Alzheimer's Disease, Dementia, and Delirium Flashcards Preview

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

Flashcards in Alzheimer's Disease, Dementia, and Delirium Deck (45)
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The focus of delirium care is

prevention and reserved for those that will harm themselves or others

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


Cognitive Impairment

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


Mild cognitive impairment

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



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


MCI Medication treatment vs Dementia

MCI not treated with any medication

Dementia can be treated with medications


Risk Factors of Dementia

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


Most common form of dementia

Alzheimer's Disease (60-80%)


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

Preserved, Preserved, Lost

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

Thinking and reasoning are preserved


Early Alzheimer's

Hippocampus (memory) is affected early

No language affect

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


Progression of Alzheiemer's (general)

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

*the areas affected are rich in cholinergic neurons


Histology of Alzheimer's

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


Amyloid beta (A-beta) protein formation

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


Neuronal cell bright parts (Tau proteins)

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

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


Cholinergic Hypothesis

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


Amyloid-Beta Hypothesis

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


Tau Hypothesis

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

*this hypothesis is gaining ground


Inflammation Hypothesis

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


The novel hypothesis

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)


AD is multifactorial with _____________

No single cause or cure

*similar to cancer in this regard


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

10 years


Early Onset AD

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


Preclinical AD

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


Mild Cognitive Impairment Due to Alzheimer's Disease

MMSE 22-26

Cognitive changes have occurred but no functional changes


Dementia due to Alzheimer's Disease

MMSE under 22

Functional Impairments have occurred


Mild AD (early-stage) Changes

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


Moderate AD (middle-stage) Changes

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


Severe AD (late-stage) Changes

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


AD vs Vascular Dementia

AD is steady decline in cognitive function, VD is not


Vascular Dementia

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)


PD and ______________ share the same pathology

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