Blood and Immunity — MCQs

Blood and Immunity Indian Medical PG Practice Questions and MCQs

Question 411: The maximum life of a transfused R.B.C. is -

A. One day
B. 15 days
C. One hour
D. 50 days (Correct Answer)

Explanation: ***50 days*** - The **practical maximum lifespan** of a **transfused red blood cell (RBC)** is approximately **50-60 days** in the recipient's circulation, representing the T50 (median survival time) for stored blood. - This is shorter than the natural lifespan of native RBCs (around 120 days) due to **storage lesions** - damage occurring during blood bank storage including ATP depletion, membrane changes, and reduced deformability. - While some transfused RBCs may survive longer, the majority do not exceed 50-60 days due to cumulative storage-related damage. *One day* - A lifespan of one day is far too short for transfused **RBCs**, which are expected to circulate for weeks to provide oxygen-carrying capacity. - This short duration would indicate immediate destruction or incompatibility, which is not the goal of a successful transfusion. *15 days* - While 15 days is longer than one day, it is still a significant underestimation of the **typical survival** of successfully transfused RBCs. - This duration would suggest suboptimal survival, though some stored RBCs might be cleared within this timeframe due to severe storage lesions. *One hour* - A lifespan of one hour for transfused **RBCs** is indicative of a severe **transfusion reaction** leading to rapid hemolysis. - This scenario represents a failed transfusion with acute destruction of donor cells, which is not the maximum life expectancy.

Question 412: If a mother has had measles, her newborn baby is immune to this disease for -

A. 1 to 3 years
B. 3 to 6 years
C. 6 to 12 months
D. 4 to 6 months (Correct Answer)

Explanation: ***Correct: 4 to 6 months*** - Maternal antibodies, primarily **IgG**, are transferred across the placenta to the fetus, providing **passive immunity** to measles - This passive immunity typically lasts for a limited period, usually around **4 to 6 months**, as the maternal antibodies gradually degrade - This is why measles vaccination is typically scheduled at 9-12 months of age in most immunization protocols *Incorrect: 1 to 3 years* - A duration of 1 to 3 years is **too long** for maternally acquired passive immunity to last against measles - After the maternal antibody protection wanes, the child's own active immune system needs to develop through vaccination or natural exposure *Incorrect: 3 to 6 years* - This timeframe represents a significant **overestimation** of the longevity of maternally transferred measles antibodies - Long-term immunity beyond infancy is achieved through the infant's own immune response via vaccination, not passive transfer *Incorrect: 6 to 12 months* - While some infants may retain detectable maternal antibodies up to 9-12 months, the **most significant protective period** is generally 4-6 months - The efficacy of protection significantly wanes after the 6-month mark, making the infant increasingly vulnerable to measles infection

Question 413: Cortisol increases all of the following components except:

A. Monocytes
B. RBCs
C. Platelets
D. Eosinophils (Correct Answer)

Explanation: ***Eosinophils*** - Cortisol causes **eosinopenia** (a decrease in eosinophils) by increasing their sequestration in tissues and promoting their apoptosis. - This effect is a classic indicator of stress and can be observed in conditions of elevated endogenous or exogenous cortisol. *Monocytes* - Cortisol typically causes a **mild monocytosis** (increase in circulating monocytes), although this effect can vary. - It impacts the trafficking and differentiation of monocytes, leading to their transient increase in the bloodstream. *RBCs* - Cortisol can lead to a slight **increase in red blood cell (RBC) count** or hemoglobin concentration. - This effect is partly due to hemoconcentration and partly by promoting erythropoiesis. *Platelets* - Cortisol generally causes a **thrombocytosis** (increase in platelet count). - This effect is thought to be mediated by various factors, including cytokine interactions and direct effects on megakaryopoiesis.

Question 414: Which of the following is a secondary mediator of anaphylaxis?

