Hematopathology — MCQs

A 45-year-old lady presented with a painless neck swelling for 3 months, associated with loss of weight and fever. FNAC of the swelling showed a polymorphous population of lymphocytes, eosinophils, plasma cells, and large binucleate cells with an owl-eye appearance of the nucleus. What is your diagnosis?

Q248Medium

Which of the following does not cause an increase in spleen size in later stages?

Q249Easy

Peripheral blood smear showing spur cells and stomatocytes is suggestive of which condition?

Q250Easy

Which of the following is false regarding echinocytes?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 241: Which of the following is not a myeloproliferative disease?

A. Polycythemia rubra vera
B. Acute myeloid leukemia (Correct Answer)
C. Chronic myeloid leukemia
D. Essential thrombocytosis

Explanation: **Explanation:** The core distinction in hematological malignancies lies between **Myeloproliferative Neoplasms (MPNs)** and **Acute Myeloid Leukemia (AML)** based on the maturation of cells. [1] **Why Option B is correct:** **Acute Myeloid Leukemia (AML)** is characterized by a "maturation arrest." It involves the rapid proliferation of immature myeloid cells (**blasts**) [2]. According to the WHO classification, a blast count of **≥20%** in the bone marrow or peripheral blood is diagnostic of AML [1]. It is an acute, aggressive process rather than a chronic myeloproliferative one. **Why other options are incorrect:** Myeloproliferative Neoplasms (MPNs) are clonal hematopoietic stem cell disorders characterized by the overproduction of one or more fully differentiated (mature) myeloid lineages. * **Chronic Myeloid Leukemia (CML):** A classic MPN defined by the Philadelphia chromosome $t(9;22)$ and the *BCR-ABL1* fusion gene, leading to increased granulocytes. * **Polycythemia Rubra Vera (PRV):** An MPN characterized by autonomous erythropoiesis, strongly associated with the **JAK2 V617F** mutation. * **Essential Thrombocytosis (ET):** An MPN involving the overproduction of platelets/megakaryocytes, also associated with *JAK2*, *CALR*, or *MPL* mutations. **High-Yield Clinical Pearls for NEET-PG:** * **The "Spent Phase":** MPNs (especially PRV and Primary Myelofibrosis) can progress to a fibrotic stage or transform into AML (Blast Crisis). * **JAK2 V617F Mutation:** Present in >95% of PRV cases and ~50-60% of ET and Primary Myelofibrosis cases. * **Hypercellularity:** Unlike AML, MPNs typically present with a hypercellular bone marrow with effective maturation and low blast counts (<20%) [3]. **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. 620. [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. 620-621. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Question 242: Which of the following is NOT associated with massive transfusion?

A. Hypothermia
B. Hypercalcemia (Correct Answer)
C. Thrombocytopenia
D. DIC

Explanation: **Explanation:** Massive transfusion is defined as the replacement of one total blood volume (approx. 10 units of PRBCs) within 24 hours. The correct answer is **Hypercalcemia** because massive transfusion actually causes **Hypocalcemia**. **1. Why Hypercalcemia is incorrect (The Correct Answer):** Stored blood contains **sodium citrate** as an anticoagulant. When large volumes of blood are infused rapidly, the citrate binds to the patient’s ionized calcium, leading to **hypocalcemia**. While the liver eventually metabolizes citrate into bicarbonate, the acute effect is a drop in calcium levels, which can lead to paresthesia, tetany, or arrhythmias. **2. Analysis of Incorrect Options:** * **Hypothermia (A):** Stored blood is kept at 4°C. Rapid infusion of large volumes of cold blood overwhelms the body’s thermoregulatory capacity, leading to a drop in core temperature. * **Thrombocytopenia (C):** Packed Red Blood Cells (PRBCs) are deficient in viable platelets and clotting factors (V and VIII) [2]. Replacing whole blood with only PRBCs leads to **dilutional thrombocytopenia** and coagulopathy. * **DIC (D):** Massive transfusion can trigger Disseminated Intravascular Coagulation due to the combination of the "lethal triad" (hypothermia, acidosis, and coagulopathy) and the underlying trauma/shock for which the transfusion was indicated [1]. **NEET-PG High-Yield Pearls:** * **Electrolyte Shifts:** Massive transfusion causes **Hypocalcemia**, **Hypomagnesemia**, and **Hyperkalemia** (due to the release of potassium from lysed RBCs during storage). * **Acid-Base Balance:** Initially, stored blood is acidic (due to lactate and citrate); however, post-transfusion, **metabolic alkalosis** may occur as citrate is metabolized to bicarbonate. * **Shift in Oxygen Curve:** Stored blood has low **2,3-DPG**, causing a **left shift** in the oxygen dissociation curve (increased O2 affinity, decreased tissue delivery). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 672-673. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625.

