Dementia (5Q) Flashcards Preview

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Flashcards in Dementia (5Q) Deck (33)
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1
Q

Dementia: risk factors

A
  1. Age
  2. Family Hx
  3. Vascular disease/ Diabetes
2
Q

Dementia: protective factors

A

Education, continuing intellectual stimulation

3
Q

Dementia: patient

A

Over 60 yo, w/ risk doubling every 5 years after that.

4
Q

Differentiate delirium from dementia

A

Delirium: acute confusional state that often occurs in response to an identifiable trigger. (eg, drugs, infection, metabolic disturbance, sleep deprivation, or other neurologic disease.
Delirium will have a fluctuating level of arousal including drowsiness or agitation that improves with removal of precipitating factor.

5
Q

Word-finding difficulty (def and lesion location)

A

a dementia symtom- refers to difficulty recalling the names of people, places, or objects (low-frequency first), resulting in speech laden with pronouns and circumlocations. NO problems with articulation, fluency, or word meaning.
Suggests lesion in temproparietal junction of L hemisphere.

6
Q

Visuospatial dysfunction (def and lesion location)

A

Symptom of dementia: results in poor navigation and getting lost in familiar places, inability to identify familiar faces or buildings, or trouble discerning object from background.
Suggests lesion in R parietal lobe.

7
Q

Short-term memory loss (def and lesion location)

A

It is what it sounds like. Suggests lesion in hippocampus.

8
Q

Executive dysfunction (def and lesion location)

A

easy distractability, impulsivity, mental inflexibility, slowed processing, impaired judgement, poor planning.
Suggests lesion in frontal lobe or subcortical areas (basal ganglia, white matter).

9
Q

What are some other Sx of dementia (not including short term memory loss, word-finding difficulty, visuospatial dysfunction, executive dysfunction)? Where do they suggest lesions?

A

Apathy- damage to frontal lobe, basal ganglia, or white matter.

Apraxia- loss of learned motor behaviors- damage in frontal or parietal (esp L) lobes.

10
Q

Why is it so important to have a baseline assessment of functional status (ADLs, IADLs) for geriatric patients?

A

Cognitive and functional decline may ONLY be noticeable when compared to pt’s baseline.

11
Q

What are the limitations of mini-mental status exams (including Folstein MMSE and Montreal Cog Assessment)?

A

They are insensitive to mild cognitive impairment, may be biased negatively by language/attention problems, does not correlate with functional capacity.

12
Q

Dementia screening guidelines for asymptomatic older patients:

A

There aren’t any! Current suggests for patients >70: Test registration (apple, book, car), clock test (hands at 11:10), short term memory (repeat 3 words after clock test). If there is any abnormality (remember <3 words or have a weird clock), then do a full MMSE.

13
Q

For whom is brain imaging indicated? What are you looking for?

A

Any patient with a new, progressive cognitive complaint. Goal is to rule out occult cerebrovascular disease, tumor, or other structural abnormality (not provide positive evidence of disease). MRI is preferred.

14
Q

When is a PET scan useful?

A

When you are trying to distinguish between several dementia causes (eg, Alzheimer and frontotemporal dementia). Specifically, PET imaging with a radiolabeled ligand for beta-amyloid is sensitive to amyloid pathology and provides positive evidence of Alzheimer).

15
Q

Alzheimer pathology

A

Plaques containing beta-amyloid peptide and neurofibrillary tangles containing tau protein occur throughout neocortex.

16
Q

Alzheimer: clinical features

A

Most common age-related neurodegenerative disease. Short term memory impairment is prominent w/ variable deficits in executive function, visuospatial function, and language

17
Q

Vascular dementia pathology

A

Multifocal ischemic changes

18
Q

Vascular dementia: clinical features

A

Progressive accumulation of cognitive deficits in association with repeated strokes. Specific sx are specific to location of strokes.

