HELLP syndrome and thrombotic thrombocytopenic purpura (TTP) are both thrombotic microangiopathies (TMAs) that produce microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and end-organ damage through microvascular thrombosis. However, their pathophysiology, treatment, and prognosis differ dramatically, making accurate differentiation a critical NP competency. HELLP syndrome arises from abnormal placentation causing endothelial dysfunction specific to pregnancy — the hallmark triad is Hemolysis (schistocytes, elevated LDH, low haptoglobin), Elevated Liver enzymes, and Low Platelets. HELLP occurs after 20 weeks gestation (typically third trimester) and resolves with delivery. TTP results from severe deficiency of ADAMTS13, a metalloprotease that cleaves ultra-large von Willebrand factor (ULvWF) multimers. Without ADAMTS13, ULvWF multimers accumulate on endothelial surfaces, causing platelet adhesion and aggregation into microvascular thrombi that shear red blood cells (producing schistocytes) and consume platelets. TTP classically presents with the pentad: thrombocytopenia, MAHA, neurological symptoms (confusion, seizures, focal deficits), renal impairment, and fever — though the full pentad is present in fewer than 10% of cases. The critical distinction is that TTP requires emergent therapeutic plasma exchange (TPE) to replace ADAMTS13, while platelet transfusion in TTP can be fatal (providing...