The urinary incontinence suggests disease progression into a more advanced stage of dementia requiring reassessment of the current treatment plan.

While disease progression is possible, the temporal relationship to oxybutynin initiation makes a drug interaction the most likely explanation for the increased confusion.

Increase donepezil dosage to overcome the cognitive decline, since higher cholinesterase inhibitor levels may compensate for the concurrent medication effect.

Increasing donepezil to overcome an anticholinergic antagonist raises side effect risk (GI disturbance, bradycardia) without addressing the root cause of the interaction.

Oxybutynin is an anticholinergic that directly opposes donepezil's cholinesterase inhibitor mechanism, likely worsening cognition through a pharmacodynamic interaction.

Donepezil increases acetylcholine at the synapse. Oxybutynin blocks muscarinic acetylcholine receptors. These medications are working against each other — the anticholinergic cancels the cholinesterase inhibitor's benefit and may worsen cognition beyond baseline. This is a classic polypharmacy trap in geriatric psychiatry. The PMHNP should identify the drug-drug interaction, communicate with the PCP, and recommend an alternative for incontinence without anticholinergic properties (e.g., mirabegron, a beta-3 agonist that treats overactive bladder without anticholinergic effects).

Discontinue donepezil since it is no longer providing cognitive benefit, as evidenced by the worsening confusion reported by the patient's daughter.

Donepezil may still be effective — the cognitive decline is likely iatrogenic from the pharmacodynamic interaction, not disease progression or treatment failure.