Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1051: Which of the following statements is not true regarding chronic myelogenous leukemia?

A. BCR-ABL fusion is involved in the oncogenesis.
B. Pseudo Gaucher cells may be present in the bone marrow examination.
C. Blast crisis in the disease may involve lymphoblasts.
D. Bone marrow biopsy is essential for confirmation of diagnosis. (Correct Answer)

Explanation: **Explanation:** The correct answer is **D**. In Chronic Myelogenous Leukemia (CML), while a bone marrow examination is often performed to assess cellularity and the percentage of blasts (to determine the phase of the disease), it is **not essential for the primary diagnosis**. The definitive diagnosis of CML is established by demonstrating the presence of the **Philadelphia chromosome (t[9;22])** or the **BCR-ABL1 fusion gene** through cytogenetics (karyotyping), FISH, or RT-PCR using **peripheral blood** samples [1]. **Analysis of other options:** * **Option A:** True. The hallmark of CML is the $t(9;22)(q34;q11)$ translocation, which creates the **BCR-ABL1** fusion gene [1]. This gene encodes a constitutively active tyrosine kinase [1] that drives uncontrolled myeloid proliferation. * **Option B:** True. **Pseudo-Gaucher cells** (histiocytes with crumpled-tissue paper cytoplasm) are often seen in CML bone marrow due to the high turnover of myeloid cells, which overwhelms the lysosomal capacity of macrophages. * **Option C:** True. CML is a disease of a pluripotent hematopoietic stem cell. Therefore, when it progresses to a **blast crisis**, the blasts can be either myeloid (~70%) or **lymphoid (~30%)** in origin. **High-Yield Clinical Pearls for NEET-PG:** * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **decreased** in CML (helps differentiate it from a Leukemoid reaction where LAP is increased). * **Peripheral Smear:** Shows a "whole spectrum" of myeloid cells (myelocytes, metamyelocytes, etc.) with a characteristic **"myelocytic bulge"** and **basophilia** [2]. * **Treatment:** Imatinib (a Tyrosine Kinase Inhibitor) is the first-line therapy [2]. * **Most common physical finding:** Splenomegaly (often massive) [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, pp. 624-625. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.

Question 1052: In the Ann Arbor staging system for Hodgkin's lymphoma, which stage is characterized by the involvement of lymph nodes on both sides of the diaphragm?

A. Stage I
B. Stage II
C. Stage III (Correct Answer)
D. Stage IV

Explanation: The **Ann Arbor Staging System** is the standard classification used to determine the extent of Hodgkin’s Lymphoma (HL) and Non-Hodgkin’s Lymphoma (NHL). It is primarily based on the number of lymph node regions involved and their relationship to the **diaphragm**. ### **Explanation of the Correct Answer** * **Stage III (Correct):** This stage is defined by the involvement of lymph node regions or structures on **both sides of the diaphragm**. This may also include involvement of the spleen (Stage IIIS). The diaphragm serves as the anatomical landmark that separates the upper (cervical, axillary, mediastinal) and lower (inguinal, para-aortic) nodal groups. ### **Analysis of Incorrect Options** * **Stage I:** Involvement of a **single** lymph node region (e.g., only cervical nodes) or a single extralymphatic organ/site (Stage IE) [1]. * **Stage II:** Involvement of **two or more** lymph node regions on the **same side** of the diaphragm (e.g., cervical and axillary nodes). * **Stage IV:** Represents **disseminated (multifocal) involvement** of one or more extralymphatic organs (e.g., bone marrow, liver, or lungs), with or without associated lymph node involvement [1]. ### **High-Yield Clinical Pearls for NEET-PG** 1. **B-Symptoms:** Each stage is sub-classified into **A** (asymptomatic) or **B** (presence of fever, drenching night sweats, and weight loss >10% in 6 months) [1]. The presence of B-symptoms generally indicates a poorer prognosis. 2. **Bulky Disease:** Often designated as **'X'**, this refers to a nodal mass >10 cm or a mediastinal mass >1/3rd of the transthoracic diameter. 3. **Most Common Site:** The most common initial presentation of HL is painless **cervical lymphadenopathy**. 4. **Staging Investigation:** While historical staging required laparotomy, the current "gold standard" for clinical staging is a **PET-CT scan**. **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. 557-558.

