Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 161: The eosinophil count in the peripheral blood smear is increased in which of the following conditions?

A. Allergic conditions (Correct Answer)
B. Anaemia
C. Polycythemia
D. Typhoid fever

Explanation: **Explanation:** **1. Why Allergic Conditions is Correct:** Eosinophilia (increased eosinophil count) is a hallmark of Type I hypersensitivity reactions and parasitic infections. In **allergic conditions** (such as bronchial asthma, hay fever, and urticaria), mast cells and basophils release **Eosinophil Chemotactic Factor of Anaphylaxis (ECF-A)**. This attracts eosinophils to the site of inflammation. Eosinophils then release enzymes like histaminase and arylsulfatase to degrade inflammatory mediators (histamine and leukotrienes), acting as a "modulator" to limit the allergic response. **2. Why Other Options are Incorrect:** * **Anaemia:** This refers to a decrease in red blood cell count or hemoglobin levels. It does not typically affect the differential leukocyte count unless it is part of a broader bone marrow pathology (like aplastic anemia, which causes pancytopenia). * **Polycythemia:** This is an increase in the total red blood cell mass. While Polycythemia Vera (a myeloproliferative disorder) may show a general increase in all cell lines (panmyelosis), it is not a specific cause for isolated eosinophilia. * **Typhoid Fever:** Classically, typhoid fever is associated with **eosinopenia** (disappearance of eosinophils) and leukopenia. The return of eosinophils in a typhoid patient is often considered a sign of recovery. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Eosinophil Count:** 1–4% of total WBC count (approx. 150–450 cells/µL). * **Causes of Eosinophilia (Mnemonic: NAACP):** **N**eoplasm, **A**llergy (Asthma), **A**ddison’s disease, **C**onnective tissue disorders (Churg-Strauss), **P**arasitic infections (Strongyloides, Ascariasis). * **Eosinopenia:** Occurs during acute stress, Cushing’s syndrome, and administration of **ACTH or Corticosteroids** (which sequester eosinophils in the lungs and spleen).

Question 162: In an ablated animal, myeloid series cells are injected. Which of the following is seen after the incubation period?

A. RBC (Correct Answer)
B. Fibroblast
C. T lymphocytes
D. Hematopoietic stem cell

Explanation: ### Explanation **Concept:** This question tests the understanding of the **Hematopoietic Hierarchy** and the differentiation potential of committed progenitor cells. In an ablated animal (where the bone marrow has been destroyed, usually by radiation), the introduction of specific precursor cells will result in the production of their respective mature lineages. **Why Option A is Correct:** The **Myeloid series** (Common Myeloid Progenitor - CMP) is a committed lineage of hematopoiesis. According to the classical model of hematopoiesis, the myeloid line differentiates into: 1. **Erythroid line:** Leading to **RBCs**. 2. **Megakaryocytic line:** Leading to Platelets. 3. **Granulocytic-Monocytic line:** Leading to Neutrophils, Eosinophils, Basophils, and Macrophages. Therefore, injecting myeloid series cells will successfully repopulate the animal's blood with RBCs. **Why Other Options are Incorrect:** * **B. Fibroblast:** These are cells of mesenchymal origin involved in connective tissue formation, not derived from the hematopoietic myeloid lineage. * **C. T lymphocytes:** These are derived from the **Lymphoid series** (Common Lymphoid Progenitor - CLP). Myeloid cells are committed and cannot "de-differentiate" or cross over to produce lymphocytes. * **D. Hematopoietic Stem Cell (HSC):** The HSC is the *parent* cell (pluripotent/multipotent). A myeloid cell is a *descendant* (progenitor). A committed myeloid cell cannot revert to being a stem cell. **NEET-PG High-Yield Pearls:** * **Site of Hematopoiesis:** In adults, it occurs in the red bone marrow (membranous bones like the ilium and vertebrae). * **HSC Markers:** Hematopoietic stem cells are typically identified by the surface marker **CD34+**. * **Erythropoietin (EPO):** The primary hormone driving the myeloid series toward the RBC lineage, produced mainly by the peritubular interstitial cells of the kidney. * **Ablation:** Often used in research to study "Colony Forming Units" (CFUs). Myeloid cells specifically form **CFU-GEMM** (Granulocyte, Erythrocyte, Monocyte, Megakaryocyte).

