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Pharmacy School 2016-17 > Alzheimer's Disease, Dementia, and Delirium > Flashcards

Alzheimer's Disease, Dementia, and Delirium Flashcards

1
Q

The focus of delirium care is

A

prevention and reserved for those that will harm themselves or others

*medication in delirium has been known to increase risk of death

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2
Q

Cognitive Impairment

A

A deficit in cognitive function (memory, ability to reason, planning, attention, language, executive function, visuospatial perception)

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3
Q

Mild cognitive impairment

A

A drop from a prior level of cognitive function

*Cognitive function declines with age

**If a scientific study does not measure a prior level of function, an MCI cannot be defined

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4
Q

Dementia

A

Mild cognitive impairment plus the loss in the ability to care for one’s self

This includes activities of daily living: Eating, bathing, grooming, toileting, transferring and cooking

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5
Q

MCI Medication treatment vs Dementia

A

MCI not treated with any medication

Dementia can be treated with medications

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6
Q

Risk Factors of Dementia

A

Genetics (Apolipoprotein E variants e2, e3 and e4; single copy of e4 increases risk by 3 fold while homozygous copy of e4 increase by 8-12 fold; family history of CV also increases risk)

Cardiovascular Disease in Middle Age (Smoking, midlife obesity, midlife hypertension, midlife hyperlipidemia, diabetes)

Mild cognitive impairment will increase risk of dementia; Education and social interaction increase cognitive reserve

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7
Q

Most common form of dementia

A

Alzheimer’s Disease (60-80%)

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8
Q

In normal aging, neurons are ________, brain mass is ________ and synaptic connections are __________.

A

Preserved, Preserved, Lost

Result is slowed retrieval of memories but no impairment of storing them

Thinking and reasoning are preserved

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9
Q

Early Alzheimer’s

A

Hippocampus (memory) is affected early

No language affect

Ventricles begin to enlarge and sulci get wider as more cells die

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10
Q

Progression of Alzheiemer’s (general)

A

Memory first, followed by language and then reasoning/understanding, lastly is dis-inhibition and behavior problems

*the areas affected are rich in cholinergic neurons

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11
Q

Histology of Alzheimer’s

A

Amyloid beta peptide abnormally fold, causing insoluble plaques that accumulate on the outside of cells

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12
Q

Amyloid beta (A-beta) protein formation

A

Amyloid Precursor Protein (APP) cleaved by b-secretase then by y-secretase to give Amyloid-beta(42) which is highly plaque forming due to insolubility

When APP is cleaved by a-secretase instead, it gives rise to b-amyloid 40 which is more soluble and less plaque forming

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13
Q

Neuronal cell bright parts (Tau proteins)

A

Hyperphosphorolated tau proteins represent the bright parts and work to stabilize microtubules

Microtubules transport molecules and nutrients within the cell, axon and dendrites

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14
Q

Cholinergic Hypothesis

A

Loss of cholinergic neurons is responsible for AD (considered a downstream event)

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15
Q

Amyloid-Beta Hypothesis

A

A-beta is the initial pathology leading to inflammation and neuronal death

*Almost all adults have A-beta and A-beta load does not correlate with AD symptoms

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16
Q

Tau Hypothesis

A

Tau-hyperphosphorylation and neurofibillary tangles is the single common pathway that leads to AD

*this hypothesis is gaining ground

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17
Q

Inflammation Hypothesis

A

Inflammation is common inn AD; Nonspecific inflammation damages neurons causing A-beta and NFT

*many believe this to be a marker of neuronal damage rather than a cause

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18
Q

The novel hypothesis

A

Impaired glucose transport (brain uses 20% of body’s energy and is only 2% of it’s weight) > Disruption of energy formation can lead to oxidative stress, free radicals, inflammation and neuronal death > insulin resistance (diabetes) and decreased brain blood flow (vascular disease)

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19
Q

AD is multifactorial with _____________

A

No single cause or cure

*similar to cancer in this regard

20
Q

There is approximately a _____________ delay between the pathology and symptoms in AD

A

10 years

21
Q

Early Onset AD

A

5% of all AD patient symptoms start before 65 years, but it can start in the 30s

Genetics is a strong influence (familial AD) - APP as well as Presenilin Genes 1 and 2 (PSEN -1, -2)

Diagnosis can be difficult and often misdiagnosed

Will need support and are often still working

No qualification for medicare

22
Q

Preclinical AD

A

MMSE of 30-26

No symptoms have occurred, only biomarker changes (e.g. A-beta or tau in the BBB or CSF; MRI of the brain)

This is controversial classification since there is no agreed upon biomarker

23
Q

Mild Cognitive Impairment Due to Alzheimer’s Disease

A

MMSE 22-26

Cognitive changes have occurred but no functional changes

24
Q

Dementia due to Alzheimer’s Disease

A

MMSE under 22

Functional Impairments have occurred

25
Q

Mild AD (early-stage) Changes

A

Problems coming up with the right word or name

Trouble remembering the names when introduced to new people

Having greater difficulty performing tasks in social or work settings

Forgetting material that one has just read

Losing or misplacing a valuable object

Increasing trouble with planning or organizing

26
Q

Moderate AD (middle-stage) Changes

A

Forgetfulness of events or about one’s own personal history

Feeling moody or withdrawn, especially in socially or mentally challenging situations

Being unable to recall their own address or telephone number or the high school or college from which they graduated

Confusion about where they are or what day it is

The need for help choosing proper clothing for the season or the occasion

Trouble controlling bladder and bowels in some individuals

Changes in sleep patterns, such as sleeping during the day and becoming restless at night

