Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 371: HBsAg is based on which principle

A. Chemiluminescence
B. Immunofluorescence
C. Immunochromatography assays
D. ELISA (Correct Answer)

Explanation: ***ELISA*** - **Enzyme-linked immunosorbent assay (ELISA)** is a widely used laboratory test to detect and quantify antigens (like HBsAg) or antibodies in a sample. - It involves an enzyme-linked antibody that reacts with a substrate to produce a detectable signal, making it highly sensitive and specific for **HBsAg detection**. *Immunochromatography assays* - These are typically **rapid diagnostic tests (RDTs)** that provide quick qualitative results, often used for point-of-care testing. - While they can detect HBsAg, they generally have lower sensitivity and specificity compared to ELISA. *Chemiluminescence* - This is a detection method used in some immunoassays where a chemical reaction emits light, often providing higher sensitivity than colorimetric detection. - While it can be incorporated into HBsAg testing platforms, it is a *detection principle* rather than the primary assay principle like ELISA itself. *Immunofluorescence* - This technique uses **fluorescently labeled antibodies** to visualize antigens in cells or tissues under a fluorescence microscope [1]. - It is used for localization and identification of antigens, but not typically the primary method for routine quantitative HBsAg serology [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 259-260.

Question 372: All are true for transplanted kidney except which of the following?

A. Humoral antibody responsible for rejection
B. HLA identity similarity seen in 1:100 people (Correct Answer)
C. Previous blood transfusion
D. CMI is responsible for rejection

Explanation: ***HLA identity similarity seen in 1:100 people*** - The **HLA (Human Leukocyte Antigen)** system is crucial for compatibility in organ transplantation; the likelihood of finding a suitable match is low [1]. - **HLA matching** significantly impacts transplant success and rejection rates, making this statement incorrect in context to what is true for transplanted kidneys [1]. *CMI is responsible for rejection* - While **cell-mediated immunity (CMI)** plays a role in rejection, it is not the only factor; humoral mechanisms also contribute significantly [1]. - This statement oversimplifies the rejection process, which can involve various **immune responses** [1]. *Previous blood transfusion* - **Previous blood transfusions** can lead to sensitization against donor antigens but do not universally apply to all transplant scenarios. - The relevance of prior transfusions varies based on patient history and the specific organ transplanted, making this statement too general. *Humoral antibody responsible for rejection* - **Humoral rejection** involves antibodies but is not exclusively responsible for all types of rejection, as T-cell mediated (CMI) responses also play a role [1]. - It is not accurate to state that humoral antibodies are the sole factor in transplant rejection [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-243.

Question 373: What is the Rose Waaler test used for?

A. Ring precipitation
B. Precipitation in gel
C. Complement fixation test
D. Passive hemagglutination test (Correct Answer)

Explanation: ***Passive hemagglutination test*** - The **Rose Waaler test** is a historical **rheumatoid factor (RF)** detection method based on **passive hemagglutination**. - It uses sheep red blood cells coated with a subagglutinating dose of rabbit anti-sheep red blood cell antibody to detect RF in patient serum. *Complement fixation test* - This assay detects the presence of **antibody** or **antigen** by observing whether **complement** is consumed in an antigen-antibody reaction. - The Rose Waaler test does not involve the measurement of complement consumption. *Precipitation in gel* - This technique, such as **immunodiffusion**, involves the formation of a visible **precipitate** when soluble antigens and antibodies diffuse through a gel matrix and meet at optimal concentrations. - The Rose Waaler test relies on agglutination of red blood cells, not precipitation in gel. *Ring precipitation* - A **ring precipitation test** involves layering an antigen solution over an antibody solution, creating an antigen-antibody complex visible as a **precipitate ring** at the interface of the two solutions. - This method is distinct from the Rose Waaler test which uses red blood cell agglutination.

Question 374: What is the number of antigens typically evaluated in comprehensive HLA matching for organ transplantation?

