5- Delirium and Dementia Flashcards by A B

other names of delirium syndrome

acute confusional state

Toxic metab encephalopathy

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signs of delirium syndrome

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

reversible

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

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common etiologies of delirium

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

usu reversible or metabolic/toxic cause

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what is a major drug cause of delirium

polypharmacy

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

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ddx of delirium

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

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evaluation of delium

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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describe dementia

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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dementia
acute or chronic
level of consciousnesss

can causes include toxic or metab

chronic, not progressive
normal level of consciousness

not usu toxic and metab causes

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reversible causes of dementia

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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irreversible causes of dementia

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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evaluation steps of dementia

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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types of dementia

cortical

alzheimer’s

frontotemporal (pick’s)

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types of dementia

subcortical

parkinson’s disease

huntington’s

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types of dementia

white matter

NPH

binswangers

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types of dementia

mixed

multi infarct dementia

CJD

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stages of alzheimer’s disease

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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causes of alzheimer’s disease

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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cholinergic hypothesis of alzheimer’s disease

early loss of cholinergic cells in basal forebrain so treat with

cholinesterase inhib
 (donepezil, rivastigmine, galantamine, memantine

guiding treatments of delirium

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

drugs for adequate sleep in delirium

1) trazodone

2) zolpidem

drugs for agitation in delirium

atypical neuroleptics

benzodiazepines

understand principles guiding treatment of dementia

cholinergic hypothesis

informed counseling
avoid drugs that worsen
cautious of alternative treatments

drugs for AD

cholinesterase inhib (donepezil, rivastigmine, galantamine)
memantine

easier to deal with __ compared to delusion or behavioral changes major symptoms of dementia

memory loss aggressiveness, delusions of fidelity

``` delirium vs dementia timing level of consciousness attention? speech difficulty? toxic metab causes? reversibility? ```

``` delirium vs. dementia acute vs. chronic fluctuating vs. normal impaired vs. normal incoherent speech vs. aphasia found vs. not reversible vs. not ```

underlying pathophys of delirium

diffuse brain dysfunction due to disruption of normal homeostasis mostly cholinergic, dopaminergic, histamin, nroadrenergic, serotoninergic

define mild cognitive impairment

memory impaired for age/education normal cognitive, no dementia intermediate btwn normal aging and Alzheimer's (incr risk for AD)

gross signs of Alzheimer's etiology of AD

1) cerebral atrophy 2) cortical neuron/synapse loss 2) major damage to limbic and assoc cortices etiology = genetic + environment

microscopic path of AD

1) neuritic (amyloid) plaques | 2) neurofibrill tangles in neocortex and hippocampus

mutations assoc with early onset AD

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

mutations assoc with late onset AD

APOE on chrom 19 E4 = higher risk E2 = protective

FTD affects where? what is spared until late dz so symptoms?

affects frontal +/- temporal lobe hippocampus spared behavioral early before memory loss

FTD suggested by early features of

frontal lobe dysfunction (disinhib, apathy, exec dysfunction, aphasia memory normal many patients first dx with bipolar disorders

Parkinson's disease 1) mechanism 2) what kind of deficit seen? and treatment?

1) loss of dopaminergic cells in midbrain SN | 2) cholinergic deficit--> use cholinesterase inhibitor

Huntington's disease 1) symtpoms 2) drugs to use?

AD dementia and chorea; early personality changes --> disinhibition, poor judgment, antisocial use neuroleptics and tetrabenazine for chorea

Binswanger's disease 1) mechanism 2) symtpoms

1) vascular dmeentia with severe cerebral white matter ischemia 2) insidious behavioral and cognitive decline acute focal onset (stroke) in 1/3

neuroimaging of binswanger's disease CT MRI

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

neuropath of binswanger's disease

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

NPH reversible? clinical triad? CT MRI signs? treatment?

reversible dementia, gait disorder, and urinary incontinence ventriculomegaly and normal cortical gyri high volume lumbar tap test improves gait and cognition

treatment of NPH

surgery = VP, VA, LP shunts | gait more likely to improve

Multi-infarct dementia combination of ? clinical course? prevent and treatment =?

combo of cortical + subcortical strokes --> dementia from accum destruction of brain tissue step wise course from new strokes ASA, heparin, warfarin, tPA, carotid surgery

CJD symptoms progression treatment?

rapid dementia with acute confusion, hallucinations, delusions, myoclonus ends in 1 yr no treatment

mechanism of CJD diagnosis of CJD what do you see on EEG and CSF

conformational change in prion --> neuronal loss, gliosis, spongiform changes diffusion MRI = deep gray matter/cortical hyperintensity EEG = periodic discharges CSF = 14-3-3 protein

treatment of cognitive impairment in dementia

cholinesterase inhib | memantine = NMDA antagonist

delirium tremens symptoms

hallucinations delusional agitation/restlessness from alcohol withdrawal

most common cause of Binswanger's disease

uncontrolled HTN