Blood and Immunity Practice Questions

Q: What antibodies are present in an individual with blood group O?

Both Anti-A and Anti-B antibodies. ### Explanation **Concept Overview: Landsteiner’s Law** The presence of antibodies in the plasma is governed by **Landsteiner’s Law**, which states that if an agglutinogen (antigen) is absent on the red blood cell (RBC) membrane, the corresponding agglutinin (antibody) must be present in the plasma. In **Blood Group O**, the RBCs lack both Antigen A and Antigen B. According to Landsteiner’s Law, because both antigens are absent, the body produces antibodies against both. Therefore, the plasma contains **both Anti-A and Anti-B antibodies**. **Analysis of Options:** * **Option C (Correct):** Individuals with Group O have neither A nor B antigens, leading to the development of both Anti-A and Anti-B antibodies (predominantly of the IgG and IgM classes). * **Option A:** Anti-A only is found in individuals with **Blood Group B**. * **Option B:** Anti-B only is found in individuals with **Blood Group A**. * **Option D:** No antibodies are found in the plasma of individuals with **Blood Group AB**, as they possess both A and B antigens on their RBCs. **High-Yield Clinical Pearls for NEET-PG:** * **Universal Donor:** Group O is the universal donor because its RBCs lack A and B antigens, preventing a reaction with the recipient's antibodies. Specifically, **O Negative** is the preferred universal donor in emergencies. * **Antibody Nature:** Naturally occurring ABO antibodies are primarily **IgM** (cannot cross the placenta). However, in Group O individuals, Anti-A and Anti-B are often **IgG**, which can cross the placenta and cause Hemolytic Disease of the Newborn (HDN). * **H-Antigen:** Group O individuals have the maximum amount of **H-substance**, which is the precursor for A and B antigens. The rare **Bombay Phenotype** lacks even the H-antigen.

Q: Blood is not a Newtonian fluid because:

Its viscosity changes with velocity.. **Explanation:** The classification of a fluid as **Newtonian** or **Non-Newtonian** depends on the relationship between shear stress and shear rate. 1. **Why the correct answer is right:** A Newtonian fluid (like water or plasma) maintains a constant viscosity regardless of the flow velocity or force applied. Blood, however, is a **Non-Newtonian fluid** because its viscosity is **inversely proportional** to its velocity (shear rate). This is primarily due to the presence of formed elements (RBCs). At low velocities, RBCs aggregate into stacks called **Rouleaux**, which increases internal friction and viscosity. As velocity increases, these aggregates break apart and RBCs undergo "deformability" (streamlining), which decreases viscosity. This specific behavior is known as **Pseudoplasticity** or "shear-thinning." 2. **Why the incorrect options are wrong:** * **Option A:** This describes a Newtonian fluid. If blood's viscosity did not change with velocity, it would be Newtonian. * **Options C & D:** Newtonian status is defined by **viscosity**, not density. While density is a physical property of blood, it does not dictate the rheological (flow) classification in this context. **High-Yield NEET-PG Pearls:** * **Fahraeus-Lindqvist Effect:** In very small blood vessels (capillaries <1.5mm), blood viscosity actually *decreases* because RBCs move to the center of the vessel (axial accumulation), leaving a cell-free plasma layer at the walls. * **Hematocrit:** This is the single most important determinant of blood viscosity. * **Temperature:** Viscosity increases as body temperature decreases (relevant in induced hypothermia or Raynaud’s phenomenon).

Q: Which of the following is not a secondary granule?