A. 10 (Correct Answer)
B. 4
C. 16
D. 22

Explanation: ***10*** - The **number of criteria for HLA matching** in organ transplantation is typically 10, consisting of 6 class I and 4 class II antigens. - Proper HLA matching is critical for minimizing the risk of **graft rejection** and ensuring **recipient compatibility** [1]. *16* - While there are various HLA antigens, a total of **16** criteria is not a standard number used for matching purposes. - This number may include other factors but does not represent the core criteria for **HLA matching**. *4* - HLA matching involves more than **4 criteria**, inadequate for reliable transplantation outcomes. - This number does not encompass the essential **class I and class II antigens** that are necessary for effective matching. *22* - A total of **22 criteria** exceeds the conventional standard for HLA matching, which is not practical or necessary. - This figure may relate to overall HLA typing but is not applicable for the matching process itself. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 179-180.

Question 375: Post-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?

A. Type -1 hypersensitivity
B. Type -2 hypersensitivity
C. Type -3 hypersensitivity (Correct Answer)
D. Type -4 hypersensitivity

Explanation: ***Type -3 hypersensitivity*** - Post-streptococcal glomerulonephritis (PSGN) is caused by **immune complex deposition**, a hallmark of type III hypersensitivity reactions [1][2][3]. - It involves the formation of **antigen-antibody complexes** following a streptococcal infection, leading to inflammation in the kidneys [1][2]. *Type -1 hypersensitivity* - Characterized by **IgE-mediated** reactions, such as allergies and anaphylaxis, which do not apply to PSGN. - It typically involves **mast cells** and histamine release, notably absent in PSGN cases. *Type -4 hypersensitivity* - Involves **T-cell mediated** responses and is related to delayed-type reactions, not applicable to PSGN. - Common examples include **contact dermatitis** and graft-versus-host disease, differing fundamentally from PSGN's mechanism. *Type -2 hypersensitivity* - Characterized by **antibody-mediated cytotoxicity**, such as in hemolytic anemia, unrelated to immune complexes in PSGN. - Typically involves direct damage to cells, contrasting with the immune complex mechanism observed in PSGN [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.

Question 376: What is the initial event in serum sickness?

A. It is associated with hypocomplementemia.
B. It is a type III hypersensitivity reaction.
C. It occurs due to exposure to heterologous antigens. (Correct Answer)
D. It can lead to leukocytoclastic vasculitis.

Explanation: ***Can lead to leukocytoclastic vasculitis*** - Serum sickness is characterized by the formation of **immune complexes**, which can trigger **leukocytoclastic vasculitis** affecting the blood vessels [1][2]. - Symptoms can include **rash, fever, and arthralgia**, typically occurring 1-3 weeks after exposure to the offending antigen [2]. *Can occur due to homologous antigen* - Serum sickness is usually a reaction to **heterologous** antigens, such as those from animal serum, not **homologous** ones. - Homologous antigens do not typically elicit the immune response seen in serum sickness; hence, this statement is incorrect. *Type 2 hypersensitivity* - Serum sickness is classified as a **Type III hypersensitivity** reaction due to the immune complex formation, not Type II [1]. - Type II is characterized by antibody-mediated destruction of **target cells**, which does not apply here. *Hypercomplementemia* - Serum sickness is associated with **hypocomplementemia** due to complement consumption from immune complex formation, not hypercomplementemia. - This can lead to **decreased complement levels** during the response, making this statement incorrect. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 172-173.

Question 377: What is the most common type of graft rejection?

A. Hyperacute
B. Acute (Correct Answer)
C. Chronic
D. Acute on chronic

Explanation: ***Acute*** - **Acute rejection** is the most common type of graft rejection, occurring in **10-40% of transplant recipients**. [1] - It typically occurs **days to weeks to months** after transplantation (most commonly within the first 6 months). [1] - Mediated primarily by **T-lymphocytes** (cellular rejection) or **antibodies** (antibody-mediated rejection) reacting against donor antigens. [1] - Usually **responsive to immunosuppressive therapy** when detected early. *Hyperacute* - **Hyperacute rejection** is rare (occurs in <1% of cases) due to routine **pre-transplant cross-matching**. - Occurs within **minutes to hours** after transplantation due to **pre-existing circulating antibodies** against donor antigens. [1] - Results in immediate thrombosis and graft necrosis, requiring **immediate graft removal**. [1] *Chronic* - **Chronic rejection** (chronic allograft dysfunction) develops **months to years** after transplantation. - It is the **most common cause of late graft failure**, but not the most common type of rejection episode. - Characterized by **gradual, progressive loss of graft function** with vascular and fibrotic changes. - **Largely irreversible** and poorly responsive to treatment. *Acute on chronic* - This is **not a primary category** of graft rejection but represents an **acute rejection episode superimposed** on a graft already undergoing chronic changes. - Reflects exacerbation in a chronically rejecting graft. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-242.

