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Alzheimers-Test 2 Flashcards

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1
Q

What are the types of dementia?

A 
Mild Cognitive Impairment (MCI)
Alzheimer’s Disease (AD)
Vascular Dementia
Lewy Body Dementia
–Parkinson’s Dementia
Frontal Lobe Dementia (Frontotemporal Dementia)
Mixed Dementia
--Vascular Dementia and AD
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2
Q

What are s/s of delirium?

A

–Sudden alterations in cognitive function, Hours to days
–Fluctuations in cognition during day
–Attention span impaired, Rarely aware of cognitive deficits
–Often accompanied by disturbances in sleep-wake cycle and psychomotor disturbances

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3
Q

What are some potential causes of delirium?

A

–underlying pathology
UTI, MI, pneumonia, pain
–May be drug induced
Benzodiazepines, anticholinergics, antihistamines, anticonvulsants, beta blockers, sympathomimetics, lithium, diuretics

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4
Q

What are the s/s of depression?

A

–Short and long-term memory are selectively impaired
–No progression/worsening of cognitive dysfunction
–Pt usually aware of deficits (often disturbed by dysfunction)

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5
Q

What is the most common form of dementia?

A

Alzheimers

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6
Q

What is Alzheimers?

A

Neurodegenerative disease characterized by non-reversible, progressive cognitive deterioration, together with declining activities of daily living and by neuropsychiatric symptoms or behavioral changes

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7
Q

What are risk factors for AD?

A
  • Age
  • Dementia in close family member
  • E4 allele of the ApoE gene
  • History of psychiatric illness
  • other: Down’s Syndrome, exposure to anesthetic agents, head injury, diabetes
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8
Q

What are the gene mutations that play a role in early onset AD?

A

1) Prensilin 1 on Chromosome 21
2) Amyloid Precursor Protein (APP) on Chromosome 1
3) Presenilin 2 on Chromosome 1

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9
Q

What do the above mutations lead to?

A

an increase in B-A4 peptide fragments of APP which forms neuritic plaques

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10
Q

What gene is involved in late onset AD?

A

Apolipoprotein E (Apo E) on Chromosome 19

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11
Q

What is the neuropathology of AD?

A

Neurofibrillary tangles (NFTs) and Neuritic plaque lesions with insoluble B-amyloid peptide core

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12
Q

What forms the NFT? What happens to these tangels?

A

abnormally phosphorylated tau protein … this protein is essential for axonal transport and stabilizes the neuron, with the abnormal tau the neurons become unstable and die

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13
Q

What presents around the areas of plaque formation in the brain?

A

Glial cells, cytokines (IL-1 and IL-6), and complement cascade

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14
Q

What does destruction of neuronal pathways from accumulation of plaques lead to?

A

to shortage of Acetylcholine

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15
Q

What is glutamate involved in?

A

neuronal pathways essential to learning & memory

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16
Q

What can B amyloid aggregation lead to?

A

disrupt transmission of glutamate and lead to excess stimulation of NMDA receptors

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17
Q

What does excess stimulation of NMDA receptors lead to?

A

high intracellular Ca++ concentration and excitotoxicity neuronal death

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18
Q

What are the earlu symptoms of AD?

A

is loss of memory (amnesia), which usually manifests as minor forgetfulness that becomes steadily more pronounced with the progression of the illness, with relative preservation of older memories.

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19
Q

What are the s/s as AD progresses?

A

cognitive impairment extends to domains of language (aphasia), skilled movements (apraxia), recognition (agnosia), and functions related to frontal and temporal lobes (decision-making and planning)

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20
Q

What is the average duration of AD?

A

7-10 years

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21
Q

What are the stages of AD?

A 
Stage 1:  No cognitive impairment
Stage 2:  Very mild cognitive decline
Stage 3:  Mild cognitive decline
Stage 4:  Moderate cognitive decline
Stage 5:  Moderately severe cognitive decline
Stage 6:  Severe cognitive decline
Stage 7:  Very severe cognitive decline
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22
Q

What typically results in death from elderly affected by AD?

A

Choking, aspiration and infection

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23
Q

How is the diagnosis of AD made?

A

Only conclusive test post-mortem
basis of history, clinical observation, memory tests and intellectual functioning over weeks or months; blood tests and neuroimaging (PET and SPECT scans) to R/O alternative diagnoses

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24
Q

What score on the MMSE classifies mild-mod AD?

