Dementias - Cohen Flashcards
risk fx dementia
aging
dementia
develop multi cognitive defects sufficient to cause impairment in occupational and social fxn
progressive and likely irreversible decline
not temporary (like delirirum)
MC cause of dementia
alhzeimers
beta-amyloid plaques
alzheimers
AB42
tau tangles
alzheimers - microtubules inside neurons
phosphorylated tau
down syndrome
almost all get alzheimers - so chromosome 21 may play a role
alzheimers
see loss of ACh
beta-amyloid
AB42
produced from APP by secretases
alzheimers epidemiology
older - >80yo in 10-25%
more common in women
homozygous at E4 allele of apoE
more prone to alzheimers
alzheimers clinical course
begins - loss of memory speech restricted to simple phrases trouble day to day affairs visuospatial decline - get lost gait disorder depression, bored, lack social inhibition
apraxia
loss of simple actions/certain tasks
-loss of connections between cortical sites
in alzheimers
mild alzheimers
safe at home, some help with activities, not a threat
moderate alzheimers
kept at home with great effort
-full or nearly full time caregiver
severe alzheimers
must go to nursing home - round clock supervision
diagnosis of alzheimers
clinical diagnosis
possible diagnostic test - inject PiB (pitt compound) and use PET scan to see amyloid deposition in brain
CSF levels of beta-amyloid decrease and tau increase
MRI - atrophy medial temporal lobe
tx of AD
cholinesterase inhibitor
- raise ACh levels
- may help symptoms
donepezil**
rivastigmine
galantamine
memantine $$$
donepezil
most widely used tx for AD - fewest adverse effects
-taken once daily
memantine
antagonist of glutamate
prevent cell death from glutamate activity
tx of AD - but $$$
mild cognitive impairment
mild AD
-still fxn in social and job roles
lots progress to AD
lewy body disease
fluctuating dementia
wild and crazy
decreased facial animation, slow, imbalance, tremor
-mild/moderate parkinsonian sx
EARLY dementia and agitation
more common in men
dementia fluctuating, visual hallucinations, parkinsonism
lewy body dementia
bad response to antipsychotic
lewy body dementia
tx of lewy body dementia
may improve with AChE drugs
lewy bodies
contain protein alpha-synuclein
clinical course of lewy body disorder
rapid decline
-death 5-7 years
psychotic behavior that fluctuates
-with visual hallucinations
diagnosis of lewy body disorder
clinical diagnosis
AChE tx somewhat effective
prior strokes with step like downhill course
multi-infarct dementia
seizures common
likely CAD, PVD, or carotid stenosis - seen on U/S
risk fx for multi-infarct dementia
HTN, diabetes, hyperlipidemia
tx of multi-infarct dementia
control risk fx - aspirin and anti-coags
fronto-temporal dementia
family of multi disorders
-early age of onset 50-60yo
decline in behavior and speech
incrased tau protein, TDP43, and ubiquitin
increased tau, TDP43, and ubiquitin
seen in fronto-temporal dementia
behavior dominant FTD
most patients
personality change
- obsessed with certain subject - sing song over and over
- over eat, over drink
- occasional become weak
no hallucinations
language predominant form of FTD
progressive aphasia
left frontal and temporal lobe - more atrophy
mute in few years
tx of FTD
antidepressant somewhat help
creutzfeldt jakob disease
prions
-proteins
rapid dementia over 1 year with myoclonic jerks
CJD
spongiform brain
EEG - triphasic waves - diffuse periodic wave pattern
14-3-3 in CSF
CJD
prion path
change in shape of proteins
normal pressure hydrocephalus
gait disturbance
incontinence
dementia
have large lateral ventricles
see normal P on spinal tap
tx of NPH
shunting
diagnosis of NPH
remove 30cc from CSF with lumbar pucture - symptoms better
