Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 311: Which of the following is NOT a peripheral lymphoid organ?

A. Lymph nodes
B. Spleen
C. Mucosa-associated lymphoid tissue
D. Thymus (Correct Answer)

Explanation: ### Explanation Lymphoid organs are categorized into two types based on their function in lymphocyte development: **Primary (Central)** and **Secondary (Peripheral)** lymphoid organs. **1. Why Thymus is the Correct Answer:** The **Thymus** and **Bone Marrow** are **Primary Lymphoid Organs**. These are the sites where lymphocytes are produced (lymphopoiesis) and undergo antigen-independent maturation. In the thymus, T-cell precursors from the bone marrow differentiate into mature, immunocompetent T-lymphocytes. Since the question asks for the organ that is *NOT* peripheral, the Thymus is the correct choice. **2. Analysis of Incorrect Options (Peripheral Organs):** Peripheral lymphoid organs are sites where mature lymphocytes reside and where **adaptive immune responses** are initiated upon encountering antigens. * **A. Lymph nodes:** Filter lymph and are the primary site for B and T cell activation against tissue-borne antigens. * **B. Spleen:** Acts as a blood filter; it is the major site for immune responses against blood-borne pathogens. * **C. Mucosa-associated lymphoid tissue (MALT):** Includes Peyer’s patches, tonsils, and appendix. These protect mucosal surfaces (GI, respiratory, and urogenital tracts). **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Hassall’s Corpuscles:** Characteristic histological feature of the Thymic medulla. * **DiGeorge Syndrome:** Congenital failure of the 3rd and 4th pharyngeal pouches to develop, leading to thymic aplasia and T-cell deficiency. * **Thymic Involution:** The thymus is largest at puberty and undergoes "age-associated involution," where lymphoid tissue is replaced by fat. * **B-cell Maturation:** While T-cells mature in the Thymus, B-cells mature in the **Bone Marrow** (in mammals) or the **Bursa of Fabricius** (in birds).

Question 312: What is the normal range for mean corpuscular hemoglobin (MCH)?

A. 5-8 pg
B. 15-18 pg
C. 28-32 pg (Correct Answer)
D. 32-38 pg

Explanation: **Explanation:** **Mean Corpuscular Hemoglobin (MCH)** represents the average amount (mass) of hemoglobin present in a single red blood cell. It is calculated by dividing the total hemoglobin by the total number of red blood cells: * **Formula:** MCH = (Hemoglobin in g/dL × 10) / RBC count in millions/µL. * **Normal Range:** The standard physiological range is **27–32 picograms (pg)** per cell. Option C (28–32 pg) is the closest and most accurate representation of this clinical value. **Analysis of Incorrect Options:** * **Option A (5-8 pg) & B (15-18 pg):** These values are pathologically low. Such levels are not seen even in severe microcytic anemias and would be incompatible with effective oxygen transport. * **Option D (32-38 pg):** This range overlaps with **MCHC** (Mean Corpuscular Hemoglobin Concentration), which is measured in g/dL or percentage. While MCH can be slightly elevated in macrocytic anemias (like Vitamin B12 deficiency), 32–38 pg is generally considered above the normal reference interval for a healthy individual. **NEET-PG High-Yield Pearls:** 1. **MCH vs. MCHC:** MCH measures the *weight* of Hb per cell (pg), while MCHC measures the *concentration* of Hb in a given volume of packed red cells (g/dL). 2. **Clinical Correlation:** MCH is decreased in **hypochromic anemias** (e.g., Iron Deficiency Anemia, Thalassemia) and increased in **macrocytic anemias** (e.g., Megaloblastic Anemia) because larger cells can hold more hemoglobin. 3. **MCHC Significance:** MCHC is the most specific indicator of true hypochromia. It is uniquely elevated in **Hereditary Spherocytosis** due to membrane loss and cellular dehydration.

Question 313: Which is the most mature normoblast?

