Block 3 Psych Exam -- Dementia (#5)

Front 1

Breakdown of etiology of dementia
(statistical % of causes)

Back 1

85% due to Alzheimer's, Vascular dementia, or a combo
15% due to variety of other conditions

Front 2

Common neuroimaging findings in "normal" elderly (2)

Back 2

Enlarged ventricles and atrophy
Ischemic changes in deep white matter and basal ganglia

Front 3

Characteristic problems of mild cognitive impairment (4)

Back 3

Finding words "on tip of tongue"
Trouble recalling names
Misplacing things
TROUBLE CONCENTRATING

Front 4

In amnestic disorder, memory disturbance must be a consequence of what?

Back 4

A general medical condition

Front 5

What part of the brain is most sensitive to ischemia?

Back 5

Hippocampi

Front 6

Amnestic syndrome can reflect disruption anywhere along what?

Back 6

Medial hemispheric circuit

Front 7

How does prevalence of dementia progress after age 65

Back 7

Prevalence doubles every 5 years

Front 8

Pick's Disease

Back 8

Frontal lobe degeneration
(This is a primary dementia)

Front 9

Far and away the most common cause of dementia

Back 9

Alzheimer's disease

Front 10

Development of aphasia in cortical vs. subcortical dementia

Back 10

Cortical -- aphasia early

Subcortical -- dysarthria early, but NO aphasia

Front 11

Relative quality of recognition vs. recall in C vs. SC dementia

Back 11

Cortical -- recognition = recall

Subcortical -- recall is worse than recognition
(if you show them something, they'll recognize it)

Front 12

Speed of thinking of in C vs. SC dementia

Back 12

Cortical -- NORMAL speed of thinking

Subcortical -- SLOWED thinking

Front 13

Proportionality of decline in executive functioning in C vs. SC dementia

Back 13

Cortical -- decline in executive functioning is proportional to other traits

Subcortical -- early decline in exec. functioning GREATER THAN other deficits

Front 14

Motor exam finding in C vs. SC dementia

Back 14

Cortical -- NORMAL motor exam early

Subcortical -- movement disorders are common

Front 15

What is the only way Alzheimer's can be diagnosed definitively?

Back 15

At autopsy

Front 16

Examples of CORTICAL dementia (3)

Back 16

Alzheimer's
Pick's Disease
Cortical strokes

Front 17

Examples of SUBCORTICAL dementia (6)

Back 17

PD
Huntington's
HIV
Depression
Alcohol
Stroke

Front 18

"Diagnosis" of Alzheimer's must show multiple cognitive deficits w/ both:

Back 18

Memory impairment AND

One (or more) of following:
Apraxia, Aphasia, Agnosia
Impaired exectuitve functioning

Front 19

Onset of Alzheimer's typically begins when?

Back 19

After age 55

Front 20

How do MMSE scores of Alzheimer's pts. change over time?

Back 20

2-3 pt. decline per year

Front 21

What is the mean post-diagnosis survival time in Alzheimer's?

Back 21

10 years

Front 22

How is memory first affected by Alzheimer's?

Back 22

Long-term memory is initially in tact
Short-term memory is impaired

Front 23

How does the EEG of Alzheimer's pts. change between stages of disease?

Back 23

Stage 1 - Normal
Stage 2 - Background slowing
Stage 3 - Diffuse slowing

Front 24

CT/MRI evolution through stages of Alzheimer's

Back 24

Stage 1 - Normal
Stage 2 - Normal or mild atrophy/ventricular enlargement
Stage 3 - Ventricular dilatation; sulcal enlargement

Front 25

Progression of PET/SPECT scans in Alzheimer's

Back 25

Starts off w/ bilateral, posterior, parietal-temporal hypometabolism

Becomes, biparietal AND frontal hypometabolism

Front 26

Pattern of neuronal loss in Alzheimer's

Back 26

Bilateral
Symmetric

Front 27

Two primary brain regions affected by Alzheimer's

Back 27

Temporal-parietal cortex
Hippocampus

Front 28

Brain regions relatively spared by Alzheimer's

Back 28

Primary motor, sensory, and visual cortices

Front 29

What/where are amyloid plaques?

Back 29

EXTRAcellular lesions
Core of beta-amyloid surrounded by dystrophic neurites

Front 30

What are neurofibrillary tangles?

Back 30

INTRAcellular lesions
Made of abnormally phosphorylated microtubules

Front 31

What are Hirano bodies?

