Blood and Immunity Practice Questions

Q: What is the average size of platelets in micrometers?

2-3 µm. ***2-3 µm*** - Platelets, also known as **thrombocytes**, are small, anucleated cell fragments crucial for **hemostasis**, and their average diameter generally falls within the range of 2-3 micrometers. - This **small size** allows them to easily navigate through capillaries and aggregate rapidly at sites of vascular injury. *3-4 µm* - While platelets can vary slightly in size, an average of 3-4 µm is generally considered a bit on the larger side and not the typical average diameter. - Larger platelets might be seen in certain conditions like **idiopathic thrombocytopenic purpura (ITP)**, but this is not the average normal size. *4-5 µm* - This range is significantly larger than the typical size of normal circulating platelets. - Platelets this large would be considered **macroplatelets** and could indicate specific pathological conditions or inherited platelet disorders. *1-2 µm* - This size range is generally considered smaller than the average normal platelet size. - Very small platelets might be seen in some specific conditions, but it's not the usual average for healthy individuals.

Q: Increase in plasma viscosity is maximally caused by which plasma protein?

Fibrinogen. ***Globulin*** - Increased levels of **globulin** proteins, particularly in inflammatory or proliferative conditions, have a significant impact on plasma viscosity due to their **high molecular weight** [1]. - **Globulins** contribute to **hyperviscosity syndrome**, which can lead to clinical symptoms like fatigue and visual disturbances [1]. *Albumin* - While **albumin** is the most abundant plasma protein, its primary role is in maintaining **oncotic pressure**, not significantly affecting plasma viscosity. - An increase in albumin does not correlate with plasma viscosity increases to the extent seen with globulins. *All have equal effect* - Different plasma proteins do not have **equal effects** on viscosity; **globulins** and **fibrinogen** particularly influence it more than **albumin**. - The impact on viscosity varies significantly with protein concentration and type, making this statement inaccurate. *Fibrinogen* - **Fibrinogen** does contribute to plasma viscosity but is typically less than that caused by globulins, especially when globulin levels are markedly elevated. - Its effect is more pronounced during **coagulation**, rather than in the general increase of plasma viscosity associated with inflammatory states. **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. 141-142.

Q: The major role of 2,3-bisphosphoglycerate in RBCs is -

Release of oxygen. ***Release of oxygen*** - **2,3-bisphosphoglycerate (2,3-BPG)** binds allosterically to **deoxyhemoglobin**, stabilizing its T (tense) state. - This binding reduces hemoglobin's affinity for oxygen, promoting the **release of oxygen** to tissues. *Acid-base balance* - While red blood cells play a role in **acid-base balance** through the bicarbonate buffer system, 2,3-BPG's primary role is not buffering. - The **chloride shift** and **carbonic anhydrase** are more directly involved in RBC acid-base regulation. *Reversal of glycolysis* - 2,3-BPG is an intermediate of the **Rapoport-Luebering shunt**, a side pathway of glycolysis. - It does not reverse glycolysis but rather is produced during glycolysis to serve a specific function in oxygen transport. *Binding of oxygen* - 2,3-BPG **decreases** hemoglobin's affinity for oxygen, thus promoting its *release* from hemoglobin, not its binding. - Oxygen binding to hemoglobin occurs primarily at the **heme iron** without 2,3-BPG.

Q: Conversion of prekallikrein to kallikrein requires which clotting factor?

XII. ***XII*** - **Factor XII (Hageman factor)** is crucial in the **intrinsic pathway** of coagulation. - It initiates the contact activation system, which includes the conversion of **prekallikrein to kallikrein**. *XIII* - **Factor XIII (fibrin-stabilizing factor)** is responsible for **cross-linking fibrin** monomers to form a stable clot. - It acts much later in the coagulation cascade, after thrombin has converted fibrinogen to fibrin. *XI* - **Factor XI (plasma thromboplastin antecedent)** is activated by factor XIIa and in turn activates factor IX in the intrinsic pathway. - While part of the intrinsic pathway, it does not directly convert prekallikrein to kallikrein. *X* - **Factor X (Stuart-Prower factor)** is a central component of the **common pathway**, activated by both intrinsic and extrinsic pathways. - Its primary role is to combine with factor Va, calcium, and phospholipids to form the **prothrombinase complex**, converting prothrombin to thrombin.

