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Clinical Neurosciences > Dementia > Flashcards

Dementia Flashcards

1
Q

disorder affecting the cerebral cortex that plays a critical role in thinking like memory and language

A

cortical dementia

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2
Q

signs of cortical dementia include

A

memory loss
aphasia
apraxia
agnosia

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3
Q

dysfunction in the parts of the brain that are beneath the cortex

A

subcortical dementia

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4
Q

the ______pathways facilitate speed and efficiency of thought

A

frontostriatal pathways

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5
Q

What is the pyramidal system

A

motor system with fibers originating from the cerebral cortex; corticospinal tract called pyramid in medulla

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6
Q

What is the extramyrapidal system

A

motor system with fibers originating from the basal ganglia and cerebellum

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7
Q

what are signs and symptoms of parkinsonism

A

tremor
bradykinesia
cogwheel rigidity
postural instability

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8
Q

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

A

dementia

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9
Q

what percentage of people get dementia over age of 65

A

10%

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10
Q

what percentage of people over the age of 85 get dementia

A

up to 50%

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11
Q

memory impairment in people who are NOT demented and have INTACT ADL’s (activity of daily living)

A

mild cognitive impairment

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12
Q

approximately what percentage of people progress to dementia

A

6-25%

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13
Q

most common dementia over the age of 65

A

alzheimer disease

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14
Q

a progressive, degenerative brain disease characterized by memory loss and loss of other cognitive function

A

alzheimer disease

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15
Q

what are the risk factors for alzhimer disease

A

down syndrome, family history of alzheimer and advanced age

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16
Q

what type of dementia is characterized by loss of short term memory early with changes in behavior, personality, judgement and ADL’s

A

alzheimer disease

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17
Q

beta secretase plays a significant role in what disease

A

Alzeheimer disease

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18
Q

cholingergic defiency in the cortex and basal forebrain is associated with

A

alzheimer disease (contributes to cognitive deficits)

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19
Q

how does glutamate contribute to the pathogenesis of alzheimer disease

A

by overstimulating various glutamate receptors leading to excitotoxicity and neuronal cell death

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20
Q

late onset alzheimer disease is assoicated with what chromosome

A

19 (most common)

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21
Q

what chromosomes are associated with early onset alzheimer disese

A

chromosomes 1,14,and 21

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22
Q

familial alzheimer disease is what type of geneic disease

A

autosomal dominant involving APP gene chromosome 21 or presenilin 1 protein gene-chromosome 14

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23
Q

how do you diagnose AD

A

clinical + histopathological-extracellular deposition of amyloid beta protein, intracellular neurofibrillary tangles and loss of neurons especially in the hippocampus

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24
Q

extracellular deposits in AD

A

neuritic plaques

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25
Q

intracellular deposits in AD

A

neurofibrillary tangles

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26
Q

donepezil

A

treatment of mild, moderate or severe dementia

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27
Q

rivastigmine

A

treatment of mild to moderate dementia and is also used for dementia related to PD

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28
Q

what are the four cholinesterase inhibitors

A

donepezil
rivastigmine
tacrine
galantamine

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29
Q

used to treat AD is a cholinesterase inhibitor and is associated with abnormal liver function tests

A

tacrine (Cognex)

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30
Q

what is measured for people being treated with tacrine

A

serum transaminases

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31
Q

what are the adverse effects of cholinesterase inhibitors

A 
nausea, vomitting diarrhea
anorexia
weight loss
bradycardia
heart block, syncope insomnia
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32
Q

what is the name of the one NMDA receptor antagonist used to treat AD

A

memantine (namenda)

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33
Q

what are the adverse effects of memantine

A

constipation
hypertension
dizziness
headache

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34
Q

are drugs a cure for alzheimers diesase

A

NO

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35
Q

parkinsonism
visual hallucinations
fluctuating cognitive impairment

A

diffuse lewy body dementia

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36
Q

decreased levodopa responsivity is a characteristic of

A

dementia with lewy bodies

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37
Q

significant fluctuations in cognition is common in

A

DLB

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38
Q

this type of dementia usually occurs before, at the same time or very shortly after development of parkinsonian signs

A

dementia with lewy bodys

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39
Q

what are the two troublesome clinical symptoms associated with DLB

A

hallucinations and agitation

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40
Q

what is the first line of drug for DLB

A

acetylcholinesterase inhibitors (rivastigmine or donepezil)

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41
Q

what is the second line of drug for DLB

A

atypical neuroleptics (clozapine, quetiapine, and aripiprazole)

