Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 131: What is the physiological result of storage of packed red blood cells?

A. Oxy-hemoglobin curve shifts to the right
B. Decrease in 2,3-diphosphoglycerate (2,3-DPG) (Correct Answer)
C. Increase in pH
D. Decrease in lactate

Explanation: ### Explanation The storage of Packed Red Blood Cells (PRBCs) leads to a series of biochemical and structural changes collectively known as the **"Storage Lesion."** **Why Option B is Correct:** During storage, RBCs continue to undergo anaerobic glycolysis, but at a reduced rate. Over time, there is a progressive **decrease in 2,3-diphosphoglycerate (2,3-DPG)** levels. Since 2,3-DPG normally facilitates oxygen unloading by stabilizing the T-state (deoxy-form) of hemoglobin, its depletion causes hemoglobin to bind oxygen more tightly. **Analysis of Incorrect Options:** * **Option A:** Because 2,3-DPG levels fall, the **Oxy-hemoglobin dissociation curve shifts to the LEFT**, not the right. This indicates an increased affinity of hemoglobin for oxygen and decreased delivery to tissues. * **Option C:** The pH actually **decreases (becomes more acidic)**. This is due to the accumulation of lactic acid and pyruvic acid from ongoing anaerobic metabolism within the storage bag. * **Option D:** There is an **increase in lactate** levels as a byproduct of anaerobic glycolysis during the storage period. **High-Yield Clinical Pearls for NEET-PG:** * **The Storage Lesion Summary:** ↓ 2,3-DPG, ↓ pH (Acidosis), ↓ ATP, ↑ Potassium (due to Na+/K+ pump failure), and ↑ Lactate. * **Shift to the Left:** Remember the mnemonic **"Left is Low"**—Low 2,3-DPG, Low Temp, Low H+ (High pH), and Low CO2 all shift the curve to the left. * **Clinical Impact:** Massive transfusion of stored blood can lead to **hyperkalemia** and **hypocalcemia** (due to citrate anticoagulant). * **Recovery:** Once transfused, 2,3-DPG levels typically begin to regenerate within 6–24 hours in the recipient’s circulation.

Question 132: Which blood group is considered the universal recipient?

A. A
B. B
C. O
D. AB (Correct Answer)

Explanation: **Explanation:** The correct answer is **AB (Option D)**. The classification of blood groups is based on the **Landsteiner Law**, which states that the antigens (agglutinogens) are present on the surface of Red Blood Cells (RBCs), while the corresponding antibodies (agglutinins) are found in the plasma. **Why AB is the Universal Recipient:** Individuals with blood group AB have **both Antigen A and Antigen B** on their RBC membranes. Crucially, their plasma contains **no anti-A or anti-B antibodies**. Because they lack these antibodies, they can receive blood from any ABO group (A, B, AB, or O) without triggering a life-threatening hemolytic transfusion reaction. Specifically, **AB Rh-positive** is the absolute universal recipient. **Analysis of Incorrect Options:** * **Option A (Group A):** Contains Antigen A and Anti-B antibodies. It can only receive from groups A and O. * **Option B (Group B):** Contains Antigen B and Anti-A antibodies. It can only receive from groups B and O. * **Option C (Group O):** Contains no antigens but has **both Anti-A and Anti-B antibodies** in the plasma. While it is the **Universal Donor** (specifically O negative), it can only receive blood from another O donor. **NEET-PG High-Yield Pearls:** 1. **Universal Donor:** O Negative (lacks A, B, and Rh antigens). 2. **Universal Recipient:** AB Positive (lacks anti-A, anti-B, and anti-Rh antibodies). 3. **Bombay Blood Group:** Lacks the H-antigen; can only receive blood from another Bombay group individual. 4. **Landsteiner’s Law Exception:** The law does not apply to the Rh system (anti-D antibodies are not naturally occurring; they develop only after exposure).

Question 133: Which of the following is NOT a known function of platelet-activating factor (PAF)?

