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- Jul 12, 2007
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First off, when learning about these two diseases, they are similar in so many ways.
Pathoma says focal infarcts are from benign htn (the pathologic feature of Hyaline arterioscelerosis) and charcot bouchard are from chronic or malignant htn (so I'm assuming the path is hyperplastic arterioscelerosis or onion skinning + fibrinoid necrosis - features of chronic htn)...BUT uworld says BOTH charcot bouchard and focal infarcts are from chronic HTN...what is correct?
So first off with with the similarities, they BOTH affect lenticulostriate arteries feeding the basal ganglia and are due to hypertension? If UWorld is correct, then I assume both are from chronic hypertension- another similarity. As far as differences, UWorld mentions the size of lesion, the ability to diagnose the hemorrhagic lesion in charcot-bouchard early but not the initial pale ischemic infarct leading to a cavitary lesion (which weeks later can be diagnosed) of the focal infarct...but my question is ultimately once again is the pathological process origin chronic HTN?
So am i missing something, because it would then seem from a pathological standpoint, pretty much if the lenticulostriate artery under chronic HTN purely causes ischema OR weakens the vessel wall enough to rupture it the point of divergence leading two two different diagnosis
Pathoma says focal infarcts are from benign htn (the pathologic feature of Hyaline arterioscelerosis) and charcot bouchard are from chronic or malignant htn (so I'm assuming the path is hyperplastic arterioscelerosis or onion skinning + fibrinoid necrosis - features of chronic htn)...BUT uworld says BOTH charcot bouchard and focal infarcts are from chronic HTN...what is correct?
So first off with with the similarities, they BOTH affect lenticulostriate arteries feeding the basal ganglia and are due to hypertension? If UWorld is correct, then I assume both are from chronic hypertension- another similarity. As far as differences, UWorld mentions the size of lesion, the ability to diagnose the hemorrhagic lesion in charcot-bouchard early but not the initial pale ischemic infarct leading to a cavitary lesion (which weeks later can be diagnosed) of the focal infarct...but my question is ultimately once again is the pathological process origin chronic HTN?
So am i missing something, because it would then seem from a pathological standpoint, pretty much if the lenticulostriate artery under chronic HTN purely causes ischema OR weakens the vessel wall enough to rupture it the point of divergence leading two two different diagnosis