Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 281: Which peptide causes increased capillary permeability and edema?

A. Histamine
B. Angiotensin II
C. Bradykinin (Correct Answer)
D. Renin

Explanation: **Explanation:** **Bradykinin (Correct Answer):** Bradykinin is a potent vasodilator peptide belonging to the kinin system. It acts primarily on **B2 receptors** to stimulate the release of nitric oxide and prostacyclin. Its hallmark physiological effect is a significant increase in **capillary permeability** by causing the contraction of endothelial cells, which creates gaps in the microvasculature. This allows fluid and proteins to leak into the interstitial space, leading to **edema**. **Analysis of Incorrect Options:** * **Histamine (Option A):** While histamine also increases capillary permeability and causes edema (e.g., in type I hypersensitivity), it is an **amine**, not a **peptide**. The question specifically asks for a peptide. * **Angiotensin II (Option B):** This is a potent **vasoconstrictor**. It generally increases blood pressure and decreases capillary hydrostatic pressure downstream, which does not typically promote edema. * **Renin (Option D):** Renin is an **enzyme** (aspartyl protease) secreted by the juxtaglomerular cells. It does not directly affect capillary permeability; its role is to convert Angiotensinogen to Angiotensin I. **NEET-PG High-Yield Pearls:** * **ACE Inhibitors & Cough:** ACE (Angiotensin-Converting Enzyme) is responsible for the breakdown of Bradykinin. ACE inhibitors lead to Bradykinin accumulation, causing the classic side effects of **dry cough** and **angioedema**. * **Hereditary Angioedema:** This condition is caused by a **C1 esterase inhibitor deficiency**, leading to overproduction of Bradykinin, resulting in episodes of severe swelling. * **Triple Response of Lewis:** Bradykinin and Histamine are both involved in the "wheal and flare" reaction following skin injury.

Question 282: Which one of the following helps in generating oxygen burst in the neutrophils?

A. NADPH oxidase (Correct Answer)
B. Superoxide dismutase
C. Catalase
D. Glutathione peroxidase

Explanation: ### Explanation **Correct Option: A. NADPH oxidase** The "Oxygen Burst" (or Respiratory Burst) is a critical process in neutrophils and macrophages used to kill phagocytosed bacteria. When a pathogen is ingested, there is a rapid increase in oxygen consumption. The enzyme **NADPH oxidase**, located in the phagosomal membrane, catalyzes the conversion of molecular oxygen ($O_2$) into **superoxide radicals** ($O_2^-$) by transferring an electron from NADPH. This superoxide is the precursor for other potent reactive oxygen species (ROS) like hydrogen peroxide and hypochlorite, which destroy the microbe. **Analysis of Incorrect Options:** * **B. Superoxide dismutase (SOD):** This enzyme actually acts as an antioxidant. It converts the superoxide radical ($O_2^-$) into hydrogen peroxide ($H_2O_2$). While it is part of the pathway, it is not the *generator* of the burst; it processes the product of NADPH oxidase. * **C. Catalase:** This is a protective enzyme that breaks down hydrogen peroxide into water and oxygen. It prevents cellular damage from ROS rather than generating the burst. * **D. Glutathione peroxidase:** This enzyme reduces hydrogen peroxide to water using reduced glutathione. It is a key component of the cellular antioxidant defense system, not the pro-oxidant burst mechanism. **Clinical Pearls for NEET-PG:** * **Chronic Granulomatous Disease (CGD):** A high-yield clinical correlation. It is 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 generate their own oxygen burst. * **MPO (Myeloperoxidase):** This enzyme uses the $H_2O_2$ produced during the burst to create **HOCl (Hypochlorous acid/Bleach)**, which is the most potent bactericidal agent in neutrophils. * **Nitroblue Tetrazolium (NBT) Test:** Used to diagnose CGD; a positive result (blue color) indicates functional NADPH oxidase.

Question 283: Which test measures the extrinsic pathway of blood clotting?

