Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 191: The spleen contains about _________% of the total blood volume?

A. 1
B. 2 (Correct Answer)
C. 5
D. 7

Explanation: **Explanation:** The spleen serves as a significant reservoir for blood, particularly in animals, though this function is less pronounced in healthy humans. In a resting adult, the spleen contains approximately **100–150 mL of blood**, which constitutes about **2% of the total blood volume** (based on an average total blood volume of 5 liters). **Why Option B is correct:** The splenic pulp contains large venous sinuses and a porous parenchyma. While the spleen is primarily known for filtering aged red blood cells, it stores roughly 2% of the total circulating blood volume. During physiological stress, such as severe exercise or hemorrhage, the splenic capsule can contract (mediated by sympathetic stimulation), discharging this stored blood into the general circulation to improve oxygen delivery. **Why other options are incorrect:** * **Option A (1%):** This value is too low; the physiological storage capacity of the spleen exceeds this amount. * **Option C (5%) & D (7%):** These values are overestimations for the spleen. However, 5–7% is more representative of the blood volume found in the **heart** or the **pulmonary circulation** at any given time. **High-Yield NEET-PG Pearls:** * **Platelet Reservoir:** While the spleen holds only 2% of total blood, it sequesters approximately **1/3rd (33%) of the body's total platelets**. This is why splenomegaly leads to thrombocytopenia (sequestration) and splenectomy leads to transient thrombocytosis. * **Pitting and Culling:** The spleen removes inclusions from RBCs (pitting) and destroys aged/abnormal RBCs (culling). * **Erythropoiesis:** The spleen is a site of hematopoiesis during the **fetal period** (months 3–7), but this ceases after birth unless pathological extramedullary hematopoiesis occurs.

Question 192: In anemia, what is the concentration of 2,3-DPG?

A. Decreased
B. Increased (Correct Answer)
C. Either decreased or increased
D. Unchanged

Explanation: **Explanation:** In anemia, the oxygen-carrying capacity of the blood is reduced due to a decrease in hemoglobin concentration. To compensate for this hypoxia, the body increases the production of **2,3-Bisphosphoglycerate (2,3-DPG)** within red blood cells. 2,3-DPG binds to the beta chains of deoxyhemoglobin, stabilizing the "T" (Tense) state. This reduces the affinity of hemoglobin for oxygen, causing a **rightward shift of the Oxygen-Dissociation Curve (ODC)**. This shift facilitates the unloading of oxygen from hemoglobin to the peripheral tissues, helping to maintain tissue oxygenation despite lower hemoglobin levels. **Analysis of Options:** * **Option B (Correct):** Increased levels of 2,3-DPG are a primary compensatory mechanism in chronic anemia, high altitude, and chronic obstructive pulmonary disease (COPD). * **Option A (Incorrect):** Decreased 2,3-DPG levels would shift the ODC to the left, increasing oxygen affinity and worsening tissue hypoxia in anemic patients. This occurs in conditions like septic shock or stored blood transfusion. * **Options C & D (Incorrect):** 2,3-DPG levels are physiologically regulated; they do not remain unchanged or fluctuate randomly during anemic stress. **High-Yield Clinical Pearls for NEET-PG:** * **Right Shift (CADET, face Right!):** **C**O2 increase, **A**cidosis (H+), **D**PG increase, **E**xercise, **T**emperature increase. * **Stored Blood:** 2,3-DPG levels **decrease** in stored blood over time. Massive transfusion of old blood can lead to impaired oxygen delivery to tissues. * **Fetal Hemoglobin (HbF):** HbF has a **lower affinity** for 2,3-DPG (due to gamma chains instead of beta), resulting in a leftward shift compared to adult HbA, allowing the fetus to pull oxygen from maternal blood.

Question 193: Th2 helper T cells function in which type of immunity?

A. Cellular immunity
B. Humoral immunity (Correct Answer)
C. Inducing cellular immunity by activation of cytotoxic T cells
D. Both humoral and cell-mediated immunity