A. Oxyphilic normoblast (Correct Answer)
B. Pronormoblast
C. Polychromatic normoblast
D. Basophilic normoblast

Explanation: **Explanation:** The process of erythropoiesis involves the maturation of a hematopoietic stem cell into a mature erythrocyte. As a normoblast matures, it undergoes specific morphological changes: the cell size decreases, the nucleus condenses (pyknosis) and is eventually extruded, and the cytoplasm shifts from basophilic (high RNA) to eosinophilic (high hemoglobin). **Why Oxyphilic Normoblast is correct:** The **Oxyphilic normoblast** (also known as the Late Normoblast or Orthochromatic Normoblast) is the final stage of the nucleated red cell series. At this stage, the cytoplasm has attained its full complement of hemoglobin, giving it a pinkish/acidophilic (oxyphilic) appearance. The nucleus is small, dense, and pyknotic, prepared for extrusion to become a reticulocyte. **Analysis of Incorrect Options:** * **B. Pronormoblast:** This is the **earliest** recognizable erythrocyte precursor. It is a large cell with a large nucleus and visible nucleoli. * **D. Basophilic Normoblast:** The second stage. It is characterized by intense cytoplasmic basophilia due to a high concentration of ribosomes for protein synthesis. * **C. Polychromatic Normoblast:** The intermediate stage where hemoglobin starts appearing. The "muddy" or greyish color is due to the mixture of pink hemoglobin and blue RNA. **NEET-PG High-Yield Pearls:** 1. **Nucleus Extrusion:** Occurs at the transition from the Oxyphilic normoblast to the Reticulocyte. 2. **First Hemoglobin Appearance:** Hemoglobin synthesis begins in the **Basophilic normoblast**, but it first becomes visible light-microscopically in the **Polychromatic normoblast**. 3. **Last stage of Mitosis:** The Polychromatic normoblast is the last stage capable of cell division. 4. **Reticulocyte:** The immediate precursor to the mature RBC; it contains residual RNA (ribosomes) which can be stained with supra-vital stains like New Methylene Blue.

Question 314: Allergic asthma and rhinitis are related to which chemokine receptor?

A. CCR1
B. CCR2
C. CCR3 (Correct Answer)
D. CCR5

Explanation: **Explanation:** The correct answer is **CCR3**. **Why CCR3 is correct:** Chemokine receptors are G-protein-coupled receptors that guide the migration of leukocytes. **CCR3** is highly and selectively expressed on **eosinophils**, basophils, and Th2 cells. It is the primary receptor for **eotaxin** (CCL11), a potent chemoattractant. In allergic conditions like asthma and rhinitis, Th2 cytokines (IL-4, IL-5) trigger the recruitment of eosinophils to the airway mucosa via the CCR3-eotaxin axis. This leads to eosinophilic inflammation, airway hyperresponsiveness, and mucosal edema, which are hallmarks of these diseases. **Why other options are incorrect:** * **CCR1:** Primarily expressed on monocytes and memory T cells. It binds to ligands like CCL3 (MIP-1α) and is involved in chronic inflammatory diseases like rheumatoid arthritis, but it is not the dominant receptor for allergic eosinophilia. * **CCR2:** This is the major receptor for **MCP-1** (Monocyte Chemoattractant Protein-1). It is essential for the recruitment of **monocytes** to sites of inflammation and is linked to atherosclerosis and insulin resistance. * **CCR5:** Expressed on T cells, macrophages, and dendritic cells. It is clinically significant as the **major co-receptor for M-tropic strains of HIV-1** (entry point into the cell). **High-Yield Pearls for NEET-PG:** * **CCR3:** Target for eosinophil recruitment (Asthma/Allergy). * **CCR5 & CXCR4:** Essential co-receptors for HIV entry. * **CXCR3:** Associated with Th1 responses and found on activated T cells. * **Eotaxin (CCL11):** The specific ligand for CCR3; its levels correlate with the severity of asthma.

Question 315: What is the main reason for the lower hemoglobin level in females compared to males?

