Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 231: Which of the following maintains oncotic pressure?

A. Globulin
B. Albumin (Correct Answer)
C. Fibrin
D. Na+

Explanation: **Explanation:** **Colloid Osmotic Pressure (Oncotic Pressure)** is the osmotic pressure exerted by plasma proteins that pulls water into the circulatory system. It is the primary force opposing hydrostatic pressure, thereby preventing edema. **Why Albumin is the Correct Answer:** Albumin is the most abundant plasma protein (comprising ~60% of total protein) and has a relatively low molecular weight (~69 kDa). According to **Van't Hoff's Law**, osmotic pressure depends on the *number* of particles in a solution rather than their mass. Because albumin is present in the highest molar concentration, it is responsible for approximately **75–80% of the total oncotic pressure** (about 22–25 mmHg). **Analysis of Incorrect Options:** * **Globulin (A):** While globulins contribute to oncotic pressure, they are larger and fewer in number than albumin. Their primary roles are immunity (immunoglobulins) and transport. * **Fibrin/Fibrinogen (C):** Fibrinogen is the largest plasma protein but is present in very low concentrations. Its primary role is blood coagulation. * **Na+ (D):** Sodium is the main determinant of **crystalloid osmotic pressure**. While it contributes significantly to total plasma osmolarity, it moves freely across capillary membranes and therefore does not exert an effective "oncotic" pull between the intravascular and interstitial compartments. **High-Yield Clinical Pearls for NEET-PG:** * **Hypoalbuminemia:** Conditions like Nephrotic syndrome (loss in urine) or Cirrhosis (decreased synthesis) lead to a drop in oncotic pressure, resulting in generalized edema and ascites. * **Starling Forces:** The balance between capillary hydrostatic pressure and plasma oncotic pressure determines the net filtration across the capillary bed. * **Normal Albumin Levels:** 3.5 to 5.0 g/dL.

Question 232: Oedema occurs when plasma protein level is below which value?

A. 8 mg/dl
B. 2 mg/dl
C. 5 mg/dl (Correct Answer)
D. 10 mg/dl

Explanation: **Explanation:** The development of oedema is primarily governed by **Starling’s Forces**, which regulate fluid exchange between capillaries and the interstitium. The two main opposing forces are Capillary Hydrostatic Pressure (pushing fluid out) and **Plasma Colloid Osmotic Pressure (COP)** (pulling fluid in). **Why 5 mg/dl is correct:** Plasma proteins, specifically **Albumin** (which contributes 70-80% of the COP), are responsible for maintaining an oncotic pressure of approximately 25-28 mmHg. When total plasma protein levels fall below **5 g/dl** (specifically when albumin falls below **2.5 g/dl**), the COP decreases significantly. This allows hydrostatic pressure to dominate, leading to the excessive filtration of fluid into the interstitial space, resulting in clinical oedema. **Analysis of Incorrect Options:** * **A & D (8 mg/dl & 10 mg/dl):** These values are within or above the normal range for total plasma proteins (Normal: 6–8 g/dl). At these levels, oncotic pressure is sufficient to prevent fluid leakage. * **B (2 mg/dl):** While oedema certainly occurs at 2 g/dl, this is a state of severe hypoproteinemia (often seen in advanced Nephrotic syndrome or Kwashiorkor). The threshold or "critical level" at which oedema *begins* to manifest is 5 g/dl. **High-Yield Clinical Pearls for NEET-PG:** * **Hypoproteinemic Oedema:** Characteristically presents as **pitting oedema** and is often first seen in lax tissue like the eyelids (periorbital oedema) or dependent parts (feet). * **Albumin vs. Globulin:** Albumin is more important for COP than globulin because it has a lower molecular weight (more molecules per unit weight) and a higher concentration. * **Mnemonic:** Remember the **"Rule of 5 & 2.5"**—Oedema occurs when Total Protein < 5 g/dl or Albumin < 2.5 g/dl.

Question 233: Which of the following anticoagulants prevent clotting of blood in the normal vascular system?

