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57 Cards in this Set

  • Front
  • Back
characteristics of dementia
gradual progression of multiple cognitive deficits
impaired ability to learn new info
short term memory is involved much greater than long term
aphasia
apraxia
agnosia
disturbance in executive functioning
failure in the execution of a learned motor task despite normal strength and coordination
apraxia
failure to recognize or identify objects despite intact sensory function
agnosia
by far the most common type of dementia
Alzheimer's disease
epidemiology of Alzheimers dementia
incidence of 1% at age 60 and double every 5 years after
associated with increased risk of developing late onset Alzheimers dementia
presence of apolipoprotein E4 allele on chromosome 19
what is associated with early onset Alzheimers dementia
abnormalities in chromosome 21, 14 and 1
1/3 of AD patients don't have ApoE4 allele
**
what disorder is associated with development of AD in virtually 100% of cases by age 40
Down's syndrome
what cortical neurons are particularly affected in Alzheimers dementia
association cortex, deeper layers of the temporal cortex and hippocampus
what neurotransmitter is affected in Alzheimers dementia
significant drop-out of the basal forebrain cholinergic neurons which project to the cerebral cortex - ACh
what do amyloid plaques do in the brain of alzheimers patients and the end result
trigger:
1. inflammation
2. hyperphosphorylation of tau protein leading to neurofibrillary tangles
3. free radical toxicity
resulting in neuronal loss and cholinergic dysfunction
senile plaques
extracellular nruonal and glial processes composed of amyloid beta protein
neurofibrillary tangles
intracellular collection of abnormal filaments that have distinction paired helical structure composed of tau protein
3 pathological features of alzheimers dementia
senile plaques
neurofibrillary tangles
granulovacuolar degeneration of hippocampal pyramidal cells
what is maintained in a patient with Alzheimers dementia
social skill
long term memory
what symptoms can present in a person with late features of alzheimers dementia
apathy
social withdrawal
depression
anxiety
agitation
delusions
hallucinations
what signs on exam can present in person with late features of alzheimers dementia
gait instability
parkinsonian features
frontal lobe release signs
what may be a better way of engaging a patient with frustration during a mental status exam
engage them informally and in conversation ask questions about their favorite sports team or TV show
imaging in Alzheimers dementia
PET scan shows hypometabolism especially in temporal-parietal regions
amyloid imaging is a specific PET scan that bind to amyloid
what should always be checked in a patient with a poor mental status exam
metabolic work-up:
electrolytes
kidney and liver function
B12 level
thyroid studies
bladder infections
what groups of drugs are used for Alzheimers dementia
acetylcholinesterase inhibitors
list the drugs used for alzheimers dementia
Donepezil
Rivastigmine
Galantamine
Memantine
Memantine
noncompetitive NMDA receptor antagonist
what should be treated in patients with late stages of alzheimers dementia
agitation
psychosis
aggressive behavior
depression
-atypical neuroleptics
Multi-infarct Dementia
multiple cortical strokes results in a stepwise decline, and associated with hemiplegia, visual field defects, aphasia, and sensory loss
associated with dementia presenting along with: dysarthria, dysphagia, emotional incontinence, and apathy
multiple subcortical strokes
why can the development of dementia in parkinson's disease greatly interfere with treatment
medications used to treat PD can cause confusion and hallucinations
patients present with early symptoms of parkinsonism and dementia
Dementia with Lewy Bodies
classic triad of dementia with lewy bodies
1. dementia with fluctuating cognition
2. recurrent visual and nonvisual hallucination
3. motor features of parkinsonism
characteristics of dementia with lewy bodies
prominent hallucinations
fewer tremors
orthostasis
hypersensitivity to neuroleptic and antiemetic medications
100% have REM behavior disorder
pathology seen in dementia with lewy bodies
1. lewy bodies seen throughout the brain, not just subcortical region like idiopathic PD
2. loss of dopamine-producing neurons in substacia nigra
3. loss of ACh producing neurons in basal nucleus
4. senile plaques
5. granulovacuolar degeneration
abnormal proteinaceous (alpha-synuclein) cytoplastmic inclusions
lewy bodies
drug of choice for dementia with lewy bodies
acetylcholinesterase inhibitors
because hallucination often worsened by medication used to treat parkinsonism (increased dopamine)
dementia associated with early behavioral problems and chorea
Hunginton's disease
when is dementia noted in HIV
late manifestation of the disease process
associated with rapidly progressive dementia, non-epileptic myoclonic jerks, and ataxia
Creutzfeldt-Jakob Disease
most prominent manifestation of CJD
dementia
most common cause for CJD
sporadic
diagnosis of CJD supported by
periodic sharp waves on EEG
raised level of 14-3-3 protein in CSF
signal changes in the basal ganglia seen on MRI
what symptoms would suggest frontotemporal dementia
early features of disinhibition and personality change
associated with thiamine deficiency
wernicke's encphalpathy
Korsakoff's syndrome
common cause of thiamine deficiency
chronic alcoholism
classic features of wenicke's encephalopathy
1. ophthalmoplegia - usually CN VI
2. encephalopathy - can progress to coma
3. gait instability - midelin truncal
what can precipitate symptoms of underlying thiamine deficiency
administration of IV glucose
associated with anterograde and retrograde memory deficit, little insight, and profound confabulation
Korsakoff's syndrome
associated with degeneration of thalamus, mamillary bodies, peri-aqueductal structures, pons
Korsakoff's syndrome
treatment of Wernicke's encephalopathy/Kofsakoff's syndrome
treat with thiamine
classic non-specific triad of symptoms in normal pressure hydrocephalus
gait apraxia - first symptom
dementia - subcortical with withdrawn, depressed symptoms
Urinary incontinence
pathology of normal pressure hydrocephalus leading to gait apraxia and urinary incontinence
failure of the arachnoid granulations to resorb CSF leading to ventricles enlarging and pushing against pathway important for control of legs and bladder
why is normal pressure hydrocephalus frequently overdiagnosed
because hydrocephalus ex-vacuo appears like enlarged ventricles, patients actually have AD with gait instability and urinary incontinence
differentiate pseudodementia (depression) from actual dementia
depression - onset may be abrupt and may fluctuate from day to day, emphasizes failures, personality changes, aware and distressed (good insight)
dementia - slow and steady progression, emphasizes achievements, cheerful, unaware and unconcerned (low insight)
symptoms often associated with withdrawal from alcohol and sedatives
delirium tremens - hallucinations, restlessness, autonomic over-activity, and irritability
characteristics of encephalopathy
acute onset
fluctuating course
sleepy
often reversible
how do know if primary aphasia is present
language deficits are far our of proportion to the memory loss, unlike dementia or encephalopathy
memory loss begins after a fall
chronic subdural hematoma
how to distinguish focal mass lesion on exam from dementia or encephalopathy
look for focal abnormalities on exam - this will not be found in person with dementia or encephalopathy