Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 21: What is true of fetal hematopoiesis in the course of pregnancy?

A. Rise in MCV
B. Rise in reticulocyte count
C. Rise in Hemoglobin content (Correct Answer)
D. Decrease in blood volume

Explanation: ### Explanation **Correct Option: C. Rise in Hemoglobin content** During fetal development, there is a progressive and significant increase in hemoglobin (Hb) concentration to meet the rising oxygen demands of the growing fetus. At 10 weeks of gestation, Hb is approximately 8–10 g/dL; by term, it rises to **14–20 g/dL**. This increase is driven by the high levels of **Erythropoietin (EPO)** produced by the fetal liver (and later the kidneys) in response to the relatively low oxygen tension ($PaO_2$) of the intrauterine environment. **Analysis of Incorrect Options:** * **A. Rise in MCV:** This is incorrect. Fetal red blood cells (RBCs) are initially **macrocytic**. As gestation progresses, the Mean Corpuscular Volume (MCV) actually **decreases**. It starts at >130 fL in the first trimester and drops to approximately 100–110 fL at birth. * **B. Rise in reticulocyte count:** The reticulocyte count is very high in early pregnancy (up to 40% at 12 weeks) due to rapid erythropoiesis but **decreases** as the fetus approaches term (dropping to 3–5% at birth). * **C. Decrease in blood volume:** This is incorrect. Fetal blood volume **increases** linearly with fetal weight throughout pregnancy to support the expanding vascular bed and placental circulation. **High-Yield Facts for NEET-PG:** 1. **Sites of Hematopoiesis:** * **Mesoblastic Stage (3–8 weeks):** Yolk sac (specifically "blood islands"). * **Hepatic Stage (6 weeks – Birth):** Liver is the chief site (peaks at 3–4 months). The spleen also contributes (12–28 weeks). * **Myeloid Stage (18 weeks onwards):** Bone marrow becomes the primary site. 2. **Fetal Hemoglobin (HbF):** Composed of $\alpha_2\gamma_2$ chains. It has a higher affinity for oxygen than adult Hb (HbA) because it binds poorly to 2,3-BPG. 3. **Nucleated RBCs:** These are commonly seen in fetal peripheral blood early on but disappear as the bone marrow matures.

Question 22: A father's blood group is 'A' and a mother's blood group is 'AB'. Which of the following blood groups is not possible in any of their child?

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

Explanation: ### Explanation The inheritance of ABO blood groups is determined by the **ABO gene**, which follows the principles of **Co-dominance** and **Multiple Allelism**. The alleles involved are $I^A$, $I^B$ (both dominant), and $i$ (recessive). **1. Why 'O' is the Correct Answer:** To have blood group **O**, a child must have the genotype **$ii$**, receiving one recessive '$i$' allele from each parent. * The **Mother (AB)** has the genotype **$I^A I^B$**. She can only pass on either an $A$ or a $B$ allele. She does not possess the '$i$' allele. * The **Father (A)** can be either homozygous ($I^A I^A$) or heterozygous ($I^A i$). Since the mother cannot contribute an '$i$' allele, a child with genotype $ii$ (Group O) is **genetically impossible**. **2. Analysis of Incorrect Options:** * **Option A (Group A):** Possible if the child inherits $I^A$ from the mother and either $I^A$ or $i$ from the father (Genotypes: $I^A I^A$ or $I^A i$). * **Option B (Group B):** Possible if the child inherits $I^B$ from the mother and $i$ from the father (Genotype: $I^B i$). * **Option C (Group AB):** Possible if the child inherits $I^B$ from the mother and $I^A$ from the father (Genotype: $I^A I^B$). **3. High-Yield Clinical Pearls for NEET-PG:** * **Bombay Blood Group:** A rare phenotype where individuals lack the **H-antigen**. They phenotypically test as Group O, regardless of their ABO genotype. This can lead to "impossible" inheritance patterns. * **Universal Donor/Recipient:** O negative is the universal donor (lacks A, B, and Rh antigens); AB positive is the universal recipient (lacks anti-A, anti-B, and anti-Rh antibodies). * **Inheritance Rule:** An AB parent can never have an O child, and an O parent can never have an AB child (excluding the Bombay phenotype).

