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154 Cards in this Set
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table 70-7 pg 1110
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1110
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What causese increased prolactin levels from AP?
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DA blockade in tuberoinfundibular tract
DA is the major prolactin-inhibiting factor |
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What can result form increased prolactin?
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galactorrhea, amenorrhea, gynecomastia
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Which AP are more likely to have increased prolactin levels?
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dose related
more common in FGA and risperidone |
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Does tolerance develop to the effects of increased prolactin?
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yes
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Which AP have no effect on prolactin?
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SGA: olanzapine, quetiapine, ziprasidone, aripiprazole
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What causes wt gain from AP?
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not sure: associated with antihistaminic effects, antimuscarinic effects, blockade of 5-HT2c receptors, activity level
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What is considered significant wt gain?
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7%
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Which AP have the most wt. gain?
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clozapine and olanzapine
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Which AP have lowest wt. gain?
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ziprasidone and aripiprazole
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What is clinical significance of wt gain?
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substantial: risk of CV mortality increases, risk factor for DM, poor adherence
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What should be done if unwanted wt gain occurs?
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switch to AP with less wt gain, dietary restriction, exercise, behavior modification programs
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When should change because of wt gain occur?
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5% increase form baseline
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Which APs have greatest risk for development of T2DM?
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clozapine and olanzapine
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New onset DM has been reported from what AP?
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risperidone, olanzapine, quetiapine, ziprasidone
aripiprazole (limited reports) |
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What is considered orthostatic hypotension?
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>20mmHg drop in systolic BP
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What cause orthostatic hypotension?
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alpha adrenergic blockade
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Which AP cause the most orthostatic hypotension?
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low potency FGA and SGA (especially IM or IV)
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Which pts have the most orthostatic hypotension?
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DM with preexisting CV diseaseand elderly
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Does tolerance develop to orthostatic hypotension?
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within 2-3 months
use lower dose or change AP to one with less alpha blockade if tolerance doesn't develop |
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Which AP cause most ECG changes?
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thioridazine, clozapine, ziprasidone
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What ECG changes might be experienced from AP?
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increased heart rate, flattened T waves, ST segment depression, prolongation of QT and PR intervals
prolongation of QTc is most clinically important |
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What is associated with QTc prolongation?
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ventricular arrhythmias (torsades de pointes)
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When should AP be d/c because of QTc prolongation?
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if interval consistently exceeds 500msec
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Which pts are at greater risk of QTc prolongation?
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elderly, preexisting cardiac or cerebrovascular disease, pts taking diuretics or meds that prolong QTc
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What pretreatment things should be done if pt is older than 50?
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pretx ECG and baseline serum K and Mg
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Which SGA have least change of lipid levels?
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risperidone, ziprasidone, aripiprazole
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Which AP has the most metabolic effects?
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olanzapine
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What is criteria for metabolic syndrome?
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TG 150 or more
HDL males (40 or less), females (50 or less) fasting glucose 100 or more BP 130/85 or more abdominal circumference greater than 40in for males and 34in for females |
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What are anticholinergic SE?
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dry mouth, constipation, tachycardia, blurred vision, inhibition or impairment of ejaculation, urinary retention, impaired memory
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Which AP cause anticholinergic SE?
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low potency FGAs, clozapine and olanzapine
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Which age group have most anticholinergic SE?
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elderly
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What are major EPS?
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dystonia, akathisia, pseudoparkinsonism, TD
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What is dystonia?
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abnormal tonicity, "muscle spasm"
prolonged tonic contractions |
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When does dystonia typically occur?
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rapid onset, usually within 24-96hrs or dosage initiation or increase
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Is dystonia life threatening?
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can be, pharyngeal laryngeal dystonias
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Which AP typically have dystonia?
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FGA
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What are risk factors for dystonia?
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young, male, high potency agent, high dosage
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What is tx for dystonia?
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IM or IV anticholinergics or BDZ
benztropine mesylate or diphenhydramine IM or IV diazepam slow IV push lorazepam IM biperiden, trihexyphenidyl clonazepam |
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What is akathisia?
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inability to sit still
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How is akathisia diagnosed?
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combining subjective complaints (describe feeling of inner restlessness or disquiet or a compulsion to move or remain constant motion) with objective symptoms (pacing, shifting, shuffling, tapping feet)
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What is tx for akathisia?
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anticholinergic agents (disappointing for akathisia, helpful if concomitant pseudoparkinsonism)
reduce AP dose (may not be realistic in acutely psychotic pt) switch to AP with lower risk for akathisia |
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Which AP cause akathisia?
