Immunology and Allergies — MCQs
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True about Severe Combined Immunodeficiency (SCID) in children is:
A 4-year-old male presents with a recent onset of rash, urticaria, and fever of 101°F. The mother reports the child has been complaining of bone pain. Physical examination reveals mild lymphadenopathy. The patient recently completed a 10-day course of cefaclor suspension for an upper respiratory infection. How should this patient be treated?
A 9-year-old girl presents with a 6-month history of difficulty combing her hair and climbing upstairs. She exhibits a positive Gower's sign and a maculopapular rash over her metacarpophalangeal joints. What is the most appropriate next investigation?
A 20-year-old male presented with eczema, recurrent skin abscesses, and recurrent lung infections. There is eosinophilia and high serum levels of IgE. What is the most likely diagnosis?
Physical examination that finds multiple palpable purpuric lesions on the legs of a 7-year-old boy is most suggestive of what condition?
Which of the following is NOT true about cartilage-hair hypoplasia syndrome?
A 9-year-old boy presented with high fever, pruritic erythematous rash, joint pain, and lymph node enlargement. He had a history of upper respiratory tract infection for which he was on cefaclor for 7 days, completing a 10-day course. What is the most likely diagnosis?
A child with an obvious rash presents with recurrent infections. Investigations revealed a decreased platelet count and reduced IgM. Which of the following is the most likely diagnosis?
Which of the following conditions is characterized by immunoglobulin deficiency?
A 9-year-old child presents with multiple itchy erythematous wheals all over the body for 2 days, with no respiratory difficulty. What is the most appropriate treatment?
Immunology and Allergies Indian Medical PG Practice Questions and MCQs
Question 21: True about Severe Combined Immunodeficiency (SCID) in children is:
- A. It is due to adenosine deaminase deficiency (Correct Answer)
- B. Humoral immunity is predominantly affected
- C. Child should receive double dose of all vaccines
- D. Patients with SCID have normal thymus
Explanation: **Explanation:** Severe Combined Immunodeficiency (SCID) is a pediatric emergency characterized by a profound defect in both **T-cell and B-cell** function. **1. Why Option A is Correct:** Adenosine Deaminase (ADA) deficiency is the **second most common cause** of SCID (autosomal recessive). ADA is an enzyme required to break down toxic metabolites (deoxyadenosine) within lymphocytes. Without it, these toxins accumulate, leading to the death of T, B, and NK cells. The most common cause overall is the **X-linked SCID** (IL-2 receptor gamma chain mutation). **2. Why Other Options are Incorrect:** * **Option B:** In SCID, **both** cellular (T-cell) and humoral (B-cell) immunity are severely affected. While B-cells may be present in some forms, they are non-functional due to the lack of T-cell help. * **Option C:** Live vaccines (e.g., BCG, OPV, MMR) are **strictly contraindicated** in SCID patients as they can cause fatal systemic infections. Even non-live vaccines are generally ineffective due to the inability to mount an immune response. * **Option D:** A hallmark of SCID is **thymic hypoplasia or dysplasia**. On a chest X-ray, the absence of a thymic shadow is a classic diagnostic clue. **Clinical Pearls for NEET-PG:** * **Presentation:** Recurrent severe infections (pneumonia, diarrhea, thrush), failure to thrive, and persistent lymphopenia (<1500 cells/mm³). * **Diagnosis:** Low absolute lymphocyte count and flow cytometry showing absent T-cells. * **Treatment:** Hematopoietic Stem Cell Transplant (HSCT) is the definitive treatment. ADA deficiency can also be treated with Enzyme Replacement Therapy (ERT) or Gene Therapy. * **Screening:** TRECs (T-cell Receptor Excision Circles) are used in newborn screening to detect SCID early.
Question 22: A 4-year-old male presents with a recent onset of rash, urticaria, and fever of 101°F. The mother reports the child has been complaining of bone pain. Physical examination reveals mild lymphadenopathy. The patient recently completed a 10-day course of cefaclor suspension for an upper respiratory infection. How should this patient be treated?
