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Immune Thrombocytopenic Purpura (ITP) — NEET PG 2026 Complete Summary

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1. DEFINITION & NOMENCLATURE

• Full name: Immune Thrombocytopenic Purpura = Idiopathic Thrombocytopenic Purpura = Werlhof's Disease
• Acquired autoimmune disorder → immune-mediated destruction of platelets + possible inhibition of platelet release from megakaryocytes
• Defined by isolated thrombocytopenia (platelet count < 1,00,000/μL) with no other identifiable cause
• Primary ITP: No known underlying condition (diagnosis of exclusion)
• Secondary ITP: Associated with SLE, HIV, Hepatitis C, CLL, H. pylori, antiphospholipid syndrome

— Robbins, Cotran & Kumar Pathologic Basis of Disease | — Harrison's Principles of Internal Medicine 22E

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2. CLASSIFICATION

• Acute ITP in children: often follows viral illness (1–4 weeks before), resolves spontaneously in >80%
• Chronic ITP in adults: defined as lasting >12 months; more common in women

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3. EPIDEMIOLOGY

• Incidence: ~100 persons per million annually
• About half are children
• Adult ITP: predominantly young women (20–40 years)
• Classic description: "disease of young women" — though any age/sex can be affected

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4. PATHOGENESIS (Most Important for MCQs)

Key Autoantibodies:

• IgG autoantibodies (most common class) directed against platelet membrane glycoproteins IIb/IIIa (most common target) and Ib/IX
• Demonstrable in plasma and on platelet surface in ~80% of patients

Mechanism of platelet destruction:

1. Autoantibodies opsonize platelets → recognized by IgG Fc receptors on phagocytes → phagocytosis
2. Primary site of removal = spleen (via splenic macrophages in red pulp)
3. Liver macrophages also contribute
4. Autoantibodies may also damage megakaryocytes → decreased platelet production (dual mechanism)

Why splenectomy works:

• Spleen = major site of opsonized platelet removal
• Splenic red pulp = rich in plasma cells → source of autoantibodies
• Splenectomy removes both destruction site AND antibody source

— Robbins, Cotran & Kumar; Schwartz's Surgery

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5. CLINICAL FEATURES

Symptoms:

• Mucocutaneous bleeding (hallmark — differentiates from coagulation factor deficiencies which cause deep tissue bleeding)
• Petechiae and ecchymoses (most common presentation)
• Epistaxis, gingival bleeding, menorrhagia, hematuria, melena, hematochezia
• Wet purpura (blood blisters in mouth) and retinal hemorrhages = signs of impending life-threatening bleeding

Correlation of platelet count with bleeding:

Key negative findings:

• Splenomegaly is ABSENT (important — its presence should prompt search for another cause)
  • Exception: up to 10% of children may have a palpable spleen tip
• No lymphadenopathy, no fever (unless secondary cause)
• Intracranial hemorrhage: ~1% incidence, usually early in disease; most feared complication

— Schwartz's Surgery; Goldman-Cecil Medicine

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6. LABORATORY FINDINGS

For Secondary ITP workup:

• HIV, Hepatitis C serology
• ANA, anti-dsDNA (for SLE)
• Serum protein electrophoresis, immunoglobulin levels
• H. pylori testing
• Direct Coombs test — if anemia present (to rule out Evans' syndrome = ITP + autoimmune hemolytic anemia)
• Bone marrow biopsy: reserved for atypical cases OR non-responders to initial therapy

— Harrison's 22E; Goldman-Cecil

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7. MORPHOLOGY / HISTOPATHOLOGY (Robbins High-Yield)

Spleen:

• Normal size (no splenomegaly)
• Congestion of sinusoids
• Enlargement of splenic follicles with prominent reactive germinal centers
• Scattered megakaryocytes within sinuses (mild extramedullary hematopoiesis)

Bone marrow:

• Modestly increased megakaryocytes
• Some immature megakaryocytes with large, non-lobulated, single nuclei

