Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1171: Hypersegmented neutrophils are characteristic findings in which of the following conditions?

A. Microcytic hypochromic anemia
B. Sideroblastic anemia
C. Megaloblastic anemia (Correct Answer)
D. Hemolytic anemia

Explanation: **Explanation:** **Megaloblastic anemia** is the correct answer because it is characterized by impaired DNA synthesis, most commonly due to Vitamin B12 or Folic acid deficiency [1], [2]. This impairment leads to **nuclear-cytoplasmic asynchrony**, where the nucleus matures slower than the cytoplasm [2], [3]. In neutrophils, this results in nuclear hypersegmentation [1], [2]. * **Definition:** A neutrophil is considered "hypersegmented" if it has **$\geq$ 6 lobes** or if more than 5% of neutrophils have **5 lobes** [1]. This is often the earliest peripheral blood sign of megaloblastic anemia, appearing even before macrocytosis (increased MCV). **Analysis of Incorrect Options:** * **A. Microcytic hypochromic anemia:** Typically caused by Iron Deficiency Anemia (IDA). The peripheral smear shows small, pale RBCs (pencil cells), not hypersegmented neutrophils. * **B. Sideroblastic anemia:** Characterized by "ring sideroblasts" in the bone marrow due to impaired heme synthesis. It does not affect leukocyte nuclear maturation. * **C. Hemolytic anemia:** Characterized by increased RBC destruction. Smear findings usually include schistocytes (microangiopathic) or spherocytes (hereditary spherocytosis), with a high reticulocyte count. **High-Yield NEET-PG Pearls:** 1. **Rule of Five:** The presence of a single neutrophil with 6 lobes is diagnostic of megaloblastic change [1]. 2. **Macropolycytes:** These are exceptionally large hypersegmented neutrophils. 3. **Other causes:** Apart from B12/Folate deficiency, hypersegmentation can be seen in **Uremia** and as a side effect of **Methotrexate** or **Hydroxyurea** therapy. 4. **Differential:** Do not confuse this with the **Pelger-Huët anomaly**, which shows hyposegmented (spectacle-shaped) nuclei. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 654-655. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 594-595.

Question 1172: Translocation (8;14) is characteristic of which of the following conditions?

A. Burkitt's lymphoma (Correct Answer)
B. Ataxia telangiectasia
C. Acute lymphoblastic leukemia (ALL)
D. Chronic myeloid leukemia (CML)

Explanation: **Explanation:** **Burkitt’s Lymphoma (Correct Answer):** The hallmark of Burkitt’s lymphoma is the **t(8;14)** translocation. This involves the transposition of the **c-MYC proto-oncogene** from chromosome 8 to the **Immunoglobulin Heavy chain (IgH)** gene locus on chromosome 14 [1]. Because the IgH promoter is highly active in B-cells, this leads to the constitutive overexpression of c-MYC, a potent transcription factor that drives rapid cellular proliferation [1]. This results in the classic "starry-sky" appearance seen on histology [3]. **Analysis of Incorrect Options:** * **Ataxia Telangiectasia:** This is an autosomal recessive genomic instability syndrome caused by mutations in the **ATM gene** (chromosome 11). It is characterized by cerebellar ataxia, telangiectasias, and immune deficiency, rather than a specific t(8;14) translocation. * **Acute Lymphoblastic Leukemia (ALL):** While ALL involves various translocations, the most characteristic ones are **t(12;21)** (associated with a good prognosis in children) or **t(9;22)** (Philadelphia chromosome, associated with a poor prognosis) [3]. * **Chronic Myeloid Leukemia (CML):** CML is defined by the **t(9;22)** translocation, known as the **Philadelphia chromosome**, which creates the *BCR-ABL1* fusion protein with constitutive tyrosine kinase activity. **High-Yield Clinical Pearls for NEET-PG:** * **Variants of Burkitt’s:** While t(8;14) is most common (80%), variant translocations include **t(2;8)** (kappa light chain) and **t(22;8)** (lambda light chain) [1]. * **Morphology:** Look for "Starry-sky" appearance (tingible body macrophages) and medium-sized B-cells with multiple nucleoli and cytoplasmic vacuoles [3]. * **EBV Association:** Strongly linked with the Endemic (African) form, typically presenting as a jaw mass [2]. The Sporadic form often presents as an abdominal/ileocecal mass [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [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. 605-606. [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. 606.

