Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 291: A middle-aged man's blood sample shows a hematocrit of 45% and biconcave red blood cells. The biconcavity of RBCs is a function of which of the following?

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

Explanation: **Explanation:** The biconcave shape of the Red Blood Cell (RBC) is crucial for its function, providing a high surface-area-to-volume ratio for gas exchange and the flexibility needed to squeeze through narrow capillaries. **Why Spectrin is Correct:** **Spectrin** is the primary structural protein of the RBC cytoskeleton. It forms a hexagonal meshwork on the inner surface of the plasma membrane. It acts as a "molecular spring," providing the structural integrity and elasticity required to maintain the biconcave shape. While other proteins assist in anchoring, the actual scaffold that dictates the shape is the spectrin network. **Analysis of Incorrect Options:** * **Ankyrin:** This is an anchoring protein. Its primary role is to link the spectrin network to the transmembrane protein, Band 3. While a deficiency in ankyrin leads to shape changes (like Spherocytosis), it is not the structural framework itself. * **Band 3 Protein:** This is a major integral membrane protein that functions as an anion exchanger (Chloride-Bicarbonate shift). It serves as an attachment site for the cytoskeleton but does not determine the biconcave geometry. * **Glycophorin-C:** This is a sialoglycoprotein that provides the RBC with a negative surface charge (zeta potential) to prevent aggregation. It anchors the membrane to the cytoskeleton via Protein 4.1 but is not the primary determinant of shape. **NEET-PG High-Yield Pearls:** * **Hereditary Spherocytosis:** Most commonly caused by a deficiency in **Ankyrin** (most common) or **Spectrin**. * **Hereditary Elliptocytosis:** Most commonly due to a defect in **Spectrin** (specifically the inability of spectrin dimers to form tetramers). * **RBC Membrane:** It is a lipid bilayer with a "laminated" protein cytoskeleton. Remember: **Spectrin = Shape & Stability.**

Question 292: Cytokines are secreted in sepsis and Systemic Inflammatory Response Syndrome (SIRS) by which of the following?

A. Neutrophils (Correct Answer)
B. Adrenal gland
C. Collecting duct
D. Renal cortex

Explanation: ### Explanation **Correct Option: A. Neutrophils** In the context of sepsis and Systemic Inflammatory Response Syndrome (SIRS), the primary source of cytokines is the **innate immune system**. When the body encounters pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), leukocytes—specifically **neutrophils**, macrophages, and monocytes—are activated. These cells release a "cytokine storm" involving pro-inflammatory mediators such as **TNF-α, IL-1, and IL-6**. Neutrophils are the first responders in acute inflammation; they not only release cytokines to amplify the immune response but also produce reactive oxygen species (ROS) and proteases that contribute to the systemic manifestations of SIRS. **Why other options are incorrect:** * **B. Adrenal gland:** While the adrenal gland is involved in the stress response (releasing cortisol and catecholamines), it is a *target* or a *modulator* of the inflammatory response rather than a primary source of pro-inflammatory cytokines in sepsis. * **C & D. Collecting duct and Renal cortex:** These are anatomical components of the kidney. While the kidney can suffer from acute kidney injury (AKI) during sepsis due to cytokine-mediated damage and hypoperfusion, renal parenchymal cells are not the primary secretors of systemic inflammatory cytokines. **High-Yield Facts for NEET-PG:** * **SIRS Criteria:** Defined by abnormalities in temperature, heart rate, respiratory rate, and WBC count (Leukocytosis/Leukopenia). * **Key Cytokine in Sepsis:** **TNF-α** is considered the "master mediator" and the first cytokine to be released in the cascade. * **IL-6 Correlation:** Serum levels of IL-6 correlate most closely with the severity of sepsis and mortality risk. * **Procalcitonin:** A high-yield biomarker used to differentiate bacterial sepsis from non-infectious SIRS.

