Hematopathology Practice Questions

Q: What processing should be done of the blood before transfusion to reduce chances of febrile non-hemolytic transfusion reaction (FNHTR)?

Leucocyte reduction. ***Leucocyte reduction*** - **Febrile non-hemolytic transfusion reactions (FNHTRs)** are primarily caused by cytokines released from donor leukocytes during storage or by recipient antibodies targeting donor leukocytes [1]. - **Leukocyte reduction** removes these donor white blood cells, thereby significantly decreasing the risk of FNHTRs. *Washing* - **Washing** removes plasma proteins and antibodies, which is useful for preventing allergic reactions or anaphylaxis in patients with IgA deficiency, but it is not the primary method for preventing FNHTRs. - While it can remove some cytokines, its main indication is different from preventing leukocyte-mediated reactions. *Irradiation* - **Irradiation** is performed to prevent **transfusion-associated graft-versus-host disease (TA-GVHD)** by inactivating donor lymphocytes, preserving their function but preventing their proliferation. - It does not primarily reduce the number of leukocytes or the associated cytokine release responsible for FNHTRs. *Glycerolization* - **Glycerolization** is a process used to cryopreserve **red blood cells** for long-term storage, often decades. - This process is essential for maintaining the viability of red blood cells in frozen storage but has no direct role in preventing FNHTRs.

Q: Storage temperature of RBC, Platelet, and Fresh Frozen Plasma (FFP) are:

RBC 2-6°C, Platelet 20-24°C, FFP -30°C. **RBC 2-6°C, Platelet 20-22°C, FFP -30°C** - **Red blood cells (RBCs)** are stored at **2-6°C** to slow metabolic activity and maintain viability for up to 42 days, depending on the anticoagulant. - **Platelets** require storage at **20-24°C** with continuous agitation to prevent aggregation and maintain their function for up to 5-7 days [1]. - **Fresh Frozen Plasma (FFP)** is stored at **-18°C or colder (often -30°C)** within 8 hours of collection to preserve labile clotting factors, particularly Factors V and VIII [2]. *RBC 20-22°C, Platelet 2-6°C, FFP -30°C* - Storing **RBCs** at **20-22°C** would lead to rapid bacterial growth and spoilage, making them unsafe for transfusion and shortening their shelf life significantly. - Storing **platelets** at **2-6°C** would cause them to lose their function due to activation and aggregation, rendering them ineffective for treating bleeding [1]. *RBC -30°C, FFP 2-6°C, Platelet 20-22°C* - Storing **RBCs** at **-30°C** without cryoprotectants would cause them to hemolyze due to ice crystal formation, destroying their integrity. - Storing **FFP** at **2-6°C** would lead to the degradation of labile clotting factors, particularly factors V and VIII, within hours, making it ineffective for coagulation deficiencies [2]. *RBC 20-22°C, FFP -30°C, Platelet 2-6°C* - Storing **RBCs** at **20-22°C** would significantly increase their metabolic rate and risk of bacterial contamination, shortening their viable storage period to only hours. - Storing **platelets** at **2-6°C** would impair their function, causing them to aggregate and become unviable for transfusion [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-583. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.

Q: A voluntary donor underwent apheresis for platelet donation for the first time after which he developed perioral tingling and numbness. This is seen because:

Due to citrate based anticoagulant. ***Due to citrate based anticoagulant*** - **Citrate** is commonly used as an anticoagulant during apheresis procedures and can chelate **ionized calcium**. - A decrease in ionized calcium levels can lead to symptoms like **perioral tingling** and **numbness** (paresthesias) due to increased neuromuscular excitability. *Due to fluid depletion* - While fluid shifts can occur during apheresis, **hypovolemia** is more likely to cause symptoms like dizziness, lightheadedness, or syncope rather than specific paresthesias. - **Fluid depletion** alone does not typically directly explain perioral tingling and numbness. *He underwent apheresis for the first time* - The novelty of the procedure does not inherently cause physiological symptoms like **perioral tingling** and **numbness**. - This is a psychological factor, not a direct cause of a specific physiological response seen in this scenario. *His platelet count was low for donation* - A donor's **low platelet count** would typically contraindicate donation or lead to a less efficient collection, but it does not cause **perioral tingling** or **numbness** during or after the procedure. - The symptoms described are related to the **anticoagulant** used, not the donor's baseline platelet levels.

Q: Why does iron deficiency anemia cause increased platelet count despite decreased erythropoiesis?