These findings are NOT specific — reflect accelerated thrombopoiesis seen in any destructive thrombocytopenia

— Robbins, Cotran & Kumar

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8. DIAGNOSIS

• Diagnosis of EXCLUSION — no single confirmatory test
• Criteria: Isolated thrombocytopenia + mucocutaneous bleeding + normal CBC except platelets + absence of splenomegaly + no secondary cause
• Peripheral smear: large platelets with otherwise normal morphology

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9. TREATMENT

When to treat:

• Platelet count >30,000/μL + asymptomatic → Observe (no treatment needed; no increased mortality)
• Treatment indicated when: symptomatic bleeding, platelets <30,000/μL, or signs of impending severe bleeding

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First-Line Treatment:

• IVIg: Fastest platelet rise (within 24–48 hours) — used in emergencies
• Corticosteroids: Most common first-line agent

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Second-Line Treatment (Refractory/Chronic ITP):

🔑 SPLENECTOMY — Most Important Second-Line Treatment

• Best long-term remission rate (~60–70% complete response)
• Indicated when: fails corticosteroids, relapses after stopping steroids, requires high steroid doses to maintain platelets
• Vaccinations before splenectomy: Pneumococcal, Meningococcal, H. influenzae type b (given ≥2 weeks before)
• Post-splenectomy: Howell-Jolly bodies appear on peripheral smear

Other Second-Line Agents:

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Emergency/Life-Threatening Bleeding:

• IVIg + IV methylprednisolone + platelet transfusion (combination)
• Platelet transfusion alone not effective due to rapid destruction — use only with concurrent IVIg/steroids

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10. SPECIAL SCENARIOS (NEET MCQ Traps)

Evans' Syndrome:

• ITP + Autoimmune Hemolytic Anemia (AIHA)
• Direct Coombs test positive
• Must rule out when ITP + anemia coexist

H. pylori and ITP:

• Geographic distribution in association
• Eradication of H. pylori can improve platelet counts in some patients
• Test and treat H. pylori in all ITP patients

ITP in Pregnancy:

• Maternal IgG crosses placenta → neonatal thrombocytopenia possible
• Differentiate from Gestational Thrombocytopenia (mild, platelet rarely <70,000, no fetal risk, resolves postpartum)
• Management: corticosteroids, IVIg; avoid splenectomy in pregnancy (if needed, second trimester preferred)

ITP vs. TTP/HUS:

ITP vs. Drug-Induced Thrombocytopenia:

• Drugs causing thrombocytopenia (common MCQ list): Heparin, quinine, quinidine, sulfonamides, rifampicin, valproate, linezolid, vancomycin, carbamazepine
• Heparin → HIT (Heparin-Induced Thrombocytopenia): IgG against PF4-heparin complex → thrombosis, NOT just bleeding

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11. ACUTE ITP IN CHILDREN (High-Yield Points)

• Most common cause of thrombocytopenia in children
• Follows viral infection (e.g., chickenpox, EBV, CMV, Parvovirus B19) by 1–4 weeks
• Self-limiting in >80% — spontaneous remission within 6 months
• Treatment: Observation if mild; oral prednisone or IVIg if platelet <20,000 or symptomatic
• No splenectomy in acute childhood ITP (not needed; resolves on own)
• Intracranial hemorrhage: rare but most dreaded complication

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12. CHRONIC ITP DEFINITION TIMELINE

