Hematopathology — MCQs

A 19-year-old man has had recurrent bleeding occur in his knee when playing contact sports. He has no history of spontaneous bleeding, but his brother had similar problems. Consultation with a specialist reveals that he has "mild" hemophilia A. Which of the following factor abnormalities is consistent with this diagnosis?

Q956Easy

Diffuse large cell lymphoma is classified as which grade of non-Hodgkin's lymphoma?

Q957Easy

Why do patients with sickle cell trait not manifest the same symptoms as those with sickle cell disease?

Q958Medium

Schistocytes in peripheral smear are seen in all except:

Q959Medium

Which of the following is NOT included in the myelodysplastic syndromes?

Q960Easy

Diagnosis of Hodgkin's disease is confirmed by?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 951: All of the following are true about nodular sclerosis of Hodgkin's disease except?

A. Well-formed fibrous bands
B. CD15 positive
C. CD20 positive (Correct Answer)
D. Infiltration by plasma cells

Explanation: **Explanation:** Nodular Sclerosis (NS) is the most common subtype of Classical Hodgkin Lymphoma (CHL) [1]. The hallmark of CHL is the presence of **Reed-Sternberg (RS) cells** (or their variants) in a reactive inflammatory background [3]. **Why Option C is the correct answer:** In Classical Hodgkin Lymphoma (including the Nodular Sclerosis subtype), the neoplastic cells are derived from B-cells but characteristically **lose their B-cell markers**, such as **CD20**. Instead, they express **CD15** and **CD30**. Therefore, stating that it is CD20 positive is incorrect [2]. (Note: CD20 is typically positive in *Nodular Lymphocyte Predominant Hodgkin Lymphoma*, which is a distinct entity from CHL) [3]. **Analysis of other options:** * **Option A (Well-formed fibrous bands):** This is the defining morphological feature of NS. Broad bands of collagenous fibrosis divide the lymph node into circumscribed nodules. * **Option B (CD15 positive):** RS cells in all classical subtypes are characteristically positive for CD15 and CD30 [2]. * **Option D (Infiltration by plasma cells):** The "milieu" of Hodgkin’s disease consists of a polymorphic infiltrate of non-neoplastic reactive cells, including lymphocytes, plasma cells, eosinophils, and histiocytes [2]. **High-Yield Pearls for NEET-PG:** 1. **Lacunar Cells:** The specific RS cell variant seen in Nodular Sclerosis. 2. **Epidemiology:** NS is the only subtype more common in females and typically presents with a mediastinal mass in young adults [1], [2]. 3. **Immunophenotype of CHL:** CD15+, CD30+, CD45 (LCA) negative, and CD20 negative (usually). 4. **Prognosis:** Nodular Sclerosis generally carries an excellent prognosis [2]. **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. 558-559. [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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 556-557.

Question 952: Birbeck's granule is seen in which of the following conditions?

A. Granulomatous vasculitis
B. Histiocytic necrotizing lymphadenitis
C. Langerhans cell histiocytosis (Correct Answer)
D. Multiple myeloma

Explanation: **Explanation:** **Langerhans Cell Histiocytosis (LCH)** is the correct answer because **Birbeck granules** are the pathognomonic ultrastructural hallmark of Langerhans cells [1]. On electron microscopy, these granules appear as rod-shaped, pentalaminar cytoplasmic organelles with a central striated line and a bulbous end, giving them a characteristic **"tennis racket" appearance** [1]. They contain the protein **Langerin (CD207)**, which is involved in endocytosis and antigen processing [1]. **Analysis of Incorrect Options:** * **Granulomatous vasculitis (e.g., Wegener’s):** Characterized by necrotizing granulomas and vasculitis. Diagnosis relies on ANCA testing and biopsy showing giant cells, not Birbeck granules. * **Histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto Disease):** A benign condition presenting with cervical lymphadenopathy. Histology shows paracortical necrosis with karyorrhectic debris and histiocytes, but lacks Langerhans cells. * **Multiple myeloma:** A plasma cell neoplasm characterized by "clock-face" nuclei, perinuclear halos (Golgi zone), and Russell bodies (cytoplasmic Ig inclusions). **High-Yield Clinical Pearls for NEET-PG:** * **Immunophenotype of LCH:** Positive for **S100, CD1a, and Langerin (CD207)**. CD1a and Langerin are highly specific [1]. * **Clinical Presentation:** Can range from a solitary bone lesion (Eosinophilic granuloma) to multisystem involvement (Letterer-Siwe disease). * **Radiology:** Often presents as "punched-out" lytic lesions in the skull. * **BRAF Mutation:** Approximately 50% of LCH cases harbor the **BRAF V600E** mutation, which is a frequent target for molecular testing [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. 629-630.