Question 1053: Which of the following features is shared in common between lymphocyte-rich and lymphocyte-predominant types of Hodgkin's lymphoma?

A. Paucity of diagnostic Reed-Sternberg cells
B. Epstein-Barr virus (EBV) association
C. Reed-Sternberg cells are CD20 positive
D. Good prognosis (Correct Answer)

Explanation: Both **Lymphocyte-Rich Hodgkin Lymphoma (LRHL)** and **Nodular Lymphocyte-Predominant Hodgkin Lymphoma (NLPHL)** are characterized by an abundance of reactive lymphocytes and a relatively low burden of neoplastic cells [1], [2]. The shared clinical hallmark of these two subtypes is an **excellent prognosis** (Option D), as they typically present at an early stage and respond very well to treatment compared to the more aggressive Mixed Cellularity or Lymphocyte Depleted subtypes [2]. **Analysis of Incorrect Options:** * **Option A:** While NLPHL has a paucity of classic RS cells (showing "Popcorn" or LP cells instead), LRHL contains **diagnostic classic Reed-Sternberg cells** [1]. * **Option B:** LRHL is associated with **EBV in approximately 40%** of cases. In contrast, NLPHL is almost **never associated with EBV** [2]. * **Option C:** In LRHL, the RS cells follow the classic Hodgkin immunophenotype (**CD15+, CD30+, CD20-**). In NLPHL, the LP cells are **CD20+ and CD45+**, but negative for CD15 and CD30. **High-Yield Pearls for NEET-PG:** * **NLPHL** is now considered a distinct entity (often called "non-classic") because its cells (LP cells) express B-cell markers (CD20) [2]. * **LRHL** is a "classic" Hodgkin lymphoma; it looks like NLPHL morphologically (nodular growth, many lymphocytes) but has the immunophenotype of CHL (CD15/CD30 positive) [1]. * **Most common subtype:** Nodular Sclerosis. * **Best prognosis:** NLPHL / Lymphocyte Rich [2]. * **Worst prognosis:** Lymphocyte Depleted [1]. **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. 559-560. [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.

Question 1054: HTLV-II has been implicated in the etiology of which condition?

A. Hairy cell leukemia (Correct Answer)
B. AIDS
C. Adult T-cell lymphoma
D. Zinc deficiency

Explanation: **Explanation:** **Human T-cell Lymphotropic Virus type II (HTLV-II)** is a retrovirus closely related to HTLV-I. While HTLV-I is the definitive causative agent of Adult T-cell Leukemia/Lymphoma (ATLL), **HTLV-II** has been specifically isolated from and implicated in the etiology of **Hairy Cell Leukemia (HCL)**, particularly certain atypical variants. Although the primary driver of HCL is the **BRAF V600E mutation**, the association with HTLV-II remains a classic high-yield association in viral oncogenesis. **Analysis of Incorrect Options:** * **B. AIDS:** This is caused by the Human Immunodeficiency Virus (HIV-1 and HIV-2), which targets CD4+ T-cells, leading to profound immunosuppression. * **C. Adult T-cell Lymphoma (ATLL):** This is caused by **HTLV-I**, not HTLV-II. HTLV-I is also associated with Tropical Spastic Paraparesis (TSP). * **D. Zinc deficiency:** This is a nutritional disorder leading to acrodermatitis enteropathica, impaired wound healing, and immune dysfunction; it has no viral etiology. **High-Yield Clinical Pearls for NEET-PG:** * **Hairy Cell Leukemia (HCL):** A B-cell neoplasm characterized by "hairy" cytoplasmic projections [1]. * **Key Marker:** **TRAP positive** (Tartrate-Resistant Acid Phosphatase). * **Immunophenotype:** CD11c, CD25, CD103, and Annexin A1 (most specific). * **Clinical Feature:** Massive splenomegaly and **"Dry tap"** on bone marrow aspiration due to increased reticulin fibrosis [1]. * **Genetic Hallmark:** **BRAF V600E** mutation is present in nearly 100% of classic HCL cases. **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. 612.

