Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 201: Coagulation time of blood is prolonged in which of the following conditions?

A. Hemophilia (Correct Answer)
B. Leukemia
C. Pernicious anaemia
D. Malignant neutropenia

Explanation: **Explanation:** **1. Why Hemophilia is Correct:** Coagulation Time (CT) measures the time required for blood to clot via the **intrinsic and common pathways**. Hemophilia (specifically Hemophilia A and B) is caused by a deficiency of clotting factors VIII and IX, respectively. These factors are critical components of the intrinsic pathway. In their absence, the formation of fibrin is significantly delayed, leading to a **prolonged Coagulation Time**. Notably, the Bleeding Time (BT) in Hemophilia remains normal because platelet function and primary hemostasis are unaffected. **2. Why the Other Options are Incorrect:** * **Leukemia:** This is a malignancy of white blood cells. While advanced leukemia can cause thrombocytopenia (low platelets) leading to a prolonged *Bleeding Time*, it does not typically affect the clotting factor cascade directly; therefore, CT remains normal. * **Pernicious Anemia:** This is caused by Vitamin B12 deficiency due to a lack of intrinsic factor. It primarily affects erythropoiesis (causing megaloblastic anemia) and does not involve the coagulation cascade. * **Malignant Neutropenia (Agranulocytosis):** This is a severe reduction in neutrophil count, making the patient highly susceptible to infections. It has no physiological impact on the blood's ability to clot. **Clinical Pearls for NEET-PG:** * **Bleeding Time (BT):** Reflects platelet function and vascular integrity. Prolonged in Thrombocytopenia and von Willebrand Disease. * **Coagulation Time (CT):** Reflects the intrinsic pathway. Prolonged in Hemophilia and during Heparin therapy. * **Prothrombin Time (PT):** Reflects the extrinsic pathway (Factor VII). Prolonged in Vitamin K deficiency and Warfarin therapy. * **Vitamin K Deficiency:** Prolongs both PT and CT because it affects factors II, VII, IX, and X.

Question 202: What is the other name for Factor X?

A. Stuart-Prower factor (Correct Answer)
B. Calcium ion
C. Plasma thromboplastin component (PTC)
D. Plasma thromboplastin antecedent (PTA)

Explanation: **Explanation:** **Factor X (Stuart-Prower Factor)** is a crucial vitamin K-dependent serine protease in the coagulation cascade. It represents the starting point of the **Common Pathway**, where both the intrinsic and extrinsic pathways converge. It was named after the two patients (Mr. Stuart and Ms. Prower) in whom the deficiency was first described. Once activated to Factor Xa (by the tenase complex), it combines with Factor Va, calcium, and phospholipids to form the **prothrombinase complex**, which converts prothrombin (II) to thrombin (IIa). **Analysis of Incorrect Options:** * **Option B: Calcium Ion** is **Factor IV**. It is essential for almost all steps of the coagulation cascade (except the initial steps of the intrinsic pathway). * **Option C: Plasma Thromboplastin Component (PTC)** is **Factor IX** (also known as Christmas Factor). Its deficiency leads to Hemophilia B. * **Option D: Plasma Thromboplastin Antecedent (PTA)** is **Factor XI**. Its deficiency leads to Hemophilia C (Rosenthal syndrome). **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin K-dependent factors:** II, VII, IX, and X (and Proteins C and S). * **Shortest half-life:** Factor VII (often the first to decrease in liver disease or Warfarin therapy). * **Longest half-life:** Factor II (Prothrombin). * **Direct Factor Xa Inhibitors:** Drugs like **Rivaroxaban and Apixaban** act directly on Factor Xa, bypassing the need for antithrombin III monitoring. * **Lab Monitoring:** Factor X is part of the common pathway; therefore, its deficiency or inhibition prolongs both **PT (Prothrombin Time)** and **aPTT (activated Partial Thromboplastin Time)**.

Question 203: Which of the following cells increases in case of parasitic infection?