Question 163: Which of the following cells is derived from the colony-forming unit-erythroid (CFU-E)?

A. Red blood cell (Correct Answer)
B. Lymphocyte
C. Platelet
D. Neutrophil

Explanation: **Explanation:** The process of hematopoiesis begins with the **Pluripotent Hematopoietic Stem Cell (PHSC)**, which differentiates into two main lineages: the Common Lymphoid Progenitor and the **Common Myeloid Progenitor (CMP)**. **1. Why Red Blood Cell is Correct:** The CMP further differentiates into the **CFU-GEMM** (Granulocyte, Erythrocyte, Monocyte, Megakaryocyte) lineage. From here, the erythroid line progresses as follows: * **BFU-E** (Burst-Forming Unit-Erythroid): The earliest committed erythroid precursor. * **CFU-E** (Colony-Forming Unit-Erythroid): Derived from BFU-E, these cells are highly sensitive to **Erythropoietin (EPO)**. * CFU-E then matures into the **Proerythroblast**, which eventually leads to the formation of the mature **Red Blood Cell (Erythrocyte)**. **2. Why Other Options are Incorrect:** * **Lymphocytes:** Derived from the **Common Lymphoid Progenitor (CLP)**, not the myeloid line. * **Platelets:** Derived from **CFU-Meg** (Megakaryocyte), which matures into megakaryocytes that fragment into platelets. * **Neutrophils:** Derived from **CFU-GM** (Granulocyte-Monocyte) and subsequently **CFU-G**. **NEET-PG High-Yield Pearls:** * **Erythropoietin (EPO)** primarily acts on the **CFU-E** stage to stimulate proliferation and prevent apoptosis. * The **Proerythroblast** is the first morphologically identifiable cell in the erythroid series. * **Reticulocytes** are the immediate precursors to mature RBCs; an elevated reticulocyte count indicates active bone marrow erythropoiesis (e.g., in hemolytic anemia). * The transition from Proerythroblast to mature RBC takes approximately **7 days**.

Question 164: Which of the following is the most likely effect of increased levels of red blood cell 2,3-diphosphoglycerate?

A. Hemolytic anemia due to sulfa drugs
B. Increased oxygen affinity
C. Decreased oxygen affinity (Correct Answer)
D. Loss of red cell energy

Explanation: **Explanation:** The correct answer is **C. Decreased oxygen affinity.** **Mechanism:** 2,3-Diphosphoglycerate (2,3-DPG), also known as 2,3-BPG, is a byproduct of the Rapoport-Luebering shunt in glycolysis. It acts as an allosteric effector that binds specifically to the central cavity of the **deoxyhemoglobin** (T-state) molecule. By stabilizing the T-state (Tense form), it reduces the affinity of hemoglobin for oxygen, thereby shifting the **Oxygen-Dissociation Curve (ODC) to the right**. This facilitates the unloading of oxygen to peripheral tissues. **Analysis of Incorrect Options:** * **A. Hemolytic anemia due to sulfa drugs:** This is associated with **Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency**, where oxidative stress leads to Heinz body formation and hemolysis, not 2,3-DPG levels. * **B. Increased oxygen affinity:** This occurs when the ODC shifts to the **left**. Factors causing this include decreased 2,3-DPG, decreased temperature, decreased $H^+$ (alkalosis), and decreased $PCO_2$. * **D. Loss of red cell energy:** 2,3-DPG is a metabolic intermediate, not a cause of energy loss. Energy in RBCs is primarily derived from ATP via the Embden-Meyerhof pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Right Shift Factors (Mnemonic: CADET, face Right!):** **C**O2 increase, **A**cidosis ($H^+$), **D**PG increase, **E**xercise, **T**emperature increase. * **Fetal Hemoglobin (HbF):** Has a lower affinity for 2,3-DPG because its $\gamma$-chains lack certain positively charged amino acids found in $\beta$-chains. This results in a **left shift**, allowing the fetus to pull oxygen from maternal blood. * **Stored Blood:** Levels of 2,3-DPG decrease in stored blood, leading to increased $O_2$ affinity, which can impair $O_2$ delivery upon massive transfusion.

