antipsych case studies pharm 1

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Author:
ssimmons
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136741
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antipsych case studies pharm 1
Updated:
2012-02-21 12:25:51
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pharm
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Description:
pharm block 7 exam 1
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  1. What type of antispychotic is chlorpromazine and what is its MOA?
    it is a "low potency" neuroleptic that acts by competitive antagonism at the dopamine D2 receptor
  2. If a pt has been on a drug like chlorpromazine and starts developing abnormal facial gestures and difficulty with speech--What effects are they experiencing and why are they occuring?
    this is called tardive dyskinesia and it is caused by months to years of taking antipsychotics that block the dopamine D2 receptor
  3. What causes tardive dyskinesia?
    in a pt that has been taking an antipsychotic that blocks the dopamine D2 receptor for months/years the receptors can develop a supersensitivity to dopamine, it may go away with an increased dosage but it will eventually just get worse
  4. If your pt develops tardive dyskinesia while taking chlorpromazine, what would be the reasoning behind switching to risperidone?
    risperidone is a "high potency" atypical antipsychotic that has a higher affinity for the 5HT2 seretonin recptor than the D2 receptor so it will cause less dopamine hypersensitivity
  5. Why would olanzapine not be a reasonable choice for a switch for a diabetic pt that has tardive dyskinesia on chlorpromazine? or haloperidol?
    olanzapine can cause hyperglycemia and potential to develop diabetes, this would not be good for a pt that already has diabetes. haloperidol is a "high potency" D2 antagonist so giving this would not be any better than the chlorpromazine
  6. How do the side effect profiles for chlorpromazine, olanzapine, and risperidone compare?
    • chlorpromazine--may cause tardive dyskinesia (EP), anticholinergic, cardiovascular effects, elevates serum prolactin, poikolothermy (impaired thermoregulation)
    • olanzapine--moderate anticholinergic, less EP, weight gain, hyperglycemia, can develop diabetes
    • respiridone--less EP side effects, less anticholinergic, minimal sedation, may increase serum prolactin and induce arrythmias

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