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psych cognitive disorders Flashcards

1
Q

def of cognitive disorder

A

signif chang in cognition from a previous level of functioning

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2
Q

two main types of cognitive disorders

A

delirium and dementia

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3
Q

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

A

most likely tertiary syphilis; order VDRL and TSH

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4
Q

delirium lasts how long?

A

can last from days to weeks, and may become chronic

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5
Q

other terms for delirium

A

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

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6
Q

how common is delirium

A

ten to thirty percent of medically admitted patients exhibit delirium

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7
Q

DSM IV criteria for delirium

A

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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8
Q

treatment of delirium

A

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

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9
Q

do NOT use benzos with delirium

A

can cause/prolong delirium

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10
Q

dementia

A

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

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11
Q

msot common cause of dementia

A

alzheimers (50 to 70 percent)

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12
Q

second most common cause of dementia

A

vascular dementia

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13
Q

dsm four criteria for dementia

A

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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14
Q

alzheimers disease epi

A

affects women three times more commonly than men; very heritable

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15
Q

alzheimers mech

A

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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16
Q

alzheimers genes

A

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

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17
Q

explanation for Alzheimers disease

A

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

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18
Q

postmortem findings in alzheimers disease

A

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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19
Q

treatment for alzheimers

A

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

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20
Q

examples of cholinesterase inhib used in AD

A

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

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21
Q

examples of NMDA antags used for AD

A

Memantine (Namenda)

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22
Q

treatment for vascular dementia

A

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

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23
Q

cause of Lewy body dementia

A

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

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24
Q

clinical manifestations of LBD

A

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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25
Q

Difference between LBD and Parkinson disease dementia

A

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

26
Q

treatment for LBD

A

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

27
Q

treatment for REM sleep behavior disorder in LBD

A

clonazepam

28
Q

Pick disease/FTD presents when

A

between 45 and 65

29
Q

genetics of FTD

A

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

30
Q

duration of illness to death in FTD

A

5 years

31
Q

clinical manifestations of FTD

A

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

32
Q

pathology of FTD

A

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

33
Q

treatment for FTD

A

anticholinergic meds and antidepressants improve behavioral sx but not cognition

34
Q

most common dementia caused by infectious disease

A

hiv assoc dementia

35
Q

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

A

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

36
Q

treatment for HIV-assoc dementia

A

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

37
Q

caudate atrophy

A

huntingtons disease

38
Q

HD gene

A

trinuc repeat on chrom 4

39
Q

treatment for HD

A

none

40
Q

lilliputian hallucinations

A

sensation that objects appear very small; seen in parkinsons disease

41
Q

parkinsons disease pathology

A

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

42
Q

what percent of PD patients develop dementia?

A

30-40 percent

43
Q

how is PD like AD

A

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

44
Q

source of CJD

A

a small number of patients have become infected through corneal transplants

45
Q

clinical features of CJD

A

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

46
Q

diagnosis of CJD

A

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

47
Q

NPH

A

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

48
Q

cause of NPH

A

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

49
Q

treatment of NPH

A

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

50
Q

most common finding in delirum

A

impairment in recent memory

51
Q

dementia with cogwheel rigidity and resting tremor

A

LBD or PD

52
Q

dementia plus diminished position and vibration sensation plus megaloblasts on CBC

A

vit B12 def

53
Q

dementia plus tremor plus abnormal LFTs plus kayser-fleisher rigns

A

wilson disease; check ceruloplasmin

54
Q

dementia plus diminished position and vibration plusArgyll robertson pupils

A

neurosyph; do CSF VDRL

55
Q

delirium timing of symptoms

A

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

56
Q

EEG changes

A

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

57
Q

senile plaques and NFTs

A

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

58
Q

a stroke to the frontal lobe

A

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

59
Q

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

A

right

60
Q

prion diseases besides CJD

A

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

61
Q

the three Ws of NPH

A

wobbyl, wet and wacky

Psych (23 decks)

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