Blood and Immunity — MCQs

A 33-year-old man presents with a 5-week history of calf pain, swelling, and low-grade fever. Serum levels of creatinine kinase are elevated. A muscle biopsy reveals numerous eosinophils and he also has peripheral blood eosinophilia. Which of the following interleukins is primarily responsible for the increase in eosinophils in this patient?

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 441: Which factor increases the affinity of hemoglobin for O2?

A. Acidosis
B. Hyperthermia
C. High pH (Correct Answer)
D. High PCO2

Explanation: ***High pH*** - A **high pH** (alkalosis) increases hemoglobin's affinity for oxygen, shifting the **oxygen dissociation curve to the left**. - This is known as the **Bohr effect**, where an increase in pH (i.e., decreased H+ concentration) enhances oxygen binding. *Acidosis* - **Acidosis** (low pH) decreases hemoglobin's affinity for oxygen, promoting oxygen release to tissues. - This effect, part of the **Bohr effect**, shifts the **oxygen dissociation curve to the right**. *Hyperthermia* - **Increased body temperature** (hyperthermia) reduces hemoglobin's affinity for oxygen. - This causes the **oxygen dissociation curve to shift to the right**, facilitating oxygen delivery to metabolically active, warm tissues. *High PCO2* - An **elevated partial pressure of carbon dioxide (PCO2)** decreases hemoglobin's affinity for oxygen. - This is also part of the **Bohr effect**, as high PCO2 leads to increased H+ concentration (lower pH), shifting the **oxygen dissociation curve to the right**.

Question 442: Which of the following statements about carboxyhemoglobin is true?

A. Causes a left shift of the Hb-O2 dissociation curve (Correct Answer)
B. None of the options
C. Takes up oxygen very quickly
D. Causes histotoxic hypoxia in tissues

Explanation: ***Correct: Causes a left shift of the Hb-O2 dissociation curve*** - Carbon monoxide (CO) binds to hemoglobin with an affinity **210-250 times greater** than oxygen, forming carboxyhemoglobin (COHb). - When CO occupies some heme sites, it causes **allosteric conformational changes** in the hemoglobin molecule, increasing the oxygen affinity of the remaining unoccupied heme sites. - This results in a **left shift of the oxygen-hemoglobin dissociation curve**, meaning hemoglobin holds oxygen more tightly and releases it less readily to tissues. - This combination of **reduced oxygen-carrying capacity** (functional anemia) and **impaired oxygen release** (left shift) makes CO poisoning particularly dangerous. *Incorrect: Takes up oxygen very quickly* - This is false; COHb does **not** take up oxygen. - CO occupies the heme binding sites, **preventing** oxygen from binding. - CO's high affinity for hemoglobin means it displaces and blocks oxygen binding, reducing the blood's oxygen-carrying capacity. *Incorrect: Causes histotoxic hypoxia in tissues* - This is incorrect; CO poisoning causes **hypoxic hypoxia** (inadequate oxygen delivery), not histotoxic hypoxia. - **Histotoxic hypoxia** is caused by agents like **cyanide**, which inhibit cellular enzymes (cytochrome oxidase) and prevent tissues from utilizing oxygen. - COHb reduces oxygen delivery but does not impair cellular oxygen utilization mechanisms. *Incorrect: None of the options* - This is incorrect because the statement about the left shift of the Hb-O2 dissociation curve is physiologically accurate and well-established in medical literature.

Question 443: Where is the primary site of synthesis for Complement component C1 inhibitor (C1-INH)?

A. Liver (Correct Answer)
B. Intestinal epithelium
C. Macrophages
D. Endothelium

Explanation: ***Liver*** - The **liver** is the principal site of synthesis for most plasma proteins, including the **complement components** and their inhibitors such as C1-INH. - **Hepatocytes** within the liver are responsible for the constant production and secretion of C1-INH into the bloodstream. *Macrophages* - While **macrophages** can produce certain complement components and cytokines, they are not the primary site for the systemic synthesis of **C1-INH**. - Macrophage-derived complement proteins often play a more localized role in immune responses. *Intestinal epithelium* - The **intestinal epithelium** is primarily involved in digestion, nutrient absorption, and acting as a barrier, not in the bulk synthesis of systemic complement inhibitors like **C1-INH**. - These cells do produce some immune-related molecules, but not C1-INH. *Endothelium* - **Endothelial cells** lining blood vessels play roles in regulating vascular tone and local inflammation, but they are not the main producers of circulating **C1-INH**. - They can express and modify certain adhesion molecules and cytokines, but large-scale protein synthesis like C1-INH occurs elsewhere.

Question 444: NO acts on platelets through?

