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pharm III exam 1 > antipsychotics > Flashcards

antipsychotics Flashcards

1
Q

List the classical antipsychotics

A
  • Chlorpromazine (Thorazine®)
  • Prochlorperazine (Compazine®)
  • Fluphenazine (Prolixin®)
  • Haloperidol (Haldol®)
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2
Q

what class is Clozapine (Clozaril®) in

A

atypical antipsychotics

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3
Q

what class is Olanzapine (Zyprexa®) in

A

atypical antipsychotics

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4
Q

what class is Quetiapine (Seroquel®) in

A

atypical antipsychotics

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5
Q

what class is Aripiprazole (Abilify®) in

A

atypical antipsychotics

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6
Q

what class is Risperidone (Risperdal®) in

A

atypical antipsychotics

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7
Q

what class is Ziprisadone (Geodon®) in

A

atypical antipsychotics

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8
Q

what class is Lithium (Eskalith®) in

A

mood stabilizer

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9
Q

what class is Valproic acid (Depakene®) in

A

mood stabilizer

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10
Q

what class is Carbamazepine (Tegretol®) in

A

mood stabilizer

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11
Q

what class is Gabapentin (Neurontin®) in

A

mood stabilizer

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12
Q

what class is Lamotrigine (Lamictal®) in

A

mood stabilizer

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13
Q

What are examples positive symptoms

A
  • hallucinations, delusions, catatonic behavior, disorganized speech and thinking
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14
Q

positive symptoms are due to what neurological pathway

A
  • over active dopamine pathway in limbic system: mesolimbic
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15
Q

what are some examples of negative symptoms

A
  • affective behavior, apathetic, withdrawn, anti-social, lack of motivation, depression
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16
Q

negative symptoms are due to what neurological pathway

A
  • under-active dopamine pathways in frontal cortex: Mesocortical
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17
Q

the mesolimibic pathway goes from where to where? what is it responsible for?

A
  • VTA (ventral tegmental area) to limbic system
  • emotion
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18
Q

The mesocortical system travels from where to where? what is it responsible for

A
  • VTA (ventral tegmental area) to frontal cortex
  • cognition and emotion
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19
Q

the Nigrostriatal pathway travels from where to where? what is it responsible for

A
  • Substantia nigra to striatum
  • motor control
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20
Q

the Tuberoinfundibular pathway travels from where to where? what is it responsible for

A
  • hypothalamus to pituitary
  • Prolactin release
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21
Q

MOA of the “classical” antipsychotics (Neuroleptics)? what dopamine system do they target? What symptoms do they relieve

A
  • block dopamine D2 receptors
  • targert mesolimbic system
  • alleviate positive symptoms
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22
Q

MOA of the “atypical” antipsychotics? what dopamine system do they target? What symptoms do they relieve

A
  • block 5-HT2A and dopamine receptors
  • target mesocortical and mesolimbic system
  • alleviate both negative and positive symptoms
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23
Q

Dopamine D2 are highly concentrated in what area of brain

A

limbic system

  • The potency for blocking the D2 receptor correlates well with the efficacy at relieving the “positive” symptoms of schizophrenia
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24
Q

effects of antipsychotics takes how long

A

6 weeks

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25
Q

general effects specific to Prochlorperazine (Compazine®)

A

antiemetic

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26
Q

most (classical and atypical) drugs also block what receptors

A
  • muscarininc
  • a-adrenergic
  • histamine

**brain and periphery

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27
Q

antipsychotic medications have what effect on seizures

A

decrease seizure threshold

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28
Q

endocrine side effects of antipsychotic medications

A
  • weight gain
  • increased prolactin secretion
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29
Q

anticholinergic, anti a-adrenergic, and anti histamine effects of antipsychotic medications

A
  • anticholinergic: dry mouth, blurred vision, tachycardia, constipation
  • anti a-adrenergic: postural hypotension
  • anti histamine effects: sedation
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30
Q

What are extrapyramidal symptoms

A
  • parkinson’s like symptoms : tremor, rigidity, dyskinesia, rocking (akathisia), pacing, restlessless, anxiety, dystonia
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31
Q

why do antipsychotic medications cause extrapyramidal symptoms

A
  • D2 antagonists block not only DA receptors in the limbic system, but also those in the nigrostriatal system (substantia nigra, striatum).
    • imbalance of striatal DA and ACh
32
Q

how are extrapyramidal symptoms treated

A
  • treat with anticholinergics such as Benztropine (Cogentin) to restore ACh/DA balance
33
Q

which class of antipsychotics tend to cause more EPS symptoms

A
  • classical antipsychotics tend to cause more EPS than atypicals
    • the higher the degree of anticholinergic activity of the drug, the less likely to cause EPS
34
Q

15-25% of patients will have tardive dyskinesia. What is this

A
  • uncontrollable, jerky movements of face and limbs
    • occurs late in disease following long-term tx
    • discontinue drug
35
Q

which two antipsychotic drugs are the least likely to cause tardive dyskinesia

A
  • Clozapine
  • Olanzapine
36
Q

What is Neuoleptic Malignant syndrome? what is it caused by

A
  • life threatening, starts with muscle rigidity, fever, changes in BP and HR
  • caused by block of Dopamine D2 receptors in the striatum and hypothalamus
37
Q

What can be used to treat Neuoleptic Malignant syndrome

A
  • Dantrolene (dantrium)
38
Q

MOA of classical antipsychotics

A
  • block Dopamine D2 receptors
39
Q

classical antipsychotics are metabolized by

A
  • CYP450s (2D6 and 3A4)
  • high first pass metabolism
40
Q

effects of classical antipsychotics last for how long

A
  • weeks after last administration
    • bad for pt compliance
41
Q

Chlorpromazine has what incidence of EPS? why?