A. Shorter erythrocyte half-life time
B. Decreased responsiveness of bone marrow stem cells to erythropoietin
C. Smaller number of bone marrow stem cells
D. Low testosterone levels in females (Correct Answer)

Explanation: **Explanation:** The primary reason for the physiological difference in hemoglobin (Hb) levels between males and females is the influence of sex hormones on erythropoiesis. **1. Why Option D is Correct:** Testosterone, which is significantly higher in males, acts as a potent stimulator of erythropoiesis through two main mechanisms: * **Direct Stimulation:** It acts directly on the bone marrow to increase the proliferation of erythroid progenitor cells. * **Indirect Stimulation:** It stimulates the kidneys to produce more **Erythropoietin (EPO)**. In contrast, females have low testosterone levels. Furthermore, **estrogen** in females has a mild inhibitory effect on erythropoiesis and can suppress the production of EPO, leading to a lower baseline Hb (approx. 12–14 g/dL in females vs. 14–16 g/dL in males). **2. Why Other Options are Incorrect:** * **Option A:** The average lifespan of an erythrocyte is approximately 120 days in both genders. There is no physiological evidence that female RBCs have a shorter half-life. * **Option B:** Bone marrow responsiveness to EPO is generally consistent across genders. The difference lies in the *quantity* of EPO produced and the hormonal "boost" provided by androgens, not the sensitivity of the stem cells. * **Option C:** The total pool of hematopoietic stem cells is not inherently smaller in females; the rate of their differentiation into the erythroid lineage is what differs due to hormonal signaling. **Clinical Pearls for NEET-PG:** * **Androgens and Anemia:** Because testosterone stimulates RBC production, synthetic androgens (like Danazol) were historically used to treat certain types of refractory anemia. * **Menstruation:** While monthly blood loss contributes to lower iron stores in females, the primary *physiological* baseline difference is hormonal. * **High-Yield Fact:** Hemoglobin levels are highest at birth (Newborn: 17–20 g/dL) due to high levels of Erythropoietin in utero (hypoxic environment).

Question 316: Leukotrienes are secreted by all of the following cells except?

A. Macrophages
B. T4 cells
C. T8 cells
D. Platelets (Correct Answer)

Explanation: **Explanation** Leukotrienes (LTs) are potent inflammatory mediators derived from arachidonic acid via the **5-lipoxygenase (5-LOX) pathway**. The synthesis of leukotrienes is primarily restricted to specific inflammatory cells that express the 5-LOX enzyme. **Why Platelets is the Correct Answer:** Platelets lack the enzyme **5-lipoxygenase** and therefore cannot synthesize leukotrienes independently. Instead, platelets possess the enzyme **12-lipoxygenase**, which produces 12-HETE. While platelets can participate in "transcellular biosynthesis" (taking up LTA4 from neutrophils to produce Lipoxins), they do not secrete leukotrienes themselves. **Analysis of Other Options:** * **Macrophages:** These are major sources of LTB4 and LTC4, which play critical roles in chemotaxis and vascular permeability during chronic inflammation. * **T4 (Helper) and T8 (Cytotoxic) Cells:** Lymphocytes, including both CD4+ and CD8+ subsets, express the 5-LOX pathway and secrete leukotrienes to modulate immune responses and leukocyte trafficking. **High-Yield Clinical Pearls for NEET-PG:** * **LTA4:** The precursor for all other leukotrienes. * **LTB4:** A potent **chemotactic agent** for neutrophils ("B for Bacteria/Binding"). * **LTC4, LTD4, LTE4:** Known as the **Slow-Reacting Substance of Anaphylaxis (SRS-A)**; they cause intense bronchoconstriction and are central to the pathogenesis of asthma. * **Zileuton:** A 5-LOX inhibitor used in asthma. * **Montelukast/Zafirlukast:** Cysteinyl leukotriene receptor (CysLT1) antagonists.

Question 317: Albumin is an important factor in maintaining osmotic pressure. Which of the following best describes albumin's characteristics relevant to this function?

