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NEURO FINAL SELF > 4 Dementia > Flashcards

4 Dementia Flashcards

1
Q

Does aging equal dementia? Does getting old cause Alzheimer’s?

A

No, but it is the primary risk factor

No

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2
Q

How much does the prevalence increase each decade starting at the age of 65 (5% risk) for dementia?

A

It doubles to about 17% at the age of 85 as it levels off

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3
Q

Normal aging is associated with what neurologically?

A
  1. mild cognitive weakness,
  2. mild cortical atrophy,
  3. mild accumulation of Alzheimer-type pathology and
  4. mild reduced cerebral blood flow
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4
Q

If getting old does not cause AD what does AD reflect?

A

pathologic changes in excess of that seen in normal aging, [AGE is a RISK FACTOR, but not ETIOLOGICAL CAUSE]

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5
Q

As people live longer through advanced medicine what will happen neurologically speaking?

A

incidence of AD and other dementias will increase

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6
Q

Besides aging, what impacts on cognitive changes in elderly people?

A

health status–physical and emotional

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7
Q

What are the main signs of normal cognitive changes in elderly people?

A

-slower processing
-novel tasks are difficult to learn
-recalling names
[benign forgetfulness]

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8
Q

What does dementia refer to?

A

acquired impairments in multiple aspects of cognition that are severe enough to interfere with normal activities

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9
Q

T-F–AD comprises majority of dementia?

A

True–65%

[AD +vascular changes is very high as well]

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10
Q

What are the signs of dementia? [there are 6 of them, they may be better just to review]

A
  1. memory loss affecting normal activity
  2. excess word finding problems
  3. diff. performing familiar tasks
  4. Disorientation to time or place
  5. changes in mood, behavior, personality
  6. Poor judgement
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11
Q

This is a list of the diseases associated with dementia. Don’t memorize but it’s a good review.

A 
AD
vascular disease
Parkinsons
Pick's
Medication Side effects
depression
Alc./Drugs
Tumor
Hydrocephalus
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12
Q

Is AD highly inheritable?

A

No .2-.3

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13
Q

Is personality highly inheritable? What about alcoholism and antisocial behavior?

A

yes 20-70%

Yes, maybe even more higher [how much does environment play a role though?]

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14
Q

Who was Dr. Alzheimers colleague in psychiatry?

A

Dr. Nissl

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15
Q

Is AD reversible? What neurons does it primarily affect? How many are estimated to have it by 2030?

A

No
Cortical Neurons
8.5 million U.S

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16
Q

What did Alzheimer find in the brain of his first patient?

A

senile plaques and neurofibrillary tangles

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17
Q

What are the main characteristics of Alzheimer’s disease?

A
  • age-related
  • IRREVERSIBLE
  • gradual
  • decline in thinking
  • DEATH of BRAIN CELLS
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18
Q

Iowa per capita has the 3rd highest what and the highest what in regards to age?

A

concentrations of 65+ and 85+. Thus, a lot of Alzheimers

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19
Q

Is there a higher prevalence of AD in women or men?

A

women

20
Q

What is the length of survival in AD post diagnosis?

A

8-10 years [will be longer from start of symptoms, but those don’t always correlate]

21
Q

Are neurofibrillary tangles intra or extracellular?

A

Intra

22
Q

Are neuritic plaques intra or extracellular?

A

extracellular

23
Q

What are the 5 things found in AD neuropathology>

A
  1. neurofibrillary tangles
  2. Neuritic Plaques
  3. Amyloid Accumulation
  4. Neurotransmitter Loss
  5. Neuronal Loss
24
Q

Why do we use the term probable AD?

A

Because clinically AD needs a biopsy to be confirmatory

25
Q

What is a neurofibrillary tangle?

A

abnormal mass of neurofilaments and abnormally phosphorylated tau protein twisted and tangles into triangle and loop shapes in cytoplasm

26
Q

What stains are best to visualize neurofibrillary triangles?

A

silver stains

27
Q

Are neurofibrillar tangles seen in normal aging? What disease are they also seen in?

A

Yes

Down’s Syndrome

28
Q

What does a NFT do in the neuron?

A

disrupt and cause death—>tombstone or ghost tangle

29
Q

What is a neuritic plaque and what do they consist of?

A

small areas of tissue degeneration in the spaces between neurons,
consists of granular deposits and remnants of neuronal processes

30
Q

What shape do neuritic plaques form? what is in the center of the shape?

A

spherical with a dense central core made of amyloid

31
Q

What cerebral cortex does AD most readily affect?

A

subcortical structures–amygdala and cholinergic neurons of the nucleus basal is of meynert [affect cholinergic innervation of the cerebral cortex]

32
Q

Is the association cortex heavily affected in AD? primary sensory cortex? motor cortex?

A

association=heavily
Sensory= minimal
Motor= least

33
Q

Where are NFTs most heavily distributed?

A

anterior portion of the parahippocampal gyrus and specifically the entorhinal cortex

[you also see concentrations in the frontal association cortex, cortex of inferior parietal, and lateral temporal lobe]

34
Q

Where are NFT generally not seen?

A

precentral gyrus, postcentral gyrus
Heschles
primary visual cortex

35
Q

How does the distribution of NPs contrast that of NFT?

A

more generally distributed throughout the cortex–greatest density is behind the central sulcus in p and t lobes.

[frontal lobes do have some]

36
Q

where is the smallest number of NPs found?

A

entorhinal cortex!

37
Q

Is dementia severity more correlated with extent of NFTs or NPs?

A

NFTs

38
Q

Where is glucose hypo metabolism seen in AD patients on PET scans?

A

bilateral temporal-parietal

[later stages demonstrate bifrontal hyometabolism]

39
Q

Where are no changes in glucose metabolism seen in AD patients?

A

sensorimotor, visual cortices, basal ganglia, and/or cerebellum

40
Q

What are the general macroscopic changes in the AD brain? general locations?

A

gyro get smaller and sulci get larger

[particularly apparent in the prefrontal lobe, parietal-occipital, and lateral temporal]

41
Q

What layers of cortex in the entorhinal do we see NFTs?

A

II and IV–>disconnecting the hippo from association and limbic cortices and thus disrupts input communication

42
Q

If sensory information cannot access the hippocampal formation via entorhinal cortex what happens?

A

hippo cannot put the stamp of approval on info and relaying it to the association cortices for long-term storage

43
Q

What 4 genes have been identified in AD?

A
  1. Amyloid protein precursor (APP)
  2. Presenilin 1 [ch.14]
  3. Presenilin 2 [ch. 1]
  4. APOE4 on ch. 19 [E4 allele is most alarming]
44
Q

What is the basic 3 drug therapy in AD?

A
  1. Cholinesterase Inhibitors
  2. NMDA Antagonist [namenda]
  3. Neuroprotection [viatminE]
45
Q

How does IVIG work in AD?

A

contains a high level of anti-amyloid antibodies

[lower levels of these antibodies are found in AD patients]

46
Q

The NINDS-ADRDA criteria for AD includes what? Mainly for review but very important

A 
>abnormal results in neuro/cog exams
>deficits in 2 or more areas of cognition
>progression of amnesia and cog
>no disturbance of consciousness
>aged 40-90
>no other brain issue that could explain

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