A. Rupture of mature graafian follicle and ovulation
B. Hemostasis and thrombosis
C. Bronchial asthma
D. Congestive heart failure (Correct Answer)

Explanation: **Explanation:** Platelet-activating factor (PAF) is a potent phospholipid-derived mediator produced by various cells, including platelets, neutrophils, monocytes, and endothelial cells. It acts via G-protein-coupled receptors to trigger diverse physiological and pathological processes. **Why Option D is Correct:** **Congestive Heart Failure (CHF)** is primarily a hemodynamic and structural disorder of the heart. While PAF has potent cardiovascular effects—such as inducing systemic hypotension and reducing myocardial contractility (negative inotropy)—it is **not** a known causative factor or a primary mediator in the pathogenesis of CHF. Therefore, it is the "except" in this list. **Why the other options are incorrect:** * **Option A (Ovulation):** PAF plays a crucial role in reproductive physiology. It is involved in the rupture of the mature Graafian follicle by stimulating the release of proteolytic enzymes and prostaglandins necessary for ovulation. * **Option B (Hemostasis and Thrombosis):** As the name suggests, PAF is one of the most potent stimulators of platelet aggregation and degranulation. It plays a central role in thrombus formation and the inflammatory response of the vascular endothelium. * **Option C (Bronchial Asthma):** PAF is a key mediator in Type I hypersensitivity. It causes potent bronchoconstriction (300–1000 times more potent than histamine) and increases vascular permeability, leading to airway edema and mucus secretion. **High-Yield Clinical Pearls for NEET-PG:** * **Source:** PAF is synthesized from membrane phospholipids by the enzyme **Phospholipase A2**. * **Potency:** It is one of the most potent known chemotactic agents for neutrophils and eosinophils. * **Anaphylaxis:** PAF is a major mediator in the pathogenesis of anaphylactic shock. * **Antagonist:** **Ginkgolide B** (derived from the Ginkgo biloba tree) is a specific PAF receptor antagonist often mentioned in pharmacology.

Question 134: Which of the following statements regarding blood coagulation is true?

A. Addition of Vitamin K to a freshly drawn blood sample delays clotting.
B. Thrombin converts fibrin to fibrinogen.
C. Heparin inhibits blood coagulation by interfering with Vitamin K metabolism in the liver.
D. Platelets are essential for blood clot formation. (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Platelets are essential for blood clot formation.** Platelets (thrombocytes) play a dual role in hemostasis. Initially, they form a **primary platelet plug** (primary hemostasis). Subsequently, they provide a phospholipid surface (**Platelet Factor 3**) essential for the activation of the coagulation cascade, which leads to the formation of a stable fibrin mesh (secondary hemostasis). Without platelets, the conversion of prothrombin to thrombin is severely impaired, and clots cannot retract. **Analysis of Incorrect Options:** * **Option A:** Vitamin K is a fat-soluble vitamin required for the **gamma-carboxylation** of factors II, VII, IX, and X in the **liver**. It has no direct effect on blood that has already been drawn (in vitro) because the clotting factors are already synthesized. * **Option B:** The process is the reverse. **Thrombin** (Factor IIa) acts as a proteolytic enzyme that converts the soluble plasma protein **fibrinogen** into insoluble **fibrin** monomers. * **Option C:** Heparin acts by activating **Antithrombin III**, which then inactivates Thrombin and Factor Xa. It is **Warfarin (Coumadin)** that inhibits blood coagulation by interfering with Vitamin K metabolism (inhibiting Vitamin K epoxide reductase). **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin K Dependent Factors:** II, VII, IX, X, Protein C, and Protein S ("1972"). * **Clot Retraction:** This process depends on the contractile protein **thrombosthenin** found in platelets. * **Calcium (Factor IV):** It is required for almost every step of the coagulation cascade except the first two steps of the intrinsic pathway. This is why EDTA/Citrate (calcium chelators) are used as anticoagulants in blood vials. * **Bleeding Time (BT)** assesses platelet function, while **Prothrombin Time (PT)** and **aPTT** assess the coagulation cascade.

Question 135: Which of the following changes does NOT occur in blood passing through the systemic capillaries?

