Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychiatry > Diagnosis and Evaluation of Dementia / Meds for Cognitive Impairment > Flashcards

Diagnosis and Evaluation of Dementia / Meds for Cognitive Impairment Flashcards

1
Q

What is the definition of dementia?

A

Decline in memory and at least 1 other cognitive function sufficient enough to affect daily life in an alert person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the major cognitive domains?

A
  1. Complex attention
  2. Executive function
  3. Learning and memory
  4. Language
  5. Perceptual-motor
  6. Social cognition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is dementia now called in the DSM 5, and what are its diagnostic criteria?

A

Major Neurocognitive Disorder

Significant decline in 1+ cognitive domains, as assessed by clinical assessment. They interfere with daily life and do not occur exclusively in delirium or as a part of another psych disorder.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Mild Neurocognitive Disorder?

A

Decline in 1+ cognitive domains, except that these deficits do not yet have to interfere with capacity for independence in daily activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are two formal mental status exams used to evaluate dementia in patients?

A
  1. MMSE - mini mental status exam

2. MOCA - montreal cognitive assessment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why are baseline laboratory assessments done in the dementia workup? Give some example labs taken and how they might be relevant.

A

Rule out reversible dementias

i.e.
Thyroid studies - hypothyroidism
Syphillis testing - rule out neurosyphillis
B12 (via methylmalonic acid) / folate levels (via homocysteine) - rule out CNS sequelae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the biomarkers in the CSF for dementia?

A

Low CSF A-beta42 (aggregates do not cross BBB into CSF very well)

Elevated CSF tau (hyperphosphorylated tau accumulates)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the PET and MRI findings in Alzheimer’s disease?

A

PET - decreased uptake into the temporoparietal cortex

MRI - Hippocampal atrophy

PET - can also assess amyloid burden in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In what conditions will you find decreased Dopamine uptake via DAT on brain scan?

A

Parkinson’s or Lewy Body Dementia

no hippocampal atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a good rapid assessment of dementia and what conditions will it discriminate well?

A

Clock Drawings Test

Will screen for Alzheimer disease and suspected frontotemporal dementia
-> frontotemporal dementia clocks will be WAYYY off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is neuropsychological testing and when is it used?

A

Extensive testing for assessment of specific focal deficits, and determining what the patient’s strengths and weaknesses are to tailor a specific rehab regimen to them. Do repeatedly to measure changes over time.

-> Done when beside assessment fails to differentiate between normal aging vs early dementia often

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When would each of the following be consulted: geriatric psychiatrist, neurologist, geriatrician?

A

Geriatric psychiatrist - severe mood / behavior problems which is not responsive to treatment, having unclear diagnosis

Neurologist - parkinsonian symptoms, early onset, focal neurological signs with rapid progression

Geriatrician - for complex medical problems (i.e. drug interactions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What three genes are associated with early onset Alzheimer’s disease (AD)?

A
  1. Amyloid Precursor Protein - Chromosome 21 (repeated in Down syndrome, high chance of AD)
  2. PS1 - presenillin1
  3. PS2 - presenillin2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What gene is a primary risk factor for Late Onset Alzheimer’s Disease and why?

A

ApoE4 - E4 variant causes ineffective removal of amyloid peptides, leading to amyloid plaque formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is genetic testing normally recommended for diagnostics / asymptomatic individuals? In what conditions is it especially warranted?

A

No

Warranted in:
Huntington’s disease
Frontotemporal dementia - has genetic component
Alzheimer’s disease <35 years (early onset, for genetic counseling)
APOE4 in AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is pseudo-dementia / what causes it?

A

Memory complains which are misdiagnosed as dementia, but are actually due to depression
-> need to be sure to ask about sadness or anhedonia

-BEWARE: depressive symptoms can be a precursor to dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of dementia is characterized by abrupt onset or stepwise deterioration?

A

Vascular dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the characteristics of frontotemporal dementia?

A

Behavioral changes, apathy, and aphasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give two causes of progressive gait disorder.

A

Vascular dementia, hydrocephalus

20
Q

Give one type of dementia other than acute delirium which can cause prominent fluctuations in the level of consciousness or cognitive abilities.

A

Dementia with Lewy bodies

21
Q

What dementias are associated with hallucinations or delusions?

A

Lewy body dementias, also delirium

22
Q

What diagnoses are associated with extrapyramidal signs or gait (acutely)

A

Vascular dementias -> affecting basal ganglia

Parkinson’s syndromes

23
Q

Give two conditions causing eye-movement abnormalities.