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42
Q

what drugs should you avoid in DLB

A

haloperidol because of neuroleptic sensitivity

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43
Q

DOC for depression in DLB

A

SSRI’s

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44
Q

history of one or more strokes with a characteristic stepwise course of memory decline

A

multi-infract dementia-“vascular dementia”

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45
Q

age of onset for vascular dementia is

A

65 years old

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46
Q

predominant involvement of the lower extremities is what type of dementia

A

vascular dementia

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47
Q

focal neurologic signs is characteristic of

A

vascular dementia

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48
Q

frontal dysfunction in vascular dementia may lead to

A

dysexecutive syndrome with abulia and apathy

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49
Q

due to prevalence of mixed pathology what should possibly be prescribed in pts with vascular dementia

A

cholinesterase inhibitors

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50
Q

subcortical arteriosclerotic encephalopathy, multiple infracts in WHITE matter

A

binswanger disease

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51
Q

what chromosome is affected in CADASIL

A

chromosome 19, notch 3 gene

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52
Q

prominent frontal lobe symptoms, early onset, behavior changes and atrophy of frontal and anterior temporal lobes

A

frontotemporal dementia

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53
Q

behavioral variant is the most common form of

A

FTD

54
Q

what is the first deficit in progressive non-fluent aphasia

A

anomia

55
Q

fluent with impaired comprehension

A

semantic dementia

56
Q

link between FTD and ALS

A

20-40% of FtD is familial and ALS and FTD linked to chromosome 9

57
Q

what percentage of people are affected in individuals with parkinson diseast over age of 60

A

1%

58
Q

symptom of parkinson disease is due to lack of

A

striatal dopamine

59
Q

what is the typical age of onset for parkinson disease

A

over 55 yo

60
Q

characterized by resting tremor, rigidity, bradykinesia and postrual instability

A

PD

61
Q

lewy bodies

A

PD

62
Q

risk of dementia with PD increases if

A

age of onset
age of pt
duration and severity of illness

63
Q

executive dysfunction, visuaspatial impairments, and verbal memory

A

PD dementia

64
Q

test of face recognition are in particular impared early in the course of

A

PD

65
Q

what has been found to be a more accurate brief bedside test for PDD

A

MOCA

66
Q

antipsychotics for PD

A

not approved for treatment of behavioral disorders in pts with dementia

67
Q

two antipsychotics for PD

A

quetiapine and clozapine

68
Q

drugs used for PD

A

cholinesterase inhibitors, rivastigmine, donepezil, NO anticholinergic meds, low dose quetiapine and clozapine

69
Q

what is age of onset for progressive supranuclear palsy

A

45-75

70
Q

symmetric onset of bradykinesia and rigidity; RARE TREMOR, vertical supranuclue gaze palzy with downward gaze abnormlaities, prominent postural instability with unexplained fall

A

progressive supranuclear palsy

71
Q

looks worried associaed with

A

PSP

72
Q

startled expression, lid retraction and masked facies

A

PSP

73
Q

MRI of PSP advanced cases reveals

A

midbrain atrophy
thinning of quadrigeminal plate
dilation of the 3rd ventricle

74
Q

what disorders should you rule out in PSP

A

whipple diases

75
Q

what is the CNS WD traid

A

dementia
vertical opthalmoplegia
myoclonus

76
Q

examples of reversible dementias

A 
normal pressure hydrocephalus
vitamin B12 deficiency
hypothyroidism
syphillis
MEDS
metabolic disorders
tumors
alcohol related
77
Q

what percentage of dementias are reversible

A

10%

78
Q

triad of normal pressure hydrocephalus

A

dementia
ataxia/apraxia
incontinence (wet, wacky, and wobbly)

79
Q

MRI of normal pressure hydrocephalus

A

ventriculomegaly out of proportion to sulcal enlargement and NO evidence of CSF flow obstruction

80
Q

how does normal pressure hydrocephalus occur

A

idiopathic(elderly)
secondary-any age after subarachnoid hemorrhage or menigitis (impaired CSF absorption and inflammation and subsequent fibrosis of the arachnoid granulations)

