week 6 Flashcards
(97 cards)
1
Q
what are psychotropic meds
A
- affect the action of CNS
- mind altering meds to change ones thinking, feelings, perceptions, behaviours
- manage symptoms of mental illness but not curative
2
Q
top 5 most frequently prescribed psychotropic drugs
A
- Xanax (alprazolam)
- Zoloft (sertraline)
- Celexa (citalopram)
- Prozac (fluoxetine)
- Ativan (lorazepam)
3
Q
for mood disorders we use…
A
antidepressants
can also use…
sedatives/anti-anxiety and antipsychotics
4
Q
for anxiety disorders we use
A
mood stabilizers
sedatives/anti-anxiety
can also use…
antidepressants
5
Q
for sleep disorders we use
A
sedatives/anti-anxiety
6
Q
for psychotic disorders we use
A
antipsychotics
7
Q
pharmacodynamics
A
biochem and physiological effects of drugs on body
We theorize how they have an effect on the body and treat mental illness but we are not 100% sure.
(MoA and effect)
8
Q
pharmacokinetics
A
actions of body on drug
(absorption, distribution, metabolism, excretion)
How long acting are they?
9
Q
pharmacogenetics
A
genetic differences inform treatment approaches
10
Q
4 neurotransmitters + what they do
A
serotonin
NE
dopamine
GABA
Drugs enhance, block, or otherwise change the action of the neurotransmitter in the CNS at the synaptic cleft
How they do this depends on the drugs MOA
11
Q
most common prescribed classes
A
Benzodiazapines and SSRIs
12
Q
for eating disorders and substance abuse we can use
A
antidepressants
13
Q
can psychotropics have overlapping use?
A
Psychotropics have overlapping use and have been found to be effective for multiple conditions. For example antidepressants are the main treatment for anxiety disorders and antipsychotics used for bipolar disorder
14
Q
what is an agonist
A
drugs that occupy receptors and activate them
15
Q
what is an antagonist
A
drugs that occupy recptors but do not activate them
Other ways through works includes enhancing neurotransission action on the receptor, reuptake inhibition, preventing the breakdown of neurotransmitters.
16
Q
agonist alone =
A
full activation
17
Q
agonist + antagonist =
A
less activation
18
Q
antagonist alone =
A
no activation
19
Q
what are anxiolytics
A
meds that enhance GABA activity
ex: relief of acute anxiety, insomnia
we will focus on fast-acting, symptomatic treatments for anxiety in this lecture. These drugs may be used alone in mild or situational anxiety, but often need to be combined with daily, longer acting medication to successfully control anxiety (antidepressants).
ex: benzodiazepines, non-benzodiazepine anxiolytic, non-benzodiazepine hypnotic
20
Q
what is GABA
A
= major inhibitory transmitter in the CNS
calm your mind
21
Q
give list of 4 benzodiazepines
A
alprazolam (xanax)
clonazepam (rivotril)
lorazepam (ativan)
diazepam (valium)
“Z-hypnotics”
zepam’s, zolam
22
Q
example non-benzodiazepine anxiolytic
A
buspirone (buspar)
23
Q
describe non-benzodiazepine hypnotic
A
diphenhydramine (ZzzQuil, Benadryl)
doxylamine (unisom)
24
Q
describe to me the pharmacologic target of benzodiazepines + what it does
A
targets = GABA receptor
allosteric modifier
- binding increases frequency w which chloride channel opens, resulting in hyperpolarization (and inhibition) of postsynaptic neuron
25
what happens w high vs low doses of benzodiazepines
low - calmness and "tranquility" which relieves acute hyperarousal, agitation
high - cause sedation and promote sleep
26
risk of adverse effects for benzodiazepines
- tolerance, dependence, and addiction are possible
- life threatening CNS depression when combined w opioids, ETOH, or other sedatives
- impairment of reflexes and attention (caution when driving)
- increase falls, delirium in elderly
27
what are benzodiazepines good for
Very good at relieving anxiety and inducing sleep – in the short term. Not a good strategy for long-term therapy for most patients for the following reasons.
28
what are zopiclone, zolpidem, zaleplon
- essentially same effects on GABA receptors as benzodiazepines
- faster onset than many BZDs (within 15-30 min or less)
- marketed as being safer or more targeted toward insomnia than BZDs, but little scientific or clinical evidence to support this
Pharmacodynamics, clinical effects, and risks are very similar to benzodiazepines.