Back 31

Cytoplasmic aggregates of actin and assoc. proteins

These affect the cytoskeletal structure

Front 32

Early Alzheimer's changes seen on PET scan

Back 32

Extensive hypometabolism in temporal-parietal cortex

INCREASED activity in hippocampal area
"revving harder to think"

Front 33

Later Alzheimer's changes seen on PET scan

Back 33

Hypometabolism spreads to frontal cortex

BUT, primary motor, sensory and visual cortices rel. spared

Front 34

Temporal-parietal hypoperfusion is NOT specific to Alzheimer's

What other conditions can cause i (3)?

Back 34

Sleep apnea
Hypoxic brain injury
Vascular Dementia

Front 35

% of Alzheimer's cases that are familial

Back 35

40%

Front 36

Concordance in Alzheimer's twins

Back 36

40% for monozygotic
SAME for dizygotic

SO, environmental factors must play a role

Front 37

Early onset cases of Alzheimer's show links to what chromosomes (2)?

Back 37

14
21

Front 38

Some late onset and sporadic cases of AD show links to what chromosome?

Back 38

19 (The gene for ApoE4)

Front 39

ApoE4

Back 39

Binds avidly to beta-amyloid
Found in plaques and tangles

1 copy causes 3x greater risk
2 copies causes 8x greater risk

Front 40

Potential etiologies for Alzheimer's (4)

Back 40

Acetylcholine deficiency
Excess glutamate
Amyloid hypothesis
ApoE hypothesis

Front 41

Key points about using cholinergic drugs in Alzheimer's

Back 41

More effective EARLY

Do NOT change rate of progression of illness

Front 42

Tacrine (Cognex)

Back 42

Reversible cholinesterase inhibitor

NOT used anymore
Most pts. couldn't tolerate the high doses
(hepatotoxicity, Inc. gastric acid, N&V)

Front 43

Donepezil (Aricept)

Back 43

Cholinesterase inhibitor

Can be take ONCE daily
NOT assoc. w/ liver toxicity

Front 44

Rivastigmine (Exelon)

Back 44

Cholinesterase inhibitor

Taken TWICE daily
NOT assoc. w/ liver toxicity

Front 45

Galantamine (Reminyl)

Back 45

BOTH a cholinesterase inhibitor
AND a nicotine receptor allosteric modulator

Front 46

ACh loss in Alzheimer's corresponds to loss of neurons where?

Back 46

Nucleus Basalis of Meynert

Front 47

Neurotransmitter that is most depleted in Alzheimer's

Back 47

ACh

Front 48

Glutamate/Excitotoxicity Hypothesis

Back 48

Too much glutamate
Thus, too great an influx of Calcium

Calcium activates enzymes that make free radicals
Free radicals injure neuron membranes and organelles

Cell is "excited to death"

Front 49

2 main treatment implications of glutamate/excitotoxicity hypothesis

Back 49

Glutamate blockade
Antioxidant Therapy

Front 50

Memantine (Namenda)

Back 50

NMDA-receptor antagonist

Approved for moderate to severe Alzheimer's
Can be combined with cholinesterase inhibitors

Front 51

Which works better in Alzheimer's?

Vitamin E or Selegline

Back 51

Both are equally effective
Both show little effect on COGNITION

BUT, can potentially slow functional decline

Front 52

Is it better to use Vitamin E and Selegline in combo, or either alone?

Back 52

The combination actually performs worse than either drug alone

Front 53

Amyloid hypothesis

Back 53

Excessive amyloid accumulation leads to destruction of neurons

Analogy to cholesterol in heart disease

Front 54

What chromosome is the Amyloid precursor gene on?

Back 54

21

Front 55

Which ApoE allele is linked with the lowest risk of AD?

Back 55

ApoE2

Front 56

What is ApoE?

Back 56

Apolipoprotein involved in clearing lipids in the bloodstream

Binds avidly to beta-amyloid

Has been found in plaques, tangles, and amyloid angiopathies

Front 57

Which ApoE allele is linked with the highest risk of AD?

Back 57

ApoE4

Analogy is made to "good" and "bad" cholesterol

Front 58

5 main steps in treatment plan for AD

Back 58

Establish alliance w/ pt. and family

Follow cognitive status and treat comorbid problems
Monitor for pt. safety

Consider anti-oxidant therapy
Consider cholinergic/glutamate blocking therapy

Front 59

Commonly prescribed in AD despite being only 20-30% effective

Back 59

Antipsychotics

Should be reserved for severe agitation and psychosis