Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 381: What color is emitted by FITC after absorbing blue light?

A. Yellow-green (Correct Answer)
B. Orange-red
C. Apple-green
D. Golden-brown

Explanation: ***Yellow-green*** - Fluorescein isothiocyanate (FITC) is a common fluorochrome used in **fluorescence microscopy** and flow cytometry. - Upon excitation by blue light (typically around 495 nm), FITC emits light in the **yellow-green spectrum**, specifically around 521 nm. - This is the **spectroscopically accurate** description of FITC's emission peak. *Orange-red* - **Orange-red emission** is characteristic of fluorochromes like **phycoerythrin (PE)** or **Texas Red**, not FITC. - These fluorochromes have different **excitation and emission maxima** compared to FITC. *Apple-green* - While FITC fluorescence is sometimes clinically described as **"apple-green"** (especially in immunofluorescence), this is a **subjective visual description** rather than a precise spectral term. - The more **spectroscopically accurate** description is **yellow-green**, which reflects FITC's specific emission peak at 521 nm. - "Apple-green" typically suggests a purer green without the yellow component. *Golden-brown* - **Golden-brown** is not a typical emission color for fluorochromes like FITC. - This color is generally associated with **pigments** or stained tissues (e.g., lipofuscin, hemosiderin), not fluorescent probes.

Question 382: Which among the following is an example of type I hypersensitivity reaction?

A. Graves' disease
B. Pernicious anemia
C. Arthus reaction
D. Casoni's test (Correct Answer)

Explanation: ***Casoni's test*** - Casoni's test is a **diagnostic skin test** for **hydatid disease** (echinococcosis), involving intradermal injection of **hydatid cyst fluid antigen**. - A positive reaction produces an **immediate wheal and flare response** (within 15-30 minutes), which is a classic manifestation of **Type I hypersensitivity** mediated by **IgE antibodies** and **mast cell degranulation** [1], [2]. - Among the given options, Casoni's test is the correct answer because it **demonstrates/elicits** a Type I hypersensitivity reaction as part of its diagnostic mechanism. *Arthus reaction* - The Arthus reaction is a localized **Type III hypersensitivity** reaction caused by pre-formed IgG antibodies forming **immune complexes** with antigens injected intracutaneously. - It results in **vasculitis**, **edema**, **necrosis**, and **erythema** at the injection site, typically appearing **3-8 hours** after antigen exposure (delayed, not immediate). *Graves' disease* - Graves' disease is an **autoimmune disorder** causing **hyperthyroidism**, due to **stimulatory autoantibodies** (TSI - thyroid-stimulating immunoglobulins) against the **TSH receptor** [1]. - It is classified as a **Type II hypersensitivity** reaction, where antibodies bind to cell surface receptors leading to abnormal cell stimulation rather than destruction [1]. *Pernicious anemia* - Pernicious anemia is a **Type II hypersensitivity** reaction where autoantibodies target **intrinsic factor** or **gastric parietal cells**, leading to **vitamin B12 malabsorption** and subsequent megaloblastic anemia. - This antibody-mediated destruction or interference with normal cell function is characteristic of Type II hypersensitivity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-213. [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. 171-172.

Question 383: Which of the following best explains the development of intravascular hemolysis in a 54-year-old woman who was given type A Rh+ blood by mistake, despite being a type B Rh+ patient, after a blood transfusion following an automobile accident?

A. Direct cytotoxic T-cell mediated lysis
B. Antibody-mediated complement fixation (Correct Answer)
C. Immune complex mediated hemolysis
D. Antibody-dependent cellular cytotoxicity

Explanation: ***Antibody-mediated complement fixation*** - Intravascular hemolysis occurs when type B blood is transfused with type A blood, triggering **IgM antibodies** to activate **complement**, leading to the destruction of transfused red blood cells [1][2]. - This mechanism is rapid and results in **hemolytic transfusion reactions**, which are life-threatening and present shortly after the transfusion [1]. *Antibody-dependent cellular cytotoxicity* - This process primarily involves **IgG antibodies** targeting cells for destruction by **NK cells** or macrophages, rather than complement activation. - It usually leads to **extravascular hemolysis** rather than intravascular hemolysis caused by complement. *Delayed-type hypersensitivity* - This immune response is mediated by **T cells** and typically occurs days to weeks after exposure, not immediately as seen in transfusion reactions. - It does not directly lead to **hemolysis** but rather to tissue damage due to cellular immunity. *Immune complex disease* - Characterized by **formation of immune complexes** leading to inflammation and sometimes tissue damage, but not specifically linked to immediate hemolytic reactions. - This mechanism is more relevant in conditions like **serum sickness**, rather than the direct hemolysis observed in this transfusion scenario. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.

Question 384: Defective phagolysosome formation is a feature of which condition?