A

10-26

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25
What score on the MMSE classifies mod-severe AD?
3-14
26
What tx may help delay the progression of AD?
Antioxidants, estrogen, NSAIDs,
27
What antioxidants are thought to slow progression and how do they work?
–Vitamin E Recent meta-analyses suggest that high-dose Vit E (>400 IU/day) may increase all-cause mortality Recommendation: If used, dose = 400 IU/day –Selegiline Improvements similar to vitamin E in 1 study Recommendation: Not recommended as adjunctive tx
28
What is the recommendation for estrogen use?
Use only in pts who have another medical reason for HRT
29
How are NSAIDs best utilized?
–Evidence of delaying disease onset and progression, slowed rate of cognitive impairment –2 years of exposure necessary for protective effect --Recommendation: Do not use as treatment at this time…. Safety profile limits the use!
30
What is a proposed tx for prevention of AD and possibly vascular dementia?
Lipid-lowering agents
31
When are the lipid lowering agents actually recommended?
only in pts who have medical reason for lipid lowering, conflicting evidence
32
What is the proposed tx algorithm for mild AD?
–Donepezil, galantamine, rivastigmine, tacrine* or memantine –+ Vitamin E
33
What is the proposed tx algorithm for mod- severe AD?
–Donepezil, galantamine, rivastigmine or tacrine* alone OR donepezil in combination with memantine –+ Vitamin E –* tacrine no longer used due to hepatotoxicity
34
What are ways to evaluate the medication response in pts with AD?
1) MMSE –Average expected decline in AD is 2-4 points per year in an untreated patient –Halting progression or improvement over a 6-12 month time period during clinical trials would be considered response 2)ADAS-Cog –Average expected decline is 4pts at 6 months and 7pts at 1 year –Halting progression or improvement at 6 months or longer considered response
35
What are the MMSE scores the correlate with AD?
Mild AD ~20-25; Moderate AD 10-20; Severe AD
36
How are the ADAS-Cog and Severe Impairement Battery tests scaled?
0-70 0-100 ** higher scores= better cognition
37
What are the pharm tx for mild- mod AD?
Cholinesterase inhibitors
38
What are the pharm tx for mod- severe AD?
–Memantine +/- cholinesterase inhibitor | –donepezil
39
What are the cholinesterase inhibitors?
``` Tacrine (Cognex) –hepatotoxicity, don’t use anymore Donepezil (Aricept)- oral Galantamine (Reminyl)- oral Rivastigmine (Exelon)- oral or patch –No P450 interactions with metabolite ```
40
What is the profile of donepezil?
Long acting, selective for AChE, reversible inhibitor
41
What are the indications for donepezil?
Mild, moderate, and severe Alzheimer’s dementia
42
How is donepezil metabolized and why is this important?
Metabolized by CYP 2D6 and 3A4 –Minimal risk of clinically significant drug-interactions –Partial renal elimination
43
What are the indications for rivastigmine?
–Mild to moderate Alzheimer’s dementia | –Mild to moderate Parkinson’s dementia
44
What is rivastigmine selective for?
AChE (G1)
45
What is the profile for rivastigmine?
Pseudo-irreversible, non-competitive T1/2 = 1.5 hours Not significantly metabolized by CYP450
46
How is rivastigmine dosed?
–1.5mg twice daily with food | –Increase by 3mg/day in 2 week intervals as tolerated, up to 6mg twice daily
47
What is the MOA of galantamine?
Reversible, competitive inhibitor of AChE | Also stimulates nicotinic receptor sites
48
What are indications for galantamine?
Mild to moderate Alzheimer’s dementia
49
What is the dosing for galantamine?
–4mg twice daily with food (not an effective dose) | –Increase by 8mg/dy at 4 week intervals as tolerated, up to 12mg twice daily
50
How is galantamine metabolized?
Metabolized by CYP450 2D6 and 3A4
51
When should galantamine not be used?
patients with renal or liver impairment
52
What are the ADRs of the cholinesterase inhibs?
``` N/V Diarrhea Anorexia Dizziness Dyspepsia Agitation ```
53
What are some cautions with the cholinesterase inhibs?
Bradycardia –Monitor carefully in pts on concomitant medications that decrease heart rate Ulcers –Increased gastric acid secretion COPD or Asthma –bronchoconstriction Exaggerate succinylcholine neuromuscular blockade during anesthesia Anticholinergic medications will negate effects of cholinesterase inhibitors
54
What is the NMDA receptor antagonist?
Memantine
55
What is the MOA of memantine?
–Moderate-affinity noncompetitive receptor antagonist | Shows neuroprotective effects, slows rate of memory loss in vascular and Alzheimer’s dementia.
56
When is memantine indicated?
moderate to severe AD (MMSE 3-14)
57
What is the dosing for memantine?
–5mg once daily | –Increase by 5mg at weekly interval to a maximum daily dose of 20mg (10mg twice daily)
58
When should there be dose reduction with memantine use?
pts with renal impairment is recommended | CrCl 40-60 ml/min 5mg twice daily
59
How is memantine metabolized? What are the drug interactions?
Minimal CYP-450 metabolism | Use caution with other NMDA-antagonists (amantadine, ketamine, dextromethorphan)
60
What are the expected ADRs of memantine?
Agitation, insomnia, diarrhea, urinary incontinence, UTI
61
What is a good combo therapy for AD?
Memantine + Donezepil | Vitamin E
62
Why is vit E recommended?
–recommended as adjunctive treatment because of antioxidant properties –Potential effectiveness and favorable side effect profile –Doses of no greater than 400 International Units / day
63
Why do we care about small changes in cognition and functiong?
COST… thousands of dollars difference with increase and decline on the MMSE
64
What is the tx for BPSD (Behavioral and Psycological Symptoms of Dementia)?
Should try non pharm first No medications are approved to treat specifically Use low doses of antipsychotics in patients with dementia –Risperidone, olanzipine

Pharm3- fixed (12 decks)

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