Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 81: Which test is used to evaluate the extrinsic pathway of coagulation?

A. Prothrombin Time (PT) (Correct Answer)
B. Clotting Time (CT)
C. Activated Partial Thromboplastin Time (aPTT)
D. Bleeding Time (BT)

Explanation: **Explanation:** The coagulation cascade is divided into the intrinsic, extrinsic, and common pathways. The **Prothrombin Time (PT)** is the specific laboratory test used to evaluate the **Extrinsic Pathway** (Factor VII) and the **Common Pathway** (Factors X, V, II, and I). It measures the time taken for plasma to clot after the addition of Tissue Thromboplastin (Tissue Factor) and Calcium. **Analysis of Options:** * **A. Prothrombin Time (PT):** Correct. It assesses the extrinsic pathway. Clinically, it is used to monitor **Warfarin** therapy and assess liver synthetic function. * **B. Clotting Time (CT):** Incorrect. This is a non-specific bedside test (e.g., Lee-White method) that measures the overall time for blood to clot but lacks the sensitivity to isolate specific pathways. * **C. Activated Partial Thromboplastin Time (aPTT):** Incorrect. aPTT evaluates the **Intrinsic Pathway** (Factors XII, XI, IX, VIII) and the common pathway. It is used to monitor **Unfractionated Heparin** therapy. * **D. Bleeding Time (BT):** Incorrect. BT assesses **Primary Hemostasis**, specifically platelet function and vascular integrity, rather than the secondary hemostasis (clotting factors) evaluated by PT/aPTT. **High-Yield Clinical Pearls for NEET-PG:** * **INR (International Normalized Ratio):** A standardized version of PT used to monitor oral anticoagulants (Warfarin). * **Vitamin K Dependent Factors:** II, VII, IX, and X. Since Factor VII has the shortest half-life, PT is the first to be prolonged in Vitamin K deficiency or early liver disease. * **Mnemonic:** **P**e**T** (2 letters) = Extrinsic (shorter name); **aPTT** (4 letters) = Intrinsic (longer name).

Question 82: Which anticoagulant is produced by mast cells?

A. Antithrombin III
B. Protein C
C. Protein S
D. Heparin (Correct Answer)

Explanation: **Explanation:** **Heparin** is the correct answer because it is a naturally occurring anticoagulant synthesized and stored in the secretory granules of **mast cells** and **basophils**. Chemically, it is a highly sulfated glycosaminoglycan. Its primary physiological role is to prevent the formation of fibrin clots by binding to and significantly accelerating the activity of Antithrombin III, which inactivates Thrombin (Factor IIa) and Factor Xa. **Analysis of Incorrect Options:** * **Antithrombin III (A):** This is a plasma glycoprotein synthesized primarily in the **liver**. It is a natural inhibitor of coagulation, but it is not produced by mast cells. * **Protein C (B) and Protein S (C):** Both are Vitamin K-dependent glycoproteins synthesized in the **liver**. Protein C, when activated by the thrombin-thrombomodulin complex, degrades Factors Va and VIIIa. Protein S acts as a cofactor for Protein C. **Clinical Pearls for NEET-PG:** * **Mast Cell Locations:** Mast cells are abundant in tissues exposed to the external environment, particularly the **lungs, liver, and skin**, which explains why these tissues are rich sources of endogenous heparin. * **Antidote:** The anticoagulant effect of heparin can be rapidly neutralized by **Protamine Sulfate** (a positively charged molecule that binds to negatively charged heparin). * **Monitoring:** Unfractionated Heparin (UFH) therapy is monitored using **aPTT** (activated Partial Thromboplastin Time). * **Histology:** Mast cell granules show **metachromasia** (change color) when stained with Toluidine blue due to the high content of heparin.

Question 83: What effect does 2,3-DPG have on the binding of oxygen and hemoglobin?

