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14 Cards in this Set
- Front
- Back
etiology for supratentorial hemispheric parenchymal bleed
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ruptured aneurysm
vascular malformation cortical/dural venous thrombosis amyloid |
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pathophys of amyloid angiopathy
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amyloid deposits in media and intima of small arteries and arterioles or cortex/meninges
there is fibrinoid degeneration and microaneurysmal dilatation --> ruptured BV |
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pathologically how is amyloid angiopathy dx'd
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stains red with congo red, wiht apple green birefringence under polarized light
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describe pathogenesis of hemorrhagic transformation of infarct
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altered BBB predisposes and then either pt had lysis, developed collateral flow, or there was correction of hypotension --> bleed
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appearance of hemorrhagic transformation of infarct
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cortical gray matter is almost always involved, +/- white matter involvement
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appearance of WM if it is involved in a hemorrhagic transformation of infarct
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WM is hypodense to nml WM on CT and is hetero in appearance (this + bleed being in a vascular distribution helps to distinguish it from lobar hemorrhage)
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pathogenesis of dolichoectasia and fusiform aneurysm
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they develop from ATH affecting media (as opposed to nml ATH dz, which affects the intima).
damage to the media --> arterial stretching, elongation extending over a long segment |
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do fusiform aneurysms rupture
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rarely, but they do cause sx 2/2 mass effect --> hemiparesis, impaired eye mov't or other cranial neuoropathy
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definition of a giant intracranial aneurysm
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>25mm
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BV most comonly involved in giant intracranial aneurysm
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40-60% inovlve th ecavernous internal carotid artery
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complications assoc with giant intracranial aneurysm
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high risk o fhemorrhage, cerebral compression and thromboembolic events
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classic appearance of partially thrombosed giant intracranial aneurysm
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target appearance on CECT
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appearance of giant intracranial aneurysm when not thrombosed
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hyperdense on NECT and have marked enhancement
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appearance of giant intracranial aneurysm on MR
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variable
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