Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define neuroses

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are typical psychotic markers (noticeable symptoms)

A

delusions and/or paranoia
hallucinations
disordered thoughts
inappropriate emotional responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what drugs can induce psychoses?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T/F men are more effected by schizophrenia

A

False, men and women are equally effected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the typical age of onset of schizophrenia?

A

15-25 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is “flat effect”

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

define anhedonia

A

inability to feel pleasure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does lack of volition mean?

A

have no will power, you have no power over decisions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T/F psychotherapy is a good monotherapy for schizophrenia

A

False, ineffective by itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does cognitive behavioral therapy improve schizophrenic patients?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what drug can schizophrenic patients self-medicate with?

A

nicotine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the main treatment used for schizophrenia?

A

antipsychotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

neuroleptics or major tranquilizers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what symptoms do antipsychotics help manage with schizophrenia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

all antipsychotics are what drug class?

A

D2 dopamine receptor antagonists or weak partial agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the mesocortical pathway (logic, judgement, and affect)?

A

ventral tegmental area to frontal and prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the mesolimbic pathway (emotion and delusions)?

A

ventral tegmental area to nucleus accumbens in limbic area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the nigrostriatal pathway (regulation of movement)?

A

substantia nigra to striatum in basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the tuberoinfundibular pathway (involved in prolactin secretion)?

A

hypothalamus to pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

explain the dopamine theory of psychosis

A

psychoses is a result from over-stimulated dopamine receptors in the cortex (reasoning) and limbic (emotional) areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how do drugs that increase dopamine levels effect psychosis?

A

increasing dopamine can worsen or cause psychoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do drugs that block dopamine release effect psychosis?

A

decreasing dopamine release can decrease psychoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

“positive” symptoms of psychosis seem to be a result of?

A

dopamine hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

“negative” symptoms of psychosis seem to be a result of?

A

reduced cortical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the “grandparent” of all antipsychotics?

A

chlorpromazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does FGA mean?

A

first generation antipsychotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

list all of the FGAs:

A

Chlorpromazine
Thioridazine
Fluphenazine
Thiothixene
Haloperidol
Pimozide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what drug class are all FGAs?

A

D2 antagonists

38
Q

which two of the FGAs have more D2 selectivity and higher affinity?

A

Haloperidol and Pimozide

39
Q

what drug class is LSD?

A

serotonin partial agonist and hallucinogen/psychotic agent

40
Q

newer antipsychotics have higher affinity for what receptors?

A

serotonin 5-HT2 receptors

41
Q

Ketamine and PCP are what drug class?
how do they effect psychosis?
what receptor do they target?

A

glutamate antagonists
can worsen or cause psychosis
NMDA receptors

42
Q

which 2nd gen antipsychotics are D2/5HT2 antagonists?

A

Clozapine
Loxapine
Olanzapine
Quetiapine
Asenapine
Risperidone
Ziprasidone
Iloperidone
Paliperidone
Lurasidone

43
Q

which 2nd gen antipsychs are weak D2 partial agonists?

A

aripiprazole
brexpiprazole

44
Q

which 2nd gen antipsychs are D2 partial agonists/5HT2 antagonists?

A

Cariprazine
Lumateperone

45
Q

which 2nd gen antipsych is a pure 5HT2 antagonist?

A

Pimavanserin

46
Q

do SGAs have higher or lower affinity for 5-HT2 receptors compared to FGA?

A

higher affinity

47
Q

do SGAs have higher or lower affinity for D2 dopamine receptors compared to FGAs?

A

somewhat lower affinity

48
Q

do SGAs have more or less SEs associated with D2 inhibition compared to FGAs?

A

less side effects

49
Q

which generation of antipsychs do we use as first line therapy?

A

SGAs

50
Q

antagonism of D2 receptors in the basal ganglia of the nigrostriatal pathway produces?

A

extrapyramidal side effects

51
Q

what are extrapyramidal side effects?

A

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
Q

the nigrostriatal pathway is involved in?

A

initiation and control of movement and muscle tone

53
Q

the nigrostriatal pathway is selectively degenerated in what disease state?

A

Parkinson’s

54
Q

the nigrostriatal pathway is involved with what types of disorders?

A

obsessive/compulsive disorders

55
Q

how do we treat extrapyramidal side effects?

A

decrease dose of antipsych, change drug, or adding anti-parkinson agents

56
Q

T/F FGAs cause less extrapyramidal side effects than SGAs

A

False, SGAs cause less extrapyramidal side effects

57
Q

the greater a drugs affinity for the muscarinic receptor is, the ______ extrapyramidal side effects they will experience

A

less

58
Q

how do muscarinic antagonists help reset the motor output imbalance caused by D2 antagonists?

