Hematopathology Practice Questions

Q: A 2-year-old child in shock presents with multiple non-blanching purple lesions of various sizes scattered on the trunk and extremities. Petechiae are noted, and oozing from the venipuncture site has been observed. The child's peripheral blood smear is shown below. Clotting studies are likely to show which of the following?

The presence of fibrin split products. ***The presence of fibrin split products*** - The clinical presentation of **shock**, **non-blanching purple lesions**, **petechiae**, and **oozing from venipuncture sites** strongly suggests **disseminated intravascular coagulation (DIC)**. - In DIC, **fibrinogen** is converted to **fibrin** and subsequently broken down by **plasmin**, leading to elevated **fibrin degradation products (FDPs)** and **D-dimers** as hallmark findings. *Increased levels of factors V and VIII* - In DIC, **coagulation factors** including **factors V and VIII** are **consumed** during the coagulation cascade, resulting in **decreased** rather than increased levels. - The **consumption coagulopathy** depletes clotting factors as they are utilized in widespread **microthrombi formation** throughout the circulation. *A decreased prothrombin level* - While **prothrombin (factor II)** levels may be decreased due to consumption in DIC, this is not the **most characteristic** or **reliable** finding. - **Fibrin split products** are more **specific** and **sensitive** markers for diagnosing DIC compared to individual factor levels. *An increased fibrinogen level* - **Fibrinogen** levels are typically **decreased** in DIC due to **consumption** during widespread **fibrin formation** and subsequent **fibrinolysis**. - The **schistocytes** visible on blood smear indicate **microangiopathic hemolytic anemia**, supporting the diagnosis of DIC where fibrinogen is consumed.

Q: Acid Citrate Dextrose (ACD) is used to store blood and preserves Red Blood Cells (RBCs) for 21 days. What are the respective storage periods when phosphate alone is added to ACD, and when adenine and phosphate are added together to ACD?

21 days and 35 days. ### Explanation The storage life of Red Blood Cells (RBCs) in a blood bank depends on the composition of the anticoagulant-preservative solution, which maintains cell viability by providing nutrients and preventing metabolic decay. **1. Understanding the Correct Answer (Option B):** * **ACD (Acid Citrate Dextrose):** The baseline storage period is **21 days**. Citrate acts as an anticoagulant, while Dextrose provides a substrate for ATP production via glycolysis. * **CPD (Citrate Phosphate Dextrose):** When **Phosphate** is added to ACD, the storage period remains **21 days**. However, Phosphate acts as a buffer to maintain pH and maintains higher levels of 2,3-DPG, ensuring better oxygen delivery post-transfusion. * **CPDA-1 (Citrate Phosphate Dextrose Adenine):** When **Adenine** is added along with Phosphate, the storage period increases to **35 days**. Adenine provides a substrate for the synthesis of ATP, which is essential for maintaining the RBC membrane integrity and the sodium-potassium pump. **2. Why Other Options are Incorrect:** * **Option A & D:** 42 days is the storage life for **Additive Solutions** (like SAGM: Saline-Adenine-Glucose-Mannitol), not CPDA-1. 35 days refers to CPDA-1, not CPD alone. * **Option C:** 28 days and 45 days are not standard storage durations for the primary anticoagulant solutions used in clinical practice. **3. Clinical Pearls for NEET-PG:** * **Storage Temperature:** Blood is stored at **2°C to 6°C**. * **The "Storage Lesion":** During storage, there is a decrease in pH, 2,3-DPG, and Sodium, while there is an **increase in Potassium** and Lactate. * **SAGM (Additive Solution):** Extends shelf life to **42 days** by providing optimal nutrients after the plasma is removed. * **Frozen RBCs:** Can be stored for up to **10 years** using Glycerol as a cryoprotectant.

Q: Which cells are characteristic of Hodgkin's disease?

