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53 Cards in this Set
- Front
- Back
What CNS Cell has selective vulnerability to hypoxia/ischemia?
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Neuron
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What part of the brain is particularly vulnerable to hypoxia/ischemia? What subsection? Which subsection is most resistant
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The Hippocampus...CA1. CA2
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What is the second most vulnerable part of the brain susceptible to hypoxia/ischemia? What cell type?
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Cerebellar Cortex. The Purkinje Layer.
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What is the third most vulnerable region of the brain to ischemia?
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Cerebral Cortex
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Neurons are the most susceptible cell to hypoxia/ischemia in the brain. Which is the next most susceptible?
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Myelin (oligiodenroglial cells)
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What cell types proliferate in ischemic damage?
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Endothelial cells, Astrocytes, microglial cells
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What is the change in neurons as a result of damage to axons because of backflow, which pushes RNA back into cell body?
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Central Chromatolysis
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Which cell type has a "fried egg" appearance?
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Oligodendrocytes
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What sort of change do Microglial cells undergo during an early stage of activation? What does this cause?
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Rod Cells. Microglial nodules and neuronophagia (encephalitis only).
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What are Gitter Cells?
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Lipid laden macrophages from degraded myelin.
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what is the difference between hypoxia and ischemia?
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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.
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What causes vasogenic edema? Is it intra- or extracellular? Why can't the lymphatics absorb the extra fluid in the brain?
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Disruption of BBB causes resorption impairment. Extracellular. There are no lymphatics in the brain.
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What causes cytotoxic Edema? Intra- or extracellular?
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Disrupted ion transport. Intracellular.
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What are the effects of uncal herniation? Which vessels does it affect?
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Compression of CN III, and results. Basilar Artery and PCA.
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What is a Duret Hemorrhage?
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A midline hemorrhage in the midbrain and pons due to compression of vessels due to uncal (trans-tentorial) herniation.
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What are the effects of a tonsillar herniation?
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Brainstem compression and resulting respiratory arrest.
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What are the effects of a Sub-falcine herniation?
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Adjacent structure compression.
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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 |
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What is the most common cause of hydrocephalus? What causes a non-communicating hydrocephalus? Communicating?
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Decrease Absorption. Mass Lesions compress ventricles. Meningitis, suba. hemorrhage disrupt arachnoid granulations.
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What are some more rare causes of hydrocephalus?
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Increased CSF production from a choroid plexus papilloma or hydrocephalus ex-vacuo from cerebral atrophy.
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What percentage of strokes are thrombotic and what percentage are embolic?
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!5-30 and 15-30
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Are thrombotic strokes typically hemorrhagic? Why or why not?
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No...complete occlusion
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Are Embolic strokes typically hemorrhagic? Why or why not?
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Yes...obstruction causes necrosis of vessel wall and embolism can allow reperfusion.
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How can you differentiate Lucunar infarcts in the internal capsule from base of pons from thalamus?
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Pure motor hemiparesis vs. ataxic hemiparesis vs pure sensory stroke
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What are the pathologic findings of stroke grossly and microscopically at 6 hrs?
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No Change, No Change
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What are the pathologic findings of stroke grossly and microscopically at 24 hrs?
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No Change, pink neurons, edema, neutrophils
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What are the pathologic findings of stroke grossly and microscopically at 48-72 hrs?
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Pale, soft, swollen (edema), blurred gray-white demarcation. Macrophages, granulation tissue
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What are the pathologic findings of stroke grossly and microscopically at 7-10 days?
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Gelatinous, friable, better demarcated. Astrocytic gliosis begins.
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What are the pathologic findings of stroke grossly and microscopically at 3-4 weeks?
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Cystic Cavity. Cystic Cavity with macrophages and surrounding gliosis.
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Remember to look at all the pictures from lecture
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ok
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What changes can be expected in global hypoxia-ischemia grossly and microscopically in 6 hrs
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No change
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What changes can be expected in global hypoxia-ischemia grossly and microscopically in 24 hrs
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No change. Pink neurons, edema, neutrophils in zones of selective vulnerability
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What changes can be expected in global hypoxia-ischemia grossly and microscopically in 7-10 days
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Watershed infarcts, laminar cortical necrosis, cerebellar necrosis, diffuse cerebral edema. Paucity of macrophages, granulation of tissue
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What changes can be expected in global hypoxia-ischemia grossly and microscopically in 3-4 weeks
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Gelatinous, friable. Astrocyte gliosis
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what are watershed infarcts?
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Cystic gliotic cortex. Variably cystic gliotic cortex.
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What is a watershed infarct?
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I'm not sure.
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What are some causes of Global hypoxia-ischemia?
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Shock, cardiac arrhythmias, Intracranial pressure
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What is the most common cause of primary intra-parenchymal hemorrhage?
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Hypertension
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What are some less common causes of intra-parenchymal hemorrhage?
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Amyloid angiopathy, arterio-venous malformations, neoplastic hemorrhage, coagulation disorders, and cocaine or amphetamines
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What is the most common location of a HTNsive intra-parenchymal hemorrhage? What are some less common causes? (You really need to memorize these)
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Basal Ganglia-putamen. Thalamus, pons, cerebral white matter, cerebellum.
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What is the acute effect of Hypertensive intra-parenchymal hemorrhage? How is it different from infarct?
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Mass effect.
Causes only scant tissue necrosis. |
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What is the chronic effect of Hypertensive intra-parenchymal hemorrhage? How is it different from infarct?
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Cystic gliotic cavity with hemosiderin.
Only scant parenchymal loss |
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what is a common occurance due to the rapid hemorraging from a HTNsive hemorrhage involves ventricals?
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Blood in ventricals.
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What is the big difference between HTNsive pontine hemorrhage and a Duret hemorrhage?
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Pontine bigger than duret.
Usually less midline than duret. |
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What are the big changes in arterioles in hypertensive patients?
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Hyaline arteriosclerosis.
Fibrinoid Necrosis (sudden change causes necrosis in hyaline areas) Charchoat-Bouchard micro-aneurysm |
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What are poor prognostic factors in HTNsive brain hemorrhage?
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Old, Decreased LOC, Large hematoma, infratentorial location, Intravascular extention
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Why is the infratentorial Compartment a bad location for HTNsive hemorrhage (or any other swelling for that matter)? Intraventricular?
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Infratentorial - Tighter than the supratentorial
Intraventricular - Expansion effects + Increased CSF pressure |
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Cerebral Amyloid angiopathy is often associated with what disease?
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Alzheimer's
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Cerebral Amyloid angiopathy is due to...
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An accumulation of amyloid in small or medium vessels
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What is the most important difference when examining grossly a brain suffering from Cerebral Amyloid angiopathy vs HTNsive hemorrhage?
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Location - CAA ones are not in the deep grey matter, they are in the hemispheres.
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What diseases put patients at high risk for an aneurysm?
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Those with polycystic renal disease and coarctation of the aorta
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How do the walls of an aneurysm appear microscopically?
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Muscle wall has variable thickness and inconsistencies in the elastic layer.
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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?
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Aterio-venous malformations
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