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| ==Pathophysiology==
| | #REDIRECT[[Hypertensive Emergency]] |
| *Rapid increase in BP leading to severe HTN causing disruption of vascular endothelium which narrows/obliterates vascular lumen
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| *RAAS activation
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| *Autoregulation of BP lost
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| ==Clinical Features==
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| *Retinal hemorrhage and exudates, papilledema
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| *Malignant nephrosclerosis causes AKI, proteinuria, hematuria
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| *Neurologic sx due to [[hypertensive encephalopathy]], [[SAH]], lacunar infarcts
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| **[[Hypertensive encephalopathy]] = cerebral edema secondary to breakthrough hyperperfusion from severe/sudden rise in BP (CPP autoregulation lost)
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| *Can cause [[microangiopathic hemolytic anemia (MAHA)]]
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| ==Diagnosis==
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| *BP, physical exam, Cr, UA, +/- CT Head or MRI Brain
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| ==Treatment==
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| *IV BP meds: nitroprusside, nicardipine, labetalol, fenoldopam
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| *If no IV meds: sublingual nifedipine or sublingual captopril; these can rapidly decrease BP in 10-30 min, beware of MI/stroke
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| *Goal: Lower BP by 25% over 2-6hr, goal DBP 100-105
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| ==See Also==
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| *[[Hypertensive emergency]], [[Hypertensive encephalopathy]]
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| *[[Microangiopathic hemolytic anemia (MAHA)]]
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| [[Category:Cards]] [[Category:Heme/Onc]]
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