A. Adenosine
B. cAMP
C. cGMP (Correct Answer)
D. TX-A2

Explanation: ***cGMP*** - **Nitric oxide (NO)** activates **guanylyl cyclase**, which then converts **GTP (guanosine triphosphate)** to **cGMP (cyclic guanosine monophosphate)**. - Increased levels of **cGMP** in platelets lead to a cascade of events that ultimately result in **platelet inhibition**, mainly by reducing intracellular calcium and inhibiting aggregation. *cAMP* - **cAMP (cyclic AMP)** is primarily involved in pathways mediated by **prostacyclin (PGI2)** and **prostaglandin E1 (PGE1)**, which activate adenylyl cyclase. - While both **cAMP** and **cGMP** are cyclic nucleotides that regulate platelet function, **NO** specifically acts via the **cGMP** pathway. *Adenosine* - **Adenosine** acts on specific surface receptors (e.g., A2A receptors) on platelets, leading to activation of **adenylyl cyclase** and an increase in **cAMP** levels, which also inhibits platelet aggregation. - However, **NO** does not directly act through **adenosine** or its receptors to exert its effects. *TX-A2* - **Thromboxane A2 (TXA2)** is a potent **pro-aggregatory** and **vasoconstrictive** agent produced by platelets. - **NO** opposes the actions of **TXA2**; it does not act through it but rather counteracts its effects to promote platelet inhibition.

Question 445: Which of the following substances does hemoglobin not bind or transport?

A. CO
B. CO2
C. O2
D. SO2 (Correct Answer)

Explanation: **SO2** - **Sulfur dioxide (SO2)** is a toxic gas primarily associated with air pollution and **acid rain**; hemoglobin does not have a binding site for or physiological role in transporting SO2. - Exposure to SO2 can cause respiratory irritation and damage, but it does not directly bind to hemoglobin like CO, O2, or CO2. *CO* - **Carbon monoxide (CO)** binds to hemoglobin with an affinity 200-250 times greater than oxygen, forming **carboxyhemoglobin**. - This strong binding prevents oxygen transport, leading to **tissue hypoxia**. *O2* - **Oxygen (O2)** is the primary physiological ligand for hemoglobin, binding to the **heme iron** to be transported from the lungs to peripheral tissues, forming oxyhemoglobin. - This binding is cooperative, meaning the binding of one O2 molecule increases hemoglobin's affinity for subsequent O2 molecules. *CO2* - **Carbon dioxide (CO2)** is transported by hemoglobin, forming **carbaminohemoglobin**, though most CO2 is transported as bicarbonate. - CO2 binds to the **amino groups** of the globin chains, not the heme iron, making it a distinct binding site from oxygen.

Question 446: Gamma globulins are synthesized in?

A. Liver
B. Spleen
C. Kidney
D. Plasma cells (Correct Answer)

Explanation: ***Plasma cells*** - **Plasma cells** are differentiated B lymphocytes that are specialized in producing and secreting large quantities of **antibodies (gamma globulins)**. - This process is a crucial part of the body's **humoral immune response** to pathogens. *Liver* - The **liver** is primarily responsible for synthesizing most other plasma proteins, such as **albumin**, **clotting factors**, and lipoproteins. - While important for protein metabolism, it does not directly synthesize **gamma globulins**. *Spleen* - The **spleen** is a secondary lymphoid organ involved in filtering blood, storing blood cells, and initiating immune responses. - It contains immune cells like B cells and plasma cells, but it is not the primary site of **gamma globulin synthesis** itself. *Kidney* - The **kidney's** main functions are filtering waste products from the blood, regulating blood pressure, and producing hormones. - It plays no direct role in the synthesis of **gamma globulins**.

Question 447: Which factor activates the extrinsic system of coagulation?

A. Factor X (Stuart-Prower factor)
B. Factor XII (Hageman factor)
C. Factor III (Tissue factor) (Correct Answer)
D. Factor XI (Plasma thromboplastin antecedent)

Explanation: ***Factor III*** - The **extrinsic pathway** of coagulation is primarily activated by **tissue factor (Factor III)** in response to vascular injury [1]. - This pathway is crucial for initiating the coagulation cascade, leading to the conversion of **prothrombin to thrombin** [1,2]. *Factor X* - Factor X is part of the **common pathway** and is activated downstream after the extrinsic system is initiated, so it cannot activate the extrinsic pathway itself [2]. - It acts as a bridge between the **intrinsic** and **extrinsic pathways**, playing no direct role in their activation. *Factor XI* - Factor XI is involved in the **intrinsic pathway** and is activated by **thrombin** or contact activation, not directly related to the extrinsic pathway. - Its role in coagulation is primarily in amplifying the response after initial activation has occurred. *Factor XII* - Also part of the **intrinsic pathway**, Factor XII is activated by contact with negatively charged surfaces, thus does not have a role in the extrinsic pathway [2]. - Like Factor XI, its activation is indirectly linked to the extrinsic coagulation process, but it does not initiate it. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 126-128. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130.