19
Q

Normal pressure hydrocephalus: clinical features

A

Gait apraxia (magnetic gait- feet stuck to floor), urinary incontinence, and dementia.

20
Q

What do you order to R/O normal pressure hydrocephalus? What are you looking for?

A

CT or MRI- showing enlarged ventricles disproportionate to sulcal widening and overall brain atrophy

21
Q

What lab tests should you order when working up suspected dementia? What are they for?

A

Serum B12 (r/o B12 neuropathy); free T4 (thyroid function); TSH. Get these in ANY pt with cog sx. RPR if worried about latent syphillis.

ApoE- get this in a young patient with cognitive impairment to raise index of suspicion for Alzheimer.

22
Q

What are some non-pharmacologic treatments for dementia?

A

Aerobic exercise (45 mins for most days of week) and frequent mental stimulation reduce the rate of functional decline.

Mental stimulation= maintaining an active role in the community (if possible) and emphasizing activities in which the patient feels confident. Note that memory improvement programs etc show little effect and that once a pt loses the ability to do something competently, they won’t recover it. Avoid frustrating activities.

23
Q

Dementia with Lewy bodies- what is it (super basic)

A

Cognitive dysfunction with Parkinson’s sx. May include psych disturbance w/ fluctuating delirium.

24
Q

First line treatment for Alzheimer’s-related cognitive decline:

A

Mild-moderate (MMSE > 17) Cholinesterase inhibitors (donepezil, rivastigmine). Start low and titrate dose up. Symptomatic tx for cognitive Sx. Not disease altering.

CI: frontotemporal dementia

25
Q

What is frontotemporal dementia

A

Complex disease that peaks in 6th decade. Behavioral variant (mainly behavioral sx- disinhibition, apathetic w/ relatively preserved memory); Semantic- deficits in word-finding, single word comprehension (may be combined with behavioral type); Progressive nonfluent aphasia: speech effortful with dysarthria, weird sounds, bad grammar.

Not on our objectives, but important because cholinesterase inhibitors, used for Alzheimer, will worsen frontotemporal dementia.

26
Q

First line treatment for dementia w/ Lewey bodies:

A

Cholinesterase inhibitors. Not disease-altering.

27
Q

2nd Line for Alzheimer’s and Dementia w/ Lewey bodies:

A

Memantine (NMDA antagonist). Not disease altering. Better for moderate-severe dementia.

28
Q

First line for depression associated w/ dementia:

A

SSRIs (not paroxetine due to anticholinergic effects)

29
Q

Tx for agitation and impulsivity in dementia (for patient safety):

A

1: Behavioral interventions- reorientation, avoid anxiety-provoking stimuli. Ensure adequate activity during day and sleep at night.
2. Make sure pt has appropriate pharmacologic tx for cognitive decline
3. LAST resort- low dose atypical antipsychotic (eg quetiapine)- use w/ caution if fall risk, parkinsonism present.

30
Q

When should a patient stop driving?

A

Any patient with mild dementia or worse should stop driving.

31
Q

Rapidly progressive dementia

A

Dementia that develops quickly with obvious decline over weeks to months. Consider atypical etiologies, including infectious.

32
Q

How should you work up rapidly progressive dementia?

A

MRI of brain w/ contrast, labs (B12, free T4, TSH, RPR, HIV, Lyme serology, rheumatologic tests, anti-thyroglobulin, anti-thyroperoxidase, paraneoplastic autoimmune antibodies, CSF studies). CSF studies include: cell count/diff, protein electrophoresis for oligoclonal IgG, PCR for Whipple’s, CMV, HSV, varicella zoster.

33
Q

What are some etiologies of rapidly progressive demantia?

A

Can be due to typical causes, but also: HIV, Lyme, Syphillis, rheumatic disease, neoplasims, Hashimoto encephalopathy, antibody-mediated paraneoplastic syndrome, Jakob-Creutzfeldt disease (cortical ribboning and restricted diffusion to caudate/ anterior putamen on diffusion-weighted MRI).