Day 2-psychopharmacotheapy Flashcards
(152 cards)
1
Q
psychopharmacotherapy
A
a subspeciality of pharmacology
2
Q
classes of psychopharm
A
antipsychotics
mood stabilizers
antidepressants
antianxiety
stimulants
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
4
Q
4 sites of drug action
A
receptors
ion channels
enzymes
carrier proteins
5
Q
receptors
A
all drugs mimic some biological action that we naturally have
6
Q
agonist
A
working with or add to the natural process
7
Q
antagonist
A
working against the natural biologic process
8
Q
selectivity
A
specific for a receptor
lock and key
9
Q
affinity
A
degree of attraction
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
11
Q
ion channels
A
drugs can block or open then
12
Q
example of ion channels
A
benzodiazepine drug facilitate GABA neurotransmitter in opening the chloride ion channel
13
Q
enzymes
A
complex proteins that catalyze specific biochemical reactions within cells and are targets for some drugs
14
Q
enzyme example
A
monoamine oxidase is an enzyme that breaks down most bioamine neurotransmitters
MAOIs inhibit the breakdown of bioamine neurotransmitters
15
Q
bioamine neurotransmitters
A
NE, DA serotonin
16
Q
too much NE
A
anxiety
17
Q
too much DA
A
psychosis or depression
18
Q
too much MAO
A
they break down serotonin causing depression
19
Q
prescribing medication
A
we don’t know what causes mental health symptom so we try all classes until one works
20
Q
carrier proteins
A
function is to take neurotransmitter back into presynaptic cell after neurotransmitter have activated receptors in the synapse
21
Q
example of carrier protein
A
SSRI mostly used for anxiety, depression, schizophrenia and PTSD
22
Q
efficacy
A
ability to produce desired response
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Q
potency
A
dose required to produce desired response
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Q
ss of effect due to biologic adaptation
A
tolerance
treatment refractory
side effects
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tolerance
your body getting used to having them and this becomes its baseline
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treatment refractory
drug resistant from the start so they don't respond to anything
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side effects
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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drug toxicity
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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therapeutic index
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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pharmacokinetics
what does the body do to a drug
ADME
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absorption
movement from the site of administration to the plasma
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ways to administer psychotropic medications
oral
IM
IV
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IM injections
short or long acting
good for non compliance
no pocketing
convinient
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first pass metabolism
before reaching the circulation
higher first pass lower response
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bioavailability
how much reached the circulation unchanged
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distribution
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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solubility of drugs
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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factors effecting distribution
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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metabolism
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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lipid soluble and metabolism
usually become more water soluble and are therefore excreted
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excretion
the elimination from the body eitehr unchanged or as metabolites
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half life
the time required for plasma concentrations of the drug to be reduced by 50%
dosing frequency based on this
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dosing
administration of medication over time so that therapeutic levels can be achieved
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steady state
drug accumulates and plateuas at a particular level
rate of accumulation is determined by half life
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reaching steady state
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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plateaus
any increase in dose doesn't improve condition
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titration
slowly working up to an effective dose
done because of severe side effects, allergy risk or narrow therapeutic indexi
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individual variations of drug effects age
alteration in gastric absorption
renal function is altered in very young and old
liver metabolism decreases with age
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ethnicity and genetic make up variability
genetics play a significant role in the metabolism of medication
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phases of drug treatment
initiation
stabilization
maintenance
discontiuation
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stabilization
from the start until you achieve a stable level that is working
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discontinuation
not common in mental health
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antipsychotic medication target symptoms
psychotic symptoms
positive and negative
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types of antipsychotics
first generation/typical
second generation/atypical. Good for positive and negative