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FGAs
occasionally with SGAs |
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Which AP have lowest risk for akathisia?
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quetiapine and clozapine
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What is tx for akathisia?
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BDZ (high prevalence of substance abuse)
BB (propranolol, nadolol, metoprolol) |
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What causes pseudoparkinsonism?
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D2 blockade in nigrostriatum
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What are the 4 cardinal symptoms of pseudoparkinsonism?
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present with one of these:
akinesia, bradykinesia, or decreased motor activity including difficulty initiating movement, extreme slowness, mask like facial expression, micrographia, slowed speech, decreased arm swing tremor (pill rolling) - predominant at rest and decreases with movement, usually involves fingers and hands cogwheel rigidity seen in limbs - jerky,ratchet like fashion when passively moved postural abnormalities and instability manifested as stooped posture, difficulty in maintatining stability when changing body position, and gait that ranges from slow and shuffling to festinating |
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What are risk factors for pseudoparkinsonism?
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increasing age, female
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What is onset of pseudoparkinsonism?
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1-2 weeks after initiation of AP or dose increase
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What is tx for pseudoparkinsonism?
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anticholinergics
Benztropine has long t1/2 so dosed once-twice daily Amantadine - dopamine agonis trihexyphenidyl, diphenhydramine, biperiden are dosed thrice daily |
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When do pseudoparkinsonism symptoms resolve?
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3-4 days after tx, 2 weeks of tx is usually required for full response
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What is benefit of amantadine compared to anticholinergics for pseudoparkinsonism?
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as efficacious with less effect on memory function
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Should meds be used prophylactically for pseudoparkinsonism?
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unnecessary for SGAs
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Whould antiparkinsonism meds be used long term for pseudoparkinsonism?
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taper and d/c 6 weeks to 3 months after symptom resolution
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What should be done if symptoms of pseudoparkinsonism return when taking FGA?
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switch to SGA
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Which SGA causes the most pseudoparkinsonism?
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risperidone
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Which AP should be used if pt experiences EPS with other SGAs?
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quetiapine, aripiprazole, clozapine
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What is TD?
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abnormal involuntary movements occurring late in onset in relation to initiation of antipsychotic therapy
buccal-lingual masticatory (BLM) syndrome or orofacial movements |
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Is TD reversible?
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sometimes is irreversible
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When do buccal lingual masticatory syndrome occur?
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typically first detectable signs of TD
begin with mild forward, backward, or lateral movements of the tongue as progresses, more obvious BLM movements appear (tongue thrusting, rolling, or fly catching movements, chewing or lateral jaw movements) |
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What complications from TD?
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oral ulceration, inability to wear denturs, inflammation and loosening of mandibular joints, eating difficulties, malnutrition
wt loss (if esophageal or respiratory manifestations, not runcal movements) |
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What facial movements are seen in TD?
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blinking, brow arching, frimacing, upward deviation of eyes, and lip smacking
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What limb movements are seen in TD?
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restless choreiform (irregular spasmodic) and distal athetosis (slow, writhing movement) of limbs
including twisting, spreading, flexion, and extension of fingers, toe tapping, toe dorsiflexion (upward turning) unusual posture, hyperextension, pelvic thrustin, axial hyperkinesia (excessive muscular activity of head and trunk), ballismus (jerking or shaking), exaggerated lordosis (bending backward), rocking, swaying |
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What movements are see more often in elderly?
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orofacial movements
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What movements are seen more often in young adults?
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truncal axial movements
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What can worsen TD movements?
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stress, attempts to suppress movements
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What can make movements disappear?
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sleep
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Is TD reversible?
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early signs are, late stage can be irreversible even with drug d/c
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What rating scales can be used to help diagnose TD?
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AIMS (abnormal involuntary movements scale)
DISCUS (dyskinesia identificationn system: condensed user scale) they aren't diagnostic |
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What are risk factors for TD?
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increasing age, acute EPS, poor AP response, diagnosis of organic mental disorder, DM, mood disorders, female
duration, daily dose, and total cumulative dose are most significant risk factors |
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What is rate of remission of TD?
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25% of pts after 5 year tx
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Does FGA or SGA have more TD?
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FGA has much more
olanzapine, risperidone, quetiapine has really low incidence clozapine has had no TD |
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How can TD be prevented?
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start with SGA
regular neurologic exams at baseline and quarterly reassess at first sign of TD |
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What has been used to treat TD?
