Antipsychotics (Ch. 5) Flashcards

1
Q

Re: nomenclature for meds, how should you refer to psych med names

A

use pharm. mechanism of action not their clinical indication

many drugs work on various disorders/syndromes/sx

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2
Q

what receptors (generally) do “antipsychotics” work on

A

serotonin and dopamine but will affect other neurotransmitter systems secondarily

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3
Q

D2 antagonists use, mechanism of action & examples

A

typical/conventional/first-generation antipsychotics

use if don’t respond to second generation or tx resistance or needed immediate/long acting injenctions

tx= bipolar mania, psychotic mania, psychotic depression, Tourette syndrome, gastroesophogeal reflux, gastroparesis, prevent n/v r/t chemo

mechanism of action= blocking D2 receptors in mesolimbic/mesostriatal pathways help positive sx of psychosis but this pathway is also for motivation & reward. “Pleasure center”. Can cause secondary negative sx

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4
Q

“Other” pharmacological properties of D2 antagonists

A

muscarinic cholinergic antagonism
antihistaminic actions (H1 antagonism)
alpha 1 adrenergic antagonism

*linked to SE more than therapeutic

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5
Q

muscarinic cholinergic antagonism SE

A

dry mouth, blurred vision, risk of paralytic ileus

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6
Q

blockage of H1 histamine SE

A

weight gain, sedation

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7
Q

blockage of alpha 1 adrenergic receptors SE

A

sedation, CV SE like orthostatic hypotension

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8
Q

Ex D2 antagonist that also strongly binds to all three muscarinic, antihistamine (H1), alpha 1 adrenergic receptors and when indicated

A

chlorpromazine
when need sedation & antipsychotic

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9
Q

what d2 antagonists are more likely to cause DIP

A

agents with weak anticholinergic (muscarinic) properties

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10
Q

what d2 antagonists are less likely to cause DIP

A

agents with stronger anticholinergic properties

but higher incidents of constipation > life-threatening paralytic ileus

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11
Q

Examples of D2 antagonists & potency

A

chlopromazine (Thorazine) - low potency
fluphenazine (Prolixin)- high potency
haloperidol (Haldol)- high potency
loxapine (Loxitane)
perphenazine (Trilafon)- high potency
pimozide (Orap)- high potency; QT issues
thioridazine (Mellaril)- high potency; QT issues
thiothixene (Navane)- high potency
trifluoperazine (Stelazine)- high potency

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12
Q

How to treat negative secondary sx of D2 antagonists

A

lower dose or switch med; adjunct meds for depression can help (5HT2A antagonists or D3 partial agonists)

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13
Q

Mesocortical dopamine D2 receptor antagonism effects

A

secondary neg sx, cognitive/affective sx since dopamine in this pathway is thought to already be low in schizophrenia leading to negative sx

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14
Q

what SE if block D2 receptors in tuberoinfundibular pathway

A

increased prolactin

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15
Q

what SE if block D2 receptors in nigrostriatal pathway

A

motor SE- DIP (bradykinesia/akinesia), akathisia, dystonia, tardive dyskinesia (chronic use)

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16
Q

what is best to treat psychosis r/t dementia or Parkinson’s

A

a 2HT2A antagonist without a D2 antagonist

17
Q

antipsychotics with high metabolic risk

A

clozapine, olanzapine

18
Q

antipsychotics with moderate metabolic risk

A

risperidone, paliperidone, quetiapine, asenapine, iloperidone

19
Q

antipsychotics with low metabolic risk

A

lurasidone, cariprazine, limateperone, ziprasidone, pimavanserin, aripiprazole, brexpiprazole

20
Q

what to measure/monitor w/ antipsychotics for cardiometabolic SE risk

A

weight/BMI, fasting glucose, fasting triglycerides, BP

family hx DM

21
Q

what medication can be considered to mitigate weight gain/cardiometabolic risk with antipsychotics

A

metformin
less consistent results with topiramate

22
Q

*What causes elevated prolactin, med common with, sx, tx

A
  • D2 blockade in the Tuberoinfundibular pathway= Hyper-prolactin
  • Common with Risperdal
  • Men= Gynecomastia, erectile dysfunction, low libido, galactorrhea
  • Women = galactorrhea and absence of menses, low libido, galactorrhea

Management
1. Reduce or discontinue med
2. Switch to a different mediation
3. If the above techniques are not feasible, add Aripiprazole to the regimen

