Exam 3: Dementia/Delirium

Question 1

Define dementia

Answer 1

A general term for the impaired ability to remember, think, or make decisions that interferes with doing everyday activities.

Question 2

what areas are affected by dementia and delirium?

Answer 2

-2) temporal lobe: Association area: short term memory, equilibrium, emotion

-13) frontal lobe: High mental functions: concentration, planning, judgement, emotional expression, creativity, inhibition

Question 3

what does the reticular activating system maintain?

Answer 3

– maintains wakefulness

**in dementia and delirium–>RAS is sometimes off kilter

Question 4

what are neurons? and how do they communicate?

Answer 4

they are functional cells of the CNS that send and receives information, they are supported by glial cells

• long axons synapses with another neuron and communication goes back and forth between neurons along the axons

Question 5

what are the three types of glial cells? and its functions

Answer 5

-microglial: phagocytes–cells that go through the CNS and check for abnormalities and correct them

-astrocytes: blood vessel support and communication

• oligodenocytes: myelin sheath production

Question 6

what are irreversible dementia?

Answer 6

• alzheimer
• frontotemporal
• Lewy body

Question 7

what are most common reversible dementia?

Answer 7

-Alcoholism (chronic)

-Medications: Anticholinergics and antihistamines (typically used inappropriately in older adults)

-Metabolic diseases: Hypothyroidism and hepatic encephalopathy (complication of etoh)

Question 8

what are the mechanisms of Irreversible degenerative dementia?

Answer 8

• Abnormal proteins that damage neurons and/or neuronal connections leading to neuronal cell death

**the global pathophysiology for dementia of the irreversible type is abnormal protein

Question 9

molecular mechanism of Alzheimer

Answer 9

• amyloid beta protein
• phosphorylated tau protein

Question 10

pathology of Alzheimer

Answer 10

amyloid plaques, neurofibrillary tangles, neuronal and synaptic loss in the brain

Question 11

molecular mechanism of dementia with Lewy bodies

Answer 11

alpha-synuclein

Question 12

pathology of dementia with Lewy bodies

Answer 12

alpha-synuclein inclusions (Lewy bodies)

Question 13

molecular mechanism of behavioral variant frontotemporal dementia

Answer 13

microtubule-associated protein tau (MAPT)

Question 14

pathology of frontotemporal dementia (3)

Answer 14

• tau inclusions
• pick bodies
• neurofibrillary tangles

Question 15

what are the most common dementias associated with?

Answer 15

Genetic risks exist but the most common dementias are associated with susceptible genes and multifactorial contributions.

Here’s the expression: “The genes load the gun and the environment and lifestyle pull the trigger.” The truly horrific, early onset, causal gene dementias typically involve an autosomal dominant allele and clear familial transmission

Question 16

manifestations of dementia

Answer 16

classics are insidious onset (core feature) and progressive decline of cognition, memory, and ability to care for self.

insidious onset–>means slow, its gradual, it sort of sneaks up on you

Question 17

what are the screening test for dementia? (2)

Answer 17

• mini mental status exam
  -montreal cognitive assessment

Question 18

Abnormal proteins associated with Alzheimer disease

Answer 18

i. Beta amyloid plaque: Amyloid precursor protein (APP), a cell wall glycoprotein, is cleaved by enzymes → beta amyloid protein fragment. Fragments aggregate outside the neuron producing amyloid plaque.
ii. Neurofibrillary tau tangles: The axon is composed of microtubules that send signals from one neuron to another. Tau protein makes up the structure of the microtubule. Tau protein structure altered, microtubules disrupted, tau collects inside the neuron.
iii. Results on beta amyloid and tau: Impaired cell to cell communication and eventually cell death.

Question 19

what is the pathophysiology of alzheimer’s dementia?

Answer 19

Abnormal proteins damage the 1. neuron cell body and 2. Axons. Neuron to neuron signaling and neuron death occurs.

Question 20

what can occur when more neurons die throughout the brain?