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preparations of antipsychotics
Oral
IM
depot-haloperidol and fluphenazine
long acting injectable-risperdal constants
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side effects antipsychotics
orthostatic hypotension
anticholinergic
metabolic syndrome/weight gain
endocrine and sexual drive decreased
blood dysstasias agranulocytosis (clozapine)
EPS
NMS
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acute agitation
5mg haloperidol and 5mg benzodiazepine
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poor response to antipsychotic medication
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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rapid elimination
their half life is much shorter than normal resulting in low blood levels
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typical antipsychotics
phenothiazines
haloperidol (haldol)h
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Haldol use
acute agitation
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atypical antipsychoticw
clozapine
risperidone
olanzapine
quetiapine
ziprasidone
aripiprazole
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clozapine
Clozaril
last resort due to agranulocytosis
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Risperidone
Risperdal
common, most potent
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olanzapine
Zyprexa
common at 5-10mg/day
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quetiapine
seroquel
bad at antipsychotic but stabilizes, mood, anxiety, depression and a sleeping aid
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medication related movement disorder
cased by blocking dopamine receptors
3 or more anti psychotics lead to high risk
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acute EPS
dystonia
Parkinsonism
akathiasia
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dystonia
involuntary muscle spasms, abnormal postures
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parkinsonism
rigidity, akinesia, tremor, mask like face, loss of spontaneous movement
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akathisia
inability to sit still, restlessness
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akinesia
slow movement
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treatment of EPS
anticholinergic medication for hystonia, parkinsonism
akathisia does not ususally repond to meds but beta blocker are the best option
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Cogentin
often in an injection of haloperidol and ativan in prediction of EPS symptoms
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chronic movement disorder
tardive dyskinesia
treatment is irreversible
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tardive dyskinesia symptoms
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
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prevention of EPS
using lowest dose possible
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prevention of tardive dyskinesia
using lowest possible dosage
minimizing use of PRN antipsychotic medication
closely monitoring individuals in high risk gropus
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high risk groups for tardive dyskinesia
late teens and early twenties
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mood stabilizers
used primarily for stabilizing mood
treating BPD I and II
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first line of BPD
lithium carbonate and divalproex sodium/valproic acid
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BPD I
patients have mania and depression
mania putting people out of life
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BPD II
patient has depression and hypomania
less severe usually a person can function in life
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lithium carbonate
action unknown but effective for BPD
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side effects of carbonate
thrist
metallic taste
increased frequency of urination
fine head and hand tremor
drowsiness and mild diarrhea
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adverse effects of lithium
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
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mood stabilizers anticonvulsants
valproates and derivates
carbamazepine
gapapentin
lamotrigine
tropiramate
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valproates and derivates
divalproex sodium
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carbamazepine
tegretol
only if not responding to others
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gabapentin
neurotensin
olanzapine
antipsychotic is more common than it is for BPD
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Lamotrigine
Lamictal
BPD II not strong enough of BPD I
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topiramate
Topamax
rarely seen for BPD
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mechanism of BPD
cause an increase GABA neurotransmitter in brain
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kindling of BPD
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
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kindling common words
every manic episode lowers the threshold for the next one
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anticonvulsant side effects
dizziness, drowsiness, tremor, visual disturbances, nausea and vomiting
weight gail (all psych med)
alopecia
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interventions for BPD
minimized by treating in low doses
given with foodi
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depressant classes
SSRI
SSNRI
SNRI (anxiety because NE is related to emotion)
TCA
MAOIs
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anxiety and depression
have a 50% comorbidity
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SSRI examples
fluoxetine
sertraline
paroxetine
fluvoxamine
citalopram
escitalopram
take 6 weeks to reach therapeutic levels
