6/16- CV Pathology and Pathophysiology Flashcards
What are Watershed zones?
Where is the worst?
Areas supplied by multiple arteries (but the very end of these arteries)
- Infarcts may result from hypotension
Worst = high posterior parietal cortex (“triple border zone area”)
What is the leading cause of ischemic strokes?
Atherosclerosis spawning emboli or thrombus formation (may be intracranial or extracranial)
What is this?
Carotid endarterectomy
- Atherosclerosis with complicated plaques
What is a “complicated” plaque?
What does it cause?
When an atherosclerotic plaque erodes through the endothelium
- Causes thrombogenesis
- May lead to emboli or breaking off or local thrombosis with occlusion of the vessel
What is a non-atherosclerotic cause of stroke?
Carotid dissection
- Blood leaves vessel, gets stuck within adventitia, and then compresses vessel lumen
Where do dissections usually occur?
Areas of trauma to the vessel
- e.g. struck in neck with baseball
- damage to back of throat (near carotid)
What are some symptoms seen in hypotensive ischemic injury?
“Watershed” or arterial border zone infarcts
- Dorsolateral aspects of the cerebral hemispheres
- “Man in a barrel” weakness
- Rims of the cerebellar hemispheres
If sufficiently severe, global damage with atrophy of neuron containing structures:
- Laminar necrosis
- Basal ganglia shrinkage
- Hydrocephalus ex vacuo
What is this?
Watershed infarct of high posterior parietal cortex (although can involve motor strip)
- Infarct = loss of tissue due to ischemia
- Enlarged sulci with shrunken gyri
What is this?
Result of global hypoperfusion
- Not much cortex left (innermost layers go first- laminar necrosis)
- No thalamus, caudate….
- Hydrocephalus ex vacuo
- Person would be unconscious; persistent vegetative state
What is this?
Sulcal depth discoloration seen in relative watershed
- Depth of sulcus is relatively less well perfused than surface
- Opposite of contusions (affect surface of gyri more)
Which cells are most vulnerable to ischemia?
Neurons >> Glia > Endothelium
- Purkinje cells of cerebellum
- Pyramidal neurons of CA1 (Sommer’s sector of the hippocampus)
- Middle layers of the cerebral cortex- laminar necrosis
Secondary mechanism of damage following ischemia?
Major contribution from excitotoxicity secondary to release of aspartate and glutamate
What is this?
Shows selective ischemic vulnerability of the neurons in the hippocampus
- Memory problems
What is this?
Acute Middle Cerebral Artery Infarct
- Discoloration in MCA territory
- Ventricular effacement
- Cingulate herniation
- Probably pretty proximal block, because so much area affected
- Pt’s life is endanger from brain swelling (may need hemi-craniectomy)
What is this?
Acute PCA stroke
- Posterior cerebral artery territory infarcts (mesial surface of temporal lobe)
- May result from emboli or thrombosis
Histopathology of Infarction: Temporal Evolution
- Day 1:
- Day 2- weeks:
- Weeks- months:
Day 1:
- Red neuron and rarefaction of neuropil (first sign/change that can be seen of infarction; light microscopy)
Day 2-weeks:
- Neuronal drop out
- Rarefaction of neuropil
- Influx of macrophages and fewer lymphocytes and poly’s
- Astrogliosis
- Vascular proliferation (beware of contrast ehancement!)
Weeks-months:
- Cystic cavity containing macrophages then CSF
- Wall of reactive astrocytes (reactive gliosis)
What is this?
Acute infarct with red neurons
- Earliest light microscopic change in CNS infarct
- Red cytoplasm
- No good Nissl substance anymore
What is this?
How long after stroke?
Remote middle cerebral artery infarct
Several months later
- Neurons/tissue cleared out by macrophages
- Large ventricle compensating for volume loss
- If this hits motor strip, person will probably be hemiparetic (face and arm worse than leg b/c ACA still okay)
What is this?
Wall of remote infarct cavity
- Macrophages (foamy cytoplasm)
- Rarefied tissue- not many cells
- Reactive astrocytes (big, bottom right) in wall; much cytoplasm- doing their best to wall off the cyst
What does this show?
Cerebral peduncle and medullary pyramid atrophy following MCA infarct
- Due to loss/degeneration of axons