A. Decrease binding of O2 and hemoglobin (Correct Answer)
B. Increased acidity in RBC
C. Decreased acidity in RBC
D. Lysis of RBC

Explanation: **Explanation:** The binding of oxygen to hemoglobin is regulated by several factors that shift the **Oxygen-Dissociation Curve (ODC)**. 2,3-Diphosphoglycerate (2,3-DPG), a byproduct of glycolysis in red blood cells, is a key physiological regulator. **Why Option A is correct:** 2,3-DPG binds specifically to the central cavity of the hemoglobin tetramer (specifically the beta chains) in its **T-state (Tense/Deoxygenated state)**. This binding stabilizes the T-state, reducing hemoglobin's affinity for oxygen. Consequently, oxygen is released more easily into the tissues. On the ODC, an increase in 2,3-DPG causes a **Right Shift**, indicating a decreased affinity and increased unloading of oxygen. **Why other options are incorrect:** * **Options B & C:** While pH (acidity) affects oxygen binding (the Bohr Effect), 2,3-DPG itself is a metabolite, not a primary regulator of intracellular pH. In fact, chronic hypoxia or high altitude increases 2,3-DPG levels to facilitate oxygen delivery, independent of direct pH changes. * **Option D:** 2,3-DPG is a normal metabolic intermediate of the Rapoport-Luebering shunt. It does not cause hemolysis or lysis of the RBC. **High-Yield Clinical Pearls for NEET-PG:** * **Right Shift (CADET, face Right!):** **C**O2 increase, **A**cidosis (H+), **D**PG (2,3-DPG) increase, **E**xercise, and **T**emperature increase. * **Fetal Hemoglobin (HbF):** HbF has a lower affinity for 2,3-DPG because its gamma chains lack the specific binding sites found in beta chains. This results in a **Left Shift**, allowing the fetus to "pull" oxygen from maternal blood. * **Stored Blood:** 2,3-DPG levels drop in stored blood, causing a Left Shift. This makes transfused blood less efficient at releasing oxygen immediately after transfusion.

Question 84: Haematocrit is the ratio of:

A. WBC to whole blood
B. Platelets to whole blood
C. RBCs to whole blood (Correct Answer)
D. Total blood cells to plasma

Explanation: **Explanation:** **Haematocrit (Hct)**, also known as **Packed Cell Volume (PCV)**, is defined as the proportion of the total blood volume that is occupied by Red Blood Cells (RBCs). When a blood sample is centrifuged, the heavier RBCs settle at the bottom, and the Hct is calculated as the height of the RBC column divided by the total height of the blood column. * **Why Option C is Correct:** RBCs constitute approximately 99% of the cellular elements in blood. Therefore, the volume of "packed cells" is clinically synonymous with the volume of RBCs. Normal values are roughly 40–50% for men and 36–44% for women. **Analysis of Incorrect Options:** * **Options A & B:** WBCs and Platelets form a very thin, white layer between the plasma and RBCs called the **"Buffy Coat"** (comprising <1% of blood volume). They are not included in the haematocrit calculation. * **Option D:** While haematocrit represents cells relative to whole blood, it specifically measures the volume of RBCs, not the ratio of all cells to plasma. **High-Yield Clinical Pearls for NEET-PG:** 1. **Wintrobe’s Tube:** The standard instrument used to determine PCV and ESR. 2. **Dehydration:** Causes a "relative" increase in Hct due to decreased plasma volume (Hemoconcentration). 3. **Anemia vs. Polycythemia:** Hct is the primary tool to screen for anemia (low Hct) and polycythemia (high Hct). 4. **Rule of Three:** In a healthy individual, **Haemoglobin (g/dL) × 3 ≈ Haematocrit (%)**. 5. **Body vs. Venous Hct:** The "Body Haematocrit" (average Hct in all vessels) is slightly lower (about 91%) than the "Venous Haematocrit" measured from a peripheral vein.

Question 85: Which of the following is NOT an action of platelet-activating factor?

