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Neuro_week3 > 5- Delirium and Dementia > Flashcards

5- Delirium and Dementia Flashcards

1
Q

other names of delirium syndrome

A

acute confusional state

Toxic metab encephalopathy

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2
Q

signs of delirium syndrome

A

rapid developing disorder of attention –> can’t maintain coherent line of thought (hyperaroused + agitation + restlessness)

1) fluctuating consciousness
2) impaired attention
3) incoherent speech

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3
Q

delirium syndrome
reversible or not?
more common form (hypo or hyper) and causes of ea

A

reversible

more common = hypoaroused with lethargy/somnolence
less common = hyperaroused = delirium tremens

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4
Q

common etiologies of delirium

A 
drugs and toxins
metab disorders
infection/inflamm
structural lesions
seizure disorders

usu reversible or metabolic/toxic cause

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5
Q

what is a major drug cause of delirium

A

polypharmacy

20-30 meds not manageable esp older patients and disrupts normal brain homeostasis

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6
Q

ddx of delirium

A

1) dementia
2) amnesia
3) aphasia
4) schizo
5) mania
6) depression

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7
Q

evaluation of delium

A

1) H and P
2) mental status
3) blood chem
4) urinalysis
5) ECG
6) CXR
7) toxicology
8) CT/MRI, LP, EEG

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8
Q

describe dementia

A

acquired and persistent impairment in intellectual functions with deficits in

1) memory
2) language
3) visuospatial skills
4) complex cog
5) emotion or personality interfere with usu social/occup fxn

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9
Q

dementia
acute or chronic
level of consciousnesss

can causes include toxic or metab

A

chronic, not progressive
normal level of consciousness

not usu toxic and metab causes

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10
Q

reversible causes of dementia

A

1) drugs/toxins/alcohol
2) mass lesions
3) NPH
4) hypothyroid
5) vitamin B12
6) neurosyphilis/SLE
7) mild TBI
8) depression

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11
Q

irreversible causes of dementia

A

1) alzheimer’s
2) FTD
3) vascular
4) huntington’s
5) parkinson’s
6) lewy body
7) CJD
8) AIDS dementia

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12
Q

evaluation steps of dementia

A

1) H and P
2) CMP, CBC, TSH, B12, RPR for syphilis
3) MRI or CT
4) lumbar, eeg, hiv, esr

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13
Q

types of dementia

cortical

A

alzheimer’s

frontotemporal (pick’s)

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14
Q

types of dementia

subcortical

A

parkinson’s disease

huntington’s

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15
Q

types of dementia

white matter

A

NPH

binswangers

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16
Q

types of dementia

mixed

A

multi infarct dementia

CJD

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17
Q

stages of alzheimer’s disease

A

live 6-12 yrs after onset; decr 3 points on MMSE/yr
I = initial amnesia, anomia (can’t recall names of everyday objects), apathy

II = marked amnesia, fluent aphasia, visuospatial dysfunction, anosognosia, neuropsych features

III = severe dementia, global aphasia, or incontinence

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18
Q

causes of alzheimer’s disease

A

genetics
all down syndrome get AD (overexpressed amyloid plaque formation)

older folks susceptible because APOE gene on chrom 19

cholinergic hypothesis = loss of ACh

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19
Q

cholinergic hypothesis of alzheimer’s disease

A

early loss of cholinergic cells in basal forebrain so treat with

cholinesterase inhib
 (donepezil, rivastigmine, galantamine, memantine
20
Q

guiding treatments of delirium

A

1) attention to etiology
2) environmental manipulations
3) adequate sleep (no nap/daytime)
4) treat agitation

