Chapter 20: Parkinson & Alzheimer Disease Drug Therapy

Parkinson's disease is analyzed through the lens of an extrapyramidal motor tract dysfunction caused by a significant neurotransmitter imbalance: a deficiency in inhibitory dopamine and an overabundance of excitatory acetylcholine within the substantia nigra. The text details various drug classes intended to restore this balance, most notably dopaminergic replacement therapies like carbidopa-levodopa. In this combination, carbidopa serves as a decarboxylase inhibitor that prevents the peripheral breakdown of levodopa, allowing a greater concentration to reach the brain for conversion into dopamine. Other treatment strategies include dopamine agonists that mimic natural neurotransmitters, MAO-B and COMT inhibitors that prolong dopamine's presence by blocking catabolic enzymes, and anticholinergics used to suppress tremors and rigidity. Shifting focus to Alzheimer’s disease, the chapter examines the decline in cognitive function related to the degeneration of cholinergic neurons, the formation of neuritic plaques, and the development of neurofibrillary tangles. Therapeutic interventions highlighted include acetylcholinesterase inhibitors like rivastigmine and galantamine to boost acetylcholine levels, along with NMDA receptor antagonists such as memantine for moderate-to-severe cases. Additionally, it introduces modern biological treatments, including monoclonal antibodies like aducanumab and lecanemab, which target the reduction of amyloid-beta plaques. Throughout the chapter, a heavy emphasis is placed on the nursing process and clinical judgment, focusing on patient safety, the management of side effects such as orthostatic hypotension and gastrointestinal distress, and critical patient education regarding dietary restrictions and fall prevention to optimize long-term care.