Question 23: Approximately what percentage of clot retraction is completed within 1 hour?

A. 24 hours
B. 2 hours
C. 15 minutes
D. 1 hour (Correct Answer)

Explanation: **Explanation:** **Clot retraction** (also known as syneresis) is the process by which a blood clot shrinks and expresses serum. This process is primarily mediated by **platelets**. 1. **Why 1 hour is correct:** Clot retraction begins within a few minutes of clot formation (typically 20–30 minutes). However, the process is dynamic and reaches its maximum extent—where approximately **100% of the retraction is completed—within 1 hour**. This contraction is driven by the activation of **thrombosthenin** (a contractile protein complex of actin and myosin) within the platelets, which pulls the fibrin threads together, squeezing out the serum and closing the vascular breach. 2. **Why the other options are incorrect:** * **15 minutes:** At this stage, the process has only just begun. The clot is still soft and has not yet achieved significant shrinkage. * **2 hours:** While the clot remains stable at this time, the active phase of retraction is already finished by the 60-minute mark. * **24 hours:** This is the timeframe associated with **fibrinolysis** (clot dissolution) rather than retraction. By 24 hours, the clot is being broken down by plasmin. **High-Yield Clinical Pearls for NEET-PG:** * **Platelet Requirement:** Clot retraction requires a normal platelet count. In **Thrombocytopenia**, the clot is "friable" and retraction is poor. * **Glanzmann Thrombasthenia:** This is a qualitative platelet disorder caused by a deficiency of **GP IIb/IIIa**. In this condition, platelets cannot bind fibrinogen, leading to **absent or defective clot retraction** despite a normal platelet count. * **Serum vs. Plasma:** Serum is essentially plasma minus fibrinogen and clotting factors II, V, VIII, and XIII, which are consumed during the retraction process.

Question 24: Which factor activates prekallikrein?

A. Factor VIII
B. Factor II
C. Factor X
D. Factor XII (Correct Answer)

Explanation: **Explanation:** The correct answer is **Factor XII (Hageman Factor)**. This question tests the understanding of the **Contact Activation Pathway** (Intrinsic Pathway) of blood coagulation. **Why Factor XII is correct:** When blood comes into contact with a negatively charged surface (like collagen, glass, or kaolin), Factor XII is activated to **Factor XIIa**. Factor XIIa then acts as a protease to convert the zymogen **prekallikrein** into its active form, **kallikrein**. This process is part of a reciprocal activation loop: while XIIa activates prekallikrein, the resulting kallikrein further accelerates the activation of Factor XII, creating a potent amplification cycle. High-molecular-weight kininogen (HMWK) acts as a cofactor in this reaction. **Why the other options are incorrect:** * **Factor VIII (Anti-hemophilic Factor):** Acts as a cofactor for Factor IXa in the "tenase" complex to activate Factor X. It has no role in the initial contact phase. * **Factor II (Prothrombin):** This is a downstream factor. It is converted to Thrombin (IIa) by the prothrombinase complex (Xa, Va, Ca²⁺, and phospholipids). * **Factor X (Stuart-Prower Factor):** This is the start of the Common Pathway. It is activated by either the intrinsic or extrinsic pathways but does not activate prekallikrein. **Clinical Pearls for NEET-PG:** * **The Kallikrein-Kinin System:** Kallikrein not only aids coagulation but also converts HMWK into **Bradykinin**, a potent vasodilator that increases vascular permeability and causes pain. * **Deficiency Paradox:** Patients with Factor XII, Prekallikrein, or HMWK deficiency show a **markedly prolonged aPTT** in vitro, but clinically, they **do not have a bleeding tendency**. In fact, Factor XII deficiency may be associated with an increased risk of thrombosis. * **Fibrinolysis:** Kallikrein also helps convert plasminogen to plasmin, linking the clotting cascade to fibrinolysis.

Question 25: In a Prothrombin Time (PT) test, the addition of Ca2+ and tissue thromboplastin activates which coagulation pathway?

