Immunopathology Practice Questions

Q: A 40-year-old man presents with a several-month history of chronic cough and fever. Radiography reveals a diffuse reticulonodular pattern. Microscopically, a transbronchial biopsy shows focal areas of inflammation containing epithelioid cell granulomas, Langerhans cells, and lymphocytes. These findings are typically indicative of which of the following types of hypersensitivity immunological responses?

Type IV. **Explanation:** The clinical presentation of chronic cough, fever, and reticulonodular patterns, combined with the histological finding of **epithelioid cell granulomas** and **Langhans giant cells**, is a classic description of **Tuberculosis** or **Sarcoidosis**. These conditions are mediated by a **Type IV (Delayed-type) Hypersensitivity reaction**. **Why Type IV is Correct:** Type IV hypersensitivity is a cell-mediated immune response (not antibody-mediated). It involves **CD4+ T-lymphocytes (Th1 cells)** which, upon encountering an antigen, release cytokines like IFN-γ. This activates macrophages, transforming them into **epithelioid cells**. These cells can fuse to form **Langhans giant cells**, ultimately resulting in the formation of a granuloma to sequester the indigestible antigen. **Why Other Options are Incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). It does not form granulomas. * **Type II (Antibody-mediated):** Involves IgG/IgM binding to fixed cell-surface antigens, leading to complement activation or ADCC (e.g., Rheumatic fever, Goodpasture syndrome). * **Type III (Immune-complex):** Caused by the deposition of antigen-antibody complexes in tissues, leading to neutrophil recruitment (e.g., SLE, Post-streptococcal glomerulonephritis). **High-Yield NEET-PG Pearls:** * **Granuloma Components:** Epithelioid cells (modified macrophages), lymphocytes, and giant cells (Langhans type in TB; Foreign body type in non-immunological reactions). * **Key Cytokine:** **IFN-γ** is the most critical cytokine for macrophage activation in Type IV reactions. * **Classic Examples:** Mantoux test (PPD), Contact dermatitis, and chronic infections like Leprosy and Tuberculosis.

Q: Which of the following conditions is not due to complement deficiency?

Paroxysmal Nocturnal Hemoglobinuria (PNH). **Explanation** The correct answer is **B. Paroxysmal Nocturnal Hemoglobinuria (PNH)**. The key to this question lies in distinguishing between a **deficiency of complement proteins** and a **deficiency of complement regulatory proteins.** 1. **Why PNH is the correct answer:** PNH is not caused by a deficiency of complement proteins themselves. Instead, it is an acquired clonal stem cell disorder caused by a mutation in the **PIGA gene**. This leads to a deficiency of **GPI-anchored proteins**, specifically **CD55 (DAF)** and **CD59 (MIRL)**. These are regulatory proteins that normally protect RBCs from complement-mediated lysis. In PNH, the complement system is intact, but the RBCs lack the "shield" to stop it from attacking them. 2. **Why the other options are incorrect:** * **SLE (Option A):** Deficiencies of early classical pathway components (**C1q, C1r, C1s, C4, and C2**) are strongly associated with SLE-like syndromes because they are essential for the clearance of immune complexes. * **Glomerulonephritis (Option C):** Deficiencies in **C3** or regulatory factors like **Factor H** lead to uncontrolled complement activation and the deposition of immune complexes in the kidney, causing glomerulonephritis. * **Neisseria infection (Option D):** Deficiencies in the late components (**C5–C9**), which form the **Membrane Attack Complex (MAC)**, specifically predispose individuals to recurrent disseminated infections by *Neisseria meningitidis* and *Neisseria gonorrhoeae*. **High-Yield Clinical Pearls for NEET-PG:** * **C2 deficiency:** The most common complement deficiency in humans. * **C3 deficiency:** The most severe; presents with recurrent pyogenic infections (encapsulated bacteria). * **CH50 Assay:** Used to screen for classical pathway deficiencies. * **PNH Diagnosis:** Gold standard is **Flow Cytometry** showing absence of CD55/CD59.

Q: Which of the following conditions requires a large antigen-antibody reaction to cause?

Autoimmune hemolytic anemia. **Explanation:** The question focuses on the quantitative requirement of antigen-antibody interactions across different hypersensitivity reactions. **Why Option B is Correct:** **Autoimmune Hemolytic Anemia (AIHA)** is a **Type II Hypersensitivity** reaction. In Type II reactions, antibodies (IgG or IgM) are directed against antigens on specific cell surfaces (the RBC membrane in this case). Because the antigen is a structural component of a cell, a **large amount of antigen-antibody reaction** is required to cause significant clinical hemolysis. The density of antigens on the cell surface and the subsequent binding of numerous antibodies are necessary to trigger effective complement activation or opsonization by splenic macrophages. **Why Other Options are Incorrect:** * **A. Serum Sickness:** This is a **Type III Hypersensitivity** reaction. It is characterized by the formation of small, soluble immune complexes that circulate and deposit in tissues. It is triggered by an **excess of antigen**, not necessarily a "large" total reaction volume. * **C & D. Urticaria and Anaphylaxis:** These are **Type I Hypersensitivity** reactions mediated by IgE. These reactions are notorious for being triggered by **minute quantities** of an antigen (allergen). A single molecule of allergen can cross-link IgE on a mast cell, leading to massive degranulation; thus, they do not require a large reaction to manifest symptoms. **NEET-PG High-Yield Pearls:** * **Type I:** IgE mediated, "Immediate," requires minimal antigen (e.g., Penicillin anaphylaxis). * **Type II:** Cytotoxic, antibody-mediated (e.g., AIHA, Goodpasture syndrome, Myasthenia Gravis). * **Type III:** Immune-complex mediated, "Ag-Ab complexes" (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV:** T-cell mediated, "Delayed" (e.g., Mantoux test, Contact dermatitis).