A. Antithrombin III (Correct Answer)
B. Plasminogen
C. Fibrinogen
D. Heparin

Explanation: ### Explanation The maintenance of blood fluidity within the normal vascular system is achieved through a delicate balance between procoagulants and natural anticoagulants. **Why Antithrombin III is correct:** Antithrombin III (AT-III) is the most important **natural circulating anticoagulant**. It is a serine protease inhibitor (serpin) that irreversibly inactivates several factors in the clotting cascade, most notably **Thrombin (Factor IIa)** and **Factor Xa**. It also inhibits Factors IXa, XIa, and XIIa. While it works independently to prevent spontaneous clot formation in normal vessels, its activity is increased several thousand-fold in the presence of heparin or heparin-like molecules on the endothelial surface. **Analysis of Incorrect Options:** * **Plasminogen (B):** This is the inactive precursor of plasmin. It is involved in **fibrinolysis** (dissolving an existing clot) rather than preventing the initial formation of a clot in the normal vascular system. * **Fibrinogen (C):** This is **Factor I**, a procoagulant. It is converted into fibrin by thrombin to form the structural mesh of a blood clot. * **Heparin (D):** While heparin is a potent anticoagulant, it is primarily found in the granules of mast cells and basophils. Endogenous heparin levels in normal circulating plasma are **negligible**; therefore, it does not function as the primary systemic anticoagulant under physiological conditions. It acts as a cofactor that enhances Antithrombin III. **High-Yield NEET-PG Pearls:** * **Antithrombin III Deficiency:** Leads to a hypercoagulable state (thrombophilia) and "Heparin Resistance," where standard doses of heparin fail to prolong the PTT. * **Protein C and S:** Other key natural anticoagulants; they specifically inactivate Factors Va and VIIIa. * **Virchow’s Triad:** Endothelial injury, stasis, and hypercoagulability are the three factors leading to intravascular thrombosis.

Question 234: Vitamin B12 is essential for what aspect of blood cell reproduction?

A. Formation of hemoglobin
B. Extrusion of the nucleus from the normoblasts
C. Formation of DNA (Correct Answer)
D. Activation of erythropoietin

Explanation: **Explanation:** **Why "Formation of DNA" is correct:** Vitamin B12 (Cobalamin) and Folic acid are essential co-factors for the synthesis of **thymidine triphosphate**, one of the four building blocks of DNA. Specifically, Vitamin B12 is required for the conversion of homocysteine to methionine, a process that regenerates tetrahydrofolate. Without B12, folate is "trapped" in an inactive form (the Methyl-folate trap), leading to impaired DNA synthesis. In the bone marrow, this results in a failure of nuclear maturation while cytoplasmic growth continues normally. **Why the other options are incorrect:** * **A. Formation of hemoglobin:** This process primarily requires **Iron**, Vitamin B6 (pyridoxine), and amino acids. B12 does not directly participate in heme or globin synthesis. * **B. Extrusion of the nucleus:** This is a late-stage physical process in erythropoiesis (transition from orthochromatic erythroblast to reticulocyte) and is not dependent on B12. * **D. Activation of erythropoietin:** Erythropoietin is a hormone produced by the peritubular interstitial cells of the **kidney** in response to hypoxia; its production is independent of Vitamin B12 levels. **High-Yield Clinical Pearls for NEET-PG:** * **Megaloblastic Anemia:** Deficiency of B12 leads to "nuclear-cytoplasmic asynchrony," where the nucleus remains immature (large and lacy) while the cytoplasm matures, resulting in macrocytes. * **Hypersegmented Neutrophils:** One of the earliest peripheral blood findings in B12/Folate deficiency (defined as >5% of neutrophils having 5 lobes or any having ≥6 lobes). * **Neurological Symptoms:** Unlike Folate deficiency, B12 deficiency causes **Subacute Combined Degeneration (SCD)** of the spinal cord due to the failure of methylmalonyl-CoA to succinyl-CoA conversion, leading to myelin damage.

Question 235: Tissue thromboplastin activates which coagulation factor?