A. Increased capillary permeability
B. Bronchodilation (Correct Answer)
C. Vasodilation
D. Erosion of gastric mucosa

Explanation: **Explanation:** Platelet-activating factor (PAF) is a potent phospholipid-derived mediator released from various cells, including platelets, endothelium, and inflammatory cells (neutrophils, eosinophils, and macrophages). It plays a central role in inflammation and anaphylaxis. **Why Bronchodilation is the Correct Answer:** PAF is a potent **bronchoconstrictor**, not a bronchodilator. In the lungs, it induces smooth muscle contraction and airway hyperreactivity, making it significantly more potent than histamine in triggering asthma-like symptoms. Therefore, Option B is the incorrect action. **Analysis of Incorrect Options:** * **A. Increased capillary permeability:** PAF causes endothelial cell contraction and gap formation, leading to protein leakage and edema. This is a hallmark of the inflammatory response. * **C. Vasodilation:** At low concentrations, PAF induces systemic vasodilation, which can lead to hypotension and shock during anaphylactic reactions. * **D. Erosion of gastric mucosa:** PAF is highly ulcerogenic. It reduces gastric blood flow and stimulates the release of other inflammatory mediators, leading to mucosal damage and ulcer formation. **High-Yield NEET-PG Pearls:** * **Potency:** PAF is 100 to 1,000 times more potent than histamine in causing bronchoconstriction and vasodilation. * **Source:** It is synthesized via the action of **Phospholipase A2** on membrane phospholipids. * **Platelet Effects:** As the name suggests, it causes platelet aggregation and the "release reaction" (degranulation of serotonin and ADP). * **Clinical Link:** PAF antagonists are a subject of research for treating septic shock and inflammatory disorders.

Question 86: T-cells mature in which of the following locations?

A. Bone marrow
B. Liver
C. Thymus (Correct Answer)
D. Lymph nodes

Explanation: **Explanation:** The maturation of T-lymphocytes is a critical process in adaptive immunity. While all lymphocytes originate from hematopoietic stem cells in the **bone marrow**, their site of maturation differs based on their type. **1. Why Thymus is correct:** Immature T-cell precursors (prothymocytes) migrate from the bone marrow to the **Thymus**. Here, they undergo "thymic education," which includes **positive selection** (ensuring they recognize self-MHC molecules) and **negative selection** (eliminating cells that react too strongly against self-antigens). This process ensures central tolerance and prevents autoimmunity. Once mature, they are released into the bloodstream as CD4+ or CD8+ T-cells. **2. Why other options are incorrect:** * **Bone marrow:** This is the site of production for all blood cells and the site of both origin and **maturation for B-cells**. * **Liver:** This is the primary site of hematopoiesis during the **fetal stage** (second trimester), but it is not a site for T-cell maturation. * **Lymph nodes:** These are **secondary lymphoid organs** where mature T-cells encounter antigens and undergo activation and proliferation, not initial maturation. **High-Yield Clinical Pearls for NEET-PG:** * **DiGeorge Syndrome:** Congenital thymic aplasia leading to profound T-cell deficiency and recurrent viral/fungal infections. * **Hassall’s Corpuscles:** Characteristic epithelial structures found in the thymic medulla. * **Involution:** The thymus is most active in childhood and undergoes fatty replacement (involution) after puberty, though T-cell production continues at a lower rate. * **Mnemonic:** **B**-cells mature in **B**one marrow; **T**-cells mature in **T**hymus.

Question 87: What is the primary function of hemoglobin regarding oxygen transport?

A. To increase oxygen delivery in the lungs and uptake at tissues.
B. To increase oxygen uptake in the lungs and delivery at tissues. (Correct Answer)
C. To increase carbon dioxide delivery at tissues and uptake in the lungs.
D. None of the above.

