Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1211: Auer rods are characteristic findings in which of the following hematological conditions?

A. Acute myeloid leukemia (Correct Answer)
B. Chronic myeloid leukemia
C. Iron deficiency anemia
D. Hodgkin's disease

Explanation: **Explanation:** **1. Why Acute Myeloid Leukemia (AML) is correct:** Auer rods are pathognomonic morphological features of **Acute Myeloid Leukemia (AML)** [1]. They are elongated, needle-shaped, pink/red-staining cytoplasmic inclusions. Biochemically, they represent **fused primary (azurophilic) granules** and contain peroxidase, lysosomal enzymes, and crystalline ribonuclease. Their presence confirms a myeloid lineage, effectively ruling out Acute Lymphoblastic Leukemia (ALL). They are most commonly seen in AML subtypes M1, M2, M3, and M4 (FAB classification) [1]. **2. Why the other options are incorrect:** * **Chronic Myeloid Leukemia (CML):** CML is a myeloproliferative neoplasm characterized by a full spectrum of maturing myeloid cells (neutrophils, myelocytes, etc.) and the Philadelphia chromosome. Auer rods are absent in the chronic phase; their appearance in CML signifies a "Blast Crisis" (transformation into AML). * **Iron Deficiency Anemia:** This is a microcytic hypochromic anemia characterized by small, pale RBCs and pencil cells. It involves the erythroid line and does not feature myeloid cytoplasmic inclusions. * **Hodgkin’s Disease:** This is a lymphoid malignancy characterized by the presence of **Reed-Sternberg (RS) cells** (owl-eye appearance) in a reactive inflammatory background, not Auer rods. **3. High-Yield Clinical Pearls for NEET-PG:** * **APL (AML-M3):** Characterized by "Faggot cells" (cells containing bundles/clumps of numerous Auer rods) [1]. This is a medical emergency due to the high risk of DIC. * **Staining:** Auer rods are strongly **Myeloperoxidase (MPO) positive** and Sudan Black B positive. * **Exclusion:** Auer rods are **never** found in lymphoblasts (ALL). Their presence is the single most reliable morphological feature to distinguish AML from ALL [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 620-622.

Question 1212: Intravascular hemolysis occurs in which of the following conditions?

A. Hereditary spherocytosis
B. Autoimmune hemolytic anemia
C. Paroxysmal nocturnal hemoglobinuria (Correct Answer)
D. Thalassemia

Explanation: **Explanation:** Hemolysis is classified into two types based on the site of red blood cell (RBC) destruction: **Intravascular** (within the blood vessels) and **Extravascular** (within the splenic or hepatic sinusoids) [1]. **Correct Answer: C. Paroxysmal Nocturnal Hemoglobinuria (PNH)** PNH is a classic example of **intravascular hemolysis** [2]. It is an acquired stem cell disorder caused by a mutation in the *PIGA* gene, leading to a deficiency of GPI-anchored proteins, specifically **CD55 (DAF)** and **CD59 (MIRL)** [2]. These proteins normally protect RBCs from complement-mediated attack. Their absence allows the Membrane Attack Complex (MAC) to form directly on the RBC surface, causing osmotic lysis within the circulation [2]. **Analysis of Incorrect Options:** * **A. Hereditary Spherocytosis:** This is a prototype of **extravascular hemolysis**. Molecular defects in membrane proteins (ankyrin, spectrin) result in spherical RBCs that are less deformable. These cells are trapped and destroyed by splenic macrophages [3]. * **B. Autoimmune Hemolytic Anemia (AIHA):** Most cases (Warm AIHA) involve IgG-coated RBCs being partially phagocytosed by splenic macrophages, leading to spherocyte formation and **extravascular** destruction [3]. (Note: Cold Agglutinin Disease can occasionally cause intravascular hemolysis, but it is primarily extravascular). * **D. Thalassemia:** This is a quantitative globin chain defect leading to "ineffective erythropoiesis" in the bone marrow and **extravascular** hemolysis of surviving RBCs in the spleen. **NEET-PG High-Yield Pearls:** * **Intravascular Markers:** Low haptoglobin, high LDH, hemoglobinuria, and hemosiderinuria [1]. * **Extravascular Markers:** Splenomegaly and jaundice (unconjugated hyperbilirubinemia) [1]. * **PNH Triad:** Hemolytic anemia, pancytopenia, and venous thrombosis (e.g., Budd-Chiari syndrome) [2]. * **Gold Standard Test for PNH:** Flow cytometry (looking for absence of CD55/CD59) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Question 1213: Which of the following statements regarding Chronic Myeloid Leukemia (CML) is true?

