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Pharm II > Antipsychotics > Flashcards

Antipsychotics Flashcards

1
Q

other names for antipsychotics? what are they most often used to tx?

A

neuroleptic or anti-schizophrenic drugs
most often used to tx schizophrenia, delirium, mania, delusional disorder, manage severe agitated states, mood disorders (bipolar), Tourette’s syndrome

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2
Q

what is psychosis? ssxs?

A

mental state in which the perception of reality is distorted
ssxs: disorganized thinking, personality changes, paranoid or delusional beliefs, hallucinations
“a severe mental d/o w/ or w/o organic damage characterized by derangement of personality and loss of contact w/reality causing mental deterioration of normal social functioning

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3
Q

psychosis has been traditionally linked to what neurotransmitter?

A

dopamine (overactivity of dopamine function in the brain, particularly in the mesolimbic pathway)

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4
Q

dopamine-blocking drugs cause what in relation to psychotic sxs? drugs that boost dopamine activity cause what in relation to psychotic sxs?

A

dopamine blocking drugs reduce the intensity of psychotic sxs
dopamine boosting drugs trigger psychosis in some people

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5
Q

what other neurotransmitter has possibly been linked to psychosis?

A

glutamate esp w/activity of the NMDA receptor
theory reinforced by fact that dissociative NMDA receptor antagonists such as Ketamine, PCP and dextromethorphan at lg overdoses induces a psychotic state

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6
Q

definition of hallucinations? can occur in what senses?

A

hallucinations are defined as sensory perceptions in the absence of external stimuli
can occur in any of the 5 senses and take on almost any form (lights, colors, tastes, smells, hearing voices, perceiving complex tactile sensations and seeing and interacting with imaginary ppl)

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7
Q

examples of secondary psychosis?

A

neuro d/os
electrolyte d/os
multiple medical conditions
drugs - use, abuse, withdrawal

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8
Q

what is intermetamorphosis?

A

intermetamorphosis: those around look like enemies

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9
Q

what is dorian grey syndrome?

A

dorian gray syndrome: one does not age

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10
Q

what is cotard’s syndrome?

A

cotard’s syndrome: delusional sense of nihilism

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11
Q

what is fregoli’s phenomenon?

A

fregoli’s phenomenon: persecutor impersonates ppl the pt knows

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12
Q

what is lilliputian hallucination?

A

lilliputian hallucination: seeing ppl as small creatures

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13
Q

what is messianic delusion?

A

messianic delusion: belief he is the messiah

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14
Q

what is mignon delusion?

A

mignon delusion: believes he belongs to Royal lineage

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15
Q

what is picture sign?

A

picture sign: ppl on the TV is inside the house

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16
Q

what is noetic delusion?

A

noetic delusion: prophetic delusion

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17
Q

what is command hallucination?

A

command hallucination: obeying orders of what is asked through auditory hallucinations

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18
Q

what is capgras syndrome?

A

capgras syndrome: identical looking impostors has replaced someone significant to the pt

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19
Q

8 neuro d/os associated w/psychosis?

A 
brain tumors
alzheimer's
multi-infarct dementia
dementia w/Lewy bodies
MS
syphilis
Parkinson's dz
Pick's dz
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20
Q

electrolyte d/os associated w/psychosis?

A 
hypo/hypercalcemia
hypo/hypernatremia
hypokalemia
hypo/hypermagnesemia
hypophosphatemia
hypoglycemia
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21
Q

medical conditions associated w/psychosis?

A 
AIDS
lupus
lyme dz
sarcoidosis
leprosy
malaria
can even develop from things such as flu or mumps
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22
Q

drugs whose use, abuse or withdrawal that have been associated w/psychosis?

A 
OTC such as dextromethorphan at high doses or antihistamines
atropine
antidepressants
antiepileptics
barbiturates
benzos
L-dopa
narcotic analgesics
EtOH
amphetamines
cannabis
cocaine
LSD
MDMA (ecstasy)
mescaline
PCP 
psilocybin
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23
Q

drugs with depressant effects on the CNS cause what in relation to psychosis?