Increased TPO production. Increased TPO production - **Iron deficiency** stimulates the production of **thrombopoietin (TPO)**, a cytokine that promotes megakaryocyte proliferation and platelet production. - This elevated TPO, often mediated by inflammatory cytokines, overrides the bone marrow's overall reduced activity in erythropoiesis. *Enhanced iron utilization* - While the body attempts to maximize iron utilization during deficiency, this mechanism primarily benefits erythropoiesis and does not directly cause **thrombocytosis**. - **Iron's role** in platelet production is indirect, mainly through its impact on overall cellular function rather than a direct stimulus for increased numbers. *Compensatory bone marrow response* - The bone marrow *does* attempt to compensate for anemia, but this primarily focuses on increasing red blood cell production, which is hindered by the **lack of iron**. - The *specific* increase in platelets is due to a distinct signaling pathway involving **TPO**, not a general compensatory response for all cell lines. *Decreased platelet destruction* - **Iron deficiency anemia** does not typically lead to a decrease in platelet destruction. - Platelet lifespan and clearance mechanisms are generally unaffected by **iron status**. *Note: Current medical literature, including leading hematology and biochemistry texts, acknowledges that iron deficiency is associated with reactive thrombocytosis, often linked to structural similarity between erythropoietin and thrombopoietin or common progenitor stimulation, though specific molecular pathways regarding hepcidin and iron-sensing are primarily focused on the erythroid lineage [1].*

Q: Which is NOT a feature of microangiopathic hemolytic anemia?

Spherocytes. ***Spherocytes*** - **Spherocytes** are typically found in conditions like **hereditary spherocytosis** or **autoimmune hemolytic anemia**, where red blood cells are damaged or improperly formed, leading to a spherical shape [1]. - In **microangiopathic hemolytic anemia (MAHA)**, red cells are fragmented by shear stress from damaged small blood vessels, resulting in **schistocytes**, not spherocytes. *High LDH* - **Lactate dehydrogenase (LDH)** is an intracellular enzyme released when red blood cells are destroyed, making **elevated LDH** a common finding in hemolytic anemias, including MAHA. - Its high levels reflect increased red cell turnover and destruction in the microvasculature. *Schistocytes* - **Schistocytes**, or fragmented red blood cells, are the **hallmark** of microangiopathic hemolytic anemia. - They are formed when red blood cells pass through damaged small blood vessels containing fibrin strands, leading to their shearing and destruction. *Low haptoglobin* - **Haptoglobin** is a plasma protein that binds free hemoglobin released during red blood cell destruction. - In hemolytic anemias like MAHA, there is increased hemoglobin release, which saturates and depletes haptoglobin, leading to **low or undetectable levels**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Q: Direct Coombs test is positive in all EXCEPT:

G6PD deficiency. ***G6PD deficiency*** - **G6PD deficiency** is an intrinsic red blood cell defect that leads to hemolytic anemia, but it does **not involve immune-mediated destruction** of red blood cells. - The **Direct Coombs test** detects antibodies or complement components bound to the surface of red blood cells; since G6PD deficiency is not immune-mediated, the test will be negative. *Rh incompatibility* - **Rh incompatibility** occurs when maternal antibodies cross the placenta and target fetal red blood cells, leading to **immune-mediated hemolysis** [1]. - The anti-D antibodies bind to fetal red blood cells, resulting in a **positive Direct Coombs test** (detecting antibody-coated fetal RBCs) [1]. *Autoimmune hemolysis* - **Autoimmune hemolysis** involves the body producing **autoantibodies** against its own red blood cells, leading to their premature destruction [3]. - These autoantibodies (e.g., IgG, IgM) bind to the red blood cell surface, making the **Direct Coombs test positive** [3]. *ABO incompatibility* - **ABO incompatibility** involves the presence of naturally occurring antibodies (e.g., anti-A, anti-B) in a recipient's plasma that react with donor red blood cells [2]. - When incompatible red blood cells are transfused, or in cases of **hemolytic disease of the newborn** due to ABO incompatibility, antibodies bind to the RBCs, resulting in a **positive Direct Coombs test** [2].

Q: What is the primary site of involvement in multiple myeloma?

Bone marrow. ***Bone marrow*** - Multiple myeloma is a **B-cell malignancy** characterized by the uncontrolled proliferation of **plasma cells** in the bone marrow [1]. - These malignant plasma cells produce an abnormal **monoclonal immunoglobulin** (M protein) and can cause lytic bone lesions [2]. *Lungs* - While lung involvement can occur in advanced or unusual cases of multiple myeloma (e.g., through extramedullary plasmacytomas), it is **not the primary site** of the disease. - Primary lung malignancies or metastases from other cancers are more common causes of lung pathology. *Liver* - **Liver infiltration** by myeloma cells is rare and usually indicates widespread disease or extramedullary involvement, not the initial or primary site. - The liver's primary role in hematologic malignancies often involves metabolism or effects on coagulation, not as a primary site of plasma cell proliferation. *Spleen* - **Splenomegaly** can sometimes be observed in multiple myeloma due to extramedullary hematopoiesis or infiltration, but it is **not the primary site** for plasma cell proliferation. - Lymphomas and leukemias are more typically associated with primary splenic involvement. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-618. [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, pp. 606-608.

Q: Which of the following statements about sickle cell disease is true?