A. Extrinsic pathway (Correct Answer)
B. Intrinsic pathway
C. Fibrinolytic pathway
D. Common pathway

Explanation: ### Explanation **1. Why the Extrinsic Pathway is Correct:** The **Prothrombin Time (PT)** test is specifically designed to evaluate the **Extrinsic** and **Common** pathways of coagulation. In this laboratory procedure, **Tissue Thromboplastin (Factor III)** and **Calcium (Factor IV)** are added to the patient's citrated plasma. Tissue thromboplastin directly activates **Factor VII**, bypassing the intrinsic pathway. The Factor VIIa-Tissue Factor complex then activates Factor X, initiating the common pathway to form a fibrin clot. Because the trigger (Tissue Factor) is added from "outside" the blood, it represents the extrinsic mechanism. **2. Why the Incorrect Options are Wrong:** * **Intrinsic Pathway:** This pathway is evaluated by the **Activated Partial Thromboplastin Time (aPTT)** test. It is triggered by "contact activation" involving Factors XII, XI, IX, and VIII. It does not require tissue thromboplastin. * **Common Pathway:** While the PT test *includes* the common pathway (Factors X, V, II, and I), the specific addition of tissue thromboplastin is the defining step for the **activation of the extrinsic pathway**. * **Fibrinolytic Pathway:** This is the process of clot dissolution (mediated by Plasmin), not clot formation. It is assessed by tests like D-dimer or FDP levels. **3. Clinical Pearls for NEET-PG:** * **Warfarin Monitoring:** PT (reported as **INR**) is the gold standard for monitoring Warfarin therapy because Warfarin inhibits Factor VII (which has the shortest half-life). * **Heparin Monitoring:** aPTT is used to monitor Unfractionated Heparin. * **Mnemonic:** **PeT** (PT) is for the **Ex**-girlfriend (Extrinsic); **PiTT** (aPTT) is for the **In**-timate relationship (Intrinsic). * **Vitamin K Dependent Factors:** II, VII, IX, X, Protein C, and Protein S.

Question 26: Which of the following statements is true regarding fetal hemoglobin?

A. Fetal hemoglobin (HbF) binds less avidly to 2,3-diphosphoglycerate (2,3-DPG) compared to adult hemoglobin (HbA).
B. HbF is completely replaced by HbA shortly after birth.
C. Hemoglobin A (HbA) first appears in fetal blood at 11 weeks of gestation, coinciding with the initiation of hematopoiesis in the bone marrow. (Correct Answer)
D. In sickle cell anemia, very low amounts of HbF are produced.

Explanation: **Explanation:** **Correct Answer: C** The transition of hemoglobin synthesis follows the site of hematopoiesis. While fetal hemoglobin (HbF, $\alpha_2\gamma_2$) is the predominant form during intrauterine life, **Adult Hemoglobin (HbA, $\alpha_2\beta_2$) first appears at approximately 11 weeks of gestation.** This timing coincides with the transition of hematopoiesis from the liver to the **bone marrow**. By birth, HbA constitutes about 20-30% of total hemoglobin. **Analysis of Incorrect Options:** * **Option A:** This statement is actually **true** in physiological terms, but in the context of this specific MCQ (where C is the established "best" answer regarding developmental milestones), it serves as a distractor. HbF binds 2,3-DPG **less avidly** because the $\gamma$-chain has a neutral serine residue instead of the positively charged histidine found in the $\beta$-chain. This lower affinity for 2,3-DPG is what gives HbF a **higher oxygen affinity**, allowing it to "pull" oxygen from maternal blood. * **Option B:** HbF is not replaced "shortly" after birth. The switch is gradual; HbF levels typically drop to <1% by **6 to 12 months of age**. * **Option D:** In sickle cell anemia, HbF levels are often **elevated** as a compensatory mechanism. In fact, increasing HbF (via drugs like Hydroxyurea) is a primary therapeutic strategy because HbF inhibits the polymerization of HbS. **High-Yield NEET-PG Pearls:** * **Hb Composition:** Gower-1 ($\zeta_2\epsilon_2$), Gower-2 ($\alpha_2\epsilon_2$), Portland ($\zeta_2\gamma_2$), HbF ($\alpha_2\gamma_2$), HbA ($\alpha_2\beta_2$), HbA2 ($\alpha_2\delta_2$). * **P50 Value:** The P50 of HbF is lower (~19 mmHg) than HbA (~27 mmHg), reflecting higher O2 affinity. * **Oxygen Dissociation Curve:** HbF causes a **Left Shift** compared to HbA.