Question 378: ABO isoantibodies are of which class?

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

Explanation: ***IgM*** - Naturally occurring **ABO isoantibodies** are predominantly of the **IgM class**. - These **pentameric antibodies** are highly effective at causing **agglutination** of incompatible red blood cells, which is crucial in transfusion reactions [1]. *IgG* - While IgG antibodies can be formed against ABO antigens (e.g., in hemolytic disease of the newborn), the **naturally occurring isoantibodies** are primarily IgM. - IgG antibodies are **monomeric** and can cross the **placenta**, which is a key difference from the primary IgM ABO antibodies. *IgD* - **IgD** antibodies are primarily found on the surface of **B cells** and play a role in B cell activation. - They are **not a primary mediator** of ABO isoantibody response or red blood cell agglutination. *IgA* - **IgA** antibodies are predominantly found in **mucosal secretions** and play a role in mucosal immunity. - While some IgA may be present, it is **not the predominant class** for naturally occurring ABO isoantibodies involved in transfusion reactions. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 154-155.

Question 379: HLA is located on ?

A. Short arm of chr-6 (Correct Answer)
B. Long arm of chr-6
C. Short arm of chr-3
D. Long arm of chr-3

Explanation: ***Short arm of chr-6*** - The **Human Leukocyte Antigen (HLA)** complex, crucial for immune recognition, is located on the **short arm of chromosome 6**. [1] - This region, specifically 6p21.3, contains highly polymorphic genes encoding MHC (Major Histocompatibility Complex) proteins. [2] *Long arm of chr-6* - The **long arm of chromosome 6** contains many genes, but the primary HLA complex is not located here. - Genes on the long arm are involved in various cellular functions, but not central to immune recognition via HLA. *Short arm of chr-3* - Genes on **chromosome 3**, including its short arm, are not associated with the primary HLA complex. - Chromosome 3 is known for genes related to conditions such as von Hippel-Lindau disease. *Long arm of chr-3* - The **long arm of chromosome 3** is not the location for the HLA complex. - This region contains genes involved in diverse cellular processes and disease associations, but not immune recognition via HLA molecules. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 55-56. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-240.

Question 380: What laboratory findings are associated with common variable hypogammaglobulinemia?

A. Low serum immunoglobulin levels (Correct Answer)
B. Decreased B cell count
C. Increased B cell count
D. Neutropenia

Explanation: ***Low serum immunoglobulin levels*** - **Common variable hypogammaglobulinemia (CVID)** is characterized by significantly **low levels of IgG, IgA, and/or IgM** due to impaired B cell differentiation into plasma cells. - This deficiency in antibodies is the hallmark of the disorder, explaining the increased susceptibility to infections. *Decreased B cell count* - While CVID involves impaired B cell function, the **B cell counts** in the peripheral blood are typically **normal** or sometimes even elevated [1]. - The problem lies in their inability to differentiate and produce adequate antibodies, not in their numerical presence [1]. *Increased B cell count* - An increased B cell count is not a characteristic finding in CVID; peripheral B cell numbers are usually normal [1]. - If B cell counts are significantly increased, other conditions such as certain **lymphoproliferative disorders** should be considered. *Neutropenia* - **Neutropenia** (low neutrophil count) is not a primary diagnostic feature of CVID, although it can occur in some patients with autoimmune complications. - The defining laboratory finding is the **deficiency of immunoglobulins**, leading to recurrent infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 249-250.

Practice by Chapter

Cells and Tissues of the Immune System

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Innate Immunity

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Adaptive Immunity

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Hypersensitivity Reactions

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Autoimmune Diseases

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Immunodeficiency Disorders

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Transplantation Immunopathology

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Immune Response to Infections

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Immunologic Laboratory Techniques

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Tumor Immunology

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