Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 11: What is true about the Rh factor?

A. There are no natural anti-Rh antibodies in serum. (Correct Answer)
B. It is seen only in females.
C. Approximately 15% of Indians are Rh positive.
D. The D antigen is the least potent Rh antigen.

Explanation: ### Explanation **1. Why Option A is Correct:** Unlike the ABO system, where antibodies (isoagglutinins) develop spontaneously within the first few months of life, the Rh system has **no naturally occurring antibodies**. Anti-D antibodies are only produced after an Rh-negative individual is "sensitized"—either through a mismatched blood transfusion or during pregnancy with an Rh-positive fetus. This is a crucial distinction in transfusion medicine. **2. Analysis of Incorrect Options:** * **Option B:** The Rh factor is an inherited protein found on the surface of red blood cells. It is autosomal dominant and not sex-linked; therefore, it occurs in both males and females. * **Option C:** In the Indian population, approximately **93–95%** of individuals are Rh-positive. Only about 5–7% are Rh-negative. (In Caucasians, the Rh-negative prevalence is higher, around 15%). * **Option D:** The Rh system consists of several antigens (C, D, E, c, d, e). The **D antigen is the most potent** and highly immunogenic. Its presence or absence determines whether a person is classified as Rh-positive or Rh-negative. **3. Clinical Pearls for NEET-PG:** * **Erythroblastosis Fetalis:** Occurs when an Rh-negative mother carries an Rh-positive fetus. Sensitization usually happens during the first delivery, affecting subsequent pregnancies. * **Prophylaxis:** To prevent sensitization, **Anti-D (RhoGAM)** is administered to Rh-negative mothers at 28 weeks of gestation and within 72 hours of delivering an Rh-positive baby. * **Landsteiner & Wiener:** They discovered the Rh factor in 1940 using the blood of Rhesus monkeys. * **Fisher-Race Nomenclature:** Postulates that Rh antigens are determined by three pairs of closely linked genes (C/c, D/d, E/e).

Question 12: Low erythropoietin levels are seen in which of the following conditions?

A. Aplastic anemia
B. Renal failure (Correct Answer)
C. Obesity
D. Hepatoma

Explanation: **Explanation:** **Correct Answer: B. Renal failure** **Underlying Concept:** Erythropoietin (EPO) is a glycoprotein hormone essential for erythropoiesis. In adults, approximately **90% of EPO is produced by the peritubular interstitial cells of the renal cortex**, while the remaining 10% is produced by the liver. In **Chronic Kidney Disease (CKD) or Renal Failure**, the destruction of these functional renal tissues leads to a primary deficiency of EPO. This results in normocytic normochromic anemia, which is a hallmark of renal failure. **Analysis of Incorrect Options:** * **A. Aplastic Anemia:** In this condition, the bone marrow fails to produce RBCs. Since the kidneys are functional and detect low oxygen delivery (hypoxia) due to anemia, they compensate by **increasing** EPO production. * **C. Obesity:** Obesity is not typically associated with low EPO levels. However, it is linked to increased hepcidin (due to chronic inflammation), which affects iron metabolism rather than EPO production. * **D. Hepatoma:** Certain tumors, such as Hepatocellular carcinoma (Hepatoma) and Renal Cell Carcinoma, can produce EPO ectopically. This leads to **elevated** EPO levels and secondary polycythemia. **High-Yield Clinical Pearls for NEET-PG:** * **Stimulus for EPO:** The primary stimulus for EPO secretion is **hypoxia** (detected by Hypoxia-Inducible Factor - HIF-1α), not the number of RBCs. * **Site of Action:** EPO acts on the **CFU-E (Colony Forming Unit-Erythroid)** progenitors in the bone marrow. * **Clinical Use:** Recombinant human EPO (Epoetin alfa) is used to treat anemia in CKD and chemotherapy patients. * **Other conditions with high EPO:** High altitude, COPD, and Cyanotic heart disease (due to physiological compensation for hypoxia).

Question 13: Which cell does not differentiate in the bone marrow?

