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Nurs 307 > Day 2-psychopharmacotheapy > Flashcards

Day 2-psychopharmacotheapy Flashcards

1
Q

psychopharmacotherapy

A

a subspeciality of pharmacology

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2
Q

classes of psychopharm

A

antipsychotics
mood stabilizers
antidepressants
antianxiety
stimulants

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3
Q

pharmacodynamics

A

where drugs act
what does the drug do to the body
how intense of an effect does it have
where does it have that effect

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4
Q

4 sites of drug action

A

receptors
ion channels
enzymes
carrier proteins

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5
Q

receptors

A

all drugs mimic some biological action that we naturally have

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6
Q

agonist

A

working with or add to the natural process

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7
Q

antagonist

A

working against the natural biologic process

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8
Q

selectivity

A

specific for a receptor
lock and key

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9
Q

affinity

A

degree of attraction

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10
Q

intrinsic activity

A

ability to produce a biologic response once it is attached to receptor
will it actually do waht we want and produce a therapeutic effect

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11
Q

ion channels

A

drugs can block or open then

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12
Q

example of ion channels

A

benzodiazepine drug facilitate GABA neurotransmitter in opening the chloride ion channel

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13
Q

enzymes

A

complex proteins that catalyze specific biochemical reactions within cells and are targets for some drugs

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14
Q

enzyme example

A

monoamine oxidase is an enzyme that breaks down most bioamine neurotransmitters
MAOIs inhibit the breakdown of bioamine neurotransmitters

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15
Q

bioamine neurotransmitters

A

NE, DA serotonin

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16
Q

too much NE

A

anxiety

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17
Q

too much DA

A

psychosis or depression

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18
Q

too much MAO

A

they break down serotonin causing depression

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19
Q

prescribing medication

A

we don’t know what causes mental health symptom so we try all classes until one works

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20
Q

carrier proteins

A

function is to take neurotransmitter back into presynaptic cell after neurotransmitter have activated receptors in the synapse

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21
Q

example of carrier protein

A

SSRI mostly used for anxiety, depression, schizophrenia and PTSD

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22
Q

efficacy

A

ability to produce desired response

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23
Q

potency

A

dose required to produce desired response

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24
Q

ss of effect due to biologic adaptation

A

tolerance
treatment refractory
side effects

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25
Q

tolerance

A

your body getting used to having them and this becomes its baseline

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26
Q

treatment refractory

A

drug resistant from the start so they don’t respond to anything

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27
Q

side effects

A

all meds have them because we have receptors distributed in all parts of the body but we only want to target the brain

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28
Q

drug toxicity

A

concentation of the drug in the body greater than the safe range and may become harmful or poisonous to the body

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29
Q

therapeutic index

A

ratio between minimum effective dose and maximum safe dose
the higher the ratio the better because more space between high and low

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30
Q

pharmacokinetics

A

what does the body do to a drug
ADME

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31
Q

absorption

A

movement from the site of administration to the plasma

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32
Q

ways to administer psychotropic medications

A

oral
IM
IV

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33
Q

IM injections

A

short or long acting
good for non compliance
no pocketing
convinient

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34
Q

first pass metabolism

A

before reaching the circulation
higher first pass lower response

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35
Q

bioavailability

A

how much reached the circulation unchanged

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36
Q

distribution

A

reflects how easy it is for a drug to pass out of teh systemic circulation and move into other types of tissues

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37
Q

solubility of drugs

A

most are water soluble and don’t go to the brain
psychiatric drugs must cross BBB and are therefore fat soluble

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38
Q

factors effecting distribution

A

amount of blood flow or perfusion within the tissue
how lipophilic the drug is
anatomic barriers like the BBB the drug must cross

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39
Q

metabolism

A

process by which the drug is altered and broken down into smaller substances (metabolites ) that are usually inactive
commonly carried out in the liver

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40
Q

lipid soluble and metabolism

A

usually become more water soluble and are therefore excreted

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41
Q

excretion

A

the elimination from the body eitehr unchanged or as metabolites

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42
Q

half life

A

the time required for plasma concentrations of the drug to be reduced by 50%
dosing frequency based on this