A

D2 antagonists block dopamine receptors in striatum, but muscarinic antagonists can block the muscarinic receptors preventing acetylcholine from binding at GABA site

59
Q

Antipsychotics that have 5-HT2 antagonism and low affinity for D2 antagonism would be expected to have more or less EPS?

A

less EPS

60
Q

why do antipsychotics with 5-HT2 antagonism prevent EPS?

A

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
Q

define tardive dyskinesia
why is it relevant?

A

involuntary movement of tongue, lips, head and neck
it occurs in half of patients using long-term antipsychs

62
Q

why does tardive dyskinesia occur?

A

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
Q

why are VMAT2 inhibitors beneficial for preventing tardive dyskinesia?

A

they prevent dopamine from being packaged into vesicles, so more dopamine will be metabolized which reduces the potential for tardive dyskinesia

64
Q

what are the names of the 2 VMAT inhibitors for tardive dyskinesia prevention?

A

Deutetrabenazine and Valbenzaine

65
Q

Pituitary D2 receptors normally inhibit?
thus, if they are blocked by a D2 antagonist, what occurs?

A

prolactin
increased prolactin release

66
Q

why is blocking D2 receptors at the pituitary an issue? (side effects)

A

increasing prolactin release can cause gyno and increased lactation, disturbed thermal regulation, amenorrhea (absence of menstruation), infertility, and sexual dysfunction

67
Q

why does blocking D2 receptors at the pituitary cause infertility?

A

prolactin suppresses ovulation

68
Q

when would we use a D2 antagonist to intentionally block D2 receptors in the pituitary?

A

to increase lactation for mothers

69
Q

when should you avoid antipsychs with high affinity for alpha-1 antagonism?

A

patients who are hypotensive

70
Q

when should you avoid antipsychs with high affinity for H1 histamine antagonism?

A

patients who need less sedation

71
Q

what are the CNS SEs of antipsychs with muscarinic cholinergic antagonism?

A

amnesia and hallucinations

72
Q

why is it important to not prescribe antipsychs that cause prolonged QT for patients currently taking a different med that causes prolonged QT?

A

may cause torsades de pointe arrythmias, increases risk of sudden cardiac death

73
Q

Elderly patients with ____ have an increased risk of death when taking antipsychs

A

dementia

74
Q

what are the side effects of neuroleptic malignant syndrome?

A

hyperthermia, diaphoresis (increased sweating), altered mental status (catatonia and stupor), fluctuating BP and pulse, tremor, and acute renal failure

75
Q

why is clozapine considered a third-line agent?

A

can cause leukopenia (low WBC count) which can lead to agranulocytosis (absolute neutrophil count is decreased)
also can cause myocarditis and cardiovascular collapse

76
Q

why is olanzapine considered a third-line agent?

A

causes weight gain and metabolic SEs

77
Q

what was olanzapine combined with to prevent the weight gain SE?

A

samidoprhan, an appetite suppresant

78
Q

what are the SEs expected from quetiapine?

A

sedation, weight gain, possible metabolic syndrome

79
Q

why is asenapine not used often? (SE)

A

can cause hypersensitivity rxns

80
Q

what is the main SE from asenapine?

A

sedation

81
Q

Risperidone:
drug class?
sedating?
SEs?

A

high affinity D2 antagonist w/ 5-HT2 antagonism
non-sedating
causes restlessness/agitation

82
Q

Paliperidone:
drug class?
SEs?

A

high affinity D2 antagonist w/ 5-HT2 antagonism
similar to risperidone

83
Q

Ziprasidone:
why was it taken off market?

A

problems with QT elongation

84
Q

Lurasidone is a good choice in?

A

pregnancy

85
Q

Iloperidone:
why is it a good drug of choice?
what is one issue with this drug? (drug class it blocks)

A

low EPS, low anti-cholinergic effects, low weight gain, low tendency for metabolic syndrome?
causes hypotension due to some alpha 1 antagonism

86
Q

what drug class are aripipazole and brexpiprazole?
what is the main issue with them and why?

A

D2 partial agonists
may increase psychoses due to D2 receptor stimulation (can increase dopamine levels, but overall limits amount of dopamine response)

87
Q

what drug class are cariprazine and lumateperone?

A

D2 partial agonists/ 5HT2 antagonists

88
Q

what is the correlation between D2 antagonism and parkinson’s?

A

D2 antagonists would increase parkinson’s symptoms

89
Q

what drug was developed to prevent parkinson’s symptoms from D2 antagonists? what drug class is it considered?

A

Pimavanserin
5HT2 inverse agonist

90
Q

which 3 antipsychs are approved as adjunct treatment for depression?

A

aripiprazole, quetiapine, and olanzapine

IDT Fall (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions