Immune Thrombocytopenic Purpura and Thrombotic Thrombocytopenic Purpura (TTP) / Hemolytic Uremic Syndrome are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.
Immune Thrombocytopenic Purpura vs Thrombotic Thrombocytopenic Purpura (TTP) / Hemolytic Uremic Syndrome at a glance
Immune Thrombocytopenic Purpura: Isolated thrombocytopenia from autoantibody-mediated platelet destruction with normal-to-increased marrow megakaryocytes.
Thrombotic Thrombocytopenic Purpura (TTP) / Hemolytic Uremic Syndrome: Thrombotic microangiopathies — TTP from ADAMTS13 deficiency, HUS classically from Shiga toxin; both produce microangiopathic hemolysis with thrombocytopenia.
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Question 1HematologyMedium
A 50-year-old male is evaluated for an isolated thrombocytopenia found on routine CBC: platelets 88K. Repeat CBC confirms platelets 90K. He is asymptomatic without bleeding. Physical exam is normal. Testing is negative for HIV and hepatitis C and positive for H. pylori. Peripheral smear shows large platelets with no clumping. Bone marrow biopsy shows increased megakaryocytes. ANA is negative. Which of the following is the most appropriate next step in management?
AOral prednisone 1 mg/kg daily
BIntravenous immunoglobulin (IVIG)
CH. pylori eradication therapy
DIntravenous rituximab therapy
Reveal answer & full explanation
Correct answer: C — H. pylori eradication therapy
AOral prednisone 1 mg/kg daily
BIntravenous immunoglobulin (IVIG)
CH. pylori eradication therapy✓
DIntravenous rituximab therapy
Why H. pylori eradication therapy is correct
Findings — isolated thrombocytopenia, increased megakaryocytes, and exclusion of other causes — are diagnostic of immune thrombocytopenic purpura (ITP)
H. pylori testing is recommended in adults with ITP; eradication leads to platelet recovery in 40-80% of H. pylori-positive ITP patients
First-line eradication (ACG 2024): bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole) x14 days when clarithromycin susceptibility is unknown; clarithromycin-based triple therapy only if susceptibility is confirmed; confirm eradication with urea breath test or stool antigen at least 4 weeks after therapy (off PPI for 2 weeks)
Platelets >30K and asymptomatic: observation plus eradication is reasonable; reserve corticosteroids or intravenous immunoglobulin (IVIG) for platelets <30K or bleeding
Why the others are wrong
Oral prednisone 1 mg/kg daily — standard first-line therapy for newly diagnosed ITP, but ASH guidance reserves corticosteroids for platelets <30K or bleeding; at 90K without symptoms, observation plus H. pylori eradication is preferred over immunosuppression
Intravenous immunoglobulin (IVIG) — used for rapid platelet elevation in patients who are bleeding or need an urgent procedure; neither applies to an asymptomatic patient with platelets of 90K
Intravenous rituximab therapy — a second-line option for ITP that relapses after or fails corticosteroids, not initial management of an untreated, asymptomatic patient with mild thrombocytopenia
Question 2HematologyMedium
A 38-year-old woman presents with fatigue, confusion, and scattered petechiae over 3 days. Temperature is 38.1°C (100.6°F) and she is intermittently disoriented. Labs show hemoglobin 8.1 g/dL, platelets 14,000/µL, and creatinine 1.6 mg/dL; LDH is markedly elevated and haptoglobin is undetectable. The peripheral smear shows numerous schistocytes, and PT, PTT, and fibrinogen are normal. The direct antiglobulin (Coombs) test is negative, and ADAMTS13 activity returns at less than 5%. Which of the following best explains the findings?
AAutoantibody-mediated splenic clearance of antibody-coated circulating platelets
BUnchecked alternative complement activation injuring vascular endothelial surfaces
CShiga toxin injuring glomerular endothelium and triggering platelet microthrombi
DUltralarge von Willebrand factor multimers aggregating platelets into thrombi
Reveal answer & full explanation
Correct answer: D — Ultralarge von Willebrand factor multimers aggregating platelets into thrombi
AAutoantibody-mediated splenic clearance of antibody-coated circulating platelets
BUnchecked alternative complement activation injuring vascular endothelial surfaces
CShiga toxin injuring glomerular endothelium and triggering platelet microthrombi
DUltralarge von Willebrand factor multimers aggregating platelets into thrombi✓
Why Ultralarge von Willebrand factor multimers aggregating platelets into thrombi is correct
The vignette is classic acquired thrombotic thrombocytopenic purpura (TTP): microangiopathic hemolytic anemia (anemia, high LDH, undetectable haptoglobin, schistocytes, negative DAT) plus severe thrombocytopenia, neurologic change, fever, and renal involvement, with normal coagulation studies.
