Autoimmune Diseases — MCQs

10 questions

Which of the following auto antibodies is most likely to be present in a patient with systemic lupus erythematosus?

All are true about Sjogren syndrome except

A 45-year-old female presents with dry eyes, dry mouth, and joint pain. Which of the following antibodies is most indicative of the suspected condition?

Which is the rheumatoid arthritis autoantibody?

A 30-year-old woman presents with thyroid swelling. On investigations, her TSH levels are found to be elevated. Postoperative reports showed lymphocytic infiltration and Hurthle cells. A most probable diagnosis is?

Which of the following cardiac complications may develop in a 33 year old woman with systemic lupus erythematosus (SLE) because of her underlying condition?

Which is not an autoimmune disease

All are true about autoimmune disease except:

Which of the following is the most important infiltrate in rheumatoid arthritis?

Q10

Cell surface molecules involved in peripheral tolerance induction are

Autoimmune Diseases Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following auto antibodies is most likely to be present in a patient with systemic lupus erythematosus?

A. Antiphospholipid
B. Anti-Ro
C. Anti- ds DNA (Correct Answer)
D. Anti-RNP

Explanation: ***Anti-ds DNA*** - **Anti-double-stranded DNA (anti-dsDNA)** antibodies are highly specific for **Systemic Lupus Erythematosus (SLE)** and are included in the classification criteria [1]. - Their levels often correlate with disease activity, especially in cases with **lupus nephritis** [1]. *Antiphospholipid* - While **antiphospholipid antibodies** can be present in SLE patients (leading to **secondary antiphospholipid syndrome**), they are not the most characteristic or diagnostic autoantibody for SLE itself. - These antibodies are primarily associated with a **prothrombotic state** and recurrent miscarriages. *Anti-Ro* - **Anti-Ro (SSA) antibodies** are associated with SLE, particularly with **cutaneous lupus**, **neonatal lupus**, and **Sjögren's syndrome**, but they are not as specific as anti-dsDNA for the general diagnosis of SLE [1]. - Patients with anti-Ro antibodies may have a higher risk of **photosensitivity** [1]. *Anti-RNP* - **Anti-RNP antibodies** are found in patients with SLE, but they are most characteristically associated with **Mixed Connective Tissue Disease (MCTD)**. - Their presence in SLE often correlates with less severe renal involvement but may indicate **myositis** or **Raynaud's phenomenon**.

Question 2: All are true about Sjogren syndrome except

A. Xerostomia
B. Lack of tear
C. Interstitial nephritis
D. Subcutaneous fibrosis (Correct Answer)

Explanation: ***Subcutaneous fibrosis*** - **Subcutaneous fibrosis** is typically associated with conditions like **systemic sclerosis** or **eosinophilic fasciitis**, not Sjögren's syndrome [2]. - Sjögren's syndrome primarily affects exocrine glands and other organ systems, but **fibrosis of subcutaneous tissue** is not a characteristic manifestation. *Xerostomia* - **Xerostomia**, or **dry mouth**, is a hallmark symptom of Sjögren's syndrome due to immune-mediated destruction of salivary glands. - This symptom can lead to dental caries, dysphagia, and difficulty speaking. *Lack of tear* - **Keratoconjunctivitis sicca**, or **dry eyes** (lack of tears), is another cardinal feature of Sjögren's syndrome, resulting from inflammation of the lacrimal glands [1]. - Patients often experience grittiness, foreign body sensation, and blurred vision due to insufficient tear production. *Interstitial nephritis* - **Interstitial nephritis** can occur in Sjögren's syndrome, particularly **tubulointerstitial nephritis**, which may lead to **renal tubular acidosis**. - Renal involvement, though less common than sicca symptoms, is a recognized extraglandular manifestation.

Question 3: A 45-year-old female presents with dry eyes, dry mouth, and joint pain. Which of the following antibodies is most indicative of the suspected condition?

A. Anti-Ro/SSA antibodies (Correct Answer)
B. Anti-histone antibodies
C. Anti-thyroid peroxidase antibodies
D. Anti-phospholipid antibodies