Question 1173: Which malignant tumor is associated with Waldenstrom macroglobulinemia?

A. Smoldering myeloma
B. Primary effusion lymphoma
C. Mycosis fungoides
D. Lymphoplasmacytic lymphoma (Correct Answer)

Explanation: **Explanation:** **Waldenström Macroglobulinemia (WM)** is a clinical syndrome defined by the presence of a monoclonal IgM protein (macroglobulin) in the blood, resulting from the bone marrow infiltration of **Lymphoplasmacytic Lymphoma (LPL)** [1]. 1. **Why Lymphoplasmacytic Lymphoma (LPL) is correct:** LPL is a mature B-cell neoplasm characterized by a mixture of small B-lymphocytes, plasmacytoid lymphocytes, and plasma cells [1]. According to the WHO classification, WM is specifically the subset of LPL that involves the bone marrow and secretes an IgM monoclonal spike. The large size of the IgM pentamer leads to the classic **hyperviscosity syndrome** associated with this disease [1]. 2. **Why other options are incorrect:** * **Smoldering Myeloma:** This is an asymptomatic precursor to Multiple Myeloma. While it involves monoclonal proteins, it is associated with IgG or IgA, not IgM, and involves pure plasma cell proliferation rather than lymphoplasmacytic cells [2]. * **Primary Effusion Lymphoma:** This is a rare B-cell lymphoma caused by HHV-8, typically presenting as malignant effusions (pleural/pericardial) in HIV-positive patients. * **Mycosis Fungoides:** This is a cutaneous T-cell lymphoma (CTCL) and has no association with IgM paraproteinemia or LPL. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Hallmark:** Over 90% of WM/LPL cases harbor the **MYD88 L265P mutation**. * **Clinical Presentation:** Visual disturbances (sausage-link retinopathy), neurological symptoms (due to hyperviscosity) [1], and hepatosplenomegaly. * **Diagnosis:** Bone marrow biopsy shows "lymphoplasmacytic" infiltrate; Serum electrophoresis shows an **IgM M-spike** [1]. * **Distinction:** Unlike Multiple Myeloma, WM typically does **not** cause lytic bone lesions or hypercalcemia. **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. 609-610. [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. 608-609.

Question 1174: Which of the following tests does NOT assess platelet function?

A. Prothrombin time (Correct Answer)
B. Bleeding time
C. Clot retraction time
D. Prothrombin deactivation

Explanation: The assessment of hemostasis is divided into primary hemostasis (platelet plug formation) and secondary hemostasis (coagulation cascade). **Why Prothrombin Time (PT) is the correct answer:** **Prothrombin Time (PT)** measures the **extrinsic and common pathways** of the coagulation cascade (Factors VII, X, V, II, and I). It evaluates the efficiency of plasma clotting factors rather than platelet activity [2]. Therefore, it does not assess platelet function. **Analysis of other options:** * **Bleeding Time (BT):** This is the classic *in vivo* test for **primary hemostasis**. It measures the time taken for a standardized skin wound to stop bleeding, which depends on platelet number and their ability to adhere and aggregate [1]. * **Clot Retraction Time (CRT):** After a clot forms, platelets use their contractile protein (**thrombosthenin**) to pull fibrin strands together, squeezing out serum [1]. Abnormal CRT indicates qualitative platelet defects (e.g., Glanzmann Thrombasthenia) or severe thrombocytopenia. * **Prothrombin Consumption Test (PCT):** (Often referred to in older texts/variations like deactivation/utilization). This test measures the amount of prothrombin remaining in the serum after clotting. Since platelets provide the phospholipid surface (Platelet Factor 3) necessary for converting prothrombin to thrombin, a failure to "consume" prothrombin indicates a platelet functional defect. **High-Yield Clinical Pearls for NEET-PG:** * **Glanzmann Thrombasthenia:** Normal platelet count, but defective GpIIb/IIIa (failure of aggregation). BT is prolonged; CRT is abnormal [3]. * **Bernard-Soulier Syndrome:** Low/Normal platelet count, giant platelets, defective GpIb (failure of adhesion). BT is prolonged [3]. * **PFA-100:** The modern "gold standard" automated replacement for Bleeding Time to screen for platelet dysfunction [2]. * **Ristocetin Aggregation:** Absent in both von Willebrand Disease and Bernard-Soulier Syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 664-665. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.