Question 1055: Chronic myeloid leukemia (CML) is characterized by all of the following except:

A. Leukocytosis
B. Thrombocytosis
C. Increased Leukocyte alkaline phosphatase (Correct Answer)
D. Increased serum Vitamin B12

Explanation: **Explanation:** Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm characterized by the uncontrolled proliferation of the myeloid lineage. **Why Option C is correct:** In CML, the **Leukocyte Alkaline Phosphatase (LAP) score is characteristically decreased or absent**. This occurs because the rapidly proliferating malignant granulocytes are biochemically abnormal and lack this enzyme. A low LAP score is a crucial diagnostic marker used to differentiate CML from a **Leukemoid Reaction**, where the LAP score is elevated (as the neutrophils are mature and functionally normal). **Analysis of Incorrect Options:** * **A. Leukocytosis:** This is a hallmark of CML [2]. Patients typically present with a massive increase in WBC count (often >100,000/µL) with a "spectrum of myeloid cells" (myeloblasts to mature neutrophils) seen on the peripheral smear [2]. * **B. Thrombocytosis:** Increased platelet counts are common in the chronic phase of CML due to the involvement of the multipotent hematopoietic stem cell [1]. * **D. Increased Serum Vitamin B12:** CML cells produce excessive amounts of **Transcobalamin I** (a B12-binding protein), leading to significantly elevated serum Vitamin B12 levels. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** Characterized by **t(9;22)**, known as the **Philadelphia Chromosome**, creating the *BCR-ABL1* fusion gene with constitutive tyrosine kinase activity [3]. * **Peripheral Smear:** Shows a "myelocyte bulge" (predominance of myelocytes and metamyelocytes) and **basophilia** (a highly specific finding for CML). * **Treatment:** The first-line treatment is **Imatinib**, a tyrosine kinase inhibitor (TKI) [2]. * **Splenomegaly:** CML often presents with massive, "huge" splenomegaly [1], [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, pp. 625-626. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612. [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 1056: Which chromosomal translocation is characteristic of Burkitt's lymphoma?

A. t(8;14) (Correct Answer)
B. t(9;22)
C. t(11;14)
D. t(14;18)

Explanation: **Explanation:** **Burkitt’s Lymphoma** is a highly aggressive B-cell non-Hodgkin lymphoma characterized by the translocation of the **c-MYC proto-oncogene** (located on chromosome 8) [1]. In approximately 80% of cases, the characteristic translocation is **t(8;14)**, where the *c-MYC* gene is moved adjacent to the **Immunoglobulin Heavy Chain (IgH)** locus on chromosome 14 [1]. This results in the constitutive overexpression of the MYC protein, a potent transcription factor that drives rapid cellular proliferation [1]. **Analysis of Incorrect Options:** * **t(9;22):** Known as the **Philadelphia Chromosome**, it creates the *BCR-ABL1* fusion gene, characteristic of **Chronic Myeloid Leukemia (CML)** and some cases of ALL. * **t(11;14):** Involves the *CCND1* (Cyclin D1) gene and the IgH locus. It is the hallmark of **Mantle Cell Lymphoma**, leading to overexpression of Cyclin D1 and cell cycle progression. * **t(14;18):** Involves the *BCL-2* anti-apoptotic gene and the IgH locus [3]. It is characteristic of **Follicular Lymphoma**, leading to the inhibition of apoptosis [3], [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Classic **"Starry-sky appearance"** (tingible body macrophages acting as "stars" against a background of dark neoplastic B-cells) [2]. * **Variants:** Endemic (African; strongly associated with **EBV**, involves the jaw), Sporadic (abdominal involvement), and Immunodeficiency-associated. * **Genetics:** While t(8;14) is most common, variant translocations include **t(2;8)** and **t(8;22)** involving kappa and lambda light chains respectively [1]. * **Marker:** Burkitt’s cells are typically Ki-67 positive in nearly 100% of cells (very high proliferation index) [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, p. 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, pp. 602-604. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562.

Question 1057: Which is the most common defectively produced antibody in multiple myeloma?