A. The size of splenomegaly is indicative of prognosis. (Correct Answer)
B. Phagocytic activity of white blood cells is reduced.
C. Sudan black stain is specific for myeloblasts.
D. All of the above.

Explanation: **Explanation:** **1. Why Option A is correct:** In Chronic Myeloid Leukemia (CML), the degree of **splenomegaly** is a well-established prognostic indicator [1]. Massive splenomegaly often correlates with a higher tumor burden, a higher percentage of blasts, and an increased risk of transformation into the accelerated phase or blast crisis [2]. It is a key component of clinical scoring systems like the **Sokal Score** and **Hasford Score**, which are used to predict survival and response to Tyrosine Kinase Inhibitors (TKIs). **2. Why the other options are incorrect:** * **Option B:** In CML, while the white blood cell count is massively elevated, the cells are mature and functionally competent [1]. Unlike in acute leukemias or certain qualitative disorders, the **phagocytic and bactericidal activity of neutrophils in CML is generally preserved** during the chronic phase [1]. * **Option C:** Sudan Black B (SBB) stain is used to identify myeloblasts by staining phospholipids in the granules. However, it is **not specific** for myeloblasts; it also stains precursors of the monocyte series and mature granulocytes. Furthermore, in the context of CML, the **Leukocyte Alkaline Phosphatase (LAP) score** (which is characteristically low) is a more specific diagnostic marker than SBB. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** CML is defined by the **t(9;22)** translocation, forming the **Philadelphia (Ph) chromosome** and the **BCR-ABL1** fusion gene [3]. * **Peripheral Smear:** Characterized by a "myelocyte bulge" (myelocytes > metamyelocytes) and **basophilia** (a hallmark of CML) [1]. * **LAP/NAP Score:** Decreased in CML; increased in Leukemoid Reaction and Polycythemia Vera. * **Drug of Choice:** **Imatinib** (a Tyrosine Kinase Inhibitor). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 625-626. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 624.

Question 1214: Lymph node biopsy of an AIDS patient shows what finding?

A. Wahin-Finkeldey cells
B. Marked follicular hyperplasia
C. 'Moth-eaten appearance'
D. All of the above (Correct Answer)

Explanation: **Explanation:** The lymph node changes in HIV/AIDS are dynamic and evolve based on the stage of the disease and the patient's immune status. 1. **Marked Follicular Hyperplasia:** In the early stages of HIV infection (Persistent Generalized Lymphadenopathy), there is an exuberant B-cell response [2]. This manifests as massive follicular hyperplasia with irregularly shaped (geographic) germinal centers. 2. **'Moth-eaten Appearance':** As the disease progresses, the germinal centers undergo "follicular lysis." Small lymphocytes from the mantle zone infiltrate the germinal centers, creating a fragmented or "moth-eaten" histological appearance [1]. 3. **Warthin-Finkeldey Cells:** These are multinucleated giant cells with eosinophilic nuclear and cytoplasmic inclusions. While classically associated with Measles, they are also frequently observed in the hyperplastic lymph nodes of HIV-infected individuals. **Why "All of the above" is correct:** All three features are characteristic histological findings in the lymphadenopathy associated with HIV/AIDS, representing different pathological processes (hyperplasia, involution, and viral cytopathic effects). **High-Yield Clinical Pearls for NEET-PG:** * **Early Stage (Stage I):** Florid follicular hyperplasia (B-cell proliferation) [2]. * **Intermediate Stage (Stage II):** Follicular involution and "moth-eaten" appearance [1]. * **Late Stage (Stage III):** Lymphocyte depletion; the node becomes "burnt out" with hyaline vascular changes, resembling Castleman disease [1]. * **Differential Diagnosis:** Warthin-Finkeldey cells are a "catch-all" high-yield fact—always think **Measles** first, but **HIV** second. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 555-556. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 257-258.

Question 1215: Microspherocytosis is seen in which of the following conditions?