A. B lymphocyte
B. T lymphocyte (Correct Answer)
C. Neutrophil
D. Basophil

Explanation: ### Explanation The correct answer is **B. T lymphocyte**. **1. Why T lymphocytes are the correct answer:** All blood cells originate from **Pluripotent Hematopoietic Stem Cells (PHSCs)** in the bone marrow. However, while T lymphocytes are *produced* in the bone marrow, they do not *differentiate* or mature there. Instead, pro-T cells migrate via the bloodstream to the **Thymus**. In the thymus, they undergo "thymic education," where they differentiate into mature T cells (CD4+ or CD8+), develop self-tolerance, and acquire their T-cell receptors (TCR). **2. Why the other options are incorrect:** * **A. B lymphocyte:** Unlike T cells, B lymphocytes undergo both production and maturation/differentiation within the **Bone marrow** (hence the name "B" cell). They only leave for secondary lymphoid organs once they are mature. * **C & D. Neutrophils and Basophils:** These are granulocytes belonging to the myeloid lineage. Their entire process of myelopoiesis—from myeloblasts to mature segmented cells—occurs completely within the bone marrow before they are released into the peripheral circulation. **3. High-Yield Clinical Pearls for NEET-PG:** * **Primary Lymphoid Organs:** Bone marrow and Thymus (where lymphocytes are formed/matured). * **Secondary Lymphoid Organs:** Lymph nodes, Spleen, Peyer’s patches, and Tonsils (where immune responses occur). * **Thymic Involution:** The thymus is most active during childhood and begins to atrophy (replaced by fat) after puberty, though T-cell production continues at a lower rate. * **DiGeorge Syndrome:** A classic clinical correlation where the failure of the 3rd and 4th pharyngeal pouches to develop leads to thymic aplasia and a profound deficiency in mature T cells.

Question 14: Von Willebrand factor protects which factor from degradation?

A. Factor V
B. Factor VI
C. Factor VII
D. Factor VIII (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Factor VIII** **Mechanism and Concept:** Von Willebrand Factor (vWF) is a large multimeric glycoprotein synthesized by endothelial cells (stored in Weibel-Palade bodies) and megakaryocytes (stored in α-granules of platelets). In the circulation, vWF serves two primary functions: 1. **Platelet Adhesion:** It acts as a bridge between platelet surface receptors (GpIb) and exposed subendothelial collagen at the site of vascular injury. 2. **Carrier Protein for Factor VIII:** vWF forms a non-covalent complex with Factor VIII (FVIII). This binding is crucial because it **stabilizes Factor VIII**, protecting it from rapid proteolytic degradation by activated Protein C and Protein S. In the absence of vWF, the half-life of Factor VIII drops significantly (from ~12 hours to <2 hours), leading to secondary deficiency of FVIII. **Analysis of Incorrect Options:** * **Factor V:** This is a cofactor for Factor Xa in the prothrombinase complex. It is structurally similar to Factor VIII but does not require vWF for stabilization; it circulates freely or is stored in platelet α-granules. * **Factor VI:** This factor does not exist in the modern coagulation cascade (it was historically assigned to activated Factor V). * **Factor VII:** This is a vitamin K-dependent factor involved in the extrinsic pathway. It circulates independently and is activated by Tissue Factor. **NEET-PG High-Yield Pearls:** * **vWD vs. Hemophilia A:** Because vWF protects Factor VIII, patients with severe von Willebrand Disease (vWD) will often show a **prolonged aPTT** due to secondary Factor VIII deficiency. * **Ristocetin Cofactor Assay:** The gold standard test for vWF function; ristocetin induces vWF-mediated platelet agglutination. * **Treatment:** Desmopressin (DDAVP) is used in mild vWD and Hemophilia A because it triggers the release of vWF and Factor VIII from endothelial stores.

Question 15: Which is a pluripotent stem cell?

A. Embryonic stem cell (Correct Answer)
B. Tissue stem cell
C. Adult stem cell
D. Hematopoietic stem cell

Explanation: ### Explanation The classification of stem cells is based on their **potency**—the ability to differentiate into different cell types. **1. Why Embryonic Stem Cells (ESCs) are correct:** Embryonic stem cells are derived from the **inner cell mass of the blastocyst**. They are **pluripotent**, meaning they have the potential to differentiate into cells of all three germ layers: **ectoderm, mesoderm, and endoderm**. While they can form any cell in the human body (neurons, muscle, hepatocytes, etc.), they cannot form extra-embryonic tissues like the placenta. **2. Analysis of Incorrect Options:** * **B & C. Tissue/Adult Stem Cells:** These are synonymous. They are found in postnatal tissues (e.g., bone marrow, gut, brain) and are typically **multipotent**. Their differentiation potential is restricted to the lineage of the tissue they reside in. * **D. Hematopoietic Stem Cell (HSC):** HSCs are a specific type of adult/multipotent stem cell. They can differentiate into all blood cell lineages (RBCs, WBCs, platelets) but cannot naturally form non-hematopoietic tissues like nerve or muscle cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Totipotent Cells:** The zygote and early blastomeres (up to the 8-cell stage). These can form an entire organism, including the placenta. * **Pluripotent Cells:** Embryonic Stem Cells (ESCs) and Induced Pluripotent Stem Cells (iPSCs). * **Multipotent Cells:** Hematopoietic stem cells and Mesenchymal stem cells. * **Unipotent Cells:** Can only produce one cell type but have self-renewal properties (e.g., muscle satellite cells, epidermal basal cells). * **Hierarchy of Potency:** Totipotent > Pluripotent > Multipotent > Unipotent.