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switch AP to clozapine
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Which AP have most sedation?
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chlorpromazine, thioridazine, mesoridazine, closapine, olanzapine, quetiapine
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What can be done to prevent daytime sedation from AP?
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dose at bedtime
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Can sedation decrease over time?
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yes
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What positive effects on cagnition are seen with AP?
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improvements in tasks involving visual motor skills, attention to task, working memory
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Which AP have more cognitive benefits?
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SGA
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What increases risk of seizure from AP?
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preexisting seizure disorder, history of drug induced seizure, abnormal EEG, preexisting CNS pathology or head trauma
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When are seizures most common?
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high doses, rapid dose increase, initiation of tx
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What is tx for seizure?
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dosage decrease, no anticonvulsant
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Which AP have highest chance of seizure?
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clozapine, chlorpromazine
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Which AP has lowest chance of seizure?
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risperidone, molindone, thioridazine, haloperidol, pimozide, trifluoperazine, fluphenazine
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What thermoregulation problems can develop from AP?
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poikilothermia (body temp adjusting to ambient temp)
hyperpyrexic (in hot weather or exercise) inhibition of sweating (may cause heat stroke) hypothermia |
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Which AP cause thermoregulation problems?
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low potency FGA and more anticholinergic SGA
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When is neuroleptic malignant syndrome more likely?
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receiving high potency FGAs, injectable or depot FGAs, dehydrated pt, phycal exhaustion, organic mental disorders
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Which AP cause NMS?
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mainly FGAs
has been reported from SGAs, including clozapine |
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How is onset of NMS?
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varies from early in tx to months later
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Can NMS occur after d/c of AP?
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yes
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What is mechanism of NMS?
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disruption of central thermoregulatory process or excess production of heat secondary to skeletal muscle conractions
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What is differential diagnosis for NMS?
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heat stroke, lethal catatonia, anesthetic associated malignant hyperthermia, anticholinergic toxicity, MAOI DI
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What are cardinal s/s of NMS?
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temp exceeding 38C (100.4F), altered level of consciousness, autonomic dysfunction (tachycardia, labile BP, diaphoresis, tachypnea, urinary or fecal incontinence), rigidity
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What lab abnormalities may be seen in NMS?
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leukocytosis, increase in CK, AST, ALT, LD, and myoglobinuria
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What is tx for NMS?
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d/c AP and supportive care
bromocriptine or amantadine(DA agonist) is used to reduce rigidity, fever, or CK dantrolene is skeletal muscle relaxant that effects temp, HR, RR, CK |
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Can AP be started back if pt has had NMS?
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rechallenge is ok, should use SGA
monitor for 2 week or more |
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What is behavioral toxicity?
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antipsychotic induced akathisia, akinesia, and dysphoria
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What is akinesia?
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diminished spontaneity, symptoms of apathy and withdrawal, often mistaken for negative symptoms
appear depressed |
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When is delirium and psychosis experienced with AP tx?
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large dose FGA or combo anticholinergic and FGA
reversible on d/c |
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What should be AP tx if pt has narrow angle glaucoma?
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AP with low anticholinergic effects
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What AP cause opaque deposits in cornea?
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phenothiazine (particularly chlorpromazine)
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What monitoring should be done if pt on phenothiazines?
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slit-lamp ophthalmologic exam
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What ophthalmologic effect is a risk for quetiapine?
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cataracts, only in animals
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What ophthalmologic effect from thioridazine?
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retinitis pigmentosa
caused by melanin deposits, may cause permanent visual impairment |
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Which AP have most hepatic AE?
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phenothiazines
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What hepatic abnormalities do phenothiazine cause?
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cholestatic hepatocanalicular jaundice, LFTs
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When should AP be changed based on LFT?
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if 3x ULN
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Do SGA have LFT abnormalities?
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uncommon
risperidone has caused cholestatic hepatitis transient LFT abnormalities with olanzapine and clozapine |
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Which AP cause urinary hesitancy and retention?
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low potency FGA and clozapine
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Who is at increased risk of urinary hesitancy and retention?
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men with BPH
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What cause urinary incontinence?
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alpha blockade
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Which AP cause most sexual dysfunction?
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FGA and risperidone
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What causes sexual dysfuntion?
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dopaminergic blockade, hyperprolactinemia, histaminergic blockade (sedation), anticholinergic effects, alpha adrenergic blockade
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When should AP be d/c based on WBC?
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less than 3000
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When should AP be d/c based on ANC?
