Food Allergies and the Upper Aerodigestive Tract — MCQs
Which immunoglobulin is known to be heat-labile?
A cook prepares sandwiches for 10 people going for a picnic. Eight out of them develop severe gastroenteritis within 4-6 hours of consuming the sandwiches. It is likely that on investigation, the cook is found to be the carrier of -
Patient following peanut consumption presented with laryngeal edema, stridor, hoarseness of voice and swelling of tongue. Most likely diagnosis is:
Match the following: A) Glossopharyngeal nerve B) Spinal accessory nerve C) Facial nerve D) Mandibular nerve 1) Shrugging of shoulder 2) Touch sensation from the posterior one-third of the tongue 3) Chewing 4) Taste from the anterior two-thirds of the tongue
Which of the following is false regarding transfusion-associated anaphylactic reactions?
A 60-year-old man presents with foul breath and regurgitates food eaten 3 days ago. What is the most likely diagnosis?
A 45-year-old patient with a known allergy to penicillin presents with an enterococcal endocarditis. The physician needs to prescribe an antibiotic but wants to ensure it is safe for a penicillin allergy. The patient has had previous allergic reactions to penicillin including rash & swelling. Which of the following drugs can be used safely in a patient allergic to penicillin?
Drug of choice for Enterococcus infection in a patient allergic to penicillin?
Which of the following are early mediators of allergic rhinitis?
Which of the following preformed toxins is involved in the mechanism of allergic rhinitis?
Food Allergies and the Upper Aerodigestive Tract Indian Medical PG Practice Questions and MCQs
Question 1: Which immunoglobulin is known to be heat-labile?
- A. IgA
- B. IgG
- C. IgM (Correct Answer)
- D. IgE
Explanation: ***IgM*** - **IgM** is known for its **heat lability** and is readily denatured at 56°C within a few minutes. - This characteristic is due to its **pentameric structure** held together by disulfide bonds and J chains, which are sensitive to thermal denaturation. - Heat lability of IgM is clinically important in complement fixation tests and other laboratory assays where heat inactivation is performed. - IgM is the first antibody produced in primary immune response and its heat sensitivity distinguishes it from other immunoglobulins. *IgA* - **IgA** exists in monomeric (serum) and dimeric (secretory) forms and shows moderate stability to heat. - Secretory IgA is relatively stable as it needs to function in harsh mucosal environments, though not as heat-resistant as IgG. - Does not exhibit the pronounced heat lability characteristic of IgM. *IgG* - **IgG** is the most stable immunoglobulin and is highly resistant to heat denaturation. - Can withstand temperatures up to 60-70°C without significant loss of activity. - Its monomeric structure with strong intramolecular bonds provides exceptional thermal stability. - Most abundant antibody in serum and has the longest half-life. *IgE* - **IgE** is actually quite stable to heat and can withstand 56°C for extended periods. - While it has a short half-life in serum (2-3 days), this is due to receptor binding rather than heat instability. - Important in type I hypersensitivity reactions and parasitic infections. - Does not show the characteristic heat lability that defines IgM.
Question 2: A cook prepares sandwiches for 10 people going for a picnic. Eight out of them develop severe gastroenteritis within 4-6 hours of consuming the sandwiches. It is likely that on investigation, the cook is found to be the carrier of -
- A. Salmonella typhi
- B. Vibrio cholerae
- C. Entamoeba histolytica
- D. Staphylococcus aureus (Correct Answer)
Explanation: ***Staphylococcus aureus*** - The rapid onset of symptoms (4-6 hours) and the development of severe gastroenteritis in multiple individuals after consuming common food items (sandwiches) strongly suggest a **preformed toxin ingestion**. - **_Staphylococcus aureus_** is a common cause of food poisoning due to its ability to produce enterotoxins that are heat-stable and cause rapid onset of nausea, vomiting, and diarrhea. *Salmonella typhi* - **_Salmonella typhi_** causes typhoid fever, which typically has an incubation period of **1-3 weeks**, much longer than the 4-6 hours seen in this case. - The symptoms of typhoid fever are also more systemic, including high fever, headache, and abdominal pain, rather than acute gastroenteritis with rapid onset. *Vibrio cholerae* - **_Vibrio cholerae_** causes cholera, characterized by **profuse watery diarrhea** with a typical incubation period of **1-5 days**. - The rapid onset of symptoms in this scenario (4-6 hours) does not align with the incubation period of cholera. *Entamoeba histolytica* - **_Entamoeba histolytica_** causes amoebiasis, which has an incubation period ranging from **several days to weeks or even months**. - It typically presents with **bloody diarrhea** and abdominal pain, and its slow onset is inconsistent with the acute event described.