Answer 20

people may express:
- memory loss
- impaired decision making
- language problems

Question 21

what is used to diagnose Alzheimer?

Answer 21

a. History, physical exam, blood work, genetic testing in people with family history, and memory (MMSE or MOCA)/psychiatric testing to rule out reversible causes of dementia.

b. Diagnostic and Statistical Manual V (DSM-V): Core characteristics insidious onset and gradual decline AND cognitive impairment in two of the following domains:

• MRI: brain atrophy, sulci (furrows) widening, gyri (folds) shrinking and ventricle enlarging
  -Positron emitting tomography (PET) using tracers to detect amyloid plaque and neurofibrillary tau tangles. Required to qualify for newer drugs that clear amyloid plaque (Aducanumab (Aduhelm)).

Question 22

lis the five Diagnostic and Statistical Manual V (DSM-V) domain for dementia

Answer 22

i. Acquiring and remembering new information: short term memory loss (first impairment)–temporal lobe
ii. Reasoning, judgement, and complex thinking–frontal lobe
iii. Visual special perception
iv. Language use and expression
v. Personality or behavior

Question 23

what area of the brain does Alzheimer affect?

Answer 23

• changes start in the temporal lobe/hippocampus (memory) and progress toe involve the entire cerebral cortex

Question 24

biomarks for Alzheimers disease (2)

Answer 24

i. Cerebrospinal fluid: Amyloid beta and tau proteins.
ii. Plasma: Still in investigative stage.

Question 25

usual age of onset for Alzheimers disease

Answer 25

~ 60 years old **On average, individual will live 4-8 years from diagnosis (~ 60) to death (5th leading cause of death for those 65+). Sometimes termed “the long goodbye.”

Question 26

does mild cognitive impairment disease mean someone has Alzheimers?

Answer 26

No Mild cognitive impairment: Changes in thinking that are recognized by patient and family and may represent a precursor to Alzheimer disease or natural effect of old age

Question 27

manifestions: Alzheimer disease: Mild

Answer 27

Individual able to function (work, drive, social interaction) and is aware of difficulties with: i. recalling recently learned material (three-word recall), name recall ii. word finding iii. losing or misplacing items iv. task completion

Question 28

manifestations: Alzheimer disease: Moderate

Answer 28

Progressive worsening of symptoms + personality changes. Needs help with ADLs. i. forgetful about personal history ii. disoriented and day/night pattern disruption, wandering iii. behavioral and psychological changes – fearful, suspicious iv. assistance needed for self-care: hygiene, clothing, toileting

Question 29

manifestations: Alzheimer disease: Severe.

Answer 29

Unable to care for self. i. Loss of awareness of experiences/surroundings/family ii. Decreased ability to communicate -> non-verbal iii. Physical motor abilities lost: Completely dependent, bedridden, impaired swallowing ( can lead to pna, which is common cause of death)

Question 30

pathophysiology of Lewy body dementia

Answer 30

Alpha synuclein protein cluster together forming Lewy bodies. Lewy bodies damage dopamine mediated cell-to-cell communication especially in the cerebral cortex, amygdala (mood), and hippocampus (memory and learning).

Question 31

what are the diagnosis for Lewy body dementia?

Answer 31

a. History and physical: Similar to Alzheimer disease. b. Single Photon emission computed tomography (SPECT) scan for dopamine transport in the brain and where dopamine is inhibited c. DSM-V: Neurocognitive disorders with Lewy bodies. Core characteristics: Insidious onset and gradual decline.

Question 32

DSM-V: Neurocognitive disorders with Lewy bodies. Diagnostic features:

Answer 32

i. Fluctuating cognition ii. Visual hallucinations: Vivid, well formed, detailed iii. Spontaneous parkinsonism starting after cognitive decline iv. REM sleep disorders: “My dream is more real than your reality.” v. Overly sensitive to antipsychotic medicines (explanation – many antipsychotics decrease dopamine worsening underlying pathophysiology of Lewy body dementia)

Question 33

usual age of onset for Lewy body dementia

Answer 33

~ 50 years old **On average, individual will live 4-8 years from diagnosis (~ age 50+) to death.