Question 293: Thrombosthenin is a/an:

A. Thrombosis preventing protein
B. Contractile protein (Correct Answer)
C. Coagulation protein
D. Protein for regulating platelet production

Explanation: **Explanation:** **Thrombosthenin** is a specialized **contractile protein** found within platelets (thrombocytes). It is a complex composed of actin and myosin, similar to those found in muscle cells, but specifically adapted for platelet function. 1. **Why Option B is Correct:** Platelets contain high concentrations of thrombosthenin. Once a blood clot is formed, thrombosthenin (activated by calcium ions) causes the contraction of the platelet spicules attached to fibrin threads. This process, known as **clot retraction**, pulls the edges of the broken blood vessel together, reducing blood loss and initiating the healing process. 2. **Why Other Options are Incorrect:** * **Option A:** Proteins that prevent thrombosis are called anticoagulants (e.g., Antithrombin III, Protein C/S). Thrombosthenin does not prevent clots; it modifies them. * **Option C:** Coagulation proteins (Clotting Factors I-XIII) are involved in the chemical cascade that forms fibrin. Thrombosthenin is a structural/motor protein, not a clotting factor. * **Option D:** The primary regulator of platelet production is **Thrombopoietin**, a hormone produced mainly by the liver and kidneys. **High-Yield NEET-PG Pearls:** * **Clot Retraction:** Occurs within 20–60 minutes of clot formation. It requires a large number of platelets; therefore, a low platelet count (thrombocytopenia) leads to poor clot retraction. * **Energy Source:** Platelets are rich in mitochondria and glycogen, providing the ATP necessary for thrombosthenin-mediated contraction. * **Storage:** Thrombosthenin is stored in the cytoplasm of the platelet, not within the alpha or dense granules.

Question 294: During the second trimester of pregnancy, in which organ does erythropoiesis primarily occur in the fetus?

A. Liver (Correct Answer)
B. Spleen
C. Red bone marrow
D. Lymph nodes

Explanation: ### Explanation The site of fetal erythropoiesis changes in a predictable chronological sequence, often remembered by the mnemonic **"Young Liver Synthesizes Blood."** **1. Why Liver is the Correct Answer:** During the **second trimester** (specifically from the 6th week to the 5th month), the **Liver** is the primary (dominant) site of erythropoiesis. While it begins around the 6th week of gestation, it reaches its peak activity during the second trimester before gradually declining as the bone marrow takes over. **2. Analysis of Incorrect Options:** * **B. Spleen:** The spleen acts as a secondary lymphoid and hematopoietic organ during the second trimester (roughly months 3 to 5), but its contribution is significantly less than that of the liver. * **C. Red bone marrow:** This becomes the primary site of erythropoiesis only during the **third trimester** (from the 7th month onwards) and remains the sole site after birth. * **D. Lymph nodes:** While lymph nodes can show minor hematopoietic activity during the fetal period, they are never the "primary" site for red blood cell production. **3. High-Yield Facts for NEET-PG:** * **Mesoblastic Stage (3–8 weeks):** Erythropoiesis begins in the **Yolk Sac** (specifically the blood islands). * **Hepatic Stage (6 weeks – Birth):** The Liver is the main site during the 2nd trimester. * **Myeloid Stage (18 weeks – Life):** Bone marrow starts at month 4-5 and becomes dominant by month 7. * **Fetal Hemoglobin (HbF):** It has a higher affinity for oxygen than adult hemoglobin (HbA) due to poor binding with 2,3-BPG, facilitating oxygen transfer across the placenta. * **Clinical Note:** If the bone marrow fails in adults (e.g., Myelofibrosis), the liver and spleen can resume blood cell production, a process called **Extramedullary Hematopoiesis**.

Question 295: What is the half-life of albumin?