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13. KEY ONE-LINERS FOR MCQs

• Antibody target: GP IIb/IIIa (most common), GP Ib/IX
• Antibody class: IgG
• Antibody demonstrable in: ~80% of patients
• Site of platelet destruction: Spleen (primary)
• Bone marrow: Increased megakaryocytes
• Spleen in ITP: Normal size (no splenomegaly)
• Best treatment for acute childhood ITP: Observation / IVIg / steroids (NOT splenectomy)
• Best long-term treatment for chronic ITP: Splenectomy
• Fastest platelet rise: IVIg
• Howell-Jolly bodies: post-splenectomy finding
• Evans syndrome: ITP + AIHA (Coombs positive)
• Wet purpura = blood blisters in oral mucosa = impending life-threatening bleed
• Antiplatelet antibody testing: NOT recommended (low sensitivity and specificity)
• Platelet count threshold for treatment initiation: <30,000/μL (or symptomatic)
• H. pylori eradication: can improve platelet counts in ITP
• Intracranial hemorrhage risk: ~1% (most feared complication)

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14. DIFFERENTIALS — QUICK COMPARISON

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What is the most common target antigen for autoantibodies in ITP?	Glycoprotein IIb/IIIa (most common); also GP Ib/IX. Antibodies are of IgG class.

In what percentage of ITP patients can antiplatelet autoantibodies be demonstrated?	~80% of patients (in plasma and bound to platelet surface)

What is the primary site of opsonized platelet destruction in ITP?	Spleen (via Fc receptor-expressing macrophages in the splenic red pulp). Liver macrophages contribute secondarily.

Why does splenectomy work in ITP? (dual mechanism)	1. Removes the primary site of opsonized platelet destruction. 2. Removes splenic red pulp plasma cells — a major source of autoantibodies.

What is the bone marrow finding in ITP?	Normal or INCREASED megakaryocytes. Some are immature with large, non-lobulated single nuclei. Rest of marrow is normal.

What is the splenic size in ITP? What does splenomegaly suggest?	Spleen is NORMAL SIZE in ITP. Splenomegaly suggests a secondary cause (e.g., lymphoma, CLL, portal hypertension) — not primary ITP.

What are the histological findings in the spleen in ITP?	Normal size; congestion of sinusoids; enlarged follicles with prominent reactive germinal centers; scattered megakaryocytes within sinuses (mild extramedullary hematopoiesis).

What is Evans' syndrome?	ITP + Autoimmune Hemolytic Anemia (AIHA). Direct Coombs test is positive. Both platelet and RBC are targeted by autoantibodies.

What is the peripheral blood smear finding in ITP?	Decreased platelets; large/giant platelets (megathrombocytes); otherwise normal morphology. No schistocytes (absence of schistocytes differentiates from TTP/HUS).

Why are antiplatelet antibody assays NOT recommended in ITP diagnosis?	Low sensitivity AND low specificity — results neither confirm nor exclude the diagnosis.

What class of immunoglobulin mediates platelet destruction in ITP, and via which receptor?	IgG autoantibodies opsonize platelets → recognized by IgG Fc receptors on splenic and hepatic macrophages → phagocytosis and destruction.

What is the dual pathological mechanism of thrombocytopenia in ITP?	1. Increased peripheral destruction of antibody-coated platelets (primary). 2. Autoantibodies binding megakaryocytes → impaired platelet production (secondary).

What secondary conditions are associated with ITP? (5 key causes)	1. SLE 2. HIV infection 3. Hepatitis C 4. CLL (B-cell neoplasms) 5. H. pylori infection. (Also: antiphospholipid syndrome, other lymphoproliferative disorders)

Acute ITP vs. Chronic ITP — key pathological and clinical differences?	Acute ITP: Children; post-viral; self-limiting (>80% remission); abrupt onset. Chronic ITP: Adults (young women); autoimmune; insidious; recurrent; defined as lasting >12 months.

What are the Howell-Jolly bodies and when do they appear in context of ITP?	Howell-Jolly bodies = nuclear remnants in RBCs, normally removed by the spleen. They appear on peripheral smear AFTER splenectomy — a post-splenectomy marker.

ITP is a diagnosis of ___. What must be excluded before diagnosing primary ITP?	Diagnosis of EXCLUSION. Must exclude: SLE, HIV, Hepatitis C, CLL, drug-induced thrombocytopenia, TTP, HUS, DIC, aplastic anemia, gestational thrombocytopenia, antiphospholipid syndrome.