Q: Serum sickness occurs after:

Injection with foreign serum. **Explanation:** Serum sickness is a classic example of a **Type III Hypersensitivity reaction** (Immune-complex mediated). It occurs when a large amount of foreign antigen is introduced into the body, leading to the formation of soluble antigen-antibody complexes that deposit in small blood vessels, activating the complement system and causing tissue damage. * **Why Option A is correct:** Serum sickness was historically described after the administration of horse serum (antitoxin) for diphtheria or tetanus. When **foreign serum** (containing foreign proteins) is injected, the body recognizes these proteins as antigens and produces antibodies (usually IgG). These antibodies bind to the circulating foreign proteins, forming complexes that deposit in joints, kidneys, and vessels, typically manifesting 7–14 days after exposure. * **Why Options B and C are incorrect:** **Own serum** (autologous) and **Normal saline** (isotonic salt solution) are not recognized as foreign by the immune system. They lack the "non-self" immunogenic proteins required to trigger an antibody response and subsequent immune-complex formation. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Fever, Rash (urticaria), and Arthralgia. * **Mechanism:** It is a **systemic** Type III hypersensitivity (unlike the Arthus reaction, which is localized). * **Complement Levels:** Characterized by **low serum complement levels** (C3 and C4) due to massive consumption during the reaction. * **Modern Triggers:** Today, it is more commonly caused by non-protein drugs like **Penicillin**, sulfonamides, or monoclonal antibodies (e.g., Rituximab).

Question 1

A 40-year-old man presents with a several-month history of chronic cough and fever. Radiography reveals a diffuse reticulonodular pattern. Microscopically, a transbronchial biopsy shows focal areas of inflammation containing epithelioid cell granulomas, Langerhans cells, and lymphocytes. These findings are typically indicative of which of the following types of hypersensitivity immunological responses?

Accepted Answer

Type IV

Answer

Type I

Answer

Type II

Answer

Type III

Question 2

Immunosuppressive drugs are less effective in which type of graft rejection?

Accepted Answer

Acute humoral rejection

Answer

Acute cellular rejection

Answer

Chronic rejection

Answer

None of the above

Question 3

Which of the following is an example of Type II hypersensitivity?

Accepted Answer

Blood transfusion reaction

Answer

Autoimmune hemolytic anemia

Answer

Allergic rhinitis

Answer

Glomerulonephritis

Question 4

What type of hypersensitivity reaction is the Arthus reaction?

Accepted Answer

Localized immune complex

Answer

Antigen-antibody reaction

Answer

Complement mediated

Answer

Antibody mediated

Question 5

Local lymph nodules are enlarged near an infected wound. Histological examination reveals an increased amount of macrophages, lymphocytes, lymphatic follicles in the cortical layer, and a large amount of plasma cells. What process in the lymphatic nodules represents these histological changes?

Accepted Answer

Antigen stimulation

Answer

Acquired insufficiency of the lymphoid tissue

Answer

Tumour transformation

Answer

Innate insufficiency of the lymphoid tissue

Question 6

Which granulomatous condition is associated with hypercalcemia?

Accepted Answer

Sarcoidosis

Answer

Tuberculosis

Answer

Berylliosis

Answer

Systemic Lupus Erythematosus

Question 7

Which of the following conditions is not due to complement deficiency?

Accepted Answer

Paroxysmal Nocturnal Hemoglobinuria (PNH)

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Glomerulonephritis

Answer

Neisseria infection

Question 8

Which of the following conditions requires a large antigen-antibody reaction to cause?

Accepted Answer

Autoimmune hemolytic anemia

Answer

Serum sickness

Answer

Urticaria

Answer

Anaphylactic reaction

Question 9

Graft versus host disease is due to?

Accepted Answer

Immunocompetent T cells in graft tissue

Answer

Immunocompetent T cells in host

Answer

Immunocompetent B cells in graft tissue

Answer

Immunocompetent B cells in host

Question 10

Serum sickness occurs after:

Accepted Answer

Injection with foreign serum

Answer

Injection with own serum

Answer

Injection with normal saline

Answer

All of the above

Immunopathology — MCQs

Immunopathology — MCQs

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