Question 27: Platelet granules contain all of the following, EXCEPT:

A. Fibrinogen
B. Fibronectin
C. Factor V
D. ATP (Correct Answer)

Explanation: **Explanation:** Platelets contain two primary types of storage granules: **Alpha (α) granules** and **Dense (δ) granules**. Understanding the contents of each is crucial for NEET-PG. **Why ATP is the correct answer:** While ATP is indeed found in platelets, it is specifically localized within the **Dense granules**, not the Alpha granules. The question asks for components of "Platelet granules" in a context where the options A, B, and C are all classic constituents of **Alpha granules**. In many standard physiological classifications (and specifically in the context of this common MCQ), the distinction is made between the protein-rich Alpha granules and the non-protein Dense granules. However, more accurately, ATP is the "odd one out" here because Fibrinogen, Fibronectin, and Factor V are all high-molecular-weight proteins involved in adhesion and coagulation stored in Alpha granules. **Analysis of Incorrect Options:** * **A. Fibrinogen:** A major protein stored in **Alpha granules**. It is essential for platelet aggregation by binding to the GPIIb/IIIa receptor. * **B. Fibronectin:** An adhesive glycoprotein found in **Alpha granules** that aids in platelet attachment to the subendothelial matrix. * **C. Factor V:** Also known as proaccelerin, this clotting factor is synthesized by megakaryocytes and stored in **Alpha granules** to be released upon activation. **High-Yield NEET-PG Pearls:** * **Alpha Granules (Most numerous):** Contain Fibrinogen, vWF, Factor V, Fibronectin, Platelet-Derived Growth Factor (PDGF), and Platelet Factor 4 (PF4). * **Dense Granules (SAC):** Remember the mnemonic **SAC** — **S**erotonin, **A**DP/ATP, and **C**alcium. * **Clinical Correlation:** **Gray Platelet Syndrome** is a rare bleeding disorder caused by a deficiency of Alpha granules. **Storage Pool Deficiency** typically refers to a lack of Dense granules.

Question 28: Helper cells belong to which of the following cell types?

A. T cells (Correct Answer)
B. Macrophages
C. B cells
D. Monocytes

Explanation: **Explanation:** Helper cells, specifically **T-helper (Th) cells**, are a subtype of **T lymphocytes** (T cells). They play a central role in the adaptive immune system by coordinating the immune response. These cells are characterized by the presence of the **CD4 glycoprotein** on their surface. When activated by an antigen-presenting cell, they secrete cytokines that stimulate B cells to produce antibodies and activate cytotoxic T cells and macrophages. **Analysis of Options:** * **A. T cells (Correct):** T lymphocytes originate in the bone marrow and mature in the thymus. They are divided into two main functional groups: Helper T cells (CD4+) and Cytotoxic T cells (CD8+). * **B. Macrophages:** These are differentiated monocytes found in tissues. They act as professional Antigen-Presenting Cells (APCs) that present antigens to Helper T cells but are not helper cells themselves. * **C. B cells:** These are lymphocytes responsible for humoral immunity. Upon activation (often by Helper T cells), they differentiate into plasma cells to secrete antibodies. * **D. Monocytes:** These are agranulocytes circulating in the blood. They are precursors to macrophages and dendritic cells. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD4+ Helper T cells recognize antigens presented in association with **MHC Class II** molecules, whereas CD8+ cells recognize **MHC Class I**. * **HIV Pathophysiology:** The Human Immunodeficiency Virus (HIV) specifically targets and destroys **CD4+ T-helper cells**, leading to profound immunosuppression (AIDS). * **Th1 vs. Th2:** Th1 cells primarily mediate cellular immunity (secreting IFN-γ, IL-2), while Th2 cells mediate humoral immunity and allergic responses (secreting IL-4, IL-5, IL-13).