Q: Converging point of both pathways in coagulation is at:

Stuart factor X. ***Stuart factor X*** [1][2] - It is the main **converging point** of the coagulation cascade, where both the intrinsic and extrinsic pathways meet to initiate the common pathway [1]. - Activated factor X leads to the conversion of **prothrombin to thrombin**, pivotal for clot formation [2]. *Factor VII* [2] - Primarily involved in the **extrinsic pathway** of coagulation, activating factor X, but does not serve as a converging point. - Its function is limited to starting the coagulation cascade, particularly upon tissue injury. *Factor IX* [2] - A key component of the **intrinsic pathway**, it leads to the activation of factor X but is not the point where both pathways converge. - It requires **factor VIII** for its activation, further illustrating its role within a specific pathway. *Factor VIII* - Also part of the **intrinsic pathway**, it acts as a cofactor for factor IX but does not integrate both pathways into a common point. - Its deficiency is associated with **Hemophilia A**, underscoring its specific pathway involvement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.

Q: What is Proaccelerin?

Factor V. ***Factor V*** - **Factor V**, also known as **proaccelerin** or **labile factor**, is a **plasma protein** that plays a crucial role in the coagulation cascade. - It is activated by thrombin to **Factor Va**, which then combines with Factor Xa, calcium, and phospholipid to form the **prothrombinase complex**, significantly enhancing thrombin generation. *Factor II* - **Factor II** is **prothrombin**, a precursor to **thrombin**, which is central to coagulation. - It is not referred to as preaccelerin. *Factor VII* - **Factor VII** is primarily involved in the **extrinsic pathway** of coagulation, becoming activated to Factor VIIa upon contact with tissue factor. - It works to activate Factor IX and Factor X, but it is not preaccelerin. *Factor X* - **Factor X**, also known as **Stuart-Prower factor**, is a key enzyme in the **common pathway** of coagulation, converting prothrombin to thrombin. - It is distinct from Factor V, which acts as a cofactor.

Q: Females have a lower RBC count compared to males due to?

Low erythropoietin. ***Low erythropoietin (relative to males)*** - The primary reason females have lower RBC counts is due to **hormonal differences**, specifically the lack of androgenic stimulation of erythropoiesis that males experience. - **Testosterone in males** directly stimulates erythropoietin production and enhances erythropoiesis, leading to higher RBC counts (males: 4.5-5.5 million/µL vs females: 4.0-5.0 million/µL). - Females have relatively lower erythropoietic drive compared to males due to the absence of significant androgenic hormones, which can be conceptualized as relatively lower erythropoietic stimulus. - This difference exists across all age groups, including pre-menarchal and post-menopausal women, confirming it is **hormonal rather than blood loss-related**. *High estrogen* - Estrogen does not significantly suppress erythropoiesis to cause lower RBC counts. - Estrogen has various effects on the hematopoietic system but is not the primary cause of the gender difference in RBC count. *Low stem cells* - Hematopoietic stem cell numbers and functionality are comparable between males and females. - There is no evidence of lower stem cell counts in females accounting for RBC differences. *Menstrual blood loss* - While menstrual blood loss can contribute to **iron deficiency anemia** in some women, it does NOT explain the baseline physiological difference in RBC counts between genders. - Most healthy menstruating women maintain normal RBC counts despite regular menstruation. - The RBC count difference exists even in pre-menarchal girls and post-menopausal women, proving menstruation is not the primary cause.

Q: In which condition is venous blood most commonly observed to have a high hematocrit in routine clinical practice?

Dehydration. Dehydration - In **dehydration**, the total body water is reduced, leading to a decrease in plasma volume [1, 5]. This concentrates the red blood cells, resulting in a relatively **high hematocrit**. [3] - This is a common finding as the body attempts to conserve fluid, making it a primary cause of **elevated hematocrit** in clinical practice. *Anemia* - **Anemia** is characterized by a decrease in the number of red blood cells or a reduced hemoglobin concentration, which would lead to a **low hematocrit**, not a high one [2]. - This condition involves insufficient oxygen-carrying capacity due to a deficiency in red blood cells or hemoglobin [2]. *Hypervolemia* - **Hypervolemia** describes an excess of fluid in the blood, which would dilute the blood components, leading to a relatively **low hematocrit** [1]. - This condition is often associated with conditions like heart failure or kidney disease, where fluid retention is common. *Acute blood loss* - In **acute blood loss**, the loss of whole blood immediately after the event would initially reduce both red blood cells and plasma proportionally, not immediately raising hematocrit [2]. - As the body attempts to compensate by shifting extravascular fluid into the circulation, this would further dilute the blood, eventually leading to a **decreased hematocrit** [2].

