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IDT Fall > Antipsychotic Agents > Flashcards

Antipsychotic Agents Flashcards

1
Q

define psychoses

A

mental disorders characterized by rifts in rational thought, inappropriate processing of sensory information, and disturbed views of reality itself. psychotic symptoms are generally not recognized as much by the sufferer

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2
Q

define neuroses

A

abnormal reaction to an external state that is generally recognized as abnormal by the sufferer

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3
Q

what are typical psychotic markers (noticeable symptoms)

A

delusions and/or paranoia
hallucinations
disordered thoughts
inappropriate emotional responses

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4
Q

what drugs can induce psychoses?

A

amphetamines, steroids, LSD, ketamine, PCP, sedative/hypnotics

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5
Q

T/F men are more effected by schizophrenia

A

False, men and women are equally effected

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6
Q

what is the typical age of onset of schizophrenia?

A

15-25 years old

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7
Q

T/F it is difficult to retain a long term prognosis for schizophrenia

A

true

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8
Q

what are “negative” or residual symptoms of schizophrenia?

A

-flat effect
-anhedonia and apathy
-lack of volition
-social and emotional withdrawal
-disorganized speech, thinking and behavior
-impaired attention
-poor self-care

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9
Q

what is “flat effect”

A

your emotions are not perceived by others and you can come across as uncaring or unresponsive

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10
Q

define anhedonia

A

inability to feel pleasure

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11
Q

what does lack of volition mean?

A

have no will power, you have no power over decisions

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12
Q

T/F occurrence of schizophrenia can have both genetic and environmental factors

A

True

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13
Q

what are examples of anatomic irregularities that may make people more susceptible to schizophrenia?

A

enlarged cerebral ventricles
reduced cortical mass
“hypofrontality”: reduced processing in the prefrontal cortex

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14
Q

what was a treatment in the 1940s and 1950s for schizophrenia? what was the negative outcome?

A

frontal lobotomy
it was permanently debilitating

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15
Q

T/F psychotherapy is a good monotherapy for schizophrenia

A

False, ineffective by itself

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16
Q

how does cognitive behavioral therapy improve schizophrenic patients?

A

improves social skills
improves life skills
may improve ability to self-assess

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17
Q

what drug can schizophrenic patients self-medicate with?

A

nicotine

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18
Q

what is the main treatment used for schizophrenia?

A

antipsychotics

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19
Q

what drug class do we use that we label as antipsychotic agents?

A

neuroleptics or major tranquilizers

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20
Q

T/F antipsychotics can eventually cure schizophrenia when combined with cognitive behavioral therapy

A

false

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21
Q

what symptoms do antipsychotics help manage with schizophrenia?

A

reduce frequency of hallucinations and delusions
improve mood, reduce anxiety and improve sleep

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22
Q

what is the timeline for effectiveness for psychosis with antipsychotics?

A

calming effects occur within minutes to hours
diminished psychotic symptoms within 24-28 hours
full antipsychotic effects evolve over 2-8 weeks
improvement may continue for up to 6 months

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23
Q

all antipsychotics are what drug class?

A

D2 dopamine receptor antagonists or weak partial agonists

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24
Q

antipsychotic _____ for D2 receptors correlates with ________
what does this mean?

A

affinity, average clinical dose
the larger of dose we can use with an antipsychotic the greater affinity that drug will have at D2 receptors