A. Neutrophils
B. Basophils
C. Eosinophils (Correct Answer)
D. Monocytes

Explanation: ### Explanation **Correct Answer: C. Eosinophils** **Mechanism and Concept:** Eosinophils are specialized granulocytes primarily responsible for combating multicellular parasites, such as helminths (worms). When a parasitic infection occurs, eosinophils undergo **degranulation**, releasing highly potent cytotoxic proteins stored in their large acidophilic granules. The most significant of these is **Major Basic Protein (MBP)**, which is directly toxic to the parasite's tegument (outer coating). They also release Eosinophil Cationic Protein (ECP) and peroxidase to destroy the pathogen. **Analysis of Incorrect Options:** * **A. Neutrophils:** These are the "first responders" and the primary cell type in **acute bacterial infections** and pyogenic inflammation. They utilize phagocytosis and respiratory burst to kill bacteria. * **B. Basophils:** These cells are primarily involved in **allergic reactions** and type I hypersensitivity. They contain histamine and heparin; while they share a common lineage with eosinophils, they are not the primary responders to parasites. * **D. Monocytes:** These are mononuclear cells that migrate into tissues to become **macrophages**. They are typically elevated in **chronic infections** (e.g., Tuberculosis) and are responsible for long-term phagocytosis and antigen presentation. **NEET-PG High-Yield Pearls:** * **Eosinophilia Definition:** Absolute Eosinophil Count (AEC) > 500 cells/µL. * **Common Causes (Mnemonic: NAAACP):** **N**eoplasia, **A**llergy (Asthma/Hay fever), **A**ddison’s disease, **A**theroembolism, **C**onnective tissue disorders, **P**arasites. * **Charcot-Leyden Crystals:** These are microscopic crystals found in the sputum of asthmatics or stool of parasite patients, formed from the breakdown of eosinophil membranes (specifically Galectin-10). * **IL-5:** This is the primary cytokine responsible for the production, activation, and chemotaxis of eosinophils.

Question 204: Which factor prevents apoptosis of Memory B cells?

A. Platelet derived Growth Factor
B. Nerve Growth Factor (Correct Answer)
C. Fibroblast Growth Factor
D. IGF

Explanation: ### Explanation **Correct Answer: B. Nerve Growth Factor (NGF)** **Mechanism and Concept:** While Nerve Growth Factor (NGF) is traditionally associated with the survival and differentiation of neurons, it plays a critical role in the immune system. Memory B cells express high-affinity receptors for NGF (specifically **TrkA**). When NGF binds to these receptors, it triggers an anti-apoptotic signaling pathway (upregulating **Bcl-2**), which prevents programmed cell death. This mechanism is essential for the long-term persistence of memory B cells in the body, ensuring a rapid secondary immune response upon re-exposure to an antigen. **Analysis of Incorrect Options:** * **A. Platelet-Derived Growth Factor (PDGF):** Primarily involved in wound healing, angiogenesis, and the proliferation of connective tissue cells (fibroblasts and smooth muscle cells). It does not have a specific role in B cell survival. * **C. Fibroblast Growth Factor (FGF):** Involved in embryonic development, tissue repair, and tumor growth. While it affects various cell types, it is not the primary factor regulating memory B cell apoptosis. * **D. Insulin-like Growth Factor (IGF):** Primarily mediates the effects of Growth Hormone and promotes systemic cell growth and proliferation, but it is not the specific factor identified for preventing memory B cell apoptosis in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Neuro-Immunology:** The interaction between NGF and B cells is a classic example of the "crosstalk" between the nervous and immune systems. * **Bcl-2 Connection:** Memory B cells survive for years because they express high levels of the anti-apoptotic protein **Bcl-2**, which is maintained by NGF. * **CD27:** Remember that **CD27** is the classic surface marker used to identify Memory B cells in humans. * **Site of Origin:** Memory B cells are primarily generated in the **Germinal Centers** of secondary lymphoid organs following T-cell dependent activation.