A. IgG (Correct Answer)
B. IgM
C. IgA
D. IgD

Explanation: **Explanation:** Multiple Myeloma (MM) is a neoplastic proliferation of a single clone of plasma cells derived from B-cells. These malignant plasma cells secrete excessive amounts of a specific monoclonal (M) protein, which is most commonly a complete immunoglobulin molecule [1]. **Why IgG is the Correct Answer:** In Multiple Myeloma, **IgG** is the most frequently produced monoclonal protein, accounting for approximately **50-60%** of all cases [5]. This is followed by IgA [1]. The overproduction of this non-functional IgG leads to a "monoclonal spike" (M-spike) on serum protein electrophoresis (SPEP) and a reciprocal decrease in normal functional antibodies, increasing the risk of infections. **Analysis of Incorrect Options:** * **IgA (Option C):** This is the second most common isotype, seen in about **20-25%** of cases [1]. It is often associated with more frequent hypercalcemia and extramedullary involvement. * **IgM (Option B):** Monoclonal IgM is rare in Multiple Myeloma [1]. Its presence is the hallmark of **Waldenström Macroglobulinemia**, a distinct lymphoproliferative disorder characterized by hyperviscosity [3]. * **IgD (Option D):** This is a rare variant (<2% of cases) and is typically associated with a more aggressive clinical course and a higher frequency of Bence-Jones proteinuria [1]. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** Remember the classic presentation: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions (punched-out lytic lesions) [2]. * **Diagnosis:** Plasma cells in bone marrow >10% is a diagnostic requirement. * **Blood Film:** Look for **Rouleaux formation** due to increased serum proteins [4]. * **Bence-Jones Proteins:** These represent free monoclonal light chains (Kappa or Lambda) excreted in the urine [4]. **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. 608-609. [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. 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. 606-607. [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. 607-608. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617.

Question 1058: All of the following are associated with Epstein-Barr virus (EBV), EXCEPT:

A. Hodgkin's disease
B. Lymphoplasmacytic lymphoma (Correct Answer)
C. Post-organ transplant lymphoma
D. Extranodal NK/T cell lymphoma, nasal type

Explanation: **Explanation:** The association between Epstein-Barr Virus (EBV) and various malignancies is a high-yield topic in hematopathology. EBV is a gamma-herpesvirus that infects B cells via the **CD21 receptor**, leading to immortalization and potential oncogenesis [1]. **Why Lymphoplasmacytic Lymphoma (LPL) is the correct answer:** LPL (often manifesting as Waldenström Macroglobulinemia) is a mature B-cell neoplasm characterized by the **MYD88 L265P mutation**. It is **not** associated with EBV infection. Its pathogenesis is driven by somatic hypermutation and specific genetic signaling pathways rather than viral transformation. **Analysis of Incorrect Options:** * **Hodgkin’s Disease:** EBV is strongly associated with Hodgkin Lymphoma, particularly the **Mixed Cellularity subtype** (up to 70% of cases) and some cases of Nodular Sclerosis. The virus is often found within the Reed-Sternberg cells. * **Post-organ transplant lymphoma (PTLD):** This is a life-threatening complication of immunosuppression. Most PTLDs are **EBV-driven B-cell proliferations** occurring because T-cell surveillance is insufficient to control EBV-infected B cells [3]. * **Extranodal NK/T cell lymphoma, nasal type:** This is an aggressive lymphoma where **EBV is present in virtually 100% of cases**. The detection of EBV (via EBER in-situ hybridization) is actually a diagnostic requirement for this entity. **NEET-PG High-Yield Pearls:** * **Other EBV associations:** Burkitt Lymphoma (Endemic type), Nasopharyngeal Carcinoma, and Oral Hairy Leukoplakia (in HIV) [2][4]. * **Receptor:** EBV binds to **CD21** (CR2) on B-cells and **MHC Class II** as a co-receptor. * **Diagnostic Test:** **EBER (EBV-encoded RNA)** in-situ hybridization is the gold standard for detecting EBV in tissue sections. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 219-220. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336. [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. 595-596. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262.

Question 1059: Prolonged prothrombin time (PT) and normal activated partial thromboplastin time (aPTT) may be seen in which of the following conditions?

