Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 211: What is the primary determinant of colloidal osmotic pressure of plasma?

A. Albumin (Correct Answer)
B. Fibrinogen
C. Globulin
D. Prothrombin

Explanation: **Explanation:** The **Colloidal Osmotic Pressure (COP)**, also known as **Oncotic Pressure**, is the osmotic pressure exerted by plasma proteins that serves to hold water within the vascular compartment, opposing hydrostatic pressure. **Why Albumin is the Correct Answer:** Albumin is the primary determinant of COP (contributing approximately **75-80%** of the total oncotic pressure) due to two main reasons: 1. **High Concentration:** It is the most abundant plasma protein (3.5–5.0 g/dL). 2. **Low Molecular Weight:** Osmotic pressure depends on the *number* of particles per unit volume rather than the mass. Being the smallest major plasma protein (~69 kDa), albumin has more molecules per gram than larger proteins like globulins. 3. **Gibbs-Donnan Effect:** Albumin is negatively charged and attracts cations (mainly Na+), further increasing the osmotic gradient. **Analysis of Incorrect Options:** * **B. Fibrinogen:** Although it has the highest molecular weight among common plasma proteins, its concentration is very low (200–400 mg/dL), making its contribution to COP negligible. * **C. Globulin:** Globulins have a higher molecular weight than albumin. While they contribute to COP, their lower molar concentration makes them less significant than albumin. * **D. Prothrombin:** This is a clotting factor present in trace amounts; it does not significantly influence plasma osmolarity. **High-Yield Clinical Pearls for NEET-PG:** * **Starling’s Forces:** A decrease in plasma albumin (hypoalbuminemia) leads to a drop in COP, resulting in the movement of fluid into the interstitial space, causing **edema** (e.g., in Nephrotic Syndrome or Liver Cirrhosis). * **Normal COP Value:** Approximately **25–28 mmHg**. * **Albumin:Globulin (A/G) Ratio:** Normally **1.2 to 1.5:1**. A reversal of this ratio is often seen in chronic liver disease or multiple myeloma.

Question 212: In which of the following conditions is the synthesis of hepcidin not reduced?

A. Hypoxia
B. Anemia
C. Hemorrhage
D. Hemosiderosis (Correct Answer)

Explanation: ### Explanation **Concept:** Hepcidin is a peptide hormone synthesized by the liver that acts as the **master regulator of iron homeostasis**. It inhibits iron absorption from the intestine and iron release from macrophages by binding to and degrading **ferroportin**. The synthesis of hepcidin is regulated by the body's iron status and erythropoietic demand: 1. **Increased Iron Stores:** Stimulates hepcidin synthesis to prevent further iron absorption (negative feedback). 2. **Increased Erythropoietic Demand/Hypoxia:** Inhibits hepcidin synthesis to increase iron availability for hemoglobin production. **Why Hemosiderosis is Correct:** **Hemosiderosis** is a condition of iron overload where excessive iron is deposited in tissues. In response to high systemic iron levels, the liver **increases** hepcidin production to block further iron absorption via the gut. Therefore, hepcidin synthesis is **not reduced**; it is significantly elevated. **Why Other Options are Incorrect:** * **Hypoxia (A):** Low oxygen levels stimulate the production of Erythropoietin (EPO) and Erythroferrone (ERFE). ERFE directly suppresses hepcidin to ensure iron is available for RBC production. * **Anemia (B):** Anemia triggers compensatory erythropoiesis. High erythropoietic activity suppresses hepcidin to mobilize iron stores. * **Hemorrhage (C):** Acute blood loss leads to both anemia and hypoxia, both of which are potent inhibitors of hepcidin synthesis to facilitate rapid erythroid recovery. ### NEET-PG High-Yield Pearls * **Mechanism of Action:** Hepcidin causes internalization and degradation of **Ferroportin** (the only known cellular iron exporter). * **Stimulators of Hepcidin:** High plasma iron, high iron stores, and **Inflammation (IL-6)**. This is the pathophysiology behind **Anemia of Chronic Disease**. * **Inhibitors of Hepcidin:** Iron deficiency, Hypoxia, and **Erythroferrone** (secreted by erythroblasts). * **Clinical Correlation:** Mutations in the HAMP gene (encoding hepcidin) lead to **Juvenile Hemochromatosis**.

