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Special Pops - Geriatrics > Degenerative Dementias > Flashcards

Degenerative Dementias Flashcards

1
Q

DSM-5 criteria for major neurocognitive disorder?

A

Must have significant cognitive decline and it must interfere with independence in everyday activities

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2
Q

Prevalence of Alzheimer’s by age?

A
  • 30% of those 85 yo
  • 11% of those 65 yo
  • 4% of those under 65
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3
Q

Genetic associations for Alzheimer’s

A
  • APOE e4 (20% US population) 1 copy increases risk 3x, 2 copies 12x risk
  • APOE e3 (60% US population) average risk
  • APOE e2 (20% US population) less risk
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4
Q

What gene puts you at most risk for Alzheimer’s?

A

APOE e4

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5
Q

What gene puts you at average risk for Alzheimer’s?

A

APOE e3

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6
Q

What gene puts you at less risk for Alzheimer’s?

A

APOE e2

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7
Q

Types of dementia

A
  • Alzheimer’s (60%): tauopathy
  • Lewy body (15%): synucleinopathy
  • Mixed (10%)
  • Vascular (5%)
  • Other (normal pressure hydrocephalus, 10%)
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8
Q

Early symptoms of Alzheimer’s

A

Memory - forgets conversations/appointments/plans

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9
Q

Later symptoms of Alzheimer’s

A

Loss of:

  1. Memory
  2. Language
  3. Visual/spatial
  4. Executive functions (including sequence capability and time perception)
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10
Q

Pathologic hallmarks of Alzheimer’s

A

Plaques and NF tangles

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11
Q

How does Alzheimer’s develop?

A
  1. Brain accumulation of amyloid (PET scan can ID it)
  2. Phosphorylated Tau (associated neuronal injury) which can be found in CSF
  3. Brain structure changes (loss of volume on MRI)
  4. More severe cognitive loss clinically
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12
Q

Lab and imaging findings of Alzheimer’s

A
  • NO serum biomarkers
  • Increased P-Tau and decreased AB 1-42 in CSF
  • PET scan showing AB amyloid deposition in brain
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13
Q

What is Tau? What is phosphorylated Tau?

A
  • Soluble protein in cell microtubules (necessary for cell function)
  • P-TAU is INSOLUBLE and toxic to cells
  • Tau is in “senile plaques” of several dementias
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14
Q

Describe Beta amyloid

A
  • Amyloid Precursor Protein (APP) is a normal cell membrane feature
  • APP metabolism usually results in soluble fragments
  • Disease associated APP breakdown produces INSOLUBLE Beta amyloid which aggregates into plaques
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15
Q

Describe PET identification of beta amyloid accuracy in Alzheimer’s

A
  • Highly sensitive (true positives)
  • Not overly specific (false positives, can be found in normal aging, MCI, other dementias)
  • CSF markers AND PET amyloid increases accuracy of diagnosis
  • PET is FDA approved for detection of amyloid
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16
Q

Prognosis of someone with MCI who is positive for PET amyloid?

A

50% of pts will convert to Alzheimer’s dementia in 3 yrs

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17
Q

Functional MRI in Alzheimer’s diagnosis

A
  • Measures O2 content and does NOT require contrast
  • New and experimental
  • Good correlation to PET
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18
Q

Routine MRI in evaluation of Alzheimer’s

A

Can measure volume loss (esp medial temporal lobes)

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19
Q

CT in evaluation of Alzheimer’s

A

Can demonstrate atrophy

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20
Q

Define mild cognitive impairment (MCI)

A
  • Some evidence of cognitive impairment but NOT progressed to dementia
  • ADLs are preserved
  • Some improvement/reversibility possible
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21
Q

Treatments for MCI/Alzheimer’s

A
  • Cholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine)
  • NMDA receptor blockers (Memantine)
  • Some synergy is found if NMDA blocker used in combo w/cholinesterase inhibitor
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22
Q

Caution of cholinesterase inhibitor use in Alzheimer’s?

A

Bradycardia - do NOT use if HR less than 60 or if heart block

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23
Q

How do cholinesterase inhibitors work in Alzheimer’s disease?

A
  • None are protective against disease progression

- They increase ACh in areas known to be deficient (nucleus basalis of Meynert and diagonal band of Broca)

24
Q

What 2 areas do cholinesterase inhibitors work on in Alzheimer’s treatment?

A
  • Nucleus basalis of Meynert

- Diagonal band of Broca

25
Q

What is the NMDA blocker used to treat Alzheimer’s?

A

Memantine

treats symptoms NOT neuroprotective

26
Q

ADEs of Memantine

A
  • AMS, agitation

- Decrease dose of renal impairment

27
Q

How to help prevent Alzheimer’s

A
  • Treat standard CV risk factors (HLD, HTN, obesity, DM)
  • Exercise
  • Cognitive reserve (ongoing intellectual pursuit)
  • Avoid smoking and high ETOH consumption
28
Q

How do standard CV risk factors influence Alzheimer’s risk?