Question 1175: What are the essential WHO criteria for polycythemia vera?

A. Tyrosine kinase JAK2 V617F and other mutations (Correct Answer)
B. Low levels of erythropoietin
C. Thrombocytosis
D. Increased MCV

Explanation: Polycythemia Vera (PV) is a chronic myeloproliferative neoplasm characterized by the autonomous overproduction of red blood cells [2]. According to the **WHO 2022 (and 2016) criteria**, the diagnosis relies on three major criteria: 1. **Elevated Hemoglobin/Hematocrit** (Hb >16.5 g/dL in men, >16.0 g/dL in women) [2]. 2. **Bone marrow biopsy** showing hypercellularity with panmyelosis (increased erythroid, granulocytic, and megakaryocytic proliferation) [1]. 3. **Presence of JAK2 V617F or JAK2 exon 12 mutation.** [1][3] **Option A** is correct because the JAK2 mutation is a **Major Criterion** present in >95% of PV cases [1]. It leads to constitutive activation of the JAK-STAT pathway, making erythroid progenitors hypersensitive to erythropoietin [3]. **Why other options are incorrect:** * **Option B:** Low serum erythropoietin (EPO) is a **Minor Criterion**, not a major one. While highly suggestive of PV, it is not as definitive as the genetic mutation. * **Option C:** Thrombocytosis is a common finding in PV (panmyelosis), but it is not a diagnostic requirement. It is more characteristic of Essential Thrombocythemia [1]. * **Option D:** PV typically presents with a **low or normal MCV** due to "relative iron deficiency" caused by the massive consumption of iron stores for hemoglobin synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common mutation:** JAK2 V617F (Exon 14) [3]. * **Clinical hallmark:** Aquagenic pruritus (itching after a hot bath) and plethora. * **Complication:** High risk of thrombotic events (Budd-Chiari syndrome) and spent phase (myelofibrosis) [1]. * **Treatment of choice:** Phlebotomy and Hydroxyurea. **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. 624-628. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615.

Question 1176: Which immunohistochemistry marker is characteristic of histiocytosis X?

A. CD1a (Correct Answer)
B. CD57
C. CD3
D. CD68

Explanation: **Explanation:** **Histiocytosis X**, now more commonly known as **Langerhans Cell Histiocytosis (LCH)**, is a clonal proliferation of Langerhans cells [1]. These cells are specialized dendritic cells normally found in the skin and mucosa. **Why CD1a is the correct answer:** Langerhans cells are characterized by the expression of specific surface markers that aid in their identification. **CD1a** and **Langerin (CD207)** are the most specific immunohistochemical markers for LCH [1]. CD1a is a glycoprotein structurally related to MHC molecules and is essential for the definitive diagnosis of this condition. **Analysis of Incorrect Options:** * **CD57:** This is a marker primarily used for **Natural Killer (NK) cells** and certain neuroendocrine tissues. It has no diagnostic utility in LCH. * **CD3:** This is the definitive pan-**T-cell marker**. While T-cells may be present in the inflammatory background of LCH lesions, the neoplastic cells themselves are CD3 negative. * **CD68:** This is a general marker for **macrophages/monocytes**. While LCH cells may show weak positivity for CD68, it is non-specific and found in various other histiocytic disorders (like Sinus Histiocytosis). It is not diagnostic for LCH. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy:** The pathognomonic finding is the **Birbeck Granule**, a "tennis-racket" shaped pentalaminar cytoplasmic organelle [1]. * **S100 Protein:** LCH cells are almost always **S100 positive** (though this is non-specific). * **Clinical Triad (Hand-Schüller-Christian disease):** Calvarial bone defects, exophthalmos, and diabetes insipidus. * **Letterer-Siwe Disease:** The aggressive, multisystem form seen in infants (<2 years). **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 1177: Beta-2 microglobulin is a marker for which condition?