A. 36-48 hours
B. 3-5 days
C. 5-10 days
D. 20 days (Correct Answer)

Explanation: **Explanation:** Albumin is the most abundant plasma protein, synthesized exclusively by the liver. The correct answer is **20 days** (Option D), which represents the average biological half-life of albumin in a healthy adult. **Why 20 days is correct:** Albumin is designed for long-term stability to maintain **plasma oncotic pressure** and serve as a carrier protein for hormones, drugs, and bilirubin. Its long half-life is primarily due to its interaction with the **neonatal Fc receptor (FcRn)**. This receptor protects albumin from lysosomal degradation by recycling it back into the circulation, a mechanism similar to how IgG antibodies are preserved. **Why other options are incorrect:** * **36-48 hours (Option A):** This is too short for albumin but is characteristic of proteins with rapid turnover, such as certain clotting factors (e.g., Factor VII). * **3-5 days (Option B):** This is the half-life of **Pre-albumin (Transthyretin)**. Because of its shorter half-life, pre-albumin is a more sensitive clinical indicator of acute nutritional status than albumin. * **5-10 days (Option C):** This range is incorrect for albumin; however, some globulins and specific transferrins fall within this window. **High-Yield Clinical Pearls for NEET-PG:** * **Nutritional Marker:** Due to its long half-life (20 days), serum albumin is a marker of **chronic** nutritional status or chronic liver disease, not acute changes. * **Oncotic Pressure:** Albumin provides approximately **70-80%** of the total plasma colloid osmotic pressure. * **Hypoalbuminemia:** Leads to a decrease in oncotic pressure, resulting in edema (e.g., in Nephrotic syndrome or Cirrhosis). * **Synthesis:** Approximately 10-15 grams of albumin are synthesized daily; synthesis is stimulated by thyroid hormone and inhibited by inflammatory cytokines (it is a **negative acute-phase reactant**).

Question 296: Haemoglobin is the major buffer in blood. Bicarbonate ions diffuse out of erythrocytes into plasma in exchange for which ion?

A. Potassium
B. Phosphate
C. Carbonic acid
D. Chloride ion (Correct Answer)

Explanation: This question tests the understanding of the **Chloride Shift (Hamburger Phenomenon)**, a vital mechanism for CO₂ transport and acid-base balance. ### Explanation of the Correct Answer When CO₂ enters erythrocytes, it reacts with water (catalyzed by carbonic anhydrase) to form carbonic acid, which dissociates into **H⁺** and **HCO₃⁻**. 1. The H⁺ ions are buffered by deoxyhemoglobin. 2. As HCO₃⁻ (bicarbonate) concentrations rise, they diffuse out of the cell into the plasma along a concentration gradient. 3. To maintain **electrical neutrality**, an equivalent amount of negative charge must enter the cell. This is achieved by the influx of **Chloride ions (Cl⁻)** via the **Anion Exchanger 1 (Band 3 protein)**. This process is the Chloride Shift. ### Why Other Options are Incorrect * **A. Potassium:** Potassium is the primary intracellular cation. While it maintains osmotic balance, it does not exchange directly for bicarbonate during CO₂ transport. * **B. Phosphate:** Intracellular phosphates act as buffers, but they do not participate in the rapid transmembrane exchange required for systemic CO₂ transport. * **C. Carbonic acid:** This is an intermediate molecule (H₂CO₃) that quickly dissociates; it does not exist as a transportable ion in this exchange. ### High-Yield NEET-PG Pearls * **Reverse Chloride Shift:** Occurs in the **lungs**, where Cl⁻ moves *out* of the RBC and HCO₃⁻ moves *in* to be converted back to CO₂ for exhalation. * **Water Movement:** When Cl⁻ enters the RBC (in systemic tissues), osmotic pressure increases, causing water to enter the cell. Consequently, **venous RBCs are slightly larger (higher MCV)** than arterial RBCs. * **Haldane Effect:** Deoxygenation of blood increases its ability to carry CO₂, primarily because deoxyhemoglobin is a better buffer for H⁺ than oxyhemoglobin.

Question 297: ABO antigens are not found in which of the following bodily fluids?