Question 243: In an ablated animal model, myeloid series cells are injected. Which of the following is observed after an incubation period?

A. RBCs (Correct Answer)
B. Fibroblasts
C. T lymphocytes
D. Hematopoietic stem cells

Explanation: This question tests the understanding of the **hematopoietic hierarchy** and the differentiation potential of committed progenitor cells. ### **Explanation** The term **"myeloid series cells"** refers to the **Common Myeloid Progenitor (CMP)** or its downstream lineage-committed cells. In an ablated animal model (where the bone marrow has been destroyed by radiation or chemicals), the injection of myeloid progenitors will lead to the production of all cells within the myeloid lineage [1]. According to the classical model of hematopoiesis, the CMP differentiates into: 1. **Erythroid lineage:** Leading to the production of **RBCs** (Correct Answer) [2]. 2. **Megakaryocytic lineage:** Leading to Platelets. 3. **Granulocytic-Monocytic lineage:** Leading to Neutrophils, Eosinophils, Basophils, and Monocytes/Macrophages [1]. ### **Analysis of Incorrect Options** * **B. Fibroblasts:** These are mesenchymal cells derived from the mesoderm/stromal lineage, not from hematopoietic myeloid progenitors. * **C. T lymphocytes:** These are derived from the **Common Lymphoid Progenitor (CLP)**. Myeloid series cells lack the potential to differentiate into the lymphoid lineage (T cells, B cells, or NK cells) [1]. * **D. Hematopoietic stem cells (HSCs):** Differentiation is a unidirectional process. Myeloid series cells are "committed" progenitors; they cannot "de-differentiate" back into pluripotent HSCs. ### **NEET-PG High-Yield Pearls** * **HSC Markers:** CD34+ and CD117+ (c-kit). They are characterized by **self-renewal** and **pluripotency** [1]. * **Erythropoiesis:** The first morphologically identifiable erythroid precursor is the **Proerythroblast** [2]. * **Site of Hematopoiesis:** In adults, it is the red bone marrow (primarily axial skeleton). In the fetus, the **liver** is the main site between 2–7 months of gestation. * **Ablation Models:** Often used in research to study **Spleen Colony Forming Units (CFU-S)**, which primarily represent myeloid differentiation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 588-590. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 585-586.

Question 244: A crisis in a patient with sickle cell disease is most likely to be caused by what condition?

A. Alkalosis
B. Acidosis (Correct Answer)
C. Increased oxygen concentration
D. Decreased CO2 concentration

Explanation: ### Explanation The primary pathophysiology of **Sickle Cell Disease (SCD)** involves a point mutation in the $\beta$-globin chain (Glu $\to$ Val at position 6), leading to the formation of Hemoglobin S (HbS). [1] Under certain physiological stressors, HbS undergoes polymerization, causing the red blood cells to "sickle," leading to vaso-occlusion and hemolysis. **Why Acidosis is the Correct Answer:** Acidosis (decreased pH) is a potent trigger for sickling. According to the **Bohr Effect**, a decrease in pH shifts the oxygen-dissociation curve to the right, reducing the affinity of hemoglobin for oxygen. This promotes the **deoxygenated state** of HbS. Deoxygenated HbS molecules have a conformational shape that allows them to polymerize into long, stiff fibers, distorting the RBC into a sickle shape. [1] Therefore, conditions like infection, dehydration, or hypoxia that lead to acidosis precipitate a vaso-occlusive crisis. [1] **Analysis of Incorrect Options:** * **Alkalosis (A):** An increase in pH shifts the oxygen-dissociation curve to the left, increasing hemoglobin's affinity for oxygen. Since oxy-HbS does not polymerize, alkalosis actually inhibits sickling. * **Increased Oxygen Concentration (C):** High oxygen levels keep HbS in the oxygenated state, which prevents polymerization. Oxygen therapy is often used in the management of crises. [1] * **Decreased $CO_2$ Concentration (D):** Low $CO_2$ (hypocapnia) typically leads to respiratory alkalosis. As established, alkalosis prevents rather than causes sickling. **High-Yield Clinical Pearls for NEET-PG:** * **Factors promoting sickling:** Hypoxia, Acidosis, Dehydration, Increased 2,3-BPG, and Hypertonic plasma (cell dehydration). [1] * **Rate of sickling:** The most critical factor determining a crisis is the **transit time** of RBCs through microvascular beds relative to the **delay time** of polymerization. * **Protective factors:** HbF (Fetal Hemoglobin) strongly inhibits the polymerization of HbS, which is why Hydroxyurea (which increases HbF) is used for treatment. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-600.