A. Increase in hematocrit
B. Decrease in pH
C. Shift of the oxygen-hemoglobin dissociation curve to the left (Correct Answer)
D. Increase in protein concentration

Explanation: ### Explanation In systemic capillaries, blood undergoes specific physiological changes as it exchanges gases and solutes with metabolically active tissues. **Why Option C is the Correct Answer:** When blood reaches systemic capillaries, it encounters high levels of **$CO_2$** and **$H^+$** (low pH) produced by tissues. These factors, along with increased temperature, decrease hemoglobin's affinity for oxygen. This results in a **Rightward Shift** of the oxygen-hemoglobin dissociation curve (the **Bohr Effect**), facilitating oxygen unloading to the tissues. Therefore, a shift to the *left* (which indicates increased affinity) does not occur here. **Analysis of Incorrect Options:** * **A. Increase in hematocrit:** As $CO_2$ enters RBCs, it is converted to $HCO_3^-$ and $H^+$. The $HCO_3^-$ leaves the cell in exchange for $Cl^-$ (**Chloride Shift/Hamburger Phenomenon**). This increase in intracellular osmotically active particles causes water to enter the RBCs, making them swell and increasing the overall hematocrit in venous blood compared to arterial blood. * **B. Decrease in pH:** Tissues release $CO_2$ and lactic acid. The hydration of $CO_2$ into carbonic acid increases the hydrogen ion concentration, leading to a drop in blood pH. * **D. Increase in protein concentration:** Due to hydrostatic pressure, a small amount of protein-free fluid filters out of the capillaries into the interstitial space. This slight loss of plasma volume leads to a relative increase in the concentration of plasma proteins (hemoconcentration). ### High-Yield NEET-PG Pearls * **Chloride Shift:** Occurs in systemic capillaries ($Cl^-$ moves **into** RBCs). * **Reverse Chloride Shift:** Occurs in pulmonary capillaries ($Cl^-$ moves **out** of RBCs). * **Left Shift Causes:** $\downarrow$ $H^+$ (alkalosis), $\downarrow$ $PCO_2$, $\downarrow$ Temperature, $\downarrow$ 2,3-BPG, and **HbF** (Fetal Hemoglobin). * **Venous Hematocrit:** Is always slightly higher (~3%) than arterial hematocrit due to RBC swelling.

Question 136: Colloidal osmotic pressure in plasma is exerted mainly by?

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

Explanation: ### Explanation **Concept Overview:** Colloidal Osmotic Pressure (COP), also known as **Oncotic Pressure**, is the osmotic pressure exerted by plasma proteins that pulls water into the circulatory system. While electrolytes are more numerous, they pass freely through capillary membranes; proteins do not, thus creating the pressure gradient necessary to maintain intravascular volume. **Why Albumin is the Correct Answer:** Albumin is the primary determinant of plasma oncotic pressure (contributing approximately **75-80%** of the total COP). This is due to two main reasons: 1. **High Concentration:** Albumin is the most abundant plasma protein (3.5–5.0 g/dL). 2. **Low Molecular Weight:** According to Van't Hoff’s law, osmotic pressure depends on the number of particles. Being smaller than globulins, more albumin molecules exist per unit of weight, exerting a greater osmotic effect. Additionally, its negative charge attracts sodium ions (**Gibbs-Donnan effect**), further increasing its osmotic power. **Analysis of Incorrect Options:** * **B. Globulin:** Although globulins are large, their concentration is lower and their molecular weight is much higher than albumin, making their contribution to COP significant but secondary. * **C. Fibrinogen:** This is the largest common plasma protein but is present in very low concentrations (200–400 mg/dL), contributing minimally to oncotic pressure. Its primary role is blood coagulation. * **D. Transferrin:** This is a beta-globulin responsible for iron transport. Its concentration is too low to significantly impact plasma oncotic pressure. **High-Yield Clinical Pearls for NEET-PG:** * **Starling’s Forces:** Edema occurs when COP falls (hypoalbuminemia) or capillary hydrostatic pressure rises. * **Hypoalbuminemia:** Seen in Nephrotic Syndrome (loss in urine), Cirrhosis (decreased synthesis), and Kwashiorkor (malnutrition), leading to generalized edema and ascites. * **Normal COP Value:** Approximately **25–28 mmHg**. Of this, ~20 mmHg is due to the proteins themselves, and ~8 mmHg is due to the Gibbs-Donnan effect.