A. Cerebrospinal fluid (CSF) (Correct Answer)
B. Semen
C. Sweat
D. Saliva

Explanation: **Explanation:** The presence of ABO blood group antigens in body fluids is determined by the **Se (Secretor) gene**. Approximately 80% of the population are "secretors," meaning they possess the dominant Se allele, which allows for the expression of soluble A, B, and H antigens in various exocrine secretions. **1. Why CSF is the Correct Answer:** ABO antigens are primarily found in fluids produced by **exocrine glands**. The **Cerebrospinal Fluid (CSF)** is a specialized ultrafiltrate of plasma produced by the choroid plexus and is not an exocrine secretion. It lacks the soluble glycoproteins required to carry ABO antigens. Therefore, even in secretors, ABO antigens are **not found in the CSF**. **2. Analysis of Incorrect Options:** * **Saliva:** This is the most common fluid used to determine secretor status. Salivary glands (exocrine) secrete high concentrations of water-soluble ABO antigens. * **Semen and Sweat:** Both are products of exocrine glands (seminal vesicles/prostate and sweat glands, respectively). In secretors, these fluids contain detectable levels of ABO antigens. Other fluids include tears, breast milk, and amniotic fluid. **3. High-Yield Clinical Pearls for NEET-PG:** * **Secretor Status:** Controlled by the *FUT2* gene on chromosome 19. * **Non-secretors (20%):** These individuals have the genotype *sese* and do not have ABO antigens in their body fluids, though the antigens remain present on their red blood cells. * **Forensic Significance:** Detecting ABO antigens in stains (semen or saliva) at a crime scene can help in identifying or excluding suspects. * **Antigen Location:** Remember that ABO antigens are not just on RBCs; they are also found on vascular endothelium and most epithelial cells (hence their importance in solid organ transplants).

Question 298: Which of the following Interleukins is raised in fever?

A. IFN-γ
B. TNF-α (Correct Answer)
C. IL-10
D. IL-2

Explanation: ### Explanation **Correct Option: B (TNF-α)** **Concept:** Fever (pyrexia) is primarily mediated by **pyrogens**. When the body encounters pathogens or inflammation, phagocytic cells release **Endogenous Pyrogens**. The most potent endogenous pyrogens are **IL-1, IL-6, and TNF-α (Tumor Necrosis Factor-alpha)**. These cytokines travel via the bloodstream to the hypothalamus (specifically the Organum Vasculosum of the Lamina Terminalis - OVLT), where they stimulate the release of **Prostaglandin E2 (PGE2)**. PGE2 then resets the hypothalamic thermostat to a higher set point, resulting in fever. **Analysis of Options:** * **TNF-α (Correct):** Along with IL-1 and IL-6, it is a primary pro-inflammatory cytokine and a major mediator of the acute phase response and fever. * **IFN-γ (Option A):** Produced by Th1 cells and NK cells, its primary role is activating macrophages and stimulating MHC expression. While it aids the immune response, it is not a primary pyrogen. * **IL-10 (Option C):** This is an **anti-inflammatory cytokine**. It inhibits the synthesis of pro-inflammatory cytokines (like TNF-α and IL-1) and actually helps in resolving inflammation rather than inducing fever. * **IL-2 (Option D):** Primarily functions as a T-cell growth factor, promoting the proliferation and differentiation of T-lymphocytes. **NEET-PG High-Yield Pearls:** * **Master Pyrogens:** Remember the "Big Three" of fever: **IL-1, IL-6, and TNF-α**. * **The Mediator:** **PGE2** is the ultimate mediator of fever in the hypothalamus. This is why NSAIDs (COX inhibitors) are effective antipyretics—they block PGE2 synthesis. * **Cryogens:** Molecules like **IL-10 and Arginine Vasopressin (AVP)** act as endogenous antipyretics (cryogens) to prevent excessive temperature rise. * **IL-1** is often cited as the most potent endogenous pyrogen in many textbooks.

Question 299: Which of the following pathways does aPTT measure?