A
  • low incidence of EPS
  • High anticholinergic activity
42
Q

MOA of Chlorpromazine

A
  • blocks DA D2 receptors
  • blocks a-adrenergic receptors and ACh
43
Q

side effects of Chlorpromazine

A
  • anticholinergic: blurred vision, dry mouth, constipation
  • decreased sz threshold
  • retinal deposits:“browning of vision”
44
Q

How does Fluphenazine compare to Chlorpromazine

A
  • both block DA D2 receptors
  • has less anticholinergic activity -> more likely to cause EPS
45
Q

MOA of Haloperidol “Vitamin H”

A
  • potent blocker of DA D2 receptor
    • also affinity for DA D1, 5-HT2, and a1 receptors
46
Q

when is Haloperidol “Vitamin H” used

A
  • used frequently in acute setting (ER)
  • can be injected
47
Q

main side effect of Haloperidol “Vitamin H”

A
  • extrapyramidal symptoms
    • no anticholinergic acitivity
    • don’t use long term
48
Q

MOA of Clozapine

A
  • blocks 5-HT2A and DA D4 receptors
    • some affinity for D2
49
Q

what happens if Clozapine is discontinued abruptly

A
  • rapid relapse
    • unique!
50
Q

side effects of Clozapine

A
  • agranulocytosis
    • ​makes it drug of last choice
    • blood must be monitored
  • EPS and tardive dyskinesia are rare
51
Q

MOA of Olanzapine

A
  • blocks 5-HT2A receptors and DA D4 and D2 receptors
  • improves positive and negative symptoms
    • used in tx of bipolar
52
Q

side effects of Olanzapine

A
  • hyperglycemia, type II diabetes
  • extrapyramidal symptoms rare
53
Q

first line drug for psychosis

A

Risperidone

54
Q

MOA of Risperidone

A
  • blocks 5-HT2A and DA D2 receptors
  • improves both positive and negative symptoms
  • no significant effect on DA neurotransmission in nigrostriatal pathway
55
Q

MOA of Ziprasidone

A
  • blocks 5-HT2A and DA D2 receptors
  • some antidepressant activity
  • 5HT1A agonist, inhibit 5 HT reuptake
56
Q

unique side effects of Ziprasidone

A
  • prolongs QT interval
  • sedation
  • Hyperprolactinemia
57
Q

MOA of Quetiapine

A
  • blocks 5-HT2A and DA D2 receptors
58
Q

side effects of Quetiapine (Seroquel)

A
  • very sedating***
    • ​used to promote sleep onset and maintenance
  • does not elevate prolactin
59
Q

MOA of Aripiprazole (abilify)

A
  • dopamine system stabilizer
    • ​dopaminergic tone is low -> DA receptors are activated
    • dopaminergic tone is high -> DA receptors are blocks
  • partial agonist for DA D2 and 5-HT1A receptors
  • antagonist for 5-HT2A
60
Q

unique side effect of Aripiprazole

A
  • decreases esophageal motility
61
Q

what is thought to be a cause of bipolar affective disorder

A
  • a lack of GABAergic activity
62
Q

DOC for bipolar affective disorder

A
  • lithium
63
Q

metabolism of Lithium

A
  • No metabolism
  • excreted by kidneys
64
Q

MOA of Lithium

A
  • suppress 2nd messengers (IP3)
    • may increase ACh, NE, and DA
65
Q

how is lithium reabsorbed?

A
  • reabsorbed by the proximal tubule in the kidney
  • competes with sodium for re-absorption
    • Na+ decreases -> Li+ absorption increases -> toxicity
    • Li+ increases -> Na+ absorption decreases -> hyponatremia
66
Q

Lithium has a small therapeutic window. what plasma levels are associated with side effects and toxicity

A
  • Plasma levels > 2 mEq/L -> N/D, tremor
  • Plasma levels > 2.5 mEq/L -> confusion, slurred speech, sz, renal failure, cardiac arrhythmias
67
Q

patients taking lithium can get diabetes insipidus. why? what is a tx?

A
  • Li+ inhibits ADH
  • treat with amiloride (blocks entry of Li+ into collecting duct)
68
Q

lithium is contraindicated in

A

pregnancy

69
Q

What happens when lithium + benzodiazepines or antipsychotics

A

SAFE

70
Q

lithium + NSAIDs ->

A
  • increase Li toxicity
71
Q

if patient can not tolerate lithium for bipolar, what is the next drug of choice

A
  • valproic acid
    • best used for rapid cycling manic/depressive phases
72
Q

side effects of valproic acid

A
  • surgical bleeding (dental)
  • teratogenic
73
Q

Which two anticonvulsants are useful for rapid cycling manic/depressive phases of bipolar disorder

A
  1. valproic acid
  2. Gabapentin
74
Q

what drug is used in combination with lithium to tx refractory bipolar disorder

A

Carbamazepine

75
Q

drug interactions with Carbamazepine

A
  • CYP450 inducer
    • increases toxicity of isoniazid, erythromycin, cimetidine etc
76
Q

unique adverse effect of Carbamazepine

A
  • steven’s johnson syndrome
    • toxic epidermal necrolysis

pharm III exam 1 (11 decks)

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