- A. Aspirin and diphenhydramine
- B. Erythromycin and diphenhydramine
- C. Intravenous penicillin and diphenhydramine
- D. Oral prednisone and diphenhydramine (Correct Answer)
Explanation: ### **Explanation** The clinical presentation of fever, urticaria, lymphadenopathy, and arthralgia (bone pain) following the administration of a medication (cefaclor) is classic for **Serum Sickness-Like Reaction (SSLR)**. **Why Option D is Correct:** SSLR is a Type III hypersensitivity reaction caused by the deposition of immune complexes in small vessels. Unlike true Serum Sickness, it does not involve circulating immune complexes or low complement levels. The mainstay of treatment is **symptomatic relief** and removal of the offending agent. * **Antihistamines (Diphenhydramine):** Used to manage pruritus and urticaria. * **Corticosteroids (Oral Prednisone):** Indicated in moderate to severe cases, especially when there is significant joint pain (arthralgia) or high fever, to rapidly reduce inflammation. **Why Other Options are Incorrect:** * **Option A:** **Aspirin** is contraindicated in children with viral-like symptoms or febrile illnesses due to the risk of **Reye Syndrome**. * **Option B:** **Erythromycin** is an antibiotic. SSLR is an immunological reaction, not an active infection; adding another antibiotic may complicate the clinical picture. * **Option C:** **Penicillin** is a common trigger for SSLR. Administering it would worsen the hypersensitivity reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Common Triggers:** Cefaclor (most common in children), Penicillins, and Sulfa drugs. * **Timing:** Symptoms typically appear **7–21 days** after drug exposure. * **Key Differentiator:** Unlike true Serum Sickness, SSLR lacks renal involvement (no proteinuria/hematuria) and complement levels (C3, C4) remain **normal**. * **Prognosis:** Excellent; symptoms usually resolve within 1–2 weeks of drug discontinuation.
Question 23: A 9-year-old girl presents with a 6-month history of difficulty combing her hair and climbing upstairs. She exhibits a positive Gower's sign and a maculopapular rash over her metacarpophalangeal joints. What is the most appropriate next investigation?
- A. Erythrocyte Sedimentation Rate (ESR)
- B. Rheumatoid Factor (RA factor)
- C. Creatine Kinase (CK) (Correct Answer)
- D. Electromyography (EMG)
Explanation: ### Explanation **Diagnosis: Juvenile Dermatomyositis (JDM)** The clinical presentation of proximal muscle weakness (difficulty climbing stairs and combing hair, positive Gower’s sign) combined with a characteristic skin rash (maculopapular rash over MCP joints, known as **Gottron’s papules**) is classic for Juvenile Dermatomyositis. **1. Why Creatine Kinase (CK) is the correct answer:** In JDM, the primary pathology is an immune-mediated inflammatory myopathy. Damage to the muscle fibers leads to the leakage of sarcoplasmic enzymes into the bloodstream. **Serum Creatine Kinase (CK)** is the most sensitive initial laboratory investigation to confirm muscle injury. It is typically elevated (often 10–50 times the normal limit) and serves as a crucial marker for both diagnosis and monitoring disease activity. **2. Why the other options are incorrect:** * **ESR (Option A):** While ESR may be elevated in inflammatory conditions, it is non-specific and can be normal in many cases of JDM. It does not confirm muscle involvement. * **Rheumatoid Factor (Option B):** RF is associated with Juvenile Idiopathic Arthritis (JIA). JDM is not typically associated with RF positivity. * **Electromyography (Option D):** EMG can show characteristic features of myopathy (short-duration, low-amplitude polyphasic potentials), but it is invasive, painful for a child, and has largely been replaced by **MRI** (the gold standard for identifying muscle edema) and CK levels in modern practice. **Clinical Pearls for NEET-PG:** * **Gottron’s Papules:** Pathognomonic erythematous, scaly plaques over the extensor surfaces of MCP and IP joints. * **Heliotrope Rash:** Violaceous discoloration of the upper eyelids with periorbital edema. * **Gower’s Sign:** Indicates proximal muscle weakness (classically seen in Duchenne Muscular Dystrophy, but also present in inflammatory myopathies). * **Definitive Diagnosis:** Muscle biopsy (shows perifascicular atrophy and perivascular inflammation), though often avoided if clinical and MRI findings are classic.
