Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 71: Which of the following, when increased, can cause a shift of the oxygen-hemoglobin dissociation curve to the left?

A. pH (Correct Answer)
B. Temperature
C. 2,3-BPG
D. pCO2

Explanation: The oxygen-hemoglobin (O2-Hb) dissociation curve represents the relationship between the partial pressure of oxygen ($pO_2$) and the percentage saturation of hemoglobin. A **shift to the left** indicates an increased affinity of hemoglobin for oxygen, meaning hemoglobin binds oxygen more tightly and releases it less readily to the tissues. ### Why pH is the Correct Answer An **increase in pH** (alkalosis) signifies a decrease in hydrogen ion ($H^+$) concentration. According to the **Bohr Effect**, a decrease in $H^+$ ions stabilizes the relaxed (R) state of hemoglobin, which has a higher affinity for oxygen. This results in a leftward shift of the curve. ### Why the Other Options are Incorrect Options B, C, and D all cause a **shift to the right** (decreased affinity, easier unloading of oxygen): * **Temperature:** Increased temperature (e.g., during fever or exercise) weakens the bond between Hb and $O_2$, shifting the curve to the right. * **2,3-BPG:** This byproduct of glycolysis binds to the beta chains of deoxygenated hemoglobin, stabilizing the Tense (T) state and promoting $O_2$ release (right shift). * **$pCO_2$:** Increased $CO_2$ leads to increased $H^+$ production (via carbonic anhydrase), which decreases affinity (right shift). ### High-Yield Clinical Pearls for NEET-PG * **Mnemonic for Right Shift:** "**CADET**, face Right!" (**C**O2, **A**cid, **D**PG/2,3-BPG, **E**xercise, **T**emperature). * **Fetal Hemoglobin (HbF):** Shifting to the **left** is a physiological adaptation in HbF, allowing the fetus to pull oxygen from maternal blood. * **$P_{50}$ Value:** A left shift **decreases** the $P_{50}$ (the $pO_2$ at which Hb is 50% saturated), while a right shift **increases** it. * **Carbon Monoxide (CO):** CO poisoning causes a **left shift** of the remaining heme sites, preventing the release of oxygen to tissues, leading to cellular hypoxia.

Question 72: The Rh factor is a:

A. Antibody (Correct Answer)
B. Mucopolysaccharide
C. Lipoprotein
D. Glycoprotein

Explanation: **Explanation:** The Rh factor (Rhesus factor) refers to a specific group of antigens found on the surface of red blood cells. However, in the context of this specific question (often seen in older physiological classifications), the term "Rh factor" is historically used to describe the **anti-Rh antibodies** (specifically Anti-D) that react with the Rh antigen. 1. **Why 'Antibody' is the correct answer:** In classical immunology nomenclature, a "factor" often refers to the reactive component in the serum. The Rh factor was discovered by Landsteiner and Wiener when they injected Rhesus monkey blood into rabbits; the rabbits produced an **antibody** (the Rh factor) that agglutinated human RBCs. In modern clinical practice, we distinguish between the Rh *antigen* (on the RBC) and the Rh *antibody* (in the serum), but for competitive exams, it is traditionally classified as an antibody. 2. **Why the other options are incorrect:** * **Mucopolysaccharide:** This describes the chemical nature of ABO blood group antigens (which are glycolipids and glycoproteins with carbohydrate side chains). * **Lipoprotein:** Rh antigens are non-glycosylated, hydrophobic proteins, but they are not classified as lipoproteins. * **Glycoprotein:** While many RBC surface markers are glycoproteins (like ABO), the Rh antigens (D, C, c, E, e) are unique because they are **pure transmembrane proteins** with no carbohydrate side chains. **High-Yield Clinical Pearls for NEET-PG:** * **Nature of Rh Antigen:** It is a non-glycosylated protein. * **Inheritance:** Rh antigens are encoded by two genes, *RHD* and *RHCE*, located on **Chromosome 1**. * **Clinical Significance:** Rh antibodies are **IgG** type. Unlike ABO antibodies, they cross the placenta, leading to **Erythroblastosis Fetalis** (Hemolytic Disease of the Newborn). * **Immunogenicity:** The **D antigen** is the most immunogenic of all non-ABO antigens.

Question 73: Which clotting factor is not affected in liver disease?