Differentiate ITP from TTP on pathological/lab basis.	ITP: No schistocytes, no hemolysis, normal PT/aPTT, normal ADAMTS-13, no organ failure. TTP: Schistocytes (MAHA), ADAMTS-13 deficiency/antibody, thrombosis in microvasculature, renal and neurological involvement.

What is the significance of "wet purpura" in ITP pathology?	Wet purpura = blood blisters in oral mucosa. Along with retinal hemorrhages, it signifies a very low platelet count and heralds impending life-threatening hemorrhage (including intracranial).

What is the incidence and timing of intracranial hemorrhage in ITP?	~1% incidence; most feared/life-threatening complication; usually occurs EARLY in the disease course.

What is the pathological basis of neonatal thrombocytopenia in maternal ITP?	Maternal IgG antiplatelet antibodies (anti-GP IIb/IIIa or Ib/IX) cross the placenta → opsonize fetal platelets → destruction by fetal splenic macrophages via Fc receptor-mediated phagocytosis. Analogous to hemolytic disease of the newborn.

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IMMUNE THROMBOCYTOPENIC PURPURA (ITP) — NEET PG 2026 Master Revision Card	DEFINITION & NAMES
• Also called: Idiopathic Thrombocytopenic Purpura / Werlhof's Disease
• Isolated thrombocytopenia (plt <1,00,000) due to autoimmune platelet destruction
• Diagnosis of EXCLUSION

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CLASSIFICATION
• Acute ITP → Children (peak 5 yrs) | post-viral | self-limiting (>80%) | abrupt onset
• Chronic ITP → Adults (young women) | insidious | recurrent | >12 months duration
• Newly diagnosed <3m | Persistent 3–12m | Chronic >12m

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PATHOGENESIS (Most MCQ-tested)
• Antibody class → IgG (most common)
• Antibody target → GP IIb/IIIa (MC) and GP Ib/IX
• Demonstrable in → ~80% of patients
• Destruction site → SPLEEN (primary) via Fc receptor macrophages; liver secondary
• Dual mechanism → ① Peripheral platelet destruction ② Megakaryocyte damage → ↓ production
• Why splenectomy works → Removes destruction site + removes autoantibody-producing plasma cells

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SECONDARY CAUSES (5 key)
SLE | HIV | Hepatitis C | CLL | H. pylori
Also: Antiphospholipid syndrome | Lymphoproliferative disorders

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CLINICAL FEATURES
• Mucocutaneous bleeding (hallmark) — NOT deep tissue bleeding
• Petechiae, ecchymoses, epistaxis, menorrhagia, gingival bleeding
• Wet purpura (oral blood blisters) + retinal hemorrhage → impending life-threatening bleed
• SPLEEN → NORMAL SIZE (splenomegaly = think secondary cause)
• Intracranial hemorrhage → ~1%, most feared, occurs early

PLATELET COUNT vs BLEEDING SEVERITY
>50,000 → Incidental | 30–50k → Easy bruising | 10–30k → Spontaneous petechiae | <10k → Internal bleeding risk

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LAB FINDINGS
• CBC → Isolated thrombocytopenia only
• Peripheral smear → Large/giant platelets (megathrombocytes); NO schistocytes
• Bone marrow → ↑ Megakaryocytes (some immature, large, non-lobulated nuclei); rest normal
• PT/aPTT → NORMAL | Bleeding time → Prolonged
• Antiplatelet antibody test → NOT recommended (low sensitivity + specificity)
• Evans syndrome workup → Direct Coombs test (ITP + AIHA)

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HISTOPATHOLOGY (Robbins)
SPLEEN → Normal size | Congested sinusoids | Enlarged follicles with reactive germinal centers | Scattered megakaryocytes in sinuses
BONE MARROW → ↑ Megakaryocytes | Some immature (large, non-lobulated, single nucleus)