A. Factor VII (Correct Answer)
B. Factor IV
C. Factor VI
D. None of the above

Explanation: **Explanation:** The coagulation cascade is divided into the Intrinsic and Extrinsic pathways, which converge into a Common pathway. This question focuses on the **Extrinsic Pathway**, which is the primary initiator of blood clotting in vivo. **1. Why Factor VII is correct:** Tissue Thromboplastin (also known as **Factor III** or Tissue Factor) is released upon subendothelial vascular injury. It acts as a high-affinity receptor and cofactor for **Factor VII**. Once Tissue Thromboplastin binds to Factor VII, it activates it to Factor VIIa in the presence of calcium ions. This **Tissue Factor-Factor VIIa complex** then goes on to activate Factor X (the start of the common pathway) and Factor IX. **2. Why other options are incorrect:** * **Factor IV:** This refers to **Calcium ions (Ca²⁺)**. While calcium is a mandatory cofactor for almost all steps of the coagulation cascade (including the activation of Factor VII), it is not the factor "activated" by thromboplastin. * **Factor VI:** This factor is **non-existent** in the modern coagulation nomenclature. It was originally thought to be "accelerin" (activated Factor V), but it was later removed from the list once its identity was clarified. * **None of the above:** Incorrect, as Factor VII is the specific target of Tissue Thromboplastin. **Clinical Pearls for NEET-PG:** * **PT vs. aPTT:** The Extrinsic pathway (Factor VII) is clinically monitored using **Prothrombin Time (PT)**. The Intrinsic pathway is monitored using **aPTT**. * **Vitamin K Dependency:** Factor VII has the **shortest half-life** (approx. 6 hours) among the Vitamin K-dependent factors (II, VII, IX, X). Therefore, PT is the first lab value to become prolonged in Vitamin K deficiency or early Warfarin therapy. * **Initiation:** Remember that the Extrinsic pathway is "extrinsic" because it requires a factor (Tissue Thromboplastin) normally found outside the blood.

Question 236: Increased Prothrombin time results from deficiency of which factor?

A. Factor IX
B. Fibrinogen (Correct Answer)
C. Factor VI
D. Factor XI

Explanation: **Explanation:** Prothrombin Time (PT) measures the integrity of the **Extrinsic** and **Common pathways** of the coagulation cascade. It specifically assesses Factors **I (Fibrinogen)**, **II (Prothrombin)**, **V**, **VII**, and **X**. 1. **Why Fibrinogen is correct:** Fibrinogen (Factor I) is the final substrate of the common pathway. Since PT measures the time taken for a fibrin clot to form, a significant deficiency in Fibrinogen will lead to a prolonged PT. 2. **Why Factor IX and XI are incorrect:** These factors belong to the **Intrinsic pathway**. Deficiencies in Factors VIII, IX, XI, or XII result in a prolonged **Activated Partial Thromboplastin Time (aPTT)**, while the PT remains normal. 3. **Why Factor VI is incorrect:** There is no "Factor VI" in the modern coagulation cascade (it was previously thought to be activated Factor V but was later removed from the nomenclature). **Clinical Pearls for NEET-PG:** * **PT** is the most sensitive screening test for **Vitamin K deficiency** and **Liver disease** because it monitors Factor VII, which has the shortest half-life (approx. 6 hours). * **Warfarin** therapy is monitored using PT/INR (Extrinsic pathway). * **Heparin** therapy is monitored using aPTT (Intrinsic pathway). * **Isolated prolonged PT** usually indicates Factor VII deficiency. * **Prolongation of both PT and aPTT** suggests a deficiency in the common pathway (Factors I, II, V, or X).