Question 245: What pre-surgical test is required for a patient with Vitamin K deficiency?

A. PT time (Correct Answer)
B. Bleeding time
C. Clotting time
D. Bleeding index

Explanation: **Explanation:** **1. Why PT (Prothrombin Time) is the correct answer:** Vitamin K is a vital fat-soluble cofactor required for the post-translational **gamma-carboxylation** of clotting factors **II, VII, IX, and X**, as well as proteins C and S [1]. Among these, **Factor VII** has the shortest half-life (~4–6 hours). Because the Prothrombin Time (PT) specifically measures the **Extrinsic and Common pathways** (Factors VII, X, V, II, and Fibrinogen), it is the first and most sensitive laboratory parameter to become prolonged in Vitamin K deficiency [1]. Monitoring PT ensures the patient’s coagulation status is optimized to prevent intraoperative hemorrhage. **2. Why the other options are incorrect:** * **Bleeding Time (BT):** This measures **platelet function** and vascular integrity. Vitamin K deficiency affects soluble clotting factors, not platelet plug formation; therefore, BT remains normal. * **Clotting Time (CT):** This is an archaic, non-specific bedside test for the intrinsic pathway. While it may be prolonged in severe deficiencies, it lacks the sensitivity and standardization required for surgical clearance. * **Bleeding Index:** This is not a standard clinical laboratory parameter used for assessing surgical coagulation risk. **3. NEET-PG High-Yield Pearls:** * **Warfarin Monitoring:** Like Vitamin K deficiency, Warfarin (a Vitamin K antagonist) is monitored using **PT/INR** [1]. * **APTT:** While Vitamin K deficiency eventually prolongs APTT (due to factors IX, X, and II), PT is always affected first. * **Differential Diagnosis:** If PT is prolonged but does not correct with Vitamin K administration, suspect severe **liver disease** (failure of synthesis) [1]. * **Newborns:** Hemorrhagic disease of the newborn occurs due to sterile gut and low Vitamin K stores; hence, prophylactic Vitamin K is given at birth [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625.

Question 246: Which of the following conditions are associated with both an elevated activated partial thromboplastin time (APTT) and an elevated prothrombin time (PT)?

A. Factor 13 deficiency
B. Severe liver disease (Correct Answer)
C. Immune thrombocytopenic purpura
D. Leiden (Factor V) deficiency

Explanation: **Explanation:** To solve coagulation profile questions, one must understand the components of the coagulation cascade: * **PT (Prothrombin Time):** Evaluates the **Extrinsic** (Factor VII) and **Common** pathways. * **aPTT (Activated Partial Thromboplastin Time):** Evaluates the **Intrinsic** (Factors XII, XI, IX, VIII) and **Common** pathways. * **Common Pathway:** Includes Factors X, V, II (Prothrombin), and I (Fibrinogen). **Why Severe Liver Disease is Correct:** The liver is the primary site for the synthesis of almost all coagulation factors (except Factor VIII and von Willebrand Factor) [1]. In severe liver disease, there is a global deficiency of clotting factors [1]. Since both the extrinsic pathway (Factor VII) and the common pathway (Factors X, V, II, I) are affected, **both PT and aPTT will be prolonged.** PT is typically the first to rise due to the short half-life of Factor VII. **Analysis of Incorrect Options:** * **Factor XIII Deficiency:** Factor XIII stabilizes the fibrin clot *after* the cascade is complete. Therefore, both PT and aPTT are **normal**. It is diagnosed using the Urea Solubility Test. * **Immune Thrombocytopenic Purpura (ITP):** This is a disorder of primary hemostasis (platelets). Coagulation profiles (PT/aPTT) remain **normal** because the secondary hemostasis (clotting factors) is intact. * **Factor V Leiden:** This is a hypercoagulable (thrombophilic) state caused by a mutation that makes Factor V resistant to inactivation by Protein C. It does not typically cause a prolongation of PT or aPTT; rather, it increases the risk of thrombosis. **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin K Deficiency:** Also causes elevated PT and aPTT (affects Factors II, VII, IX, X) [1]. * **Isolated PT elevation:** Think Factor VII deficiency or early Warfarin therapy. * **Isolated aPTT elevation:** Think Hemophilia A (VIII), B (IX), or Heparin therapy. * **Mixing Study:** If a prolonged PT/aPTT corrects with normal plasma, it indicates a **factor deficiency**; if it does not correct, it indicates the presence of an **inhibitor** (e.g., Lupus anticoagulant). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583, 624-626.