Question 16: The biconcave shape of RBC is due to the binding of spectrin to which protein?

A. Ankyrin (Correct Answer)
B. Actin
C. Myosin
D. Adducin

Explanation: **Explanation:** The biconcave shape of the Red Blood Cell (RBC) is critical for its flexibility and high surface-area-to-volume ratio, allowing it to deform through narrow capillaries. This shape is maintained by a complex sub-membranous cytoskeleton. **Why Ankyrin is Correct:** The primary structural framework of the RBC consists of **Spectrin** (alpha and beta chains). However, spectrin is not directly attached to the lipid bilayer. It is anchored to the cell membrane via a bridge protein called **Ankyrin**. Ankyrin binds to the beta-chain of spectrin and links it to the cytoplasmic domain of **Band 3** (an integral membrane protein). This Spectrin-Ankyrin-Band 3 complex is the "vertical" anchor that stabilizes the membrane; a defect here leads to loss of membrane surface area and the formation of spherocytes. **Analysis of Incorrect Options:** * **Actin:** While actin filaments bind to the distal ends of spectrin to form a "junctional complex," it facilitates horizontal stability rather than the primary vertical anchoring to the membrane. * **Myosin:** Though present in small amounts in the RBC cytoskeleton to assist in contractility, it is not the primary anchor for spectrin. * **Adducin:** This is a regulatory protein that promotes the binding of spectrin to actin at the junctional complex, but it does not link spectrin to the membrane. **Clinical Pearls for NEET-PG:** * **Hereditary Spherocytosis:** Most commonly caused by a deficiency or defect in **Ankyrin** (approx. 50% of cases), followed by Band 3 or Spectrin. * **Hereditary Elliptocytosis:** Usually results from defects in **Spectrin** (horizontal interactions) or Protein 4.1. * **Energy Requirement:** The biconcave shape is an active process requiring ATP; depleted ATP levels lead to an "Echinocyte" (spiculated) shape.

Question 17: What is the lifespan of fetal red blood cells?

A. Same as adult red blood cells
B. One-fourth of adult red blood cells
C. One-half of adult red blood cells
D. Two-thirds of adult red blood cells (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (Two-thirds of adult red blood cells)**. **1. Underlying Medical Concept:** The lifespan of a normal adult red blood cell (RBC) is approximately **120 days**. In contrast, fetal RBCs have a significantly shorter lifespan of approximately **80 to 90 days**. Mathematically, 80 days is roughly two-thirds of 120 days. This shorter survival is attributed to several physiological factors: * **Metabolic differences:** Fetal RBCs have lower levels of certain enzymes (like phosphofructokinase) and lower ATP concentrations. * **Oxidative stress:** They are more prone to oxidative damage. * **Membrane characteristics:** Fetal RBC membranes are less deformable, making them more susceptible to sequestration and destruction in the splenic circulation. **2. Analysis of Incorrect Options:** * **Option A (Same as adult):** Incorrect. Fetal RBCs are more fragile and metabolically distinct, leading to faster turnover. * **Option B (One-fourth):** Incorrect. This would imply a lifespan of only 30 days, which is seen in severe pathological states (like certain hemolytic anemias), not normal fetal physiology. * **Option C (One-half):** Incorrect. While 60 days is short, it underestimates the actual 80-90 day survival of full-term fetal RBCs. **3. NEET-PG High-Yield Pearls:** * **Neonatal Jaundice:** The shorter lifespan of fetal RBCs, combined with a higher total RBC mass (polycythemia) and an immature liver (low glucuronyl transferase activity), is the primary cause of **physiological jaundice** in newborns. * **Hemoglobin Shift:** Fetal hemoglobin (HbF: $\alpha_2\gamma_2$) has a higher affinity for oxygen than adult hemoglobin (HbA: $\alpha_2\beta_2$) because it binds poorly to 2,3-BPG. * **Preterm Infants:** The RBC lifespan is even shorter in premature neonates, often ranging from **35 to 50 days**.

Question 18: The Arneth count is used to quantify which of the following?