A. Low molecular weight and high blood concentration (Correct Answer)
B. Low molecular weight and low blood concentration
C. High molecular weight and low blood concentration
D. High molecular weight and high blood concentration

Explanation: **Explanation:** The primary determinant of **Colloid Osmotic Pressure (Oncotic Pressure)** in the plasma is the number of particles present per unit volume, rather than the size of the particles. This is governed by **Van’t Hoff’s Law**. **Why Option A is Correct:** Albumin accounts for approximately **75–80% of the total plasma oncotic pressure** (approx. 25–28 mmHg). This dominance is due to two factors: 1. **High Concentration:** It is the most abundant plasma protein (3.5–5.0 g/dL). 2. **Low Molecular Weight:** Among the major plasma proteins (Albumin ≈ 69 kDa vs. Globulins ≈ 90–150 kDa vs. Fibrinogen ≈ 340 kDa), albumin is the smallest. Because it is small, a given mass of albumin contains a **higher number of individual molecules** compared to an equal mass of larger proteins, thereby exerting greater osmotic pull. **Analysis of Incorrect Options:** * **B & C:** Low blood concentration would result in decreased oncotic pressure, leading to edema (as seen in nephrotic syndrome or liver failure). * **D:** While albumin has a "high" weight compared to electrolytes, in the context of plasma proteins, it is considered the **lowest** molecular weight fraction. If it had a high molecular weight, there would be fewer molecules per gram, reducing its osmotic efficiency. **NEET-PG High-Yield Pearls:** * **Donnan Effect:** Albumin is negatively charged at physiological pH. It attracts cations (like $Na^+$), which further increases the osmotic pressure by ~50% more than the protein alone would account for. * **Synthesis:** Exclusively in the **liver**. * **Clinical Correlation:** Hypoalbuminemia leads to a drop in oncotic pressure, causing fluid to move from the intravascular to the interstitial space (**Edema/Ascites**). * **Half-life:** Approximately **20 days**.

Question 318: Which of the following procoagulants is not normally circulating in the plasma?

A. Prothrombin
B. Fibrinogen
C. Antithrombophilic factor (Factor VIII)
D. None of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **None of the above** because all the listed factors (Prothrombin, Fibrinogen, and Factor VIII) are normal constituents of the plasma, circulating in their inactive forms (zymogens) or as cofactor proteins. **1. Underlying Medical Concept** The coagulation cascade consists of a series of plasma proteins (clotting factors) that circulate in the blood in an **inactive state** to prevent spontaneous thrombosis. They are only activated at the site of vascular injury. Since all the options listed are standard clotting factors synthesized by the liver (or endothelial cells in the case of Factor VIII), they are all normally found in circulation. **2. Analysis of Options** * **A. Prothrombin (Factor II):** This is a vitamin K-dependent alpha-globulin synthesized by the liver. It is a constant component of plasma that is converted to thrombin during the common pathway. * **B. Fibrinogen (Factor I):** This is the most abundant coagulation factor in the plasma. It is a soluble protein that is converted into insoluble fibrin threads by the action of thrombin. * **C. Antithrombophilic factor (Factor VIII):** This factor circulates in the plasma bound to von Willebrand factor (vWF). It acts as a crucial cofactor in the intrinsic pathway (specifically the "tenase" complex). **3. High-Yield Facts for NEET-PG** * **The "Exception" Rule:** The only clotting factor that is **not** normally circulating in the plasma is **Tissue Factor (Factor III)**. It is an integral membrane protein found in subendothelial cells and is only exposed to the blood following vascular injury to initiate the extrinsic pathway. * **Site of Synthesis:** All clotting factors are produced in the liver except **Factor VIII** (produced by endothelial cells) and **vWF** (produced by endothelial cells and megakaryocytes). * **Calcium (Factor IV):** It is the only inorganic ion in the coagulation cascade. * **Vitamin K-dependent factors:** II, VII, IX, and X (and proteins C and S).

Question 319: Which of the following is an inhibitor of platelet aggregation?