Question 213: 2,3-DPG levels are decreased in which of the following conditions?

A. Anemia
B. Acidosis (Correct Answer)
C. High altitude
D. Exercise

Explanation: **Explanation:** The level of **2,3-Bisphosphoglycerate (2,3-DPG)** in red blood cells is a critical regulator of hemoglobin's affinity for oxygen. 2,3-DPG binds to the beta chains of deoxyhemoglobin, stabilizing the "T" (Tense) state and shifting the oxygen-dissociation curve to the **right**, facilitating oxygen unloading to tissues. **Why Acidosis is the Correct Answer:** The synthesis of 2,3-DPG is catalyzed by the enzyme **phosphoglycerate mutase**. This enzyme is highly sensitive to pH; it is **inhibited by a decrease in pH (acidosis)**. Therefore, in states of acidosis, the glycolytic pathway in RBCs is slowed, leading to decreased production of 2,3-DPG. This serves as a compensatory mechanism: while acidosis itself shifts the curve to the right (Bohr effect), the resulting decrease in 2,3-DPG shifts it back to the left, helping maintain equilibrium. **Analysis of Incorrect Options:** * **Anemia:** In anemia, there is a functional hypoxia. The body compensates by **increasing** 2,3-DPG levels to enhance oxygen delivery to tissues. * **High Altitude:** Low partial pressure of oxygen triggers an **increase** in 2,3-DPG to facilitate better peripheral unloading of oxygen. * **Exercise:** Strenuous exercise leads to increased metabolism and temporary hypoxia, which stimulates an **increase** in 2,3-DPG levels. **NEET-PG High-Yield Pearls:** * **Stored Blood:** 2,3-DPG levels **decrease** in stored blood (bank blood). Transfusing large amounts of old blood can impair oxygen delivery to tissues due to a leftward shift of the curve. * **Fetal Hemoglobin (HbF):** HbF has a **lower affinity** for 2,3-DPG because its gamma chains lack the specific binding sites found in beta chains. This results in HbF having a higher affinity for oxygen than adult hemoglobin (HbA). * **Mnemonic:** Factors that shift the curve to the **Right** (increase 2,3-DPG): **CADET**, face Right! (**C**O2, **A**cid, **D**PG, **E**xercise, **T**emperature).

Question 214: Regarding the oxygen-hemoglobin dissociation curve, which statement is true?

A. The affinity of oxygen with hemoglobin decreases as hemoglobin attaches to oxygen in a linear fashion.
B. One hemoglobin molecule attaches to two molecules of 2,3-DPG.
C. Oxygen affinity will be equal in both HbF and HbA in the absence of 2,3-DPG. (Correct Answer)
D. Carboxyhemoglobin increases the release of oxygen in the blood, causing a rightward shift of the oxygen dissociation curve.