A. Prothrombin time (Correct Answer)
B. Activated partial thromboplastin time
C. Bleeding time
D. Clotting time

Explanation: **Explanation:** The coagulation cascade is divided into the intrinsic, extrinsic, and common pathways. The **Prothrombin Time (PT)** specifically measures the **Extrinsic Pathway** (Factor VII) and the **Common Pathway** (Factors X, V, II, and I). It is performed by adding thromboplastin (tissue factor) and calcium to the patient’s plasma. **Analysis of Options:** * **A. Prothrombin Time (PT):** Correct. It is the most sensitive test for the extrinsic pathway. It is also used to monitor **Warfarin** therapy and assess liver synthetic function. * **B. Activated Partial Thromboplastin Time (aPTT):** Incorrect. This measures the **Intrinsic Pathway** (Factors XII, XI, IX, VIII) and the common pathway. It is used to monitor **Unfractionated Heparin**. * **C. Bleeding Time (BT):** Incorrect. This measures **platelet function** and vascular integrity, not the coagulation cascade. It is prolonged in conditions like Von Willebrand Disease or thrombocytopenia. * **D. Clotting Time (CT):** Incorrect. This is a non-specific, bedside test (e.g., Lee-White method) that reflects the overall time taken for blood to clot, primarily influenced by the intrinsic pathway, but it lacks the sensitivity of PT/aPTT. **High-Yield Clinical Pearls for NEET-PG:** * **INR (International Normalized Ratio):** A standardized version of PT used to monitor oral anticoagulants (Warfarin). * **Vitamin K Dependent Factors:** II, VII, IX, and X. Since Factor VII has the shortest half-life, PT is the first to be prolonged in Vitamin K deficiency or early liver disease. * **Mnemonic:** **PeT** (PT = Extrinsic) and **PiTT** (aPTT = Intrinsic).

Question 284: The process whereby white blood cells can squeeze through pores in capillary walls is called what?

A. Diffusion
B. Diapedesis (Correct Answer)
C. Osmosis
D. Pinocytosis

Explanation: ### Explanation **Correct Answer: B. Diapedesis** **Mechanism:** Diapedesis (also known as **leukocyte extravasation**) is the process by which white blood cells (WBCs), particularly neutrophils and monocytes, squeeze through the narrow intercellular junctions of the capillary endothelium to reach the site of inflammation or tissue injury. This is a highly regulated process involving: 1. **Margination and Rolling:** Mediated by **selectins**. 2. **Adhesion and Activation:** Mediated by **integrins** (ICAM-1/VCAM-1). 3. **Transmigration (Diapedesis):** Mediated by **PECAM-1** (CD31). Once outside the vessel, the cells move toward the injury site via **chemotaxis**. **Why Incorrect Options are Wrong:** * **A. Diffusion:** This is the passive movement of solutes (like O₂ or CO₂) from an area of high concentration to low concentration. It does not involve the active squeezing of whole cells. * **C. Osmosis:** This refers specifically to the movement of water molecules across a semi-permeable membrane. * **D. Pinocytosis:** Also known as "cell drinking," this is a form of endocytosis where the cell membrane folds inward to ingest extracellular fluid and small molecules. **High-Yield Clinical Pearls for NEET-PG:** * **Neutrophils** are the first cells to undergo diapedesis in acute inflammation, followed by **monocytes/macrophages**. * **Leukocyte Adhesion Deficiency (LAD):** A clinical condition where a defect in integrins (LAD-1) or selectin ligands (LAD-2) prevents diapedesis, leading to recurrent bacterial infections and delayed umbilical cord separation. * **CD31 (PECAM-1)** is the specific molecule found at endothelial junctions that facilitates the "squeezing" process.

Question 285: Delay in blood coagulation results from which of the following?

A. Human thrombin
B. Heparin (Correct Answer)
C. Ferric chloride
D. Vitamin K

Explanation: **Explanation:** The correct answer is **Heparin**. Blood coagulation is a complex cascade of enzymatic reactions that leads to the formation of a fibrin clot. Delaying or preventing this process requires the inhibition of key clotting factors. **Why Heparin is correct:** Heparin is a potent **anticoagulant** produced naturally by mast cells and basophils. It works by binding to and activating **Antithrombin III**. This complex then inactivates several serine proteases in the coagulation cascade, most notably **Thrombin (Factor IIa)** and **Factor Xa**. By neutralizing these factors, heparin effectively prevents the conversion of fibrinogen to fibrin, thereby delaying or preventing clot formation. **Why the other options are incorrect:** * **Human Thrombin:** This is an active clotting factor (Factor IIa) that converts fibrinogen into fibrin. Adding thrombin would **accelerate** coagulation, not delay it. * **Ferric Chloride:** This is a **styptic agent**. It acts as a local hemostatic by causing rapid protein precipitation and vessel occlusion, which promotes clot formation to stop bleeding. * **Vitamin K:** This is an essential cofactor for the **gamma-carboxylation** of Factors II, VII, IX, and X. A deficiency in Vitamin K delays clotting, but its presence is necessary for the synthesis of functional procoagulants. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Heparin acts primarily on the **Intrinsic and Common pathways**. * **Monitoring:** The efficacy of Unfractionated Heparin (UFH) is monitored using **aPTT** (activated Partial Thromboplastin Time). * **Antidote:** The specific antagonist for heparin overdose is **Protamine Sulfate**. * **LMWH:** Low Molecular Weight Heparin (e.g., Enoxaparin) mainly inhibits Factor Xa and does not require routine aPTT monitoring.