21
Q

drugs for adequate sleep in delirium

A

1) trazodone

2) zolpidem

22
Q

drugs for agitation in delirium

A

atypical neuroleptics

benzodiazepines

23
Q

understand principles guiding treatment of dementia

cholinergic hypothesis

A

informed counseling
avoid drugs that worsen
cautious of alternative treatments

24
Q

drugs for AD

A 
cholinesterase inhib (donepezil, rivastigmine, galantamine)
memantine
25
Q

easier to deal with __ compared to delusion or behavioral changes

major symptoms of dementia

A

memory loss

aggressiveness, delusions of fidelity

26
Q 
delirium vs dementia
timing
level of consciousness
attention?
speech difficulty?
toxic metab causes?
reversibility?
A 
delirium vs. dementia
acute vs. chronic
fluctuating  vs. normal
impaired vs. normal 
incoherent speech vs. aphasia
found vs. not 
reversible vs. not
27
Q

underlying pathophys of delirium

A

diffuse brain dysfunction due to disruption of normal homeostasis

mostly cholinergic, dopaminergic, histamin, nroadrenergic, serotoninergic

28
Q

define mild cognitive impairment

A

memory impaired for age/education
normal cognitive, no dementia

intermediate btwn normal aging and Alzheimer’s (incr risk for AD)

29
Q

gross signs of Alzheimer’s

etiology of AD

A

1) cerebral atrophy
2) cortical neuron/synapse loss
2) major damage to limbic and assoc cortices

etiology = genetic + environment

30
Q

microscopic path of AD

A

1) neuritic (amyloid) plaques

2) neurofibrill tangles in neocortex and hippocampus

31
Q

mutations assoc with early onset AD

A

onset before age 65
APP on chrom 21
PSEN-1 on chrom 14
PSEN-2 on chrom 1

32
Q

mutations assoc with late onset AD

A

APOE on chrom 19
E4 = higher risk
E2 = protective

33
Q

FTD affects where?

what is spared until late dz

so symptoms?

A

affects frontal +/- temporal lobe

hippocampus spared

behavioral early before memory loss

34
Q

FTD suggested by early features of

A

frontal lobe dysfunction (disinhib, apathy, exec dysfunction, aphasia

memory normal

many patients first dx with bipolar disorders

35
Q

Parkinson’s disease
1) mechanism

2) what kind of deficit seen? and treatment?

A

1) loss of dopaminergic cells in midbrain SN

2) cholinergic deficit–> use cholinesterase inhibitor

36
Q

Huntington’s disease
1) symtpoms

2) drugs to use?

A

AD
dementia and chorea; early personality changes –> disinhibition, poor judgment, antisocial

use neuroleptics and tetrabenazine for chorea

37
Q

Binswanger’s disease
1) mechanism

2) symtpoms

A

1) vascular dmeentia with severe cerebral white matter ischemia

2) insidious behavioral and cognitive decline
acute focal onset (stroke) in 1/3

38
Q

neuroimaging of binswanger’s disease

CT
MRI

A

CT = low density white matter lesions

2) MRI = patchy or confluent white matter; hyperintensities on T2, proton density, FLAIR

ventriculomegaly

39
Q

neuropath of binswanger’s disease

A

white matter volume loss esp periventricular = hydrocephalus ex vacuo

thick and hyalinized small vessels

ischemic demyelination esp of association fibers (spare U fibers)

incomplete infarct of white matter

40
Q

NPH
reversible?

clinical triad?

CT MRI signs?

treatment?

A

reversible

dementia, gait disorder, and urinary incontinence

ventriculomegaly and normal cortical gyri

high volume lumbar tap test improves gait and cognition

41
Q

treatment of NPH

A

surgery = VP, VA, LP shunts

gait more likely to improve

42
Q

Multi-infarct dementia
combination of ?

clinical course?

prevent and treatment =?

A

combo of cortical + subcortical strokes –> dementia from accum destruction of brain tissue

step wise course from new strokes

ASA, heparin, warfarin, tPA, carotid surgery

43
Q

CJD
symptoms

progression

treatment?

A

rapid dementia with acute confusion, hallucinations, delusions, myoclonus

ends in 1 yr

no treatment

44
Q

mechanism of CJD

diagnosis of CJD
what do you see on EEG and CSF

A

conformational change in prion –> neuronal loss, gliosis, spongiform changes

diffusion MRI = deep gray matter/cortical hyperintensity

EEG = periodic discharges

CSF = 14-3-3 protein

45
Q

treatment of cognitive impairment in dementia

A

cholinesterase inhib

memantine = NMDA antagonist

46
Q

delirium tremens symptoms

A

hallucinations
delusional
agitation/restlessness

from alcohol withdrawal

47
Q

most common cause of Binswanger’s disease

A

uncontrolled HTN

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