Anatomy and Physiology XIII Flashcards
How is vasospasm due to blood breakdown of subarachnoid hemorrhage treated?
With nimodipine (calcium channel blocker) (p.424)
What most commonly causes intraparenchymal (hypertensive) hemorrhages?
Systemic hypertension most commonly (p.424)
Name three causes of intraparenchymal hemorrhages other than the most common cause.
Amyloid angiopathy, vasculitis, neoplasm (p.424)
Where do intraparenchymal hemorrhages most commonly occur?
In the basal ganglia and internal capsule, but can also be lobar (p.424)
What is another name for intraparenchymal hemorrhages of the internal capsule?
Charcot-Bouchard aneurysms of the lenticulostriate vessels (p.424)
After how much time of hypoxia does irreversible brain damage begin?
After 5 minutes of hypoxia (p.425)
What areas of the brain are most vulnerable to hypoxia?
The hippocampus, neocortex, cerebellum, and watershed areas (p.425)
What is seen in brain tissue of ischemic disease/ stroke 12-48 hours after the ischemic event?
Red neurons (p.425)
What is seen in brain tissue of ischemic disease/ stroke 24-72 hours after the ischemic event?
Necrosis and neutrophils (p.425)
What is seen in brain tissue of ischemic disease/ stroke 3-5 days after the ischemic event?
Macrophages (p.425)
What is seen in brain tissue of ischemic disease/ stroke 1-2 weeks after the ischemic event?
Reactive gliosis and vascular proliferation (p.425)
What is seen in brain tissue of ischemic disease/ stroke greater than 2 weeks after the ischemic event?
Glial scar (p.425)
Describe the CT findings of stroke.
Dark on non-contrast CT in approx. 24 hour.s. Bright areas on noncontrast CT indicate hemorrhage (tPA is contraindicated) (p.425)
Describe the MRI findings of stroke.
Bright on diffusion-weighted MRI in 3-30 minutes and remains bright for 10 days (p.425)
How does atherosclerosis lead to ischemic brain disease/ stroke?
Thrombi lead to ischemic stroke with subsequent necrosis. Cystic cavity forms with reactive gliosis (p.425)