Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 401: The type of allergic reaction seen in allergic fungal sinusitis is -

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

Explanation: ***Type 1 and Type 3*** - **Allergic fungal sinusitis (AFS)** is primarily characterized by **IgE-mediated hypersensitivity (Type I)** against fungal antigens, manifesting as immediate allergic responses [1]. - **Immune complex formation and deposition (Type III hypersensitivity)** also plays a significant role, contributing to chronic inflammation and tissue damage in the sinuses [2]. - These are considered the **predominant mechanisms** in AFS pathogenesis for clinical and examination purposes. *Type 1 and Type 2* - While **Type I hypersensitivity** (IgE-mediated) is a key component of AFS, **Type II hypersensitivity** (cytotoxic, antibody-dependent) is not involved [1]. - Type II reactions involve antibodies binding to cell surface antigens causing direct cell destruction, which is not a mechanism in AFS [1]. *Type 2 and Type 3* - **Type II hypersensitivity** is not a mechanism in AFS, as the disease does not involve antibody-mediated cellular cytotoxicity [1]. - Although **Type III hypersensitivity** is involved, the absence of Type I (the primary mechanism) makes this option incorrect [2]. *Type 4 and Type 1* - **Type I hypersensitivity** is the primary mechanism in AFS [1]. **Type IV hypersensitivity** (delayed-type, T-cell mediated) may play a contributory role in chronic inflammation. - However, the **classic teaching emphasizes Types I and III** as the predominant hypersensitivity reactions in AFS, with Type I (IgE-mediated) and Type III (immune complex) being the primary drivers of the clinical presentation and pathology [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215.

Question 402: Which of the following types of hypersensitivity reactions is primarily involved in Farmer's lung?

A. Type III
B. Type IV (Correct Answer)
C. Type I
D. Type II

Explanation: ***cd*** - Farmer's lung is primarily a **Type III hypersensitivity** reaction [1], which involves the formation of **immune complexes** from inhaled organic antigens, leading to inflammation. - The exposure to moldy hay or organic dust results in **alveolitis**, which characterizes this condition [2]. *ac* - Type I hypersensitivity is **IgE-mediated**, typically causing **immediate allergic reactions**, such as asthma or anaphylaxis. - It does not manifest as chronic lung conditions like Farmer's lung, which has different immunological mechanisms. *ab* - Type II hypersensitivity involves **IgG or IgM antibodies** targeting specific cell surface antigens, leading to cell destruction or dysfunction. - Conditions like hemolytic anemia or autoimmune disorders are examples but are unrelated to Farmer's lung. *bd* - Type IV hypersensitivity is a **cell-mediated response** involving T cells, commonly seen in infections or contact dermatitis. - While it plays a role in certain lung conditions [2], it does not correlate with the immune complex involvement seen in Farmer's lung. **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 Lung, pp. 701-702.

Question 403: Which type of cells are primarily involved in the infiltration seen in rheumatoid arthritis?

A. T-cells
B. B cells
C. NK-cells
D. T-cells and B cells (Correct Answer)

Explanation: ***T-cells*** - In rheumatoid arthritis, **T-cells** play a crucial role in the **pathogenesis**, contributing to inflammation and joint destruction [1]. - Activated **CD4+ T-cells** are particularly prominent, facilitating the inflammatory processes in the synovium [1]. *NK-cells* - While **Natural Killer (NK) cells** are involved in innate immunity, they are not the predominant infiltrating cells in rheumatoid arthritis. - The condition is primarily driven by **adaptive immune responses**, especially involving T-cells and antibodies. *B cells* - **B cells** contribute to the disease by producing antibodies, but they are not the primary cell type infiltrated [1]. - In rheumatoid arthritis, their role is more about antibody-mediated damage rather than being the dominant infiltrating cells. *Both B & T Cells* - Although both T and B cells are present in rheumatoid arthritis, **T-cells** are the specifically significant infiltrating cells associated with the inflammation. - The focus on **T-cells** highlights the specific adaptive immune response that characterizes this disease [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1212-1214.

Question 404: Job's syndrome is which of the following types of immunodeficiency disease?