BPI. ### Explanation In neutrophils (Polymorphonuclear leukocytes), granules are classified based on their contents and the timing of their appearance during granulopoiesis. **1. Why BPI is the Correct Answer:** **Bactericidal/Permeability-Increasing protein (BPI)** is a constituent of **Primary (Azurophilic) granules**, not secondary granules. Primary granules are the first to appear (at the promyelocyte stage) and contain potent antimicrobial agents like Myeloperoxidase (MPO), Defensins, BPI, and Neutral Proteases (Elastase, Cathepsin G). BPI specifically targets Gram-negative bacteria by binding to lipopolysaccharides (LPS). **2. Analysis of Incorrect Options (Secondary Granules):** Secondary (Specific) granules appear later (at the myelocyte stage) and contain markers used to identify mature neutrophils. * **Lactoferrin:** A key secondary granule protein that sequesters iron, preventing bacterial growth. * **Alkaline Phosphatase (NAP/ALP):** A classic marker for secondary granules. Its levels are clinically used to differentiate Leukemoid reactions (High NAP) from Chronic Myeloid Leukemia (Low NAP). * **Lysozyme:** Found in **both** primary and secondary granules. Since it is a major component of secondary granules, it is not the "odd one out" compared to BPI, which is strictly primary. **3. High-Yield Clinical Pearls for NEET-PG:** * **Primary Granule Marker:** Myeloperoxidase (MPO). * **Secondary Granule Marker:** Lactoferrin and Vitamin B12-binding protein. * **Tertiary Granules:** Contain Gelatinase and Cathepsins; they are involved in tissue degradation and migration. * **Chediak-Higashi Syndrome:** Characterized by giant lysosomal granules due to a defect in vesicle trafficking (LYST gene). * **Specific Granule Deficiency:** A rare condition leading to recurrent pyogenic infections due to the absence of secondary granules.

Q: What is the approximate percentage of Hemoglobin F (HbF) at birth?

70%. **Explanation:** **Understanding the Concept:** Hemoglobin F (HbF, $\alpha_2\gamma_2$) is the predominant hemoglobin during fetal life due to its high affinity for oxygen, which facilitates oxygen transfer from maternal blood across the placenta. The switch from fetal ($\gamma$-globin) to adult ($\beta$-globin) synthesis begins around 30 weeks of gestation. At the time of birth, a full-term neonate typically has **70% to 80% HbF**, with the remaining 20–30% being adult hemoglobin (HbA). **Analysis of Options:** * **Option C (70%) is Correct:** This represents the standard physiological level of HbF in a term neonate. * **Option A (20%) & B (50%):** These levels are too low for a newborn. HbF levels drop to approximately 50% by 1 month of age and reach adult levels (<1%) by 6–12 months. * **Option D (90%):** While HbF is nearly 90–95% at 30 weeks gestation, the progressive switch to HbA reduces this to ~70% by the time the baby is born at term. **NEET-PG High-Yield Pearls:** 1. **The "Switch":** HbF levels decline rapidly after birth. By **6 months of age**, HbF usually drops to **<5%**. 2. **Clinical Significance:** Beta-hemoglobinopathies (like **Beta-Thalassemia Major** and **Sickle Cell Anemia**) do not manifest clinically until 6 months of age, as the protective effect of HbF wanes and the defective HbA production becomes dominant. 3. **Structure:** HbF consists of two alpha ($\alpha$) and two gamma ($\gamma$) chains. 4. **P50 Value:** HbF has a lower P50 (approx. 19 mmHg) compared to HbA (approx. 27 mmHg), reflecting its higher oxygen affinity.

Q: All of the following are actions of Cytotoxic T-cells except?

They can phagocytose cells.. ### Explanation **Correct Answer: C. They can phagocytose cells.** **1. Why Option C is Correct (The Underlying Concept):** Cytotoxic T-cells (CD8+ T-cells) are the "assassins" of the adaptive immune system, but they are **not phagocytes**. Phagocytosis—the process of engulfing and digesting large particles or whole cells—is a characteristic function of the innate immune system, primarily performed by **neutrophils, macrophages, and dendritic cells**. Cytotoxic T-cells eliminate target cells by inducing **apoptosis** (programmed cell death) through chemical signaling and membrane disruption, rather than ingestion. **2. Analysis of Incorrect Options:** * **Option A:** Cytotoxic T-cells are specialized to recognize and destroy virally infected cells, transplanted foreign tissues (allografts), and tumor cells. They recognize these via MHC Class I molecules. * **Option B:** CD8 is a transmembrane glycoprotein that serves as a co-receptor for the T-cell receptor (TCR). It specifically binds to the **MHC Class I** molecule, ensuring the T-cell attacks the correct target. * **Option D:** Upon activation, these cells release **perforins** (which create holes in the target cell membrane) and **granzymes/lymphotoxins** (which enter the cell to trigger the caspase cascade), leading to DNA fragmentation and cell death. **3. NEET-PG High-Yield Pearls:** * **MHC Restriction:** Remember the "Rule of 8": **CD8** cells bind **MHC I** (8x1=8), while **CD4** cells bind **MHC II** (4x2=8). * **Fas Ligand:** Besides perforins, CD8+ cells can induce apoptosis by binding their **Fas ligand** to the **Fas receptor** on a target cell. * **Cytokine Production:** While their primary role is killing, activated CD8+ cells also secrete **IFN-γ**, which inhibits viral replication and activates macrophages.