A. Leukotriene B4 (Correct Answer)
B. Protease
C. Histamine
D. Eosinophilic chemotactic factor

Explanation: ***Leukotriene B4*** - **Leukotrienes** are synthesized from **arachidonic acid** via the 5-lipoxygenase pathway during an anaphylactic reaction, making them **secondary mediators**. - **Leukotriene B4** is a potent **chemoattractant for neutrophils** and contributes to the inflammatory response in anaphylaxis. - Note: The **cysteinyl leukotrienes (LTC4, LTD4, LTE4)** are the primary leukotrienes responsible for **bronchoconstriction** and increased vascular permeability in anaphylaxis. *Protease* - **Proteases**, such as **tryptase**, are **preformed mediators** stored in mast cell granules and are rapidly released upon activation. - They are considered **primary mediators** due to their immediate release following mast cell degranulation. *Histamine* - **Histamine** is a classic **preformed mediator** stored in mast cell granules and is one of the first substances released during anaphylaxis. - Its rapid release causes immediate effects such as **vasodilation**, **bronchoconstriction**, and increased vascular permeability. *Eosinophilic chemotactic factor* - **Eosinophilic chemotactic factor (ECF-A)** is a **preformed mediator** stored in mast cell granules. - While it attracts eosinophils, it is released immediately from granules upon mast cell activation, classifying it as a **primary mediator**.

Question 415: Percentage of COHb that usually causes death:

A. > 70%
B. > 60%
C. > 80% (Correct Answer)
D. > 50%

Explanation: ***> 80%*** - While significant symptoms occur at lower levels, **COHb levels above 80%** typically cause profound central nervous system depression leading to **cardiac arrest and death**. - This level indicates almost complete displacement of oxygen from hemoglobin, leading to severe **tissue hypoxia**. *> 70%* - At **COHb levels above 70%**, individuals are often in a **coma**, experiencing severe **cardiac dysfunction** and respiratory failure. - Death is highly probable at this level, though it is not the universally accepted threshold for lethality as higher percentages are more definitive for causing death. *> 60%* - At **COHb levels above 60%**, patients typically experience **coma, convulsions**, and significant **cardiovascular compromise**. - While extremely dangerous and often fatal, **COHb levels above 80%** are more reliably associated with death. *> 50%* - At **COHb levels above 50%**, individuals often experience **coma, seizures**, and severe **metabolic acidosis**. - While critical and life-threatening, death is less common at this percentage compared to those above 70% or 80%, as aggressive medical intervention may still be effective.

Question 416: ABO antigens are not found in:

A. Semen
B. CSF (Correct Answer)
C. Saliva
D. Tears

Explanation: ***CSF*** - ABO antigens are typically expressed on the surface of **red blood cells** and in the secretions of individuals classified as **secretors**. - **Cerebrospinal fluid (CSF)** is generally devoid of these antigens. *Semen* - ABO antigens can be found in **semen**, particularly in individuals who are secretors. - This is due to the presence of **secreted bodily fluids** containing soluble forms of these antigens. *Saliva* - **Saliva** is a well-known source of soluble ABO antigens in secretor individuals. - The presence of these antigens in saliva is often used in **forensic testing** and blood group determination. *Tears* - Similar to other bodily secretions, **tears** can contain soluble ABO antigens in secretor individuals. - This is part of the general secretion of these antigens into exocrine fluids.

Question 417: Basophils are activated by:

A. Cell-bound IgE (Correct Answer)
B. Neutrophils
C. Killer inhibitory peptide
D. IL-5

Explanation: ***Cell-bound IgE*** - Basophils express **Fc receptors** for **IgE** on their cell surface. - When **allergens** bind to IgE antibodies already attached to these receptors, it triggers **basophil activation** and degranulation, releasing inflammatory mediators. *Neutrophils* - **Neutrophils** are phagocytic cells primarily involved in the anti-bacterial immune response and do not directly activate basophils. - They are distinct leukocyte populations with different roles in immunity. *Killer inhibitory peptide* - **Killer inhibitory peptides** (KIRs) are receptors found on **Natural Killer (NK) cells** that inhibit their cytotoxic activity when bound to MHC class I molecules. - They are not involved in the activation of basophils. *IL-5* - **Interleukin-5 (IL-5)** is a cytokine primarily involved in the **growth**, differentiation, and activation of **eosinophils**. - While basophils can be influenced by various cytokines, IL-5 is not their primary activator.