Question 237: The biconcave shape of RBC is useful in all aspects except:

A. Helps in passing through capillaries
B. Helps in cellular metabolism (Correct Answer)
C. Increased surface area for gas diffusion
D. Prevents osmotic lysis

Explanation: ### Explanation The biconcave shape of a Red Blood Cell (RBC) is a specialized structural adaptation designed to optimize its primary function: gas transport. **Why "Helps in cellular metabolism" is the correct answer:** The biconcave shape is a physical structural feature and has **no direct role in cellular metabolism**. In fact, mature RBCs lack mitochondria and a nucleus; they generate energy (ATP) exclusively through anaerobic glycolysis (Embden-Meyerhof pathway). Metabolism is governed by cytoplasmic enzymes and the availability of glucose, not the geometric shape of the cell membrane. **Analysis of Incorrect Options:** * **Helps in passing through capillaries:** The biconcave shape provides a high **surface-area-to-volume ratio**, allowing the RBC to be highly flexible and deformable. This allows a 7.5 µm cell to squeeze through narrow splenic sinusoids and capillaries as small as 3–5 µm without rupturing. * **Increased surface area for gas diffusion:** Compared to a sphere of the same volume, a biconcave disc has significantly more surface area. This maximizes the area available for the rapid exchange of $O_2$ and $CO_2$ across the membrane. * **Prevents osmotic lysis:** The "excess" membrane area allows the RBC to swell into a spherical shape when placed in a hypotonic solution. If the RBC were already spherical, any intake of water would lead to immediate membrane rupture (lysis). **High-Yield Clinical Pearls for NEET-PG:** * **Hereditary Spherocytosis:** A deficiency in membrane proteins (Spectrin, Ankyrin) causes RBCs to lose their biconcave shape and become spherical. These cells are less deformable and are prematurely destroyed in the spleen (extravascular hemolysis). * **Mean Corpuscular Volume (MCV):** The average volume of an RBC is **80–100 fL**. * **Average Diameter:** The diameter of a normal RBC is **7.2–7.8 µm** (Average 7.5 µm). * **Rouleaux Formation:** The biconcave shape facilitates the "stacking" of RBCs, which is seen in states of high ESR (e.g., chronic inflammation or Multiple Myeloma).

Question 238: Osmotic fragility of RBCs is increased in which of the following conditions?

A. Hereditary Spherocytosis (Correct Answer)
B. Sickle cell anemia
C. Thalassemia
D. Paroxysmal Nocturnal Hemoglobinuria (PNH)

Explanation: ### Explanation **1. Why Hereditary Spherocytosis is Correct:** Osmotic fragility refers to the susceptibility of RBCs to burst when exposed to hypotonic solutions. In **Hereditary Spherocytosis**, there is a genetic defect in membrane proteins (like **Ankyrin**, Spectrin, or Band 3). This leads to a loss of membrane surface area, forcing the cell to adopt a **spherical shape**. Spheres have the lowest surface-area-to-volume ratio, meaning they have no "reserve" capacity to expand when water enters the cell via osmosis. Consequently, they rupture at higher saline concentrations than normal biconcave cells, indicating **increased osmotic fragility**. **2. Why the Other Options are Incorrect:** * **Sickle Cell Anemia & Thalassemia:** In these conditions, RBCs are often "flatter" (target cells) or have abnormal hemoglobin. These cells have a **higher** surface-area-to-volume ratio than normal cells. They can accommodate more water before stretching the membrane to the breaking point. Therefore, they show **decreased** osmotic fragility. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** PNH is a stem cell defect involving increased sensitivity to **complement-mediated lysis** (due to deficiency of CD55/CD59), not osmotic stress. The diagnostic test for PNH is the Flow Cytometry or the Ham’s test, not the osmotic fragility test. **3. NEET-PG High-Yield Pearls:** * **Incubation:** Osmotic fragility is significantly enhanced by incubating the blood at 37°C for 24 hours. * **The "MCHC" Clue:** Hereditary Spherocytosis is one of the few conditions where the **Mean Corpuscular Hemoglobin Concentration (MCHC) is increased**. * **Confirmatory Test:** While osmotic fragility is the classic test, the **EMA (Eosin-5-maleimide) binding test** via flow cytometry is now the gold standard for diagnosing Hereditary Spherocytosis. * **Splenectomy:** This is the definitive treatment to prevent hemolysis, as the spleen is the primary site where these fragile spherocytes are destroyed.

Question 239: Although more than 400 blood groups have been identified, the ABO Rh blood group systems remain the most important in clinical medicine because?

