Haldol decanoate fda

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The mechanism of action of all first-generation antipsychotics (FGAs) appears to be postsynaptic blockade of brain dopamine D2 receptors. Evidence supporting this mechanism includes strong antagonism of D2 receptors in both cortical and striatal areas [ 1 ], a high correlation between D2 receptor binding and clinical potency [ 2 ], and a consistent requirement of 65 percent D2 receptor occupancy for antipsychotic efficacy in functional imaging studies [ 3 ]. The nonspecific localization of FGA dopamine binding throughout the central nervous system is consistent with their risk of movement disorders and prolactinemia. Aside from their common activity as D2 antagonists, each FGA has distinct effects on neuronal 5-HT2a, alpha-1, histaminic, and muscarinic receptors, which generally correspond to their individual side effect profiles, as shown in the table ( table 1 ).

The intravenous route is not FDA approved and is generally not recommended except when no other alternatives are available. Intravenous administration appears to be associated with a higher risk of QT prolongation and torsade de pointes (TdP) than other forms of administration. The manufacturer recommends ECG monitoring for QT prolongation and arrhythmias if IV administration is required. A dose in the range of 1 to 5 mg IV has been suggested, with the dose being repeated at 30 to 60 minute intervals, if needed. A maximum IV dose has not been established. The lowest effective dose should be used in conjunction with conversion to oral therapy as soon as possible.

Haldol decanoate fda

haldol decanoate fda

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