A. Multiple Myeloma (Correct Answer)
B. Mycosis fungoides
C. B-Cell lymphoma
D. Mantle cell lymphoma

Explanation: **Explanation:** **Beta-2 microglobulin ($\beta$2M)** is a low-molecular-weight protein that forms the light chain component of the **MHC Class I molecule**, present on the surface of all nucleated cells. **Why Multiple Myeloma is the correct answer:** In Multiple Myeloma (MM), there is a high turnover of malignant plasma cells, leading to increased shedding of $\beta$2M into the serum. In NEET-PG, it is high-yield to remember that $\beta$2M is the **most important prognostic marker** for Multiple Myeloma [1]. It is a core component of the **International Staging System (ISS)** for MM: * **Stage I:** $\beta$2M < 3.5 mg/L * **Stage II:** $\beta$2M 3.5–5.5 mg/L * **Stage III:** $\beta$2M > 5.5 mg/L Higher levels correlate with a higher tumor burden and renal impairment [1]. **Analysis of Incorrect Options:** * **Mycosis Fungoides:** This is a T-cell lymphoma of the skin. While LDH may be elevated, $\beta$2M is not a specific diagnostic or staging marker used in clinical practice for this condition. * **B-Cell Lymphoma & Mantle Cell Lymphoma:** While $\beta$2M can be elevated in various lymphoproliferative disorders due to cell turnover, it is not the primary or definitive marker for these conditions. For these, LDH and specific immunophenotyping (e.g., CD5, CD20, Cyclin D1) are more relevant. **Clinical Pearls for NEET-PG:** * $\beta$2M levels are also elevated in **renal failure** because it is normally filtered by the glomerulus; thus, its levels must be interpreted cautiously in patients with kidney disease [1]. * **Mnemonic for ISS Staging:** Remember the cut-offs **3.5 and 5.5**. * Other key markers in MM: **M-Spike** (Electrophoresis), **Bence-Jones proteins** (Urine) [1], [2], and **CD138/CD38** (Flow cytometry) [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. 606-609. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-618.

Question 1178: For acute leukemia, the blast cell count should be greater than what percentage?

A. 10%
B. 20% (Correct Answer)
C. 30%
D. 40%

Explanation: **Explanation:** The diagnosis of **Acute Leukemia** (both AML and ALL) is primarily based on the presence of blast cells in the bone marrow or peripheral blood. According to the **WHO Classification of Tumors of Haematopoietic and Lymphoid Tissues**, the mandatory threshold for a diagnosis of acute leukemia is a blast count of **≥20%** [1]. **Why 20% is correct:** Historically, the threshold was higher, but the WHO lowered it to 20% to ensure earlier diagnosis and treatment [1]. It is important to note a high-yield exception: in **Acute Myeloid Leukemia (AML)**, if specific recurrent genetic abnormalities are present—such as t(8;21), inv(16), or t(15;17)—the diagnosis of AML can be made **regardless of the blast percentage**, even if it is less than 20% [2]. **Analysis of Incorrect Options:** * **10% (Option A):** This is below the diagnostic threshold for acute leukemia. Patients with 10-19% blasts are typically classified under **Myelodysplastic Syndromes (MDS)** with excess blasts [1]. * **30% (Option C):** This was the diagnostic threshold under the older **FAB (French-American-British) classification**. Modern practice follows the WHO criteria of 20%. * **40% (Option D):** This is significantly higher than the required diagnostic limit and does not represent a standard classification cutoff. **Clinical Pearls for NEET-PG:** * **Auer Rods:** Their presence is pathognomonic for myeloblasts (AML), most commonly seen in the M3 subtype (APML) [2]. * **Marrow Cellularity:** Acute leukemia is usually associated with a hypercellular marrow. * **Flow Cytometry:** Essential for lineage differentiation (e.g., CD13/CD33 for myeloid; CD10/CD19 for B-cell ALL). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614. [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, p. 620.

Question 1179: Post-transplant lymphoproliferative disorder is most commonly associated with which cell type?