A. Factor II
B. Factor IV
C. Factor IX
D. Factor VIII (Correct Answer)

Explanation: **Explanation:** The liver is the primary site for the synthesis of almost all coagulation factors. However, **Factor VIII (Anti-hemophilic factor)** is the notable exception. While it is produced by various tissues, its primary source is the **vascular endothelial cells** (specifically in the liver sinusoids and other extrahepatic sites), rather than the hepatocytes. Therefore, in chronic liver disease, Factor VIII levels do not decrease; in fact, they often **increase** due to a compensatory mechanism or decreased clearance by the diseased liver. **Analysis of Options:** * **Factor II (Prothrombin):** Synthesized in hepatocytes and is Vitamin K-dependent. Its levels drop significantly in liver failure. * **Factor IV (Calcium):** This is an inorganic ion obtained from the diet and bone metabolism, not synthesized by the liver. However, in the context of "clotting factors synthesized by the liver," Factor VIII is the classic physiological exception taught for exams. * **Factor IX (Christmas Factor):** A Vitamin K-dependent factor synthesized exclusively by hepatocytes. Its deficiency is seen early in liver dysfunction. **High-Yield Clinical Pearls for NEET-PG:** 1. **Vitamin K Dependent Factors:** II, VII, IX, and X (all synthesized in the liver). 2. **Shortest Half-life:** Factor VII has the shortest half-life (4–6 hours), making **Prothrombin Time (PT)** the best early indicator of acute liver cell failure. 3. **Factor VIII and vWF:** Both are produced by endothelial cells (Weibel-Palade bodies) and remain elevated or normal in liver cirrhosis. 4. **Factor V:** Unlike Factor VIII, Factor V is synthesized in the liver. Comparing Factor V and Factor VIII levels can help differentiate between Vitamin K deficiency (Factor V normal) and true liver disease (Factor V low).

Question 74: During a cardiac intervention, numerous endothelial cells are dislodged from the lining of the popliteal vein. What substance allows platelet adhesion to the exposed collagen fibers?

A. Factor IX
B. Fibronectin
C. Tissue factor
D. Von Willebrand factor (Correct Answer)

Explanation: ### Explanation The correct answer is **Von Willebrand factor (vWF)**. **1. Why Von Willebrand factor is correct:** Hemostasis occurs in three stages: vascular spasm, primary hemostasis (platelet plug), and secondary hemostasis (coagulation). When endothelial cells are dislodged, the underlying **sub-endothelial collagen** is exposed. Platelets cannot bind directly to collagen under high-shear stress conditions. **Von Willebrand factor (vWF)**, synthesized by endothelial cells (stored in **Weibel-Palade bodies**) and megakaryocytes, acts as a molecular bridge. It binds to the exposed collagen on one side and to the **Glycoprotein Ib (GpIb)** receptor on the platelet surface on the other. This "tethering" is the critical first step of platelet adhesion. **2. Why the other options are incorrect:** * **Factor IX:** This is a component of the intrinsic pathway of the coagulation cascade (secondary hemostasis). Its deficiency leads to Hemophilia B. It is involved in fibrin formation, not initial platelet adhesion. * **Fibronectin:** While fibronectin is an adhesive glycoprotein found in plasma and the extracellular matrix that can aid in cell-matrix interactions, it is not the primary mediator for platelet-collagen binding in the high-flow environment of the vasculature. * **Tissue factor (Factor III):** This is released from damaged extravascular cells and triggers the **extrinsic pathway** by activating Factor VII. It is essential for thrombin generation but does not mediate platelet adhesion to collagen. **3. High-Yield Clinical Pearls for NEET-PG:** * **Bernard-Soulier Syndrome:** Deficiency of GpIb receptor (platelets cannot bind to vWF). * **Von Willebrand Disease:** The most common inherited bleeding disorder; characterized by a defect in platelet adhesion and a prolonged Bleeding Time (BT). * **Storage:** vWF is stored in **Weibel-Palade bodies** of endothelial cells and **alpha-granules** of platelets. * **Dual Role:** vWF also acts as a carrier protein for **Factor VIII**, protecting it from degradation. Therefore, vWD can sometimes present with a prolonged aPTT.

Question 75: Which of the following is present in plasma but absent in serum?

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

Explanation: ### Explanation The fundamental difference between plasma and serum lies in the process of **coagulation**. **1. Why Fibrinogen is the Correct Answer:** Plasma is the liquid, cell-free part of blood that has been treated with anti-coagulants. Serum, however, is the liquid remains of whole blood after it has been allowed to clot. During the clotting process, **Fibrinogen** (Clotting Factor I), which is a soluble protein present in plasma, is converted into **insoluble Fibrin** by the action of thrombin. This fibrin forms the meshwork of the blood clot. Therefore, when the clot is removed, the resulting serum contains no fibrinogen (and lacks other clotting factors like II, V, and VIII). **2. Analysis of Incorrect Options:** * **A & B (Albumin and Globulin):** These are the major plasma proteins. They do not participate in the coagulation cascade and remain unchanged in both plasma and serum. * **C (Lecithin):** This is a phospholipid (phosphoglyceride) found in cell membranes and transported in the blood. It is not consumed during clotting and is present in both plasma and serum. **3. NEET-PG High-Yield Pearls:** * **Formula to remember:** Serum = Plasma – Clotting Factors (primarily Fibrinogen). * **Electrophoresis:** On serum protein electrophoresis, the "fibrinogen peak" is absent. If you see a peak between the beta and gamma regions in a sample labeled "serum," it suggests the sample is actually plasma or incomplete clotting has occurred. * **Clinical Use:** Serum is preferred for most serological tests and clinical chemistry (e.g., electrolytes, cholesterol) because the absence of fibrinogen prevents the sample from clotting again during automated testing, which could clog the machinery.