A
  • There is often evidence of both vascular and Alzheimer’s dementia
  • Beta amyloid is increased with many of these CV factors
29
Q

How does cognitive reserve help prevent Alzheimer’s?

A

High levels of education and ongoing intellectual pursuit are a/w decreased Beta amyloid deposition

30
Q

Neuroprotective strategy of Alzheimer’s

A

NONE proven - Mediterranean diet suggest possible positive trend

31
Q

Vitamins and dietary additives to prevent Alzheimer’s?

A

If a patient is not deficient, there is NO extra value

32
Q

How should late stage behavioral problems in dementia be approached?

A
  • AVOID BZDs and anticholinergics (side effects)

- Use DA blockers, antipsychotics

33
Q

Risk of antipsychotic use in late stage dementia?

A
  • Atypical antipsychotics had increased risk of death
  • Mortality was highest with Haldol (but also high with Risperidone and Olanzapine)
  • Always monitor QTc interval
34
Q

Risk of DA blocker use in late stage dementia?

A
  • EPSEs including TD/parkinsonism/sedation and falls

- Tardive dyskinesia has NO reliable treatment and will remain for years

35
Q

Define apathy

A
  • “Loss of” condition

- It is unlike depression (which has considerable emotional distress)

36
Q

How to treat apathy in dementia patients?

A

Anecdotal evidence suggests:

  • DA antidepressants (Sertraline, Bupropion)
  • Stimulants (Ritalin)
  • DA agonists (Carbidopa/Levodopa)
37
Q

How does Lewy body dementia present?

A
  • Rapidly evolving (less than 1 yr) memory loss a/w parkinsonian features
  • Lack of response to DA therapy
38
Q

What happens to Lewy body dementia patients if given a DA blocker?

A

Frozen (severely rigid)

39
Q

What type of disease is Parkinson’s and how does it present with dementia?

A
  • Synuleinopathy
  • 30% become demented later on (slow evolution)
  • Pts DO respond to DA treatment like Carbo/Levo (unlike Lewy body dementia)
40
Q

Describe Parkinson plus syndromes

A
  • Similar to Parkinson’s
  • All are refractory to DA treatment
  • All are rigid
  • All can dement
41
Q

What are the Parkinson plus syndromes?

A
  • PSP (progressive supranuclear palsy)
  • MSA (multi system atrophy)
  • CBD (cortical basilar degeneration)
42
Q

Describe progressive supranuclear palsy

A
  • Parkinson plus syndrome (rapidly progressive, less than 1 yr)
  • Dementia
  • Severe rigidity
  • Vertical gaze palsy
43
Q

Describe multi system atrophy

A
  • Parkinson plus syndrome

- Rigid with cerebellar ataxia

44
Q

Describe cortical basilar degeneration

A
  • Parkinson plus syndrome
  • Severely lateralized motor rigidity
  • Sensory deficits
45
Q

Describe frontal temporal dementia

A
  • Rapid evolution of dementia with frontal lobe dysfunction (disinhibition, mood decline)
  • ALS like loss of motor function (30% pts)
46
Q

Describe primary progressive aphasia

A
  • Neurodegenerative disease
  • Primary loss of language (before loss of other domains)
  • Slow progression over years
  • Eventually converts to global severe dementia
47
Q

What are the 3 features of normal pressure hydrocephalus (NPH)?

A
  1. Gait apraxia (magnet foot steppage)
  2. Memory impairment
  3. Urinary incontinence
    * *Rare condition!
48
Q

What vasculitis conditions can cause dementia and how do they affect the brain?

A
  • Lupus: brain involvement and strokes
  • Sjogrens: brain vasculopathy
  • Behcet’s: meningoencephalitis
49
Q

What has an increased association with ovarian teratoma?

A

Paraneoplastic syndrome

50
Q

How does paraneoplastic syndrome present?

A

NMDA receptor antibody positive in serum and CSF

51
Q

What anti-Hu and anti-CV2 antibodies associated with?

A

Lung small cell cancer

52
Q

What are anti-MA2 antibodies associated with?

A

Testicular cancer

53
Q

Describe prion disease

A
  • Rapid dementia progression (wks to months)
  • Myoclonus
  • Positive MRI, EEG
  • Abnormal 14-3-3 protein in CSF
  • Highly contagious
    (e. g. mad cow disease)
54
Q

What is the triad of Wernicke’s encephalopathy?

A

-Ataxia (gait > limbs)
-Nystagmus
-AMS
(only 20% pts have all 3)

55
Q

What are the 5 areas of damage associated with B12 deficiency?

A
  1. Mentation (memory mainly)
  2. Optic nerve dysfunction
  3. Cerebellar ataxia
  4. Posterior column defects
  5. Peripheral neuropathy
    * Hyperreflexia
56
Q

What confirms diagnosis of B12 deficiency?

A

Methylmalonic acid

Special Pops - Geriatrics (9 decks)

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