Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 111: Which factor initiates in vitro coagulation?

A. Factor XII (Correct Answer)
B. Factor XI
C. Factor X
D. Factor VII

Explanation: **Explanation:** The process of blood coagulation occurs via two primary pathways: the **Intrinsic Pathway** and the **Extrinsic Pathway**. **Why Factor XII is correct:** In an *in vitro* (laboratory/test tube) environment, coagulation is initiated when blood comes into contact with a "foreign" negatively charged surface, such as glass or kaolin. This process is known as the **Contact Activation Pathway**. **Factor XII (Hageman factor)** is the specific plasma protein that binds to these surfaces, undergoing a conformational change to become activated (Factor XIIa). This triggers the intrinsic cascade (XII → XI → IX → VIII → X). **Analysis of Incorrect Options:** * **Factor XI:** While part of the intrinsic pathway, it is activated by Factor XIIa, not by the glass surface itself. * **Factor X:** This is the start of the **Common Pathway**. It is the point where both intrinsic and extrinsic pathways converge, but it does not initiate the process *in vitro*. * **Factor VII:** This factor initiates the **Extrinsic Pathway** *in vivo*. It requires **Tissue Factor (Factor III)**, which is released upon vascular injury, rather than contact with a glass surface. **High-Yield NEET-PG Pearls:** * **Factor XII Deficiency:** Interestingly, patients with Factor XII deficiency show a prolonged PTT (Partial Thromboplastin Time) in the lab but **do not** have a clinical bleeding tendency *in vivo*. * **In Vivo Initiation:** In the living body, the Extrinsic Pathway (Factor VII + Tissue Factor) is the primary initiator of coagulation. * **Vitamin K Dependent Factors:** II, VII, IX, and X. * **Lab Tests:** PT (Prothrombin Time) monitors the Extrinsic pathway; aPTT monitors the Intrinsic pathway.

Question 112: Citrate is a useful anticoagulant because of its ability to

A. Buffer basic groups of coagulation factors
B. Bind factor XII
C. Bind vitamin K
D. Chelate calcium (Correct Answer)

Explanation: **Explanation:** **Why the correct answer is right:** Calcium (Factor IV) is an essential cofactor in the coagulation cascade. It is required for almost all steps of the clotting process, including the activation of Factor IX, Factor X, and the conversion of prothrombin to thrombin. Citrate (usually as Sodium Citrate) acts as an anticoagulant by **chelating (binding) free calcium ions** in the blood. By forming an insoluble complex with calcium, citrate reduces the concentration of ionized calcium below the threshold required for the clotting enzymes to function, thereby preventing the formation of a fibrin clot. **Why the incorrect options are wrong:** * **A. Buffer basic groups:** Citrate is a weak acid salt, but its anticoagulant property is strictly due to ion binding, not pH buffering of coagulation factors. * **B. Bind factor XII:** Factor XII (Hageman factor) is the initiator of the intrinsic pathway. While some substances like heparin inhibit factors, citrate specifically targets calcium, not Factor XII. * **C. Bind vitamin K:** Vitamin K is necessary for the hepatic synthesis of Factors II, VII, IX, and X. Drugs like Warfarin interfere with Vitamin K; citrate does not interact with Vitamin K or its synthesis. **Clinical Pearls for NEET-PG:** * **Standard Ratio:** For routine coagulation studies (PT/aPTT), sodium citrate is used in a **1:9 ratio** (1 part citrate to 9 parts blood). * **Reversibility:** The effect of citrate is easily reversed by adding calcium, which is why it is the preferred anticoagulant for blood transfusions and coagulation testing. * **Citrate Toxicity:** In massive blood transfusions, "Citrate Toxicity" can occur, leading to **hypocalcemia** (symptoms include tetany and prolonged QT interval) because the excess citrate chelates the patient's own serum calcium. * **Other Chelators:** EDTA is another common chelator used in CBC vials, but it is not used for coagulation studies as it can irreversibly damage some clotting factors.

