

MAO-A selective, reversible, competitive inh MAOIs

A

MOCLOBEMIDE

CLORGYLINE

121
Q

MAOI with irreversible SE

A

PHENELZINE

TRANYLCYPROMINE

122
Q

atropine-like effects of MAOIs

A

postural hypotension
dry mouth
blurred vision
urinary retention

123
Q

CNS stimulation effects of MAOIs

A

weight gain
restlessness
insomia

124
Q

MOCLOBEMIDE SE

A

milder, transient

125
Q

MAO A selective and irreversible inhibitor

A

CLORGYLINE

126
Q

very effective but have potentially unacceptable side effect (antihistaminic, anticholinergic, antiadrenergic)

A

tricyclic antidepressants

127
Q

minimun supply of TCA to cause death

A

one week

128
Q

moa of TCAs

A

nonselective
bind to 5-HT and NE reuptake transporters preventing reuptake of monoamines from the synaptic cleft and their subsequent degradation

129
Q

reuptake blockade of TCAs lead to

A

accumulation of 5-HT and NE in the synaptic cleft

conc returns to normal range

130
Q

greater Na uptake, less 5HT uptake

A

IMIPRAMINE

131
Q

more 5-HT uptake, less Na uptake

A

CLOMIPRAMINE

132
Q

Na uptake= 5-HT uptake

A

AMITRIPTYLINE

133
Q

high Na uptake, NO 5-HT uptake

A

DESIPIRAMINE

134
Q

effects of TCAs

A

atropine like effects

  • postural hypotension
  • dry mouth
  • blurred vision
  • urinary retention

alpha1 antagonism
-postural hypotension

h1 antagonism
-sedation

poor dental health

135
Q

TCAs indication

A

treat affective or mood disorders

136
Q

main effect of TCAs

A

block the uptake of monoamines by nerve terminals by competing for the binding site of the carrier protein

137
Q

poor dental effect SE of TCAs are common among

A

middle-aged and elderly patients

138
Q

SSRI indication

A

anxiety and depressive symptoms

139
Q

most common SE of SSRIs

A

GI upset, sexual dysfunction, anxiety, restlessness, nervousness, insomia, fatigue, sedation, dizziness

very little risk of cardiotoxicities

140
Q

discontinuation syndrome in SSRIs

A

agitation
nausea
disequilibrium
dysphoria

141
Q

moa of SSRIs

A

bind at the 5-HT reuptake transporter preventing reuptake and subsequent degradation of 5-HT

small amounts of 5-HT are still degraded

142
Q

most prescribed antidepressant

A

SSRIs

as efficacious as TCAs but without anticholinergic SE

143
Q

unwanted SE of SSRIs

A

nausea
anorexia
insomnia
sexual dysfunction

144
Q

PAROXETINE (PAXIL, SEROXAT) pros

A

sedating properties, good inital relief from anxiety and insomnia
short half-life with no active metabolite

145
Q

PAROXETINE cons

A 
significant CYP2D6 inhibition
sedation
weight gain
more anticholinergic effects
more likely to cause discontinuation syndrome
146
Q

SERTRALINE (ZOLOFT) pros

A

very weak P450 interactions
short half-life with lower build up of metabolites
less sedating as compared to PAROXETINE
for OCD

147
Q

SERTRALINE cons

A

maximum absorption requires full stomach

increased number of GI adverse drug reactions

148
Q

FLUOXETINE (PROZAC) pros

A

long half-life with increased incidence of discontinuation syndromes
good for patients with noncompliance issues
increased energy
for tapering someone off SSRI to prevent discontinuation syndrome, one 20mg

149
Q

FLUOXETINE cons

A

active metabolite build-up
significant P450 interactions
increase anxiety and insomia upon initial activation
induce mania than other SSRIs

150
Q

CITALOPRAM (CELEXA) pros

A

low overall inh of P450 enzymes
few drug-to-drug interactions
low incidence of discontinuation syndrome d/t intermediate half-life

