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PSYCH CLERKSHIP > Chapter 8_Neurocognitive Disorders (NCDs) > Flashcards

Chapter 8_Neurocognitive Disorders (NCDs) Flashcards

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1
Q

What are the six cognitive domains that can be affected by NCDs?

A

learning and memory, language, complex attention, perceptual motor skills, social interaction, and executive function

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2
Q

What is another way to think of delirium?

A

Acute brain failure. It is a medical emergency associated with high mortality; it often goes unrecognized

aka toxic/metabolic encephalopathy, acute organic brain syndrome, acute confusional state, acute toxic psychosis, ICU psychosis

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3
Q

Risk factors for delirium

A
  • advanced age
  • polypharmacy (including psychotropic meds like benzos and anticholinergics)
  • limited mobility
  • history of previous delirium
  • male gender
  • severe or terminal illness
  • alcohol use
  • malnutrition
  • pain
  • preexisting cognitive impairment/depression
  • multiple medical comorbidities
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4
Q

What are the 5 categories of delirium?

A
  • substance intoxication delirium
  • substance withdrawal delirium
  • medication-induced delirium
  • delirium due to another medical condition
  • delirium due to multiple etiologies
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5
Q

delirium+hemiparesis or other focal neuro signs

dx and test?

A

CVA or mass lesion

head ct/brain MRI

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6
Q

delirium +elevated bp+papilledema

dx and test?

A

hypertensive papilledema

head ct/brain MRI

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7
Q

delirium + dilated pupils + tachycardia

A

substance intoxication

UDS

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8
Q

delirium+fever+nuchal rigidity+photophobia

A

meningitis

LP

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9
Q

delirium+tchycardia+tremor+thyromegaly

A

thyrotoxicosis

Free TSH, T3, T4

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10
Q

How does delirium present?

A
  • deficits in attention and awareness
  • cognitive deficits develop acutely over hours to days
  • symptoms fluctuate throughout course of the day (usually worse at night)
  • deficits in recent memory/language abnormalities/perceptual disturbances (usually visual)
  • differing degrees of psychomotor activity
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11
Q

Three types of delirium based on psychomotor activity?

A
  • mixed type (most common): activity remains stable at baseline or fluctuates rapidly between hyper and hypo
  • hyopactive (most likely to go undetected): decreased activity; lethargy/drowsiness
  • hyperactive: agitation, mood lability, uncooperativeness; often seen in drug withdrawal or toxicity
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12
Q

How does delirium show up on EEG?

A

generally manifests are diffuse background slowing on EEG

exception: DELIRIUM TREMENS; FAST ACTIVITY on EEG

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13
Q

What are some useful labs for evaluating a patient with delirium?

A

fingerstick blood glucose, pulse ox, ABG, ECG, UDS, blood alcohol level, therapeutic drug levels, hepatic panel, thyroid hormone level, chest xray, head CT/MRI, EEG, LP

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14
Q

Treatment for delirium

A

TREAT UNDERLYING CAUSE

can give haloperidol for agitation

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15
Q

When to use benzos to treat delirium?

A

ONLY FOR ALCOHOL OR BENZO WITHDRAWAL!

do not use for anything else because they can worsen delirium via disinhibition or oversedation

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16
Q

Difference between mild and major NCDs

A

Patients with major NCDs require assistance with IADLS, while patients with minor NCDs do not

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17
Q

Cognitive impairment with stepwise increase in severity + focal neurologoical signs

A

vascular dx

head ct/brain MRI

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18
Q

cognitive impairment + cogwhell rigidity + resting tremor

A

Lewy body disease/Parkinsons

clinical dx

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19
Q

cognitive impairment + gait apraxia + urinary incontinence + dilated cerebral ventricles

A

Normal pressure hydrocephalus

Head CT + brain MRI

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20
Q

cognitive impairment + fatigue + cold intolerance + coarse hair + constipation

A

hypothyroidism

TSH, free T4

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21
Q

Cognitive impairment + paresthesias + diminished position and vibration sensation + megaloblasts on CBC

A

Vitamin B12 deficiency

Serum B12

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22
Q

Cognitive impairment + tremor + Kayser-Fleischer rings + abnormal LFTs

A

Wilson’s dx

cerumoplasmin

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23
Q

Cognitive impairment + diminished position and vibration sensation + Argyll Robertson Pupils (accomodation response present, but no light)

A

Neurosyphillis

CSF FTA-ABS and VDRL

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24
Q

A good quick screening test useful for delirium?

A

Mini Mental State Exam (MMSE)

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25
Q

What are the components of MMSE?

A

Orientation, registration (naming objects), attention (DLROW), recall (3 objects within 5 minutes), language (repetition, comprehension, writing)

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26
Q

What is the most underlying cause of major NCD?

A

Alzheimer’s disease

27
Q

Clinical manifestations of Alzheimer’s

A

gradual progressive decline
primary domains affected: memory, learning, language
-motor and sensory symptoms seen late in course of dx, death within 10 years of dx

28
Q

Etiologies of Alzheimer’s (name 2)

A
  1. accumulation of beta amyloid plaques and intraneuronal tau protein tangles
  2. 1% autosomal dominant single gene mutation (amyloid precursor protein) = early onset

down syndrome = higher risk for developing early onset AD

29
Q

What is the only way to dx Alzheimer’s

A

postmortem pathological exam of the brain

30
Q

Cure/treatment for Alzheimer’s

A

no cure yet :(

31
Q

What are treatment options for AD?

