week 12 part 2 Flashcards

1
Q

dementia

A

a group of progressive neurodegenerative chronic diseases
- impaired cognitive function

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2
Q

Alzheimer’s disease pathophysiology

A
  • progressive cortical atrophy
    0 critical loss of synapses that is especially pronounced in the hippocampus
  • amyloid plaque and tangle formation that builds up in the brain
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3
Q

beta-amyloid plaque

A
  • APP in found in the synapses of neurons
    (9 transmembranes)
  • enzymes come in a clever protein and now in the wrong place
  • now you have a clump together cause dysfunction and apoptosis
  • trigger immune response and results in neuron destruction
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4
Q

tangle

A
  • tangle manifest from normal functioning gone wrong
    -microbules dissociates
    -tau protein becomes over phosphorylated causing a misfolded
    -now become sticky and twist together
    -spread across synapses into healthy neurons and cause tau misfolding
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5
Q

Alzeimers disease pathophysiology

A

the inflammatory response adds to the destruction f neurons
Glial cells (microglia) are activated by plaques and tangles and release cytokines that attack
neurons. Glial cells also begin to phagocytose synapses of neurons, impacting transmission

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6
Q

flow chart

A
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7
Q

risk factors

A

nonmodifiable
-age and genetics
modifiable
-hypertension, obesity, smoking, depression, diet, hearing loss

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8
Q

insulin resistance

A

-risk of dementia of you have type 2 diabetes
-Insulin resistance due to impaired insulin signaling is a common characteristic of
both Type 2 Diabetes Mellitus and Alzheimer’s Disease

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9
Q

Cardiovascular health & dementia risk

A

Shared clinical risk factors
* Hypertension
* High Cholesterol
* Obesity
* Type 2 Diabetes
* Chronic Inflammation

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10
Q

vascular cognitive impairment and vascular dementia

A
  • decline of cognition corresponding to vascular
    ischemic events
    -
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11
Q

coup contrecoup injury

A

brain hits opposite sides of the skull

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12
Q

torque injury

A
  • head and neck twists
    -neurons of the reticular formation are most often affected
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13
Q

Concussion - Pathophysiology

A
  1. Many neurons injured due to blowing and/or shearing
  2. Spontaneous action potential firing (axons begin to leak ions)
  3. Excess Neurotransmitter Release
  4. Many neurons stimulated
  5. Massive increase in metabolic activity
  6. Neurons are damaged: remain in a low metabolic state for a period of time
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