Question 113: Adding glucose to stored blood causes what?

A. Prevention of hemolysis
B. Nutrition to red blood cells (Correct Answer)
C. Increased acidosis of stored blood
D. Prevention of hyperkalemia

Explanation: ### Explanation **Correct Answer: B. Nutrition to red blood cells** Red Blood Cells (RBCs) are unique because they lack mitochondria and rely exclusively on **anaerobic glycolysis** (the Embden-Meyerhof pathway) to generate energy in the form of ATP. ATP is essential for maintaining the structural integrity of the RBC membrane and the function of the Na⁺/K⁺-ATPase pump. When blood is stored *ex vivo*, the RBCs continue their metabolic activity. Adding glucose provides the necessary substrate for glycolysis, ensuring the cells remain viable and functional during storage. **Analysis of Incorrect Options:** * **A. Prevention of hemolysis:** While glucose indirectly helps maintain membrane integrity, hemolysis is primarily prevented by the **citrate** (which prevents clotting) and the **refrigeration temperature** (which slows metabolism). Glucose alone cannot stop the physical or chemical breakdown of cells over time. * **C. Increased acidosis:** This is a *side effect* of glucose metabolism, not the reason for adding it. As RBCs consume glucose via anaerobic glycolysis, they produce **lactic acid**, which actually *increases* the acidity (decreases pH) of stored blood. * **D. Prevention of hyperkalemia:** Stored blood actually develops **hyperkalemia** over time. As ATP levels eventually drop, the Na⁺/K⁺ pumps fail, causing potassium to leak out of the RBCs into the plasma. Adding glucose slows this process but does not prevent it. **High-Yield NEET-PG Pearls:** * **CPD (Citrate Phosphate Dextrose):** The standard preservative. Citrate is the anticoagulant; Phosphate acts as a buffer; **Dextrose (Glucose)** provides nutrition. * **Storage Life:** CPD extends storage to 21 days; **CPDA-1** (adding Adenine) extends it to 35 days by further assisting ATP synthesis. * **Storage Lesion:** This term refers to the biochemical changes in stored blood, including **decreased pH, decreased 2,3-BPG** (shifting the O₂ dissociation curve to the left), and **increased plasma Potassium.**

Question 114: Which of the following is responsible for adhesion of platelets to the vessel wall?

A. Factor IX
B. Von Willebrand factor (Correct Answer)
C. Fibrinogen
D. Fibronectin

Explanation: ### Explanation **Correct Answer: B. Von Willebrand factor (vWF)** **Mechanism of Platelet Adhesion:** When a blood vessel is injured, the subendothelial collagen is exposed. Platelets do not bind directly to collagen with high affinity under high-shear conditions (like in arteries). Instead, **Von Willebrand factor (vWF)** acts as a molecular bridge. One end of the vWF molecule binds to the exposed **subendothelial collagen**, while the other end binds to the **Glycoprotein Ib-IX-V (GpIb)** receptor on the platelet surface. This initial attachment is known as **platelet adhesion**, the first step in forming a primary hemostatic plug. **Analysis of Incorrect Options:** * **A. Factor IX:** This is a clotting factor involved in the **intrinsic pathway** of the coagulation cascade. Its deficiency leads to Hemophilia B (Christmas disease). It is involved in secondary hemostasis (fibrin formation), not initial platelet adhesion. * **C. Fibrinogen (Factor I):** Fibrinogen is primarily responsible for **platelet aggregation** (platelet-to-platelet binding) by linking **GpIIb/IIIa** receptors on adjacent platelets. It is also the precursor to fibrin. * **D. Fibronectin:** While fibronectin is an adhesive glycoprotein found in plasma and the extracellular matrix that can aid in cell attachment, it is not the primary or rate-limiting mediator for platelet-vessel wall adhesion in high-flow states. **High-Yield NEET-PG Pearls:** * **Adhesion:** Mediated by **vWF** binding to **GpIb**. Deficiency of GpIb results in **Bernard-Soulier Syndrome** (characterized by giant platelets and thrombocytopenia). * **Aggregation:** Mediated by **Fibrinogen** binding to **GpIIb/IIIa**. Deficiency of GpIIb/IIIa results in **Glanzmann Thrombasthenia**. * **vWF Source:** It is synthesized and stored in **Weibel-Palade bodies** of endothelial cells and **alpha-granules** of platelets. * **Ristocetin Cofactor Assay:** Used to test vWF function; ristocetin induces platelet agglutination only in the presence of vWF.

