Hematopathology Practice Questions

Q: Why is citrate phosphate dextrose (CPD) better than acid citrate dextrose (ACD) for storage of blood?

Contains phosphate and dextrose. ***Contains phosphate and dextrose*** - CPD contains **phosphate**, which acts as a buffer and helps maintain crucial 2,3-bisphosphoglycerate (2,3-BPG) levels in red blood cells, improving oxygen delivery capacity. - The presence of **dextrose** provides a substrate for glycolysis, which is essential for ATP production and red blood cell viability during storage. - This combination allows CPD to extend blood storage life to approximately **35 days** compared to ACD's **21 days**. *Maintains pH stability during storage* - Both ACD and CPD help maintain pH stability due to their **citrate** content, which acts as an anticoagulant and buffer. - However, CPD's phosphate component offers superior buffering capacity, but pH maintenance alone is not the primary distinguishing advantage. - This is a shared characteristic of both solutions, not the key reason CPD is preferred. *Prevents hemolysis in stored blood* - Both CPD and ACD prevent hemolysis by chelating **calcium**, which prevents coagulation and maintains red blood cell integrity. - While both solutions successfully prevent hemolysis, this is not the distinguishing feature that makes CPD superior. - The primary advantage of CPD lies in its better support of red blood cell metabolism and viability through phosphate and dextrose. *Reduces metabolic activity in stored blood* - This is **incorrect** - the purpose of anticoagulant solutions is to preserve blood components, not to reduce metabolic activity. - The dextrose in CPD is provided precisely to **fuel essential metabolic activity** (glycolysis) to sustain red blood cells during storage. - While refrigeration at 1-6°C slows metabolism, CPD actively supports rather than reduces the metabolic processes necessary for RBC survival.

Q: Glanzmann thrombasthenia is due to defect in:-

Gp IIb/IIIa. ***Gp IIb/IIIa*** - Glanzmann thrombasthenia is a **rare, inherited bleeding disorder** characterized by a defect or deficiency in the **glycoprotein IIb/IIIa (Gp IIb/IIIa) complex** on the platelet surface [1]. - This complex is crucial for platelet aggregation as it acts as the receptor for **fibrinogen**, which links activated platelets together [1]. *Gp VI* - **Glycoprotein VI (Gp VI)** is a collagen receptor on platelets, important for initial **platelet adhesion and activation** at sites of vascular injury. - Defects in Gp VI are associated with milder bleeding disorders, not Glanzmann thrombasthenia. *Thromboxane A2* - **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and **platelet aggregator** synthesized by platelets. - Disorders in TXA2 synthesis or response, such as aspirin-induced platelet dysfunction, cause bleeding but are biochemically distinct from Glanzmann thrombasthenia. *Gp Ia/IIa* - The **glycoprotein Ia/IIa (Gp Ia/IIa) complex** (also known as integrin ̡2̢1) is another **collagen receptor** on platelets, mediating platelet adhesion to collagen. - Defects in Gp Ia/IIa lead to a different type of mild bleeding disorder, affecting initial adhesion rather than aggregation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.

Q: All of the following decrease in iron deficiency anemia except:

TIBC. ***TIBC*** - In **iron deficiency anemia**, the body attempts to maximize iron absorption and transport, leading to an **increase** in **Total Iron Binding Capacity (TIBC)** [1]. - TIBC reflects the amount of **transferrin** available to bind iron; more transferrin is produced when iron stores are low [1]. *Serum iron* - **Serum iron** measures the iron circulating in the blood bound to transferrin. - In **iron deficiency anemia**, the overall amount of circulating iron is **decreased** due to insufficient iron stores [1]. *Ferritin* - **Ferritin** is a storage protein for iron, reflecting the body's iron stores [2]. - In **iron deficiency anemia**, iron stores are depleted, resulting in a **decreased** serum ferritin level [1]. *Transferrin saturation* - **Transferrin saturation** is the percentage of transferrin binding sites occupied by iron. - In **iron deficiency anemia**, with low serum iron and increased TIBC, the percentage of binding sites occupied by iron is **lowered** [1].

Q: Tumor cells in chronic lymphocytic leukemia or small lymphoblastic lymphoma (CLL/SLL) arise from which of the following?

