psych cognitive disorders Flashcards by Joe Shmoe

def of cognitive disorder

signif chang in cognition from a previous level of functioning

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two main types of cognitive disorders

delirium and dementia

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57 yo M with tremor, EPS, frontal dizziness, and sluggish pupillary reflexes

most likely tertiary syphilis; order VDRL and TSH

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delirium lasts how long?

can last from days to weeks, and may become chronic

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other terms for delirium

encephalopathy; acute organic brain syndrome; acute confusional state; acute toxic psychosis; and ICU psychosis

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how common is delirium

ten to thirty percent of medically admitted patients exhibit delirium

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DSM IV criteria for delirium

disturbance of consciousness, change in cognition, develips over a short period of time (hrs to days) and tends to fluctuate throughout the course of the day

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treatment of delirium

orient the patient; lights on and window shades up; meds can be used symptomatically (haloperidol)

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do NOT use benzos with delirium

can cause/prolong delirium

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dementia

impairment of memory and other cognitive functions without alteration in the level of consciousness

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msot common cause of dementia

alzheimers (50 to 70 percent)

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second most common cause of dementia

vascular dementia

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dsm four criteria for dementia

multiple cognitive deficits manifested by both memory impairment and one or more of aphasia, apraxia, agnosia, loss of exec functioning; deficits do not occur exclusively during delirium

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alzheimers disease epi

affects women three times more commonly than men; very heritable

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alzheimers mech

decrease in ach due to loss of noradrenergic neurons in the basal ceruleus and decreased choline acetyltransferase (reqd for Ach synthesis)

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alzheimers genes

account for only 5% of cases; presenelin I, presenelin II, amyloid precursor protein APP; major susceptibility gene is APOe4

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explanation for Alzheimers disease

amyloid cascade hypoth; exce of Abeta peptides either by overproduction or diminished clearance

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postmortem findings in alzheimers disease

diffuse atrophy with enlarge ventricles and flattened sulci; senile plaques and NFTs; (plaques but no tangles correlate with severity of dementia)

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treatment for alzheimers

cholinestase inhib can slow cognitive decline for 6-12 mos; also NMDA antags can be used

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examples of cholinesterase inhib used in AD

Tacrine (Cognex); donepezil (Aricept); rivastigmine (Exelon); galantamine (Razadyne)

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examples of NMDA antags used for AD

Memantine (Namenda)

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treatment for vascular dementia

cholinesterase inhib have been shown to be successful; antihypertensive tx; tx symptoms as necessary

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cause of Lewy body dementia

Lewy bodies and Lewy neurites (aggregations of alpha synuclein) in the brain, primarily in the basal gang

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clinical manifestations of LBD

progressive cognitive decline; waxing and waning of cognition is core feature; VH of animals and people; paranoid delusions; parkinsonis; sens to neuroleptics; REM sleep behavior disorder is common

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Difference between LBD and Parkinson disease dementia

LBD is onset of dementia within 12 mos of parkinsonism sx; dementia that begins more than 12 mos after the parkinsonism sx is classified as Parkinson disease dementia

treatment for LBD

cholinesterase inhib help improve VH; psychostimulants, levodopa/carbidopa, and dopamine agonists may improve cognition, apathy and psychomotor slowing

treatment for REM sleep behavior disorder in LBD

clonazepam

Pick disease/FTD presents when

between 45 and 65

genetics of FTD

about 25% are familial and may be assoc with mutation in the progranulin or MAPT gent

duration of illness to death in FTD

5 years

clinical manifestations of FTD

changes in personality and social conduct; disinhibited behavior; echolalia, overeating, oral exploration of objects; lack emotional warmth; poor insight; preservation fo memory, language, and spatial functions

pathology of FTD

marked atrophy of the frontal and temporal lobes; neuron loss, microvacuolization, and astrocytic gliosis in cortical layer II

treatment for FTD

anticholinergic meds and antidepressants improve behavioral sx but not cognition

most common dementia caused by infectious disease

hiv assoc dementia

what is the cuase of dementia in HIV-assoc dementia?

the infections as well as direct effects of the virus on cells

treatment for HIV-assoc dementia

HAART improves cognition and prolongs life; also psychostimulants target fatigue and psychomotor retardation

caudate atrophy

huntingtons disease

HD gene

trinuc repeat on chrom 4

treatment for HD

none

lilliputian hallucinations

sensation that objects appear very small; seen in parkinsons disease

parkinsons disease pathology

neuron loss in the substantia nigra, which provides dopamine to the basal gang

what percent of PD patients develop dementia?

30-40 percent

how is PD like AD

senile plaques and NFTs, loss of neurons, and decr choline acetyltransferase

source of CJD

a small number of patients have become infected through corneal transplants

clinical features of CJD

rapidly progressive dementia 6-12 mos after onset of sx; myoclonus is seen in most patients; basal gang and cerebellar dysfunction; personality changes; coma, death

diagnosis of CJD

rapidly progressive dementia and periodic generalized sharp waves on EEG plus at least two of: myoclonus, cortical blindness, ataxia, pyramidal, or EPS; muscle atrophy, mutism

NPH

enlarged ventricles with incr CSF pressure; gait distubrance; urinary incont; dementia

cause of NPH

can be idiopathic or secondary to obstruction of CSF reabsorption sites due to trauma, infx, or hemorrhage

treatment of NPH

relieve pressure with shunt; of the clinical triad, dementia is least likely to improve

most common finding in delirum

impairment in recent memory

dementia with cogwheel rigidity and resting tremor

LBD or PD

dementia plus diminished position and vibration sensation plus megaloblasts on CBC

vit B12 def

dementia plus tremor plus abnormal LFTs plus kayser-fleisher rigns

wilson disease; check ceruloplasmin

dementia plus diminished position and vibration plusArgyll robertson pupils

neurosyph; do CSF VDRL

delirium timing of symptoms

usually worse at night, whereas in dementia the sx are stable throughout the day

EEG changes

fast waves or generalized slowing seen in delirium; not seen in dementia

senile plaques and NFTs

not unique to Alzheimers; also seen in Down syndrome and normal aging

a stroke to the frontal lobe

can lead to sx of schizophrenia, bipilar I disorder, and depression

FTD leads to a more rapid progression to death than in alzherimers dementia

right

prion diseases besides CJD

kuru; Gertmann-Straussler syndrome, fatal familial insomnia, and bovine spongiform encephalopathy (mad cow disease)

the three Ws of NPH

wobbyl, wet and wacky

psych cognitive disorders Flashcards

(61 cards)