Question 24: A 20-year-old male presented with eczema, recurrent skin abscesses, and recurrent lung infections. There is eosinophilia and high serum levels of IgE. What is the most likely diagnosis?
- A. Job's syndrome (Correct Answer)
- B. Shwachman's disease
- C. Wiskott-Aldrich syndrome
- D. Nezelof syndrome
Explanation: ### Explanation The clinical presentation of **eczema, recurrent skin abscesses (cold abscesses), recurrent sinopulmonary infections, and elevated serum IgE** is the classic triad of **Job’s Syndrome** (Hyper-IgE Syndrome). **1. Why Job’s Syndrome is Correct:** Job’s syndrome is most commonly an **autosomal dominant** disorder caused by a mutation in the **STAT3 gene**. This leads to a failure of Th17 cell differentiation and impaired neutrophil chemotaxis. The hallmark features include: * **Skin:** Severe eczema and "cold" staphylococcal abscesses (lack of warmth/redness due to impaired inflammatory response). * **Lungs:** Recurrent pneumonia often leading to **pneumatoceles**. * **Laboratory:** Extreme eosinophilia and IgE levels often >2000 IU/mL. * **Facies:** Coarse facial features, retained primary teeth, and scoliosis. **2. Why the Other Options are Incorrect:** * **Shwachman-Diamond Syndrome:** Characterized by exocrine pancreatic insufficiency, bone marrow failure (neutropenia), and skeletal abnormalities. It does not present with high IgE or severe eczema. * **Wiskott-Aldrich Syndrome:** While it features eczema and high IgE, it is defined by the triad of **Thrombocytopenia (small platelets)**, Eczema, and Immunodeficiency. The absence of bleeding tendencies/low platelets makes this less likely. * **Nezelof Syndrome:** An older term for a type of combined immunodeficiency (T-cell deficiency) with abnormal thymus development. It presents with severe viral/fungal infections rather than the specific IgE/abscess profile. **3. NEET-PG High-Yield Pearls:** * **Mnemonic (FATED):** **F**acies (coarse), **A**bscesses (cold), **T**eeth (retained primary), **E**levated IgE, **D**ermatological (eczema). * **Inheritance:** Autosomal Dominant (STAT3) is most common; an Autosomal Recessive form (DOCK8 deficiency) also exists but lacks skeletal/dental involvement. * **Key Radiographic Finding:** Pneumatoceles (thin-walled air-filled cysts in the lungs).
Question 25: Physical examination that finds multiple palpable purpuric lesions on the legs of a 7-year-old boy is most suggestive of what condition?
- A. Bleeding secondary to excess corticosteroids
- B. Hemorrhage secondary to hypersensitivity vasculitis (Correct Answer)
- C. Erythema secondary to active hyperemia
- D. Telangiectasia secondary to a congenital malformation
Explanation: **Explanation:** The clinical presentation of **palpable purpura** in a child, particularly localized to the lower extremities, is the hallmark of **Henoch-Schönlein Purpura (HSP)**, the most common form of **hypersensitivity vasculitis** in children. 1. **Why Option B is Correct:** Palpable purpura occurs when there is inflammation of small blood vessels (vasculitis), leading to vessel wall damage and the leakage of red blood cells into the dermis (**hemorrhage**). Unlike flat petechiae, these lesions are palpable because the inflammatory process causes localized edema and cellular infiltration. In HSP, this is typically an IgA-mediated immune complex deposition in the vessel walls. 2. **Why Incorrect Options are Wrong:** * **Option A:** Excess corticosteroids typically cause skin thinning, easy bruising (ecchymosis), and striae due to collagen breakdown, but not inflammatory palpable purpura. * **Option C:** Erythema from active hyperemia (increased blood flow) blanches under pressure (diascopy). Purpura does not blanch because the blood is extravasated outside the vessels. * **Option D:** Telangiectasias are permanent dilatations of pre-existing small blood vessels. They are blanchable, non-palpable, and do not represent acute hemorrhage. **NEET-PG High-Yield Pearls:** * **HSP Tetrad:** Palpable purpura (without thrombocytopenia), arthritis/arthralgia, abdominal pain (intussusception risk), and renal involvement (IgA nephropathy). * **Diagnosis:** Primarily clinical. If a biopsy is done, it shows **leukocytoclastic vasculitis** with IgA deposition on immunofluorescence. * **Platelet Count:** Crucially, the platelet count in HSP is **normal**; this distinguishes it from Immune Thrombocytopenic Purpura (ITP), where purpura is non-palpable and platelets are low.