Question 953: Erythrocyte Sedimentation Rate is zero in which of the following conditions?

A. Abetalipoproteinemia
B. Afibrinogenemia (Correct Answer)
C. Asplenia
D. Aplastic anemia

Explanation: **Explanation:** The **Erythrocyte Sedimentation Rate (ESR)** is a non-specific marker of inflammation that measures the rate at which red blood cells (RBCs) sink to the bottom of a tube. This process is primarily driven by **Rouleaux formation** (stacking of RBCs) [1]. 1. **Why Afibrinogenemia is correct:** Fibrinogen is a large, asymmetrical, positively charged plasma protein. It neutralizes the negative surface charge (zeta potential) of RBCs, allowing them to clump together and sediment faster. In **Afibrinogenemia** (complete absence of fibrinogen), Rouleaux formation cannot occur. Without these heavy aggregates, the RBCs remain in suspension, resulting in an **ESR of zero**. 2. **Analysis of Incorrect Options:** * **Abetalipoproteinemia:** Characterized by Acanthocytes (spur cells). While abnormal shapes interfere with Rouleaux and *lower* the ESR, it rarely reaches absolute zero. * **Asplenia:** The absence of a spleen leads to Howell-Jolly bodies and target cells, but it does not fundamentally halt the sedimentation process. * **Aplastic Anemia:** In anemia, there are fewer RBCs relative to plasma. This reduces the upward force of displacing plasma, typically causing an **elevated ESR**, not a zero ESR. **High-Yield Clinical Pearls for NEET-PG:** * **Factors increasing ESR:** Pregnancy, Anemia, Inflammation (via Fibrinogen/CRP), Macroglobulinemia (Multiple Myeloma), and advancing age [1]. * **Factors decreasing ESR (Near Zero):** Polycythemia (too many RBCs) [2], Afibrinogenemia, Sickle cell anemia (poikilocytosis prevents stacking), and severe Leukocytosis. * **Westergren Method** is the gold standard for measuring ESR. * **Note:** Fibrinogen is the most important plasma protein contributing to ESR, followed by globulins. **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. 607-608. [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.

Question 954: What is true about acquired disorders of coagulation?

A. Shows specific clotting factor deficiency
B. Shows defects in platelets as well (Correct Answer)
C. Are less frequent than inherited disorders
D. Hemarthrosis is specifically seen

Explanation: **Explanation:** Acquired disorders of coagulation (e.g., Liver disease, Vitamin K deficiency, DIC) differ significantly from inherited disorders (e.g., Hemophilia) in their pathophysiology and clinical presentation [1]. **Why Option B is Correct:** Acquired coagulation disorders are typically **multifactorial**. For instance, in **Liver Disease** (the most common acquired cause), there is not only a deficiency of multiple clotting factors (II, VII, IX, X, Protein C/S) but also a significant **defect in platelets** [2]. This includes **thrombocytopenia** (due to hypersplenism and decreased thrombopoietin) and **thrombocytopathy** (impaired platelet function) [3]. Similarly, in **DIC**, there is a simultaneous "consumptive" loss of both clotting factors and platelets [4]. **Analysis of Incorrect Options:** * **Option A:** Inherited disorders usually involve a **specific** single factor deficiency (e.g., Factor VIII in Hemophilia A). Acquired disorders involve **multiple** factor deficiencies [1]. * **Option C:** Acquired disorders are **far more frequent** in clinical practice than inherited ones [1]. Liver disease and anticoagulant use are common, whereas Hemophilia is rare. * **Option D:** **Hemarthrosis** (bleeding into joints) is a hallmark of **inherited** secondary hemostatic defects (Hemophilia). Acquired disorders more commonly present with ecchymosis, mucosal bleeds, or oozing from puncture sites [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Liver Disease:** All factors are decreased except **Factor VIII** and **von Willebrand Factor** (produced by endothelium). * **Vitamin K Deficiency:** Affects Factors **II, VII, IX, X** and Proteins **C and S** [2]. * **Mixing Studies:** Used to differentiate factor deficiency (corrects) from acquired inhibitors/antibodies (does not correct) [2]. * **PT vs. aPTT:** PT is usually the first to be prolonged in liver disease due to the short half-life of **Factor VII**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 622-623. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 619-620. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 955: A 19-year-old man has had recurrent bleeding occur in his knee when playing contact sports. He has no history of spontaneous bleeding, but his brother had similar problems. Consultation with a specialist reveals that he has "mild" hemophilia A. Which of the following factor abnormalities is consistent with this diagnosis?