23
Q

*Neuroleptic Malignant Syndrome (NMS)- what is it? Sx, risks, tx

A
  • Life-threatening idiopathic reaction to antipsychotic medications (more common w/ FGAs)
  • Medical Emergency w/ 20% mortality rate if untreated
  • *Generally apparent 2 weeks of treatment initiation
    F= Fever
    A= Autonomic Instability (Tachycardia, HTN, Diaphoresis)
    L= Leukocytosis
    T= Tremor
    E= Elevated CPK
    R= Rigidity (lead pipe)
    E= Excessive sweating (diaphoresis)
    D= Delirium (mental status changes)

Risk factors: High doses, high potency, LAIs, Young males early in treatment with high potency antipsychotics

Management
1. D/C medication
2. Supportive care (hydration, IV benzos- for relaxation; cooling blankets)
3. Administer sodium dantrolene, bromocriptine, amantadine
4. ECT can be effective

24
Q

*tardive dyskinesia- what is it? Sx, risks, tx

A

Tardive= D2 Blockade in the Nigrostriatal Pathway =late occurring

  • Involuntary Choreoathetoid movements of face, mouth, lips (lip smacking) tongue (fly catcher tongue)
    and other body parts (facial grimacing, eye blinking, trunk, limbs etc. )
  • Occurs in patients who have used neuroleptics for months to years (Sooner in older adults)
  • Risk factors: older age, women, patients with affective disorders, patients with substance abuse hx;
    FGA, duration of txt, higher dose, African American
  • Affects about 20-30% of patients who on antipsychotics or months or years.
  • Up to 50% of cases will remit (without further antipsychotic use)
  • Mostly irreversible

Management: Dose reduction; D/C med; switch to an atypical antipsychotic; Clonazepam, Amantidine,
Tetrabenazine.
2017: First FDA approved treatment for TD (Valbenazine=Ingrezza); Deutetrabenazine (Austedo)

AIMS (Abnormal Involuntary Movement Scale) testing initially then Q3-6 months

Risk factors: High doses, long duration, old age, women, hx of EPS, substance abuse (heavy smoking),
diabetes

Patient Education: TD symptoms may initially worsen transiently as medication dosages are lowered.
Consider switching to Clozaril (Lowest risk of TD)

25
*Lithium type of med, therapeutic range, what's toxic level & potentially lethal level? Sx
mood stabilizer acutely stimulates the NMDA receptor, increasing glutamate availability in the postsynaptic neuron. After chronic administration, lithium induces NMDA downregulation, this way lithium modulates glutamate neurotransmission.` Narrow therapeutic index(0.6-1.2 mEq/L) Toxic >1.5 Potentially Lethal =>2.0 * Early: Nausea, vomiting, diarrhea, coarse tremors, ataxia * Late: Seizures, Coma, death
26
*Tegretol- therapeutic level, SEs, labs needed before and during
mood stabilizer increases the inhibitory neurotransmitter GABA (gamma amino butyric acid) and decreases excitatory neurotransmitter glutamate Therapeutic Level= 8-12 mcg/ml Rare= Depakote induced thrombocytopenia Elevation of liver enzymes causing hepatitis Labs before initiating: Pregnancy test, CBC, LFTs Regular Labs: CBC, LFTs
27
*Depakote- therapeutic level/when to check, SE, labs
Therapeutic level = 80-120 ug/ml Check level after 4-5 days S/E: Nausea, diarrhea, Abdominal cramping, sedation, tremor, hair loss Rare= Depakote induced thrombocytopenia Labs: CBC, LFTs Watch for s/s of Hyperammonemia – confusion, lethargy, abnormal posture- ataxia, seizure, agitation etc. – Check ammonia level first
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*what concern would there be if depakote & tegretol admin together
hepatotoxicity
29
*Tegretol autoinduction
TEGRETOL AUTO-INDUCTION * Tegretol level range=remember auto-induction of its own metabolism may start 3-5 days after initiation = therefore decreases plasma levels * Can produce Ataxia even at therapeutic doses
30
*Factors that can increase Lithium levels
* NSAIDS (e.g. ibuprofen) * Aspirin * Thiazide diuretics * Dehydration (especially in the elderly) * Salt deprivation * Sweating (salt loss) * Impaired renal functioning * Ace Inhibitors * Antihypertensives
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