Q: Red bone marrow is involved in erythropoiesis from which gestational period?

After 5 months intrauterine. ### Explanation The process of hematopoiesis (blood cell formation) during intrauterine life occurs in three distinct chronological stages: the Mesoblastic, Hepatic, and Myeloid stages. **1. Why Option C is Correct:** The **Myeloid stage** begins around the **5th month (20th week)** of intrauterine life. At this point, the bone marrow becomes the primary site of erythropoiesis. By the 7th month, the bone marrow takes over as the dominant site, a role it maintains throughout the remainder of gestation and postnatal life. **2. Analysis of Incorrect Options:** * **Option A (3 weeks to 3 months):** This corresponds to the **Mesoblastic stage**. Erythropoiesis begins in the **yolk sac** around the 3rd week of gestation. These are nucleated red cells. * **Option B (3 months to 5 months):** This corresponds to the **Hepatic stage**. The **liver** is the chief site of blood cell formation during the second trimester, peaking at 3–4 months. The spleen also contributes significantly during this period. * **Option D (After 5 months):** While technically true, it lacks the specific "intrauterine" context required to distinguish it from postnatal development in a gestational timeline question. **3. NEET-PG High-Yield Pearls:** * **First site of hematopoiesis:** Yolk sac (mesoderm). * **Primary site in mid-trimester:** Liver (starts at 6 weeks, peaks at 3–4 months). * **Transition:** Bone marrow starts at 4–5 months but becomes the **exclusive** site only after birth. * **Post-natal rule:** In children, all bones have red marrow. By age 20, red marrow is restricted to membranous bones (vertebrae, sternum, ribs, ilium) and the proximal ends of the humerus and femur. * **Extramedullary hematopoiesis:** If the bone marrow fails in adults, the liver and spleen can resume their fetal hematopoietic function.

Q: What is the approximate lifespan of fetal red blood cells?

80 days. **Explanation:** The correct answer is **80 days (Option C)**. **1. Why 80 days is correct:** The lifespan of red blood cells (RBCs) is significantly shorter in neonates and fetuses compared to adults. In a full-term neonate, the average lifespan of an RBC is approximately **60 to 90 days** (averaging 80 days). This shortened survival is due to several physiological factors: * **Metabolic differences:** Fetal RBCs have lower levels of certain enzymes (like ATP and phosphofructokinase). * **Membrane characteristics:** They exhibit increased susceptibility to lipid peroxidation and mechanical fragility. * **Size:** Fetal RBCs are macrocytic (larger MCV), making them more prone to splenic sequestration. **2. Why other options are incorrect:** * **Option A (60 days):** While some preterm infants may have an RBC lifespan as short as 35–50 days, 80 days is the standard physiological average for a term fetus/neonate. * **Option B (100 days):** This is an intermediate value and does not represent the standard physiological mean for any specific age group. * **Option D (120 days):** This is the classic lifespan of **adult RBCs**. In NEET-PG, it is crucial to distinguish between adult and fetal values. **3. High-Yield Clinical Pearls for NEET-PG:** * **Physiological Jaundice:** The shorter lifespan of fetal RBCs (80 days) combined with a higher total RBC mass and an immature liver (low UGT enzyme activity) is the primary reason for the development of physiological jaundice in newborns. * **Fetal Hemoglobin (HbF):** Composed of $\alpha_2\gamma_2$ chains. It has a higher affinity for oxygen because it binds poorly to 2,3-BPG. * **Erythropoiesis Sites:** 0–2 months (Yolk sac), 2–7 months (Liver/Spleen), 7–9 months (Bone marrow). The liver is the predominant site in the second trimester.