A. abnormal factor VIII function
B. decreased levels of functional factor VIII (Correct Answer)
C. decreased factor IX level
D. decreased von Willebrand factor

Explanation: **Explanation:** **1. Why the Correct Answer is Right:** Hemophilia A is an X-linked recessive bleeding disorder caused by a deficiency or dysfunction of **Coagulation Factor VIII**. In this clinical scenario, the patient has "mild" hemophilia A. The severity of hemophilia is determined by the plasma levels of functional Factor VIII [1]: * **Severe:** <1% activity (spontaneous bleeding). * **Moderate:** 1–5% activity (bleeding with minor trauma) [1]. * **Mild:** 5–40% activity (bleeding only after significant trauma or surgery). The range of activity for mild disease is generally cited as 6% to 50% [1]. The patient’s symptoms (bleeding only during contact sports) and family history (X-linked pattern) are classic for a **quantitative decrease in functional Factor VIII**. **2. Why Incorrect Options are Wrong:** * **Option A:** While abnormal function (qualitative defect) can occur, the vast majority of Hemophilia A cases are due to a **quantitative deficiency** (decreased levels) of the protein [1]. * **Option C:** A decreased level of Factor IX is the hallmark of **Hemophilia B** (Christmas Disease). While clinically indistinguishable from Hemophilia A, the question specifically specifies Hemophilia A. * **Option D:** Decreased von Willebrand factor (vWF) characterizes **von Willebrand Disease (vWD)**. While vWF stabilizes Factor VIII, vWD typically presents with mucosal bleeding (epistaxis, menorrhagia) and an autosomal dominant inheritance, unlike the hemarthrosis (joint bleeding) seen here. **3. NEET-PG High-Yield Pearls:** * **Inheritance:** X-linked recessive (affects males; females are carriers) [1]. * **Lab Findings:** Prolonged **aPTT** (intrinsic pathway), Normal PT, Normal Bleeding Time, and Normal Platelet count. * **Mixing Study:** The prolonged aPTT will **correct** when mixed with normal plasma (indicating a deficiency, not an inhibitor). * **Treatment:** Recombinant Factor VIII concentrate; Desmopressin (dDAVP) can be used in mild cases to release stored Factor VIII from endothelial cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671.

Question 956: Diffuse large cell lymphoma is classified as which grade of non-Hodgkin's lymphoma?

A. Low grade
B. Intermediate grade (Correct Answer)
C. High grade
D. None of the above

Explanation: **Explanation:** Diffuse Large B-Cell Lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma (NHL) worldwide. Its classification is based on the **Working Formulation**, which categorizes NHL into three grades based on clinical aggressiveness and morphology: low, intermediate, and high grade. 1. **Why Intermediate Grade is Correct:** DLBCL is characterized by large, atypical lymphoid cells with a diffuse growth pattern. Clinically, it is aggressive and rapidly growing but potentially curable with intensive chemotherapy (like R-CHOP) [2]. In the Working Formulation, diffuse large cell lymphomas are the prototypical examples of **Intermediate Grade** lymphomas. 2. **Why Low Grade is Incorrect:** Low-grade lymphomas (e.g., Follicular lymphoma, SLL/CLL) are "indolent." They grow slowly over years and are often incurable but managed as chronic diseases. DLBCL grows too rapidly to be classified here [1]. 3. **Why High Grade is Incorrect:** High-grade lymphomas (e.g., Burkitt lymphoma, Lymphoblastic lymphoma) have extremely high mitotic rates and doubling times measured in days. While DLBCL is aggressive, it does not typically reach the extreme proliferation levels of Burkitt lymphoma. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common:** DLBCL is the most common NHL in adults [2]. * **Immunophenotype:** Usually CD19+, CD20+, CD22+, and CD45+. * **Genetic Association:** Often involves mutations in the **BCL-6** gene (3q27) or rearrangements of **BCL-2** [1]. * **Richter Transformation:** The progression of a low-grade lymphoma (like CLL) into DLBCL is known as Richter’s transformation—a favorite topic for examiners. **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. 563-564. [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. 604-605.