Question 205: Affinity for O2 in the blood depends on?

A. 2,3-diphosphoglycerate (Correct Answer)
B. 3-phosphoglycerate
C. ATP
D. cAMP

Explanation: **Explanation:** The affinity of hemoglobin for oxygen is primarily regulated by the **Oxygen-Dissociation Curve (ODC)**. The correct answer is **2,3-diphosphoglycerate (2,3-DPG)**, also known as 2,3-bisphosphoglycerate (2,3-BPG). **1. Why 2,3-DPG is correct:** 2,3-DPG is a byproduct of glycolysis in red blood cells (via the Rapoport-Luebering shunt). It binds to the beta chains of deoxyhemoglobin, stabilizing the **T-state (Tense state)**, which has a low affinity for oxygen. An increase in 2,3-DPG shifts the ODC to the **right**, promoting oxygen unloading to the tissues. Conversely, a decrease in 2,3-DPG shifts the curve to the **left**, increasing oxygen affinity. **2. Why other options are incorrect:** * **3-phosphoglycerate:** This is an intermediate in the standard Embden-Meyerhof glycolytic pathway but does not have a direct regulatory effect on hemoglobin affinity. * **ATP:** While ATP is the energy currency of the cell and present in RBCs, it is not the primary physiological regulator of the ODC. * **cAMP:** This is a secondary messenger involved in hormonal signaling and does not interact with hemoglobin to alter oxygen binding. **High-Yield Clinical Pearls for NEET-PG:** * **Right Shift (Decreased Affinity):** Remember **"CADET, face Right!"** — **C**O2 increase, **A**cidosis (H+), **D**PG increase, **E**xercise, and **T**emperature increase. * **Stored Blood:** Levels of 2,3-DPG decrease in stored blood. Transfusing old blood can lead to poor tissue oxygenation because the hemoglobin holds onto O2 too tightly (Left shift). * **Fetal Hemoglobin (HbF):** HbF has a higher affinity for O2 than adult hemoglobin (HbA) because it binds 2,3-DPG poorly due to the presence of gamma chains instead of beta chains.

Question 206: Which of the following is secreted by neutrophils?

A. Superoxide dismutase
B. Myeloperoxidase (Correct Answer)
C. Lysosomal enzyme
D. Catalase

Explanation: **Explanation:** **Neutrophils** are the primary effector cells of the innate immune system, specialized for the destruction of invading pathogens through phagocytosis and the respiratory burst. **Why Myeloperoxidase (MPO) is Correct:** Myeloperoxidase is a heme-containing enzyme stored in the **primary (azurophilic) granules** of neutrophils. During the respiratory burst, NADPH oxidase produces superoxide radicals, which are converted to hydrogen peroxide ($H_2O_2$). MPO then catalyzes the reaction between $H_2O_2$ and chloride ions ($Cl^-$) to produce **hypochlorous acid (HOCl)**—the active ingredient in household bleach and a potent bactericidal agent. This MPO-halide system is the most efficient bactericidal mechanism in neutrophils. **Analysis of Incorrect Options:** * **Superoxide dismutase (SOD) & Catalase:** These are **antioxidant enzymes** found within the cytoplasm of various cells. Their primary role is to neutralize reactive oxygen species (ROS) to protect the cell from oxidative damage, rather than being "secreted" for pathogen destruction. * **Lysosomal enzymes:** While neutrophils do contain lysosomes (acid hydrolases), the term is too broad. Myeloperoxidase is the specific, hallmark enzyme secreted during the degranulation process of the respiratory burst that defines neutrophil function. **High-Yield Clinical Pearls for NEET-PG:** * **MPO Deficiency:** The most common inherited neutrophil primary granule deficiency; patients are usually asymptomatic except for a predisposition to *Candida* infections. * **Markers:** MPO is a key histochemical marker used to differentiate **Acute Myeloid Leukemia (AML)** from Acute Lymphoblastic Leukemia (ALL). * **P-ANCA:** Perinuclear Anti-Neutrophil Cytoplasmic Antibodies (found in Microscopic Polyangiitis and Churg-Strauss) are specifically directed against myeloperoxidase.