29
pt education for zopiclone, zolpidem, zaleplon
- take when ready to sleep, expect effects for at least 8 hours
- daytime sedation/impairment possible
- common side effect: bitter taste in mouth
- Should be used short term (2- 4 weeks)
- Expect poor sleep if stopped abruptly after long-term use
30
what is clinical role of buspirone
short term relief of anxiety
A maintenance treatment for generalized anxiety disorder. It is usually a second-line treatment – less effective than antidepressants and needs to be taken 2-3x daily. Otherwise has a lot in common with antidepressants – acts via serotonin, not sedating, not habit forming.
31
MoA for buspirone
partial serotonin agonist
32
advantages of buspirone
No strong sedative-hypnotic properties
Less danger of interactions with alcohol and other sedatives
Dependence does not develop
May be better tolerated than alternatives
33
what 2 neurotransmitters play a major role in regulating mood
Norepinephrine (get up + go) and serotonin (calm + happy) play a major role in regulating mood
All increase the synaptic level of one or both neurotransmitters
34
3 hypothesis of antidepressants’ mechanisms of action
1. The monoamine hypothesis of depression
"fixing the missing chemicals makes you feel better"
- Deficiency in one or more of the 3 neurotransmitters (serotonin, norepinephrine, dopamine)
- Increasing the neurotransmitters alleviates depression
2. The monoamine receptor hypothesis of depression
"your brain gets extra sensitive bc of the chemical storage)
- Low levels of neurotransmitters cause postsynaptic receptors to be up-regulated (increased sensitivity or number)
- Increasing neurotransmitters by antidepressants results in down-regulation (desenstiization)
3. Increase production of neurotropic factors
"help your brain grow new connections to feel better"
- regulate the survival of neurons and enhance sprouting of axons to from new synaptic connections
35
antidepressants are used for maintenance therapy for people with...
anxiety disorders as well
36
tell me about antidepressants
All antidepressants boost the activity of endogenous serotonin and norepinephrine, but in different ways. Different groups of antidepressants are names after the mechanism by which they increase serotonin or norepinephrine levels. All groups of antidepressants are similarly effective. However, older antidepressants have A LOT more side effects than newer ones, and are rarely used. SSRIs and SNRIs are most commonly used today
37
what are monoamine oxidase inhibitors (MAOIs)
- increase synaptic serotonin and NE by blocking monoamine oxidase enzyme
antidepressant
MAOIs increase levels of both serotonin and norepinephrine by A LOT. While effective, they carry risks of dangerous side effects. MAO enzyme is needed to break down many substances in the body. One substance called tyramine, is unrelated to depression but can build up to dangerous levels in the presence of MAOs. Hypertensive crisis can be life-threatening. Tyramine comes from foods especially cheeses, cured meats, and alcohol and must be avoided. MAOIs can also be dangerous when combined with other drugs – serotonin syndrome is a potentially serious drug interaction which can cause convulsions and altered mental status.
38
2 types of MAOIs in canada
phenelzine, tranylcrypromine
39
side effect risk of MAOIs
- hypertensive crisis (dietary restriction to avoid tyramine necessary)
- serotonin syndrome (if combined w other serotonergic drugs)
40
MAOI acronym for meds (trade names)
"No Popular Meds"
Nardil, Parnate, Marplan
41
what needs to be avoided in MAOIs
barbiturates, tricyclic antidepressants, antihistamines, CNS depressants, antihypertensives, OTC cold meds
42
MAOIs hypertensive crisis symptoms + what they can't eat
sweating, tremors, dizziness, increased BP, pounding or fast heartbeat
tyramine foods - cheese, wine, pickled foods
43
what do tricyclic antidepressant (TCAs)
- increase synaptic serotonin and NE by blocking reuptake inhibitors
Increase serotonin and norepinephrine in a different way and to a lesser extent than MAOIs. They lack some of the dangerous side effects of MAOIs. They effect other receptors throughout the body which cause mild but very bothersome side effects. While generally safe they are toxic in overdose and may result in death. They are rarely used to treat depression these days for these reasons but have been found to be helpful for managing chronic pain and insomnia and you will likely see them used in very low doses in many patients.
44
tricyclic antidepressant (TCAs) examples
Amitriptyline, nortriptyline, desipramine, imipramine, clomipramine
45
what are side effects of tricyclic antidepressant (TCAs) + overdose can cause + used for...
Muscarinic – dry mouth, constipation
Histaminic – sedation, weight gain
Alpha - hypotension
Overdose can cause arrhythmias and death
Used for chronic pain, insomnia
46
what do Selective Serotonin Reuptake Inhibitors (SSRIs)
Increase synaptic serotonin by blocking SERT reuptake transporter
Fluoxetine, sertraline, paroxetine, citalopram, escitalopram
More selective action than TCAs
Comparable efficacy with fewer side effects
Increased adherence to treatment
Low toxicity in overdose
SSRIs inhibit SERT only, increasing serotonin. They do not act on muscarinic or histaminic receptors like TCAs do.