Question 957: Why do patients with sickle cell trait not manifest the same symptoms as those with sickle cell disease?

A. 50% HbS is required for the occurrence of sickling. (Correct Answer)
B. HbA prevents sickling.
C. 50% sickles are formed.
D. HbA prevents polymerization of HbS.

Explanation: ### Explanation **1. Why the Correct Answer is Right:** Sickle cell trait (HbAS) is characterized by a hemoglobin profile typically consisting of **60% HbA and 40% HbS** [1]. The fundamental reason patients with the trait are asymptomatic under physiological conditions is that **sickling is a concentration-dependent process**. In vivo sickling generally requires a concentration of HbS greater than **50%** [1]. Because the level of HbS in heterozygotes (trait) remains below this critical threshold, the red blood cells do not undergo polymerization or sickling unless exposed to extreme conditions like severe hypoxia (e.g., unpressurized aircraft) or hypertonicity (e.g., renal medulla) [2]. **2. Analysis of Incorrect Options:** * **Option B:** HbA does not "prevent" sickling in an absolute sense; it simply dilutes the concentration of HbS. If HbS levels were high enough, sickling would occur regardless of HbA presence. * **Option C:** Sickling is an "all-or-none" phenomenon at the cellular level based on HbS concentration and oxygen tension. It is not that "50% of cells" sickle; rather, the cells generally resist sickling altogether at trait levels [2]. * **Option D:** While HbA does not actively promote polymerization, it is **HbF (Fetal Hemoglobin)** that is the potent inhibitor of HbS polymerization. HbA is considered "permissive" but less effective at preventing polymerization than HbF. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Renal Exception:** The only site where sickling occurs in trait patients is the **renal medulla** (due to extreme hypoxia and hypertonicity), leading to **painless hematuria** and hyposthenuria. * **Protective Effect:** Sickle cell trait provides a survival advantage against *Plasmodium falciparum* malaria. * **Screening:** The **Solubility Test** (Sodium dithionite) is positive in both Trait and Disease, but **Hb Electrophoresis** is required to differentiate them (HbAS vs. HbSS). * **Polymerization Factors:** The rate of sickling is increased by **dehydration** (increased MCHC), **acidosis**, and **fever** [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. 643-644. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.

Question 958: Schistocytes in peripheral smear are seen in all except:

A. Disseminated Intravascular Coagulation (DIC)
B. Sickle cell anemia (Correct Answer)
C. Thrombotic Thrombocytopenic Purpura (TTP)
D. Hemolytic Uremic Syndrome (HUS)

Explanation: ### Explanation **1. Why Sickle Cell Anemia is the Correct Answer:** Schistocytes are fragmented red blood cells (RBCs) formed due to mechanical trauma as they pass through obstructed or damaged small blood vessels. **Sickle Cell Anemia** is characterized by **Sickle cells (drepanocytes)**, which result from the polymerization of Hemoglobin S under deoxygenated conditions [1]. While it is a hemolytic anemia, the hemolysis is primarily extravascular (in the spleen) or due to shape deformation, not mechanical fragmentation [3]. Therefore, schistocytes are not a characteristic feature of Sickle Cell Anemia. **2. Analysis of Incorrect Options (Where Schistocytes ARE seen):** Options A, C, and D are all classic examples of **Microangiopathic Hemolytic Anemia (MAHA)**. In these conditions, fibrin strands or platelet thrombi deposit within the microvasculature [2]. As RBCs attempt to squeeze through these "mesh-like" obstructions, they are physically sheared, resulting in schistocytes (helmet cells, triangle cells). * **DIC:** Widespread activation of coagulation leading to fibrin clots. * **TTP:** Deficiency of ADAMTS13 leading to large vWF multimers and platelet thrombi [2]. * **HUS:** Shiga toxin-induced endothelial damage leading to microthrombi (common in children). **3. NEET-PG High-Yield Pearls:** * **Definition:** Schistocytes are the hallmark of **MAHA** and **Mechanical Heart Valve** induced hemolysis. * **Morphology:** Look for "Helmet cells" or "Bite cells" (though bite cells are more specific to G6PD deficiency) [4]. * **Differential Diagnosis of Schistocytes:** DIC, TTP, HUS, HELLP syndrome, Malignant Hypertension, and Prosthetic Heart Valves. * **Sickle Cell Smear:** Look for Sickle cells, **Howell-Jolly bodies** (due to autosplenectomy), and target cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 642-643.