Explanation: ### Explanation **1. Why Option C is Correct:** The primary reason Fetal Hemoglobin (HbF) has a higher oxygen affinity than Adult Hemoglobin (HbA) *in vivo* is its poor binding to **2,3-Bisphosphoglycerate (2,3-DPG)**. HbF contains $\gamma$-chains instead of $\beta$-chains; these $\gamma$-chains lack certain positively charged amino acids (specifically, Histidine is replaced by Serine at position 143), reducing the binding site's affinity for the negatively charged 2,3-DPG. Since 2,3-DPG normally functions to stabilize the "T-state" (low affinity) and promote oxygen unloading, its absence allows both HbA and HbF to revert to their intrinsic high-affinity states. Stripped of 2,3-DPG, their affinity for oxygen becomes essentially equal. **2. Why Other Options are Incorrect:** * **Option A:** The binding is **not linear**; it is **sigmoidal** due to **positive cooperativity**. As each oxygen molecule binds, the affinity for the next oxygen molecule *increases*, not decreases. * **Option B:** One hemoglobin tetramer binds to **only one** molecule of 2,3-DPG in the central cavity between the two $\beta$-chains. * **Option C:** Carboxyhemoglobin (CO-Hb) causes a **leftward shift**. CO binds to Hb with 210x the affinity of $O_2$ and prevents the remaining $O_2$ from being released to tissues, leading to cellular hypoxia. **3. NEET-PG High-Yield Pearls:** * **Right Shift (Reduced Affinity/Increased Unloading):** "CADET, face Right!" (**C**O2, **A**cidosis/H+, **D**PG, **E**xercise, **T**emperature). * **Left Shift (Increased Affinity/Decreased Unloading):** HbF, Hypothermia, Alkalosis, CO poisoning, Methemoglobinemia. * **P50 Value:** The $PO_2$ at which Hb is 50% saturated. Normal adult value is **26.7 mmHg**. A right shift increases P50; a left shift decreases P50.

Question 215: What is the half-life of monocytes in circulation?

A. 6 hours
B. 12 hours
C. 24 hours
D. 1-3 days (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. 1-3 days** **Underlying Medical Concept:** Monocytes are the largest cells of the normal blood and are produced in the bone marrow. Once released into the peripheral circulation, they remain there for a relatively short duration compared to their total lifespan. In humans, the average half-life of a circulating monocyte is approximately **24 to 72 hours (1–3 days)**. After this period, they migrate through the capillary walls into the extravascular tissues, where they differentiate into specific **tissue macrophages** (e.g., Kupffer cells in the liver, alveolar macrophages in the lungs). Once they become macrophages, their lifespan increases significantly to months or even years. **Analysis of Incorrect Options:** * **A & B (6–12 hours):** This timeframe is more characteristic of **Neutrophils**. Neutrophils have a very short half-life in circulation (averaging 6–10 hours) before they enter tissues or are cleared. * **C (24 hours):** While 24 hours is within the range, "1–3 days" is the standard textbook definition (e.g., Guyton and Hall) and more accurately reflects the physiological variability of monocyte transit time. **High-Yield Facts for NEET-PG:** * **Monocyte-Macrophage System:** Formerly known as the Reticuloendothelial System (RES). * **Size:** Monocytes are the largest leukocytes in a peripheral smear (12–20 μm) and possess a characteristic kidney or horseshoe-shaped nucleus. * **Function:** They are professional phagocytes and act as **Antigen Presenting Cells (APCs)** by presenting fragments of antigens to T-lymphocytes via MHC II molecules. * **Ratio:** In a normal differential count, monocytes constitute about 2–8% of total WBCs.

Question 216: Which enzyme is responsible for the respiratory burst reaction?

A. Dehydrogenase
B. Peroxidase
C. Hydroxylase
D. NADPH-oxidase (Correct Answer)

Explanation: **Explanation:** **Respiratory Burst (Oxidative Burst)** is a critical process in innate immunity where phagocytes (neutrophils and macrophages) rapidly increase their oxygen consumption to produce reactive oxygen species (ROS) to kill ingested pathogens. **Why NADPH Oxidase is Correct:** The key enzyme initiating this process is **NADPH oxidase** (located in the phagosomal membrane). It catalyzes the transfer of an electron from NADPH to molecular oxygen ($O_2$), reducing it to the **Superoxide anion ($O_2^-$)**. This is the "rate-limiting" and first step of the respiratory burst. Superoxide is then converted to hydrogen peroxide ($H_2O_2$) by superoxide dismutase, and subsequently to hypochlorite (bleach) by myeloperoxidase. **Analysis of Incorrect Options:** * **A. Dehydrogenase:** While Glucose-6-Phosphate Dehydrogenase (G6PD) is essential for generating the NADPH required for this reaction, it is not the enzyme that directly produces the respiratory burst. * **B. Peroxidase:** Myeloperoxidase (MPO) acts *downstream* of NADPH oxidase. It converts $H_2O_2$ and chloride ions into hypochlorous acid (HOCl). While important for microbicidal activity, it is not the enzyme responsible for the initial "burst" of oxygen consumption. * **C. Hydroxylase:** These enzymes are involved in various metabolic pathways (e.g., steroid synthesis or collagen formation) but do not play a primary role in the phagocytic respiratory burst. **High-Yield Clinical Pearls for NEET-PG:** * **Chronic Granulomatous Disease (CGD):** Caused by a genetic deficiency in **NADPH oxidase**. Patients suffer from recurrent infections with **catalase-positive organisms** (e.g., *S. aureus*, *Aspergillus*) because they cannot produce superoxide. * **Diagnostic Test for CGD:** The **Nitroblue Tetrazolium (NBT) dye test** (fails to turn blue) or the more modern **Dihydrorhodamine (DHR) flow cytometry** test. * **Sequence of ROS:** $O_2 \xrightarrow{\text{NADPH Oxidase}} O_2^- \xrightarrow{\text{SOD}} H_2O_2 \xrightarrow{\text{MPO}} HOCl$.