A. Congenital spherocytosis
B. Autoimmune acquired hemolytic anemia
C. Thalassemia
D. All of the above (Correct Answer)

Explanation: **Explanation:** Microspherocytes are small, dark-staining red blood cells (RBCs) that have lost their central pallor and biconcave shape, becoming spherical. This occurs due to a **reduction in the surface-area-to-volume ratio**, usually resulting from the loss of portions of the RBC membrane [1]. 1. **Congenital Spherocytosis (HS):** This is the classic cause. Mutations in membrane proteins (Spectrin, Ankyrin, Band 3) lead to membrane instability. As these cells pass through splenic cords, pieces of the membrane are "nipped off" by macrophages, forcing the cell into a spherical shape [1]. 2. **Autoimmune Hemolytic Anemia (AIHA):** In warm-antibody AIHA (IgG), splenic macrophages recognize the Fc portion of antibodies coating the RBC. Instead of engulfing the whole cell, they "bite off" fragments of the membrane (partial erythrophagocytosis), resulting in microspherocytes [2]. 3. **Thalassemia:** While Thalassemia is primarily characterized by microcytic hypochromic cells and target cells, **microspherocytes** can be seen, particularly in HbH disease or severe forms, due to the removal of Heinz bodies (precipitated globin chains) by the spleen, which reduces the cell membrane surface area [3]. **Clinical Pearls for NEET-PG:** * **MCHC:** Microspherocytosis is the only condition where the Mean Corpuscular Hemoglobin Concentration (MCHC) is typically **increased** (>36 g/dL). * **Osmotic Fragility Test:** This is the gold standard screening test; spherocytes are more fragile and lyse earlier in hypotonic saline [4]. * **Coombs Test:** Used to differentiate the causes. HS is **Coombs negative**, while AIHA is **Coombs positive**. * **Other causes:** Microspherocytes are also a hallmark of **thermal/burn injuries** (due to direct heat damage to the membrane). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 642-643. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.

Question 1216: Which of the following is NOT a form of histiocytosis?

A. Letterer-Siwe syndrome
B. Chloroma (Correct Answer)
C. Hand-Schüller-Christian triad
D. Eosinophilic granuloma

Explanation: **Explanation:** The correct answer is **Chloroma** because it is a manifestation of myeloid leukemia, not a histiocytic disorder. **1. Why Chloroma is the correct answer:** A **Chloroma** (also known as **Granulocytic Sarcoma** or Myeloid Sarcoma) is an extramedullary solid tumor mass composed of primitive myeloid cells (myeloblasts). It is most commonly associated with **Acute Myeloid Leukemia (AML)**, particularly the M4 and M5 subtypes. The name "Chloroma" derives from its greenish appearance due to the presence of the enzyme **myeloperoxidase (MPO)**. **2. Why the other options are incorrect:** Options A, C, and D are the three classic clinical presentations of **Langerhans Cell Histiocytosis (LCH)**, a clonal proliferation of dendritic cells (histiocytes) [1]: * **Letterer-Siwe syndrome:** The acute disseminated form, typically seen in infants (<2 years). It involves multiple organs (skin, liver, spleen) and has a poor prognosis. * **Hand-Schüller-Christian triad:** The chronic disseminated form, characterized by the classic triad of **diabetes insipidus, exophthalmos, and lytic bone lesions** (skull). * **Eosinophilic granuloma:** The benign, localized form, usually presenting as solitary or few lytic bone lesions in older children or adults. **High-Yield Clinical Pearls for NEET-PG:** * **LCH Marker:** The pathognomonic electron microscopy finding in LCH is the **Birbeck granule** (tennis-racket shaped) [1]. * **Immunohistochemistry (IHC):** LCH cells are characteristically positive for **CD1a, S100, and CD207 (Langerin)** [1]. * **Chloroma Association:** Frequently associated with the chromosomal translocation **t(8;21)** in AML. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 629-630.

Question 1217: Which of the following is NOT a minor diagnostic criterion for multiple myeloma?