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Citalopram
Celexia
takes 4 weeks to reach therapeutic levels but is very expensive
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SSNRI
venlafaxine
Desvenlafaxine
Buloxetinev
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venlafaxine
Effexor
also treats panic disorder and social anxiety disorder
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Desvenlafaxine
Pristiq
also treats anxiety and panic disorder
expensive
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duloxetine
Cymbalta
also treats anxiety and certain types of chronic pain
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SSRI/SSNRI side effects
headache
anxeity
transiety nausea
vomting
diarrhea
weight gain
sexual dysfunction
serononin syndrome
sedation at high doses
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serotonin syndrome
agitation
confusion
rapid heart rate
dilated pupils
muscle rigidity
high fever seizures
108
when to administer SSRI
morning
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TCA examples
amitripyline
nortriptyline
clomipramine
doxepin
trimipramine
110
TCAs
not very common
only when patiens are unresponsive to SSRI, SSNRI
narrow therpeutic index
puts a person at higher risk of suicidal ideation
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TCA common side effects
sedation
orthostatic hypotension
anticholinergic
112
other side effects of TCA
tremor
restlessness
insomnia
confusion
pedal edema
headache
seizures
blood dyscrasias
sexual dysfunction
cardiotoxicity
113
MAOIs action
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
food and MAOIs
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
side effects of MAOIs
dry mouth, nausea, constipation, drowsiness and light headedness
drug to drug interaction
116
other antidepressants
mirtaapine
trazodone
nefazodone
buprorion
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Mirtazapine and Trazodone
Pereron
off label use for sedation and sleeping aid
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Bupropion
smoking cessation
Wellbutrin
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anxiety anxiety and sedative hypnotic medication
benzodiazepines and non benzodiazepines
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Benzos
diazepam
lorazepam
alprazolam
clonazepam
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Diazepam
valium
alcohol withdrawals because fast acting
LTC drug of choice
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Lorazepam
Ativan
agitation, aggression and anxiety
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clonazepam
Klonopin
most common
less rebounding syndrome or rush
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non benzos
buspirone
zopiclone
125
Rush
going from very anxious to very calm
a feeling that can lead to addiction
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benzodiazepines MOA
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
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effects of benzos
pronounced in the limbic system, thalamus, hypothalamus
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side effects of benzos
sedation and CNS depression
cognitive impairment
developing tolerance and dependency
withdrawal symptoms
alcohol potentiates CNS depression
avoid in the elderly
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use of benzos
short term
130
stimulants
amphetamines
used in treating narcolepsy, ADHD and obesity
exact MOA unknown
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amphetamines example
destroamphetamine
methylphenidate
pemoline
132
dextroamphetamine
Dexedrine
half life 6-7 hours
133
methylphenidate
Ritalin
half life 2-4 hours
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Pemoline
Cylert
half life 12 hours
135
stimulants off label use
adjunction iwth other depressants to treat depression and also relieve lethary and reduce cognitive deficits
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side effects of stimulants
insomnia, nervousness, restlessness, tachycardia, heart problems, risk for growth suppression
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medication non adherence patient teaching
identify reason
importance of medication regimen
if its due to side effects review dose or change medication class
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importance of medication adherence
attitude towards medication
insight
side effects
139
managing non responders
optimize dose and ensure adequate trial
switching meds
augmentation
combination
atypical antipsychotics
ETC
140
switching
antidepressant within same class or other class
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augmentation
adding non antidepressant medication
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combination
using 2 or more antidepressants
143
ECT
imitate generalized seizure by an electrical current
short acting anesthetic and muscle relaxant given
repeat procedure 2-3x per week
mechanism unknown
144
use of ECT
rapid relief of depressive symptoms
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side effects of ECT
memory loss (short and long term)
hypo or hypertension
bradycardia or tachycardia and minor arrhythmias immediately after
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effectiveness of ECT
80%
SSRI 40-50%
147
new somatic therapies
repetitive transcranial magnetic stimulation and vagus nerve stimulation
148
vagus nerve stimulation
involves a device to stimulate the Vagus nerve with electrical impulses
an implantable option to treat epilepsy and depression
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light therapy/photo therapy
resets circadian rhythm
used for seasonal affective disorder
150
nutritional therapies
neurotransmitter necessary for normal, healthy functioning of the brain nutrients produced fromamino acids taken from food
151
ketamine treatment
very effective for depression and suicidal behaviors but not covered by health care
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