Question 959: Which of the following is NOT included in the myelodysplastic syndromes?

A. Angiogenic myeloid metaplasia
B. Thrombocythemia
C. Erythroleukemia (Correct Answer)
D. Megaloblastic hyperplasia

Explanation: **Explanation** Myelodysplastic Syndromes (MDS) are a group of clonal hematopoietic stem cell disorders characterized by cytopenias, ineffective hematopoiesis, and dysplastic morphological changes in one or more cell lines [1]. **Why Erythroleukemia is the correct answer:** Erythroleukemia (formerly FAB M6) is classified under **Acute Myeloid Leukemia (AML)**, not MDS [2]. According to the WHO classification, the diagnosis of AML requires a blast count of $\geq 20\%$ in the bone marrow or peripheral blood [1]. While MDS can transform into AML (secondary AML), erythroleukemia represents a frank malignancy rather than a pre-leukemic dysplastic state [2]. **Analysis of other options:** * **Angiogenic myeloid metaplasia:** This term is often associated with the older nomenclature of Myelofibrosis, but in the context of this specific classic question, it refers to the hypervascularity and stromal changes seen during the progression of dysplastic marrow [1]. * **Thrombocythemia:** While "Essential Thrombocythemia" is a Myeloproliferative Neoplasm (MPN), isolated high platelet counts or megakaryocytic dysplasia can be features of specific MDS subtypes (like 5q- syndrome) [3]. * **Megaloblastic hyperplasia:** This is a hallmark morphological feature of MDS. Unlike nutritional B12/Folate deficiency, the megaloblastic changes in MDS are "refractory" and result from disordered DNA synthesis within the malignant clone [1]. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Bone marrow aspiration and biopsy showing dysplasia in $>10\%$ of a specific cell line [1]. * **Common Cytogenetic Abnormality:** Deletion 5q (5q- syndrome), which typically carries a better prognosis and responds to **Lenalidomide**. * **Ring Sideroblasts:** Seen in MDS with SF3B1 mutations; requires Perls' Prussian Blue stain. * **Transformation:** MDS is considered a "pre-leukemic" state; the risk of transformation to AML depends on the blast percentage and cytogenetics (IPSS-R score) [1]. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 607-608. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615.

Question 960: Diagnosis of Hodgkin's disease is confirmed by?

A. CT scan
B. Bone marrow biopsy
C. Lymph node biopsy (Correct Answer)
D. Lymphangiography

Explanation: **Explanation:** The gold standard for the diagnosis of Hodgkin Lymphoma (HL) is an **excisional lymph node biopsy**. This is because the diagnosis relies on the histopathological identification of characteristic **Reed-Sternberg (RS) cells** (large, multinucleated cells with "owl-eye" nucleoli) within a specific cellular background of non-neoplastic inflammatory cells (lymphocytes, plasma cells, eosinophils) [1]. A core needle biopsy is often insufficient as it may miss the sparse RS cells or fail to show the architectural pattern required for subtyping [2]. **Analysis of Incorrect Options:** * **A. CT Scan:** This is a radiologic modality used for **staging** (detecting lymphadenopathy and organ involvement) and monitoring treatment response, but it cannot provide a tissue diagnosis. * **B. Bone Marrow Biopsy:** This is performed to determine the **stage** of the disease (Stage IV if involved). While it may show involvement in advanced cases, it is not the primary diagnostic tool [3]. * **D. Lymphangiography:** This is an obsolete imaging technique formerly used to visualize the lymphatic system. It has been entirely replaced by CT and PET scans for staging. **High-Yield Pearls for NEET-PG:** * **Classic RS Cell Marker:** CD15+ and CD30+ (CD45 negative). * **Lymphocyte Predominant HL:** Characterized by "Popcorn cells" (L&H cells) which are CD20+ and CD45+ [4]. * **Most Common Subtype:** Nodular Sclerosis (often presents with mediastinal mass in young females) [2]. * **Best Prognosis:** Lymphocyte Rich; **Worst Prognosis:** Lymphocyte Depleted [4]. * **Staging System:** Ann Arbor Staging (modified by Cotswolds). **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. 614-616. [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. 618. [4] 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.

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