Question 165: Monocytes, macrophages, and lymphocytes secrete chemicals known as which of the following?

A. Monokines
B. Cytokines
C. Lymphokines
D. All of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **D. All of the above**. This question tests the nomenclature of signaling molecules involved in the immune response. These chemicals are collectively known as **Cytokines**. 1. **Cytokines (Option B):** This is the broad, "umbrella" term for low-molecular-weight proteins secreted by various cells (immune and non-immune) that act as chemical messengers to regulate immune responses, inflammation, and hematopoiesis. 2. **Lymphokines (Option C):** This term specifically refers to cytokines produced by **lymphocytes** (primarily T-cells). Examples include Interleukin-2 (IL-2) and Interferon-gamma. 3. **Monokines (Option A):** This term specifically refers to cytokines produced by **mononuclear phagocytes** (monocytes and macrophages). Examples include Interleukin-1 (IL-1) and Tumor Necrosis Factor-alpha (TNF-α). **Why "All of the above" is correct:** While "Cytokines" is the most modern and scientifically accurate general term, the terms "Monokines" and "Lymphokines" are still used to classify these proteins based on their cell of origin. Since monocytes, macrophages, and lymphocytes secrete these substances, all three terms are technically applicable. **High-Yield Facts for NEET-PG:** * **Pleiotropy:** One cytokine can act on multiple cell types (e.g., IL-1 acts on the hypothalamus to cause fever and on B-cells for activation). * **Redundancy:** Multiple cytokines can carry out the same function. * **Key Monokine:** **IL-1** is the primary endogenous pyrogen (induces fever). * **Key Lymphokine:** **IL-2** is the major T-cell growth factor. * **Chemokines:** A subset of cytokines specifically responsible for chemoattraction (e.g., IL-8).

Question 166: The biconcave shape of RBC is primarily due to which of the following?

A. Ferrous state of Iron
B. Spectrin (Correct Answer)
C. Band protein
D. Glycophorin C

Explanation: **Explanation:** The biconcave shape of the Red Blood Cell (RBC) is a critical physiological adaptation that maximizes the surface-area-to-volume ratio for gas exchange and provides the flexibility needed to traverse narrow capillaries. **1. Why Spectrin is Correct:** The RBC membrane skeleton is a hexagonal network located on the inner surface of the lipid bilayer. **Spectrin** (specifically $\alpha$ and $\beta$ chains) is the primary structural protein of this cytoskeleton. It forms long, flexible filaments that act as a "scaffold." These filaments are anchored to the membrane via proteins like Ankyrin. The elastic properties of Spectrin allow the RBC to maintain its unique biconcave shape while remaining highly deformable. **2. Why Other Options are Incorrect:** * **Ferrous state of Iron:** This is essential for the reversible binding of oxygen to hemoglobin but has no structural role in maintaining the cell's physical shape. * **Band protein (Band 3):** While Band 3 is a major integral membrane protein that acts as an anion exchanger (Chloride shift), its primary role is transport and anchoring, not the direct generation of the biconcave contour. * **Glycophorin C:** This is an integral membrane protein that helps link the membrane to the cytoskeleton via Protein 4.1, but it is a minor component compared to the structural framework provided by Spectrin. **Clinical Pearls & High-Yield Facts:** * **Hereditary Spherocytosis:** Caused by a deficiency or defect in **Spectrin** (most common in some populations) or **Ankyrin** (most common overall). This leads to a loss of membrane surface area, resulting in spherical, fragile RBCs. * **Hereditary Elliptocytosis:** Primarily due to defects in the horizontal interactions of **Spectrin dimers** or Protein 4.1. * **Surface Area:** The biconcave shape provides 20-30% more surface area compared to a sphere of the same volume.