Question 247: A 45-year-old lady presented with a painless neck swelling for 3 months, associated with loss of weight and fever. FNAC of the swelling showed a polymorphous population of lymphocytes, eosinophils, plasma cells, and large binucleate cells with an owl-eye appearance of the nucleus. What is your diagnosis?

A. Nodular sclerosis
B. Mixed cellularity (Correct Answer)
C. Lymphocyte rich
D. Lymphocyte depleted

Explanation: **Explanation:** The clinical presentation of a middle-aged patient with B-symptoms (fever, weight loss) and a painless neck swelling is classic for **Hodgkin Lymphoma (HL)** [2]. The FNAC findings are diagnostic: the "large binucleate cells with an owl-eye appearance" are classic **Reed-Sternberg (RS) cells** [2], while the "polymorphous population" of reactive cells (lymphocytes, eosinophils, plasma cells) defines the inflammatory background [1]. **Why Mixed Cellularity (MC) is correct:** The **Mixed Cellularity** subtype is characterized by a "mixed" inflammatory infiltrate (eosinophils, plasma cells, histiocytes) and frequent, easily identifiable classic RS cells [1]. It is strongly associated with **EBV infection** (approx. 70% of cases) and often presents with systemic B-symptoms, as seen in this patient [1]. **Why other options are incorrect:** * **Nodular Sclerosis:** The most common subtype; characterized by broad bands of collagen fibrosis and **Lacunar variant** RS cells [1]. It typically involves the mediastinum in young females. * **Lymphocyte Rich:** Shows a background predominantly of small lymphocytes with very few RS cells [3]. It has a very good prognosis. * **Lymphocyte Depleted:** The rarest and most aggressive form. It is characterized by abundant, pleomorphic RS cells and a **paucity** of background lymphocytes [3]. It is often seen in HIV-positive patients. **High-Yield Clinical Pearls for NEET-PG:** * **RS Cell Markers:** CD15+ and CD30+ (except in Nodular Lymphocyte Predominant HL, which is CD20+ and CD45+). * **Eosinophilia** in MC subtype is due to the secretion of **IL-5** by RS cells. * **Prognosis:** Lymphocyte Rich (Best) > Nodular Sclerosis > Mixed Cellularity > Lymphocyte Depleted (Worst) [3]. **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. 614-618. [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, p. 616. [3] 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.

Question 248: Which of the following does not cause an increase in spleen size in later stages?

A. Sickle cell anaemia (Correct Answer)
B. Cirrhosis
C. Infectious mononucleosis
D. Hairy cell leukaemia

Explanation: In the context of splenic pathology, the correct answer is **Sickle Cell Anaemia (SCA)** because it is the only condition listed that leads to a decrease in spleen size (splenic atrophy) over time. ### **1. Why Sickle Cell Anaemia is Correct** In the early stages of SCA (especially in children), the spleen may be enlarged due to the sequestration of sickled red blood cells [2]. However, repeated episodes of vaso-occlusion lead to multiple splenic infarcts [1]. Over time, this results in progressive fibrosis, scarring, and shrinkage of the organ. By adulthood, the spleen becomes a small, shrunken, siderofibrotic nodule—a process known as **Autosplenectomy** [1]. Histologically, these shrunken spleens often show **Gandy-Gamna bodies** (siderofibrotic nodules containing calcium and iron). ### **2. Why Other Options are Incorrect** * **Cirrhosis:** Causes **congestive splenomegaly** due to portal hypertension. The spleen remains enlarged in later stages. * **Infectious Mononucleosis:** Caused by EBV, it leads to lymphoid hyperplasia. While the risk of splenic rupture is high, the spleen is enlarged, not shrunken. * **Hairy Cell Leukaemia:** Characteristically presents with **massive splenomegaly** due to infiltration of the red pulp by "hairy" B-cells. ### **3. NEET-PG High-Yield Pearls** * **Massive Splenomegaly (>1000g):** Chronic Myeloid Leukaemia (CML), Myelofibrosis, Malaria, Kala-azar, and Hairy Cell Leukaemia. * **Gandy-Gamna Bodies:** Also seen in portal hypertension and sickle cell anaemia. * **Howell-Jolly Bodies:** Found on peripheral smears of patients with SCA, indicating functional or physical asplenia [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. 631-632. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645.