A

drugs w/depressant effects on CNS tend to not cause psychosis and can actually decrease or lessen impact of sxs in some ppl

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24
Q

withdrawal from barbiturates or EtOH can cause what?

A

delirium, psychosis, other potentially lethal withdrawal effects

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25
Q

two categories of neuroleptic/antipsychotic drugs?

A

first generation/typical

second generatio/atypical

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26
Q

two typical/first generation antipsychotics classes we care about?

A

phenothiazines

thioxanthenes

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27
Q

how do first generation antipsychotics work vs second generation?

A

first generation: D2 antagonism

second generation: 5HT2A/D2 antagonism

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28
Q

4 atypical antipsychotic med classifications?

A 
butyrophenone class 
dibenzodazepine class
thienobenzodiazepine class
others
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29
Q

main MOA of typical and atypical neuroleptic drugs?

A

blockade of dopamine receptors in the brain

may affect various receptor subtypes of NE, Ach, histamine

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30
Q

aside from blocking dopamine in the brain, how else do atypical neuroleptics work?

A

serve as antagonists or partial antagonists to serotonin receptors

31
Q

what are atypicals?

A

heterogeneous group of otherwise unrelated drugs united by the fact that they work differently from typical antipsychotics

32
Q

aripiprazole and amisulpride, two newer antipsychotics have what MOA?

A

no serotonergic activity, instead have partial dopamine agonism

33
Q

what is now considered 1st line tx for schizophrenia?

A

atypical anti-psychotics

34
Q

two defining characteristics of an atypical antipsychotic?

A

decreased propensity of these agents to cause extrapyramidal SEs and absence of sustained prolactin elevation

35
Q

main difference btw typicals and atypicals?

A

typicals block D1, 2, 3, 4 dopamine receptors and cause extrapyramidal disturbances
atypicals block 5HT2 serotonin receptors, block a2 adrenoceptors, block D4 dopamine, weak action on D2 receptors and do NOT cause extrapyramidal disturbances

36
Q

atypicals have more of an affinity for what receptors?

A

D4 over D2 receptors

this is why they are less likely to cause tardive dyskinesia

37
Q

chief antipsychotic effects of the neuroleptics appears to be related to the blocking of what neurotransmitter at what receptor?

A

dopamine block at the D2 receptors

38
Q

how is dopamine endogenously inactivated?

A

inactivated by reuptake via dopamine transporter, then breakdown by catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO)
dopamine that isn’t broken down by enzymes is repackaged into vesicles for reuse

39
Q

other name for typical antipsychotics?

A

major tranquilizers b/c can tranquilize and sedate

40
Q

are typical antipsychotics selective?

A

relatively non-selective in regards to the mesolimbic pathway, also block dopamine receptors in mesocortical pathway, tuberoinfundibular pathway and nigrostriatal pathway

41
Q

antipsychotics act how? psycho-stimulants act how?

A

antipsychotics are often dopamine receptor antagonists

psycho-stimulants are typically indirect agonists of dopamine receptors

42
Q

SEs of neuroleptics?

A 
tremors/Parkinsonian effects
tardive dyskinesia
postural hypotension
blurred vision, dry mouth, constipation and urinary retention 
sexual dysfunction
increased prolactin release
drowsiness
43
Q

generally speaking which class of antipsychotics have a lower likelihood of tardive dyskinesia as a SE?

A

atypicals

but unclear if this is true b/c they have been in use for much less time than the typicals

44
Q

what is dyskinesia? what does tardive mean?

A

involuntary movement, facial grimacing, involuntary movements of the limbs
tardive means the dyskinesia continues on or first appears after the drugs are no longer being taken

45
Q

tx of tardive dyskinesia?

