Aziz: Dementia Flashcards
(36 cards)
Which structures in the brain are involved in the circuitry of cognition?
cortex basal ganglia cerebellum thalamus pons
What are the cognitive domains that need to be assessed in a patient with dementia?
memory attention executive function language visuospatial abilities behavior functional status
What is the best screening test for patients with dementia?
MMSE
**can also use MOCA, mini cog, or clock drawing
What is mild cognitive impairment?
cognitive impairment that doesn’t interfere with activities of daily living and is not severe enough to meet criteria for dementia
T/F: Mild cognitive impairment can affect a single domain or multiple domains
True
What percentage of patients with mild cognitive impairment eventually convert to dementia in 6 years?
80%
3 risk factors for the progression of mild cognitive impairment to dementia?
- apolipoprotein allele carrier
- poor performance on semantic cueing memory test
- reduced hippocampal volumes
What is dementia? What causes it?
progressive deterioration of cognitive function that results in impairment of social and occupational functioning; caused by relentless brain tissue (neuron) degeneration
List a few types of dementia that we spoke about
Alzheimer dementia dementia with Lewy bodies frontotemporal dementia vascular dementia Parkinson disease dementia
What are some risk factors for Alzheimer dementia?
age female sex low level of education down syndrome head trauma apoE genetics
What might you notice histologically about the neurons in a patient with dementia?
formation of plaques in the interstitial space between neurons
neuronal cells are unhealthy and plump
What happens to the cortex in patients with Alzheimer’s disease?
cortical atrophy
Symptoms of Alzheimer disease?
memory loss that disrupts daily life +
at least one of the following:
aphasia, apraxia, agnosia, disurbed executive function
In Alzheimer’s, the cognitive abnormalities must represent a change from a previous higher level of function, be (blank), & impair (blank)
Gradual onset and continued decline
Not present exclusively during a period of (blank).
progressive; functioning; delirium
What tests should be done on a patient with dementia?
CBC glucose, electrolytes, BUN/creatinine, liver functioning serum vit B12 thyroid function tests noncontrast CT or MRI depression screening
Tests that should not be performed routinely on patients with dementia?
syphilis screening EEG lumbar puncture linear or volumetric MRI or CT SPECT APOe genotyping
T/F: ApoE-e4 testing does not add substantially to the diagnosis of Alzheimer’s, and is not recommended as a part of routine screening
True
3 stages of Alzheimer disease?
pre-symptomatic phase
symptomatic, pre-dementia phase
dementia phase **insidious onset over months to years with a progressive history of cognitive decline
What will the CSF AB1-42 be like if a patient has Alzheimer’s? Wht will phosphorylated tau and total tau be like?
CSF AB1-42 will be low (being used up in the formation of neurotic plaques)
tau will be high, because with neuronal atrophy, tau will leak out and will be high
What are some aspects of the total care for patients with dementia?
home care institutionalized care hospital care clinic care community care
Dementia complications?
inadequate nutrition reduced hygiene difficulty taking meds deteriorating emotional health difficulty communicating delusions and hallucinations sleep difficulties
How do we treat Alzheimer’s dementia?
AChE inhibitors like Rivastigamine and Donepezil and Galantamine
OR
Memantine which is an NMDA antagonist (blocks activation of these receptors to avoid excitotoxicity and too much neuron death)
What is the cholinergic theory of AD?
Alzheimer’s dementia is associated with decreased cholinergic activity
AChE inhibitors slow the breakdown of ACh to keep it present in the synapses longer!
What is the glutamate hypothesis of AD?
glutamate is released in large amounts in dead or dying neurons; increased extracellular glutamate increases NMDA receptor activity and can lead to excitotoxicity and death in downstream neurons