Question 115: All of the following are macrophages except—

A. Monocyte
B. Lymphocyte (Correct Answer)
C. Kupffer cell
D. Microglia

Explanation: **Explanation:** The question tests the concept of the **Mononuclear Phagocyte System (MPS)**, formerly known as the Reticuloendothelial System. This system consists of monocytes and their tissue-specific derivatives, which are specialized for phagocytosis and antigen presentation. **Why Lymphocyte is the correct answer:** Lymphocytes (B-cells, T-cells, and NK cells) are part of the **adaptive immune system** (and innate in the case of NK cells), but they are **not phagocytic cells**. They function through antibody production or cell-mediated cytotoxicity rather than engulfing and digesting pathogens. Therefore, they do not belong to the macrophage lineage. **Analysis of Incorrect Options:** * **Monocyte:** These are the precursor cells found in the blood. Once they migrate into tissues, they differentiate into mature macrophages. * **Kupffer Cells:** These are specialized, resident macrophages located in the **liver** (sinusoids). They are essential for clearing bacteria and debris from the portal circulation. * **Microglia:** These are the resident macrophages of the **Central Nervous System (CNS)**. They act as the primary active immune defense in the brain and spinal cord. **High-Yield Clinical Pearls for NEET-PG:** * **Tissue-Specific Macrophages to Remember:** * **Lung:** Alveolar macrophages (Dust cells). * **Skin:** Langerhans cells. * **Bone:** Osteoclasts. * **Kidney:** Mesangial cells. * **Placenta:** Hofbauer cells. * **Key Marker:** CD14 is a common surface marker used to identify monocytes and macrophages. * **Function:** Macrophages are the primary source of **Interleukin-1 (IL-1)**, which induces fever.

Question 116: Which coagulation factor is not present in serum?

A. II (Correct Answer)
B. IV
C. X
D. VII

Explanation: **Explanation:** The fundamental difference between **plasma** and **serum** lies in the presence of clotting factors. Serum is defined as plasma minus the clotting factors that are consumed during the coagulation process. **Why Option A is Correct:** Coagulation **Factor II (Prothrombin)** is a key component of the common pathway. During the clotting process, Prothrombin is converted into its active form, **Thrombin (IIa)**, which then converts fibrinogen into a fibrin mesh. Because Factor II is utilized and converted to form the clot, it is **absent in serum**. Other factors consumed during clotting (and thus absent in serum) include factors **I, V, VIII, and XIII**. **Why the other options are incorrect:** * **Option B (Factor IV):** This is Calcium. While it is essential for almost all steps of the coagulation cascade, it is an ion and remains present in the serum after the clot has formed. * **Option C & D (Factors X and VII):** These are part of the stable factors. While they are activated during the cascade (to Xa and VIIa), they are not entirely consumed in the same manner as Prothrombin or Fibrinogen and can still be detected in serum. **High-Yield NEET-PG Pearls:** * **Mnemonic for factors absent in serum:** "1, 2, 5, 8, 13" (The factors consumed during clotting). * **Serum vs. Plasma:** Plasma contains Fibrinogen; Serum does **not**. * **Vitamin K Dependent Factors:** II, VII, IX, and X (Note: Only II is consumed; VII, IX, and X are present in serum). * **Factor I (Fibrinogen)** is the most abundant clotting factor in plasma but is completely absent in serum as it becomes the fibrin clot.