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TREATMENT
WHEN TO TREAT → Plt <30,000 OR symptomatic bleeding
Plt >30,000 + asymptomatic → Observe (no increased mortality)

FIRST LINE
• Prednisolone 1–1.5 mg/kg/day (most common first line)
• Dexamethasone 40 mg/day × 4 days (pulse)
• IVIg 1–2 g/kg → Fastest platelet rise (emergency use)
• Anti-D (Rh₀D Ig) 50–75 µg/kg → Only Rh+ve, non-splenectomized patients

SECOND LINE
• SPLENECTOMY → Best long-term remission (~60–70%) | Pre-op vaccines: Pneumococcal + Meningococcal + Hib (≥2 weeks before)
• Rituximab → Anti-CD20 | depletes B cells | ↓ antibody production
• Romiplostim / Eltrombopag → TPO receptor agonists | ↑ platelet production
• Azathioprine | Cyclophosphamide | Danazol | Dapsone | Vincristine

EMERGENCY (life-threatening bleed)
IVIg + IV Methylprednisolone + Platelet transfusion (combined)

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HIGH-YIELD ASSOCIATIONS
• Evans syndrome → ITP + AIHA (Coombs +ve)
• Howell-Jolly bodies → Post-splenectomy peripheral smear finding
• Neonatal ITP → Maternal IgG crosses placenta → fetal platelet destruction (analogous to HDN)
• H. pylori eradication → Can improve platelet counts
• Wet purpura → Imminent life-threatening hemorrhage
• Antiplatelet Ab test → NOT done (useless)

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KEY DIFFERENTIALS
ITP vs TTP → ITP: no schistocytes, no hemolysis, normal ADAMTS-13 | TTP: schistocytes, ADAMTS-13 ↓, pentad (fever + MAHA + thrombocytopenia + renal failure + neuro signs)
ITP vs DIC → ITP: normal PT/aPTT, normal fibrinogen | DIC: ↑PT/aPTT, ↑D-dimer, ↓fibrinogen, schistocytes
ITP vs Aplastic anemia → ITP: isolated thrombocytopenia | AA: pancytopenia, hypocellular marrow
ITP vs Gestational thrombocytopenia → GT: mild (plt >70k), no fetal risk, resolves postpartum

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ONE-LINE MCQ ANCHORS
① Antibody → IgG anti-GP IIb/IIIa
② Demonstrable in → 80% patients
③ Destruction site → Spleen
④ BM finding → ↑ Megakaryocytes
⑤ Spleen size → NORMAL
⑥ Fastest Plt rise → IVIg
⑦ Best long-term Rx → Splenectomy
⑧ No schistocytes → differentiates from TTP/HUS/DIC
⑨ Antiplatelet Ab test → NOT recommended
⑩ Wet purpura → impending CNS bleed