Question 26: Which of the following is NOT true about cartilage-hair hypoplasia syndrome?
- A. Neutropenia
- B. Depigmented hair
- C. Non-functioning T cells (Correct Answer)
- D. None of the above
Explanation: **Explanation:** **Cartilage-Hair Hypoplasia (CHH)**, also known as McKusick type metaphyseal chondrodysplasia, is an autosomal recessive disorder caused by mutations in the **RMRP gene**. 1. **Why Option C is the correct answer (The "NOT true" statement):** While CHH is characterized by a cellular immunodeficiency, it typically involves a **reduction in the number of T cells** (lymphopenia) rather than a total absence of function. The T cells that are present usually retain some level of functionality, although there is impaired proliferation. Therefore, stating that the T cells are "non-functioning" is medically inaccurate in the context of this syndrome. 2. **Analysis of Incorrect Options:** * **Option A (Neutropenia):** This is a **true** clinical feature of CHH. Patients frequently present with cyclic or persistent neutropenia, which contributes to their increased susceptibility to infections. * **Option B (Depigmented hair):** This is a **true** hallmark of the disease. The "hair hypoplasia" aspect manifests as fine, sparse, light-colored (hypopigmented/depigmented), and brittle hair due to a reduction in the hair shaft diameter. **Clinical Pearls for NEET-PG:** * **Triad:** Short-limbed dwarfism (metaphyseal dysplasias), sparse/light hair, and immunodeficiency. * **Genetics:** Mutation in the **RMRP gene** (encodes the RNA component of RNase MRP enzyme). * **Key Complications:** High risk of severe **Varicella** infections, increased incidence of malignancies (especially lymphomas), and Hirschsprung disease. * **Radiology:** Metaphyseal flaring and irregularities, particularly at the knees.
Question 27: A 9-year-old boy presented with high fever, pruritic erythematous rash, joint pain, and lymph node enlargement. He had a history of upper respiratory tract infection for which he was on cefaclor for 7 days, completing a 10-day course. What is the most likely diagnosis?
- A. Serum sickness-like illness (Correct Answer)
- B. Hemolytic-uremic syndrome
- C. Kawasaki disease
- D. Type III hypersensitivity
Explanation: ### Explanation **Correct Answer: A. Serum sickness-like illness (SSLI)** **Why it is correct:** Serum sickness-like illness is a **Type III hypersensitivity reaction** (immune-complex mediated) commonly triggered by drugs, most notably **cefaclor** in children. The classic triad includes **fever, rash (urticarial or pruritic erythematous), and arthralgia/arthritis**, often accompanied by lymphadenopathy. Symptoms typically appear 7–21 days after drug exposure. Unlike true serum sickness, SSLI does not involve circulating immune complexes, vasculitis, or renal lesions, and complement levels (C3, C4) remain normal. **Why the other options are incorrect:** * **B. Hemolytic-uremic syndrome (HUS):** Characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, usually following bloody diarrhea (*E. coli* O157:H7). It does not present with a pruritic rash or joint pain. * **C. Kawasaki disease:** Requires fever for ≥5 days plus 4/5 clinical criteria (conjunctivitis, mucosal changes, strawberry tongue, extremity changes, and cervical lymphadenopathy). While it features rash and fever, the specific association with cefaclor and the nature of the joint pain point more strongly toward SSLI. * **D. Type III hypersensitivity:** While SSLI is *mechanistically* a Type III hypersensitivity reaction, the question asks for the **diagnosis**. "Serum sickness-like illness" is the specific clinical diagnosis, whereas Type III hypersensitivity is the underlying immunologic mechanism. **Clinical Pearls for NEET-PG:** * **Most common trigger:** Cefaclor (highest incidence in pediatrics), followed by penicillins and sulfonamides. * **Key distinction:** Unlike true Serum Sickness (caused by heterologous proteins like anti-thymocyte globulin), SSLI lacks renal involvement and low complement levels. * **Management:** Discontinuation of the offending drug and supportive care (antihistamines/NSAIDs). It is self-limiting.