Question 34

what does both Alzheimers and Lewy body lack?

Answer 34

they both lack dopamine, but it impacts different areas of the brain

Question 35

compare and contrast Lewy body dementia and Parkinson disease

Answer 35

- Lewy body dementia: cognitive changes precede motor symptoms - Parkinson disease: motor symptoms precede cognitive changes

Question 36

what is the classification of frontotemporal dementia?

Answer 36

Heterogeneous condition associated with degeneration of the frontal and temporal lobes. a. Behavioral variant FTD (bvFTD) b. Primary progressive aphasia: i. Semantic variant ii. Non-fluent variant

Question 37

pathophysiology of frontotemporal dementia

Answer 37

Tau inclusions and neurofibrillary tangles damage and destroy cells of the frontal and temporal lobe. Dead neurons clump together to form Pick cells. Localized decreased brain volume, deep sulci and narrow gyri.

Question 38

diagnosis of FTD

Answer 38

a. History and physical: Similar to Alzheimer disease. b. Based on clinical presentation/manifestations.

Question 39

usual age of onset for FTD

Answer 39

Insidious onset, gradual decline often starting age 45+, mean survival ~ 5 years.

Question 40

clinical presentation/manifestations: Behavioral variant FTD (4)

Answer 40

- Loss of executive function: Problems planning and sequencing (thinking through which steps come first, second, and so on) Difficulty prioritizing tasks or activities. - Perseveration/compulsiveness; Hyperorality: Repeating the same activity or saying the same word over and over. - Disinhibition: Acting impulsively or saying or doing inappropriate things without considering how others perceive the behavior - Apathy/inertia; loss of sympathy/empathy: Becoming disinterested in family or activities they used to care about.

Question 41

clinical presentation/manifestations: Semantic version PPA (primary progressive aphasia)

Answer 41

Fluency of speech intact with impaired single word comprehension. May cross over to poor/indistinct representations in drawn objects e.g. “Would you like a hamburger?” “What’s a hamburger?” “Draw a bird.” Drawn picture lacks detail of beak, wings, and tail.

Question 42

clinical presentation/manifestations: Non-fluent version PPA (primary progressive aphasia)

Answer 42

minimal speech with comprehension intact

Question 43

define delirium

Answer 43

A syndrome characterized by an acute change in attention, awareness and cognition. Delirium commonly occurs in hospitalized patients with premorbid factors and precipitating events (presenting illness or hospitalization) **it is acute not insidious

Question 44

State four major mechanisms of delirium.

Answer 44

1. Neuronal networks disrupted: Increased brain vulnerability and decreased brain resilience. Age and neurological diseases (acute or chronic) 2. Vascular dysfunction and metabolic insufficiency: Brain energy requirements not met: Impaired oxygen and glucose delivery and/or increased cerebral metabolic demand. 13 3. Inflammatory effect of glial cells: Pathogen associated (PAMP) or damage associated molecular patterns (DAMP) initiate widespread inflammatory response and tissue damage. 4. Drugs & stressors → neurotransmitter imbalance

Question 45

List the five DSM-V domains for delirium

Answer 45

a. disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment). b. disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and fluctuates in severity during the course of a day. c. additional disturbance in cognition (e.g. memory deficit, disorientation, language, visuospatial ability, or perception). d. disturbances in criteria a and c are not better explained by a pre-existing, established or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of arousal, such as coma. e. evidence from the history, physical examination or laboratory findings that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal, or exposure to a toxin, or is due to multiple etiologies.

Question 46

what are prevention models for delirium?

Answer 46

1. hospital elder life program (HELP) 2. ABCDEF bundle

Question 47

what is hospital elder life program?

Answer 47

A multi-disciplinary team approach that addresses the following risks for delirium in hospitalized, older adults: visual and hearing impairment, immobility, disorientation, sleep deprivation (non-pharmacological) and dehydration. visual and hearing impairment, Outcomes: Reduction in delirium (5%) and fewer falls