151
Q

CITALOPRAM cons

A 
sedatin due to mild antagonism at H1 receptors
GI SE (<SERTALINE)
152
Q

inhibit serotonin and NE reuptake like the TCAs but without the antihistamine, anti-adrenergic, or anticholinergic SE

A

SNRIs

153
Q

SSRIs indication

A

depression
anxiety
neuropathic pain

154
Q

moa of SNRIs

A

bind to serotonin and NE reuptake transporters contributing to alleviation of depression

small amts of 5-HT and NE continue to be degraded in the synaptic cleft

155
Q

VENLAFAXINE (EFFEXOR) pros

A

minimal drug interactions
almost no P450 activity
short half-life, fast clearance avoids build-up (good for geriatric populations)

156
Q

VENFLAXINE cons

A

10-15 mmHg dose dependent inc in diastolic BP
significant nausea
bad discontinuation syndrome- taper is recommended after 2 wks of admin
cause QT prolongation
sexual SE in >30%

157
Q

DULOXETINE (CYMBALTA) pros

A

for physical symptoms of depression

less BP increase as compared to VENLAFAXINE

158
Q

DULOXETINE (CYMBALTA) cons

A

CYP2D6 and CYP1A2 inhibitor

cannot break capsule as active ingredient not stable within stomach

159
Q

NaSSA moa

A

bind to and inhibit both adrenaline alpha 2 autoreceptors and noradrenaline alpha 2 heteroceptors

block 5HT2 and 5HT3 receptors on the postsynaptic membrane

160
Q

bind to and inhibit both adrenaline alpha 2 autoreceptors and noradrenaline alpha 2 heteroceptors leads to

A

prevention of negative feedback effect of synaptic NE on 5-HT and NE neurotransmission- neurotransmission sustained

161
Q

block 5HT2 and 5HT3 receptors on the postsynaptic membrane causes

A

enhanced 5-HT1 mediated neurotransmission

162
Q

new antidepressant that is the only member of NaSSA class

A

MIRTAZAPINE

163
Q

most common SE of MIRTAZAPINE

A

sedation due to H1 block

increased appetite with weight gain

164
Q

sympathomimetic effect of MIRTAZAPINE

A

dry mouth

165
Q

good augmentation of SSRIs

A

MIRTAZAPINE (REMERON)

166
Q

can be utilized as a hypnotic at lower doses secondary to antihistaminic effects

A

MIRTAZAPINE

167
Q

MIRTAZAPINE cons

A

inc serum cholesterol levels by 20% in 15% of patients and triglycerides in 6% of patients
very sedating at doses 30mg and above
weight gain

168
Q

mood stabilizers classes

A

LITHIUM

anticonvulsants

169
Q

mood stabilizers indication

A 
bipolar
cyclothymia
schizoaffective
impulse control
intermittent explosive disorders
170
Q

dopamine pathways in mania

A

inc dopamine transmission from sub nigra to neostriatum

dopamine activity from the ventral tegmentum and tuberoinfundibular remains unchanges

171
Q

GABA pathway in mania

A

GABAnergic inh at all levels
GABA interneurons are abundant in the brain 50%
dec GABA function in all pathways in depressed and manic states

172
Q

NE pathway in Mania

A

increased transmission of NE from the caudal nuclei and locus cereleus to all areas of the brain

173
Q

serotonin pathway in mania

A

increased transmission of serotonin from both the caudal and rostral raphe nuclei to all areas of the brain