Question 418: In a platelet poor plasma sample calcium and tissue thromboplastin are added. This is used to assess which of the following pathways?

A. Common
B. Intrinsic
C. Extrinsic (Correct Answer)
D. Fibrinolytic

Explanation: ***Extrinsic*** - The addition of **tissue thromboplastin** (containing tissue factor) and **calcium** to platelet-poor plasma directly activates the extrinsic pathway of coagulation. - This combination is used in the **prothrombin time (PT)** test, which specifically measures the integrity of the extrinsic and common pathways. *Common* - While the common pathway is utilized in this test, the direct activators of tissue thromboplastin and calcium specifically initiate the extrinsic pathway, which then feeds into the common pathway. - The PT test assesses the common pathway, but the initial trigger for the test setup outlined is the extrinsic arm. *Intrinsic* - The intrinsic pathway is initiated by factors present within the blood, such as contact with a negatively charged surface (e.g., glass), and is assessed by the **activated partial thromboplastin time (aPTT)**. - Tissue thromboplastin is not a component of the intrinsic pathway activation cascade. *Fibrinolytic* - The fibrinolytic pathway is responsible for the breakdown of clots and involves plasminogen activators and plasmin. - The addition of calcium and tissue thromboplastin is designed to initiate clot formation, not clot breakdown.

Question 419: Von Willebrand factor is secreted by which of the following?

A. Platelets
B. Fibroblasts
C. Macrophages
D. Endothelial cells (Correct Answer)

Explanation: ***Endothelial cells*** - **Von Willebrand factor (vWF)** is primarily synthesized and secreted by **endothelial cells** lining blood vessels. - It is stored in **Weibel-Palade bodies** within endothelial cells and is released upon stimulation, playing a crucial role in **hemostasis**. *Platelets* - While **platelets** can bind to and carry vWF, they do not synthesize it. - Platelets have **vWF receptors** (e.g., glycoprotein Ib) that allow them to adhere to vWF at sites of vascular injury. *Fibroblast* - **Fibroblasts** are connective tissue cells that produce components of the extracellular matrix, such as collagen and elastin. - They are not involved in the synthesis or secretion of **vWF**. *Macrophages* - **Macrophages** are immune cells involved in phagocytosis and antigen presentation. - They do not produce **vWF**; their primary role is in immune surveillance and removal of cellular debris.

Question 420: Which factor is not involved in the intrinsic coagulation pathway?

A. Factor IX
B. Factor X
C. Factor VII (Correct Answer)
D. Factor VIII

Explanation: ***Factor VII*** - **Factor VII** is a key component of the **extrinsic coagulation pathway**, which is initiated by **tissue factor** released upon vascular injury. - It forms a complex with tissue factor and calcium, which then activates Factor X to begin the common pathway. *Factor IX* - **Factor IX** is an integral part of the **intrinsic coagulation pathway**, activated by **Factor XIa** in the presence of calcium and phospholipids. - Once activated (Factor IXa), it forms a complex with **Factor VIIIa** to activate Factor X. *Factor X* - **Factor X** is a component of the **common coagulation pathway**, acting as the point where both the intrinsic and extrinsic pathways converge. - It is activated by both the intrinsic (Factor IXa/VIIIa complex) and extrinsic (Factor VIIa/tissue factor complex) pathways, forming **Factor Xa**. *Factor VIII* - **Factor VIII** is a crucial cofactor in the **intrinsic coagulation pathway**, where its activated form, **Factor VIIIa**, dramatically enhances the activity of Factor IXa. - It circulates bound to **von Willebrand factor** and is released and activated by thrombin.

Practice by Chapter

Composition and Functions of Blood

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Erythrocytes and Hemoglobin

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Leukocytes and Immune Function

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Platelets and Hemostasis

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Blood Groups and Transfusion

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Coagulation and Fibrinolysis

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Hematopoiesis

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Innate Immunity

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Adaptive Immunity

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Immunological Memory and Tolerance

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