Question 207: At what age do children typically acquire antibodies against ABO antigens?

A. At birth
B. 6 Months (Correct Answer)
C. 2 Years
D. 5 Years

Explanation: **Explanation:** The development of ABO antibodies (isoagglutinins) is a classic high-yield concept in hematology. Unlike most antibodies, ABO antibodies are not present at birth; they are "naturally occurring" but require environmental exposure to develop. **Why 6 Months is Correct:** At birth, a newborn’s serum lacks its own ABO antibodies. These antibodies (primarily IgM) begin to appear around **3 to 6 months of age**. They are produced in response to exposure to A-like and B-like polysaccharides found in common intestinal bacteria and food. Antibody titers continue to rise throughout childhood, reaching peak levels between 5 and 10 years of age. **Analysis of Incorrect Options:** * **A. At Birth:** Newborns do not produce their own ABO antibodies. Any ABO antibodies detected in a neonate are typically maternal IgG that crossed the placenta (relevant in ABO hemolytic disease of the newborn). * **C & D. 2 Years and 5 Years:** While antibody titers are higher at these ages, the *initial acquisition* occurs much earlier. By age 2, a child already has a well-established repertoire of isoagglutinins. **Clinical Pearls for NEET-PG:** * **Antibody Type:** ABO antibodies are predominantly **IgM** (which do not cross the placenta), whereas Rh antibodies are **IgG** (which do cross the placenta). * **Landsteiner’s Law:** States that if an agglutinogen (antigen) is present on RBCs, the corresponding agglutinin (antibody) must be absent; conversely, if an antigen is absent, the antibody must be present. This law applies to the ABO system but **not** the Rh system. * **Reverse Grouping:** Because infants lack these antibodies, "reverse grouping" (testing serum against known RBCs) is unreliable until the child is at least 4–6 months old.

Question 208: The blood in the vessels normally does not clot because of which of the following?

A. Vitamin K antagonists are present in plasma
B. Thrombin has a positive feedback on plasminogen
C. Sodium citrate in plasma chelates calcium ions
D. Vascular endothelium is smooth and coated with glycocalyx (Correct Answer)

Explanation: **Explanation:** The prevention of intravascular clotting (hemostasis) under normal physiological conditions is primarily due to the **thromboresistant properties of the vascular endothelium**. **Why Option D is Correct:** The vascular endothelium acts as a physical and chemical barrier. Its **smoothness** prevents the contact activation of Factor XII (Intrinsic pathway) and the adhesion of platelets. Furthermore, the endothelium is coated with the **glycocalyx**, a layer of mucopolysaccharides that are negatively charged. Since platelets are also negatively charged, the glycocalyx creates an electrostatic repulsion that prevents platelets from adhering to the vessel wall. Additionally, the endothelium secretes **Prostacyclin (PGI₂)** and **Nitric Oxide (NO)**, which inhibit platelet aggregation. **Why Other Options are Incorrect:** * **Option A:** Vitamin K antagonists (like Warfarin) are pharmacological agents used to treat clotting disorders; they are not naturally present in plasma to prevent normal clotting. * **Option B:** Thrombin actually converts fibrinogen to fibrin (clot formation). While it can activate Protein C (anticoagulant), it does not have a direct "positive feedback" on plasminogen to prevent initial clotting. * **Option C:** Sodium citrate is an *ex vivo* anticoagulant used in blood bags and labs. It is not found naturally in human plasma. **High-Yield Clinical Pearls for NEET-PG:** * **Thrombomodulin:** A protein on the endothelial surface that binds to thrombin, diverting it from a pro-coagulant to an anti-coagulant by activating **Protein C**. * **Antithrombin III:** A circulating plasma protein that inactivates thrombin and Factor Xa; its action is enhanced several thousand-fold by **Heparin**, which is produced by mast cells and basophils. * **Virchow’s Triad:** Endothelial injury, stasis of blood flow, and hypercoagulability are the three factors that lead to pathological thrombus formation.