Question 137: Fibrinogen is present in which of the following granules of platelets?

A. Alpha granules (Correct Answer)
B. Beta granules
C. Gamma granules
D. Delta granules

Explanation: **Explanation:** Platelets contain three main types of storage granules: **Alpha granules**, **Dense (Delta) granules**, and **Lysosomes (Lambda granules)**. **Why Alpha Granules are correct:** Alpha granules are the most numerous granules in platelets. They primarily store **large proteins** essential for coagulation and tissue repair. **Fibrinogen** is a key protein stored here, alongside von Willebrand factor (vWF), Platelet Factor 4 (PF4), Platelet-Derived Growth Factor (PDGF), and Factor V. During platelet activation, these granules undergo exocytosis, releasing fibrinogen to facilitate platelet aggregation via the GpIIb/IIIa receptor. **Analysis of Incorrect Options:** * **Delta Granules (Dense bodies):** These store **small non-protein molecules** necessary for platelet activation and recruitment. The mnemonic **"SAC"** is useful: **S**erotonin, **A**DP/ATP, and **C**alcium. They do not contain fibrinogen. * **Beta and Gamma Granules:** These are not standard classifications for platelet storage granules. While lysosomes are sometimes referred to as lambda granules (containing hydrolytic enzymes), "Beta" and "Gamma" are distractors in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Gray Platelet Syndrome:** A rare bleeding disorder caused by a congenital deficiency of **Alpha granules**, leading to large, "pale" or gray-appearing platelets on a peripheral smear. * **Hermansky-Pudlak Syndrome:** A disorder characterized by a deficiency of **Dense (Delta) granules**, presenting with oculocutaneous albinism and bleeding tendencies. * **P-selectin:** An adhesion molecule located on the inner membrane of Alpha granules that is expressed on the platelet surface only after activation (used as a marker for activated platelets).

Question 138: Thromboxane A2 is secreted by which of the following cells?

A. Macrophages
B. Platelets (Correct Answer)
C. Smooth muscle cells
D. Reticuloendothelial cells

Explanation: **Explanation:** **Thromboxane A2 (TXA2)** is a potent eicosanoid produced primarily by **platelets**. The process begins when membrane phospholipids are converted into arachidonic acid by Phospholipase A2. In platelets, the enzyme **Cyclooxygenase-1 (COX-1)** converts arachidonic acid into Prostaglandin H2, which is then specifically acted upon by **Thromboxane Synthase** to produce TXA2. Physiologically, TXA2 plays a critical role in hemostasis by acting as a powerful **platelet aggregator** and a potent **vasoconstrictor**. It helps in the formation of the temporary platelet plug. **Analysis of Options:** * **Macrophages (A):** While they produce various eicosanoids (like Prostaglandin E2 and Leukotrienes) during inflammation, they are not the primary source of TXA2. * **Smooth Muscle Cells (C):** These cells are the *targets* of TXA2 (causing contraction), but they do not secrete it. They primarily produce Prostacyclin (PGI2) in the vascular endothelium, which opposes TXA2. * **Reticuloendothelial cells (D):** These are part of the immune/phagocytic system (e.g., Kupffer cells, splenic macrophages) and are not involved in the TXA2-mediated clotting cascade. **High-Yield Clinical Pearls for NEET-PG:** * **Aspirin Mechanism:** Low-dose Aspirin irreversibly inhibits COX-1 in platelets. Since platelets are anuclear and cannot synthesize new enzymes, TXA2 production is inhibited for the lifetime of the platelet (7–10 days), providing its anti-thrombotic effect. * **TXA2 vs. PGI2:** Remember them as opposites. **TXA2** (Platelets) = Pro-aggregation + Vasoconstriction. **PGI2** (Endothelium) = Anti-aggregation + Vasodilation. * **VWF vs. TXA2:** Von Willebrand Factor is for platelet *adhesion*, while TXA2 is for platelet *aggregation*.