An increased risk of wandering and becoming lost

Personality and behavioral changes, including suspiciousness and delusions or compulsive, repetitive behavior like hand-wringing or tissue shredding

27
Q

Severe AD (late-stage) Changes

A

Require full time, around the clock assistance with daily personal care

Lose awareness of recent experiences as well as of their surroundings

Require high levels of assistance with daily activities and personal care

Experience changes in physical abilities, including the ability to walk, sit, and eventually swallow

Have increasing difficulty communicating

Become vulnerable to infections, especially pneumonia

28
Q

AD vs Vascular Dementia

A

AD is steady decline in cognitive function, VD is not

29
Q

Vascular Dementia

A

Accounts for around 10-20% of all dementias and is caused by cerebrovascular infarcts or narrowing of the arteries that is progressive

Symptoms are dependent on where infarct is; memory generally preserved until later; motor symptoms can co-occur

Symptom progression is stepwise and associated with a new infarct or narrowing of an artery

Often co-occurs with other dementias (co-prevalence with AD is very common due to sharing of many risk factors)

30
Q

PD and ______________ share the same pathology

A

Lewy Body Dementia

Caused by abnormal folding of alpha-synuclein protein

Inattention, executive dysfunction and visuospatial impairment

Visual hallucinations are more common; memory loss is more prominent

Lewy bodies are seen in later PD and often develop into Lewy body dementia

31
Q

Frontotemporal Dementia

A

Was called Pick’s disease as described by Arnold Pick

Accounts for 2% of all dementias

One of the most common forms of early-onset dementia, as prevalent as AD in those under 65

Social behavior and personality changes (disinhibition, apathy, loss of empathy)

Aphasia (difficulty finding words, halting speech)

Often confused with depression

Does well on cognitive testing, memory and executive function are preserved

32
Q

Treatment options

A

*all approved for AD, but we used them for dementia

Cholinesterase Inhibitors (Donepzil, Galatamine, Rivastigmine, Tacrine - no longer marketed due to hepatotoxicity)

NMDA antagonist (memantine) - FDA approved for moderate to severe AD

33
Q

ChEIs

A

Cholinesterase Inhibitors MOA: Increase ACh at synaptic cleft helping with loss of cholinergic neurons

All have same efficacy (does not increase functioning, about 6 months of delayed symptoms)

None are disease modifying (if removed from treatment, patient would return to lower level of functioning as if they were never on drug)

Choice is based on tolerability (Donepezil appears to be more tolerated than oral Rivastigmine, Galantamine is in between)

34
Q

Cholinesterase Inhibitors Adverse Effects

A

Cholinergic Side Effects

GI: NVD (up to 50% for Rivastigmine; dose limiting, increase dose every 4-6 weeks)

Anorexia, weight loss, abdominal pain

Bradycardia, dizziness, syncope, falls, accidents

Muscle tremor, weakness, and urinary incontinence (only 3%)

Insomnia, vivid dreams (up to 15%)

35
Q

Donepezil (dosage form, strength, etc.)

A

Tablet or ODT

5mg orally, once daily

Target dose 10mg/day, increased every 4-6 weeks, up to 23mg after 3 months of treatment

Generic available

36
Q

Rivastigmine Patch (dosage form, strength, etc.)

A

Patch

  1. 6 mg/24 hours starting
  2. 5 mg/24 hours starting dose, increased after 4 weeks

Can cause rash so rotate sites; fewer side effects than tablet

37
Q

Rivastigmine Oral

A

Tablet or oral solution

Start at 1.5 mg twice daily

Target 6 mg twice daily (increased 2-4 weeks by 1.5 mg twice daily)

Give with meals

Generic avilable

38
Q

Galantamine (dosage form, strength, etc.)

A

IR, tab or solution, ER

Start 4 mg bid (8 mg qd for ER)

Target 12 mg bid (or 24 qd) and may be increased by intervals of 4 mg (8mg) monthly

Give with meals

Generic Available

39
Q

Memantine

A

NMDA receptor modulator

Overstimulation by glutamate can cause excitotoxicity and neuronal death (memantine only binds once the ion channel is open, blocks the channel and prevents overstimulation)

Hypothetically could be disease modifying

Can be added to ChE inhibitor (only modest improvement and usually reserved for severe dementia)

*efficacy is no greater than ChE inhibitor alone in monotherapy

40
Q

Memantine AEs and Considerations

A

Efficacy similar to ChE inhibitors

AE are very mild in comparison

41
Q

Treatment Summary

A

ChE inhibitors are first line (generic available, efficacy is same, high rate of AEs with rivastigmine tablet having the most)

Memantine is second-line (first generic now available, some improvement in efficacy in combo, better tolerated than ChE inhibitors )

42
Q

Targets for Research (B-A)

A

B-A cascade (AN1792 vaccine against B-A protein ended due to encephalopathy, no improvement in cognition)

IVIG administration showed less brain atrophy and less loss of cognitive function at 1 year, but not 2 years (less progressed to AD)

Posiphen prevents APP formation while vaccines clear B-A from the brain

43
Q

Targets for Research (Tau)

A

Aggregation inhibitors (Methylthionium chloride)

Phase 2 trials showed an 81% decrease in progression compared to placebo

TRx0237 is a prodrug for Methylthionium chloride in phase 3 trials

44
Q

Targets for Research (Insulin)

A

SR-Exenatide in phase 1

Nasal insulin phase 2/3 studies in MCI and early AD patients, however, currently the study is halted for unknown reasons

Kaiser is studying Metformin in diabetic patients and decreased risk of AD

45
Q

Targets for Research (Inflammation)

A

Statins, NSAQIDs, unsuccessful and probably too far down AD pathway

Pharmacy School 2016-17 (22 decks)

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