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IMMUNE THROMBOCYTOPENIC PURPURA — NEET PG 2026 Master Revision	<b>NAMES:</b> Idiopathic Thrombocytopenic Purpura / Werlhof's Disease<br>Isolated thrombocytopenia (plt &lt;1,00,000) | Diagnosis of EXCLUSION<br><br><b>CLASSIFICATION:</b><br>Acute → Children (peak 5 yrs) | post-viral | self-limiting &gt;80% | abrupt<br>Chronic → Adults (young women) | insidious | recurrent | &gt;12 months<br>Timeline: Newly diagnosed &lt;3m | Persistent 3–12m | Chronic &gt;12m<br><br><b>PATHOGENESIS:</b><br>Antibody class → IgG | Target → GP IIb/IIIa (MC), GP Ib/IX<br>Demonstrable in → 80% patients<br>Destruction site → SPLEEN (primary) via Fc receptor macrophages<br>Dual mechanism → ① Peripheral destruction ② Megakaryocyte damage → ↓ production<br>Splenectomy works → removes destruction site + autoantibody-producing plasma cells<br><br><b>SECONDARY CAUSES:</b> SLE | HIV | Hepatitis C | CLL | H. pylori | Antiphospholipid syndrome<br><br><b>CLINICAL:</b><br>Mucocutaneous bleeding (hallmark) — NOT deep tissue<br>Petechiae | Ecchymoses | Epistaxis | Menorrhagia | Gingival bleeding<br>Wet purpura + Retinal hemorrhage → impending life-threatening bleed<br>Spleen → NORMAL SIZE (splenomegaly = think secondary cause)<br>Intracranial hemorrhage → 1%, most feared, occurs early<br><br><b>PLATELET COUNT vs BLEEDING:</b><br>&gt;50k → Incidental | 30–50k → Easy bruising | 10–30k → Spontaneous petechiae | &lt;10k → Internal bleed risk<br><br><b>LAB:</b><br>CBC → Isolated thrombocytopenia only<br>Smear → Large/giant platelets (megathrombocytes) | NO schistocytes<br>BM → ↑ Megakaryocytes (some immature, large, non-lobulated nuclei) | rest normal<br>PT/aPTT → NORMAL | Bleeding time → Prolonged<br>Antiplatelet Ab test → NOT recommended (low sensitivity + specificity)<br>Evans syndrome → Direct Coombs test (ITP + AIHA)<br><br><b>HISTOPATHOLOGY (Robbins):</b><br>Spleen → Normal size | Congested sinusoids | Enlarged follicles with reactive germinal centers | Megakaryocytes in sinuses<br>BM → ↑ Megakaryocytes | Immature forms with large non-lobulated single nucleus<br><br><b>TREATMENT:</b><br>Treat when → Plt &lt;30,000 OR symptomatic | Plt &gt;30k + asymptomatic → Observe<br><br>First line:<br>Prednisolone 1–1.5 mg/kg/day (most common)<br>Dexamethasone 40 mg/day × 4 days (pulse)<br>IVIg 1–2 g/kg → Fastest platelet rise (emergency)<br>Anti-D (Rh₀D Ig) → Only Rh+ve, non-splenectomized<br><br>Second line:<br>Splenectomy → Best long-term remission (60–70%) | Pre-op vaccines: Pneumococcal + Meningococcal + Hib (≥2 wks before)<br>Rituximab → Anti-CD20 | depletes B cells | ↓ antibody<br>Romiplostim / Eltrombopag → TPO-RA | ↑ platelet production<br>Azathioprine | Cyclophosphamide | Danazol | Dapsone | Vincristine<br><br>Emergency: IVIg + IV Methylprednisolone + Platelet transfusion (combined)<br><br><b>KEY ASSOCIATIONS:</b><br>Evans syndrome → ITP + AIHA (Coombs +ve)<br>Howell-Jolly bodies → Post-splenectomy<br>Neonatal ITP → Maternal IgG crosses placenta (analogous to HDN)<br>H. pylori eradication → can improve platelet counts<br><br><b>DIFFERENTIALS:</b><br>vs TTP → ITP has NO schistocytes, normal ADAMTS-13 | TTP: schistocytes, ADAMTS-13 ↓, pentad<br>vs DIC → ITP: normal PT/aPTT, normal fibrinogen | DIC: ↑PT/aPTT, ↑D-dimer, ↓fibrinogen<br>vs Aplastic anemia → ITP: isolated thrombocytopenia | AA: pancytopenia, hypocellular marrow<br>vs Gestational thrombocytopenia → GT: plt &gt;70k, no fetal risk, resolves postpartum<br><br><b>MCQ ANCHORS:</b><br>① IgG anti-GP IIb/IIIa ② 80% patients ③ Spleen = destruction site ④ BM → ↑ megakaryocytes<br>⑤ Spleen size → NORMAL ⑥ Fastest rise → IVIg ⑦ Best long-term → Splenectomy<br>⑧ No schistocytes → rules out TTP/HUS/DIC ⑨ Antiplatelet Ab → NOT done ⑩ Wet purpura → CNS bleed risk

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