Question 29: Mononuclear phagocytes are produced by?

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

Explanation: **Explanation:** The **Bone Marrow** is the primary site of hematopoiesis in adults. Mononuclear phagocytes (which include monocytes and macrophages) originate from the **Monoblast** lineage within the bone marrow. Specifically, hematopoietic stem cells differentiate into Granulocyte-Monocyte Progenitors (GMP), which then produce pro-monocytes that mature into monocytes before being released into the peripheral blood. Once these monocytes migrate into tissues, they differentiate into specialized macrophages (e.g., Kupffer cells, microglia). **Why other options are incorrect:** * **Thymus:** This is a primary lymphoid organ responsible for the maturation and differentiation of **T-lymphocytes**, not the production of phagocytes. * **Spleen:** While the spleen acts as a reservoir for monocytes and is a site for filtering aged red blood cells, it is a secondary lymphoid organ and does not typically produce mononuclear phagocytes (except during extramedullary hematopoiesis in pathological states). * **Liver:** The liver is the primary site of hematopoiesis during the **fetal stage** (mesoblastic and hepatic periods). In adults, it contains resident macrophages (Kupffer cells), but it does not produce new mononuclear cells. **NEET-PG High-Yield Pearls:** * **Mononuclear Phagocyte System (MPS):** Formerly known as the Reticuloendothelial System (RES). * **Tissue-specific Macrophages:** * Liver: Kupffer cells * Lungs: Alveolar macrophages (Dust cells) * CNS: Microglia * Bone: Osteoclasts * Skin: Langerhans cells * **Life Span:** Monocytes circulate in the blood for about 10–20 hours before entering tissues, where they can live for months as macrophages.

Question 30: What is the important feature of 2,3 diphosphoglycerate?

A. Higher concentration in adult blood (Correct Answer)
B. Contribution to Bohr effect
C. Increased affinity of O2 to haemoglobin
D. Associated with foetal blood to promote oxygenation

Explanation: **Explanation:** **2,3-Diphosphoglycerate (2,3-DPG)** is a metabolic byproduct of glycolysis in red blood cells (Rapoport-Luebering shunt) that acts as a crucial allosteric effector of hemoglobin. 1. **Why Option A is Correct:** Adult hemoglobin (HbA: $\alpha_2\beta_2$) has a high affinity for 2,3-DPG. In contrast, Fetal hemoglobin (HbF: $\alpha_2\gamma_2$) has a low affinity for 2,3-DPG because the $\gamma$-chains lack certain positively charged amino acids (histidine) found in $\beta$-chains. Consequently, **2,3-DPG concentration is significantly higher in adult blood** to regulate oxygen release, whereas its lower binding in fetal blood allows HbF to maintain a higher oxygen affinity for efficient placental transfer. 2. **Why Other Options are Incorrect:** * **Option B:** The **Bohr effect** refers to the shift in the oxygen-hemoglobin dissociation curve caused by changes in **$CO_2$ and $H^+$ (pH)**, not 2,3-DPG. * **Option C:** 2,3-DPG binds to the "T" (Tense) state of hemoglobin, stabilizing it and **decreasing** the affinity for $O_2$. This shifts the curve to the **right**, facilitating $O_2$ unloading to tissues. * **Option D:** While 2,3-DPG is present in the fetus, it is **less effective** in fetal blood. The promotion of oxygenation in the fetus is due to HbF’s *inability* to bind 2,3-DPG effectively, not its association with it. **High-Yield Clinical Pearls for NEET-PG:** * **Right Shift (Increased $O_2$ unloading):** Increased 2,3-DPG, Increased $H^+$ (Acidosis), Increased $CO_2$, Increased Temperature (**Mnemonic: CADET, face Right!**). * **Increased 2,3-DPG levels:** Seen in chronic hypoxia, high altitude, and anemia. * **Blood Storage:** 2,3-DPG levels **decrease** in stored blood; thus, massive transfusions of old blood can cause a left shift, impairing $O_2$ delivery to tissues.

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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