Explanation: ### Explanation **Correct Option: B. Humoral immunity** The primary function of **Th2 (T-helper 2) cells** is to mediate **humoral immunity** by stimulating B-lymphocytes. When a naive CD4+ T cell encounters an antigen presented by an APC (Antigen Presenting Cell) in the presence of **Interleukin-4 (IL-4)**, it differentiates into a Th2 cell. Th2 cells secrete a specific profile of cytokines: * **IL-4:** Induces B-cell antibody class switching to **IgE**. * **IL-5:** Activates **eosinophils** (crucial for anti-helminthic responses). * **IL-13:** Stimulates mucus secretion and IgE production. * **IL-10:** An anti-inflammatory cytokine that inhibits Th1 responses. **Analysis of Incorrect Options:** * **A & C:** **Cellular immunity** and the activation of **cytotoxic T cells (CD8+)** are the primary domains of **Th1 cells**. Th1 cells secrete IFN-γ and IL-2, which activate macrophages and CD8+ cells to fight intracellular pathogens (e.g., *M. tuberculosis*). * **D:** While the immune system is integrated, Th2 cells are functionally specialized for humoral responses. The "Th1/Th2 balance" dictates the direction of the immune response; Th2 does not drive cell-mediated immunity. --- ### High-Yield Clinical Pearls for NEET-PG * **Cytokine Mnemonic:** "Hot T-Bone stEAk" * IL-**1**: **Hot** (Fever) * IL-**2**: Stimulates **T** cells * IL-**3**: **Bone** marrow stimulation * IL-**4**: Ig**E** stimulation (Th2) * IL-**5**: Ig**A** stimulation & Eosinophils (Th2) * **Leprosy Link:** Tuberculoid leprosy involves a **Th1** response (contained), whereas Lepromatous leprosy involves a **Th2** response (disseminated/poor prognosis). * **Atopy:** Overactivity of Th2 cells is the underlying pathophysiology in asthma, hay fever, and atopic dermatitis.

Question 194: During homeostasis, how do platelets affect the coagulation process?

A. Platelet adhesion to exposed endothelium
B. Clot retraction
C. Activation of prothrombinase complex
D. All of the above (Correct Answer)

Explanation: Platelets are central to the process of hemostasis, acting as both a physical plug and a biochemical catalyst for the coagulation cascade. **Explanation of the Correct Answer:** The correct answer is **D (All of the above)** because platelets contribute to every phase of clot formation and stabilization: 1. **Platelet Adhesion (Option A):** When a vessel is injured, platelets adhere to the subendothelial collagen via **von Willebrand Factor (vWF)** and GP Ib/IX/V receptors. This is the initiating step of the primary hemostatic plug. 2. **Activation of Prothrombinase Complex (Option C):** Activated platelets flip their membrane phospholipids to expose **Phosphatidylserine**. This provides a catalytic surface for the assembly of the "Prothrombinase complex" (Factors Xa, Va, and $Ca^{2+}$), which accelerates the conversion of prothrombin to thrombin by 100,000-fold. 3. **Clot Retraction (Option B):** Once the fibrin mesh is formed, the **thrombosthenin** (actin and myosin) within platelets contracts. This pulls the edges of the injured vessel together and squeezes out serum, making the clot smaller and more stable. **Why other options are not "wrong" but incomplete:** Options A, B, and C are all physiological functions of platelets. Since all three contribute significantly to the overall process of hemostasis and coagulation, "All of the above" is the most comprehensive choice. **High-Yield Clinical Pearls for NEET-PG:** * **Bernard-Soulier Syndrome:** Deficiency of GP Ib (defect in adhesion). * **Glanzmann Thrombasthenia:** Deficiency of GP IIb/IIIa (defect in aggregation). * **Platelet Factor 3 (PF3):** The phospholipid surface provided by platelets essential for the intrinsic and common pathways. * **Aspirin:** Irreversibly inhibits COX-1, preventing the synthesis of **Thromboxane A2 (TXA2)**, a potent platelet aggregator.

Question 195: Which of the following is also known as Factor X?

A. Hageman factor
B. Stuart-Prower factor (Correct Answer)
C. Christmas factor
D. Tissue factor

Explanation: **Explanation:** Coagulation factors are proteins in the blood that control bleeding through a complex cascade. **Factor X (Stuart-Prower factor)** is a critical high-yield component of this cascade because it marks the beginning of the **Common Pathway**. It is a serine protease that, once activated (Xa), complexes with Factor Va, calcium, and phospholipids to form the *prothrombinase complex*, which converts prothrombin to thrombin. **Analysis of Options:** * **Stuart-Prower factor (Factor X):** Named after the two patients (Mr. Stuart and Miss Prower) in whom the deficiency was first described. It is vitamin K-dependent and synthesized in the liver. * **Hageman factor (Factor XII):** This is the first factor of the **Intrinsic Pathway**. It is activated by contact with negatively charged surfaces like collagen or glass. * **Christmas factor (Factor IX):** A vitamin K-dependent factor in the intrinsic pathway. Its deficiency leads to **Hemophilia B** (Christmas disease). * **Tissue factor (Factor III):** Also known as thromboplastin, it is the primary initiator of the **Extrinsic Pathway** following vascular injury. **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin K-dependent factors:** II, VII, IX, and X (Mnemonic: "1972"). * **Common Pathway Factors:** X, V, II (Prothrombin), and I (Fibrinogen). * **Lab Correlation:** Factor X activity is assessed by both PT (Prothrombin Time) and aPTT (activated Partial Thromboplastin Time) because it sits at the junction of both pathways. * **Direct Factor Xa Inhibitors:** Drugs like **Rivaroxaban** and **Apixaban** are increasingly tested as modern anticoagulants.

