Dementia Flashcards
disorder affecting the cerebral cortex that plays a critical role in thinking like memory and language
cortical dementia
signs of cortical dementia include
memory loss
aphasia
apraxia
agnosia
dysfunction in the parts of the brain that are beneath the cortex
subcortical dementia
the ______pathways facilitate speed and efficiency of thought
frontostriatal pathways
What is the pyramidal system
motor system with fibers originating from the cerebral cortex; corticospinal tract called pyramid in medulla
What is the extramyrapidal system
motor system with fibers originating from the basal ganglia and cerebellum
what are signs and symptoms of parkinsonism
tremor
bradykinesia
cogwheel rigidity
postural instability
acquired persistent decline of intellectual functioning; impaired memory and atleast one other cognitive domain, impairs ADL’s, NO clouding of the sensorium and NO underlying psychiatric disease
dementia
what percentage of people get dementia over age of 65
10%
what percentage of people over the age of 85 get dementia
up to 50%
memory impairment in people who are NOT demented and have INTACT ADL’s (activity of daily living)
mild cognitive impairment
approximately what percentage of people progress to dementia
6-25%
most common dementia over the age of 65
alzheimer disease
a progressive, degenerative brain disease characterized by memory loss and loss of other cognitive function
alzheimer disease
what are the risk factors for alzhimer disease
down syndrome, family history of alzheimer and advanced age
what type of dementia is characterized by loss of short term memory early with changes in behavior, personality, judgement and ADL’s
alzheimer disease
beta secretase plays a significant role in what disease
Alzeheimer disease
cholingergic defiency in the cortex and basal forebrain is associated with
alzheimer disease (contributes to cognitive deficits)
how does glutamate contribute to the pathogenesis of alzheimer disease
by overstimulating various glutamate receptors leading to excitotoxicity and neuronal cell death
late onset alzheimer disease is assoicated with what chromosome
19 (most common)
what chromosomes are associated with early onset alzheimer disese
chromosomes 1,14,and 21
familial alzheimer disease is what type of geneic disease
autosomal dominant involving APP gene chromosome 21 or presenilin 1 protein gene-chromosome 14
how do you diagnose AD
clinical + histopathological-extracellular deposition of amyloid beta protein, intracellular neurofibrillary tangles and loss of neurons especially in the hippocampus
extracellular deposits in AD
neuritic plaques
intracellular deposits in AD
neurofibrillary tangles
donepezil
treatment of mild, moderate or severe dementia
rivastigmine
treatment of mild to moderate dementia and is also used for dementia related to PD
what are the four cholinesterase inhibitors
donepezil
rivastigmine
tacrine
galantamine
used to treat AD is a cholinesterase inhibitor and is associated with abnormal liver function tests
tacrine (Cognex)
what is measured for people being treated with tacrine
serum transaminases
what are the adverse effects of cholinesterase inhibitors
nausea, vomitting diarrhea anorexia weight loss bradycardia heart block, syncope insomnia
what is the name of the one NMDA receptor antagonist used to treat AD
memantine (namenda)
what are the adverse effects of memantine
constipation
hypertension
dizziness
headache
are drugs a cure for alzheimers diesase
NO
parkinsonism
visual hallucinations
fluctuating cognitive impairment
diffuse lewy body dementia
decreased levodopa responsivity is a characteristic of
dementia with lewy bodies
significant fluctuations in cognition is common in
DLB
this type of dementia usually occurs before, at the same time or very shortly after development of parkinsonian signs
dementia with lewy bodys
what are the two troublesome clinical symptoms associated with DLB
hallucinations and agitation
what is the first line of drug for DLB
acetylcholinesterase inhibitors (rivastigmine or donepezil)
what is the second line of drug for DLB
atypical neuroleptics (clozapine, quetiapine, and aripiprazole)
what drugs should you avoid in DLB
haloperidol because of neuroleptic sensitivity
DOC for depression in DLB
SSRI’s
history of one or more strokes with a characteristic stepwise course of memory decline
multi-infract dementia-“vascular dementia”
age of onset for vascular dementia is
65 years old
predominant involvement of the lower extremities is what type of dementia
vascular dementia
focal neurologic signs is characteristic of
vascular dementia
frontal dysfunction in vascular dementia may lead to
dysexecutive syndrome with abulia and apathy
due to prevalence of mixed pathology what should possibly be prescribed in pts with vascular dementia
cholinesterase inhibitors
subcortical arteriosclerotic encephalopathy, multiple infracts in WHITE matter
binswanger disease
what chromosome is affected in CADASIL
chromosome 19, notch 3 gene
prominent frontal lobe symptoms, early onset, behavior changes and atrophy of frontal and anterior temporal lobes
frontotemporal dementia
behavioral variant is the most common form of
FTD
what is the first deficit in progressive non-fluent aphasia
anomia
fluent with impaired comprehension
semantic dementia
link between FTD and ALS
20-40% of FtD is familial and ALS and FTD linked to chromosome 9
what percentage of people are affected in individuals with parkinson diseast over age of 60
1%
symptom of parkinson disease is due to lack of
striatal dopamine
what is the typical age of onset for parkinson disease
over 55 yo
characterized by resting tremor, rigidity, bradykinesia and postrual instability
PD
lewy bodies
PD
risk of dementia with PD increases if
age of onset
age of pt
duration and severity of illness