Reed-Sternberg cells. **Explanation:** **Reed-Sternberg (RS) cells** are the diagnostic hallmark of Hodgkin Lymphoma (HL) [1]. These are large, multinucleated or polylobed B-cells, typically featuring a "mirror-image" nuclei with prominent, eosinophilic, owl-eye nucleoli. While they are the neoplastic component, they usually constitute only 1–5% of the total tumor mass, with the remainder being a reactive inflammatory background. **Analysis of Options:** * **Lacunar cells (Option A):** These are a specific *variant* of RS cells seen primarily in the **Nodular Sclerosis** subtype of HL. While characteristic of that subtype, the classic RS cell is the defining feature for Hodgkin’s disease as a whole. * **Giant cells (Option C):** This is a non-specific term. While RS cells are large, "giant cells" typically refer to Langhans giant cells (Tuberculosis) or Foreign Body giant cells, which are not diagnostic of HL. * **Eosinophils (Option D):** These are commonly found in the reactive background of HL (recruited by IL-5 secreted by RS cells), especially in the Mixed Cellularity subtype, but they are not the neoplastic or diagnostic cells. **High-Yield Pearls for NEET-PG:** * **Immunophenotype:** Classic RS cells are typically **CD15+ and CD30+**, but **CD20- and CD45-**. * **Popcorn Cells (L&H cells):** These are variants seen in **Nodular Lymphocyte Predominant HL**; they are CD20+ and CD45+, but CD15- and CD30-. * **Bimodal Age Distribution:** HL shows peaks in the 20s and again after age 50. * **EBV Association:** Most strongly linked with the Mixed Cellularity subtype.

Q: Non-immune hemolytic anemia occurs in which of the following conditions?

Plasmodium vivax infection. **Explanation:** Hemolytic anemia is broadly classified into **Immune** (mediated by antibodies) and **Non-immune** (mediated by mechanical, infectious, or metabolic factors). **Why Option B is Correct:** *Plasmodium vivax* (Malaria) causes **non-immune hemolytic anemia** through direct mechanical destruction of red blood cells (RBCs) [1]. The parasite invades the RBC, consumes hemoglobin, and eventually causes the cell to rupture (erythrocytic schizogony). Additionally, the spleen sequesters and destroys both parasitized and non-parasitized RBCs due to increased fragility and oxidative stress. Since this process is driven by the pathogen and not by autoantibodies, it is non-immune. **Why the Other Options are Incorrect:** * **A. SLE:** This is a classic cause of **Autoimmune Hemolytic Anemia (AIHA)**, typically mediated by IgG antibodies (Warm AIHA). It is a "Type II Hypersensitivity" reaction. * **C. CLL:** This is the most common malignancy associated with **Warm AIHA** [2]. The neoplastic B-cells produce autoantibodies against RBC antigens. * **D. CML:** While CML causes anemia, it is typically due to bone marrow infiltration (myelophthisis) or anemia of chronic disease, not primary hemolysis. It is not a classic cause of immune or non-immune hemolytic anemia. **NEET-PG High-Yield Pearls:** * **Direct Antiglobulin Test (Coombs Test):** Positive in immune hemolysis (SLE, CLL) and **negative** in non-immune hemolysis (Malaria, G6PD deficiency, HUS/TTP). * **Malaria & RBCs:** *P. vivax* and *P. ovale* selectively infect **reticulocytes** (young RBCs), whereas *P. falciparum* infects RBCs of all ages, leading to higher parasitemia. * **Microangiopathic Hemolytic Anemia (MAHA):** Another high-yield non-immune cause characterized by **schistocytes** on peripheral smear.

Q: A 7-year-old child presents with fever, bleeding gums, and fatigue for 4 days. On examination, she has splenomegaly. CBC shows Hb of 6 gm%, TLC 75,000/µL, and platelet count of 35,000/µL. Bone marrow aspiration shows these cells comprising 50% of marrow cells. What is the diagnosis?

Acute leukemia. ***Acute leukemia*** - **Bone marrow blasts comprising 50%** of marrow cells confirms acute leukemia (≥20% blasts required for diagnosis). - Classic pediatric presentation with **fever**, **bleeding gums**, **fatigue**, **splenomegaly**, and **pancytopenia** (anemia, thrombocytopenia with elevated WBC count). *Infectious mononucleosis* - Typically caused by **Epstein-Barr virus** with **atypical lymphocytes** on blood smear, not blast cells. - **Bone marrow blasts** would not comprise 50% of cells; lymphadenopathy is more common than splenomegaly. *Myelofibrosis* - **Bone marrow fibrosis** leads to **dry tap** on aspiration, not cellular marrow with 50% blasts. - Characterized by **teardrop-shaped RBCs** and **leukoerythroblastic picture** on peripheral smear. *Juvenile CML* - **Chronic phase** typically shows **massive leukocytosis** (>100,000/µL) with **left shift** and **basophilia**. - **Bone marrow** shows **hypercellularity** with **<5% blasts**, not 50% as seen in this case.