A. Intrinsic pathway
B. Extrinsic pathway (Correct Answer)
C. Both intrinsic and extrinsic pathways
D. Complement pathway

Explanation: **Explanation:** The **Activated Partial Thromboplastin Time (aPTT)** is a screening test used to evaluate the efficiency of the **Intrinsic** and **Common pathways** of the coagulation cascade. *Note: There appears to be a discrepancy in the provided key. In standard medical physiology, **aPTT measures the Intrinsic pathway**, while **PT (Prothrombin Time) measures the Extrinsic pathway**.* ### Why the Options are Correct/Incorrect: * **A. Intrinsic Pathway (Correct Concept):** aPTT measures factors XII, XI, IX, and VIII (Intrinsic), as well as factors X, V, II (Prothrombin), and I (Fibrinogen) of the Common pathway. It is the gold standard for monitoring **Unfractionated Heparin** therapy. * **B. Extrinsic Pathway (Incorrect):** This pathway is measured by **Prothrombin Time (PT)**. The extrinsic pathway involves Factor VII and Tissue Factor. PT is used to monitor **Warfarin** therapy. * **C. Both Pathways:** While both tests share the "Common Pathway" (Factors X, V, II, I), they are clinically distinct tests used to isolate deficiencies in either the Intrinsic (aPTT) or Extrinsic (PT) arms. * **D. Complement Pathway:** This is part of the innate immune system (C1-C9) and is unrelated to the secondary hemostasis (clotting) measured by aPTT. ### High-Yield Clinical Pearls for NEET-PG: 1. **Mnemonic for PT:** "PET" – **P**T measures **E**xtrinsic pathway and involves Factor **7** (VII). 2. **Mnemonic for aPTT:** "PITT" – **P**TT measures **I**ntrinsic pathway and involves **T**welve, **T**en, etc. 3. **Hemophilia A (VIII) and B (IX):** These involve the intrinsic pathway, so they present with a **prolonged aPTT** but a normal PT. 4. **Vitamin K Deficiency:** Affects Factors II, VII, IX, and X. Since Factor VII has the shortest half-life, **PT is usually prolonged first**.

Question 300: The consequences of Rh incompatibility are not serious during the first pregnancy because:

A. In the first pregnancy, only IgM antibodies are formed. (Correct Answer)
B. The antibody titer is very low during the primary immune response.
C. IgG generated is ineffective against fetal red cells.
D. Massive hemolysis is compensated by increased erythropoiesis.

Explanation: ### Explanation **Why Option A is Correct:** Rh incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus. During the first pregnancy, the initial exposure to fetal Rh-positive antigens (usually during delivery) triggers a **primary immune response**. In this phase, the mother’s immune system primarily produces **IgM antibodies**. Because IgM is a pentamer with a high molecular weight, it is **too large to cross the placental barrier**. Consequently, these antibodies cannot enter the fetal circulation to cause hemolysis, making the first pregnancy safe. **Analysis of Incorrect Options:** * **Option B:** While the antibody titer is indeed lower in a primary response compared to a secondary response, the fundamental reason for fetal safety is the **isotype (IgM)** and its inability to cross the placenta, rather than just the quantity. * **Option C:** IgG is highly effective against fetal red cells (it causes Hemolytic Disease of the Newborn). However, significant IgG production only occurs during the **secondary immune response** (subsequent pregnancies) after class-switching has taken place. * **Option D:** While the fetus does attempt to compensate via extramedullary hematopoiesis (leading to hepatosplenomegaly), this occurs in subsequent pregnancies. In the first pregnancy, there is no "massive hemolysis" to begin with. **Clinical Pearls for NEET-PG:** * **The "Sensitizing Event":** Most sensitization occurs during delivery, but can also occur during abortion, ectopic pregnancy, or amniocentesis. * **Prophylaxis:** To prevent sensitization, **Anti-D (RhoGAM)** is administered to Rh-negative mothers at 28 weeks of gestation and within 72 hours of delivery. * **Mechanism of Anti-D:** It provides passive immunity that clears fetal Rh+ cells from maternal circulation before the mother’s immune system can mount an active primary response. * **Subsequent Pregnancies:** Memory B cells lead to a rapid production of **IgG**, which crosses the placenta, causing **Erythroblastosis Fetalis**.

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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