Explanation: **Explanation:** The primary function of hemoglobin (Hb) is to act as a specialized transport protein that significantly increases the oxygen-carrying capacity of blood. **1. Why Option B is Correct:** In the **lungs** (high $PO_2$), hemoglobin exhibits high affinity for oxygen, allowing it to bind rapidly to oxygen molecules—a process known as **uptake**. Once the blood reaches the **peripheral tissues** (low $PO_2$), the affinity of hemoglobin for oxygen decreases, facilitating the release or **delivery** of oxygen to the cells for aerobic metabolism. Without hemoglobin, the amount of oxygen dissolved in plasma would be insufficient to meet the metabolic demands of the body. **2. Why Other Options are Incorrect:** * **Option A:** This is logically reversed. Oxygen is "taken up" in the lungs and "delivered" to the tissues, not vice versa. * **Option C:** This describes the transport of carbon dioxide, but the direction is incorrect. $CO_2$ is taken up at the tissues (as a metabolic byproduct) and delivered to the lungs for excretion. While hemoglobin does transport some $CO_2$ (as carbaminohemoglobin), its *primary* role in this context is oxygen transport. **3. NEET-PG High-Yield Pearls:** * **Oxygen-Dissociation Curve (ODC):** Hemoglobin follows a **sigmoid-shaped** curve due to "cooperative binding." * **P50 Value:** The $PO_2$ at which hemoglobin is 50% saturated is approximately **26.6 mmHg**. * **Bohr Effect:** An increase in $CO_2$ and $H^+$ (acidity) at the tissue level shifts the ODC to the **right**, decreasing Hb affinity and enhancing oxygen delivery. * **Capacity:** 1 gram of pure Hb can carry approximately **1.34 ml** of oxygen.

Question 88: Bicarbonate moves out of RBC in peripheral tissues in exchange for which ion?

A. Na+
B. H2PO4-
C. Cl- (Correct Answer)
D. SO42-

Explanation: ### Explanation The correct answer is **C. Cl-**. This phenomenon is known as the **Chloride Shift** or the **Hamburger Phenomenon**. #### 1. Why Cl- is Correct In peripheral tissues, CO₂ diffuses into the RBC and reacts with water (catalyzed by **Carbonic Anhydrase**) to form H₂CO₃, which dissociates into **H+** and **HCO₃⁻**. * To prevent the buildup of reaction products and maintain the concentration gradient, HCO₃⁻ must leave the cell. * As HCO₃⁻ (an anion) moves out, the cell becomes electropositive. To maintain **electroneutrality**, **Chloride (Cl⁻)** ions move from the plasma into the RBC. * This exchange is mediated by the **Anion Exchanger 1 (AE1)**, also known as **Band 3 protein**. #### 2. Why Other Options are Incorrect * **A. Na+:** Sodium is the primary extracellular cation. While it helps maintain osmotic balance, it is not directly exchanged for bicarbonate via the Band 3 protein during the chloride shift. * **B. H2PO4- & D. SO42-:** While these are anions, their concentrations in the plasma are too low, and the RBC membrane lacks specific high-velocity transport channels for them to play a significant role in the rapid exchange required for systemic gas transport. #### 3. Clinical Pearls & High-Yield Facts * **Reverse Chloride Shift:** Occurs in the **lungs**. HCO₃⁻ moves *into* the RBC and Cl⁻ moves *out* so that CO₂ can be regenerated and exhaled. * **Water Follows Cl-:** When Cl⁻ enters the RBC in peripheral tissues, water follows osmotically. Consequently, **venous RBCs are slightly larger (higher MCV)** than arterial RBCs. * **Haldane Effect:** The unloading of O₂ from hemoglobin (forming deoxyhemoglobin) increases hemoglobin's ability to carry CO₂ and buffer H+, facilitating the Chloride Shift. * **Key Protein:** Remember **Band 3 protein**; it is a common target for NEET-PG questions regarding RBC membrane physiology.

Question 89: ABO antigens are not present in which of the following?