47
side effects of SSRIs
Side effects
Nausea and vomiting (transient)
Anxiety (transient)
Sexual dysfunction
Discontinuation symptoms if abruptly stopped
48
Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) what are they
Increase synaptic serotonin and (at higher doses) norepinephrine by blocking SERT and NET reuptake transporters
Little to no activity at muscarinic, histamine, alpha receptors
Additional clinical applications: menopausal symptoms, neuropathic pain
49
SNRI examples
Venlafaxine, duloxetine, desvenlafaxine
50
SNRI side effects
Similar to SSRIs
Dose-dependent hypertension
51
Bupropion (Wellbutrin)
Dopamine-norepinephrine reuptake inhibitor
Mildly stimulating – administer in morning
Used for smoking cessation - inhibits nicotinic acetylcholine receptors
Well tolerated but risk of seizures in overdose
52
Mirtazapine (Remeron)
Alpha2 receptor antagonist – increases release of serotonin, norepinephrine from axon
Sedating – administer at bedtime
Increases appetite
Often well tolerated by elderly patients
53
when do antidepressants work?
take a while for them to feel the benefits
week 1: tough week, ppl can experience side effects (nausea, increased anxiety, dizziness, etc) are transient so they should go away
week 2: more physical symptoms of depression start to normalize (more reg sleep schedule, more awake and refreshed, appetite improved, aches and pain may go away)
week 3-8: mood and cognitive benefits, negative feelings would gradually decrease, cognitively sharp, more motivated to engage in everything
54
what do mood stabilizers do
Reduce the symptoms of mania/hypomania, depression, or BOTH
Most common clinical use = management of bipolar or schizoaffective disorders
Also used “off label” for impulse control disorders, personality disorders, and behavioural disorders
Mechanisms of action are not completely understood
- May act by affecting electrical conductivity in neurons
- May reduce excitatory neurotransmitter glutamate and exert an antimanic effect
55
lithium mood stabilizer
Reduces symptoms of mania AND depression
Best evidence for reducing suicide in people living with bipolar disorder
56
lithium mech of action
May affect electrical conductivity in neurons
May reduce excitatory neurotransmitter glutamate
Mechanism of action not fully understood – appears to do many things in the brain but not clear what aspect results in benefit. May regulate receptor expression for glutamate and dopamine (excitatory) may increase GABA activity (inhibitory), may have other effects…
57
what is the therapeutic index of lithium
“Narrow therapeutic index” – monitoring of blood levels necessary, very toxic in overdose or if dehydrated
58
side effects of lithium
Leukocytosis
Increased urination
tremors
hypothyroidism
increased thirst
underactive memory
mothers (teratogenic)
side effects can make it difficult to tolerate
59
Divalproex/valproic acid
Mania AND depression
Common side effects = weight gain, hair growth
Teratogenic – avoid in young women
Mood Stabilizers: Anticonvulsants
60
lamotrigine
Primary treats depression
Dose must be increased slowly (q2weeks) to avoid Steven Johnson Syndrome
Severe, exfoliative skin rash, usually associated with fever, malaise, abnormal bloodwork
May be fatal!
Mood Stabilizers: Anticonvulsants
61
mood stabilizers safety
Require close monitoring (baseline and every 6 to 12 months once stable):
Serum lithium levels (5 days after starting the medication + with dose changes, if signs of toxicity)
CBC, LFTs, thyroid
Kidney function
62
rare side effects of mood stabilizers
Aplastic anemia (stops producing blood cells)
Thrombocytopenia
Low WBC
Kidney damage
Bradycardia or arrhythmia
63
antipsychotics tell me about them + the 2 groups
2 groups:
typical / first generation – marketed 1950s – 80s
atypical / second generation – marketed 1990s - present
Used to reduce symptoms of psychosis, schizophrenia, acute agitation
“Atypical” agents also commonly used for bipolar disorder, treatment resistant unipolar depression
64
mesolimbic
INCREASED dopamine in SCZ hallucinations, delusions
65
mesocortical
INCREASED dopamine in SCZ
66
tuberoinfundibular
unrelated, dopamine regulates prolactin and milk production
67
Nigrostriatal
unrelated, dopamine regulates movement
68
first generation antipsychotics are...
are D2 antagonists
69
first generation agents antipsychotic
Strong antagonists at the D2 dopamine receptor
- Effective for reducing positive symptoms (delusions, hallucinations etc.)