A. humoral immunodeficiency
B. Disorder of phagocytosis (Correct Answer)
C. Cellular immunodeficiency
D. Disorder of complement

Explanation: ***Disorder of phagocytosis*** - Job's syndrome (Hyper-IgE syndrome) is primarily classified as a **disorder of phagocytosis** due to defective **neutrophil chemotaxis** - The hallmark feature is **impaired neutrophil migration** to sites of infection, leading to recurrent **staphylococcal skin abscesses** and **pneumonias with pneumatocele formation** - Caused by **STAT3 mutations** (autosomal dominant form), which affect multiple immune pathways but clinically manifest predominantly as phagocyte dysfunction - Classic triad: **elevated IgE** (>2000 IU/mL), **recurrent skin and lung infections**, and **characteristic facies** *Cellular immunodeficiency* - While STAT3 mutations do affect T-cell function (particularly Th17 differentiation), the **primary clinical manifestation** is phagocyte dysfunction - Pure cellular immunodeficiencies like **DiGeorge syndrome** present with viral and fungal infections, which are not the predominant feature in Job's syndrome - The classification is based on the **dominant clinical defect**, which in Job's syndrome is impaired neutrophil chemotaxis *humoral immunodeficiency* - Despite markedly elevated IgE levels, patients have relatively preserved **antibody production** against most pathogens - Humoral deficiencies like **X-linked agammaglobulinemia** present with low immunoglobulin levels and recurrent encapsulated bacterial infections - The elevated IgE in Job's syndrome is a consequence of dysregulated cytokine signaling, not a primary antibody production defect *Disorder of complement* - Complement disorders result from defects in the **complement cascade proteins** (C1-C9) - These typically present with recurrent **Neisseria infections** or autoimmune phenomena like SLE - Job's syndrome does not involve complement pathway defects and presents with characteristic staphylococcal infections

Question 405: Which antibody is primarily involved in warm antibody autoimmune hemolytic anemia?

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

Explanation: ***IgG*** - **Warm antibody autoimmune hemolytic anemia (wAIHA)** is predominantly mediated by **IgG antibodies** [1]. - These IgG antibodies bind optimally at **37°C (body temperature)**, leading to extravascular hemolysis (primarily in the spleen) [1]. *IgM* - **IgM antibodies** are primarily involved in **cold agglutinin disease**, a type of cold autoimmune hemolytic anemia. - They bind optimally at **lower temperatures (below 37°C)** and often cause intravascular hemolysis. *IgE* - **IgE antibodies** are primarily associated with **allergic reactions** and **parasitic infections**. - They do not play a significant role in the pathophysiology of autoimmune hemolytic anemias. *IgA* - While **IgA antibodies** can occasionally be found in some cases of AIHA, they are generally considered a **minor contributor** and not the primary antibody class in wAIHA. - Their presence often signifies a **mixed-type AIHA** rather than pure warm AIHA. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Question 406: Which of the following best denotes classical complement pathway activation in immune inflammatory conditions?

A. C2, C4 and C3 decreased (Correct Answer)
B. C2 and C4 normal, C3 is decreased
C. C3 normal and C2, C4 decreased
D. C2, C4, C3 all are elevated

Explanation: ***C2, C4 and C3 decreased*** - Activation of the **classical complement pathway** consumes upstream components C2 and C4, leading to their depletion [2]. - The activation also consumes C3 as all complement pathways converge at C3, thus its levels will also be decreased [1]. *C2 and C4 normal, C3 is decreased* - This pattern is more indicative of **alternate pathway activation** or a C3 deficiency, where classical pathway components (C2, C4) are not primarily involved [3]. - In classical pathway activation, C2 and C4 would be depressed due to their role early in the cascade. *C3 normal and C2, C4 decreased* - While C2 and C4 being decreased is consistent with **classical pathway activation**, the C3 component would also be decreased as it is consumed by the **C3 convertase** [1]. - A normal C3 level would imply either very early or ineffective classical pathway activation, which is unlikely given significant C2 and C4 consumption. *C2, C4, C3 all are elevated* - Elevated levels of complement components typically occur during the **acute phase response** in inflammatory conditions, but this indicates increased production, not consumption due to activation. - Active consumption in an immune inflammatory condition would lead to **decreased serum levels** of these components, not increased levels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [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. 162-163. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535.