Question 286: Why does albumin provide the maximum contribution to oncotic pressure generation?

A. High molecular weight, low concentration
B. Low molecular weight, high concentration (Correct Answer)
C. High molecular weight, high concentration
D. Low molecular weight, low concentration

Explanation: **Explanation:** The generation of **Oncotic Pressure** (Colloid Osmotic Pressure) in the plasma is governed by **Van’t Hoff’s Law**, which states that osmotic pressure depends on the **number of particles** (molarity) in a solution rather than the size or mass of the particles. 1. **Why Option B is Correct:** * **High Concentration:** Albumin is the most abundant plasma protein (3.5–5 g/dL), accounting for approximately 60% of total plasma proteins. * **Low Molecular Weight:** Compared to globulins (high MW) and fibrinogen, albumin has a relatively low molecular weight (~69,000 Da). Because it is smaller, a given mass of albumin contains a significantly higher number of individual molecules than the same mass of larger proteins. * **Result:** The combination of high mass concentration and low molecular weight ensures the highest molar concentration of particles, allowing albumin to contribute **75–80%** of the total plasma oncotic pressure (~25 mmHg). 2. **Why Other Options are Incorrect:** * **Options A & C (High MW):** Larger molecules like globulins are fewer in number per gram. If albumin had a high MW, the particle count would drop, reducing oncotic pressure. * **Options A & D (Low Concentration):** Low concentration (as seen in hypoalbuminemia) leads to a decrease in oncotic pressure, resulting in edema. **High-Yield Clinical Pearls for NEET-PG:** * **Starling Forces:** Oncotic pressure is the primary force "pulling" fluid into the capillaries, opposing Hydrostatic pressure. * **Gibbs-Donnan Effect:** Albumin is negatively charged and attracts cations (like $Na^+$) into the vessel. This increases the effective oncotic pressure by an additional 30-40% beyond what the protein molecules alone would provide. * **Clinical Correlation:** In **Nephrotic Syndrome** or **Liver Cirrhosis**, albumin levels fall, leading to a drop in oncotic pressure and the development of generalized edema (Anasarca).

Question 287: Which immunoglobulin is predominantly found in Peyer's patches?

A. IgM
B. IgG
C. IgA (Correct Answer)
D. IgD

Explanation: **Explanation:** **Correct Option: C (IgA)** Peyer’s patches are organized lymphoid tissues located in the lamina propria of the small intestine (ileum). They serve as the primary induction sites for the **Mucosal Immune System**. The predominant immunoglobulin produced here is **Secretory IgA (sIgA)**. B-cells in the Peyer’s patches undergo class-switching specifically to IgA in response to local cytokines (like TGF-β). This IgA is then transported across the intestinal epithelium to neutralize pathogens and toxins before they can penetrate the mucosal barrier. **Incorrect Options:** * **IgM (Option A):** While IgM is the first antibody produced during a primary immune response and is found on the surface of naive B-cells, it is not the dominant isotype associated with specialized mucosal lymphoid tissue like Peyer's patches. * **IgG (Option B):** IgG is the most abundant antibody in the **systemic circulation** (serum) and provides long-term immunity, but it is not the primary defender of the gut mucosa. * **IgD (Option D):** IgD is primarily found on the surface of mature B-lymphocytes as an antigen receptor; its secreted form has no significant role in mucosal immunity. **High-Yield NEET-PG Pearls:** * **M-Cells (Microfold cells):** These are specialized cells overlying Peyer’s patches that sample antigens from the intestinal lumen via transcytosis. * **J-Chain:** Secretory IgA is a **dimer** held together by a J-chain; this structure allows it to resist proteolysis by digestive enzymes. * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients often present with recurrent sinopulmonary and gastrointestinal infections.

Question 288: Which cell type lacks Human Leukocyte Antigen (HLA)?

