Antipsychotics Flashcards
What are the cardiac conduction abnormalities found with typical and atypical antipsychotics respectively? Why?
Typical = QRSd and QTc prolongation (Na and K blocking) Atypical = QTc prolongation (K blocking)
What pathway is responsible for the movement disorders associated with antipsychotic use?
Nigrostriatal pathway
What is the basis for using anticholinergics in treated acute dystonic reactions?
Dopamine acts as an inhibitor to movement, which involves ACh. If block ACh, then similar to what dopamine does normally
What type of symptoms are atypical antipsychotics better at treating?
Negative symptoms
What is the classic side effect of chlorpromazine?
Agranulocytosis
What is the classic side effect of Loxapine
Seizures
What is the classic side effect of Haldol
NMS
What is the classic side effect of Clozapine
Agranulocytosis
What is the classic side effect of Olanzapine
DM, DKA
What is unique about asenapine, and what role does this play in an overdose?
given SL since not absorbed through the GI tract. If swallowed as an attempt to OD, then little to no effect
What is the classic side effect of Risperidone
Unusual arrhythmias
What is the classic side effect of Quetiapine
Sedation
Potent alpha blocker
What is the classic side effect of ziprasidone
QTc prolongation
What is the classic side effect of Iloperidone
QTc prolongation
What is the classic side effect of Lurasidone
Hypotension
Which atypical antipsychotic does not significantly prolong the QTc?
Brexpiprazole
What classic sign of Parkinson’s is not seen with neuroleptic induces parkinsonism?
Pill-rolling tremor
What is the Vd and protein binding of antipsychotics, and what is the clinical relevance of this?
High Vd and high protein binding = no dialysis
What is the relationship between dose/blood levels of antipsychotics, and s/sx in OD?
No correlation
What two systems are mostly affected with antipsychotic ODs?
CV
Neuro
What are the hemodynamic effects of antipsychotic ODs? (2)
hypotension from alpha blocking
Direct myocardial depression
What are the major CNS s/sx of antipsychotic OD?
sedation to coma
Peripheral anti-cholinergic effects
What is the treatment for antipsychotic overdose? (hypotension, arrhythmias)
NE for hypotension
Lidocaine for ventricular arrhythmias
What classes of antiarrhythmics should be avoided in cases of antipsychotic overdose? Why?
Type I and III, since these block Na and Na/K channels respectively, which will only worsen the arrythmia
Compare serotonin syndrome and NMS in terms of: onset
NMS = slow (days to weeks)
Serotonin syndrome = fast (hours)
Compare serotonin syndrome and NMS in terms of: muscular findings
NMS = rigidity SS = Clonus, hyperreflexia
What are the two major precipitating events associated with NMS?
Medication changes
Depot form of drug
What lab is classically elevated with NMS?
CPK
What is the treatment for NMS?
Supportive, BDZ, decrease muscle use
What is the treatment for hyperprolactinemia?
Bromocriptine
What is the receptor that is defunct with malignant hyperthermia?
Ryanodine receptor
What is the treatment for malignant hyperthermia?
Dantrolene and cooling
What are the two drugs that are used to treat acute dystonic reaction?
Diphenhydramine
Benztropine
What is the treatment for akathisia?
Anticholinergics
BDZs
What is oculogyric crisis?
Inability to move eyes
What is the new drug that is approved to treat tardive dyskinesia? MOA?
- 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”