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less than 1000
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Which AP report most agranulocytosis?
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chlorpromazine and thioridazine and clozapine
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When does agranulocytosis occur?
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first 8 weeks
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How does agranulocytosis present initially?
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local infection with sore throat, leukoplakia, erythema, ulceration of pharynx
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What increases risk of agranulocytosis?
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increasing age and female
greatest risk is between months 1 and 6 of tx |
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What monitoring for clozapine?
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weekly WBC for 6 months, every 2 weeks for months 7-12, then monthly if WBC normal
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When should clozapine be d/c?
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if WBC less than 2000-300 and ANC less than 500-1000 and monitor daily
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What has been used to decrease granulocytosis?
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colony stimulating factor filgrastim
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When do allergic reactions to AP typically occur?
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in first 8 weeks
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What is tx for allergic reaction?
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d/c and topical steroids
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Which AP cause photosensitivity?
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phenothiazines (FGA and SGA)
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Why do they cause photosensitivity?
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phenothiazine absorbs UV light and energy, resulting in the formation of free radicals which damage skin
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Which AP cause blue gray or purplish skin?
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high dose of low potency phenothiazine long term administration
especially chlorpromazine |
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What usually occurs with the blue gray or purplish skin?
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corneal or lens pigmentation
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What is sialorrhea?
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drooling
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Which AP causes sialorrhea?
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clozapine
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What is tx for sialorrhea?
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alpha agonists (clonidine)
antimuscarinics (benztropine) |
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How does mild intoxication of AP present?
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sedation, hypotension, and miosis
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How dose severe intoxication of AP present?
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agitation, delirium, motor retardation, seizures, cardiac arrhythmias, respiratory arrest, coma
dystonias and pseudoparkinsonism |
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What is tx for overdose?
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supportive measures, gastric lavage, acivated charcoal
phenytoin and sodium bicarb for tx of quinidine like cardiac conduction effects on QRS or QTc |
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How should AP be used in pregnancy?
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need more studying
haloperidon is best studies and shows no relationship between use and teratogenicity clozapine and quetiapine cause wt gain and may cause gestational DM |
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How is AP used in nursing?
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clozapine has high milk concentrations
AP not CI, but lowest dose should be used and monitor infant |
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Why does metclopramide cause DI with AP?
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is is DA antagonist and pts more likely to experience akathisia and other EPS
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WHat DI do SSRIs have?
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enzyme inhibition and pharmacodynamic mechanism
5-HT2 receptors are on presynaptic dopaminergic neurons and their activation leads to decreased dopamin release from presynaptic terminal. SSRIs activate receptors and decrease dopamine release and add to dopaminolytic effects of AP. SSRIs can precipitate akathisia or EPS |
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What DI can cause and increased QTc prolongation?
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diuretics
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How is risperidone metabolized?
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CYP2D6 to 9-OH-risperidone (paliperidone)
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What cyp DI for clozapine and olanzapine?
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inhibitors of CYP1A2: cimetidine, fluvoxamine, fluoroquinolone AB
no serious interactions with olanzapine, why large therapeutic index carbamazepine can increase olanzapine elimination by 50%, cigarette smoking is inducer CYP1A2 so cause lower olanzapine concentrations |
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What causes increased clozapine levels?
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fluvoxamine is the most, up to 5x
fluoxetine and erythromycine |
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What causes decreased clozapine levels?
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smoking and carbamazepine
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What DI for ziprasidone?
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CYP3A4 inhibitors (ketoconazole) only slightly increase concentration because mainly metabolized by aldehyde oxidase
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What are DI for aripiprazole?
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CYP2D6 inhibitors (quinidine) and CYP3A4 inhibitors (ketoconazole) cause modest elvations of aripiprazole
carbamazepine decrease concentrations |
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table 70-9 pg 1116
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table 70-9 pg 1116
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How many pts have reccurrent episode of schizo?
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80%
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Which AP causes most decrease in suicidality?
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clozapine
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Which scales are used only in clinical trials?
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BPRA and PANSS
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Which scales are used in clinical practice?
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four item positive symptom rating scalse (PSRS)
brief negative symptom assessment (BNSA) |
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What baseline parameters before starting AP?
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family history, wt, ht, BMI, waist circumference, BP, FPB, fasting lipid profile
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How often should Wt be monitored?
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monthly for first 3 months, quarterly therafter
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How ofter should others be monitored?
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at 3 months, then annually
if lipids normal, can monitor less often |
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table 70-10 pg 1119
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1119
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