A

remove the drug for 3-6 mos to see if this resolves the issue, but problem may fail to improve or may even exacerbate
trial the pt on tetrabenazine

46
Q

new black box warning on atypical antipsychotics?

A

warn about risks of hyperglycemia and DM

47
Q

two antipsychotics associated w/greatest effects on wt gain and decreased insulin sensitivity? two with the least effects on wt gain and insulin resistance?

A

most effects: cozapine, olanzapine

least effects: ziprasidone, aripiprazole

48
Q

rare SE of antipsychotics? ssxs? how to tx?

A

neuroleptic malignant syndrome: catonia, fluctuating BP, dysarthria, fever - can last 8 hrs to 40 days
fatal if antipsychotic drug not immediately discontinued and pt should receive tx w/dopamine agonist such as bromocriptine

49
Q

two lab values that raise with neuroleptic malignant syndrome?

A

WBC and creatine phosphokinase plasma concentration will be reported dt increased muscular activity and rhabdomyolysis

50
Q

other effect neuroleptic drugs have?

A

anti-emetic effects that are mediated by blocking D2 dopaminergic receptors in chemoreceptor trigger zone of the medulla

51
Q

class of chlorpromazine/thorazine? indications? MOA?

A

class: typical neuroleptic
indications: psychosis, mania, schizophrenia, nausea, vomiting, intractable hiccoughs
MOA: chiefly D2 dopaminergic receptor site blockade, alpha-adrenergic blockade and H1 blockade (anti-histamine effects)

52
Q

SE of chlorpromazine/thorazine? increased risk of what? leads to what?

A

SE: onset of parkinsonian sxs, extrapyramidal signs such as tardive dyskinesia
increased release of prolactin common occurs as result of dopamine blockade - can result in galactorrhea and amenorrhea in women and infertility in men and women

53
Q

class of prochlorperazine/compazine? indications? MOA?

A

class: typical neuroleptic
indications: psychosis as well as vertigo, N/V, particularly when associated w/migraine h/as
MOA: primarily H1-histamine receptor antagonist as well as alpha adrenergic receptor antagonist and D2 dopaminergic receptor antagonist

54
Q

SEs of prochlorperazine/compazine? effect on seizure threshold?

A

SEs: significant drowsiness, dry mouth, constipation, urinary retention, lowers seizure threshold, extrapyramidal sxs only seen when given in higher doses over a longer period of time

55
Q

class of haloperidol/haldol? indications? MOA? how to give?

A

class: typical neuroleptic
indications: psychosis, Tourette’s syndrome, Huntington’s dz, acute agitated behavior
MOA: chiefly D2 dopaminergic receptor site blockade
give carefully so as to reduce excessive sedation and tardive dyskinesia

56
Q

SEs of haloperidol/haldol? what potentially fatal effect?

A

SEs: chiefly parkinsonian-like sxs and extrapyramidal effects, tremors common, potentially fatal neuroleptic malignant syndrome!

57
Q

class of clozapine/clozaril? indications? MOA? how to give?

A

class: atypical neuroleptic
indications: schizophrenia, esp when other anti-psychotic agents have failed or have produced undesirable SEs
MOA: multiple receptor site blockade yet greatest effects at D2 and 5HT2 (serotonin) receptor sites
give PO, rapid absorption and extensive metabolism

58
Q

clozapine/clozaril has been superior in treating what condition? what ‘holds it back’ from being more useful in other conditions?

A

superior for treating schizophrenia

large SE profile makes it 3rd in line to use other than in schizophrenia (causes agranulocytosis, myocarditis)

59
Q

if using clozapine/clozaril what do you have to monitor?

fatal SEs?

A

have to do weekly blood draws for ~5 mos followed by four weekly tests thereafter
echocardiograms are recommended every 6 mos to exclude cardiac damage

60
Q

class of respiradone/risperdal? indications? MOA? metabolized by what pathway?

A

class: atypical neuroleptic
indications: psychosis
MOA: unknown, presumed to be combo of dopamine and serotonin receptor blockade
metabolized in liver by P450 enzyme and metabolites are active

61
Q

SEs of respiradone/risperdal? how to taper off?