Question 117: The biconcave shape of red blood cells is primarily maintained by which protein complex?

A. Ankyrin
B. Spectrin (Correct Answer)
C. Band 3 protein
D. Glycophorin-C

Explanation: **Explanation:** The biconcave shape of the Red Blood Cell (RBC) is essential for maximizing surface area for gas exchange and providing the flexibility needed to navigate through narrow capillaries. This shape is primarily maintained by the **cytoskeletal framework** located just beneath the lipid bilayer. **1. Why Spectrin is the Correct Answer:** **Spectrin** is the major constituent of the RBC cytoskeleton. It consists of alpha and beta chains that form a long, flexible hexagonal lattice. This network acts like a "molecular spring," providing the structural integrity and elasticity required for the RBC to deform and then snap back into its biconcave shape. Without functional spectrin, the cell defaults to a spherical shape. **2. Analysis of Incorrect Options:** * **Ankyrin (Option A):** While crucial, Ankyrin acts as an **adapter protein**. Its primary role is to anchor the spectrin lattice to the transmembrane protein Band 3. It is the "link," not the primary structural scaffold itself. * **Band 3 Protein (Option B):** This is a multipass transmembrane protein that functions as an **anion exchanger** (HCO3⁻/Cl⁻). It provides an attachment point for the cytoskeleton but does not create the biconcave framework. * **Glycophorin-C (Option D):** This is a sialoglycoprotein that helps attach the cytoskeleton to the membrane via Protein 4.1, but its primary role relates to membrane charge and blood group antigens. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hereditary Spherocytosis:** Most commonly caused by a deficiency or defect in **Ankyrin** (most common) or **Spectrin**. This leads to a loss of membrane surface area, resulting in spherical, fragile RBCs that are destroyed in the spleen. * **Hereditary Elliptocytosis:** Typically associated with defects in **Spectrin** (specifically the horizontal interactions) or **Protein 4.1**. * **Vertical vs. Horizontal Interactions:** Defects in *vertical* interactions (Ankyrin/Band 3) lead to Spherocytosis; defects in *horizontal* interactions (Spectrin dimers) lead to Elliptocytosis.

Question 118: At what stage do neutrophils first appear in peripheral blood?

A. Myeloblast
B. Promyelocyte
C. Myelocyte
D. Band forms (Correct Answer)

Explanation: **Explanation:** The correct answer is **Band forms**. This question tests the understanding of granulopoiesis and the transition of cells from the bone marrow to the systemic circulation. **Why Band forms are correct:** Granulopoiesis follows a specific maturation sequence: Myeloblast → Promyelocyte → Myelocyte → Metamyelocyte → Band form → Mature Neutrophil (Segmented). Under normal physiological conditions, the bone marrow acts as a barrier, releasing only mature neutrophils and a small percentage (3-5%) of **Band forms** (immature neutrophils with non-segmented, curved nuclei) into the peripheral blood. Band forms represent the final stage of maturation before full segmentation and are the earliest stage routinely seen in a normal peripheral smear. **Why other options are incorrect:** * **Myeloblast:** This is the first identifiable myeloid precursor. It is confined to the bone marrow. Its presence in peripheral blood is always pathological (e.g., Acute Myeloid Leukemia). * **Promyelocyte:** Characterized by primary (azurophilic) granules, these cells stay within the marrow. * **Myelocyte:** This is the last stage capable of mitosis and the stage where secondary (specific) granules first appear. Like the stages above, it is restricted to the bone marrow in healthy individuals. **High-Yield Clinical Pearls for NEET-PG:** * **Left Shift:** An increase in band forms (>10%) in the peripheral blood is termed a "shift to the left," typically indicating an acute bacterial infection or inflammation. * **Myelocyte Stage:** High-yield fact—this is the stage where **specific granules** (e.g., alkaline phosphatase, lactoferrin) first appear. * **Leukemoid Reaction:** The presence of early precursors like myelocytes or metamyelocytes in the blood, often seen in severe infections, mimicking leukemia but with a high LAP (Leukocyte Alkaline Phosphatase) score.