Question 217: What is the typical volume of blood per kilogram of body weight in a child?

A. 60-70 ml (Correct Answer)
B. 100-150 ml
C. 150-200 ml
D. 200-250 ml

Explanation: **Explanation:** The total blood volume (TBV) in humans varies significantly based on age, body composition, and physiological state. The correct answer is **60-70 ml/kg**, which represents the standard physiological range for an older child or adolescent. **1. Why Option A is Correct:** As a child grows, their body composition changes. While neonates have a very high proportion of water and blood relative to their weight, this ratio decreases as they mature. In children and adolescents, the blood volume stabilizes to approximately **70 ml/kg** (ranging between 60-80 ml/kg depending on the specific age and lean body mass), which is slightly higher than the adult average of 65-70 ml/kg. **2. Why Other Options are Incorrect:** * **Option B (100-150 ml):** This is excessively high for a child. However, a **preterm neonate** can have a blood volume of approximately **90-100 ml/kg**. * **Options C & D (150-250 ml):** These values are physiologically impossible under normal conditions. Such high volumes would lead to circulatory overload and heart failure. **High-Yield Clinical Pearls for NEET-PG:** * **Age-wise TBV Distribution:** * **Preterm Neonate:** ~90-100 ml/kg * **Term Neonate:** ~80-90 ml/kg * **Infant:** ~75-80 ml/kg * **Child:** ~70-75 ml/kg * **Adult Male:** ~70 ml/kg * **Adult Female:** ~65 ml/kg (lower due to higher body fat percentage). * **Clinical Application:** Calculating TBV is critical in pediatrics for managing fluid resuscitation, estimating allowable blood loss during surgery, and determining dosages for blood component therapy (e.g., 10 ml/kg of packed RBCs typically raises hemoglobin by 2-3 g/dL).

Question 218: In an adult man, what is the approximate total amount of hemoglobin in the circulating blood in grams?

A. 350
B. 500
C. 900 (Correct Answer)
D. 1000

Explanation: To determine the total amount of hemoglobin (Hb) in the circulating blood, we must apply the standard physiological values for an average adult male (approx. 70 kg). ### **The Calculation** 1. **Total Blood Volume:** The average blood volume in an adult male is approximately **5 liters** (or 70 ml/kg). 2. **Hemoglobin Concentration:** The normal average Hb concentration is **14–16 g/dL** (deciliter = 100 ml). 3. **The Formula:** Total Hb = (Hb concentration per 100 ml) × (Total blood volume in ml / 100). * Calculation: $15\text{ g/dL} \times 50\text{ dL} = \mathbf{750\text{--}900\text{ grams}}$. Among the given options, **900 grams** (Option C) is the most accurate representation of the upper limit for a healthy adult male. ### **Analysis of Incorrect Options** * **A (350g) & B (500g):** These values are too low. 350g would imply a blood volume of only 2.3L or severe anemia. * **D (1000g):** This value is slightly higher than the physiological average, typically seen only in cases of polycythemia or in very large individuals with high muscle mass. ### **High-Yield NEET-PG Pearls** * **Iron Content:** Each gram of Hb contains **3.34 mg of iron**. Therefore, the total body iron stored in Hb is approximately 2.5–3 grams. * **Oxygen Carrying Capacity:** 1 gram of Hb carries **1.34 ml of oxygen** (Hufner's constant). * **Life Span:** The average lifespan of an RBC is **120 days**, after which Hb is broken down into heme and globin in the Reticuloendothelial system (Spleen). * **Fetal Hb (HbF):** Has a higher affinity for oxygen than adult Hb (HbA) due to poor binding with 2,3-BPG.