Question 76: What is the biological anticoagulant?

A. EDTA
B. Sodium citrate
C. Hirudin (Correct Answer)
D. Double oxalate mixture

Explanation: **Explanation:** The correct answer is **Hirudin** because it is a naturally occurring, biological substance produced by the salivary glands of medicinal leeches (*Hirudo medicinalis*). **Why Hirudin is the correct answer:** Hirudin is a potent **direct thrombin inhibitor**. Unlike heparin, it does not require Antithrombin III as a cofactor. It binds directly to thrombin, preventing the conversion of fibrinogen into fibrin, thereby inhibiting blood clot formation. Since it is derived from a living organism, it is classified as a **biological anticoagulant**. **Analysis of Incorrect Options:** * **EDTA (Ethylene Diamine Tetra-acetic Acid):** This is a synthetic chemical anticoagulant used in labs (Purple top tubes). It works by **chelating calcium** (removing Ca²⁺ ions), which is essential for the coagulation cascade. * **Sodium Citrate:** A synthetic chemical anticoagulant used in coagulation studies (Blue top) and blood banking. Like EDTA, it works by **chelating calcium**. * **Double Oxalate (Wintrobe’s Mixture):** A mixture of Ammonium and Potassium oxalate. It is a synthetic agent that works by **precipitating calcium** as calcium oxalate. **High-Yield Clinical Pearls for NEET-PG:** * **In-vivo and In-vitro:** Heparin is the only anticoagulant used both in the body and in the lab. EDTA, Citrate, and Oxalate are used **only in-vitro** (outside the body). * **Drug of Choice:** EDTA is the anticoagulant of choice for **Hematological investigations** (CBC/ESR) as it preserves blood cell morphology. * **Blood Transfusion:** Sodium Citrate is the anticoagulant of choice for **blood storage** in blood banks. * **Recombinant Hirudin:** Lepirudin and Desirudin are synthetic analogs used clinically in patients with Heparin-Induced Thrombocytopenia (HIT).

Question 77: Ferritin stores are present in the following sites except?

A. Intestine (Correct Answer)
B. Liver
C. Spleen
D. Bone

Explanation: ### Explanation The correct answer is **A. Intestine**. **1. Why Intestine is the correct answer:** Iron is stored in the body primarily in the form of **Ferritin** (soluble) and **Hemosiderin** (insoluble). While the mucosal cells of the small intestine (enterocytes) contain ferritin, it is considered a **"labile" or temporary pool** rather than a storage site. Iron in the intestine is either absorbed into the blood or lost when the mucosal cells are desquamated (sloughed off) every few days. Therefore, the intestine is not a site for long-term iron storage. **2. Analysis of Incorrect Options:** The Reticuloendothelial System (RES) and hepatocytes are the primary long-term reservoirs for iron: * **B. Liver:** The liver is the **primary storage site** for iron. Hepatocytes and Kupffer cells store the majority of the body's ferritin. * **C. Spleen:** Splenic macrophages recycle iron from aged red blood cells and store it as ferritin. * **D. Bone:** Bone marrow macrophages store iron to make it readily available for erythropoiesis (hemoglobin synthesis). **3. NEET-PG High-Yield Pearls:** * **Most sensitive index** for iron deficiency anemia (IDA): **Serum Ferritin** (it decreases before changes in hemoglobin or RBC morphology occur). * **Apoferritin + Iron = Ferritin.** * **Hepcidin:** The "Master Regulator" of iron metabolism; it inhibits iron release by binding to **Ferroportin**. * **Daily Iron Loss:** Approximately 1 mg/day (via desquamation of skin and intestinal cells). * **Site of maximum iron absorption:** Duodenum and upper jejunum.

Question 78: What is true regarding blood group A?

A. Can be safely transfused with blood group AB.
B. Will have only A offsprings if the parent is A.
C. Can receive safe O group transfusion. (Correct Answer)
D. Irrespective of the parent, all the child would be A group.