Question 209: Colostrum is rich in which immunoglobulin?

A. IgA (Correct Answer)
B. IgE
C. IgG
D. IgM

Explanation: **Explanation:** **1. Why IgA is the Correct Answer:** Colostrum, the first milk produced by the mammary glands immediately after delivery, is exceptionally rich in **Secretory IgA (sIgA)**. This immunoglobulin is specifically designed to survive in mucosal environments. It provides **natural passive immunity** to the neonate by coating the gastrointestinal and respiratory tracts, preventing the attachment and penetration of pathogens (a process known as immune exclusion). This is crucial because a newborn’s own immune system is still immature. **2. Why Other Options are Incorrect:** * **IgE:** Primarily involved in Type I hypersensitivity reactions (allergies) and defense against helminthic parasitic infections. It is found in very low concentrations in serum and secretions. * **IgG:** This is the only immunoglobulin that **crosses the placenta** (via neonatal Fc receptors) to provide prenatal passive immunity. While present in breast milk in small amounts, it is not the predominant isotype in colostrum. * **IgM:** This is the first antibody produced during a primary immune response and is the largest (pentamer). It does not cross the placenta or occur in high concentrations in secretions like colostrum. **3. NEET-PG High-Yield Pearls:** * **IgA Structure:** In secretions, IgA exists as a **dimer** connected by a J-chain and a secretory component (which protects it from enzymatic digestion in the gut). * **Placental Transfer:** Remember: **"G crosses the Gradient"** (IgG crosses the placenta). * **Milk vs. Colostrum:** While both contain IgA, the concentration is highest in colostrum. * **Breastfeeding Benefit:** It reduces the incidence of infantile diarrhea and respiratory infections due to this passive transfer of sIgA.

Question 210: Eosinophils are activated by which of the following cytokines?

A. Interleukin-1 (IL1)
B. Interleukin-5 (IL5) (Correct Answer)
C. Interleukin-4 (IL4)
D. Interleukin-6 (IL6)

Explanation: ### Explanation **Correct Option: B. Interleukin-5 (IL5)** Interleukin-5 is the most specific and potent cytokine for eosinophil regulation. It is primarily produced by **Th2 cells** and mast cells. IL-5 acts as a selective growth factor that stimulates the production, differentiation, maturation, and activation of eosinophils in the bone marrow. It also promotes their recruitment into tissues and inhibits their apoptosis, leading to eosinophilia in conditions like parasitic infections and allergic asthma. **Analysis of Incorrect Options:** * **A. Interleukin-1 (IL1):** Produced mainly by macrophages, IL-1 is a pro-inflammatory cytokine responsible for inducing fever (endogenous pyrogen) and activating T-cells and neutrophils. * **C. Interleukin-4 (IL4):** While IL-4 is also produced by Th2 cells, its primary role is inducing B-cell class switching to **IgE**. Although IgE is involved in allergic responses alongside eosinophils, IL-4 does not directly activate eosinophils as specifically as IL-5. * **D. Interleukin-6 (IL6):** This is a multifunctional cytokine involved in the acute phase response, stimulating the liver to produce C-reactive protein (CRP) and promoting B-cell differentiation into plasma cells. **High-Yield Facts for NEET-PG:** * **Mnemonic:** Remember **"IL-5 drives Eosinophils to thrive."** * **Eosinophil Granules:** Contain Major Basic Protein (MBP) and Eosinophil Cationic Protein (ECP), which are toxic to helminths. * **Clinical Correlation:** **Mepolizumab** and **Reslizumab** are monoclonal antibodies against IL-5 used in the treatment of severe eosinophilic asthma. * **Charcot-Leyden Crystals:** These are microscopic crystals found in the sputum of asthmatics, formed from the breakdown of eosinophil membranes (Galectin-10).

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