Question 219: Von Willebrand's factor is synthesized in which one of the following?

A. Vascular endothelium (Correct Answer)
B. Macrophages
C. Liver
D. Eosinophils

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 Vascular Endothelium is Correct:** vWF is primarily synthesized in two locations: 1. **Vascular Endothelial Cells:** Here, it is stored in specialized secretory organelles called **Weibel-Palade bodies**. 2. **Megakaryocytes:** It is synthesized here and subsequently stored in the **$\alpha$-granules of platelets**. Upon vascular injury, vWF is released from these sites to initiate platelet adhesion. **Why Other Options are Incorrect:** * **Macrophages:** These are phagocytic cells of the immune system and do not synthesize clotting factors. * **Liver:** While the liver is the primary site for the synthesis of most coagulation factors (like Fibrinogen, Prothrombin, and Factors VII, IX, X), it is **not** the source of vWF. This is a common "trap" in exams. * **Eosinophils:** These are granulocytes involved in allergic reactions and parasitic infections; they have no role in vWF production. **High-Yield Clinical Pearls for NEET-PG:** * **vWF and Factor VIII:** vWF stabilizes Factor VIII in circulation, increasing its half-life. In von Willebrand Disease (vWD), Factor VIII levels may also be low. * **Ristocetin Cofactor Assay:** This is the gold standard test for vWF function; Ristocetin induces platelet agglutination only in the presence of vWF. * **Desmopressin (DDAVP):** Used in treatment as it stimulates the release of vWF from Weibel-Palade bodies. * **vWD:** It is the most common inherited bleeding disorder.

Question 220: What is not caused by platelet activating factor?

A. Vasoconstriction
B. Bronchodilation (Correct Answer)
C. Causes platelet aggregation
D. Transmits signals between cells

Explanation: **Explanation:** Platelet Activating Factor (PAF) is a potent phospholipid-derived mediator released by various cells, including platelets, neutrophils, monocytes, and endothelial cells. It plays a central role in inflammation and allergic responses. **Why Bronchodilation is the correct answer:** PAF is a powerful **bronchoconstrictor**, not a bronchodilator. In the lungs, it induces contraction of airway smooth muscle and increases mucus secretion. It is significantly more potent than histamine in inducing bronchial hyperreactivity, making it a key mediator in the pathogenesis of asthma and anaphylaxis. **Analysis of Incorrect Options:** * **A. Vasoconstriction:** While PAF causes systemic vasodilation (leading to hypotension), it can cause localized vasoconstriction in specific vascular beds, such as the pulmonary and coronary arteries. * **C. Causes platelet aggregation:** This is the primary function for which it was named. PAF binds to G-protein-coupled receptors on platelets, leading to shape change, granule release, and aggregation. * **D. Transmits signals between cells:** PAF acts as a signaling molecule (intercellular mediator) that coordinates the response between inflammatory cells and the vascular endothelium. **High-Yield Clinical Pearls for NEET-PG:** * **Potency:** PAF is roughly 1,000 to 10,000 times more potent than histamine in causing bronchospasm and increasing vascular permeability. * **Vascular Effect:** It causes increased capillary permeability (edema) by inducing endothelial cell contraction. * **Chemotaxis:** It is a strong chemoattractant for neutrophils and eosinophils. * **Inhibitors:** PAF receptor antagonists are being studied for the treatment of inflammatory conditions and septic shock.

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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