Autosomal recessive. ### Autosomal recessive - Sickle cell disease is inherited in an **autosomal recessive pattern**, meaning an individual must inherit two copies of the abnormal gene (HbS) to develop the disease. - This mode of inheritance is crucial for genetic counseling and understanding family risk. [1] ### Sickled cells are flexible - **Sickled cells are rigid** and inflexible, unlike normal red blood cells, which contributes to their inability to easily pass through small blood vessels. [1] - Their stiffness is a key factor in the pathology of vaso-occlusion, as they tend to clog capillaries. ### Vaso-occlusion is rare - **Vaso-occlusion is a hallmark** and frequent complication of sickle cell disease, leading to painful crises and organ damage. [1] - The rigid, sickled red blood cells block blood flow in small vessels, causing ischemia and infarction in various tissues. ### Chronic hemolysis does not occur - **Chronic hemolysis is a prominent feature** of sickle cell disease, as the sickled red blood cells are fragile and have a shortened lifespan, leading to constant destruction. [1] - This ongoing destruction of red blood cells causes **anemia**, jaundice, and can contribute to gallstone formation. [1]

Q: Which protein is a key marker of Reed-Sternberg cells in Hodgkin's lymphoma?

CD15. ***CD15*** - **CD15** (along with **CD30**) is a characteristic **immunophenotypic marker** of **Reed-Sternberg cells** in **classical Hodgkin's lymphoma** [1]. - The classic immunophenotype is **CD30+/CD15+/CD45-/CD20-** (CD20 may be weakly positive in some cases). - **CD30 is the most sensitive marker** (positive in >95% of cases), while **CD15 is positive in 75-85%** of classical Hodgkin's lymphoma cases. - Both markers together aid in the definitive diagnosis and differentiation of Hodgkin's lymphoma from other lymphomas. *CD19* - **CD19** is an important **B-cell marker** expressed on normal B lymphocytes and in most B-cell non-Hodgkin lymphomas, but it is typically **negative** in Reed-Sternberg cells [1]. - Its presence usually points away from Hodgkin's lymphoma and towards a B-cell lineage malignancy. *CD20* - **CD20** is another key **B-cell marker** found on the surface of normal B lymphocytes and **most B-cell non-Hodgkin lymphomas**. - Reed-Sternberg cells usually **lack CD20 expression** (or show only weak positivity in 20-40% of cases), helping to distinguish Hodgkin's lymphoma from B-cell non-Hodgkin lymphomas [1]. *CD45* - **CD45** (also known as leukocyte common antigen, LCA) is expressed on nearly all **hematopoietic cells**, including most lymphomas. - However, **Reed-Sternberg cells are typically negative or only weakly positive for CD45**, which is a significant diagnostic feature that helps differentiate Hodgkin's lymphoma from many non-Hodgkin lymphomas [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. 614-618.

Question 1

What processing should be done of the blood before transfusion to reduce chances of febrile non-hemolytic transfusion reaction (FNHTR)?

Accepted Answer

Leucocyte reduction

Answer

Washing

Answer

Irradiation

Answer

Glycerolization

Question 2

Storage temperature of RBC, Platelet, and Fresh Frozen Plasma (FFP) are:

Accepted Answer

RBC 2-6°C, Platelet 20-24°C, FFP -30°C

Answer

RBC 20-22°C, Platelet 2-6°C, FFP -30°C

Answer

RBC -30°C, FFP 2-6°C, Platelet 20-22°C

Answer

RBC 20-22°C, FFP -30°C, Platelet 2-6°C

Question 3

A voluntary donor underwent apheresis for platelet donation for the first time after which he developed perioral tingling and numbness. This is seen because:

Accepted Answer

Due to citrate based anticoagulant

Answer

Due to fluid depletion

Answer

He underwent apheresis for the first time

Answer

His platelet count was low for donation

Question 4

Why does iron deficiency anemia cause increased platelet count despite decreased erythropoiesis?

Accepted Answer

Increased TPO production

Answer

Enhanced iron utilization

Answer

Compensatory bone marrow response

Answer

Decreased platelet destruction

Question 5

Which is NOT a feature of microangiopathic hemolytic anemia?

Accepted Answer

Spherocytes

Answer

High LDH

Answer

Schistocytes

Answer

Low haptoglobin

Question 6

Direct Coombs test is positive in all EXCEPT:

Accepted Answer

G6PD deficiency

Answer

Rh incompatibility

Answer

Autoimmune hemolysis

Answer

ABO incompatibility

Question 7

Which is TRUE about JAK2 V617F mutation?

Accepted Answer

Seen in PV, ET, and PMF but rare in CML.

Answer

Seen in ET.

Answer

Rare in CML.

Answer

Common in PV but not specific.

Question 8

What is the primary site of involvement in multiple myeloma?

Accepted Answer

Bone marrow

Answer

Lungs

Answer

Liver

Answer

Spleen

Question 9

Which of the following statements about sickle cell disease is true?

Accepted Answer

Autosomal recessive

Answer

Sickled cells are flexible

Answer

Vaso-occlusion is rare

Answer

Chronic hemolysis does not occur

Question 10

Which protein is a key marker of Reed-Sternberg cells in Hodgkin's lymphoma?

Accepted Answer

CD15

Answer

CD19

Answer

CD20

Answer

CD45

Hematopathology — MCQs

Hematopathology — MCQs

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