174
Q

above basalin BPD

A

mania
hypomania
mixed states

175
Q

baseline BPd

A

euthymia

176
Q

below baseline BPD

A

depression

sybsyndromal syndrome

177
Q

class A stabilizers list

A 
LITHIUM
VALPROATE
CARBAMEZIPINE
OLANZAPINE
RISPERIDONE
QUETIAPINE
178
Q

class A stabilizers function

A

prevent mania without causing depression

179
Q

class B mood stabilizers list

A

LAMOTRIGINE
LITHIUM
OLANZAPINE

180
Q

class B mood stabilizers function

A

prevent depression without causing mania

181
Q

traditional mood stabilizers

A

LITHIUM
VALPROATE
CARBAMEZEPINE

182
Q

only medication to reduce suicide rate

A

LITHIUM

183
Q

indication of LITHIUM

A

long-term prohylaxis of both mania and depressive episodes in bd 1 patients

184
Q

factors predicting response to LITHIUM

A

prior long-term response or family member with good response
classic pure mania
mania is followed by depression

185
Q

moa of LITHIUM

A

mimics sodium but not pumped out by the NATPase
serotonin transmission +
dopamine transmission -
suppression of adenylate cyclase activation by some NTs and hormones
inh phosphatidyl inositol turnover by blocking the hydrolysis of intermediate inositol phosphatases, IP2 to IP1 and to inositol, involved in the generation of IP3 and DAG wc act as 2nd NT receptors

186
Q

how to use LITHIUM

A

get baseline creatinine (TSH, CBC)

check pregnancy

187
Q

steady state of LITHIUM is achieved by

A

5 days
check 12 hours after last dose
check TSH q 3 months and creatinine 6 months
goal: blood level of 0.6- 1.2

188
Q

eibstein’s anomaly

A

seen in LITHIUM use at 1st trimester

189
Q

most common AE of LITHIUM

A

GI distress- reduced appetite, nausea, vomiting, diarrhea

  • thyroid ab
  • nonsignificant leukocytosis
  • polyuria or polydypsia 2’ to ADH antagonism
  • interstitial renal fibrosis
  • hair loss, acne
190
Q

classification of toxic effects of LITHIUM

A

mild (1.0-1.5)
moderate (1.6-2.5)
severe (>2.5)

191
Q

as effective as LITHIUM in mania

A

VALPROIC ACID

192
Q

factors affecting positive response in VALPROIC ACID

A 
rapid cycling patients (females)
comorbid substance issues
mixed patients
patients with comorbid anxiety disorders
LITHIUM nephrotoxicity
better tolerated than LITHIUM
193
Q

moa of VALPROIC acid

A

decreased GABA catabolism by inhibiting GABA transaminase

blockade of t type calcium channels

194
Q

lab tests before VALPROIC acid tx

A

LFTs, pregnancy test, CBC

195
Q

steady state of VALPROIC Acid

A

4-5 days

check 12 hours after last dose and repeat CBCs and LFTs

196
Q

goal in VALPROIC acid tx

A

level of 50-125

197
Q

VALPROIC acid AE

A 
thrombocytopenia and platelet dysfunction
hepatotoxicity
nausea, vomiting, weight gain
transaminitis
sedation
tremor
inc neural tube defect- TERATOGENIC
hair loss
cyp450 inhibitor
198
Q

first line agent for acute mania and mania prophylaxis

A

CARBAMEZIPINE

199
Q

indication for CARBAMEZIPINE

A

rapid cyclers

mixed patients

200
Q

lab test before CARBAMEZIPINE tx

A

LFTs, CBC, EKG

201
Q

steady state of CARBAMEZIPINE

A

5 days
check 12 hours after last dose, repeat CBC, LFTs
check level and adjust dosing after 1month because of self induced metabolism

202
Q

target for Carbamezipine

A

4-12mcg/ml

203
Q

most common SE of CARBAMEZIPINE

A

rash

204
Q

CARBAMEZIPINE other SE

A 
nausea, vomiting, transaminitis
sedation, dizziness, ataxia, confusion
AV conduction delays
aplastic anemia and agranulocytosis
water retention 
With CYP450 inducer can lead to inc metab
heteroinducer
205
Q

drugs that decrease CBZ levels

A

neuroleptics
barbiturates
PHENYTOIN
TCAs

206
Q

has specific efficacy for bipolar depression

A

LAMOTRIGINE (LAMICTAL)

