Cognitive disorders Flashcards

1
Q

What is delirium? DSM Dx?

A

waxing/waning changes over the course of a day:

  • change in level of consciousness with reduced ability to focus, sustain, or shift attention
  • change in cognition or development of a perceptual disturbance

tends to be worse at night “sun-downing”

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2
Q

how does delirium differ than dementia in terms of onset, course, alertness, prognosis, and EEG changes?

A

Both have memory impairment, cognitive changes, and behavioral problems

DELIRIUM
onset: rapid (hrs-days)
course: waxing/waning
alertness: hypo- or hyper-active 
prognosis: reversible 
EEG: changes: generalized slowing or fast waves
DEMENTIA
onset: slow (months-years)
course: stable decline
alertness: stable
prognosis: irreversible
EEG: no changes
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3
Q

how does delirium differ than psychotic disorders in terms of perceptual changes and level of consciousness?

A

DELIRIUM
perceptual changes: visual hallucinations
level of consciousness: waxing/waning

PSYCHOTIC d/o
perceptual changes: auditory hallucinations, delusions
level of consciousness: alert

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4
Q

2 typical sx of delirium

A

visual hallucinations

short attention span

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5
Q

What is diagnostic of all patients with delirium?

A

EEG - generalized slowing or fast waves

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6
Q

Which psychotropic Rx can be used to treat the agitative symptoms of delirium? Which ones do you want to avoid and why?

A

anti-psychotics: haloperidol

want to avoid benzodiazepines because they will often cause, prolong, or exacerbate the delirium!

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7
Q

typical and atypical anti-psychotics have a black box warning. what is it?

A

increases mortality in the elderly

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8
Q

what is dementia? DSM?

A

impairment of memory and other cognitive functions without an alteration in the level of consciousness; progressive and irreversible

requires the development of MULTIPLE cognitive deficits:

  • memory impairment
  • cognitive ∆s (aphasia, apraxia, agnosia, changes in executive functioning)

causes significant impairment in social/occupational functioning
decline from previous level of functioning

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9
Q

two most common forms of dementia

A
alzheimers (cortical atrophy and enlarged ventricles)
vascular dementia (deep WM lacunar infarcts)
others:
lewy body dementia
Pick/Fronto-temporal dementia
HIV-associated dementia
Huntington Disease
Parkinson Disease
Creutzfeldt-Jakob Disease (CJD)
Normal Pressure Hydrocephalus
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10
Q

work-up for reversible causes of dementia

A
CBC
electrolytes
TFT
VDRL/RPR
B12/folate
Brain CT/MRI
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11
Q

what causes reversible dementia?

A

hypothyroidism

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12
Q

The mental status exam can be used to assess dementia. What value is suggestive of dementia?

A

< 25

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13
Q

pathophysiology of Alzheimers disease - 2

A

decreased ACh due to

  • loss of noradrenergic neurons in the basal ceruleus
  • decrease in choline acetyltransferase (req’d for ACh synthesis)

results in gradual + progressive decline in cognitive functions (esp memory and language), personality changes, mood swings, paranoia, and ultimately death

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14
Q

In Alzheimers disease, what are the functional symptoms that are the last to go?

A

motor and sensory systems

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15
Q

treatment for Alzheimers disease - 2

A

the disease is characterized by decreased ACh, therefore it is logical to use Rx that increases ACh, such as

  • Cholinesterase inhibitors (AChEi) - tacrine, donepezil, rivastigmine, galantamine
  • NMDA antagonists - memantine
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16
Q

justification for using high potency antipsychotics in patients with alzheimer’s. Downsides to using this?

why should you avoid low-potency antipsychotics?

A

high potency antipsychotics can help with aggression, hostility, violence, but can increase EPS and increase risk of CVA (stroke)

low potency antipsychotics can result in anticholinergic and orthostatic side effects

17
Q

alzheimers susceptibility genes

A

APO34

18
Q

adults with down syndrome are at risk of developing…?

A

alzheimers disease

19
Q

what is vascular dementia caused by?

