Exam 1 Cognitive Disorders Flashcards

1
Q

Gradual onset and progression, aphasia, amnesia, apraxia, agnosia, executive dysfunction, visuospatial impairment, concreteness, indifference, preserved motor function

A

Alzheimers disease

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2
Q

Gradual onset and progression, aphasia, apraxia, agnosia, executive dysfunction, relative retention of memory and visuospatial skills until later stages, personality changes, disinhibition, apathy, atypical depression, preserved motor function

A

Frontotemporal dementia ie Picks disease

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3
Q

Abrupt onset, stepwise progression, fluctuating course, preservation of personality, emotional incontincenc, depression, focal neurologic s/sx, vascular risk factors

A

Vascular Dementia aka multi-infarct dementia

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4
Q

Gradual onset and progression, aphasia, amnesia, apraxia, agnosia, fluctuating severity, suddon onset parkinson’s features and visual hallucinations, fluctuating cognitive function

A

Lewy Body dementia

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5
Q

Cortical and subcortical feautres, psychomotor retardation, apathy, inattention, poor memory, ataxia, gait disturbance (falls), urinary incontinence

A

NPH

  • Falls, urinary incontinence, signs neuro-cognitive decline
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6
Q

What is delirium

A

Acute, rapidly progressive change in cognition characterized by inattention and disturbance of consciousness in which dx fluctuate over 24 hrs

AKA encephalopathy or acute confusional state

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7
Q

What are risks for developing delirium

A
Cognitive impairment
70+ yo
Poor functional status
hearing/visual impairment
dehydration, sleep deprivation, infection
Metabolic derangment, polypharmacy
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8
Q

DSM-IV criteria for Delirium includes what?

A
  1. Altered level of arousal
  2. Memory Impairment
  3. Disorientation
  4. Perceptual Disturbance
  5. Language disturbance/incoherent speech
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9
Q

What types of Delirium are possible

A

Hyperactive (41%)
Hypoactive (11%)
Mixed Disorder (48%)

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10
Q

Describe Hyperactive delirium

A

comprises 41% of delirium cases

  • hallucinations
  • delusions
  • agitation
  • combativeness
  • Incoherent, rambling speech
  • disturbed sleep/wake cycle
  • hypersensitivity to light/sound
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11
Q

Describe Hypoactive delirium

A

comprises 11% of delirium cases, subtle, often overlooked, misdx
- inattention, sedation, depressed, withdrawn, loss of appetite, flat affect

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12
Q

Besides delirium, what other potential ddx are there?

A

a) Delirium secondary to: medical condition, substance abuse/withdrawal
b) Substance intoxication
c) substance withdrawl
d) dementia
e) Psych disorder (psychotic disorder, schizophrenia, mood disorder with psychotic feature
f) malingering/factitious disorder

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13
Q

Important factors in the assessment of delirium include

A

Primary Survery

  1. Good H&P (med/nursing records, medication hx, outside informant)
  2. MSE

Secondary Survey**

Thorough Med workup

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14
Q

What is often helpful vs not always necessary in assessment of delirium

A

Often helpful: Hx, PE, MSE, CBC, Metab panel, UA, EKG, CXR

Sometimes: EEG (diffuse slowing), CT, Cultures without known cause, LP

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15
Q

Components of the MMSE include

A
Orientation to time and place
Recall
Registration
Attention and Calculation
Language
Repetition
Complex commands
27-30 = no cognitive impairment
21-26 = mild cog impairment
11-20 = moderate cog impairment
<10 = severe
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16
Q

what is the primary principle of delirium tx

A
treat underlying medical cause*
maintain stability
avoid use of restraints
ID and eliminate offending meds
educate family and caregivers
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17
Q

what are non-pharmacologic tx options for delirium

A

replace hearing aids/glasses

  • private room
  • around the clock attendant/sitter
  • calm and reassuring behavior
  • reorienting devices
  • re-establish sleep/wake cycle
  • educate family
  • expedite return to familiar environment
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18
Q

when should you treat someone with delirium

A
  1. Severe agitation
  2. Combative behavior
  3. Behavior that severely interferes with care

*agitation, combative, interfering = treat

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19
Q

what should you be aware of with the delirium pharmacologic tx

A

BLACK BOX warning for sudden cardiac death

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20
Q

List the various antipsychotic meds

A
Haloperidol (trad'l) IV/IM/PO
Zyprexa (IM/PO/SL)
Seroquel (PO)
Risperdal (PO)
BZ
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21
Q

Haloperidol: use, side effects

A
  • traditional antipsychotic
  • available IV/IM/PO
  • EPS likely - treat with Cogentin (Benztropine), an anticholinergic to reduce EPS PD like sx
  • prolonged QTI –> torsades, sudden cardiac death
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22
Q

What are the second generation antipsychotics

A
Zyprexa (IM/PO/SL)
Seroquel (PO)
Risperdal (PO)
*fewer EPS (bc antichol activity)
*less likely to prolong QTI
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23
Q

what is the perspective on pharm tx of delirium with antipsychotics?