Question 119: What is the predominant site of erythropoiesis during the sixth month of gestation?

A. Yolk sac
B. Liver (Correct Answer)
C. Bone marrow
D. Thymus

Explanation: The process of erythropoiesis during fetal development occurs in distinct overlapping stages, often remembered by the mnemonic **"Young Liver Synthesizes Blood."** ### **1. Why Liver is the Correct Answer** The **hepatic stage** of erythropoiesis begins around the 6th week of gestation and reaches its peak activity during the **second trimester (3rd to 6th month)**. During the sixth month, the liver remains the primary erythropoietic organ, although the bone marrow is just beginning to take over this function. By the end of the second trimester, the liver is the predominant site for producing red blood cells. ### **2. Analysis of Incorrect Options** * **A. Yolk sac:** This is the site of the **Mesoblastic stage**. It is the first site of hematopoiesis, starting at the 3rd week, but it ceases to be active by the end of the first trimester (around 10–12 weeks). * **C. Bone marrow:** The **Myeloid stage** begins in the bone marrow around the 4th to 5th month. However, it only becomes the *predominant* site after the 7th month of gestation and remains the primary site for the rest of postnatal life. * **D. Thymus:** While the thymus is involved in T-lymphocyte maturation, it is never a primary site for erythropoiesis (RBC production). ### **3. High-Yield Clinical Pearls for NEET-PG** * **Chronology:** Yolk sac (3rd week) → Liver (6th week; peak at 3–6 months) → Spleen (3rd to 7th month) → Bone Marrow (starts at 4th month; dominant from 7th month onwards). * **Spleen's Role:** The spleen contributes to erythropoiesis primarily between the 3rd and 6th months but is always secondary to the liver. * **Post-natal site:** In adults, hematopoiesis is restricted to the **axial skeleton** (vertebrae, sternum, ribs, and pelvis). * **Extramedullary Hematopoiesis:** In certain pathological states (e.g., Thalassemia, Myelofibrosis), the liver and spleen can resume their fetal erythropoietic function.

Question 120: A person with anti-A and anti-B isoagglutinins in their serum belongs to which blood group?

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

Explanation: ### Explanation The correct answer is **D. O**. This question is based on **Landsteiner’s Law**, which states that if an agglutinogen (antigen) is present on the red blood cell (RBC) membrane, the corresponding agglutinin (antibody) must be absent from the serum, and vice versa. **Why Option D is Correct:** Individuals with **Blood Group O** have neither Antigen A nor Antigen B on their RBC surfaces. According to Landsteiner’s Law, because these antigens are absent, the body produces both **anti-A and anti-B isoagglutinins** (antibodies) in the serum. These antibodies are typically IgM in nature and develop within the first few months of life. **Why Other Options are Incorrect:** * **Option A (Blood Group A):** These individuals have Antigen A on RBCs and only **anti-B** antibodies in the serum. * **Option B (Blood Group B):** These individuals have Antigen B on RBCs and only **anti-A** antibodies in the serum. * **Option C (Blood Group AB):** These individuals have both Antigen A and B on RBCs; therefore, they have **no isoagglutinins** in their serum (making them the "Universal Recipient"). **High-Yield Clinical Pearls for NEET-PG:** * **Universal Donor:** Group O (specifically O negative) is the universal donor because it lacks A and B antigens. * **Bombay Blood Group:** A rare phenotype where the H-antigen is absent. These individuals have anti-A, anti-B, and **anti-H** antibodies, meaning they can only receive blood from another Bombay phenotype individual. * **Antibody Type:** Naturally occurring ABO antibodies are primarily **IgM** (cannot cross the placenta), whereas Rh antibodies are **IgG** (can cross the placenta, leading to Erythroblastosis Fetalis). * **Secretors:** About 80% of the population secretes ABO antigens in body fluids like saliva and semen.

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