Q: Which isotope is used to measure RBC volume?

Cr 51. ***Cr 51*** - **Chromium-51** attaches irreversibly to the beta chain of hemoglobin, making it an ideal tracer for measuring **red blood cell volume** and survival. - After injection, the labeled red blood cells distribute throughout the circulation, and their dilution allows for the calculation of the total **RBC mass**. *H-3* - **Tritium (H-3)** is typically used as tritiated water to measure **total body water**, as it readily equilibrates throughout all fluid compartments. - It does not specifically bind to red blood cells for mass measurement. *D2O* - **D2O (heavy water)** is used to measure **total body water** content, similar to tritiated water. - It exchanges with water in the body and diffuses into all fluid compartments, rather than targeting red blood cells. *I-135* - While various **iodine isotopes** are used in medicine, such as **I-131** for thyroid imaging or therapy, **I-135** is not a commonly used isotope for measuring red blood cell volume. - Other tracers like **radio-iodinated human serum albumin** (e.g., I-125 HSA) can be used to measure plasma volume, not specifically RBC volume.

Q: Which cytokine activates eosinophils?

IL-5. ***IL-5*** - **Interleukin-5 (IL-5)** is the primary cytokine responsible for activating **eosinophils**, stimulating their **production, maturation, and release** from the bone marrow. - It also enhances eosinophil survival and function at sites of inflammation, particularly in **allergic reactions** and **parasitic infections**. *IL-1* - **Interleukin-1 (IL-1)** is a **pro-inflammatory cytokine** primarily involved in fever, acute phase responses, and activating lymphocytes, but not directly in eosinophil activation. - It plays a role in general immune responses and inflammation by activating various cell types, including **macrophages and endothelial cells**. *IL-4* - **Interleukin-4 (IL-4)** is crucial for **Th2 differentiation** and isotype switching to IgE in B cells, promoting allergic responses. - While involved in allergic reactions, it primarily affects B cell and T cell function rather than direct activation of eosinophils, though it can support their development indirectly. *IL-6* - **Interleukin-6 (IL-6)** is a **pro-inflammatory cytokine** involved in acute phase reactions, hematopoiesis, and immune responses. - It is critical for B cell differentiation and T cell activation but does not directly activate eosinophils.

Question 1

What is the average size of platelets in micrometers?

Accepted Answer

2-3 µm

Answer

4-5 µm

Answer

3-4 µm

Answer

1-2 µm

Question 2

Increase in plasma viscosity is maximally caused by which plasma protein?

Accepted Answer

Fibrinogen

Answer

Albumin

Answer

All have equal effect

Answer

Globulin

Question 3

The major role of 2,3-bisphosphoglycerate in RBCs is -

Accepted Answer

Release of oxygen

Answer

Acid-base balance

Answer

Reversal of glycolysis

Answer

Binding of oxygen

Question 4

Conversion of prekallikrein to kallikrein requires which clotting factor?

Accepted Answer

XII

Answer

XIII

Answer

X

Answer

XI

Question 5

Converging point of both pathways in coagulation is at:

Accepted Answer

Stuart factor X

Answer

Factor VIII

Answer

Factor IX

Answer

Factor VII

Question 6

What is Proaccelerin?

Accepted Answer

Factor V

Answer

Factor VII

Answer

Factor II

Answer

Factor X

Question 7

Females have a lower RBC count compared to males due to?

Accepted Answer

Low erythropoietin

Answer

High estrogen

Answer

Low stem cells

Answer

Menstrual blood loss

Question 8

In which condition is venous blood most commonly observed to have a high hematocrit in routine clinical practice?

Accepted Answer

Dehydration

Answer

Anemia

Answer

Hypervolemia

Answer

Acute blood loss

Question 9

Which isotope is used to measure RBC volume?

Accepted Answer

Cr 51

Answer

H-3

Answer

D2O

Answer

I-135

Question 10

Which cytokine activates eosinophils?

Accepted Answer

IL-5

Answer

IL-1

Answer

IL-4

Answer

IL-6

Blood and Immunity — MCQs

Blood and Immunity — MCQs

On this page

Practice by Chapter

Want unlimited practice?