Q: A patient with Myeloproliferative Neoplasm presents with decreased white cell count and decreased platelets. What is the most likely diagnosis?

Myelofibrosis. **Explanation:** The correct answer is **Myelofibrosis (Primary Myelofibrosis)**. **Why it is correct:** While most Myeloproliferative Neoplasms (MPNs) initially present with an increase in cell counts, Primary Myelofibrosis (PMF) is unique due to its progression into a **"spent phase."** In PMF, neoplastic megakaryocytes release cytokines like TGF-β, which stimulate fibroblasts to deposit collagen in the bone marrow [1]. This progressive **fibrosis** replaces the hematopoietic space, leading to bone marrow failure. Consequently, patients develop **cytopenias** (decreased WBCs and platelets) and extramedullary hematopoiesis (massive splenomegaly) [1]. **Why other options are incorrect:** * **Chronic Myeloid Leukemia (CML):** Characterized by marked leukocytosis (predominantly neutrophils and myelocytes) and often thrombocytosis. Cytopenia is rare unless the patient enters a Blast Crisis. * **Polycythemia Vera (PV):** Defined by an absolute increase in red cell mass, often accompanied by leukocytosis and thrombocytosis (panmyelosis). * **Essential Thrombocytosis (ET):** Primarily presents with a significantly elevated platelet count; WBC and RBC counts are usually normal or slightly increased. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **Dacrocytes (Tear-drop RBCs)** and a **Leukoerythroblastic picture** (immature WBCs and nucleated RBCs). * **Bone Marrow:** Characterized by a **"Dry Tap"** on aspiration due to extensive fibrosis (Silver stain/Reticulin stain is used for diagnosis). * **Genetics:** Associated with **JAK2 V617F** (approx. 50%), CALR, or MPL mutations. * **Splenomegaly:** PMF causes some of the largest spleens in clinical practice due to compensatory extramedullary hematopoiesis [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 615-616.

Q: Which of the following cytogenetic abnormalities is NOT seen in acute myelodysplastic syndrome?

Monosomy 9. ### Explanation The question asks for the cytogenetic abnormality **not** typically associated with Myelodysplastic Syndromes (MDS). **1. Why Monosomy 9 is the Correct Answer:** Monosomy 9 (loss of an entire chromosome 9) is an extremely rare finding in MDS. While deletions of the long arm of chromosome 9 (**del 9q**) can be seen in AML (often associated with t(8;21)), **Monosomy 9** is not a characteristic or recurrent feature of MDS. In contrast, MDS is defined by specific recurrent chromosomal losses (monosomies or interstitial deletions) and specific gains [1]. **2. Analysis of Incorrect Options:** * **Trisomy 8:** This is the most common **gain** of a chromosome in MDS. It is considered an intermediate-risk cytogenetic abnormality [1]. * **Deletion of 5q (del 5q):** This is one of the most common and characteristic deletions in MDS. The "5q- syndrome" is a distinct clinical entity characterized by macrocytic anemia, thrombocytosis, and erythroid hypoplasia with a favorable prognosis [1]. * **Deletion of 20q (del 20q):** This is a common recurrent deletion in MDS and other myeloproliferative neoplasms. It is generally associated with a good prognosis when it occurs as an isolated abnormality [1]. **3. NEET-PG High-Yield Pearls:** * **Most common cytogenetic abnormalities in MDS:** del(5q), Monosomy 7/del(7q), Trisomy 8, and del(20q) [1]. * **Good Prognosis:** Isolated del(5q), isolated del(20q), and normal karyotype [1]. * **Poor Prognosis:** Monosomy 7 or Complex karyotype (≥3 abnormalities) [1]. * **MDS Hallmark:** Ineffective hematopoiesis leading to peripheral cytopenias despite a hypercellular bone marrow [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. 622-624.

Q: Low TIBC is seen in which of the following conditions?