A. Lymphocytes
B. Lobes in neutrophils (Correct Answer)
C. Granules in eosinophils
D. White blood cells in bone marrow

Explanation: **Explanation:** The **Arneth count** (or Arneth index) is a hematological method used to evaluate the maturity of **neutrophils** by counting the number of **lobes in their nuclei**. Under normal conditions, a mature neutrophil typically has 2 to 5 lobes. As a neutrophil ages, the number of nuclear lobes increases. The Arneth count categorizes 100 neutrophils into five classes based on lobe count: * **Class I:** 1 lobe (immature/band forms) * **Class II:** 2 lobes * **Class III:** 3 lobes * **Class IV:** 4 lobes * **Class V:** 5 or more lobes (mature/older forms) **Analysis of Options:** * **Option A & C:** The Arneth count specifically assesses nuclear morphology, not the presence of granules (eosinophils) or the cell type (lymphocytes). * **Option D:** While bone marrow activity influences the count, the Arneth count is performed on a peripheral blood smear, not the marrow itself. **Clinical Pearls for NEET-PG:** 1. **Shift to the Left:** An increase in immature neutrophils (Class I & II). This occurs in **acute pyogenic infections**, where the bone marrow releases young cells rapidly to fight infection. 2. **Shift to the Right:** An increase in older neutrophils (Class IV & V). This is a classic finding in **Megaloblastic Anemia** (Vitamin B12 or Folate deficiency), characterized by **hypersegmented neutrophils** (more than 5 lobes). 3. **Cooke’s Criterion:** A similar classification used to identify hypersegmentation; if >5% of neutrophils have 5 lobes or any have 6 lobes, it is clinically significant.

Question 19: What is a major source of Von Willebrand factor (vWF)?

A. Erythrocytes
B. Neutrophils
C. Endothelial cells (Correct Answer)
D. Monocytes

Explanation: **Explanation:** **Von Willebrand factor (vWF)** is a large multimeric glycoprotein essential for primary hemostasis. It acts as a molecular bridge between the subendothelial collagen and platelets (via the GpIb receptor) and serves as a carrier protein for Factor VIII. **Why Endothelial Cells are the Correct Answer:** The primary sources of vWF are **vascular endothelial cells** and **megakaryocytes**. Within endothelial cells, vWF is synthesized and stored in specialized cigar-shaped organelles called **Weibel-Palade bodies**. When the endothelium is injured, these bodies release vWF into the subendothelium and plasma to initiate platelet adhesion. (Note: In megakaryocytes/platelets, vWF is stored in **alpha-granules**). **Analysis of Incorrect Options:** * **A. Erythrocytes:** Red blood cells are primarily involved in oxygen transport and do not synthesize or store clotting factors. * **B. Neutrophils:** These are granulocytes involved in innate immunity and phagocytosis; they do not produce vWF. * **D. Monocytes:** While they play a role in inflammation and can express Tissue Factor, they are not a source of vWF. **High-Yield Clinical Pearls for NEET-PG:** * **vWF Function:** It stabilizes **Factor VIII**; in Von Willebrand Disease (vWD), Factor VIII levels may be low, leading to a prolonged aPTT. * **Diagnostic Marker:** vWF is used as an immunohistochemical marker for vascular tumors (e.g., angiosarcoma). * **Desmopressin (DDAVP):** This drug is used in treatment as it stimulates the release of vWF from Weibel-Palade bodies. * **ADAMTS13:** This enzyme cleaves large vWF multimers; its deficiency leads to Thrombotic Thrombocytopenic Purpura (TTP).

Question 20: Histamine is mainly found within storage granules of mast cells, but it is also found in other tissues. Which of the following is a site where histamine is found?

A. Gastric mucosa (Correct Answer)
B. Oral mucosa
C. Inner epithelium
D. All of the above

Explanation: ### Explanation **1. Why Gastric Mucosa is Correct:** While histamine is primarily stored in the granules of **mast cells** and **basophils**, it is also synthesized and stored in non-mast cell sites. In the gastrointestinal tract, histamine is found in high concentrations within the **Enterochromaffin-like (ECL) cells** of the gastric mucosa. The underlying physiological concept is the **regulation of gastric acid secretion**. Gastrin, released from G-cells, stimulates ECL cells to release histamine. This histamine then acts via **H2 receptors** on neighboring parietal cells to stimulate the secretion of Hydrochloric acid (HCl). This paracrine function makes the gastric mucosa a major site of histamine localization outside the immune system. **2. Why Other Options are Incorrect:** * **Oral Mucosa & Inner Epithelium:** While these tissues contain mast cells (which house histamine), they are not considered primary "storage sites" or specialized producers of histamine in the same physiological capacity as the gastric mucosa. The question asks for a specific site where histamine is "found" as a characteristic feature of that tissue’s function. **3. NEET-PG High-Yield Pearls:** * **Synthesis:** Histamine is formed by the decarboxylation of the amino acid **L-histidine** by the enzyme *histidine decarboxylase*. * **Receptor Specificity:** * **H1:** Involved in allergy, bronchoconstriction, and vasodilation. * **H2:** Primarily involved in **gastric acid secretion**. * **H3:** Presynaptic autoreceptors in the CNS. * **Clinical Correlation:** **Proton Pump Inhibitors (PPIs)** and **H2-blockers** (like Ranitidine) are used to manage peptic ulcer disease by inhibiting the pathway initiated in the gastric mucosa. * **Other Sites:** Histamine is also found in the **hypothalamus**, where it functions as a neurotransmitter to maintain wakefulness.

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