Question 407: Which of the following immune hypersensitivity reactions is responsible for Myasthenia Gravis?

A. Type I Hypersensitivity
B. Type II Hypersensitivity (Correct Answer)
C. Type III Hypersensitivity
D. Type IV Hypersensitivity

Explanation: ***Type II Hypersensitivity*** - Myasthenia gravis is primarily mediated by **autoantibodies against acetylcholine receptors** [1], characteristic of **Type II hypersensitivity** reactions [3]. - This leads to a reduction in **neuromuscular transmission**, causing muscle weakness and fatigue [1][2]. *Type III Hypersensitivity* - Involves the formation of **immune complexes** that can deposit in tissues, leading to conditions like **lupus** or **glomerulonephritis**. - Myasthenia gravis does not exhibit significant **immune complex** pathology. *Type IV Hypersensitivity* - This is a **delayed-type hypersensitivity reaction**, typically involved in conditions like **tuberculosis** and **contact dermatitis**. - Myasthenia gravis is not primarily mediated by **T-cell** activation which typifies Type IV hypersensitivity. *Type I Hypersensitivity* - Also known as **immediate hypersensitivity** [3], it typically involves **IgE** and reactions like **asthma** and **anaphylaxis**. - Myasthenia gravis does not result from **IgE-mediated** immune responses. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 408: Cell surface molecules involved in peripheral tolerance induction are

A. CD40 and CD40L
B. CD34 and CD51
C. B7 and CD28 (Correct Answer)
D. B7 and CD3

Explanation: ***B7 and CD28*** - B7 is crucial for providing a **costimulatory signal** to T cells via interaction with CD28, promoting **T cell activation** and peripheral tolerance [1][2]. - This interaction is essential in preventing autoimmune responses by ensuring T cells require both antigen and costimulatory signals for full activation [1][3]. *B7 and CD3* - CD3 is a part of the T cell receptor (TCR) complex, primarily involved in **T cell activation**, not specifically in peripheral tolerance. - The interaction of B7 with **CD3** does not provide the costimulatory signal necessary for peripheral tolerance [3]. *CD34 and CD51* - CD34 is primarily involved in **hematopoietic stem cell trafficking** and does not play a role in T cell tolerance mechanisms. - CD51 is associated with **integrins** and plays a role in adhesion rather than in peripheral tolerance induction. *CD40 and CD40L* - While CD40-CD40L interactions are important for **B cell activation** and other immune responses, they are not directly involved in the inductive mechanisms of **peripheral tolerance** in T cells. - They primarily mediate costimulatory signals in **adaptive immunity**, not specifically for tolerance purposes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 204-206. [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. 157-158. [3] 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. 176-177.

Question 409: In a patient with Chronic Granulomatous Disease (CGD) experiencing recurrent bacterial and fungal infections, which specific function of phagocytic leukocytes is primarily impaired due to a defect in the NADPH oxidase system?

A. Migration to infection sites
B. Phagocytosis of pathogens
C. Production of reactive oxygen species (Correct Answer)
D. Presentation of antigens to lymphocytes

Explanation: ***Production of reactive oxygen species*** - Chronic Granulomatous Disease (CGD) is characterized by a defect in the **NADPH oxidase system**, which is crucial for generating a **respiratory burst**. - This respiratory burst is essential for producing **reactive oxygen species (ROS)** like superoxide radicals, which are vital for killing phagocytosed bacteria and fungi [1]. *Migration to infection sites* - The ability of phagocytes to **migrate to infection sites (chemotaxis)** is generally intact in CGD patients. - Defects in migration are more typically associated with conditions like **Leukocyte Adhesion Deficiency**. *Phagocytosis of pathogens* - Phagocytes in CGD can **engulf pathogens (phagocytosis)** normally [1]. - The defect lies in the **intracellular killing** mechanism *after* phagocytosis, not in the uptake itself [1]. *Presentation of antigens to lymphocytes* - Antigen presentation is a function primarily of **antigen-presenting cells (APCs)** like dendritic cells and macrophages, which is generally unaffected in CGD. - This process is crucial for initiating an **adaptive immune response**, a separate function from the innate pathogen killing defect in CGD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91.

Practice by Chapter

Cells and Tissues of the Immune System

Practice Questions

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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