Neuro AD done

Question 0

AD really stands for ___________, but we can say __________ to remeber it.

Answer 0

Alzheimer’s disease.

Aggressive dimentia, because this is what it is, dimentia.

Question 1

A condition of progressive dementia resulting in:

Answer 1

• Impaired memory•
Cognition
• Behavior

Question 2

AD is NOT

Answer 2

accelerated aging

Question 3

What kind of dimentia is the most common for the elderly?

Answer 3

AD

Question 4

Is AD a natural part of aging?

Answer 4

No

Question 5

Is AD fatal?

Answer 5

Yes

Question 6

Does exposure to aluminum cause AD.

Answer 6

No

Question 7

Only the elderly get AD?

Answer 7

No

Question 8

Does aspartame cause AD?

Answer 8

No

Question 9

Are there any therapies to stop the progression of AD?

Answer 9

No

Question 10

Risk Factors

Answer 10

• Age
• Genetics
• Family History
• Gender: Women > Men
• Level of education (a protective factor)• Higher education less incidence, because they stimulate their brains more.
• History of head injury/trauma, so there is damage there.
• Exposure to heavy metals & toxins, same as in heavy metal concerts that they shake their heads alot.

Question 11

Converging studies reveal that risk factors for CVA &cardiovascular disease

Answer 11

overlap with AD

Question 12

• High cholesterol & LDL, HTN, DM
• inc levels of homocysteine, a risk factor for heart
disease, is associated w/ risk of AD
• Suppression of cholesterol by statin drugs reducesformation of plaques & lowers risk of AD

Answer 12

.

Question 13

• Smoking triples the risk of AD

Answer 13

• # of β-amyloid neuritic plaques w/ amount of smoking

So there are tarry blackness on one’s lungs, so there are tarry blackness in one’s brain.

Question 14

• Social Risk Factors: Loneliness linked to AD

• Environmental Risk Factors:
• Exposure to second-hand smoke• Environmental pollutants

• Hormone Therapy in any form before age 65• Lowers the risk by half

Answer 14

.

Question 15

What are some suggested causes for AD?

Answer 15

Cause is unkown.

But genetics is a strong indicator.
An improper processing of amyloid.
And aging.

Question 16

What are four areas of the brain that are affected by AD and the associated dysfunctions that we would expect?

Answer 16

• Limbic system,emotions.
• Hippocampus, STM to LTM
• Thalamus, sensory deficit
• Hypothalamus, Monitors body temp & appetite, and the body’s in-ternal clock

Question 17

What is the firsts tructure to see damage from AD.

Answer 17

The cerebral cortex

Question 18

What are two seposits that are found in the brain?

Answer 18

Amyloid and neurofibrillary tangles

Question 19

Other Neuropathic Findings are?

Answer 19

• Widespread cortical depletion of ACh, its like Ach, my head hurt and it now all ADs up.
• Areas of brain involved initially include hippocampus, neocortex, amygdala, & basal nucleus of Meynert
• Eventually spread to cerebral cortex
• Cerebral atrophy

Question 20

How many types of dimentia do we have? And whata ee these types?

Answer 20

Two,

Acute and chronic.

Question 21

Explain acute dimentia.

Answer 21

sudden, reversible• 10% of all dementias are transient

Its like a cold, it comes on quickly and it goes away.

Question 22

Explain chronic dimentia.

Answer 22

• Chronic dementia – gradual, irreversible
• Degenerative diseases (AD, PD, Huntington’s, NPH, etc)
• Multi-infarct dementia / vascular dementia
• Infections (AIDS, Neurosyphilis)
• Head Trauma
• Alcoholic dementia

Question 23

Characteristics of Reversible Dementia

Use the anacronym, DIEMENTIA

Answer 23

• Drug use (meds S/E)
• Emotional disorders (depression)
• Metabolic disorders (electrolyte imbalance)
• Endocrine disorders (hyper/hyposecretions)
• Nutritional disorders (Vitamin B12 deficiency)• Trauma or tumor
• Infection (UTI, acute bronchitis)
• Alcoholism

Question 24

Ten Warning Signs of AD are?

Answer 24

1. Recent memory loss affecting job skills hipposcampus 2. Difficulty performing familiar tasks hipoocampus 3. Problems with speech & language, 4. Disorientation of time & place, hipoocampus, 5. Poor or decreased judgment 6. Problems with abstract thinking 7. Misplacing things, hippocampus 8. Changes in personality hippocampus 9. Mood & behavior changes, hippocampus 10. Loss of initiative There seems to be alot of problems with the issue of the memeory.

Question 25

Cahnges between satge I and stage II and stage III AD?