207
Q

moa of LAMOTRIGINE

A

Na and glutamate antagonist
prolongs inactivation of VG Na+ channels
acts presynaptically on VG Ca2+, decreasing glutamate release

208
Q

lab test for LAMOTRIGINE

A

LFTs

209
Q

initiation of titration for LAMOTRIGINE

A

start with 25mg daily for 2 weeks, then inc to 50mg for 2 weeks then inc to 100mg
because faster titration has higher incidence of rash

210
Q

advice for LAMOTRIGINE tx

A

not to stop esp 5days or more - must start at 25mg again

211
Q

most severe AE of LAMOTRIGINE

A

toxic epidermal necrolysis

SJS

212
Q

used to treat many diagnosis including panic disorder, generalized anxiety disorder, substance related disorder and their withdrawal, insomnias, parasomnias

A

anxiolytics or sedatives

213
Q

often used for CNS deprssant withdrawal protocols such as ETOH withdrawal

A

BENZODIAZEPINES

214
Q

BENZODIAZEPINES indications

A

insomnia
parasomnia
anxiety disorders

215
Q

duration of BENZODIAZEPINES

A

very short, shorter than half life

within a few hours

216
Q

BENZODIAZEPINES SE

A 
somnolence
cognitive deficits
amnesia
disinhibition
tolerance
dependence
217
Q

effect of BENZODIAZEPINES

A

anxiolytic
hypnotic
myorelaxant
amnesia

218
Q

BENZODIAZEPINES clinical use

A 
anxiety
panic disorder
phobias
insomnias
muscle spasms
premedication for op
sedation for minor surgeries
219
Q

benzodiazepine react with

A

with booster site on GABA receptors

220
Q

BENZODIAZEPINE moa

A

potentiate the inhibitory effects of GABA

221
Q

body’s natural hyonotic and tranquiliser

A

GABA

222
Q

BENZODIAZEPINE AE

A 
oversedation
memory impairment when used as premedication before surgery
paradoxical stimulant effects 
depression, emotional blunting
floppy infant syndrome
223
Q

floppy infant syndorme

A 
lax muscles
oversedation 
failure to suckle
hyperexcitability
high pitch crying
feding difficulties
224
Q

floppy infant syndrome may persist

A

in 2weeks

225
Q

antipsychotic drugs general classification

A 
phenothiazines
thioxanthene derivatives
butyrophenone derivatives
bensizoxazole
benzamide
benzothiazepine
dibenzoxapines
dihydroindolone
diphenylbutylpiperidine
arylpiperidone
remoxipride
226
Q

antipsychotics-Phenothiazines classification

A

aliphatic
piperazines
piperidines

227
Q

antipsych-phenothiazines-Aliphatics

A
228
Q

antipsych-phenothiazine-Piperazines

A

PROCHLORPERAZINE (compazine)

229
Q

antipsych-phenothiazines-Piperidines

A
230
Q

antipsych-Thioxanthine derivatives

A

THIOXANTHENE

THIOTHIXINE

231
Q

antipsych-Butyrophenone derivatives

A
232
Q

antipsych-Dibenzoxapines

A

LOXAPINE

233
Q

antipsych-Bensizoxazole

A

RISPERIDONE

234
Q

antipsych-Dihydroindolone

A

MOLINDONE

235
Q

antipsych-diphenylbutylpiperidine

A

PIMOZIDE

236
Q

antipsych-Benzamide

A

SULPIRIDE

237
Q

antipsych-Benzothiazepine

A

QUETIAPINE

238
Q

antipsych-Arylpiperylindole

A

SERTINDOLE

239
Q

aliphatic side chains in antipsychotic drugs

A

CHLORPROMAZINE
less extrapyramidal
more sedation, hypotension, tachycardia

240
Q

piperidine ring in antipsychotics

A

THIORIDAZINE
more histaminic
more anticholinergic
similar to aliphatic phenothiazines

