Antipsychotics Flashcards

1
Q

What are the cardiac conduction abnormalities found with typical and atypical antipsychotics respectively? Why?

A
Typical = QRSd and QTc prolongation (Na and K blocking)
Atypical = QTc prolongation (K blocking)
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2
Q

What pathway is responsible for the movement disorders associated with antipsychotic use?

A

Nigrostriatal pathway

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3
Q

What is the basis for using anticholinergics in treated acute dystonic reactions?

A

Dopamine acts as an inhibitor to movement, which involves ACh. If block ACh, then similar to what dopamine does normally

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4
Q

What type of symptoms are atypical antipsychotics better at treating?

A

Negative symptoms

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5
Q

What is the classic side effect of chlorpromazine?

A

Agranulocytosis

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6
Q

What is the classic side effect of Loxapine

A

Seizures

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7
Q

What is the classic side effect of Haldol

A

NMS

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8
Q

What is the classic side effect of Clozapine

A

Agranulocytosis

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9
Q

What is the classic side effect of Olanzapine

A

DM, DKA

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10
Q

What is unique about asenapine, and what role does this play in an overdose?

A

given SL since not absorbed through the GI tract. If swallowed as an attempt to OD, then little to no effect

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11
Q

What is the classic side effect of Risperidone

A

Unusual arrhythmias

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12
Q

What is the classic side effect of Quetiapine

A

Sedation

Potent alpha blocker

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13
Q

What is the classic side effect of ziprasidone

A

QTc prolongation

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14
Q

What is the classic side effect of Iloperidone

A

QTc prolongation

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15
Q

What is the classic side effect of Lurasidone

A

Hypotension

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16
Q

Which atypical antipsychotic does not significantly prolong the QTc?

A

Brexpiprazole

17
Q

What classic sign of Parkinson’s is not seen with neuroleptic induces parkinsonism?

A

Pill-rolling tremor

18
Q

What is the Vd and protein binding of antipsychotics, and what is the clinical relevance of this?

A

High Vd and high protein binding = no dialysis

19
Q

What is the relationship between dose/blood levels of antipsychotics, and s/sx in OD?

A

No correlation

20
Q

What two systems are mostly affected with antipsychotic ODs?

A

CV

Neuro

21
Q

What are the hemodynamic effects of antipsychotic ODs? (2)

A

hypotension from alpha blocking

Direct myocardial depression

22
Q

What are the major CNS s/sx of antipsychotic OD?

A

sedation to coma

Peripheral anti-cholinergic effects

23
Q

What is the treatment for antipsychotic overdose? (hypotension, arrhythmias)

A

NE for hypotension

Lidocaine for ventricular arrhythmias

24
Q

What classes of antiarrhythmics should be avoided in cases of antipsychotic overdose? Why?

A

Type I and III, since these block Na and Na/K channels respectively, which will only worsen the arrythmia

25
Q

Compare serotonin syndrome and NMS in terms of: onset

A

NMS = slow (days to weeks)

Serotonin syndrome = fast (hours)

26
Q

Compare serotonin syndrome and NMS in terms of: muscular findings

A
NMS = rigidity
SS = Clonus, hyperreflexia
27
Q

What are the two major precipitating events associated with NMS?

A

Medication changes

Depot form of drug

28
Q

What lab is classically elevated with NMS?

A

CPK

29
Q

What is the treatment for NMS?

A

Supportive, BDZ, decrease muscle use

30
Q

What is the treatment for hyperprolactinemia?

A

Bromocriptine

31
Q

What is the receptor that is defunct with malignant hyperthermia?

A

Ryanodine receptor

32
Q

What is the treatment for malignant hyperthermia?

A

Dantrolene and cooling

33
Q

What are the two drugs that are used to treat acute dystonic reaction?

A

Diphenhydramine

Benztropine

34
Q

What is the treatment for akathisia?

A

Anticholinergics

BDZs

35
Q

What is oculogyric crisis?

A

Inability to move eyes

36
Q

What is the new drug that is approved to treat tardive dyskinesia? MOA?

A
  • Valbenazine
  • VMAT inhibitor–“Although the exact cause of tardive dyskinesia is unknown, it is hypothesized that it may result from neuroleptic-induced dopamine hypersensitivity. By selectively reducing the ability of VMAT2 to load dopamine into synaptic vesicles,[6] the drug reduces overall levels of available dopamine in the synaptic cleft, ideally alleviating the symptoms associated with dopamine hypersensitivity”