A. Chediak-Higashi syndrome (Correct Answer)
B. Fanconi Anemia
C. Ataxia telangiectasia
D. Chronic granulomatous disease

Explanation: ***Chediak-Higashi syndrome*** - This condition is characterized by **defective phagolysosome formation** due to mutations in the LYST gene, leading to impaired killing of pathogens [1]. - Clinical features include **partial oculocutaneous albinism** and **neurological deficits**, along with recurrent infections [1]. *Chronic granulomatous disease* - It primarily involves a defect in the **NADPH oxidase enzyme**, leading to ineffective respiratory burst and inability to kill certain bacteria. - Patients experience recurrent infections from **catalase-positive organisms**, not primarily due to phagolysosome defects. *Ataxia telangiectasia* - This is an inherited disorder affecting DNA repair mechanisms and results in **neurological issues** and **immunodeficiency** but not specifically phagolysosome dysfunction. - Common features include **ataxia**, **telangiectasias**, and an increased risk of malignancies, rather than recurrent infections from phagocyte defects. *Fanconi Anemia* - This condition is associated with **bone marrow failure** and increased susceptibility to cancer, particularly **acute myeloid leukemia**, rather than phagolysosomal dysfunction. - Clinically, it presents with **hypoplastic anemia**, **short stature**, and **skeletal anomalies**, not recurrent infections due to impaired phagolysosome function. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Question 385: Which of the following statements about transplant rejection reactions is false:

A. Acute rejection is readily reversible with appropriate treatment
B. Liver is extremely sensitive to hyperacute rejection (Correct Answer)
C. Hyperacute rejection is uncommon
D. Chronic rejection is a major cause of late graft loss

Explanation: ***Hyperacute rejection is uncommon*** - Hyperacute rejection occurs within minutes of transplantation and is mostly associated with **pre-existing antibodies** against donor antigens, making it relatively rare with proper donor-recipient matching [1]. - Improvements in **cross-matching** techniques have led to a decrease in its incidence, reinforcing that it is not commonly encountered in modern transplants. *Acute rejection is readily reversible with appropriate treatment* - Acute rejection can be effectively treated but is not universally **reversible**, depending on the timing and severity of the rejection episode [1]. - It typically requires **immunosuppressive therapy** [2], which may not always fully restore graft function. *Chronic rejection invariably leads to loss of the graft* - Chronic rejection is a slower process that may not always lead to **immediate loss**, as some grafts can survive with reduced function for extended periods. - It's a progressive process often associated with **gradual dysfunction** rather than acute failure. *Liver is more resistant to Hyperacute rejection due to its dual blood supply.* - While the liver's dual blood supply can afford some protection, this characteristic does not completely **prevent** hyperacute rejection. - Other factors, such as the presence of **specific antibodies**, play a more significant role in hyperacute reactions than just blood supply. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-243. [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. 180-181.

Question 386: Which of the following histologic alterations is most characteristic of Sjögren's syndrome?

A. Proliferation of the ductal epithelium.
B. Atrophy of the glands due to lymphocytic infiltration.
C. Intense lymphocytic infiltration of the gland replacing the acinar structures. (Correct Answer)
D. All of the options.

Explanation: ***All of the above.*** - Sjogren's syndrome involves different histologic alterations, making this correct as it encompasses all possible histological changes associated with the condition. - The alterations include **lymphocytic infiltration**, **gland atrophy**, and **ductal proliferation**, which collectively characterize the glandular changes in this autoimmune disorder [1]. *Intense lymphocytic infiltration of the gland replacing the acinar structures, but preserving the lobular.* - While there is indeed **lymphocytic infiltration** [1], it does not fully describe the atrophy and other changes typical of Sjogren's syndrome. - It inaccurately suggests that **lobular structures remain intact**, which may not always be the case as acinar structures are often affected. *Atrophy of the glands sequential to the lymphocytic infiltration.* - Although gland atrophy can occur, this option fails to include the significant **lymphocytic infiltration** [1], which is crucial to the histological diagnosis. - The primary finding in Sjogren's is more about the immune cell infiltration rather than merely gland atrophy following it. *Proliferation of the ductal epithelium and myoepithelium.* - This option misrepresents the typical findings in Sjogren's syndrome, as while ductal changes can occur, **proliferation** is not a hallmark feature. - It overlooks the **lymphocytic infiltration and acinar damage** [1] that are more characteristic of the disease process. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 235-236.

Question 387: Type I hypersensitivity includes all of the following except:

A. Extrinsic asthma
B. Hay fever
C. Autoimmune hemolytic anemia (Correct Answer)
D. Anaphylaxis

Explanation: ***Autoimmune hemolytic anemia*** - This condition is a **Type II hypersensitivity reaction**, mediated by **IgG or IgM antibodies** targeting antigens on red blood cells, leading to their destruction [2]. - Type I hypersensitivity involves **IgE-mediated mast cell degranulation**, which is not the primary mechanism in autoimmune hemolytic anemia [2], [3]. *Anaphylaxis* - **Anaphylaxis** is a severe, systemic **Type I hypersensitivity** reaction, triggered by the release of histamine and other mediators from mast cells and basophils [5]. - It is an IgE-mediated response to allergens, leading to widespread physiological changes like **bronchoconstriction** and **vasodilation** [1]. *Extrinsic asthma* - **Extrinsic asthma** is a classic example of **Type I hypersensitivity**, where exposure to specific allergens (e.g., pollen, dust mites) triggers an IgE-mediated response [1], [4]. - This leads to **bronchospasm** and airway inflammation following mast cell degranulation in the airways [5]. *Hay fever* - Also known as **allergic rhinitis**, **hay fever** is an IgE-mediated **Type I hypersensitivity** reaction to airborne allergens like pollen [1], [4]. - It manifests as nasal congestion, sneezing, and watery eyes due to **mast cell activation** in the nasal passages. **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. 171-172. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212.