A

microvascular disease that produces multiple small infarcts -> accumulation of these infarcts will result in a step-wise deterioration/loss of function into dementia

20
Q

risk factors of vascular dementia?

A
stroke
DM
HTN
APOe4
male sex
21
Q

third most common form of dementia and its cause

A

lewy body dementia - lewy bodies and lewy neurites (alpha-synuclein aggregates)

22
Q

5 main clinical manifestations of lewy body dementia

A
waxing and waning, but progressive cognitive decline
visual hallucinations
Parkinsonism
sensitivity to neuroleptics
REM sleep behavior disorder
23
Q

pathological causes of pick disease/frontotemporal dementia (FTD)

subsequent clinical manifestations?

A

marked atrophy of frontal/temporal lobes due to neuronal loss, microvacuolization, and astrocytic gliosis in cortical layers

profound changes in personality and social conduct:

  • disinhibited verbal, physical, and sexual behavior
  • echolalia, overeating, oral exploration of inanimate objects
  • poor insight about behavioral problems
  • lack of emotional warmth, empathy, or sympathy
24
Q

pick disease/frontotemporal dementia (FTD)

A

anticholinergic Rx and antidepressants have consistently shown to improve behavioral sx but not cognition

25
Q

what causes HIV-associated dementia?

risk factors?

A

infections due to neutropenia and direct effect of the virus on the cells

risk factors: duration of illness, low CD4 counts, high viral loads

26
Q

clinical manifestations of of HIV-associated dementia

A

rapid decline in all aspects: depression, social functioning (apathy, withdrawal), memory and cognition, concentration, behavior, motor ability and pscyhomotor retardation

27
Q

one is the one function that is usually preserved in HIV-associated dementia?

A

language

28
Q

when is the average age of onset for huntington’s disease? symptoms?

what other psychiatric comorbidities is usually associated with huntington’s?

A

35-50 - choreiform movements, muscular hypertonicity, depression, psychosis

alcoholism and suicide (high rates)

29
Q

pathological cause of huntington’s disease

how is the diagnosis made? 2

A

trinucleotide CAG repeats on chromosome 4

genetic testing + MRI (caudate atrophy)

30
Q

treatment for huntington’s disease?

A

none

31
Q

what is lilliputian hallucinations? In what disease does it normally occur in?

associated sx?

A

sensations that objects appear very small

temporal lobe epilepsy

associated sx: strange smells, lip smacking, temporary loss of consciousness

32
Q

pathological cause of Parkinson’s disease

A

loss of dopaminergic neurons in the Substantia Nigra (which provides dopamine input to the basal ganglia) –> Parkinsonism (bradykinesia, cogwheel rigidity, resting tremor, masklike facies, shuffling gait, dysarthyria)

senile plaques and neurofibillary tangles
decrease choline acetyltransferase

33
Q

what do most parkinson’s patients suffer from?

A

depression - >50%

34
Q

What is Creutzfeldt-Jakob Disease? What are some of the symptoms?

A

rapidly progressive degenerative disease caused by accumulation of prions ->

  • early on: personality changes, immature behavior, paranoia
  • rapidly progressive dementia
  • myoclonus (sudden spasms of muscles)
35
Q

How is Creutzfeldt-Jakob Disease diagnosed?

A

1) rapidly progressive dementia
2) EEG - peridoic generalized sharp waves
3) at least 2 of the following:
- myoclonus
- cortical blindness (loss of vision due to occipital cortex damage)
- ataxia, (extra)pyramidal signs
- muscle atrophy
- mutism

36
Q

Potentially reversible cause of dementia? what causes this?

A

normal pressure hydrocephalus - idiopathic or secondary to obstruction of CSF reabsorption sites due to trauma, infection, hemmorhage

37
Q

what do you see on MRI in patients with normal pressure hydrocephalus?

A

enlarged ventricles with increased CSF pressure

38
Q

clinical manifestations of normal pressure hydrocephalus?

A
Wet = urinary incontinence
Wobbly = gait disturbance (first) 
Wacky = dementia, mild with insidious onset
39
Q

treatment of normal pressure hydrocephalus?

A

ventroperitoneal shunt