- Not as helpful for negative symptoms (apathy, avolition, etc) and in some cases may worsen these
Associated with motor abnormalities (extrapyramidal adverse effects)
70
example of first generation agents antipsychotics
Methotrimeprazine (Nozinan)
Loxapine (Loxapac)
Trifluoperazine (Stelazine)
Haloperidol (Haldol)
71
pseudoparkinsonism
(motor abnormalities from first gen antipsychotics)
- stopped posture
- shuffling gait
- rigidity
- bradykinesia
- tremors at rest
- pill-rolling motion of the hand
somewhat treatable
72
acute dystonia
- facial grimacing
- involuntary upward eye movement
- muscle spasms of tongue, face, neck, back
- laryngeal spasms
treatable
(motor abnormalities from first gen antipsychotics)
73
akathisia
- restless
- trouble standing still
- paces the floor
- feet in constant motion, rocking back and forth
unpleasant and hard to treat
(motor abnormalities from first gen antipsychotics)
74
tardive dyskinesia
- protrusion and rolling of tongue
- sucking and smacking movements of lips
- chewing motion
- facial dyskinesia
- involuntary movements of body and extremities
becomes permanent if not addressed even w med discontinuation
(motor abnormalities from first gen antipsychotics)
75
parkinsonism what is it
Dopamine antagonism can mimic Parkinson’s Disease symptoms
Shuffling gait
Rigidity or tremor
Mask face (expressionless face)
Drooling
76
how do we treat parkinsonism
Benztropine, diphenhydramine
Reduce dose or change antipsychotic
77
what is dystonia
Sudden, sustained, and painful muscle contractions
May affect eyes, neck, facial muscles, trunk, more rarely limbs
78
treatment for dystonia
Treatment = benztropine, diphenhydramine, and/or benzodiazepine
Give by IM injection for rapid relief
79
akathisia
Inner feeling of restlessness, “doom”
Unable to sit still (stands and sits repeatedly), move or pace constantly
VERY unpleasant – may lead to suicidal ideation
80
treatment akathisia
Benzodiazepine (Lorazepam)
Beta blocker (propranolol)
Reduce antipsychotic dose or change medications
81
tardive dyskinesia
**Involuntary** movements of orofacial muscles
Embarrassing and often permanent
Movements include:
Protruding tongue
Puckering of lips
Chewing
Grimacing
82
treatment of tardive dyskinesia
No medications.
Remove the current med and try an atypical medication
83
second generation agents for antipsychotics
Weaker dopamine antagonist than FGAs
Serotonin antagonists
Fewer extrapyramidal side effects than FGAs
First line treatment for psychosis
Marketed as being more effective for negative symptoms – no strong evidence
84
clozapine
The FIRST “atypical” antipsychotic – introduced 1970s
Clinical use = treatment resistant schizophrenia
More effective than other agents
Lowest risk of extrapyramidal symptoms
85
side effects of clozapine
MANY side effects
Neutropenia & serious infections – weekly bloodwork
Hypotension & tachycardia – slow dose increase
Myocarditis – ECG if chest pain
Constipation
Weight gain
86
side effects of atypical antipsychotic drugs
- sexual side effects
- cataracts
- wt gain
- DM
- hyperlipidemia
- extrapyramidal symptoms
- prolongation QTC interval
- myocarditis
87
atypical antipsychotic side effects
WARNING: increases metabolic syndrome
Increased weight, blood glucose and triglycerides
Clozapine, olanzapine, quetiapine most likely to cause this
metabolic syndrome: HTN, insulin resistance, high triglycerides, low HDL cholesterol, visceral obesity
88
clonzapine, olanzapine, quetiapine side effects
Sedation
Constipation
Weight gain
Orthostasis
89
paliperidone and risperidone side effects
Gynecomastia
Prolactin elevation
EPS
90
what can these four drugs cause: aripiprazole, asenapine, brexpiprazole, lurasidone
Akathisia
91
for D2 block say adverse effects + pharmacology
D2 = dopaminergic
antipsychotic effect
EPS (extrapyramidal side effects)
increased prolactin - gynecomastia (men) galactorrhea
amenorrhea
92
muscarinic cholinergic block say adverse effects + pharmacology
dry mouth
blurred vision
urinary retention
constipation
tachycardia
93
H1 block say adverse effects + pharmacology
H1 block = histamine
sedation
substantial wt gain
orthostasis
94
5-HT2 say adverse effects + pharmacology
5-HT2 = serotonin
antipsychotic effects
wt gain
hypotension
ejaculatory dysfunction
95
GABA say adverse effects + pharmacology
lowers seizure threshold
96
a2 say adverse effects + pharmacology
sexual dysfunction
priapism
97
a1 block say adverse effects + pharmacology
orthostatic hypotension
dizziness
antipsychotic effect
reflux tachycardia
failure to ejaculate