Question 388: Which one is found in Henoch-Schönlein purpura?

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

Explanation: ***IgA*** - **Henoch-Schönlein purpura (HSP)** is an **IgA-mediated vasculitis**, meaning that **IgA immune complex deposition** is central to its pathology. - These IgA deposits are found in the walls of small blood vessels in affected organs, including the skin, gut, joints, and kidneys, leading to the characteristic symptoms. *IgM* - While IgM antibodies are involved in the **initial immune response** and can be found in some autoimmune conditions, they are **not the primary immunoglobulin** associated with HSP pathogenesis. - Conditions like **Waldenström macroglobulinemia** or some autoimmune hemolytic anemias are more typically linked to IgM involvement. *IgG* - IgG antibodies are the **most abundant immunoglobulins** in the body and are involved in many immune responses and autoimmune diseases, such as **systemic lupus erythematosus** or **rheumatoid arthritis**. - However, IgG is **not the defining immunoglobulin** for HSP. *IgE* - IgE antibodies are primarily associated with **allergic reactions** and **parasitic infections**. - Conditions like **asthma**, **anaphylaxis**, or **atopic dermatitis** involve IgE, not vasculitis like HSP.

Question 389: What is the consequence of preformed antibodies in organ transplantation?

A. Delayed T-cell mediated rejection
B. Long-term graft dysfunction due to chronic inflammation
C. Post-transplant antibody-mediated rejection
D. Immediate graft failure due to preformed antibodies (Correct Answer)

Explanation: ***Hyperacute rejection*** - This occurs immediately after transplant due to **preformed antibodies** reacting against donor antigens, leading to rapid allograft failure [1]. - It is typically associated with **complement activation** and often results in thrombosis of the graft vessels [1]. *Acute rejection* - Primarily mediated by **T cells** rather than preformed antibodies, occurring days to months after transplantation [2]. - Involves a **cellular immune response**, unlike hyperacute rejection which is antibody-mediated [2]. *Acute humoral rejection* - Also involves antibodies but develops **days to weeks** post-transplant rather than immediately like hyperacute rejection. - This type is characterized by a **specific antibody response** and complement activation, but is not due to preformed antibodies. *Chronic rejection* - A long-term process that develops over months to years due to **persistent immune-mediated injury** to the graft, leading to gradual loss of function. - Involves mechanisms such as **tissue fibrosis and vascular changes**, differing from the immediate action of preformed antibodies in hyperacute rejection. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242.

Question 390: Which of the following tests would be most beneficial in the diagnosis of a patient suspected of having chronic granulomatous disease of childhood?

A. E rosette - forming assay
B. Cell-mediated cytolysis
C. Nitroblue tetrazolium (NBT) test (Correct Answer)
D. Determination of CD4: CD8 ratio

Explanation: ***Nitroblue tetrazolium (NBT) test*** - The **NBT test** is the **specific diagnostic test** for **chronic granulomatous disease (CGD)** as it directly assesses the defective pathophysiology. - CGD results from defective **NADPH oxidase**, preventing phagocytes from producing a **respiratory burst** needed to kill intracellular pathogens. - In the NBT test, normal phagocytes reduce the yellow NBT dye to blue **formazan** via superoxide production. In CGD, this reaction **fails**, confirming the diagnosis. - This functional assay directly demonstrates the **oxidative burst defect** characteristic of CGD. *E rosette - forming assay* - This assay identifies **T lymphocytes** by their ability to bind sheep red blood cells. - It evaluates **cellular immunity** and T cell numbers, not phagocyte function. - CGD is a **phagocytic disorder**, not a T cell deficiency, making this test irrelevant for diagnosis. *Cell-mediated cytolysis* - This test measures the killing ability of **cytotoxic T lymphocytes (CTLs)** and **NK cells** against target cells. - It assesses **adaptive and innate cellular immunity** but does not evaluate the **phagocytic oxidative burst** that is defective in CGD. *Determination of CD4: CD8 ratio* - This ratio evaluates the balance between **helper (CD4+)** and **cytotoxic (CD8+)** T cell subsets. - It is useful for diagnosing **HIV infection, autoimmune diseases**, and monitoring immunosuppression. - It does not assess **phagocyte function** and is not relevant to the diagnosis of CGD.

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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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