Explanation: **Explanation:** The ABO blood grouping system is determined by the presence of specific antigens (agglutinogens) on the surface of Red Blood Cells (RBCs) and naturally occurring antibodies (agglutinins) in the plasma. **Why Option C is Correct:** Blood group O is known as the **Universal Donor**. Individuals with group O lack both A and B antigens on their RBCs. Therefore, when group O blood is transfused into a person with group A, the recipient’s anti-B antibodies have no B-antigens to attack, preventing a hemolytic transfusion reaction. **Analysis of Incorrect Options:** * **Option A:** Group A blood cannot be safely transfused into a Group AB recipient *in all contexts*, but more importantly, the reverse is definitely false. If a Group A person receives AB blood, their **anti-B antibodies** will attack the B-antigens on the donor cells, causing hemolysis. * **Options B & D:** These are genetically incorrect. A person with blood group A can have the genotype **AA (homozygous)** or **AO (heterozygous)**. If a parent is AO and the other parent is O (OO) or B (BO), they can produce offspring with group O or B. The inheritance follows Mendelian laws, not a fixed rule that all children will be group A. **Clinical Pearls for NEET-PG:** * **Universal Donor:** O negative (due to lack of A, B, and Rh antigens). * **Universal Recipient:** AB positive (due to lack of anti-A, anti-B, and anti-D antibodies). * **Landsteiner’s Law:** If an agglutinogen is present on RBCs, the corresponding agglutinin must be absent in the plasma. * **Bombay Blood Group:** Lacks H-antigen; can only receive blood from another Bombay group individual.

Question 79: Abnormal increase in the number of RBCs is known as:

A. Leukocytosis
B. Polycythemia (Correct Answer)
C. Anemia
D. Thrombocytosis

Explanation: **Explanation:** **Correct Answer: B. Polycythemia** Polycythemia is defined as an abnormal increase in the total number of red blood cells (RBCs) in the systemic circulation, often reflected by an elevated hemoglobin level and hematocrit (PCV). It is categorized into **Primary Polycythemia** (e.g., Polycythemia Vera, a myeloproliferative neoplasm caused by a JAK2 mutation) and **Secondary Polycythemia** (driven by increased Erythropoietin due to chronic hypoxia, such as in high altitudes or COPD). **Analysis of Incorrect Options:** * **A. Leukocytosis:** Refers to an increase in the total **White Blood Cell (WBC)** count above the normal range (usually >11,000/µL), typically seen during infections or inflammation. * **C. Anemia:** The physiological opposite of polycythemia; it is a condition characterized by a **decrease** in the number of RBCs or the hemoglobin concentration, leading to reduced oxygen-carrying capacity. * **D. Thrombocytosis:** Refers to an abnormally high **platelet** count (usually >450,000/µL), which can be reactive or due to bone marrow disorders. **NEET-PG High-Yield Pearls:** * **Polycythemia Vera (PV):** Characterized by "Panmyelosis" (increase in all three cell lines) and a low serum Erythropoietin (EPO) level. * **Relative Polycythemia (Gaisbock syndrome):** An apparent increase in RBC count due to decreased plasma volume (dehydration), not an actual increase in RBC mass. * **Clinical Sign:** Patients often present with "aquagenic pruritus" (itching after a warm bath) and hyperviscosity symptoms.

Question 80: Factor V Leiden is resistant to direct inactivation by:

A. Thrombin-thrombomodulin complex
B. Antithrombin
C. Activated protein C (Correct Answer)
D. All of the above

Explanation: **Explanation:** **Factor V Leiden** is the most common inherited cause of hypercoagulability (thrombophilia). It results from a specific point mutation (G1691A) in the Factor V gene, where the amino acid **Arginine is replaced by Glutamine at position 506**. **Why Activated Protein C (APC) is the correct answer:** In the normal anticoagulation pathway, **Activated Protein C (APC)** inactivates procoagulant factors Va and VIIIa by cleaving them at specific sites. The mutation in Factor V Leiden alters the cleavage site (Arg506) where APC normally binds. Consequently, Factor V remains in its active form for longer, leading to a state of "APC Resistance" and an increased risk of venous thromboembolism (VTE). **Analysis of Incorrect Options:** * **A. Thrombin-thrombomodulin complex:** This complex is responsible for *activating* Protein C into APC. It does not directly inactivate Factor V; rather, it initiates the pathway that leads to its inactivation. * **B. Antithrombin:** Antithrombin primarily inhibits Thrombin (IIa) and Factor Xa. While it is a major natural anticoagulant, its primary target is not Factor V. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Clinical Presentation:** Recurrent Deep Vein Thrombosis (DVT) and Pulmonary Embolism. * **Diagnosis:** Suspected when a patient has a shortened Activated Partial Thromboplastin Time (aPTT) that does not prolong significantly upon the addition of APC (APC Resistance Test). * **Genetic Confirmation:** PCR is the gold standard to identify the G1691A mutation. * **Risk:** Heterozygotes have a 5-10 fold increased risk of VTE; homozygotes have up to an 80-fold increased risk.

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