Question 28: A child with an obvious rash presents with recurrent infections. Investigations revealed a decreased platelet count and reduced IgM. Which of the following is the most likely diagnosis?
- A. Idiopathic Thrombocytopenic Purpura
- B. Thrombotic Thrombocytopenic Purpura
- C. Wiskott-Aldrich Syndrome (Correct Answer)
- D. DiGeorge anomaly
Explanation: **Explanation:** The clinical presentation described—**recurrent infections, thrombocytopenia (low platelets), and a rash (eczema)**—is the classic triad of **Wiskott-Aldrich Syndrome (WAS)**. **1. Why Wiskott-Aldrich Syndrome is correct:** WAS is an **X-linked recessive** primary immunodeficiency caused by a mutation in the **WASp gene**, which is essential for actin cytoskeleton remodeling in hematopoietic cells. This leads to: * **Micro-thrombocytopenia:** Small-sized platelets and low platelet counts (leading to bleeding/purpura). * **Immunodeficiency:** Characterized by **low IgM**, normal/high IgA and IgE, and variable IgG levels. This results in recurrent infections with encapsulated organisms. * **Eczema:** The "obvious rash" mentioned in the question. **2. Why the other options are incorrect:** * **Idiopathic Thrombocytopenic Purpura (ITP):** Presents with isolated thrombocytopenia (usually large platelets) and bleeding, but does not cause recurrent infections or specific immunoglobulin deficiencies. * **Thrombotic Thrombocytopenic Purpura (TTP):** Characterized by the pentad of microangiopathic hemolytic anemia, thrombocytopenia, neurological symptoms, fever, and renal failure. It is not an immunodeficiency disorder. * **DiGeorge Anomaly:** Primarily a T-cell defect due to 22q11.2 deletion. It presents with CATCH-22 features (Cardiac defects, Abnormal facies, Thymic hypoplasia, Cleft palate, and Hypocalcemia). It does not typically present with thrombocytopenia. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked Recessive (only males affected). * **Platelet Morphology:** WAS is the only condition where platelets are **small** (decreased Mean Platelet Volume). * **Mnemonic (WATER):** **W**iskott **A**ldrich, **T**hrombocytopenia, **E**czema, **R**ecurrent infections. * **Risk:** Increased risk of autoimmune diseases and B-cell lymphomas. * **Treatment:** Hematopoietic stem cell transplant is the definitive cure.
Question 29: Which of the following conditions is characterized by immunoglobulin deficiency?