A

SEs: extrapyramidal effects, tardive dyskinesia, constipation, sedation, wt gain, hyperglycemia, diabetes, increased risk for stroke in elderly pts
slow withdrawal recommended to reduce incidence of acute psychosis

62
Q

class of olanzapine/zyprexa? indications? MOA? how to give?

A

class: atypical neuroleptic
indications: schizophrenia, esp when other antipsychotic agents have failed or have produced undesirable SEs
MOA: multiple receptor site blockade yet greatest effects at D2 and 5HT2 receptor sites
give PO, rapid absorption, extensive metabolism

63
Q

olanzapine is structurally similar to? olanzapine’s affinity for serotonin vs dopamine? affinity to histamine, cholinergic muscarininic and alpha adrenergic receptors?

A

clozapine
but olanzapine has higher affinity for 5HT2 serotonin receptors than D2 dopamine receptors
lower affinity for histamine, cholinergic muscarinic and alpha adrenergic receptors

64
Q

SEs of olanzapine/zyprexa?

A

SEs: relatively diminished extra-pyramidal SEs compared to other neuroleptic agents, wt gain, hyperglycemia, diabetes, increased risk for stroke in elderly

65
Q

what 2 antipsychotics should not be given to elderly pts w/dementia? why?

A

olanzapine and risperidone dt increased risk of stroke

66
Q 
class of aripiprazole/abilify? indications?
MOA?
A

class: 2nd generation class of atypical antipsychotics
indications: schizophrenia, bipolar d/o, clinical depression
MOA: partial dopamine agonist of w/additional antidepressant properties

67
Q

ssxs of mania?

A

elevated, expansive or irritable moods accompanied by increased activity, rapid speech, thoughts and feelings of grandiosity, distractibility and decreased need for sleep, may include risk for physical harm
pts that cycle btw depression and mania are dx w/bipolar d/o

68
Q

what are used prophylactically in treating bipolar d/o and in tx of manic episodes? MOA?

A

lithium salts
MOA: distributed in CNS, interacts w/a # of neurotransmitters and receptors, decreasing NE release and increasing serotonin synthesis
may dampen transmission by NE as well as diminish response to glutamate

69
Q

class of lithium carbonate/eskalith? indications? MOA? how to give? cleared by what? therapeutic index?

A

class: lithium salt
indications: bipolar d/o, manic episodes, schizophrenia
MOA: interacts w/# of neurotransmitters and receptors, decreases NE release and increasing serotonin synthesis may dampen transmission by NE as well as glutamate
give orally, cleared by KDs, very small therapeutic index so need to monitor blood levels of lithium

70
Q

plasma concentrations of lithium? overdose at what level?

A

goal is 0.6-1.2 mmol Li+
overdose at 1.5 mmol of Li+ = fatal and toxic effects include tremor, ataxia, dysarthria, nystagmus, renal impairment, convulsions

71
Q

SEs of lithium carbonate/eskalith? MC renal effect of lithium?

A

major problem is lack of compliance, esp SEs of wt gain, cognitive impairment, short-term memory deficits
MC renal effect is impaired concentration capacity dt reduced renal response to antidiuretic hormone, nephrotic diabetes insipidus, hypothyroidism

72
Q

ssxs that lithium dose is too high?

A

lethargy, confusion, diarrhea, abd pain, N/V, ataxia, severe tremors, as levels increase, seizures develop and cardiotoxicity can occur

73
Q

two methods of initiating lithium tx?

A
  1. administering a single dose of lithium, obtain a serum level 24 hrs later, use a nomogram to predict the appropriate daily dose
  2. can be started in low, divided doses to minimize SEs, depending on the pts wt and age, then the dose should be titrated upward to a serum concentration of 0.5 mEq/L
    * levels should be checked after each dosage increase

Pharm II (18 decks)

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