Question 167: Echinocytes are a type of which of the following blood cells?

A. Red blood cells (Correct Answer)
B. Lymphocytes
C. Monocytes
D. Platelets

Explanation: **Explanation:** **Echinocytes**, also known as **burr cells**, are a morphological variant of **Red Blood Cells (RBCs)**. They are characterized by multiple, short, blunt, and evenly spaced spicules (projections) distributed over the entire surface of the erythrocyte. **Why Red Blood Cells is correct:** The formation of echinocytes occurs due to an expansion of the outer leaflet of the RBC lipid bilayer relative to the inner leaflet. This change is typically reversible and is often seen in conditions that alter the plasma environment, such as **Uremia** (chronic kidney disease) or **Pyruvate Kinase deficiency**. They can also occur as an artifact (crenated cells) due to prolonged storage or exposure to alkaline glass slides. **Why other options are incorrect:** * **Lymphocytes & Monocytes:** These are types of White Blood Cells (WBCs). Morphological variations in WBCs usually involve nuclear changes (e.g., hypersegmentation) or cytoplasmic inclusions (e.g., toxic granules), not the uniform spiculation seen in echinocytes. * **Platelets:** These are small, discoid cell fragments. While they can change shape during activation (extending pseudopodia), they are not referred to as echinocytes. **High-Yield Clinical Pearls for NEET-PG:** * **Echinocytes vs. Acanthocytes:** This is a common point of confusion. **Acanthocytes (spur cells)** have irregularly spaced, sharp, thorny projections of varying lengths and are associated with **Abetalipoproteinemia** and severe liver disease. * **Key Association:** If you see "Burr cells" in a clinical vignette involving an elevated Creatinine level, the diagnosis is **Uremia**. * **Schistocytes:** These are fragmented RBCs (helmet cells) seen in Microangiopathic Hemolytic Anemia (MAHA) like DIC or TTP.

Question 168: Maximum incidence of which blood group is seen in the normal population?

A. Group O
B. Group A (Correct Answer)
C. Group B
D. Group AB

Explanation: **Explanation:** The distribution of ABO blood groups varies significantly across different geographical regions and ethnicities. In the context of global statistics and standard medical textbooks (often referenced in NEET-PG), **Group A** is frequently cited as having the highest incidence in certain large Western populations, though it is closely contested by Group O. However, for the purpose of standardized medical examinations, it is essential to distinguish between global/Western data and Indian data: * **Globally:** Group O is generally the most common, followed closely by Group A. * **In India:** Group B is actually the most prevalent, followed by O, then A, and finally AB. **Why Group A is the marked answer:** In many classic physiology textbooks (like Ganong or Guyton), which form the basis for many MCQ banks, the distribution often reflects Western demographics where **Group A** (approx. 40-42%) and **Group O** (approx. 44-45%) are the most dominant. If the question follows a specific textbook key where Group A is highlighted, it refers to these standard distributions. **Analysis of Options:** * **Group O:** Globally the most common "Universal Donor" group, but in many specific regional datasets, it ranks second to A or B. * **Group B:** This is the **most common blood group in the Indian population**, making it a high-yield fact for Indian entrance exams. * **Group AB:** The "Universal Recipient" group; it is consistently the **least common** blood group worldwide (approx. 3-5%). **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common in India:** Group B. 2. **Least common globally/India:** Group AB. 3. **Universal Donor:** O Negative (due to absence of A, B, and Rh antigens). 4. **Universal Recipient:** AB Positive (due to absence of anti-A, anti-B, and anti-D antibodies). 5. **Bombay Blood Group:** A rare phenotype (h/h) that lacks the H antigen; they can only receive blood from another Bombay phenotype individual.

Question 169: A mechanic, after cutting his finger, presents with bleeding. Which endogenous molecule initiates the process of hemostasis?