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25
What is the mesocortical pathway (logic, judgement, and affect)?
ventral tegmental area to frontal and prefrontal cortex
26
What is the mesolimbic pathway (emotion and delusions)?
ventral tegmental area to nucleus accumbens in limbic area
27
What is the nigrostriatal pathway (regulation of movement)?
substantia nigra to striatum in basal ganglia
28
What is the tuberoinfundibular pathway (involved in prolactin secretion)?
hypothalamus to pituitary
29
explain the dopamine theory of psychosis
psychoses is a result from over-stimulated dopamine receptors in the cortex (reasoning) and limbic (emotional) areas
30
how do drugs that increase dopamine levels effect psychosis?
increasing dopamine can worsen or cause psychoses
31
how do drugs that block dopamine release effect psychosis?
decreasing dopamine release can decrease psychoses
32
"positive" symptoms of psychosis seem to be a result of?
dopamine hyperactivity
33
"negative" symptoms of psychosis seem to be a result of?
reduced cortical activity
34
what is the "grandparent" of all antipsychotics?
chlorpromazine
35
what does FGA mean?
first generation antipsychotics
36
list all of the FGAs:
Chlorpromazine Thioridazine Fluphenazine Thiothixene Haloperidol Pimozide
37
what drug class are all FGAs?
D2 antagonists
38
which two of the FGAs have more D2 selectivity and higher affinity?
Haloperidol and Pimozide
39
what drug class is LSD?
serotonin partial agonist and hallucinogen/psychotic agent
40
newer antipsychotics have higher affinity for what receptors?
serotonin 5-HT2 receptors
41
Ketamine and PCP are what drug class? how do they effect psychosis? what receptor do they target?
glutamate antagonists can worsen or cause psychosis NMDA receptors
42
which 2nd gen antipsychotics are D2/5HT2 antagonists?
Clozapine Loxapine Olanzapine Quetiapine Asenapine Risperidone Ziprasidone Iloperidone Paliperidone Lurasidone
43
which 2nd gen antipsychs are weak D2 partial agonists?
aripiprazole brexpiprazole
44
which 2nd gen antipsychs are D2 partial agonists/5HT2 antagonists?
Cariprazine Lumateperone
45
which 2nd gen antipsych is a pure 5HT2 antagonist?
Pimavanserin
46
do SGAs have higher or lower affinity for 5-HT2 receptors compared to FGA?
higher affinity
47
do SGAs have higher or lower affinity for D2 dopamine receptors compared to FGAs?
somewhat lower affinity
48
do SGAs have more or less SEs associated with D2 inhibition compared to FGAs?
less side effects
49
which generation of antipsychs do we use as first line therapy?
SGAs
50
antagonism of D2 receptors in the basal ganglia of the nigrostriatal pathway produces?
extrapyramidal side effects
51
what are extrapyramidal side effects?
akathisia: inability to sit still dystonia: abnormal muscle tone causing involuntary muscle contraction pseudo-parkinsonism: stiff muscles and tremors tardive dyskinesia's: involuntary facial movements
52
the nigrostriatal pathway is involved in?
initiation and control of movement and muscle tone
53
the nigrostriatal pathway is selectively degenerated in what disease state?
Parkinson's
54
the nigrostriatal pathway is involved with what types of disorders?
obsessive/compulsive disorders
55
how do we treat extrapyramidal side effects?
decrease dose of antipsych, change drug, or adding anti-parkinson agents
56
T/F FGAs cause less extrapyramidal side effects than SGAs
False, SGAs cause less extrapyramidal side effects
57
the greater a drugs affinity for the muscarinic receptor is, the ______ extrapyramidal side effects they will experience
less
58
how do muscarinic antagonists help reset the motor output imbalance caused by D2 antagonists?
D2 antagonists block dopamine receptors in striatum, but muscarinic antagonists can block the muscarinic receptors preventing acetylcholine from binding at GABA site
59
Antipsychotics that have 5-HT2 antagonism and low affinity for D2 antagonism would be expected to have more or less EPS?
less EPS
60
why do antipsychotics with 5-HT2 antagonism prevent EPS?
they decrease the amount of dopamine entering the pre-synaptic cleft which will decrease the amount of dopamine in the synapse preventing too much dopamine from entering the post-synaptic neuron
61