executive dysfunction, visuaspatial impairments, and verbal memory
PD dementia
test of face recognition are in particular impared early in the course of
PD
what has been found to be a more accurate brief bedside test for PDD
MOCA
antipsychotics for PD
not approved for treatment of behavioral disorders in pts with dementia
two antipsychotics for PD
quetiapine and clozapine
drugs used for PD
cholinesterase inhibitors, rivastigmine, donepezil, NO anticholinergic meds, low dose quetiapine and clozapine
what is age of onset for progressive supranuclear palsy
45-75
symmetric onset of bradykinesia and rigidity; RARE TREMOR, vertical supranuclue gaze palzy with downward gaze abnormlaities, prominent postural instability with unexplained fall
progressive supranuclear palsy
looks worried associaed with
PSP
startled expression, lid retraction and masked facies
PSP
MRI of PSP advanced cases reveals
midbrain atrophy
thinning of quadrigeminal plate
dilation of the 3rd ventricle
what disorders should you rule out in PSP
whipple diases
what is the CNS WD traid
dementia
vertical opthalmoplegia
myoclonus
examples of reversible dementias
normal pressure hydrocephalus vitamin B12 deficiency hypothyroidism syphillis MEDS metabolic disorders tumors alcohol related
what percentage of dementias are reversible
10%
triad of normal pressure hydrocephalus
dementia
ataxia/apraxia
incontinence (wet, wacky, and wobbly)
MRI of normal pressure hydrocephalus
ventriculomegaly out of proportion to sulcal enlargement and NO evidence of CSF flow obstruction
how does normal pressure hydrocephalus occur
idiopathic(elderly)
secondary-any age after subarachnoid hemorrhage or menigitis (impaired CSF absorption and inflammation and subsequent fibrosis of the arachnoid granulations)
how do you diagnose normal pressure hydrocephalus
H and P
MRI or CT Scan
Indium cisternogram
treatment of normal pressure hydrocephalus
shunt
what are three rapidly progressing dementias
CJD
HIV
chronic meningitis
extrapyramidal features and startled induced myoclonus indicative of
CJD
CSF indiciates ______ in CJD
14-3-3 protein
EEG-pattern of periodic sharp waves or spikes
CJD
degenerative brain disease from history of concussions
chronic traumatic encephalopathy
cognitive impairment, depression and irrational and impulsive emotional behavior
chronic trauamtic encephalopathy
abnormal tau deposition
chronic tramautic encephalopathy
increased behavior problems in evening/night
sundowning
typically dimented and instiitionalized pts
sundowning
how is sundowning managed
reorientating the patient and INCREASED lighting
disturbance of consciousness, cognitive change not accounted for by preexisting dementia, develops over a short time period and symptoms fluctuate over the day
Delirium
acute, transient, potentially reversible confusional state
delirium
delirum occurs in what percentage of patients
10-50% of surgical patients
risk factors for delirium include
underlying brain disease such as CVA, dementia
confusion asessment method
acute onset and fluctuating course and
in-attention and either
disorganized thinking OR altered level of consciousness
greater than how many errors indicates an abnormality with the A test
greater than 2
A test, test for
inattention
environmental treatment for delirum
clock
calendar
lighting
medications for delerium
thiamine
haloperidol, atypical antipsychotics and benzodiaxepines
500 mg/dl alcohol
respiratory paralysis
400 mg/dlalcohol
coma
300 mg/dl alcohol
stupor with combativeness, incoherent speech, omiting
150-200 mg/dl
slurred speach, ataxia, anger, diplopia, labile mood, dorwsiness
50-150 mg/dl
euphoria, shyness, friedliness, impaired concentration and judgement
tremulousness
most common alcohol withdraw symptom, insomnia, agitation, increased sympathetic activity
formication
crawling feeling
occurs 48-72 hours after the last drink and usually follows seizures, if a seizure occurs during DTs think of another cause (ex: meningitis)
delirium tremens
characteristic of DT
similar to withdrawal but also have fever, tachycardia, sweating
mortality associated with DT is usually from
cirrhosis,shock, and pneumonia
treatment of delirium tremens
prevention sedation with benzodiazepine, phenobarbital fluids, electrolytes, glucose nutrition, vitamins treat underlying condition
acute syndrome, thiamine defiency, diffuse axonal neuronal and myelin loss, petechial hemorrhages, global confusion, impaied memory, inattentiveness, abnormal eye movements, ataxia
wernicke encephalopathy
what should be concidered in the differential diagnosis in all patients with acute delirium or acute ataxia
wernicke encephalopathy
what is the treatment for wenicke encepahlopathy
thiamine
transketolase deficiency indicates
thimaine deficiency
can be precipitated by giving IV glucose to thiamine deficient patients before glucose in susceptible pts
wernicke encepahlopaty
amnesia, confabulation, impaired sight, lesion in dorsal medial nucleus of thalamus, mammillary bodies and brain stem, usually memory deficits remain despite treatment
korsakoff syndrome
altered brain function from metabolic abnormalties which are a consequence of liver dysfunction
hepatic encephalopathy
what is the best characterized neurotixin that preciptates HE
ammonia
clinical features of hepatic encepahlopathy
distrubed sleep bradykinesia asterixis rigidity hyperative DTS
stage 1 HE
euphoria confusion sleep disorder
stage 2 HE
lethargy, confusion, asterixis
stage 3 HE
marked confusion, slurred speech, sleep
stage 4 HE
coma
treatment of HE
eliminate underlying cause if possible
drugs to reduce serum ammonia
lactulose and neomycin
confusion, ataxia and nystagmus
wernicke encepahlopathy
dementia ataxia incontinence
normal pressure hydrocephalis
ataxia, areflexia, ophthalmoparesis
miller fisher variabt of GBS