81
Q

how do you diagnose normal pressure hydrocephalus

A

H and P
MRI or CT Scan
Indium cisternogram

82
Q

treatment of normal pressure hydrocephalus

A

shunt

83
Q

what are three rapidly progressing dementias

A

CJD
HIV
chronic meningitis

84
Q

extrapyramidal features and startled induced myoclonus indicative of

A

CJD

85
Q

CSF indiciates ______ in CJD

A

14-3-3 protein

86
Q

EEG-pattern of periodic sharp waves or spikes

A

CJD

87
Q

degenerative brain disease from history of concussions

A

chronic traumatic encephalopathy

88
Q

cognitive impairment, depression and irrational and impulsive emotional behavior

A

chronic trauamtic encephalopathy

89
Q

abnormal tau deposition

A

chronic tramautic encephalopathy

90
Q

increased behavior problems in evening/night

A

sundowning

91
Q

typically dimented and instiitionalized pts

A

sundowning

92
Q

how is sundowning managed

A

reorientating the patient and INCREASED lighting

93
Q

disturbance of consciousness, cognitive change not accounted for by preexisting dementia, develops over a short time period and symptoms fluctuate over the day

A

Delirium

94
Q

acute, transient, potentially reversible confusional state

A

delirium

95
Q

delirum occurs in what percentage of patients

A

10-50% of surgical patients

96
Q

risk factors for delirium include

A

underlying brain disease such as CVA, dementia

97
Q

confusion asessment method

A

acute onset and fluctuating course and
in-attention and either
disorganized thinking OR altered level of consciousness

98
Q

greater than how many errors indicates an abnormality with the A test

A

greater than 2

99
Q

A test, test for

A

inattention

100
Q

environmental treatment for delirum

A

clock
calendar
lighting

101
Q

medications for delerium

A

thiamine

haloperidol, atypical antipsychotics and benzodiaxepines

102
Q

500 mg/dl alcohol

A

respiratory paralysis

103
Q

400 mg/dlalcohol

A

coma

104
Q

300 mg/dl alcohol

A

stupor with combativeness, incoherent speech, omiting

105
Q

150-200 mg/dl

A

slurred speach, ataxia, anger, diplopia, labile mood, dorwsiness

106
Q

50-150 mg/dl

A

euphoria, shyness, friedliness, impaired concentration and judgement

107
Q

tremulousness

A

most common alcohol withdraw symptom, insomnia, agitation, increased sympathetic activity

108
Q

formication

A

crawling feeling

109
Q

occurs 48-72 hours after the last drink and usually follows seizures, if a seizure occurs during DTs think of another cause (ex: meningitis)

A

delirium tremens

110
Q

characteristic of DT

A

similar to withdrawal but also have fever, tachycardia, sweating

111
Q

mortality associated with DT is usually from

A

cirrhosis,shock, and pneumonia

112
Q

treatment of delirium tremens

A 
prevention
sedation with benzodiazepine, phenobarbital
fluids, electrolytes, glucose
nutrition, vitamins
treat underlying condition
113
Q

acute syndrome, thiamine defiency, diffuse axonal neuronal and myelin loss, petechial hemorrhages, global confusion, impaied memory, inattentiveness, abnormal eye movements, ataxia

A

wernicke encephalopathy

114
Q

what should be concidered in the differential diagnosis in all patients with acute delirium or acute ataxia

A

wernicke encephalopathy

115
Q

what is the treatment for wenicke encepahlopathy

A

thiamine

116
Q

transketolase deficiency indicates

A

thimaine deficiency

117
Q

can be precipitated by giving IV glucose to thiamine deficient patients before glucose in susceptible pts

A

wernicke encepahlopaty

118
Q

amnesia, confabulation, impaired sight, lesion in dorsal medial nucleus of thalamus, mammillary bodies and brain stem, usually memory deficits remain despite treatment

A

korsakoff syndrome

119
Q

altered brain function from metabolic abnormalties which are a consequence of liver dysfunction

A

hepatic encephalopathy

120
Q

what is the best characterized neurotixin that preciptates HE

A

ammonia

121
Q

clinical features of hepatic encepahlopathy

A 
distrubed sleep
bradykinesia
asterixis
rigidity
hyperative DTS
122
Q

stage 1 HE

A

euphoria confusion sleep disorder

123
Q

stage 2 HE

A

lethargy, confusion, asterixis

124
Q

stage 3 HE

A

marked confusion, slurred speech, sleep

125
Q

stage 4 HE

A

coma

126
Q

treatment of HE

A

eliminate underlying cause if possible

127
Q

drugs to reduce serum ammonia

A

lactulose and neomycin

128
Q

confusion, ataxia and nystagmus

A

wernicke encepahlopathy

129
Q

dementia ataxia incontinence

A

normal pressure hydrocephalis

130
Q

ataxia, areflexia, ophthalmoparesis

A

miller fisher variabt of GBS

Clinical Neurosciences (16 decks)

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