A. T cell
B. B cell (Correct Answer)
C. Null cell
D. NK cell

Explanation: **Explanation:** Post-transplant lymphoproliferative disorder (PTLD) refers to a spectrum of conditions ranging from benign lymphoid hyperplasia to malignant lymphoma occurring in patients following solid organ or hematopoietic stem cell transplantation. **Why B cell is correct:** The vast majority (**>85-90%**) of PTLD cases are of **B-cell origin**. The primary driver is the **Epstein-Barr Virus (EBV)**. In the setting of therapeutic immunosuppression (especially T-cell depletion), the host’s cytotoxic T-cells can no longer control EBV-infected B-cells [1]. This leads to the unchecked proliferation of EBV-transformed B-lymphocytes, which can progress from polyclonal expansions to monoclonal B-cell lymphomas (most commonly Diffuse Large B-cell Lymphoma). **Why other options are incorrect:** * **T cell:** While T-cell PTLDs do exist, they are rare (<10-15% of cases), typically occur later after transplantation, and are often not associated with EBV. * **NK cell:** These are extremely rare subtypes of PTLD. * **Null cell:** This term refers to lymphocytes lacking traditional B or T cell surface markers; they do not represent the standard pathology of PTLD. **High-Yield Clinical Pearls for NEET-PG:** * **Most common viral association:** EBV (Epstein-Barr Virus) [1]. * **Risk Factors:** Degree of immunosuppression, EBV-seronegative recipient receiving an organ from an EBV-seropositive donor (primary infection). * **Management:** The first line of management is often the **reduction of immunosuppressive therapy**, which allows the host immune system to recover and target the proliferating B-cells. * **Common Histology:** Diffuse Large B-cell Lymphoma (DLBCL) is the most frequent morphological subtype. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 368-369.

Question 1180: A patient presents with painless lymphadenopathy. A biopsy reveals binucleated owl-shaped nuclei with a clear vacuolated area. Immunohistochemistry shows positivity for CD15 and CD30. What is the most probable diagnosis?

A. Nodular sclerosis (Correct Answer)
B. Large granular lymphocytic lymphoma
C. Lymphocyte depletion type
D. Lymphocyte predominant Hodgkin lymphoma

Explanation: ### Explanation **Correct Answer: A. Nodular Sclerosis** The clinical presentation and histopathology described are classic for **Classical Hodgkin Lymphoma (cHL)**. The "binucleated owl-shaped nuclei" are pathognomonic **Reed-Sternberg (RS) cells** [1], [3]. These cells typically express **CD15** and **CD30**, but are negative for CD45 and CD20. Among the subtypes of cHL, **Nodular Sclerosis** is the most common variant (60-70% of cases). It is characterized by the presence of **Lacunar cells** (RS cells in a clear, vacuolated space caused by formalin fixation artifact) and collagen bands dividing the lymph node into nodules [1], [4]. It frequently involves the mediastinum and has a predilection for young females [2], [4]. **Why other options are incorrect:** * **B. Large granular lymphocytic lymphoma:** This is a T-cell or NK-cell malignancy characterized by mature lymphocytes with abundant cytoplasm and azurophilic granules. It does not feature RS cells or CD15/CD30 positivity. * **C. Lymphocyte depletion type:** While this is a subtype of cHL with CD15/CD30+ RS cells, it is the rarest form, typically seen in elderly or HIV+ patients, and is characterized by a paucity of background lymphocytes rather than the "lacunar" morphology implied by the vacuolated area [5]. * **D. Lymphocyte predominant Hodgkin lymphoma (NLPHL):** This is a distinct entity. The characteristic cells are **"Popcorn cells"** (L&H cells) which are **CD20+ and CD45+**, but **CD15 and CD30 negative** [1]. **High-Yield Clinical Pearls for NEET-PG:** * **RS Cell Markers:** CD15+, CD30+, CD45-, CD20- (except in NLPHL). * **Bimodal Age Distribution:** Hodgkin Lymphoma peaks at 15–35 years and again after 50 years [3]. * **EBV Association:** Most strongly associated with the Mixed Cellularity subtype [2]. * **Prognosis:** Lymphocyte Predominant has the best prognosis; Lymphocyte Depletion has the worst. Nodular Sclerosis generally has an excellent prognosis [2]. **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, p. 616. [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. 616-618. [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. 614-616. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 558-559. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560.

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Thrombotic Disorders

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