A

no other good alternative

  • use for appropriate reasons
  • get baseline EKG, start low and go slow, monitor electrolytes and correct, monitor BP/orthostatics
  • educate family and get informed consent
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24
Q

Besides antipsychotics, what medication class can be used to treat delirium

A

BZ

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25
Q

SE of BZ

A

deleterious cognitive SE - avoid at all costs; can worsen depression, cause delirium

  • over Rx
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26
Q

what are BZ indicated for

A

alcohol/drug delirium

Diazepam and Lorazepam

*side note, according to pharm: treat alcoholic seziures with Lorazepam and Phenytoin, prevent with Diazepam and Chlordiazepoxide

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27
Q

what are different forms of delirium/ special considerations to be aware of

A

postop delirium
sundowning
alcohol withdrawal/DT

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28
Q

what is sundowning

A

delirium precipitated by hospitalization, sensory deprivation or medications
*worse at night

29
Q

How is alcohol related to delirium

A

alcohol withdrawal –> DT (delirium tremens)

  • MEDICAL EMERG
  • signs DTs are extreme autonomic hyperactivity with delirium
  • later signs = confusion, psychosis, agitation, seizures
  • mainly seen in heavy, chronic drinkers, pt with prior detox, seizures or DT
30
Q

what is dementia

A

chronic progressive decline of memory impairment and 1+:

a) aphasia (absence speech - understanding or expression)
b) apraxia (absent learned motor skills)
c) agnosia (absence of sensory understanding or recognition)
d) disturbance in executive functioning

deficits severe enough to cause functional impairment

Delirium NOT PRESENT

Irreversible

31
Q

What are causes of dementia

A

a) Alzheimers disease (AD) 50%
b) Vascular dementia (25%)
c) Neurodegen process: (Lewybody, PD dementia, frontotemporal/picks dz)
e) secondary to medical condition (huntingtons, TBI, infecitons, anoxia, Creutzfeldt-Jakob, HIV, MS)

*with or w/o behavioral disturbance

32
Q

AD (alzheimers dementia) - when and how does it develop, findings?

A

Typically after 50 yo; under 65 = early onset

  • slow progression, lose 3 pt/yr on MMSE
  • higher rates in pt with repeated head trauma or Downs
  • familial role
    findings: myoclonus and gait disorder late findings

CT/MRI/Histo

33
Q

what are sx of Parkinson’s Dementia (neurodegenerative dementia), how freq is it, and what makes it worse

A

20-60% Parkinson’s pt dev PD

  • tremor, rigidity, bradykinesia, postural instability, micrographia, slow mvmt, cogwheel rigidity
  • exacerbated by depression
34
Q

What is dementia with Lewy Body sx? cause?

A

Neurodegenerative dementia *protein deposits in brain

Parkinson’s features and visual hallucinations

35
Q

What is Pick’s disease (frontotemporal) characterized by

A

Neurodegenerative dementia –> change in personality/behavioral disinhibition
*prominent primitive reflexes on exam

36
Q

What are the characteristics of Vascular dementia and how is it dx?

A

aka multi-infarct dementia

  • vascular risk factors
  • neuro deficit from previous CVA usually
  • imaging to dx (MRI)
37
Q

What is Creutzfeldt Jakob dz triad

A
  1. dementia
  2. involuntary mvmt
  3. periodic EEG activity (diffuse slowing pattern)
38
Q

What are the characteristics of Creutzfeldt-Jakob dz? who does it affect and how? cause? tx?

A

Triad of dementia, involuntary mvmt and periodic EEG activity

  • typ 40-60 yo
  • prions: transmisison via corneal transplant, CSF
  • rapid (wk-mth) fatal
  • no tx
39
Q

what are characteristic brain pathologies associated with Creutzfeldt Jakob dx

A

brain shrinkage and deterioration (rapid), spongiform pathology of brain

40
Q

components of Huntington’s dementia

A

AD gene
onset 30-40
choreiform mvmt
Boxcar ventricles on imaging

41
Q

Features of HIV dementia include? cause?

A

direct result of HIV (can isolate in CSF)
= forgetfulness, slowness, poor problem solving/concentration, apathy, delirium, tremor ataxia

*remember to look for infectious causes

42
Q

reversible dementias include

A
NPH (norm pressure hydrocephalus)
B12 deficiency
Hypothyroidism
Depression
Syphilis
43
Q

what is mild cognitive impairment? characteristics? risk?

