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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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