A. It was first identified.
B. It has four different types of blood groups.
C. A, B and Rh antigens are most immunogenic. (Correct Answer)
D. They are inherited.

Explanation: ### Explanation The clinical significance of a blood group system is determined by its **immunogenicity**—the ability of an antigen to provoke an immune response (antibody production). **1. Why Option C is Correct:** While hundreds of antigens exist on the erythrocyte surface, the **A, B, and D (Rh) antigens** are the most potent immunogens. In the ABO system, individuals naturally possess pre-formed "isoagglutinins" (antibodies) against the antigens they lack. In the Rh system, although antibodies are not naturally occurring, the D-antigen is so highly immunogenic that an Rh-negative individual exposed to even a small amount of Rh-positive blood has an 80% probability of developing anti-D antibodies. This leads to severe **Acute Hemolytic Transfusion Reactions** or **Hemolytic Disease of the Fetus and Newborn (HDFN)**. **2. Why Other Options are Incorrect:** * **Option A:** Being the first identified (by Landsteiner in 1900) is a historical fact, not a clinical reason for its importance. * **Option B:** The number of phenotypes (four in ABO) does not dictate clinical risk; many minor systems have multiple phenotypes but rarely cause reactions. * **Option D:** All blood group antigens (Kell, Duffy, Kidd, etc.) are inherited via Mendelian genetics; this is not a unique feature of the ABO/Rh systems. **3. High-Yield Clinical Pearls for NEET-PG:** * **Landsteiner’s Law:** States that if an agglutinogen (antigen) is present on RBCs, the corresponding agglutinin (antibody) must be absent from the plasma (applies strictly to the ABO system). * **Universal Donor:** O Negative (no A, B, or D antigens). * **Universal Recipient:** AB Positive (no anti-A, anti-B, or anti-D antibodies). * **Bombay Blood Group (Oh):** Lacks the H-antigen; these individuals produce anti-H antibodies and can only receive blood from another Bombay phenotype donor. * **Most Immunogenic Rh Antigen:** D > c > E > C > e.

Question 240: Which of the following factors is NOT derived from endothelial cells?

A. Thrombomodulin
B. Protein S
C. Prostacyclin
D. Thromboxane A2 (Correct Answer)

Explanation: **Explanation:** The correct answer is **Thromboxane A2 (TXA2)**. The vascular endothelium plays a dual role in hemostasis, primarily maintaining an anti-thrombotic surface under physiological conditions while facilitating coagulation upon injury. **1. Why Thromboxane A2 is the correct answer:** Thromboxane A2 is a potent vasoconstrictor and platelet aggregator. It is synthesized and released primarily by **activated platelets** (via the cyclooxygenase pathway), not by endothelial cells. Its primary function is to promote clot formation, opposing the effects of endothelial-derived factors. **2. Why the other options are incorrect:** * **Thrombomodulin:** This is a specific receptor expressed on the **luminal surface of endothelial cells**. It binds to thrombin, converting it from a procoagulant enzyme into an anticoagulant that activates Protein C. * **Protein S:** While primarily synthesized in the liver, Protein S is also synthesized and secreted by **vascular endothelial cells** and megakaryocytes. It acts as a non-enzymatic cofactor for activated Protein C (APC). * **Prostacyclin (PGI2):** This is the major prostaglandin synthesized by **endothelial cells**. It is a potent vasodilator and inhibitor of platelet aggregation, acting as a physiological antagonist to Thromboxane A2. **High-Yield Clinical Pearls for NEET-PG:** * **The PGI2:TXA2 Balance:** In health, the endothelium-derived PGI2 inhibits platelet aggregation. In endothelial injury, this balance shifts toward TXA2, favoring clot formation. * **Other Endothelial Products:** Nitric Oxide (vasodilator), von Willebrand Factor (vWF - stored in Weibel-Palade bodies), and Tissue Plasminogen Activator (t-PA). * **Aspirin Mechanism:** Low-dose aspirin irreversibly inhibits COX-1 in platelets, reducing TXA2 levels. Since platelets lack a nucleus, they cannot synthesize new enzymes, leading to a prolonged anti-platelet effect.

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