A
  • cholinesterase inhibitors (i.e denopezil) can slow deterioration
  • NMDA receptor antagonist can provide modest benefit
  • agitation and aggression treated with antipsychotics
  • supportive care with caregiver
32
Q

Danger of antipsychotics in patients with dementia?

A

Black box warning - increased risk of death/mortality

33
Q

Second most common cause of NCD after AD?

A

vascular disease aka vascular cognitive impairment

34
Q

How does cognitive decline happen in vascular disease?

A
  • large/small vessel strokes in cortical or subcortical structures respectively
  • microvascular disease affecting periventricular white matter
35
Q

Risk factors for vascular disease?

A 
hypertension
DM
smoking
obesity
hyperlipidema
atrial fib
old age
36
Q

How to treat vascular cognitive impairment?

A

No cure/effective treatment
Try to manage risk factors and prevent strokes
symptomatic management

37
Q

Classical presentation of vascular NCD?

A

stepwise loss of function corresponding with microinfarcts

38
Q

Pathologic features of Lewy body disease (LBD)

A

pathologic aggregrations of ALPHA-SYNUCLEIN and Lewy neutrites in the brain (primarily basal ganglia)

39
Q

Core features of LBD

A
  • waxing and waning attention/alertness
  • visual hallucinations (vivid, gnomes, dwarves)
  • development of EPS after cognitive symptoms
40
Q

What are some secondary/suggestive features of LBD?

A

REM sleep behavior disorder - violent movements during sleep in response to dreams
Antipsychotic sensitivity

41
Q

Treatment for LBD?

A
  • cholinesterase inhibitors for cognitive/behavioral symptoms
  • quatiapine or clozapine for psychotic symptoms (low dose, watch out for EPS or NMS)
  • levodopa for parkinsonism
  • melatonin for REM sleep disorder
42
Q

Pathology seen in frontotemporal degeneration (FTD)?

A

Marked atrophy of the frontal and temporal lobes

43
Q

What are the two variants of FTD?

A

Behavioral - DISINHIBITED behavior (sexual, verbal, physical), overeating/sucking on objects, lack of emotional warmth, apathy, decline in social/executive function

language- difficulties in speech and comprehension

44
Q

T/F: Most patients with FTD also have significant deficits in learning/memory and perceptual motor function

A

FALSE. relative sparing of learning/memory and pereceptual motor function

45
Q

How to treat behavioral symptoms of FTD?

A

Serotonergic meds may help reduce disinhibition, anxiety, impulsivity,

46
Q

What is the most common infectious agent known to cause NCD?

A

HIV!

47
Q

How to treat NCD due to HIV?

A

HAART may be beneficial

psychostimulants to treat symptoms

48
Q

Genetic pathology of Huntingtons disease?

A

trinucleotide CAG repeats in huntingtin (HTT) protein on chromosome 4

autosomal dominant

49
Q

Triad of clinical manifestations in Huntington’s

A

Motor - chorea, bradykinesia
cognitive - decline in executive function (precedes motor symptoms)
psychiatric - depression, apathy, irritablity, obsessions, impulsivity, INCREASED SUICIDE RISK

50
Q

How to dx?

A

Family hx of HD or genetic testing showing increased CAG repeats

51
Q

How to treat movement symptoms and psychiatric symptoms of HD?

A

movement - tetrabenazine

psych - atypicals

52
Q

Parkinson’s is due to depletion of ….. in the basal ganglia

A

DOPAMINE

53
Q

Motor signs of Parkinson’s

A

cogwhell rigidity, in bloc turning, postural instability, bradykinesia, resting tremor, masked faces

54
Q

Cognitive and psychiatric manifestations of Parkinsons

A

executive dysfunction, visuospatial impairments, depression, anxiety, personality cahnges, visual hallucinations, paranoid delusions (either from dx itself or meds)

cognitive decline appears AFTER motor symptoms

55
Q

Which two symptoms are required for PD dx?

A

presence of bradykinesia and tremor/rigidity

56
Q

How to treat PD?

A

motor symptoms with carbidopa-levodopa and or dopamine agonists (watch out for psychosis!)

cholineserase inhibitors for cognitive symptoms

quetiapine and clozapine useful in psychotic symptoms (don’t use other antipsychotics because of EPS)

57
Q

A form of subacute spongiform encephalopathy caused by proteinaceous infectious particles

A

PRION DISEASE (CJD)

58
Q

Diagnosis of prion disease?

A
  • RAPID PROGRESSIVE COGNITIVE DECLINE
  • at least 2: MYOCLONUS, visual/cerebellar signs (ataxia, nystagmus, hypokinesa)
  • supportive findings on EEG (sharp wave complexes, lesions in putamin/caudate nucleus on MRI, or 144-3-3- protein in CSF
59
Q

Any treatment for prion disease?

A

Nope, Most die in a year. poor raibon

60
Q

Pathology of normal pressure hydrocephalus?

A

enlarged ventricles on imaging with localized CSF pressure but normal opening pressures on LP

61
Q

Etiology of NPH?

A

idiopathic or secondary to CSF obstruction due to infetion (meningitis) or hemorrhage (subaarachnoid or intraventricular)

62
Q

Manifestations of NPH?

A

Wobbly - gait disturbance (first)
Wet - urinary incontinence
Wacky - cognitive impairment (insidiious), executive dysfunction; least likely to improve

63
Q

How to treat NPH?

A

VP shunt may improve symptoms

PSYCH CLERKSHIP (10 decks)

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