- A. Wiskott Aldrich syndrome
- B. X linked hypogammaglobulinemia
- C. Kawasaki disease
- D. All of the above (Correct Answer)
Explanation: This question tests the understanding of primary and secondary immune alterations in pediatric conditions. While some conditions are primary immunodeficiencies, others involve transient or functional deficiencies. **Explanation of the Correct Answer:** The correct answer is **All of the above** because each condition involves a significant reduction in specific or total immunoglobulin levels: 1. **X-linked Hypogammaglobulinemia (Bruton’s Agammaglobulinemia):** This is a primary B-cell deficiency caused by a mutation in the **BTK gene**. It results in a near-total absence of B-cells and a profound deficiency of all immunoglobulin classes (IgG, IgA, IgM, IgD, and IgE). 2. **Wiskott-Aldrich Syndrome (WAS):** This is a triad of eczema, thrombocytopenia, and immunodeficiency. It is characterized by a specific pattern of immunoglobulin deficiency: typically **low IgM**, normal to high IgG, and **elevated IgA and IgE**. The low IgM levels make these patients susceptible to encapsulated organisms. 3. **Kawasaki Disease:** While primarily a systemic vasculitis, acute Kawasaki disease is associated with a functional immune dysregulation. Studies have shown that during the acute phase, there can be a transient decrease in serum IgG levels, and more importantly, **Intravenous Immunoglobulin (IVIG)** is the gold standard treatment precisely because it compensates for the immune imbalance and prevents coronary artery aneurysms. **Clinical Pearls for NEET-PG:** * **Wiskott-Aldrich Syndrome:** Remember the mnemonic **TIE** (Thrombocytopenia, Infections, Eczema). The genetic defect is in the **WASP gene** (X-linked). * **Bruton’s:** Look for a male infant (X-linked) presenting after 6 months of age (once maternal IgG wanes) with absent tonsils and recurrent sinopulmonary infections. * **Kawasaki Disease:** The most common cause of acquired heart disease in children. Diagnostic criteria include fever for ≥5 days plus 4 out of 5 clinical signs (Conjunctivitis, Rash, Edema/Erythema of hands/feet, Adenopathy, Mucosal changes - "CREAM").
Question 30: A 9-year-old child presents with multiple itchy erythematous wheals all over the body for 2 days, with no respiratory difficulty. What is the most appropriate treatment?
- A. Antihelminthics
- B. Systemic corticosteroids
- C. Antihistamines (Correct Answer)
- D. Adrenaline
Explanation: ### Explanation **Correct Option: C (Antihistamines)** The clinical presentation of itchy, erythematous wheals (hives) without systemic involvement is diagnostic of **Acute Urticaria**. The underlying pathophysiology involves Type I Hypersensitivity, where mast cell degranulation releases histamine, leading to vasodilation and increased capillary permeability. **Second-generation H1-antihistamines** (e.g., Cetirizine, Loratadine) are the first-line treatment as they effectively block H1 receptors, reducing itching and wheal formation with minimal sedation. **Why other options are incorrect:** * **A. Antihelminthics:** While parasitic infections (like *Ascaris*) can cause urticaria, they are not the immediate treatment for an acute symptomatic presentation. They are considered only if the history suggests infestation or if urticaria becomes chronic. * **B. Systemic Corticosteroids:** These are reserved for severe cases, refractory urticaria, or when associated with angioedema. They are not first-line for simple, uncomplicated wheals. * **D. Adrenaline:** This is the life-saving drug of choice for **Anaphylaxis**. Since the patient has no respiratory difficulty (no airway compromise or wheezing) and no hemodynamic instability, adrenaline is not indicated. **Clinical Pearls for NEET-PG:** * **Acute vs. Chronic:** Urticaria is "acute" if it lasts <6 weeks and "chronic" if >6 weeks. * **Drug of Choice:** Non-sedating H1 blockers are preferred over first-generation antihistamines (like Pheniramine) due to a better safety profile. * **Anaphylaxis Red Flags:** Always check for "ABC" (Airway, Breathing, Circulation) compromise. If present, the immediate step is **Intramuscular Adrenaline (1:1000)**. * **Common Triggers:** In children, viral infections are the most common cause of acute urticaria, followed by food and medications.
Practice by Chapter
Development of Immune System
Practice Questions
Primary Immunodeficiency Disorders
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Secondary Immunodeficiency Disorders
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Allergic Rhinitis
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Asthma in Children
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Atopic Dermatitis
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Food Allergies
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Drug Allergies
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Anaphylaxis
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Urticaria and Angioedema
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Autoimmune Disorders
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Immunotherapy
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