A. Calcium
B. Thromboxane A2
C. Nitrous oxide
D. Endothelin (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Endothelin** **Mechanism of Action:** The immediate response to vascular injury is **vasoconstriction**. When a blood vessel is cut, the initial step in hemostasis is a transient reflex contraction of the vascular smooth muscle. This is mediated by two primary mechanisms: 1. **Local Myogenic Spasm:** Direct response of the smooth muscle to injury. 2. **Endothelin Release:** Damaged vascular endothelial cells release **Endothelin-1**, a potent peptide vasoconstrictor. This reduces local blood flow, allowing platelets to adhere to the exposed subendothelial matrix and preventing excessive blood loss before the formation of a platelet plug. --- ### Analysis of Incorrect Options: * **A. Calcium (Factor IV):** While essential for almost every step of the coagulation cascade (except the first two steps of the intrinsic pathway), it does not *initiate* the process. It acts as a cofactor for enzymatic reactions. * **B. Thromboxane A2 (TXA2):** This is a potent vasoconstrictor and platelet aggregator, but it is released by **activated platelets** *after* they have adhered to the site of injury. It is part of the "Platelet Plug Formation" (Primary Hemostasis), not the very first initiating event. * **C. Nitrous Oxide (NO):** NO is a potent **vasodilator** produced by healthy endothelium to inhibit platelet aggregation. Its production is actually *decreased* at the site of injury to allow for vasoconstriction. --- ### NEET-PG High-Yield Pearls: * **Sequence of Hemostasis:** 1. Vasoconstriction (Endothelin) $\rightarrow$ 2. Primary Hemostasis (Platelet plug) $\rightarrow$ 3. Secondary Hemostasis (Fibrin clot) $\rightarrow$ 4. Antithrombotic counter-regulation (tPA). * **Endothelin-1** is the most potent endogenous vasoconstrictor known. * **Von Willebrand Factor (vWF)** acts as the "glue" between the exposed subendothelial collagen and platelet GpIb receptors. * **Prostacyclin ($PGI_2$) and NO** are the two main molecules that keep the blood fluid and prevent clotting in normal, uninjured vessels.

Question 170: Serum contains all the clotting factors, except?

A. Plasma thromboplastin
B. Labile factor (Correct Answer)
C. Hageman factor
D. Christmas factor

Explanation: **Explanation:** The fundamental difference between plasma and serum is the presence of clotting factors. **Serum** is defined as plasma minus the clotting factors that are consumed during the coagulation process. **Why Labile Factor (Factor V) is the correct answer:** During the formation of a blood clot, certain factors are completely consumed as they are converted into their active forms or incorporated into the fibrin meshwork. These consumed factors are **I (Fibrinogen), II (Prothrombin), V (Labile factor), VIII (Anti-hemophilic factor), and XIII (Fibrin stabilizing factor).** Since Factor V is "labile" and utilized during the conversion of prothrombin to thrombin, it is absent in serum. **Analysis of Incorrect Options:** * **A. Plasma Thromboplastin (Factor XI):** This factor is not consumed during the clotting process and remains present in the serum. * **C. Hageman Factor (Factor XII):** This factor initiates the intrinsic pathway but is not consumed; it remains in the serum. * **D. Christmas Factor (Factor IX):** Like Factor XI and XII, Factor IX is a stable factor that is not consumed during clot formation and is therefore found in serum. **High-Yield Facts for NEET-PG:** * **Formula:** Serum = Plasma – (Fibrinogen + Factors II, V, VIII, XIII). * **Factors present in Serum:** VII, IX, X, XI, and XII (Stable factors). * **Prothrombin Time (PT)** measures Factors I, II, V, VII, and X. * **Clinical Pearl:** If a patient has a bleeding disorder, we test plasma, not serum, because serum lacks the essential clotting proteins required for diagnostic assays.

Practice by Chapter

Composition and Functions of Blood

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Erythrocytes and Hemoglobin

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Leukocytes and Immune Function

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Platelets and Hemostasis

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Blood Groups and Transfusion

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Coagulation and Fibrinolysis

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Hematopoiesis

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Innate Immunity

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Adaptive Immunity

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Immunological Memory and Tolerance

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