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53 Cards in this Set

  • Front
  • Back
What CNS Cell has selective vulnerability to hypoxia/ischemia?
Neuron
What part of the brain is particularly vulnerable to hypoxia/ischemia? What subsection? Which subsection is most resistant
The Hippocampus...CA1. CA2
What is the second most vulnerable part of the brain susceptible to hypoxia/ischemia? What cell type?
Cerebellar Cortex. The Purkinje Layer.
What is the third most vulnerable region of the brain to ischemia?
Cerebral Cortex
Neurons are the most susceptible cell to hypoxia/ischemia in the brain. Which is the next most susceptible?
Myelin (oligiodenroglial cells)
What cell types proliferate in ischemic damage?
Endothelial cells, Astrocytes, microglial cells
What is the change in neurons as a result of damage to axons because of backflow, which pushes RNA back into cell body?
Central Chromatolysis
Which cell type has a "fried egg" appearance?
Oligodendrocytes
What sort of change do Microglial cells undergo during an early stage of activation? What does this cause?
Rod Cells. Microglial nodules and neuronophagia (encephalitis only).
What are Gitter Cells?
Lipid laden macrophages from degraded myelin.
what is the difference between hypoxia and ischemia?
Hypoxia is decreased oxygen to the brain. Ischemia is decreased blood flow. Thus, ischemia will result in accumulation of toxins, etc because there is also a decreased outflow.
What causes vasogenic edema? Is it intra- or extracellular? Why can't the lymphatics absorb the extra fluid in the brain?
Disruption of BBB causes resorption impairment. Extracellular. There are no lymphatics in the brain.
What causes cytotoxic Edema? Intra- or extracellular?
Disrupted ion transport. Intracellular.
What are the effects of uncal herniation? Which vessels does it affect?
Compression of CN III, and results. Basilar Artery and PCA.
What is a Duret Hemorrhage?
A midline hemorrhage in the midbrain and pons due to compression of vessels due to uncal (trans-tentorial) herniation.
What are the effects of a tonsillar herniation?
Brainstem compression and resulting respiratory arrest.
What are the effects of a Sub-falcine herniation?
Adjacent structure compression.
Name the area of swelling in the brain that results in the following:
1. Uncal Herniation
2. Tonsillar Herniation
3. Sub-Falcine Herniation
1. Mesial Temporal lobe

2. Cerebral tonsil

3. Cingulate gyrus
What is the most common cause of hydrocephalus? What causes a non-communicating hydrocephalus? Communicating?
Decrease Absorption. Mass Lesions compress ventricles. Meningitis, suba. hemorrhage disrupt arachnoid granulations.
What are some more rare causes of hydrocephalus?
Increased CSF production from a choroid plexus papilloma or hydrocephalus ex-vacuo from cerebral atrophy.
What percentage of strokes are thrombotic and what percentage are embolic?
!5-30 and 15-30
Are thrombotic strokes typically hemorrhagic? Why or why not?
No...complete occlusion
Are Embolic strokes typically hemorrhagic? Why or why not?
Yes...obstruction causes necrosis of vessel wall and embolism can allow reperfusion.
How can you differentiate Lucunar infarcts in the internal capsule from base of pons from thalamus?
Pure motor hemiparesis vs. ataxic hemiparesis vs pure sensory stroke
What are the pathologic findings of stroke grossly and microscopically at 6 hrs?
No Change, No Change
What are the pathologic findings of stroke grossly and microscopically at 24 hrs?
No Change, pink neurons, edema, neutrophils
What are the pathologic findings of stroke grossly and microscopically at 48-72 hrs?
Pale, soft, swollen (edema), blurred gray-white demarcation. Macrophages, granulation tissue
What are the pathologic findings of stroke grossly and microscopically at 7-10 days?
Gelatinous, friable, better demarcated. Astrocytic gliosis begins.
What are the pathologic findings of stroke grossly and microscopically at 3-4 weeks?
Cystic Cavity. Cystic Cavity with macrophages and surrounding gliosis.
Remember to look at all the pictures from lecture
ok
What changes can be expected in global hypoxia-ischemia grossly and microscopically in 6 hrs
No change
What changes can be expected in global hypoxia-ischemia grossly and microscopically in 24 hrs
No change. Pink neurons, edema, neutrophils in zones of selective vulnerability
What changes can be expected in global hypoxia-ischemia grossly and microscopically in 7-10 days
Watershed infarcts, laminar cortical necrosis, cerebellar necrosis, diffuse cerebral edema. Paucity of macrophages, granulation of tissue
What changes can be expected in global hypoxia-ischemia grossly and microscopically in 3-4 weeks
Gelatinous, friable. Astrocyte gliosis
what are watershed infarcts?
Cystic gliotic cortex. Variably cystic gliotic cortex.
What is a watershed infarct?
I'm not sure.
What are some causes of Global hypoxia-ischemia?
Shock, cardiac arrhythmias, Intracranial pressure
What is the most common cause of primary intra-parenchymal hemorrhage?
Hypertension
What are some less common causes of intra-parenchymal hemorrhage?
Amyloid angiopathy, arterio-venous malformations, neoplastic hemorrhage, coagulation disorders, and cocaine or amphetamines
What is the most common location of a HTNsive intra-parenchymal hemorrhage? What are some less common causes? (You really need to memorize these)
Basal Ganglia-putamen. Thalamus, pons, cerebral white matter, cerebellum.
What is the acute effect of Hypertensive intra-parenchymal hemorrhage? How is it different from infarct?
Mass effect.

Causes only scant tissue necrosis.
What is the chronic effect of Hypertensive intra-parenchymal hemorrhage? How is it different from infarct?
Cystic gliotic cavity with hemosiderin.

Only scant parenchymal loss
what is a common occurance due to the rapid hemorraging from a HTNsive hemorrhage involves ventricals?
Blood in ventricals.
What is the big difference between HTNsive pontine hemorrhage and a Duret hemorrhage?
Pontine bigger than duret.
Usually less midline than duret.
What are the big changes in arterioles in hypertensive patients?
Hyaline arteriosclerosis.

Fibrinoid Necrosis (sudden change causes necrosis in hyaline areas)

Charchoat-Bouchard micro-aneurysm
What are poor prognostic factors in HTNsive brain hemorrhage?
Old, Decreased LOC, Large hematoma, infratentorial location, Intravascular extention
Why is the infratentorial Compartment a bad location for HTNsive hemorrhage (or any other swelling for that matter)? Intraventricular?
Infratentorial - Tighter than the supratentorial

Intraventricular - Expansion effects + Increased CSF pressure
Cerebral Amyloid angiopathy is often associated with what disease?
Alzheimer's
Cerebral Amyloid angiopathy is due to...
An accumulation of amyloid in small or medium vessels
What is the most important difference when examining grossly a brain suffering from Cerebral Amyloid angiopathy vs HTNsive hemorrhage?
Location - CAA ones are not in the deep grey matter, they are in the hemispheres.
What diseases put patients at high risk for an aneurysm?
Those with polycystic renal disease and coarctation of the aorta
How do the walls of an aneurysm appear microscopically?
Muscle wall has variable thickness and inconsistencies in the elastic layer.
What is a cluster of developmentally abnormal vessels taht directly connect arterial to venous system located anywhere in the CNS, especially in the posterior cerebral hemisphere?
Aterio-venous malformations