Question 139: Haemostasis depends upon all the following, EXCEPT?

A. Calcium
B. Prothrombin
C. Vitamin B (Correct Answer)
D. Vitamin K

Explanation: **Explanation:** Haemostasis is the physiological process that stops bleeding at the site of vascular injury. It involves a complex interplay between the vessel wall, platelets, and coagulation factors. **Why Vitamin B is the correct answer:** Vitamin B (specifically the B-complex group) is primarily involved in energy metabolism, red blood cell synthesis (B12 and Folate), and neurological function. It does **not** play a direct role in the coagulation cascade or the formation of a fibrin clot. Therefore, haemostasis does not depend on Vitamin B. **Analysis of other options:** * **Calcium (Factor IV):** It is essential for almost all steps of the coagulation cascade (except the initial stages of the intrinsic pathway). It acts as a bridge between phospholipids and clotting factors. * **Prothrombin (Factor II):** This is a plasma protein produced by the liver. It is converted into **thrombin**, the key enzyme that transforms soluble fibrinogen into insoluble fibrin strands to form a stable clot. * **Vitamin K:** This is a vital fat-soluble vitamin required for the post-translational gamma-carboxylation of **Factors II, VII, IX, and X**, as well as Protein C and S. Without Vitamin K, these factors are synthesized but remain biologically inactive. **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin K Antagonist:** Warfarin acts by inhibiting Vitamin K epoxide reductase, preventing the activation of Clotting Factors II, VII, IX, and X. * **Chelating Agents:** Substances like EDTA and Citrate prevent blood clotting in vitro by binding to **Calcium**, making it unavailable for the coagulation cascade. * **Vitamin B12/Folate Deficiency:** Leads to Megaloblastic Anemia, not bleeding disorders. However, severe deficiency can cause pancytopenia, which may lead to thrombocytopenia (low platelets) and subsequent bleeding.

Question 140: Which substance is present in both serum and plasma?

A. Fibrinogen
B. Factor II
C. Factor VII (Correct Answer)
D. Factor V

Explanation: ### Explanation The fundamental difference between **plasma** and **serum** lies in the clotting process. Plasma is the liquid, cell-free part of blood treated with anticoagulants, containing all coagulation factors. Serum is the liquid remains after blood has clotted; therefore, it lacks fibrinogen and the factors consumed during the coagulation cascade. **Why Factor VII is the correct answer:** Coagulation factors are categorized into those that are consumed during clot formation and those that remain in the serum. **Factor VII** (Proconvertin) is a stable factor that is **not consumed** during the clotting process. Therefore, it is present in both plasma and serum. Other factors remaining in serum include Factors VII, IX, X, XI, and XII. **Analysis of Incorrect Options:** * **A. Fibrinogen (Factor I):** This is completely converted into a fibrin mesh during clotting. It is present in plasma but entirely absent in serum. * **B. Factor II (Prothrombin):** This is consumed as it is converted into Thrombin to facilitate the cleavage of fibrinogen. * **D. Factor V (Proaccelerin):** This is a "labile factor" and a cofactor in the prothrombinase complex. It is consumed during the clotting process and is absent in serum. **High-Yield Facts for NEET-PG:** * **Consumed Factors (Absent in Serum):** I, II, V, VIII, and XIII. (Mnemonic: *“1, 2, 5, 8, 13 are used up”*). * **Serum = Plasma – (Fibrinogen + Clotting Factors II, V, VIII, XIII).** * **Vitamin K Dependent Factors:** II, VII, IX, and X. Among these, Factor VII has the shortest half-life (approx. 4–6 hours), making the PT/INR a sensitive indicator of early liver dysfunction or Vitamin K deficiency.

Practice by Chapter

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Blood Groups and Transfusion

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Coagulation and Fibrinolysis

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Hematopoiesis

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Immunological Memory and Tolerance

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