Q: Bleeding time is prolonged in which of the following conditions?

Von-Willebrand disease. **Explanation:** The **Bleeding Time (BT)** is a clinical test that assesses the **primary hemostatic pathway**, which involves the interaction between the vascular wall and platelets (platelet plug formation). **1. Why Von-Willebrand Disease (vWD) is correct:** Von Willebrand Factor (vWF) is essential for platelet adhesion to the subendothelial collagen via the GpIb receptor. In vWD, the deficiency or dysfunction of vWF leads to defective platelet adhesion. Since BT measures the time taken for a platelet plug to form, it is characteristically **prolonged** in vWD. Additionally, vWF acts as a carrier protein for Factor VIII; thus, vWD is unique because it can show both a prolonged BT and a prolonged aPTT. **2. Why the other options are incorrect:** * **Haemophilia A (Factor VIII deficiency) & Christmas Disease (Haemophilia B/Factor IX deficiency):** These are disorders of the **secondary hemostatic pathway** (coagulation cascade). In these conditions, platelet function is normal, so the Bleeding Time is **normal**. However, the Clotting Time (CT) and aPTT are prolonged. * **Vitamin K Deficiency:** Vitamin K is required for the gamma-carboxylation of Factors II, VII, IX, and X. This affects the coagulation cascade, leading to a prolonged Prothrombin Time (PT) and aPTT, but the **Bleeding Time remains normal** as platelet function is unaffected. **NEET-PG High-Yield Pearls:** * **BT** = Platelet function/number (Prolonged in Thrombocytopenia, vWD, Bernard-Soulier). * **CT/aPTT** = Coagulation factors (Prolonged in Haemophilia, Vitamin K deficiency). * **vWD** is the most common inherited bleeding disorder. * **Bernard-Soulier Syndrome** also shows prolonged BT and is often confused with vWD, but it involves a deficiency of the GpIb receptor itself.

Q: Which of the following is NOT a platelet aggregator?

Prostaglandin D2 (PGD2). **Explanation:** Platelet aggregation is a tightly regulated process involving a balance between pro-aggregatory (pro-thrombotic) and anti-aggregatory (anti-thrombotic) substances. **Why Prostaglandin D2 (PGD2) is the correct answer:** PGD2 is a potent **inhibitor** of platelet aggregation. It acts by binding to the DP1 receptor on the platelet surface, which stimulates adenylate cyclase to increase intracellular cyclic AMP (cAMP) levels. Elevated cAMP prevents platelet activation and aggregation. Other potent inhibitors include **Prostacyclin (PGI2)** and **Nitric Oxide (NO)**. **Analysis of Incorrect Options:** * **ADP (Adenosine diphosphate):** This is a powerful physiological aggregator. It is released from platelet dense granules and binds to P2Y1 and P2Y12 receptors, leading to further platelet recruitment. * **Thromboxane (TXA2):** Produced via the COX-1 pathway, TXA2 is one of the most potent platelet aggregators and vasoconstrictors. It is the primary target of Aspirin (which irreversibly inhibits COX-1). * **Steroids:** While not primary physiological aggregators like ADP, steroids (specifically glucocorticoids) can increase platelet count and enhance platelet reactivity/aggregation in certain clinical contexts, making them "pro-aggregatory" rather than inhibitors. **NEET-PG High-Yield Pearls:** * **The "Rule of cAMP":** In platelets, **High cAMP = Inhibition** of aggregation. In contrast, **Low cAMP/High Calcium = Activation**. * **PGI2 vs. TXA2:** These are functional antagonists. PGI2 (from endothelium) inhibits aggregation; TXA2 (from platelets) promotes it. * **Platelet Granules:** ADP is stored in **Dense granules** (along with Calcium and Serotonin), while vWF and Fibrinogen are in **Alpha granules**.

Q: All of the following promote platelet aggregation except?