A. Monocyte
B. Thrombocyte
C. Neutrophil
D. Red blood cell (Correct Answer)

Explanation: **Explanation:** The **Human Leukocyte Antigen (HLA)** system, also known as the Major Histocompatibility Complex (MHC), is a set of surface proteins found on almost all **nucleated cells** in the human body. These antigens are essential for the immune system to distinguish "self" from "non-self." **Why Red Blood Cells (RBCs) are the correct answer:** Mature Red Blood Cells are unique because they **lack a nucleus** and most organelles. Since HLA/MHC Class I molecules are synthesized and expressed based on nuclear genetic coding, RBCs do not express HLA on their surface. Instead, RBCs express their own specific surface antigens, primarily the ABO and Rh systems. **Analysis of Incorrect Options:** * **A. Monocyte:** These are nucleated white blood cells that function as professional antigen-presenting cells (APCs). They express both **MHC Class I** (found on all nucleated cells) and **MHC Class II** (found on APCs). * **B. Thrombocyte (Platelet):** Although platelets are fragments of megakaryocytes and lack a nucleus, they **do express HLA Class I** antigens on their surface. This is a high-yield distinction; HLA expression on platelets is clinically significant in cases of "platelet refractoriness" following multiple transfusions. * **C. Neutrophil:** As nucleated granulocytes, neutrophils express HLA Class I molecules. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Found on all nucleated cells + Platelets. (HLA-A, B, C). * **MHC Class II:** Found only on Antigen Presenting Cells (Macrophages, B-cells, Dendritic cells). (HLA-DP, DQ, DR). * **Exception:** The **Trophoblast** is a notable nucleated cell type that lacks classical HLA-A and B to prevent maternal immune rejection of the fetus. * **RBCs and Transfusion:** Because RBCs lack HLA, HLA-matching is not required for simple red cell transfusions; however, it is critical for organ transplants and platelet transfusions.

Question 289: Platelet adhesion to collagen occurs via which of the following?

A. Factor VIII
B. Factor IX
C. von Willebrand factor (Correct Answer)
D. Fibronectin

Explanation: **Explanation:** Platelet plug formation occurs in three distinct stages: **Adhesion, Activation, and Aggregation.** **1. Why von Willebrand factor (vWF) is correct:** When a blood vessel is injured, subendothelial collagen is exposed. Platelets do not bind directly to collagen efficiently under high-shear conditions (like in arteries). Instead, **von Willebrand factor (vWF)** acts as a molecular bridge. It binds to the exposed collagen on one side and to the **Glycoprotein Ib-IX-V (GpIb)** receptor on the platelet surface on the other. This specific interaction is the critical first step in **platelet adhesion**. **2. Why the other options are incorrect:** * **Factor VIII:** While Factor VIII circulates in the blood bound to vWF (which stabilizes it), it functions in the intrinsic pathway of the coagulation cascade to activate Factor X, not in platelet adhesion. * **Factor IX (Christmas Factor):** This is a serine protease in the coagulation cascade. Its deficiency causes Hemophilia B. It is involved in secondary hemostasis, not primary platelet adhesion. * **Fibronectin:** While fibronectin is an adhesive glycoprotein found in the extracellular matrix and plasma that can aid in cell-matrix interactions, it is not the primary mediator of platelet-collagen adhesion in the context of high-shear blood flow. **Clinical Pearls for NEET-PG:** * **Bernard-Soulier Syndrome:** Caused by a deficiency of the **GpIb** receptor; characterized by giant platelets and failure of adhesion. * **von Willebrand Disease (vWD):** The most common inherited bleeding disorder; results in impaired adhesion. * **Platelet Aggregation:** Mediated by **GpIIb/IIIa** receptors using **Fibrinogen** as a bridge (Targeted by drugs like Abciximab). * **Ristocetin Cofactor Assay:** Used to test vWF function; ristocetin induces platelet agglutination only in the presence of vWF.

Question 290: Which of the following is a common step in the coagulation pathway?

A. Activation of factor VII
B. Activation of factor VIII
C. Activation of factor IX
D. Activation of factor X (Correct Answer)

Explanation: ### Explanation The coagulation cascade is divided into three pathways: the **Intrinsic**, **Extrinsic**, and **Common** pathways. **Why Option D is Correct:** The **Common Pathway** begins with the activation of **Factor X (Stuart-Prower factor)**. Both the intrinsic and extrinsic pathways converge at this point. Once Factor X is activated to **Xa** (by the Tenase complexes), it combines with Factor Va, calcium, and phospholipids to form the **Prothrombinase complex**. This complex converts Prothrombin (II) into Thrombin (IIa), which ultimately converts Fibrinogen (I) into a stable Fibrin clot (Ia). Therefore, Factor X activation is the definitive "common step." **Analysis of Incorrect Options:** * **Option A (Factor VII):** This is unique to the **Extrinsic pathway**. It is activated by Tissue Factor (Factor III) following vascular injury. * **Options B & C (Factors VIII & IX):** These are components of the **Intrinsic pathway**. Factor IXa, along with its cofactor VIIIa, forms the "Intrinsic Tenase complex" to activate Factor X. Deficiencies in these lead to Hemophilia A and B, respectively. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Common Pathway:** "1 × 2 × 5 = 10" (Factors I, II, V, and X are involved). * **Rate-limiting step:** The conversion of Prothrombin to Thrombin is the most critical rate-limiting step in thrombus formation. * **Monitoring:** The Extrinsic pathway is monitored by **PT/INR** (Warfarin), while the Intrinsic pathway is monitored by **aPTT** (Heparin). * **Vitamin K Dependent Factors:** II, VII, IX, and X (plus Protein C and S). Note that Factor VII has the shortest half-life.

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