Answer 25

They are basicaly the progression of each other. That I is the start of the memory loss but we cannot really fnd any imaging problems. II there mild • Moderately Enlarged Ventricles• Cortical Shrinkage • Hippocampal Shrinkage. And III is severe • Severely Enlarged Ventricles • Extreme Cortical Shrinkage • Extreme Hippocampal Shrink-age

Question 26

Stage I: Early Stage (1-3 years)

Answer 26

* Forgetfulness & mild memory deficit * Difficulty w/ novel or complex tasks, new tasks * Apathy & social withdrawal, lack of spontaneity * Repeating same thing over & over again, maybe because the person forgot that they had done it. * Emotional lability, moodiness, hypochondriasis * Time disorientation * judgment, problem solving, abstract thinking * May display catastrophic reactions to stressful events

Question 27

Stage II: Moderate Stage (3-10 yrs)

Answer 27

• Moderate to severe objective memory deficit, a more severe progression of stage I • Disorientation to time & place, more of stage I • Restless & wanders aimlessly, sundowning, paranoia, hallucinations, sleep pattern disturbances, impulse control • Personality & behavioral changes, mpre of stage I • Language disturbance, visuoconstructive difficulty & apraxia • Inability to learn new things, very similar to stage I • Requires supervision, major A big change is that they wonder and they hallucinate and now require supervision

Question 28

Stage III: Late Stage (8-10 yrs)

Answer 28

• Intellectual functions virtually untestable • Verbal communication severely limited • Incapable of self-care • Physical impairment • Difficulty swallowing • Weight loss • Incontinence of B/B • Inability to recognize family members • Return of primitive reflexes: • Reversal of encephalization process of childhood, whereby primitive reflexes fade as higher cortical ar-eas take control over lower subcortical centers • In AD, positive release from higher control re- emergence of primitive reflexes • “Once a man, twice a child” That a person is a child a man and now a child again.

Question 29

Stage IV: Terminal Stage

Answer 29

* Loss of all abilities – speech, motor, perceptual• Unaware of environment * Mute * Abulic * Bedridden * Joint contractures * Pathological reflexes * Myoclonus * Loss of “self” Stage III was reverting back to a child, but now he is like reverting back to even before birth, not living.

Question 30

Diagnosis

Answer 30

• Definitive diagnosis of AD can only be made on autopsy. • Current tools for diagnosing AD: • Detailed patient history – symptoms • Detailed history of illness from family/friends • R/O other non-AD causes thru physical & neurological exams and lab tests • CT or MRI to r/o strokes, tumors • Conduct neuropsychological testing to assessmemory, language, & other cognitive domains So see if they have had a history of this, and see if they are exhibiting any of the signs and symptoms of this disease.

Question 31

Criteria for “Probable” AD (accuracy of 85%)

Answer 31

• Dementia confirmed by clinical & neuropsych exam • Problems in at least 2 areas of cognition • Progressive worsening of memory & other cognitive domains • No disturbances of consciousness (no “blacking out”) • Sx beginning btw ages 40 to 90, usually after 65 • No other d/o that can account for the dementia

Question 32

Some aging older adults develop memory deficits | greater than their expected age norm, but w/o personal-ity changes or cognitive problems that characterize AD

Answer 32

* Not considered to have AD, but are said to have MildCognitive Impairment (MCI). * 40% of MCI will develop AD w/in ~3 years.

Question 33

Medical Management

Answer 33

• Anticholinesterase therapy (Cognex, Aricept, Exelon, Razadyne) • Used to block the enzyme that normally degradesthe neurotransmitter ACh • Memantine (Namenda) • Regulates excess glutamate activity • Glutamate also involved in memory functions • Used for treatment of moderate to severe AD • Amphetamines (Ritalin or Dexedrine) • Given for abulia or inattention • Benzodiazepines (Ativan) • Given for behavior control related to agitation and confusion • Anti-Inflammatories (NSAIDS, glucocorticoids) • Limit neurodegeneration • Neuroprotective & Neurotrophic factors • Nerve Growth Factors (NGF) • Enhances survival of cholinergic neurons• Antioxidants – also neuroprotective • Vitamins E & C • Co-enzyme Q10

Question 34

Which med is the one that is approved for all stages?

Answer 34

Donepezil | Aricept

Question 35

Memantine Namenda Has side effects of?

Answer 35

Headache, constipation, confusion and dizziness.

Question 36

Tacrine | Cognex

Answer 36

Possible liver damage, nausea, and vomiting

Question 37

Galantamine, Razadyne Donepezil, Aricept Rivastigimine, Exelon Side effects.

Answer 37

Nausea, vomiting, loss of appetite and increased frequency of bowel movements.