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43
Q

dosing

A

administration of medication over time so that therapeutic levels can be achieved

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44
Q

steady state

A

drug accumulates and plateuas at a particular level
rate of accumulation is determined by half life

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45
Q

reaching steady state

A

when the rate of drug input is equal to the rate of drug elimination
maintenace dosing
5x the elimination half life for a drug after regular dosing started

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46
Q

plateaus

A

any increase in dose doesn’t improve condition

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47
Q

titration

A

slowly working up to an effective dose
done because of severe side effects, allergy risk or narrow therapeutic indexi

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48
Q

individual variations of drug effects age

A

alteration in gastric absorption
renal function is altered in very young and old
liver metabolism decreases with age

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49
Q

ethnicity and genetic make up variability

A

genetics play a significant role in the metabolism of medication

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50
Q

phases of drug treatment

A

initiation
stabilization
maintenance
discontiuation

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51
Q

stabilization

A

from the start until you achieve a stable level that is working

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52
Q

discontinuation

A

not common in mental health

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53
Q

antipsychotic medication target symptoms

A

psychotic symptoms
positive and negative

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54
Q

types of antipsychotics

A

first generation/typical
second generation/atypical. Good for positive and negative

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55
Q

preparations of antipsychotics

A

Oral
IM
depot-haloperidol and fluphenazine
long acting injectable-risperdal constants

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56
Q

side effects antipsychotics

A

orthostatic hypotension
anticholinergic
metabolic syndrome/weight gain
endocrine and sexual drive decreased
blood dysstasias agranulocytosis (clozapine)
EPS
NMS

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57
Q

acute agitation

A

5mg haloperidol and 5mg benzodiazepine

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58
Q

poor response to antipsychotic medication

A

obtaining antipsychotic plasma levels in patients who hhave had poor response despite a trial with an adequate dose/duration of medication can be helpful to rule out adherence, idenntify rapid elimination, confirm true treatment resistance

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59
Q

rapid elimination

A

their half life is much shorter than normal resulting in low blood levels

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60
Q

typical antipsychotics

A

phenothiazines
haloperidol (haldol)h

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61
Q

Haldol use

A

acute agitation

62
Q

atypical antipsychoticw

A

clozapine
risperidone
olanzapine
quetiapine
ziprasidone
aripiprazole

63
Q

clozapine

A

Clozaril
last resort due to agranulocytosis

64
Q

Risperidone

A

Risperdal
common, most potent

65
Q

olanzapine

A

Zyprexa
common at 5-10mg/day

66
Q

quetiapine

A

seroquel
bad at antipsychotic but stabilizes, mood, anxiety, depression and a sleeping aid

67
Q

medication related movement disorder

A

cased by blocking dopamine receptors
3 or more anti psychotics lead to high risk

68
Q

acute EPS

A

dystonia
Parkinsonism
akathiasia

69
Q

dystonia

A

involuntary muscle spasms, abnormal postures

70
Q

parkinsonism

A

rigidity, akinesia, tremor, mask like face, loss of spontaneous movement

71
Q

akathisia

A

inability to sit still, restlessness

72
Q

akinesia

A

slow movement

73
Q

treatment of EPS

A

anticholinergic medication for hystonia, parkinsonism
akathisia does not ususally repond to meds but beta blocker are the best option

74
Q

Cogentin

A

often in an injection of haloperidol and ativan in prediction of EPS symptoms

75
Q

chronic movement disorder

A

tardive dyskinesia
treatment is irreversible

76
Q

tardive dyskinesia symptoms

A

irregular, repetitive involuntary movements of the mouth, face and tonge, including chewing, tongue protrusion, lip smacking, puckering of the lips and rapid eye blinking
abnormal finger movements are common

77
Q

prevention of EPS

A

using lowest dose possible

78
Q

prevention of tardive dyskinesia

A

using lowest possible dosage
minimizing use of PRN antipsychotic medication
closely monitoring individuals in high risk gropus