A
  1. Progressive supranuclear palsy

2. Wernicke’s encephalopathy - (ataxia, confusion, ophthalmoplegia)

24
Q

How does Alzheimer’s generally prevent differently than other dementias?

A

AD: Has a much slower (insidious) onset, with prominent early memory loss. Motor coordination / strength are generally preserved. Atrophy seen on MRI (especially medial temporal lobe = hippocampus).

Other dementias have a rapid or stepwise progression, generally occur younger than 65 years old, and affect focal CNS / motor systems far more than memory.

25
Q

How do plaques and tangles interfere with the brain in AD as insoluble aggregates?

A

Interfere with glucose transport -> lead to neuronal cell death
-> these especially deposit along cortical memory pathways

26
Q

What types of receptors are lost in the hippocampus and cortex in Alzheimer’s disease?

A

Nicotinic acetylcholine receptors

27
Q

What is the most significant risk factor for AD for everyone? Do females or males get it more? Other factors?

A

Age

Females get it more. Other factors include vascular / head trauma, low education, and inactivity

28
Q

What type of neurological findings will be seen in vascular dementia, and what will neuroimaging show?

A

Focal neurological findings

Neuroimaging shows infarcts

29
Q

What are the features of Lewy Body dementia?

A

Decreased attention / fluctuating cognition
Visual hallucinations
Motor features of parkinsonism
Lewy bodies in cerebral cortex

30
Q

What describes the drug reactivity of Lewy Body dementia patients?

A

Neuroleptic sensitivity

-> more likely to develop side effects to antipsychotics since they block dopamine, which is already low

31
Q

What is the most common cause of Frontotemporal dementia and what are its symptoms?

A

Pick’s disease

Prominent behavior changes w/ disinhibition (loss of prefrontal cortex)

Language disturbances -> aphasia, from loss of Broca’s and Wernicke’s.

Neuroimaging shows focal atrophy

32
Q

Why is PET scan useful in diagnosing frontotemporal dementia?

A

Shows hypo-perfusion prior to structural changes.

33
Q

What is the best way to assess improvements of cognitive impairment following treatment?

A

Talking to family members -> rating scales are imprecise

34
Q

What are the three stages of Alzheimer’s disease?

A

Stage 1 - presymptomatic, cognition is intact by amyloid is increasing

Stage 2 - Minor cognitive impairment (CI) - impairment is only episodic

Stage 3 - Major cognitive impairment - treatment generally begins

35
Q

What are the goals of raising acetylcholine in AD thought to do, and are any acetylcholinesterase inhibitors more effective?

A

Goals - enhance memory, slow decline in function

All are equally effective, tailor based on side effects

36
Q

What are the common side effects of all acetylcholinesterase inhibitors?

A

Nausea, vomiting, anorexia (weight loss), urinary incontinence

Abnormal dreams, Bradycardia, and orthostatic hypotension

37
Q

What are the three primary AChE’s used for treatment of Alzheimer’s? Which one has no CYP interactions?

A

Alzheimer’s GALA - Galantamine
Reverse the Stigma - Rivastigmine - no CYP interactions
Done the Puzzle - Donepezil

38
Q

Which cholinesterase inhibitor is approved for the treatment of cognitive impairment in PD? Why else was it developed?

A

Only Rivastigmine - also developed to have less GI side effects via using transdermal patch

39
Q

What Alzheimer’s treatment targets glutamate and when is it used? Is it good for other dementias?

A

Memantine - used for moderate to severe AD
-> uncompetitive NMDA antagonist. Can be used in combination with donepezil

Yes, even AChE’s are also good in other dementias which aren’t alzheimer’s disease

40
Q

When can you start using AChE’s?

A

Mild to Moderate AD (but not mild cognitive impairment)

41
Q

What is BPSD and what are some common reversible precipitants?

A

Behavioral and Psychological Symptoms in Dementia -> acting out in dementia

  • > Environmental changes (being in a nursing home)
  • > Medication side effects or withdrawal
  • > Pain
42
Q

What drugs are first line for treatment of BPSD, and some second line options?

A

First line: SSRIs or SNRIs

Second line options:
Anticonvulsants
Beta blockers
Buspirone
Trazodone
BENZOS
Gabapentin
43
Q

When would antipsychotics be used to treat BPSD? What are the issues?

A

When they are at a risk to themselves or others

Issue: Cardiovascular side effects (stroke risk)

44
Q

How should drug administration with BPSD be done, and when should you taper?

A

Done lowly and slowly

Taper after 3 months of stability

45
Q

What are the first-line nonpharmacological approaches for BPSD?

A

Manage general discomfort, have family visit more, make the patient generally happier with their life, etc

Psychiatry (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions