COSI 357 Midterms: Pathophysiology

What is a TPA?

TPA: tissue plasminogen activator  → clot buster → needs to be within 4 hours of the clot happening in an ischemic stroke

Are you more likely to survive an ischemic or hemorrhagic stroke?

• More likely to survive ischemic stroke than an hemorrhagic stroke 

  • More easier to control a blockage than a hemorrhagic 

• If you survive a hemorrhagic stroke you are more likely to recover faster

  • If you survive it means that they've clipped the aneurysm and the bleeding has stopped 

  • Once the bleeding has stopped new pathways are going to be created → brain may need to compensate in a different way but it will get there 

    • Same could happen with ischemic if the TPA is administered but most of the time people don't go to the hospital in time 

How to check to know if someone is having a stroke?

• 1. Smile → want to see the symmetry of facial muscles → if one side is drooping it tells us something may be going on 

• 2. Raise Eyebrows → eyebrows should move up in symmetry → if only one moves up something is wrong 

• 3. Have them put their hands straight out and have them push up and down on hands → check symmetry of strength 

What can a TBI result in?

• Can result in increased intracranial pressure 

  • Hematoma → swelling of astrocytes 

  • Axonal Injury → if axons are being sheared we will have slow action potentials 

What are the neuropathological changes seen in alzheimer’s disease?

Alzheimer disease
• Most common cause of irreversible dementia
• Neuropathological changes
• Neurofibrillary tangles and neuritic plaques
• Temporal and frontal lobes, hippocampus and adjacent areas
• Tangles are first noticed in entorhinal cortex, hippocampal structures, basal forebrain, and cortical then cortical association areas as the disease progresses
• Plaques fist appear in cortical areas of frontal, temporal, and occipitial lobes
• Neuronal atrophy is also present

What are the two hallmarks of AD?

plaques and tangles

The brains of people with AD have an abundance of two
abnormal structures:
An actual AD plaque An actual AD tangle
• beta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cells
• neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell AD and the Brain

How are beta-amyloid plaques created?

Amyloid precursor protein (APP) is the precursor to amyloid plaque.
1. APP sticks through the neuron
membrane.
2. Enzymes cut the APP into fragments
of protein, including beta-amyloid.
3. Beta-amyloid fragments come together
in clumps to form plaques.
In AD, many of these clumps form,
disrupting the work of neurons. This
affects the hippocampus and other areas
of the cerebral cortex.

Describe the role of tau in forming the neurofibrillary tangles?

Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules to collapse, and tau proteins clump together to form neurofibrillary tangles

Are amyloid plaques unique to AD?

• Amyloid plaques are not unique to AD
• Prion Disease (e.g, Creutzfelf-Jakob AKA mad-cow
disease)
• Dementia pugilistica (AKA Boxers Syndrome)
• Can be found in brains of people with an AD diagnosis
• Necessary for dx, but not sufficient to account for
the degree of associated cognitive impairment

Are tangles unique to AD?

Also not unique to AD
 Frontotemporal dementia
 Corticobasal degeneration
 Progressive supranuclear palsy
 Dementia pugilistica
 Can be found in brains of individuals without AD
Tangles seem to be the pathological lesion most
closely correlated with the degree of dementia

What causes alzheimers disease?

No one knows what causes AD to begin, but we do know
a lot about what happens in the brain once AD takes hold.

Discuss the pathophysiology of Parkinson’s disease

• Parkinson's Disease 

  • Problem with our substantia nigra –. Part of brain responsible for creating dopamine 

  • Initiating motor movement and smooth movement 

  • People who have PD something that is very characteristic is the shuffle walk 

    • Hard time starting and then when they do their moves are fast and small 

      • Hyperkinetic dysarthria 

      • Medication that helps increase dopamine in area → but for it to be effective you need to take it 4 times a day and it can sometimes adversely affect things like memory and learning 

  • Problems with autonomic nervous system

    • Involuntary control are out of whack 

      • Drastic changes in blood pressure 

  • Motor first and then memory and learning issues later on 

• Starts somewhere and then there is a cascade effect that affects all other parts of the brain