79
Q

high risk groups for tardive dyskinesia

A

late teens and early twenties

80
Q

mood stabilizers

A

used primarily for stabilizing mood
treating BPD I and II

81
Q

first line of BPD

A

lithium carbonate and divalproex sodium/valproic acid

82
Q

BPD I

A

patients have mania and depression
mania putting people out of life

83
Q

BPD II

A

patient has depression and hypomania
less severe usually a person can function in life

84
Q

lithium carbonate

A

action unknown but effective for BPD

85
Q

side effects of carbonate

A

thrist
metallic taste
increased frequency of urination
fine head and hand tremor
drowsiness and mild diarrhea

86
Q

adverse effects of lithium

A

toxicity so measure blood levels
monitor salt intake and dehydration because as salt increases lithium decrease
monitor creatinine concentration
monitor thyroid hormones every 6 months
avoid in pregnancy
monitor CBC q6month

87
Q

mood stabilizers anticonvulsants

A

valproates and derivates
carbamazepine
gapapentin
lamotrigine
tropiramate

88
Q

valproates and derivates

A

divalproex sodium

89
Q

carbamazepine

A

tegretol
only if not responding to others

90
Q

gabapentin

A

neurotensin
olanzapine
antipsychotic is more common than it is for BPD

91
Q

Lamotrigine

A

Lamictal
BPD II not strong enough of BPD I

92
Q

topiramate

A

Topamax
rarely seen for BPD

93
Q

mechanism of BPD

A

cause an increase GABA neurotransmitter in brain

94
Q

kindling of BPD

A

a commonly used model for the development of seizures and epilepsy in which the duration and behavioral involvemetn of induced seizures increases after seizures are induced repeatedly
in the context of manic episodes too

95
Q

kindling common words

A

every manic episode lowers the threshold for the next one

96
Q

anticonvulsant side effects

A

dizziness, drowsiness, tremor, visual disturbances, nausea and vomiting
weight gail (all psych med)
alopecia

97
Q

interventions for BPD

A

minimized by treating in low doses
given with foodi

98
Q

depressant classes

A

SSRI
SSNRI
SNRI (anxiety because NE is related to emotion)
TCA
MAOIs

99
Q

anxiety and depression

A

have a 50% comorbidity

100
Q

SSRI examples

A

fluoxetine
sertraline
paroxetine
fluvoxamine
citalopram
escitalopram
take 6 weeks to reach therapeutic levels

101
Q

Citalopram

A

Celexia
takes 4 weeks to reach therapeutic levels but is very expensive

102
Q

SSNRI

A

venlafaxine
Desvenlafaxine
Buloxetinev

103
Q

venlafaxine

A

Effexor
also treats panic disorder and social anxiety disorder

104
Q

Desvenlafaxine

A

Pristiq
also treats anxiety and panic disorder
expensive

105
Q

duloxetine

A

Cymbalta
also treats anxiety and certain types of chronic pain

106
Q

SSRI/SSNRI side effects

A

headache
anxeity
transiety nausea
vomting
diarrhea
weight gain
sexual dysfunction
serononin syndrome
sedation at high doses

107
Q

serotonin syndrome

A

agitation
confusion
rapid heart rate
dilated pupils
muscle rigidity
high fever seizures

108
Q

when to administer SSRI

A

morning

109
Q

TCA examples

A

amitripyline
nortriptyline
clomipramine
doxepin
trimipramine

110
Q

TCAs

A

not very common
only when patiens are unresponsive to SSRI, SSNRI
narrow therpeutic index
puts a person at higher risk of suicidal ideation

111
Q

TCA common side effects

A

sedation
orthostatic hypotension
anticholinergic

112
Q

other side effects of TCA

A

tremor
restlessness
insomnia
confusion
pedal edema
headache
seizures
blood dyscrasias
sexual dysfunction
cardiotoxicity

113
Q

MAOIs action

A

inhibit the enzyme that is responsbile from the metabolism of serotonin, D and NE and tyramine
causes increased levels of NE and serotonin in the CNS