A. Lytic bone lesions
B. Plasmacytosis greater than 20%
C. Plasmacytoma on biopsy (Correct Answer)
D. Monoclonal globulin spike on serum electrophoresis of > 2.5 g/dl for IgG, >1.5 g/dl for IgA

Explanation: To answer this question correctly, one must recall the **Salmon-Durie Diagnostic Criteria** for Multiple Myeloma, which categorizes findings into Major and Minor criteria. ### **Explanation of the Correct Answer** **Option C (Plasmacytoma on biopsy)** is a **Major Criterion**, not a minor one. According to the Salmon-Durie system, a tissue biopsy proven to contain a plasmacytoma (a localized collection of malignant plasma cells) is one of the three major pillars of diagnosis [4], alongside bone marrow plasmacytosis >30% and high-level M-protein spikes [3]. ### **Analysis of Incorrect Options (Minor Criteria)** * **Option A (Lytic bone lesions):** This is a classic **Minor Criterion**. It represents the "B" in the CRAB acronym (Bone lesions) and signifies end-organ damage [1]. * **Option B (Plasmacytosis 10–30%):** Bone marrow involvement between 10% and 30% is a **Minor Criterion**. (Note: >30% is Major) [1]. * **Option D (M-protein spike):** A monoclonal spike of **<3.5 g/dL for IgG** or **<2.0 g/dL for IgA** is considered a **Minor Criterion**. The values provided in the option fall within the minor range [3]. ### **High-Yield Clinical Pearls for NEET-PG** * **Diagnosis Requirement:** Diagnosis of Multiple Myeloma requires: (1 Major + 1 Minor) OR (3 Minor criteria including A + B). * **CRAB Criteria:** Modern diagnosis (IMWG) focuses on **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [5]. * **Peripheral Smear:** Look for **Rouleaux formation** due to increased serum proteins (decreased zeta potential) [2]. * **Urinalysis:** Bence-Jones proteins (free light chains) are detected by the heat precipitation test, not by standard dipsticks [2]. * **Radiology:** "Punched-out" lytic lesions are best seen on a skeletal survey; **Technetium-99 bone scans are often negative** because they detect osteoblastic activity, which is absent in myeloma [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 607-608. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 608-609. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 606-607. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617.

Question 1218: What is the most characteristic finding in megaloblastic anemia?

A. Target cell
B. Macrocyte
C. Microovalocyte
D. Macroovalocyte (Correct Answer)

Explanation: ### Explanation **Megaloblastic anemia** is a subset of macrocytic anemia caused by impaired DNA synthesis, most commonly due to Vitamin B12 or Folate deficiency [1, 2]. This impairment leads to **nuclear-cytoplasmic asynchrony**, where the nucleus matures slower than the cytoplasm, resulting in larger, abnormal precursor cells [1, 3]. **Why Macroovalocytes are the Correct Answer:** While several conditions cause large red blood cells (macrocytes), the presence of **Macroovalocytes** (large, oval-shaped erythrocytes) is the hallmark morphological feature of megaloblastic anemia [1]. These cells are formed due to defective erythropoiesis in the bone marrow. When combined with **hypersegmented neutrophils** (defined as >5% of neutrophils having 5 lobes or at least one neutrophil with 6 lobes), the diagnosis of megaloblastic anemia is highly specific [1, 2]. **Analysis of Incorrect Options:** * **A. Target Cells (Codocytes):** These are characterized by a central spot of hemoglobin and are typically seen in Thalassemia, Liver disease, and post-splenectomy states. * **B. Macrocyte:** This is a generic term for any RBC with an MCV >100 fL. While present in megaloblastic anemia, macrocytes can also be seen in non-megaloblastic states like alcoholism, hypothyroidism, and pregnancy. They are usually round, not oval. * **C. Microovalocyte:** These are small, oval cells often seen in iron deficiency anemia or certain hereditary conditions; they are the opposite of the large cells seen in megaloblastic anemia. **NEET-PG High-Yield Pearls:** * **Earliest Sign:** The appearance of hypersegmented neutrophils in the peripheral smear is often the earliest sign of megaloblastic anemia [2]. * **Bone Marrow:** Shows "Blue Marrow" due to intense erythroid hyperplasia and "sieve-like" chromatin in megaloblasts [1, 3]. * **Howell-Jolly Bodies:** These nuclear remnants are frequently seen in the RBCs of megaloblastic anemia patients due to dysfunctional erythropoiesis. * **MCV:** Usually significantly elevated, often >110–120 fL. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 654-655.