Explanation: ***Anti-Ro/SSA antibodies*** - The patient's symptoms of **dry eyes (xerophthalmia)**, **dry mouth (xerostomia)**, and **joint pain** are classic manifestations of **Sjögren's syndrome**, a chronic autoimmune disease. [1] - **Anti-Ro/SSA antibodies** are highly specific for Sjögren's syndrome, particularly in patients with primary Sjögren's. [1] *Anti-histone antibodies* - These antibodies are most commonly associated with **drug-induced lupus erythematosus**, a condition characterized by lupus-like symptoms that develop after exposure to certain medications. - The clinical presentation of dry eyes and dry mouth is not the primary distinguishing feature of drug-induced lupus. *Anti-thyroid peroxidase antibodies* - These antibodies are a hallmark of **Hashimoto's thyroiditis**, an autoimmune disease affecting the thyroid gland and leading to hypothyroidism. [2] - While Sjögren's syndrome can coexist with other autoimmune conditions, anti-thyroid peroxidase antibodies do not directly indicate Sjögren's. *Anti-phospholipid antibodies* - These antibodies are primarily associated with **antiphospholipid syndrome**, a thrombophilic disorder characterized by arterial or venous thrombosis and/or adverse pregnancy outcomes. - They are not directly indicative of the sicca symptoms seen in Sjögren's syndrome.

Question 4: Which is the rheumatoid arthritis autoantibody?

A. Anti DLE
B. Anti CCP (Correct Answer)
C. Anti ds DNA
D. Anti histone

Explanation: ***Anti CCP*** - **Anti-Citrullinated Protein Antibodies (CCP)** are highly specific for **rheumatoid arthritis** and are used for diagnosing this condition. - A positive **Anti-CCP** test can indicate the presence of **rheumatoid arthritis** even before clinical symptoms appear. *Anti histone* - This antibody is primarily associated with **drug-induced lupus erythematosus**, not rheumatoid arthritis. - It identifies a **response** to medications, rather than being a specific marker for a rheumatic condition like RA. *Anti DLE* - Suggests antibodies related to **discoid lupus erythematosus**, not rheumatoid arthritis. - These antibodies do not correlate with inflammatory joint disease or diagnosis of RA. *Anti ds DNA* - Commonly associated with **systemic lupus erythematosus** (SLE) rather than rheumatoid arthritis [1]. - While relevant for lupus, it lacks specificity for diagnosing rheumatic arthritis; ANA testing is noted as not useful in diagnosing RA specifically [1].

Question 5: A 30-year-old woman presents with thyroid swelling. On investigations, her TSH levels are found to be elevated. Postoperative reports showed lymphocytic infiltration and Hurthle cells. A most probable diagnosis is?

A. Hashimoto's thyroiditis (Correct Answer)
B. Graves' disease
C. Follicular thyroid carcinoma
D. Medullary thyroid carcinoma

Explanation: ***Hashimoto's thyroiditis*** - The presence of **lymphocytic infiltration** and **Hurthle cells** on postoperative pathology is characteristic of Hashimoto's thyroiditis [1,2]. - Elevated **TSH levels** indicate hypothyroidism, which aligns with the autoimmune nature of Hashimoto's affecting thyroid hormone production [1]. *Graves disease* - Typically presents with **hyperthyroidism**, leading to suppressed TSH levels rather than elevation. - Characterized by **thyroid enlargement** and the presence of **autoantibodies** like TSI, not lymphocytic infiltration. *Follicular carcinoma* - While it can cause **thyroid swelling**, it is usually associated with **malignant characteristics** rather than Hurthle cells and lymphocytic infiltration. - TSH levels can be normal, as it does not principally engage in autoimmune thyroid destruction like Hashimoto's. *Medullary carcinoma thyroid* - Originates from **C cells** producing calcitonin, and typically presents with elevated calcitonin levels, not TSH. - Characteristic findings include **C-cell hyperplasia** or **neoplastic changes**, which do not match the presented lymphocytic infiltration. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1090-1092. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 427-428.

Question 6: Which of the following cardiac complications may develop in a 33 year old woman with systemic lupus erythematosus (SLE) because of her underlying condition?

A. Mitral valve prolapse
B. Libman-Sacks endocarditis (Correct Answer)
C. Hemorrhagic pericarditis
D. Infective endocarditis

Explanation: ***Libman-Sacks endocarditis*** - Libman-Sacks endocarditis is a **non-infectious valvular vegetation** that is highly characteristic of **systemic lupus erythematosus (SLE)** [3]. - These vegetations can lead to **valvular incompetence** or **stenosis**, primarily affecting the **mitral and aortic valves** [1]. *Mitral valve prolapse* - While mitral valve prolapse can occur in SLE patients, it is a relatively common condition in the general population and is **not as specifically linked** to SLE pathology as Libman-Sacks endocarditis. - It involves the **leaflet(s) of the mitral valve bulging** back into the left atrium during systole, which causes a **mid-systolic click and late systolic murmur**, but does not represent the specific immune-mediated damage seen in SLE. *Hemorrhagic pericarditis* - Pericarditis is a common cardiac manifestation in SLE, leading to **inflammation of the pericardium**, but it is typically **serous or fibrinous**, not usually hemorrhagic. - **Hemorrhagic pericarditis** is more often associated with conditions like malignancy, tuberculosis, or trauma, and is not a typical presentation of SLE. *Infective endocarditis* - **Infective endocarditis** is caused by microbial infection of the heart valves, resulting in **vegetations containing bacteria or fungi** [2]. - While SLE patients can be at increased risk for infections due to immunosuppression, the vegetations of Libman-Sacks endocarditis are **sterile (non-infectious)** and distinct in their underlying pathophysiology [1].