Question 249: Peripheral blood smear showing spur cells and stomatocytes is suggestive of which condition?

A. Alcoholic hepatitis
B. Chronic liver disease (Correct Answer)
C. Chronic kidney disease
D. Hemolytic uremic syndrome

Explanation: **Explanation:** **1. Why Chronic Liver Disease (CLD) is correct:** In Chronic Liver Disease, abnormal lipid metabolism leads to an increased cholesterol-to-phospholipid ratio in the red blood cell (RBC) membrane. This excess cholesterol accumulates in the outer leaflet of the lipid bilayer, causing the membrane to expand and form irregular projections. * **Spur Cells (Acanthocytes):** These are RBCs with irregular, thorny projections of varying lengths. They are hallmark findings in severe liver disease (specifically "Spur Cell Anemia") [1]. * **Stomatocytes:** These are RBCs with a slit-like or "mouth-shaped" central pallor. In CLD, they occur due to membrane expansion and alterations in the sodium-potassium pump [1]. **2. Why other options are incorrect:** * **Alcoholic Hepatitis:** While it can show some membrane changes, it more typically presents with **Target cells** or macrocytosis. Spur cells are more characteristic of the end-stage architectural damage seen in cirrhosis/CLD [2]. * **Chronic Kidney Disease (CKD):** The classic peripheral smear finding in CKD (uremia) is **Burr cells (Echinocytes)**, which have small, uniform, and symmetric projections, unlike the irregular projections of spur cells. * **Hemolytic Uremic Syndrome (HUS):** This is a microangiopathic hemolytic anemia (MAHA) characterized by **Schistocytes** (fragmented RBCs/helmet cells) due to mechanical shearing in microthrombi. **3. NEET-PG High-Yield Pearls:** * **Target Cells (Codocytes):** Seen in "HALT" (HbC disease, Asplenia, Liver disease, Thalassemia). * **Acanthocytes:** Also seen in Abetalipoproteinemia (McLeod syndrome). * **Echinocytes (Burr cells):** Think Uremia, Pyruvate Kinase deficiency, or drying artifacts on a slide. * **Zieve’s Syndrome:** A triad of Alcoholic hepatitis, Hyperlipidemia, and Hemolytic anemia (often with spur cells). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 387-388. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 850-851.

Question 250: Which of the following is false regarding echinocytes?

A. Irregular spicules on RBC surface (Correct Answer)
B. Seen in liver disorders
C. Both of the above
D. None of the above

Explanation: **Explanation:** **Echinocytes**, also known as **Burr cells**, are characterized by **regular, short, blunt, and evenly spaced spicules** (projections) across the entire surface of the red blood cell. 1. **Why Option A is the correct (false) statement:** The hallmark of an echinocyte is the **regularity** of its projections. In contrast, **Acanthocytes** (spur cells) possess **irregular**, varying-length, and unevenly spaced spicules. Therefore, stating that echinocytes have "regular spicules" is factually incorrect, making it the right choice for this "false regarding" question. 2. **Why Option B is true:** Echinocytes are classically seen in **uremia** (most common association), but they are also frequently observed in **chronic liver disease**, pyruvate kinase deficiency [1], and as an artifact (glass effect/drying). 3. **Why Options C and D are wrong:** Since Option A is a false statement and Option B is a true statement, these collective options do not apply. **High-Yield Clinical Pearls for NEET-PG:** * **Echinocytes (Burr Cells):** Think **Uremia** and **Regular** projections. They are often reversible. * **Acanthocytes (Spur Cells):** Think **Abetalipoproteinemia** and **Irregular** projections. They are irreversible. * **Mechanism:** Echinocytes form due to expansion of the outer leaflet of the RBC lipid bilayer relative to the inner leaflet. * **Artifact Alert:** If you see echinocytes in every field of a peripheral smear, suspect an artifactual change due to increased pH or storage. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.

Practice by Chapter

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Thrombotic Disorders

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