Question 1219: The heme portion of the hemoglobin molecule consists of:

A. Porphyrin ring with a molecule of Fe in the center
B. A polypeptide chain containing Fe
C. A pyrole ring with four molecules of Fe in the center
D. Four porphyrin rings, each containing a molecule of Fe in the center (Correct Answer)

Explanation: ### Explanation **1. Why Option D is Correct:** Hemoglobin is a tetrameric protein composed of four globin chains. Each globin chain is non-covalently bound to one **heme group**. A single heme group consists of one **protoporphyrin IX ring** with a single atom of **ferrous iron ($Fe^{2+}$)** coordinated at its center [2]. Since a complete hemoglobin molecule contains four globin chains, it must contain **four heme groups** (four porphyrin rings and four iron atoms). This structure allows one hemoglobin molecule to bind up to four molecules of oxygen. **2. Why the Other Options are Incorrect:** * **Option A:** This describes a *single* heme group. While technically accurate for one unit, the question asks for the heme portion of the *hemoglobin molecule* as a whole, which is a tetramer. * **Option B:** This is a definition of a metalloprotein or a globin chain, but it is not the definition of heme. Heme is a prosthetic group, not a polypeptide. * **Option C:** A porphyrin ring is composed of **four pyrrole rings** linked together. A single pyrrole ring cannot hold four iron atoms; rather, four pyrrole rings form one porphyrin ring to hold one iron atom. **3. NEET-PG High-Yield Clinical Pearls:** * **Iron State:** Iron must be in the **ferrous state ($Fe^{2+}$)** to bind oxygen [1]. If oxidized to the **ferric state ($Fe^{3+}$)**, it forms **methemoglobin**, which cannot bind $O_2$. * **Rate-Limiting Step:** The first step of heme synthesis (Succinyl CoA + Glycine → $\delta$-ALA) is catalyzed by **ALA synthase**, requiring **Vitamin $B_6$ (Pyridoxine)** as a cofactor. Deficiency leads to Sideroblastic Anemia. * **2,3-BPG:** This molecule binds to the central cavity of the hemoglobin tetramer, stabilizing the "T" (Tense) state and promoting oxygen unloading (shifting the dissociation curve to the right). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 589-590. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 658.

Question 1220: Which of the following is seen in idiopathic thrombocytopenic purpura?

A. Thrombocytosis
B. Increased prothrombin time
C. Increased bleeding time (Correct Answer)
D. Increased clotting time

Explanation: **Explanation:** **Idiopathic Thrombocytopenic Purpura (ITP)** is an acquired autoimmune disorder characterized by the immune-mediated destruction of platelets (via anti-GP IIb/IIIa antibodies) and impaired platelet production [1]. **Why the correct answer is right:** * **Increased Bleeding Time (BT):** Bleeding time is a clinical indicator of **platelet function and number** (primary hemostasis) [2]. In ITP, the hallmark is isolated thrombocytopenia (low platelet count). When the platelet count falls below the critical threshold, the formation of the primary platelet plug is delayed, leading to a prolonged bleeding time. **Why the incorrect options are wrong:** * **Thrombocytosis (A):** This refers to an *increase* in platelet count. ITP is defined by thrombocyto**penia** (decreased count). * **Increased Prothrombin Time (PT) (B):** PT measures the extrinsic and common pathways of the coagulation cascade (secondary hemostasis). Since ITP is a platelet disorder and not a coagulation factor deficiency, PT remains normal [1]. * **Increased Clotting Time (CT) (D):** CT (or aPTT) measures the intrinsic and common pathways. Like PT, these remain unaffected in ITP because the coagulation factors are intact [1]. **NEET-PG High-Yield Pearls:** * **Bone Marrow Findings:** Characterized by **increased megakaryocytes** (compensatory hyperplasia) with many immature forms [2]. * **Diagnosis of Exclusion:** ITP is diagnosed only after ruling out other causes of thrombocytopenia [1]. * **Clinical Presentation:** Typically presents with mucocutaneous bleeding (petechiae, purpura, epistaxis) in a patient with a normal-sized spleen (splenomegaly is usually absent) [2]. * **Treatment:** First-line therapy is typically **Corticosteroids** or IVIG. Splenectomy is considered for refractory cases [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 619-621.

Practice by Chapter

Anemias: Classification and Approach

Practice Questions

Hemolytic Anemias

Practice Questions

Myeloproliferative Neoplasms

Practice Questions

Myelodysplastic Syndromes

Practice Questions

Acute Leukemias

Practice Questions

Chronic Leukemias

Practice Questions

Lymphomas and Lymphoid Neoplasms

Practice Questions

Plasma Cell Disorders

Practice Questions

Bleeding Disorders

Practice Questions

Thrombotic Disorders

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free