Question 448: What is the role of Factor X in the coagulation cascade?

A. Initiates the intrinsic pathway of coagulation
B. Activates Factor X in the intrinsic pathway
C. Converts prothrombin to thrombin in the common pathway (Correct Answer)
D. Serves as cofactor for Factor VII in extrinsic pathway

Explanation: ***Stuart-Prower factor*** - Factor X is also known as **Stuart-Prower factor**, essential for the common pathway of the coagulation cascade [1][2]. - It converts prothrombin to thrombin, facilitating the formation of **fibrin clots** [1]. - Factor X requires vitamin K for post-translational modification into its functional form [2]. *Tissue factor* - Tissue factor (TF) is involved in the **extrinsic pathway** of coagulation, activated by injury [1]. - It serves to initiate the clotting process by activating **Factor VII**, not Factor X directly [1]. *Christmas factor* - Christmas factor is another name for **Factor IX**, which plays a role in the intrinsic pathway of coagulation [1]. - It is primarily associated with **Hemophilia B**, whereas Factor X is part of the common pathway. *Hageman factor* - Hageman factor refers to **Factor XII**, which initiates the intrinsic pathway upon contact with negatively charged surfaces [1]. - It does not directly convert to Factor X in the clotting cascade. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.

Question 449: What is the main feature of chemotaxis as observed in white blood cells?

A. Increased random movement of neutrophils
B. Increased adhesiveness to intima
C. Increased phagocytosis
D. Unidirectional locomotion of neutrophils (Correct Answer)

Explanation: ***Unidirectional locomotion of neutrophils*** - **Chemotaxis** refers to the **directional movement** of cells, such as neutrophils, towards a chemical attractant. - This process is crucial for recruiting immune cells to sites of infection or inflammation. *Increased random movement of neutrophils* - While neutrophils do exhibit random movement, **chemotaxis** specifically describes **directed movement** along a chemical gradient, not merely an increase in random motion. - **Random movement** without a specific direction does not effectively guide immune cells to a specific target. *Increased adhesiveness to intima* - **Adhesion to the intima** (endothelial cells) is an initial step in the process of leukocyte extravasation, allowing cells to roll and stick to vessel walls. - However, it is primarily mediated by adhesion molecules and is distinct from the **directional migration** defined by chemotaxis. *Increased phagocytosis* - **Phagocytosis** is the process by which cells engulf pathogens or cellular debris. - While essential for immune function, it is a separate function that occurs **after** the cell has migrated to its target via chemotaxis.

Question 450: A 33-year-old man presents with a 5-week history of calf pain, swelling, and low-grade fever. Serum levels of creatinine kinase are elevated. A muscle biopsy reveals numerous eosinophils and he also has peripheral blood eosinophilia. Which of the following interleukins is primarily responsible for the increase in eosinophils in this patient?

A. IL-4
B. IL-5 (Correct Answer)
C. IL-6
D. IL-2

Explanation: ***IL-5*** - **Interleukin-5 (IL-5)** is the **most potent and direct cytokine** responsible for the **differentiation, maturation, activation, and survival of eosinophils**. - IL-5 is produced primarily by **Th2 cells**, mast cells, and eosinophils themselves, and acts directly on eosinophil progenitors in the bone marrow. - In this patient with eosinophilic myositis (likely parasitic infection such as trichinosis), **IL-5 is the primary mediator** of the peripheral blood eosinophilia and tissue eosinophil infiltration. - **Clinical correlation:** Anti-IL-5 therapies (mepolizumab, reslizumab) are used to treat hypereosinophilic conditions, confirming IL-5's central role. *IL-4* - **Interleukin-4 (IL-4)** is produced by Th2 cells and mast cells and promotes the **differentiation of naive T cells into Th2 cells**. - While IL-4 initiates the Th2 immune response that eventually leads to IL-5 production, it does **not directly stimulate eosinophil production or recruitment**. - IL-4 is more involved in IgE class switching and allergic inflammation rather than direct eosinophil regulation. *IL-6* - **Interleukin-6 (IL-6)** is a pleiotropic cytokine involved in the **acute phase response**, inflammation, and hematopoiesis. - While it has broad effects on immune cells, it is **not primarily responsible** for eosinophil production or recruitment. - Elevated in many inflammatory conditions but not specific for eosinophilia. *IL-2* - **Interleukin-2 (IL-2)** is primarily involved in the **proliferation and differentiation of T lymphocytes** and activation of natural killer (NK) cells. - It plays no significant direct role in eosinophil production or recruitment. - More important for T cell-mediated immunity rather than eosinophilic responses.

Practice by Chapter

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