Dementia Flashcards
Dementia
an acquired syndrome of decline in memory and other cognitive functions sufficient to affect daily life in an alert person, usually behavioral disturbances too
Diagnosis of dementia
DSM-V-TR, spouse, rating scales, autopsy, brain atrophy and neuronal loss (dec acteylcholine)
Risk factors of dementia
age, fam hx, hx of head trauma
Alzheimer’s disease
60-70% of all dementias, presence of B-amyloid and tau proteins, slow, progressive decline in cog ability, initial impairment w/ short term memory, difficulty learning new info, aphasia, impaired visuospacial fct
Lewy Body Dementia
Lewy body plaques, limbic and neocortical areas outside the substantia nigra, presents w/ fluctuations in alertness/attentian and confused states, visual hallucination are common, parkinsonia, orthostatic hypoTN, syncope
Vascular dementia
abrupt onset with stepwise, causal decline in cog function, based on vascular insults, language and memory retrieval difficulties, symptoms largely reliant on location of injury
parkinson’s dementia
pts w/ parkinson’s have 6x chance of dementia diagnosis, motor disturbances accompanies and often precedes symptoms, gait dysfunction, visual disturbances, frequent falls
What should you avoid when possible
antihistamine, oxybutnin, tolterodine, cyclobenzaprine, TCAs
AD treatment of cog sx
acetylcholinesterase inhibitors, NMDA antagonist
AD treatment of BPSD
non-pharm therapy, antipsychotics, antidepressants, antionvulsants/ mood stabilizers, benzos
Non-pharm treatment
exercise body/brain, mediterranean diet, music, orientation reinforcement, communication, attention to safety
Basic principles of care for AD
Keep requests and demands simple, avoid confrontation, remain calm, firm, supportive, frequent reminders, explanations, orientation cues, adjust to expectations, patience!
AChEI aimed to
increase acetylcholine, correct the cholinergic deficiency hypothesis of amnesia
Nucleus basalis of meynert
located in basal forebrain, principle site of cholinergic cell bodies for axons that project to the hippocampus, amygdala and throughout the neocortex, it is the degeneration of these cells that leads ot AD
MOA of AChEI
inhibit acetylcholinesterase, inhibit degradation of acetylcholine and thus increase acetylcholine concentrations in nerve synapses, doesn’t affect underlying neurodegenerative process
Efficacy of AChEIs
most effective when started early, used for mild to moderate, and moderate to severe AD; may see benefit for 1-3 years
ADRs of AChEIs
nausea, vomiting, diarrhea, wt loss, can exacerbate GI bleed
AChEIs
Donepezil (Aricept), Rivastigmine (Exelon), Galantamine (Razadyne), combo Donepezil/Memantine (Namzaric)
Donepezil (Aricept)
better tolerated and more convenient dosing, indicated for mild to severe AD, CNS selective, reversible inhibitor of AChE
Dosing of Donepezil (Aricept)
5 mg qHS for 4-6 weeks, then increase to 10 mg qHS
Rivastigmine (Exelon)
less tolerable compared to donepezil, less DI, CNS selective, pseudo-irreversible for AChE and BuChE, mild to severe AD and Parkinson’s dementia, hard on GI
Rivastigmine (Exelon) patch
less GI SE, better for compliance, 4.6mg/24 hours (4 weeks, can titrate up) and 9.5mg/24 hours
Galantamine (Razadyne)
reversible, competitive AChEI, more DIs, 3A4 & 2D6 metabolism, should not be used in severe renal and hepatic impairment, mild to moderate disease
Memantine (Namenda) effects
block Ca entry when extracellular glutamate is low, allows intracellular Ca levels to return to normal, when glutamate is increased in response to an action potential, glutamate displaces memantine, causing brief Ca entry
Pathophysiolody of NMSA receptor in AD
activated state, slow but steady leakage of glutamate from the pre synaptic neuron keeps the NNMDA receptor in constantly activated state allows excess influx of Ca which leads to persistant neuroexcitation and cell death
Memantine (Namenda) therapy
renally eliminated, ADRs: constipation, dizziness, HA, confusion, agitation, HTN; for mod to severe AD most often in combo w/ AChEI, 10 mg BID
Memantine/ Donepezil (Namzaric)
mod to severe AD, 10 mg donepezil+ memantine 10 mg BID or 28 mg once daily
Vitamin E
possiple protective effects, recent results of meta analysis suggests increase in all cuase mortality when dose >400 IU/day
Ginko Biloba
antioxidant properties, questionable effectiveness, shown to stabilize of improve cog performance and social behavior for 6-12 months w/ uncomplicated AD, also antiplatelet effects (caution)
Anti-inflammatory agents
epidemiological studies suggest possible protective effect by dec B amyloid plaque development, long term risks
Lipid lowering agents
possible protective effect, statins dec B amyloid production in vitro, generally not recommended outside of reducing cholesterol
Treating lewy body dementia
AChEIs considered DOC, avoid typical and atypical antipsychotics
Treating vascular dementia
control vascular risk factors, HTN, DM, hyperlipidemia, PVD, stop smoking, AChEIs DOC
Treating Parkinson’s dementia
AChEI show improvement in cognition, alertness, apathy, and aggression, may need to inc antiparkinsonian medications, can try memantine
Common behavioral symptoms
psychotic, delusions, hallucinations, inappropriate behaviors, agitation, wandering, sexual behaviors, depression
Treating BPSD non pharm
identify behavior, understand cause, adapt environment, remove triggers, orientation, treat pain, clear infections
Adverse effects of antipsychotics
falls, fractures, delirium, oversedation, stroke
approach to treatment of BPSD
reserve until non-pharm has failed, initiate low doses, monitor closely for efficacy, work w/ pt and caregiver to individualize and simplify the drug regimen, should not be long term
Antipsychotics useful for
temporary agitation and delirium/psychosis
Haloperidol (Haldol)
PO/IM, blocks post synaptic mesolimbic D1/D2 receptors, ADRs: extrapyramidal symptoms, QT prolongation, sedation, works quickly, not for parkinson’s
Boxed warning with Haloperidol
increased risk of death