Question 196: Which antigen is lacking in an Rh-negative person?

A. C
B. D (Correct Answer)
C. d
D. E

Explanation: **Explanation:** The Rh blood group system is the second most important system in transfusion medicine. It is based on the presence or absence of specific proteins (antigens) on the surface of red blood cells. **Why Option B is Correct:** The Rh status of an individual (Rh-positive or Rh-negative) is determined specifically by the presence or absence of the **D antigen**. The D antigen is the most immunogenic of all non-ABO antigens. Therefore, an **Rh-negative** person is defined by the complete absence of the D antigen on their erythrocyte membrane. **Analysis of Incorrect Options:** * **Options A and D (C and E):** These are other major antigens within the Rh system (C, c, E, e). While they are part of the Fisher-Race nomenclature, they do not determine whether a person is clinically classified as "Rh-positive" or "Rh-negative." * **Option C (d):** In medical genetics, "d" is a notation used to indicate the **absence** of the D antigen. There is no actual "d antigen" or "d protein." It is a hypothetical designation used to denote the D-negative phenotype. **High-Yield Clinical Pearls for NEET-PG:** * **Immunogenicity:** The D antigen is highly antigenic. If an Rh-negative individual is exposed to Rh-positive blood (via transfusion or pregnancy), they will develop anti-D antibodies (isoimmunization). * **Erythroblastosis Fetalis:** This occurs when an Rh-negative mother carries an Rh-positive fetus. The mother’s anti-D antibodies (IgG) cross the placenta and attack fetal RBCs. * **Prophylaxis:** Anti-D immunoglobulin (RhoGAM) is administered to Rh-negative mothers to prevent sensitization. * **Inheritance:** The Rh system is governed by two closely linked genes on **Chromosome 1**: *RHD* and *RHCE*.

Question 197: Which type of haemoglobin is alkali resistant?

A. HbA
B. HbA2
C. HbS
D. HbF (Correct Answer)

Explanation: **Explanation:** The correct answer is **HbF (Fetal Haemoglobin)**. **Why HbF is Alkali Resistant:** The resistance of haemoglobin to denaturation by strong alkaline solutions (like Potassium Hydroxide) is known as the **Singer’s Alkali Denaturation Test**. HbF is uniquely resistant to alkali because of its structural composition, specifically the presence of **gamma ($\gamma$) chains**. In an alkaline medium, adult haemoglobin (HbA) denatures and precipitates rapidly, whereas HbF remains stable. This property is clinically utilized to detect the presence of fetal blood in maternal circulation or to diagnose conditions like Thalassemia where HbF levels are elevated. **Analysis of Incorrect Options:** * **HbA ($\alpha_2\beta_2$):** This is the major adult haemoglobin. It is highly sensitive to alkali and denatures within 1–2 minutes when exposed to a high pH. * **HbA2 ($\alpha_2\delta_2$):** A minor adult haemoglobin (normal <3.5%). Like HbA, it lacks gamma chains and is not alkali-resistant. * **HbS:** This is the variant found in Sickle Cell Anemia (glutamate replaced by valine at the 6th position of the $\beta$ chain). It is also sensitive to alkali denaturation. **High-Yield NEET-PG Pearls:** * **Structure:** HbF consists of two alpha ($\alpha$) and two gamma ($\gamma$) chains ($\alpha_2\gamma_2$). * **Oxygen Affinity:** HbF has a **higher affinity for oxygen** than HbA because it binds poorly to 2,3-BPG. This allows the fetus to extract oxygen from maternal blood. * **Apt Test:** A clinical test used to differentiate fetal blood from maternal blood in neonatal gastric aspirate or vaginal bleeding, based on HbF’s alkali resistance. * **Switch:** The transition from HbF to HbA begins at 30 weeks of gestation and is usually complete by 6 months of age.

Question 198: What is the term for an increase in the number of red blood cells?

