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Neuro > Neuro AD done > Flashcards

Neuro AD done Flashcards

0
Q

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

A

Alzheimer’s disease.

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

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1
Q

A condition of progressive dementia resulting in:

A

• Impaired memory•
Cognition
• Behavior

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2
Q

AD is NOT

A

accelerated aging

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3
Q

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

A

AD

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4
Q

Is AD a natural part of aging?

A

No

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5
Q

Is AD fatal?

A

Yes

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6
Q

Does exposure to aluminum cause AD.

A

No

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7
Q

Only the elderly get AD?

A

No

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8
Q

Does aspartame cause AD?

A

No

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9
Q

Are there any therapies to stop the progression of AD?

A

No

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10
Q

Risk Factors

A
  • 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.
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11
Q

Converging studies reveal that risk factors for CVA &cardiovascular disease

A

overlap with AD

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12
Q

• 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

A

.

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13
Q

• Smoking triples the risk of AD

A

• # 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.

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14
Q

• 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

A

.

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15
Q

What are some suggested causes for AD?

A

Cause is unkown.

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

16
Q

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

A
  • Limbic system,emotions.
  • Hippocampus, STM to LTM
  • Thalamus, sensory deficit
  • Hypothalamus, Monitors body temp & appetite, and the body’s in-ternal clock
17
Q

What is the firsts tructure to see damage from AD.

A

The cerebral cortex

18
Q

What are two seposits that are found in the brain?

A

Amyloid and neurofibrillary tangles

19
Q

Other Neuropathic Findings are?

A
  • 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
20
Q

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

A

Two,

Acute and chronic.

21
Q

Explain acute dimentia.

A

sudden, reversible• 10% of all dementias are transient

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

22
Q

Explain chronic dimentia.

A
  • Chronic dementia – gradual, irreversible
  • Degenerative diseases (AD, PD, Huntington’s, NPH, etc)
  • Multi-infarct dementia / vascular dementia
  • Infections (AIDS, Neurosyphilis)
  • Head Trauma
  • Alcoholic dementia
23
Q

Characteristics of Reversible Dementia

Use the anacronym, DIEMENTIA

A
  • 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
24
Q

Ten Warning Signs of AD are?

A
  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.

25
Q

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

A

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

26
Q

Stage I: Early Stage (1-3 years)

A
  • 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
27
Q

Stage II: Moderate Stage (3-10 yrs)

A

• 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

28
Q

Stage III: Late Stage (8-10 yrs)

A

• 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.

29
Q

Stage IV: Terminal Stage

A
  • 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.

30
Q

Diagnosis

A

• 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.

31
Q

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

A

• 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

32
Q

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

A
  • Not considered to have AD, but are said to have MildCognitive Impairment (MCI).
  • 40% of MCI will develop AD w/in ~3 years.
33
Q

Medical Management

A

• 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

34
Q

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

A

Donepezil

Aricept

35
Q

Memantine
Namenda

Has side effects of?

A

Headache, constipation, confusion and dizziness.

36
Q

Tacrine

Cognex

A

Possible liver damage, nausea, and vomiting

37
Q

Galantamine, Razadyne
Donepezil, Aricept
Rivastigimine, Exelon

Side effects.

A

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

Neuro (21 decks)

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