Question 7: Which is not an autoimmune disease

A. SLE
B. Grave's disease
C. Myasthenia Gravis
D. Sickle cell disease (Correct Answer)

Explanation: ***Sickle cell disease*** - This is a **genetic disorder** caused by a mutation in the **beta-hemoglobin gene**, leading to abnormal hemoglobin (hemoglobin S) and sickle-shaped red blood cells. - It is an **inherited blood disorder**, not an autoimmune condition where the immune system attacks the body's own tissues. *SLE (Systemic Lupus Erythematosus)* - SLE is a **chronic autoimmune connective tissue disease** that can affect multiple organ systems. - It is characterized by the production of **autoantibodies** against various self-antigens, such as anti-dsDNA and anti-Sm antibodies. *Grave's disease* - This is an **autoimmune disorder** that leads to **hyperthyroidism**. - It is caused by the production of **autoantibodies** (thyroid-stimulating immunoglobulins) that mimic TSH and stimulate the thyroid gland to produce excessive thyroid hormones. *Myasthenia Gravis* - Myasthenia Gravis is an **autoimmune neuromuscular disease** characterized by fluctuating muscle weakness. - It is caused by **autoantibodies** that block or destroy acetylcholine receptors at the neuromuscular junction, impairing nerve-to-muscle communication.

Question 8: All are true about autoimmune disease except:

A. Higher incidence among males (Correct Answer)
B. T cells recognize self-antigen
C. Polyclonal B cell activation
D. Hashimoto's thyroiditis is an example

Explanation: ***Higher incidence among males*** - Autoimmune diseases (Ads) generally have a **higher incidence among females** than males, challenging the statement that they are more common in males [1]. - For example, conditions like **Systemic Lupus Erythematosus (SLE)** and **Rheumatoid Arthritis (RA)** show a pronounced female predominance [1]. *T cells recognize self-antigen* - This statement is true; in autoimmune diseases, **autoreactive T cells** fail to undergo proper selection and differentiation, leading them to recognize and attack **self-antigens** [2]. - This recognition often mediates tissue damage, as seen in **Type 1 Diabetes** where T cells target pancreatic beta cells [2]. *Polyclonal B cell activation* - This is also true; autoimmune diseases often involve **polyclonal B cell activation**, leading to the production of various **autoantibodies** that target self-components. - This broad activation contributes to the diverse clinical manifestations and systemic nature of many autoimmune conditions like **Systemic Lupus Erythematosus**. *Hashimoto's thyroiditis is an example* - This statement is true; **Hashimoto's thyroiditis** is a classic example of an **organ-specific autoimmune disease** where autoantibodies and autoreactive T-cells attack thyroid gland components [3]. - It results in **hypothyroidism** due to chronic inflammation and gradual destruction of thyroid follicles [3]. **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. 175-178. [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. 176-177. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1089-1090.

Question 9: Which of the following is the most important infiltrate in rheumatoid arthritis?

A. Dendritic cells
B. CD4+ Helper cells
C. Macrophages (Correct Answer)
D. Neutrophils

Explanation: ***Macrophages*** - **Macrophages** are crucial in rheumatoid arthritis synovium due to their role in producing **pro-inflammatory cytokines** like TNF-̑, IL-1, and IL-6, which drive joint destruction [1], [2]. - They also contribute to the **pannus formation** and degrade cartilage and bone through the release of proteases [1]. *Dendritic cells* - While present in the synovium, **dendritic cells primarily function as antigen-presenting cells**, initiating T-cell responses. - Their direct contribution to tissue damage and chronic inflammation is less prominent than that of macrophages. *CD4+ Helper cells* - **CD4+ T helper cells** orchestrate the immune response by activating B cells and macrophages, but they are not the primary effector cells causing direct tissue damage [3]. - They secrete cytokines that promote inflammation but do not directly participate in tissue degradation. *Neutrophils* - **Neutrophils are abundant in the synovial fluid** during acute flares, contributing to inflammation and breakdown of cartilage through the release of enzymes. - However, their role in the chronic, sustained synovial inflammation and tissue destruction characteristic of RA is less significant compared to macrophages. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.

Question 10: 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.

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