A. Neutropenia
B. Leukemia
C. Polycythemia (Correct Answer)
D. Anemia

Explanation: **Explanation:** **Correct Answer: C. Polycythemia** Polycythemia refers to an absolute or relative increase in the red blood cell (RBC) mass, typically manifested by an elevated hemoglobin level, hematocrit, or RBC count. It is broadly classified into **Primary Polycythemia** (e.g., Polycythemia Vera, a myeloproliferative neoplasm caused by a JAK2 mutation) and **Secondary Polycythemia** (driven by increased Erythropoietin due to chronic hypoxia, such as in high altitudes or COPD). **Analysis of Incorrect Options:** * **A. Neutropenia:** This refers to an abnormally low count of neutrophils (a type of white blood cell), which increases the risk of bacterial infections. * **B. Leukemia:** This is a group of blood cancers characterized by the malignant transformation and rapid proliferation of abnormal white blood cells in the bone marrow. * **D. Anemia:** This is the functional opposite of polycythemia, defined as a decrease in the total amount of RBCs or hemoglobin in the blood, leading to reduced oxygen-carrying capacity. **High-Yield Clinical Pearls for NEET-PG:** * **Polycythemia Vera (PV):** Characterized by "Panmyelosis" (increase in all three cell lines: RBCs, WBCs, and Platelets). A classic symptom is **aquagenic pruritus** (itching after a warm bath). * **Erythropoietin (EPO) Levels:** EPO is **low** in Primary Polycythemia (due to negative feedback) but **high** in Secondary Polycythemia. * **Gaisböck Syndrome:** Also known as "Relative Polycythemia," where the RBC count appears high due to decreased plasma volume (e.g., dehydration or stress) rather than an actual increase in RBC production.

Question 199: The 'red reaction' in the triple response is due to which of the following mechanisms?

A. Local edema
B. Capillary dilation (Correct Answer)
C. Axon reflex
D. Decreased permeability of capillaries

Explanation: The **Triple Response of Lewis** is a physiological reaction of the skin to mechanical injury (like firm stroking). It consists of three distinct stages: the Red Reaction, the Flare, and the Wheal. ### 1. Why "Capillary Dilation" is Correct The **Red Reaction** is the first component of the triple response, appearing within 10 seconds. It is caused by the **dilation of precapillary sphincters and capillaries** in the immediate area of the stimulus. This localized vasodilation is mediated by the release of histamine and other autacoids from mast cells due to direct mechanical trauma. ### 2. Analysis of Incorrect Options * **A. Local Edema:** This describes the **Wheal**, the third stage of the response. It occurs due to increased capillary permeability leading to fluid exudation into the interstitial space. * **C. Axon Reflex:** This is the mechanism behind the **Flare** (the second stage). It involves an antidromic impulse traveling through sensory nerve fibers, causing widespread arteriolar dilation beyond the site of injury. * **D. Decreased permeability:** This is incorrect because the triple response involves an *increase* in permeability (leading to the wheal), not a decrease. ### 3. High-Yield Facts for NEET-PG * **Sequence:** Red Reaction (Capillary dilation) → Flare (Arteriolar dilation via Axon reflex) → Wheal (Increased permeability/Exudation). * **Mediator:** **Histamine** is the primary chemical mediator involved in all three stages. * **The Axon Reflex** is unique because it does not involve the CNS; it is a local peripheral nerve reflex. * **Clinical Correlation:** The triple response is exaggerated in **Dermatographism**, a form of physical urticaria.

Question 200: Erythropoietin levels are increased by:

A. Decreased PO2 (Correct Answer)
B. Decreased PCO2
C. Decreased Hb
D. Decreased pH

Explanation: **Explanation:** The primary stimulus for the production of **Erythropoietin (EPO)** is **renal tissue hypoxia** (low oxygen tension). **1. Why Decreased PO2 is Correct:** The kidneys (specifically the peritubular interstitial cells in the cortex) act as the body's "oxygen sensor." When the partial pressure of oxygen (**PO2**) in the blood decreases, it stabilizes a transcription factor called **Hypoxia-Inducible Factor-1α (HIF-1α)**. Under normal oxygen levels, HIF-1α is degraded; however, in hypoxia, it accumulates and travels to the nucleus to trigger the transcription of the EPO gene. This leads to increased RBC production to improve oxygen-carrying capacity. **2. Why Incorrect Options are Wrong:** * **Decreased PCO2:** Low carbon dioxide (hypocapnia) typically occurs during hyperventilation. It does not directly stimulate EPO; in fact, it causes respiratory alkalosis, which shifts the oxygen-dissociation curve to the left, potentially increasing hemoglobin's affinity for oxygen. * **Decreased Hb:** While anemia (low Hb) eventually leads to increased EPO, it is not the *direct* molecular trigger. It is the resulting **tissue hypoxia** (decreased oxygen delivery) caused by the low Hb that stimulates the kidneys. In the context of physiological triggers, decreased PO2 is the most fundamental stimulus. * **Decreased pH:** Acidosis (low pH) shifts the oxygen-dissociation curve to the right (Bohr effect), facilitating oxygen unloading to tissues. It does not serve as a primary stimulus for EPO synthesis. **High-Yield Facts for NEET-PG:** * **Site of Production:** 85-90% in the **peritubular interstitial cells of the kidney**; 10-15% in the **liver** (Kupffer cells and hepatocytes). * **Mechanism:** EPO acts via the **JAK-STAT pathway** on erythroid progenitor cells (CFU-E) in the bone marrow. * **Clinical Correlation:** Patients with Chronic Kidney Disease (CKD) develop normocytic normochromic anemia due to EPO deficiency, requiring recombinant human EPO therapy.

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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