114
Q

food and MAOIs

A

need a low tyramine diet and avoid high tyramine foods such as aged cheese, sausage
causes a serious spike in BP and requires emergent treatment

115
Q

side effects of MAOIs

A

dry mouth, nausea, constipation, drowsiness and light headedness
drug to drug interaction

116
Q

other antidepressants

A

mirtaapine
trazodone
nefazodone
buprorion

117
Q

Mirtazapine and Trazodone

A

Pereron
off label use for sedation and sleeping aid

118
Q

Bupropion

A

smoking cessation
Wellbutrin

119
Q

anxiety anxiety and sedative hypnotic medication

A

benzodiazepines and non benzodiazepines

120
Q

Benzos

A

diazepam
lorazepam
alprazolam
clonazepam

121
Q

Diazepam

A

valium
alcohol withdrawals because fast acting
LTC drug of choice

122
Q

Lorazepam

A

Ativan
agitation, aggression and anxiety

123
Q

clonazepam

A

Klonopin
most common
less rebounding syndrome or rush

124
Q

non benzos

A

buspirone
zopiclone

125
Q

Rush

A

going from very anxious to very calm
a feeling that can lead to addiction

126
Q

benzodiazepines MOA

A

enhance the effects of GABA by increasing the frequency of the chloride ion channel opening thereby increasing the inhibitory effect of the neurotransmitter GABA on neuronal activity

127
Q

effects of benzos

A

pronounced in the limbic system, thalamus, hypothalamus

128
Q

side effects of benzos

A

sedation and CNS depression
cognitive impairment
developing tolerance and dependency
withdrawal symptoms
alcohol potentiates CNS depression
avoid in the elderly

129
Q

use of benzos

A

short term

130
Q

stimulants

A

amphetamines
used in treating narcolepsy, ADHD and obesity
exact MOA unknown

131
Q

amphetamines example

A

destroamphetamine
methylphenidate
pemoline

132
Q

dextroamphetamine

A

Dexedrine
half life 6-7 hours

133
Q

methylphenidate

A

Ritalin
half life 2-4 hours

134
Q

Pemoline

A

Cylert
half life 12 hours

135
Q

stimulants off label use

A

adjunction iwth other depressants to treat depression and also relieve lethary and reduce cognitive deficits

136
Q

side effects of stimulants

A

insomnia, nervousness, restlessness, tachycardia, heart problems, risk for growth suppression

137
Q

medication non adherence patient teaching

A

identify reason
importance of medication regimen
if its due to side effects review dose or change medication class

138
Q

importance of medication adherence

A

attitude towards medication
insight
side effects

139
Q

managing non responders

A

optimize dose and ensure adequate trial
switching meds
augmentation
combination
atypical antipsychotics
ETC

140
Q

switching

A

antidepressant within same class or other class

141
Q

augmentation

A

adding non antidepressant medication

142
Q

combination

A

using 2 or more antidepressants

143
Q

ECT

A

imitate generalized seizure by an electrical current
short acting anesthetic and muscle relaxant given
repeat procedure 2-3x per week
mechanism unknown

144
Q

use of ECT

A

rapid relief of depressive symptoms

145
Q

side effects of ECT

A

memory loss (short and long term)
hypo or hypertension
bradycardia or tachycardia and minor arrhythmias immediately after

146
Q

effectiveness of ECT

A

80%
SSRI 40-50%

147
Q

new somatic therapies

A

repetitive transcranial magnetic stimulation and vagus nerve stimulation

148
Q

vagus nerve stimulation

A

involves a device to stimulate the Vagus nerve with electrical impulses
an implantable option to treat epilepsy and depression

149
Q

light therapy/photo therapy

A

resets circadian rhythm
used for seasonal affective disorder

150
Q

nutritional therapies

A

neurotransmitter necessary for normal, healthy functioning of the brain nutrients produced fromamino acids taken from food

151
Q

ketamine treatment

A

very effective for depression and suicidal behaviors but not covered by health care

152
Q
A

Nurs 307 (1 decks)

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