A. Thrombocytopenia
B. Disseminated Intravascular Coagulation (DIC)
C. Vitamin K deficiency (Correct Answer)
D. Aspirin toxicity

Explanation: ### Explanation **Correct Answer: C. Vitamin K deficiency** **Mechanism:** Prothrombin Time (PT) measures the **Extrinsic** and **Common pathways**, while activated Partial Thromboplastin Time (aPTT) measures the **Intrinsic** and **Common pathways**. Vitamin K is essential for the gamma-carboxylation of Factors II, VII, IX, and X [1]. * **Factor VII** has the shortest half-life of all coagulation factors. * In early Vitamin K deficiency (or early liver disease), Factor VII levels drop first [1, 3]. Since Factor VII is unique to the extrinsic pathway, the **PT becomes prolonged** while the aPTT remains within the normal range. As the deficiency progresses and levels of II, IX, and X drop, both PT and aPTT will eventually be prolonged. **Analysis of Incorrect Options:** * **A. Thrombocytopenia:** This is a quantitative platelet disorder. It affects the bleeding time (BT) but has no effect on the coagulation cascade (PT and aPTT remain normal) [4]. * **B. Disseminated Intravascular Coagulation (DIC):** DIC involves widespread consumption of all clotting factors and platelets [2]. Therefore, it typically presents with **prolongation of both PT and aPTT**, along with low fibrinogen and elevated D-dimers [2]. * **D. Aspirin toxicity:** Aspirin irreversibly inhibits cyclooxygenase (COX-1), affecting platelet aggregation. It prolongs the bleeding time but does not affect PT or aPTT. **High-Yield Clinical Pearls for NEET-PG:** * **Warfarin Monitoring:** Warfarin inhibits Vitamin K epoxide reductase. Like early Vitamin K deficiency, it prolongs PT first (monitored via INR) [3]. * **Mixing Studies:** If PT/aPTT is prolonged, a mixing study (adding normal plasma) is done. If it corrects, it indicates **factor deficiency**; if it doesn't, it indicates an **inhibitor** (e.g., Lupus anticoagulant). * **Isolated aPTT prolongation:** Think of Hemophilia A (VIII), Hemophilia B (IX), or Von Willebrand Disease (due to low VIII). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667.

Question 1060: What is the characteristic marker for hairy cell leukemia?

A. CD30
B. CD103 (Correct Answer)
C. CD1
D. CD4

Explanation: **Explanation:** **Hairy Cell Leukemia (HCL)** is a rare, chronic B-cell lymphoproliferative disorder characterized by the proliferation of mature B-cells with hair-like cytoplasmic projections [1]. **Why CD103 is the correct answer:** CD103 (an alpha-E integrin) is considered the most specific immunophenotypic marker for HCL. The diagnosis is typically confirmed via flow cytometry showing a "bright" expression of mature B-cell markers (CD19, CD20, CD22) along with a specific quartet of markers: **CD103, CD11c, CD25, and annexin A1.** Among these, Annexin A1 is the most specific immunohistochemical marker, while CD103 is the classic flow cytometry hallmark. **Analysis of Incorrect Options:** * **CD30:** A marker for activated lymphocytes; it is the hallmark for **Hodgkin Lymphoma** (Reed-Sternberg cells) and **Anaplastic Large Cell Lymphoma (ALCL)**. * **CD1:** Specifically CD1a is a marker for **Langerhans Cell Histiocytosis (LCH)** and cortical thymocytes. * **CD4:** A marker for **T-helper cells**. It is expressed in T-cell lineages and is relevant in conditions like Mycosis Fungoides or Adult T-cell Leukemia/Lymphoma (ATLL). **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Splenomegaly (often massive), Pancytopenia, and "Dry tap" on bone marrow aspiration (due to increased reticulin fibrosis) [1]. * **TRAP Stain:** Historically diagnosed using Tartrate-Resistant Acid Phosphatase (TRAP) positivity. * **Genetic Mutation:** Virtually 100% of cases harbor the **BRAF V600E** mutation. * **Treatment:** Highly sensitive to purine analogs like **Cladribine** (Drug of choice). **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. 612.

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