Anemia of chronic disease. Explanation: Total Iron Binding Capacity (TIBC) is a functional measurement of the amount of Transferrin available to bind iron. It is generally inversely proportional to body iron stores. 1. Why Anemia of Chronic Disease (ACD) is correct: In ACD, the body produces high levels of Hepcidin (an acute-phase reactant) in response to inflammation. [1] Hepcidin sequesters iron within macrophages and hepatocytes, leading to low serum iron. [2] Simultaneously, the liver decreases the production of Transferrin to "starve" potential pathogens of iron. Since TIBC measures Transferrin levels, a decrease in Transferrin results in a Low TIBC. 2. Why the other options are incorrect: * Iron Deficiency Anemia (IDA): This is the classic "opposite" of ACD. [1] When iron stores are depleted, the liver compensates by increasing Transferrin production to maximize iron transport. Thus, IDA is characterized by a High TIBC. * Fanconi Anemia & Aplastic Anemia: These are bone marrow failure syndromes. They involve a primary defect in stem cells (pancytopenia) rather than a defect in iron metabolism. In these conditions, TIBC is usually normal or decreased (due to iron overload from multiple transfusions), but they are not the classic textbook examples for TIBC differentiation like ACD. [3] High-Yield Clinical Pearls for NEET-PG: * Ferritin: The most sensitive indicator for IDA (Low Ferritin). In ACD, Ferritin is Normal or High (as it is an acute-phase reactant). * Transferrin Saturation: Low in both IDA and ACD. * Soluble Transferrin Receptor (sTfR): Elevated in IDA but Normal in ACD. This is the best test to differentiate the two when they coexist. * Summary Table: * IDA: ↓ Iron, ↑ TIBC, ↓ Ferritin. * ACD: ↓ Iron, ↓ TIBC, ↑ Ferritin. [3]

Question 1

A 2-year-old child in shock presents with multiple non-blanching purple lesions of various sizes scattered on the trunk and extremities. Petechiae are noted, and oozing from the venipuncture site has been observed. The child's peripheral blood smear is shown below. Clotting studies are likely to show which of the following?

Accepted Answer

The presence of fibrin split products

Answer

Increased levels of factors V and VIII

Answer

A decreased prothrombin level

Answer

An increased fibrinogen level

Question 2

Acid Citrate Dextrose (ACD) is used to store blood and preserves Red Blood Cells (RBCs) for 21 days. What are the respective storage periods when phosphate alone is added to ACD, and when adenine and phosphate are added together to ACD?

Accepted Answer

21 days and 35 days

Answer

35 days and 42 days

Answer

28 days and 45 days

Answer

35 days and 28 days

Question 3

Which cells are characteristic of Hodgkin's disease?

Accepted Answer

Reed-Sternberg cells

Answer

Lacunar cells

Answer

Giant cells

Answer

Eosinophils

Question 4

Non-immune hemolytic anemia occurs in which of the following conditions?

Accepted Answer

Plasmodium vivax infection

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Chronic Lymphocytic Leukemia (CLL)

Answer

Chronic Myeloid Leukemia (CML)

Question 5

A 7-year-old child presents with fever, bleeding gums, and fatigue for 4 days. On examination, she has splenomegaly. CBC shows Hb of 6 gm%, TLC 75,000/µL, and platelet count of 35,000/µL. Bone marrow aspiration shows these cells comprising 50% of marrow cells. What is the diagnosis?

Accepted Answer

Acute leukemia

Answer

Infectious mononucleosis

Answer

Myelofibrosis

Answer

Juvenile CML

Question 6

A patient with Myeloproliferative Neoplasm presents with decreased white cell count and decreased platelets. What is the most likely diagnosis?

Accepted Answer

Myelofibrosis

Answer

Chronic myeloid leukemia

Answer

Polycythemia vera

Answer

Essential thrombocytosis

Question 7

Richter transformation is the conversion of?

Accepted Answer

CLL into DLBCL

Answer

DLBCL into CLL

Answer

SLL into CLL

Answer

CLL into SLL

Question 8

A thrombotic event is seen in all of the following conditions except?

Accepted Answer

Immune thrombocytopenic purpura (ITP)

Answer

Paroxysmal nocturnal hemoglobinuria (PNH)

Answer

Disseminated intravascular coagulation (DIC)

Answer

Heparin-induced thrombocytopenia (HIT)

Question 9

Which of the following cytogenetic abnormalities is NOT seen in acute myelodysplastic syndrome?

Accepted Answer

Monosomy 9

Answer

Trisomy 8

Answer

Deletion of 20q

Answer

Deletion of 5q

Question 10

Low TIBC is seen in which of the following conditions?

Accepted Answer

Anemia of chronic disease

Answer

Iron deficiency anemia

Answer

Fanconi anemia

Answer

Aplastic anemia

Hematopathology — MCQs

Hematopathology — MCQs

On this page

Practice by Chapter

Want unlimited practice?