ADAMTS13 is the metalloprotease that cleaves von Willebrand factor (vWF). When it is deficient (usually from an acquired autoantibody), ultralarge vWF multimers accumulate, bind and aggregate platelets, and form platelet-rich microthrombi that shear red cells (schistocytes) and cause organ ischemia.
ADAMTS13 activity less than 10% (here less than 5%) confirms TTP; emergent plasma exchange plus glucocorticoids is the treatment.
Why the others are wrong
Shiga toxin injuring glomerular endothelium and triggering platelet microthrombi is the mechanism of STEC-HUS, which follows bloody diarrhea, predominates in young children, causes prominent acute kidney injury rather than neurologic findings, and does not produce ADAMTS13 activity less than 10%.
Unchecked alternative complement activation injuring vascular endothelial surfaces is atypical HUS; it features prominent renal failure, often a complement-mutation or family history, and normal-to-mildly-reduced ADAMTS13, not the less-than-10% activity seen here.
Autoantibody-mediated splenic clearance of antibody-coated platelets is the mechanism of immune thrombocytopenia (ITP), which causes isolated thrombocytopenia with a normal smear and no hemolysis, schistocytes, or organ dysfunction.
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Isolated thrombocytopenia from autoantibody-mediated platelet destruction with normal-to-increased marrow megakaryocytes.
Thrombotic microangiopathies — TTP from ADAMTS13 deficiency, HUS classically from Shiga toxin; both produce microangiopathic hemolysis with thrombocytopenia.
Classic presentation
Isolated thrombocytopenia with petechiae and wet purpura in an otherwise well child 1-3 weeks after a viral illness, or in a young adult woman.; Mucocutaneous bleeding: petechiae, ecchymoses, epistaxis, gingival bleeding, menorrhagia; Hematuria, GI bleeding less common; Intracranial hemorrhage rare but most feared (~1% in adults); Often…
Microangiopathic hemolytic anemia + thrombocytopenia + schistocytes on smear + normal coagulation studies — assume TTP/HUS until proven otherwise.; Classic TTP pentad (rarely all 5; even 2 of 5 in correct context warrants treatment): microangiopathic hemolytic anemia, thrombocytopenia, neurologic symptoms (confusion, headache, focal…
Workup / key labs
Isolated thrombocytopenia (<100,000/μL) with otherwise normal CBC and smear, and exclusion of secondary causes. Diagnosis of exclusion.; CBC — isolated thrombocytopenia; Hb and WBC normal (unless bleeding-related anemia); Peripheral smear — large platelets (immature, recently released); RULE OUT schistocytes (TTP/HUS/DIC), blasts…
Microangiopathic hemolytic anemia + thrombocytopenia + schistocytes ± end-organ dysfunction. TTP confirmed by ADAMTS13 activity <10%; STEC-HUS by positive stool studies; aHUS by exclusion + complement workup.; CBC — anemia, thrombocytopenia (often <50K in TTP, <100K in HUS); Peripheral smear — schistocytes (helmet cells, fragmented…
Imaging
Not routinely indicated; imaging directed at suspected secondary cause
Head CT/MRI if neurologic symptoms (exclude hemorrhage before plasma exchange line placement); Renal ultrasound if persistent AKI
First-line treatment
Observation alone for platelets >30,000/μL without bleeding (adults) — most authoritative guidelines (ASH 2019); Glucocorticoids — first-line for platelets <30K or bleeding: prednisone 1 mg/kg/day OR dexamethasone 40 mg/day × 4 days (high-dose dexamethasone often preferred for faster response and shorter course); IVIG 1 g/kg × 1-2 days…
TTP (acquired): EMERGENCY plasma exchange (PLEX) — initiate as soon as TTP suspected; do not wait for ADAMTS13 result. Replaces deficient ADAMTS13 and removes autoantibody. Daily until platelet count >150K for ≥2 days; TTP: high-dose glucocorticoids (methylprednisolone 1 g IV × 3 days or prednisone 1 mg/kg) to suppress autoantibody;…
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