A
"pre-dementia"
Characterized by:
1. Memory complaints (subj)
2. mild Memory impairment (obj)
3. preserved cognitive function and intact ADL's

*increase risk of ALL types of dementia

44
Q

how to diagnose dementia?

A

H&P*** clinical! postmortem pathology only definitive test

  • lab eval
  • neuro imaging
  • cognitive testing (neuropsych testing, MMSE, Kokman) “cerebral atrophy”
45
Q

H&P for dementia…

A

best way to dx

  • use outside informants
  • often only way to differentiate bw diff types of dementai

Lewy body, AD, vascular, Picks, creutzfeldt-jakob

46
Q

H&P: lewy body

A

fluctuations in cognitive function, sudden onset parkinsonian features, visual hallucinations

47
Q

H&P AD (alzheimers dementia)

A

progressive decline

48
Q

H&P: Vascular dementia

A

signs previous stroke/risk factors

49
Q

H&P: Picks dz

A

Progressive nonfluent aphasia, Behavioral disinhibition (frontotemporal neurodeg)

50
Q

H&P: creutzfeldt jakob

A

rapid/progressive, involuntary mvmts (not unlike Tardive dyskinesia)
*fatal

51
Q

what lab eval should be ordered for dementia dx?

A

*draw to r/o other/reversible causes
CBC/CMP, TSH, B12, folate, homocysteine, SED rate, HIV, RPR (syphilis)

CSF eval

52
Q

is neuroimaging for dementia recommended?

A

controversial
“cerebral atrophy” questionable clinical sig

AAN rec structural neuroimaging with either noncontrast head CT or MRI in routine intiial eval of all pt with dementia (r/o reversible cause)

53
Q

Neuropsych testing, main sig test for us to know?

A

MMSE

*neuropsych testing wide range of specificity and sensitivity

54
Q

what are components of neuropsych testing

A
Attention
Orientation
Executive functioning
Memory (short and long)
Intelligence
Language
Problem solving

A.O.E.M.I.L.P. is neuropsych testing for me

*best when performed on increased risk population

55
Q

mgmt of dementia includes

A

treat cognitive sx
behavior mgmt
education/caregiver support
prevention (avoid excess BZ)

56
Q

Pharmacologic mgmt of Dementia includes

A

Cholinesterase inhibitors:

  1. Donepezil (Aricept)
  2. Rivastigmine (Exelon)
  3. Galantamine (Razadyne)

NMDA antagonists
1. Memantien (Namenda)

57
Q

Indications for prescribing cholinesterase inhibitors for dementia mgmt

A

off label use:

  • prevention in mild uncharacterized cognitive impairment
  • Lewy body neurodegenerative dementia
  • multi-infarct vascular dementia

*besides LB and vascular, no other dementia supports cholinesterase inhibitor use

58
Q

Dementia mgmt supplements/other tx includes

A

May have benefit:
*Vit E, Selegiline, fish oil, ginkgo biloba

Little evidence: Vit B, hormone replacement, NSAIDS, coconut oil

59
Q

how can you prevent dementia

A

no modifiable risk factor known (except avoid BZ, educate pt)

Promising: cognitive training, exercise

Ntr: Mediterranean diet, Omega 3, veggies

60
Q

Dementia vs delirium

A

Dementia: memory impairment, progressive insidious onset

Delirium: memory impairment, disturbance of consciousness, acute onset, fluctuation during 24 hr, attention deficit

61
Q

What are amnestic disorders

A

impaired ability/inability to learn new info, recall

causes marked impair in social or occupational functioning
*must not occur in setting of delirium/dementia

62
Q

Associated features of amnestic disorders include

A

confusion, disorientation, confabulation (make up details), rarely disoriented to self, lack insight to memory deficits, apathy

63
Q

Causes of amnesia..

A

head injury, alcohol, BZ, sedative (ambien, lunesta), postictal, ECT, focal tumors or infarct, infections (HSV encephalitis), cerebral anoxia (carbon monoxide poisoning), postconcussive, transient global amnesia

64
Q

Define transient global amnesia

A

abrupt loss of the ability to recall events or to remember new info lasting 6-24 hr

*memory usually returns EXCEPT for gap

65
Q

what are the alcohol amnestic disorders

A

wernickes encephalopathy and Korsakoffs syndrome

66
Q

Features of Wernickes encephalopathy include

A

thiamine deficiency
TRIAD: ophthalmoplegia, ataxia, nystagmus

ACUTE!!! = wernicke

67
Q

Features of Korsakoffs syndrome

A

really progression or second stage of Wernicke Korsakoff Syndrome

  • chronic
  • further thiamine def usually associated with prolonged alcohol abuse
  • irreversible
  • psychosis can be present aka Korsakoffs psychosis
68
Q

How do you treat amnestic disorders

A

mainly supportive
remove offending agent
alcohol detox/rehab
supportive psychotherapy, pharmacotherapy