Alzheimer’s Disease Angela Singh, PharmD Associate Professor of Pharmacy Practice Florida A&M...
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Transcript of Alzheimer’s Disease Angela Singh, PharmD Associate Professor of Pharmacy Practice Florida A&M...
Alzheimer’s Disease
Angela Singh, PharmD
Associate Professor of Pharmacy Practice
Florida A&M University
College of Pharmacy & Pharmaceutical Sciences
Objectives Understand the pathophysiology of Alzheimer’s Disease (AD)
Identify cognitively impairing medications when given a patient list
List the available products used for the management of AD including brand and generic names
Describe the mechanism of action of pharmacotherapy for AD
Identify potential drug interactions while reviewing a patient profile
Recommend solutions for adverse effects experienced by patients receiving therapy for AD
What is dementia?
Types of Dementia
Alzheimer’s Disease (AD)Lewy Body Dementia Vascular DementiaParkinson’s Related Dementia
Alzheimer’s Disease (AD)
Most common form of dementia Increasing prevalence with increasing age Characterized by
Presence of amyloid plaquesPresence of neurofibrillary tanglesLoss of Cortical neurons
Pathophysiology
Pathophysiology
MRI Scan
Differential Diagnosis
Anemia Hypothyroidism Low Vitamin D Levels Infections
UTI HIV
Use of Cognitively Impairing Medications
Depression versus AD
DEPRESSION Abrupt in onset Short duration Previous psychiatric
history Complaints of memory
loss “I don’t know” answers Fluctuating cognitive loss Equal memory loss for
remote and recent memory
Depressed mood occurs first
DEMENTIA Insidious in onset Long duration No psychiatric history Often unaware of
memory loss Near miss answers Stable cognitive loss;
progressive over time Memory loss is greatest
for recent events Memory loss occurs first
What are some medications that are cognitively impairing?
Diagnostic Test
Mini Mental Status Examination Formal Neuropsychiatric Testing MRI or CT scans Lab
CBC Thyroid Vitamin B-12 Iron Urinalysis Syphilis HIV
AD: Clinical Features
Impairment of Memory Changes in Personality Impairment of Judgment Loss of Language Skills Loss of Executive Function Social Withdrawal Apathy Loss of orientation
Pharmacotherapy
Acetylcholinesterase Inhibitors
How do these agents work? Take 4-6 weeks for onset of therapeutic effect to be
seen. Patient should be on the agent a minimum of 3
months without improvement before changing to another agent.
Donepezil (Aricept®) Rivastigmine (Exelon®) Galantamine (Razadyne®) Tacrine (Cognex®)
Donepezil (Aricept®)
Indicated for the management of mild to severe AD Drug Interactions
Anticholinergics 3A4 & 2D6 Inhibitors/Inducers
It is given once daily due to its long half-life. Available as a tablet and an orally disintegrating tablet
(ODT). Common Side Effects: nausea, vomiting, diarrhea,
insomnia (8%), vivid dreams, dizziness. Give in the morning with food.
Rivastigmine (Exelon®)
An inhibitor of both acetylcholinesterase and butyrylcholinesterase.
Indicated for management of mild to moderate AD Drug Interactions
Anticholinergics 3A4 & 2D6 Inhibitors/Inducers
Short elimination half-life necessitates twice daily dosing.
Available as liquid, pill, patch. Side Effects: GI side effects are more frequent
(48% - 50%), dizziness, insomnia. Must be given with food.
Galantamine (Razadyne ®)
Selectively inhibits acetylcholinesterase and also modulates nicotinic receptors.
Indicated for mild to moderate disease Drug Interactions
Anticholinergics 3A4 & 2D6 Inhibitors/Inducers
Available as a ER capsule, solution, tablet Due to its short elimination half-life, two doses are
required daily when using the tablet or solution. The ER capsule is dosed once daily. Side effects: nausea, vomiting, diarrhea, dizziness.
Memantine (Namenda®)
An N-methyl-D-aspartate antagonist approved for moderate to severe Alzheimer’s disease.
Pathophysiology of AD: Basis for Memantine
Glutamate is the main excitatory neurotransmitter in the CNS.
One type of glutamate receptor includes the NMDA (N-methyl-D-Aspartate) receptors; once activated, they generate a long-lasting influx of calcium into neurons which is thought to be involved in a cellular process that underlies learning and memory.
In AD, an increase of glutamate is thought to lead to excessive activation of NMDA receptors with consequent intracellular accumulation of calcium initiating a cascade of events which leads to neuronal death.
Mechanism of Action of Memantine
An NMDA receptor antagonist Reduces overstimulation of the NMDA receptors
(caused by abnormally high concentrations of glutamate) and restore normal receptor-signaling function.
By reducing excitotoxicity will prevent neuronal calcium overload therefore preventing further cell damage and cell death.
Memantine
Indicated for moderate to severe AD Formulations include tablets, ER tablets,
solution. Side Effects
Dizziness, tachycardia, diarrhea, insomnia, headache, restlessness, akathisia, nausea
Questions
Angela Singh, PharmD 599-3369 [email protected] Office #345