Mature B cell. ***Mature B cell*** - CLL/SLL is characterized by the accumulation of **monoclonal B lymphocytes** that are morphologically mature but functionally incompetent. [1] - These malignant cells exhibit a mature immunophenotype, expressing **CD5, CD19, CD20 (dim), and CD23**, indicating their origin from a post-germinal center or memory B cell lineage. [1] *Naive B cell* - Naive B cells are typically found circulating in the blood and lymph nodes; while they are B cells, the specific immunophenotype and genomic features of CLL/SLL cells point to a more differentiated origin. - Although CLL/SLL cells express some markers of naive B cells, their overall profile, particularly the expression of **CD23**, is more consistent with a mature or activated B cell stage. [1] *Centrocytes of germinal center* - Malignancies arising from centrocytes of germinal centers often include **follicular lymphoma**, which presents with distinct clinical and immunophenotypic features from CLL/SLL. - Centrocytes are typically involved in somatic hypermutation and class switching, processes relevant to later stage B cell development, but not the direct origin of CLL/SLL. *Progenitor B-cell* - Progenitor B-cells are early developmental stages of B cells, and their malignant transformation leads to conditions like **B-cell acute lymphoblastic leukemia (B-ALL)**. [1] - B-ALL presents with immature blast cells and a different immunophenotype (e.g., lack of CD23), distinct from the mature lymphoid cells seen in CLL/SLL. [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. 596-598.

Q: Which of the following anticoagulant preservatives can be used to store blood, so that it can be kept for 35 days?

Citrate phosphate dextrose-adenine (CPD-A). ***Citrate phosphate dextrose-adenine (CPD-A)*** - **CPD-A** is the most common anticoagulant preservative used for whole blood storage, allowing it to be stored for up to **35 days**. - The addition of **adenine** provides a substrate for red blood cell metabolism, helping to maintain **ATP levels** and extend viability. *Acid citrate dextrose (ACD)* - **ACD** was an earlier anticoagulant solution that allowed blood to be stored for **21 days**. - While effective, it does not support red blood cell viability for as long as CPD-A due to the lack of **adenine**. *CP2D - citrate phosphate double dextrose* - **CP2D** is similar to CPD but contains **double the amount of dextrose**, which can slightly improve red blood cell viability. - However, CP2D typically allows for blood storage of **21 days**, not the 35 days provided by CPD-A. *CPD Citrate phosphate dextrose* - **CPD** was an advancement over ACD, allowing blood to be stored for **21 days**. - While it improved upon ACD, it does not contain **adenine**, which is crucial for extending storage to **35 days**.

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.

Question 1

Why is citrate phosphate dextrose (CPD) better than acid citrate dextrose (ACD) for storage of blood?

Accepted Answer

Contains phosphate and dextrose

Answer

Maintains pH stability during storage

Answer

Prevents hemolysis in stored blood

Answer

Reduces metabolic activity in stored blood

Question 2

Glanzmann thrombasthenia is due to defect in:-

Accepted Answer

Gp IIb/IIIa

Answer

Gp VI

Answer

Thromboxane A2

Answer

Gp Ia/IIa

Question 3

All of the following decrease in iron deficiency anemia except:

Accepted Answer

TIBC

Answer

Serum iron

Answer

Ferritin

Answer

Transferrin saturation

Question 4

Tumor cells in chronic lymphocytic leukemia or small lymphoblastic lymphoma (CLL/SLL) arise from which of the following?

Accepted Answer

Mature B cell

Answer

Naive B cell

Answer

Centrocytes of germinal center

Answer

Progenitor B-cell

Question 5

Which of the following anticoagulant preservatives can be used to store blood, so that it can be kept for 35 days?

Accepted Answer

Citrate phosphate dextrose-adenine (CPD-A)

Answer

Acid citrate dextrose (ACD)

Answer

CP2D - citrate phosphate double dextrose

Answer

CPD Citrate phosphate dextrose

Question 6

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 7

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 8

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 9

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 10

Which is NOT a feature of microangiopathic hemolytic anemia?

Accepted Answer

Spherocytes

Answer

High LDH

Answer

Schistocytes

Answer

Low haptoglobin

Hematopathology — MCQs

Hematopathology — MCQs

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