Prostacyclin. **Explanation:** The core concept in platelet physiology is the balance between pro-aggregatory and anti-aggregatory substances. **Why Prostacyclin is the Correct Answer:** **Prostacyclin ($PGI_2$)** is a potent **inhibitor** of platelet aggregation and a vasodilator. It is synthesized by intact vascular endothelial cells. It acts by increasing intracellular **cAMP** levels within platelets, which stabilizes them and prevents activation. This ensures that platelets do not adhere to healthy, non-injured vessel walls. **Analysis of Incorrect Options:** * **Plasmin:** While primarily known for fibrinolysis (clot breakdown), plasmin has a dual role. At certain concentrations, it can activate platelets by cleaving Protease-Activated Receptors (PARs), thereby promoting aggregation. * **Thrombospondin:** This is an adhesive glycoprotein released from the $\alpha$-granules of activated platelets. It acts as a molecular "glue" that stabilizes fibrinogen binding to the GPIIb/IIIa receptor, thus promoting aggregation. * **Platelet Activating Factor (PAF):** As the name suggests, it is one of the most potent mediators of platelet activation and aggregation, released from various immune cells and the endothelium during injury. **High-Yield Clinical Pearls for NEET-PG:** * **The "Push-Pull" Mechanism:** Thromboxane $A_2$ ($TXA_2$) and Prostacyclin ($PGI_2$) are physiological antagonists. $TXA_2$ (from platelets) promotes aggregation/vasoconstriction, while $PGI_2$ (from endothelium) inhibits aggregation/promotes vasodilation. * **Aspirin's Role:** Low-dose aspirin irreversibly inhibits COX-1 in platelets, reducing $TXA_2$ levels. Since platelets lack a nucleus, they cannot regenerate the enzyme, leading to an anti-thrombotic effect. * **cAMP vs. Calcium:** Increased **cAMP** (via $PGI_2$) inhibits platelets, whereas increased **intracellular Calcium** (via $TXA_2$ or ADP) promotes aggregation.

Question 1

What antibodies are present in an individual with blood group O?

Accepted Answer

Both Anti-A and Anti-B antibodies

Answer

Anti-A antibody only

Answer

Anti-B antibody only

Answer

No antibodies

Question 2

Blood is not a Newtonian fluid because:

Accepted Answer

Its viscosity changes with velocity.

Answer

Its viscosity does not change with velocity.

Answer

Its density does not change with velocity.

Answer

Its density changes with velocity.

Question 3

Which of the following is not a secondary granule?

Accepted Answer

BPI

Answer

Lactoferrin

Answer

Alkaline phosphatase

Answer

Lysozyme

Question 4

What is the approximate percentage of Hemoglobin F (HbF) at birth?

Accepted Answer

70%

Answer

20%

Answer

50%

Answer

90%

Question 5

All of the following are actions of Cytotoxic T-cells except?

Accepted Answer

They can phagocytose cells.

Answer

They destroy translated and other foreign cells.

Answer

They display the glycoprotein CD8.

Answer

They act by using perforins and produce lymphotoxins.

Question 6

Red bone marrow is involved in erythropoiesis from which gestational period?

Accepted Answer

After 5 months intrauterine

Answer

3 weeks to 3 months intrauterine

Answer

3 months to 5 months intrauterine

Answer

After 5 months

Question 7

What is the approximate lifespan of fetal red blood cells?

Accepted Answer

80 days

Answer

60 days

Answer

100 days

Answer

120 days

Question 8

Bleeding time is prolonged in which of the following conditions?

Accepted Answer

Von-Willebrand disease

Answer

Haemophilia

Answer

Christmas disease

Answer

Vitamin K-deficiency

Question 9

Which of the following is NOT a platelet aggregator?

Accepted Answer

Prostaglandin D2 (PGD2)

Answer

Adenosine diphosphate (ADP)

Answer

Thromboxane

Answer

Steroids

Question 10

All of the following promote platelet aggregation except?

Accepted Answer

Prostacyclin

Answer

Plasmin

Answer

Thrombospondin

Answer

Platelet activating factor

Blood and Immunity — MCQs

Blood and Immunity — MCQs

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