241
Q

piperazine substituent in antipsychotics

A 
FLUPHENAZINE
more potent
more extrapyramidal
less sedating
less autonomic effects
242
Q

mood stabilizing drugs

A

LITHIUM CARBONATE
CARBAMEZIPINE
VALPROATE DISODIUM

243
Q

psychosedative and anti anxiety drugs

A

propanediols
benzodiazeoines
h1 receptor blocker with mild psychosedative action

244
Q

antianx-Propanediols

A

MEPROBAMATe

245
Q

antianx-Benzodiazepines

A
246
Q

antianx-H1 receptor blocker with mild psychosedative action

A

DIPHENHYDRAMINE HCL

TRIPELENAMINE

247
Q

antidepressants

A 
TCA
2nd gen
3rd gen
SSRI
MAOI- nonselective, reversible
248
Q

Antidep-TCA

A
249
Q

antidep-2nd gen

A
250
Q

antidep-3rd gen

A

VENFLAXINE
MIRTAZAPINE
NEFAZODONE

251
Q

antidep-SSRIs

A
252
Q

antidep-nonselective MAOI

A

hydrazide derivatives: PHENELZINE, ISOCARBOXAZID

non: TRANYLCYPROMINE

253
Q

antidep-reversible inh of MAo-a

A

MECLOBEMIDE

BROFAROMINE

254
Q

selective MAO B inh are used as

A

agents against Parkinsons dse

255
Q

nonselective older, typical or first gen neuroleptic that binds to D1 D2 5-HT2 H1 alpha2 adrenergic receptors

A

HALOPERIDOL

256
Q

efficacy of neuroleptics is thought to be due to

A

antagonism of dopamine receptors in the mesolimbic and mesofrontal systems

257
Q

AE of typical neuroleptics

A

tachycardia, impotence, dizziness (nonselective interaction at the alpha adrenoreceptor), sedation, weight gain (H1 receptor blockade)

258
Q

atypical antipsychotics effective for negative symptoms

A

CLOZAPINE
OLANZAPINE
RISPERIDONE

259
Q

Resperidone can bind to which receptors?

A

D2, 5-HT2, alpha2

260
Q

atypical neuroleptics have little or no affinity to which receptor?

A

D1

261
Q

dopaminergic AE of antipsychotics

A

extrapyramidal dystonia- akathisia, pseudoparkinsonian, tardive dyskenisia
hyperprolactinemia- galactorrhea, gynecomastia

262
Q

antimuscarinic-cholinergic AE of antipsychotics

A

visual- blurred vision, narrow angle glaucoma
Gi- dry mouth, constipation
GU- urinary retention, delayed or retrograde ejaculation
CNS- memory dysfunction, delirium
CVS- sinus tachycardia
skin- decreased sweating

263
Q

antihistaminic AE of antipsychotics

A

sedation

hypotension

264
Q

anti alpha1 AE of antipsychotics

A

postural hypotension, dizziness

reflex tachycardia

265
Q

calcium channel blockade AE of antipsychotics

A

neuroleptic malignant syndrome
inh of ejaculation
arrhythmias

266
Q

no known receptor mediation AE of antipsychotics

A 
hematologic
agranulocytosis
GI
anorexia
nausea and vomiting
CNS
seizures
depression
visual
pigmentary retinopathy (THIORIDAZINE)
skin
discoloration
photosensitivity
immune
allergic rxns
267
Q

extrapyramidal SE (acute dystonia, Parkinson syndrome) of antipsychotics treatment

A

DIPHENHYDRAMINE
BIPERIDEN
BETA BLOCKERS

268
Q

SE akathisia treatment

A

PROPRANOLOL or other beta blockers

270
Q

key pathways affected by dopamine in the brain

A

mesocortical
mesolimbic
nigrostriatal
tuberoinfundibular

Pharmacology (8 decks)

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