A. TXA2
B. PGI2 (Correct Answer)
C. PGG2
D. All of the above

Explanation: ### Explanation The balance between platelet aggregation and inhibition is crucial for maintaining vascular homeostasis. The correct answer is **PGI2 (Prostacyclin)**. **1. Why PGI2 is correct:** Prostacyclin (PGI2) is synthesized by vascular **endothelial cells**. It acts as a potent **vasodilator** and a strong **inhibitor of platelet aggregation**. It functions by increasing intracellular cyclic AMP (cAMP) levels within platelets, which stabilizes them and prevents the release of clotting factors. In a healthy vessel, PGI2 ensures that the blood remains fluid and does not clot against the vessel wall. **2. Why the other options are incorrect:** * **TXA2 (Thromboxane A2):** Produced by platelets via the COX-1 pathway, TXA2 is a potent **platelet aggregator** and vasoconstrictor. It is the functional antagonist to PGI2. * **PGG2 (Prostaglandin G2):** This is a transient intermediate in the arachidonic acid cascade. It is a precursor to both TXA2 and PGI2 but does not function as an inhibitor of aggregation itself; rather, it is converted into active prostanoids. **3. NEET-PG High-Yield Pearls:** * **The "PGI2 vs. TXA2" Balance:** Hemostasis depends on the ratio of these two. Aspirin (low dose) irreversibly inhibits COX-1 in platelets, reducing TXA2 levels. Since platelets lack a nucleus, they cannot regenerate COX-1, leading to an anti-thrombotic effect. * **Source Distinction:** Remember: **E**ndothelium produces **E**nhanced flow (PGI2), while **P**latelets produce **P**lug formation (TXA2). * **cAMP vs. Calcium:** Increased cAMP (by PGI2) inhibits aggregation, whereas increased cytosolic Calcium (triggered by TXA2) promotes aggregation.

Question 320: Which antigen is absent in Bombay blood group?

A. Hb (Correct Answer)
B. Ac
C. B
D. D

Explanation: **Explanation:** The **Bombay Blood Group (Oh phenotype)** is a rare blood phenotype characterized by the absence of the **H antigen**. **1. Why Option A is Correct:** In the ABO blood group system, the H antigen is the precursor molecule upon which A and B antigens are built. The H antigen is produced by the action of the *H gene* (FUT1), which adds L-fucose to a precursor substance. Individuals with the Bombay phenotype are homozygous recessive (**hh**); they lack the H gene and therefore cannot produce the H antigen. Since the H antigen is the necessary substrate for A and B transferases, these individuals also lack A and B antigens on their red cells, even if they possess the A or B genes. **2. Analysis of Incorrect Options:** * **Option B (A) & Option C (B):** While it is true that A and B antigens are absent in the Bombay group, the fundamental defect is the absence of the **H antigen**. In many versions of this question, "H" is the intended answer (noted here as Hb/H). * **Option D (D):** The D antigen refers to the **Rh system**. The Bombay phenotype is independent of the Rh system; a Bombay individual can be Rh-positive or Rh-negative. **Clinical Pearls for NEET-PG:** * **Discovery:** First described by Dr. Y.M. Bhende in Mumbai (1952). * **Serology:** They test as "O" group in forward grouping but their serum contains **anti-A, anti-B, and potent anti-H antibodies**. * **Transfusion:** They can only receive blood from another Bombay phenotype individual because the anti-H in their plasma will cause a fatal hemolytic reaction if they receive regular O-group blood (which has the most H antigen). * **Genetics:** It is an example of **Recessive Epistasis**.

Practice by Chapter

Composition and Functions of Blood

Practice Questions

Erythrocytes and Hemoglobin

Practice Questions

Leukocytes and Immune Function

Practice Questions

Platelets and Hemostasis

Practice Questions

Blood Groups and Transfusion

Practice Questions

Coagulation and Fibrinolysis

Practice Questions

Hematopoiesis

Practice Questions

Innate Immunity

Practice Questions

Adaptive Immunity

Practice Questions

Immunological Memory and Tolerance

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free