define tardive dyskinesia why is it relevant?
involuntary movement of tongue, lips, head and neck it occurs in half of patients using long-term antipsychs
62
why does tardive dyskinesia occur?
when we reduce the amount of dopamine in synaptic cleft and block the D2 receptors, the body will undergo "supersensitization" where more D2 receptors will be produced to regulate and cause not enough signal to occur
63
why are VMAT2 inhibitors beneficial for preventing tardive dyskinesia?
they prevent dopamine from being packaged into vesicles, so more dopamine will be metabolized which reduces the potential for tardive dyskinesia
64
what are the names of the 2 VMAT inhibitors for tardive dyskinesia prevention?
Deutetrabenazine and Valbenzaine
65
Pituitary D2 receptors normally inhibit? thus, if they are blocked by a D2 antagonist, what occurs?
prolactin increased prolactin release
66
why is blocking D2 receptors at the pituitary an issue? (side effects)
increasing prolactin release can cause gyno and increased lactation, disturbed thermal regulation, amenorrhea (absence of menstruation), infertility, and sexual dysfunction
67
why does blocking D2 receptors at the pituitary cause infertility?
prolactin suppresses ovulation
68
when would we use a D2 antagonist to intentionally block D2 receptors in the pituitary?
to increase lactation for mothers
69
when should you avoid antipsychs with high affinity for alpha-1 antagonism?
patients who are hypotensive
70
when should you avoid antipsychs with high affinity for H1 histamine antagonism?
patients who need less sedation
71
what are the CNS SEs of antipsychs with muscarinic cholinergic antagonism?
amnesia and hallucinations
72
why is it important to not prescribe antipsychs that cause prolonged QT for patients currently taking a different med that causes prolonged QT?
may cause torsades de pointe arrythmias, increases risk of sudden cardiac death
73
Elderly patients with ____ have an increased risk of death when taking antipsychs
dementia
74
what are the side effects of neuroleptic malignant syndrome?
hyperthermia, diaphoresis (increased sweating), altered mental status (catatonia and stupor), fluctuating BP and pulse, tremor, and acute renal failure
75
why is clozapine considered a third-line agent?
can cause leukopenia (low WBC count) which can lead to agranulocytosis (absolute neutrophil count is decreased) also can cause myocarditis and cardiovascular collapse
76
why is olanzapine considered a third-line agent?
causes weight gain and metabolic SEs
77
what was olanzapine combined with to prevent the weight gain SE?
samidoprhan, an appetite suppresant
78
what are the SEs expected from quetiapine?
sedation, weight gain, possible metabolic syndrome
79
why is asenapine not used often? (SE)
can cause hypersensitivity rxns
80
what is the main SE from asenapine?
sedation
81
Risperidone: drug class? sedating? SEs?
high affinity D2 antagonist w/ 5-HT2 antagonism non-sedating causes restlessness/agitation
82
Paliperidone: drug class? SEs?
high affinity D2 antagonist w/ 5-HT2 antagonism similar to risperidone
83
Ziprasidone: why was it taken off market?
problems with QT elongation
84
Lurasidone is a good choice in?
pregnancy
85
Iloperidone: why is it a good drug of choice? what is one issue with this drug? (drug class it blocks)
low EPS, low anti-cholinergic effects, low weight gain, low tendency for metabolic syndrome? causes hypotension due to some alpha 1 antagonism
86
what drug class are aripipazole and brexpiprazole? what is the main issue with them and why?
D2 partial agonists may increase psychoses due to D2 receptor stimulation (can increase dopamine levels, but overall limits amount of dopamine response)
87
what drug class are cariprazine and lumateperone?
D2 partial agonists/ 5HT2 antagonists
88
what is the correlation between D2 antagonism and parkinson's?
D2 antagonists would increase parkinson's symptoms
89
what drug was developed to prevent parkinson's symptoms from D2 antagonists? what drug class is it considered?
Pimavanserin 5HT2 inverse agonist
90
which 3 antipsychs are approved as adjunct treatment for depression?
aripiprazole, quetiapine, and olanzapine

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