A. Saliva
B. Cerebrospinal fluid (CSF) (Correct Answer)
C. Blood
D. Tear

Explanation: **Explanation:** The ABO blood group system is based on the presence of specific carbohydrate antigens (A and B) on the surface of red blood cells. However, these antigens are not restricted to erythrocytes; they are widely distributed throughout the body. **1. Why CSF is the correct answer:** ABO antigens are notably **absent in the Cerebrospinal Fluid (CSF)**. The blood-brain barrier (BBB) and the blood-CSF barrier are highly selective. Since ABO antigens are primarily found on cell membranes or as large glycoconjugates in secretions, they do not cross into the CSF. Furthermore, the central nervous system lacks the expression of these antigens on its parenchymal cells. **2. Analysis of incorrect options:** * **Blood (Option C):** This is the primary site. Antigens are found on RBCs, WBCs, and platelets. * **Saliva and Tears (Options A & D):** In approximately **80% of the population (known as "Secretors")**, ABO antigens are found in a water-soluble form in body fluids. This is governed by the **Se gene (FUT2)**. These secretors will have A, B, or H antigens in their saliva, tears, sweat, semen, and digestive juices. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Secretor Status:** Controlled by the *Se* gene on chromosome 19. If a person is a "secretor," their blood type can be determined using their saliva—a fact often used in forensic medicine. * **Distribution:** ABO antigens are also found on the surface of vascular endothelial cells and most epithelial cells (except in the CNS). * **Bombay Phenotype (hh):** These individuals lack the H antigen (the precursor for A and B). They will not have A or B antigens in their blood or secretions, even if they possess the A or B genes. * **Universal Rule:** If a question asks where ABO antigens are *absent*, the most common high-yield answers are **CSF and Hair** (except the hair root).

Question 90: Which of the following is NOT a function of the reticuloendothelial system?

A. Antibody production
B. Destruction of RBCs
C. Bilirubin metabolism (Correct Answer)
D. Phagocytosis

Explanation: The **Reticuloendothelial System (RES)**, now more commonly known as the **Mononuclear Phagocyte System (MPS)**, consists of phagocytic cells (monocytes and macrophages) located in reticular connective tissue, primarily in the spleen, liver (Kupffer cells), and lymph nodes. ### **Why "Bilirubin Metabolism" is the Correct Answer** While the RES is responsible for the **formation** of bilirubin (by breaking down hemoglobin from old RBCs), it does **not** perform bilirubin **metabolism** (conjugation). Bilirubin metabolism—specifically the conjugation of unconjugated bilirubin with glucuronic acid—is a metabolic function exclusive to the **hepatocytes** (parenchymal cells of the liver), not the phagocytic cells of the RES. ### **Explanation of Incorrect Options** * **A. Antibody production:** Macrophages in the RES act as Antigen-Presenting Cells (APCs). They process pathogens and present antigens to B-lymphocytes, which then differentiate into plasma cells to produce antibodies. * **B. Destruction of RBCs:** This is a primary function. The "graveyard of RBCs" (the spleen) is a major component of the RES, where macrophages sequester and destroy senescent (old) erythrocytes. * **C. Phagocytosis:** This is the hallmark functional characteristic of the RES. These cells ingest and destroy bacteria, viruses, and foreign particulate matter to clear the circulation. ### **High-Yield Clinical Pearls for NEET-PG** * **Components of RES:** Includes Kupffer cells (liver), Microglia (CNS), Alveolar macrophages (lungs), Mesangial cells (kidney), and Osteoclasts (bone). * **Heme Breakdown:** RES converts Heme → Biliverdin → **Unconjugated Bilirubin**. * **Key Distinction:** RES = Bilirubin *Production*; Hepatocytes = Bilirubin *Conjugation/Excretion*. * **Storage:** The RES also plays a role in iron metabolism by storing iron as ferritin or hemosiderin following RBC destruction.

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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