Question 3: Patient following peanut consumption presented with laryngeal edema, stridor, hoarseness of voice and swelling of tongue. Most likely diagnosis is:
- A. Foreign body bronchus
- B. Angioneurotic edema (Correct Answer)
- C. Foreign body larynx
- D. Pharyngeal abscess
Explanation: ***Angioneurotic edema*** - The rapid onset of **laryngeal edema**, **stridor**, **hoarseness**, and **tongue swelling** following peanut consumption points to an allergic reaction, specifically **anaphylaxis** causing angioedema [1], [2]. - This is a life-threatening condition due to potential **airway obstruction**. *Foreign body bronchus* - While a foreign body could cause **stridor** if large enough to impact the trachea, symptoms like **laryngeal edema** and **tongue swelling** are not typical. - It usually presents with sudden coughing, wheezing, and possibly dyspnea, often without rapid-onset, diffuse swelling. *Foreign body larynx* - A foreign body in the larynx might cause hoarseness and stridor, but **laryngeal edema** and **tongue swelling** are not primary features of a simple foreign body obstruction. - The history of peanut ingestion and rapid systemic inflammatory response makes an allergic reaction more likely [2]. *Pharyngeal abscess* - A pharyngeal abscess typically develops more slowly, with symptoms including **severe sore throat**, **fever**, and **difficulty swallowing**. - It would not usually present with the rapid onset of severe **laryngeal edema** and **tongue swelling** immediately after peanut consumption.
Question 4: Match the following: A) Glossopharyngeal nerve B) Spinal accessory nerve C) Facial nerve D) Mandibular nerve 1) Shrugging of shoulder 2) Touch sensation from the posterior one-third of the tongue 3) Chewing 4) Taste from the anterior two-thirds of the tongue
- A. A-3 , B-1 , C-4 , D-2
- B. A-2 , B-3 , C-4 , D-1
- C. A-4 , B-1 , C-2 , D-3
- D. A-2 , B-1 , C-4 , D-3 (Correct Answer)
Explanation: ***A-2 , B-1 , C-4 , D-3*** - **A) Glossopharyngeal nerve (CN IX)** is responsible for **general sensation and taste from the posterior one-third of the tongue** [1]. (2). - **B) Spinal Accessory nerve (CN XI)** innervates the **sternocleidomastoid** and **trapezius muscles**, which are involved in shrugging the shoulders (1). - **C) Facial nerve (CN VII)** carries **taste sensation from the anterior two-thirds of the tongue** [1] (4) via the chorda tympani. - **D) Mandibular nerve (V3)**, a branch of the trigeminal nerve, innervates the muscles of mastication, enabling **chewing** (3). *A-3 , B-1 , C-4 , D-2* - This option incorrectly associates the **glossopharyngeal nerve** with chewing, which is a function of the mandibular nerve (V3). - It also incorrectly associates the **mandibular nerve** with touch sensation from the posterior one-third of the tongue, which is a function of the glossopharyngeal nerve [1]. *A-2 , B-3 , C-4 , D-1* - This option incorrectly links the **spinal accessory nerve** with chewing; this nerve primarily controls shoulder and neck movements. - It also incorrectly assigns shrugging of the shoulder to the **mandibular nerve** instead of the spinal accessory nerve. *A-4 , B-1 , C-2 , D-3* - This choice incorrectly attributes **taste from the anterior two-thirds of the tongue** to the glossopharyngeal nerve, which supplies the posterior one-third [1]. - It also incorrectly links **touch sensation from the posterior one-third of the tongue** to the facial nerve, which is involved in taste from the anterior two-thirds [1].
Question 5: Which of the following is false regarding transfusion-associated anaphylactic reactions?
- A. Different from allergy
- B. Epinephrine is the drug of choice
- C. Washed blood products prevent it
- D. Seen in IgG deficient individuals (Correct Answer)
Explanation: ***Seen in IgG deficient individuals*** - Transfusion-associated **anaphylactic reactions** are most commonly seen in **IgA-deficient individuals** who develop **anti-IgA antibodies** and receive blood products containing IgA. - Anaphylaxis occurs when these pre-formed IgA antibodies react with donor IgA, leading to mast cell degranulation and severe allergic symptoms. *Different from allergy* - Transfusion-associated **anaphylactic reactions** are a severe form of allergic reaction, often distinguished by their **rapid onset** and life-threatening nature [1]. - While all allergies involve an immune response to an allergen, anaphylaxis represents the most extreme systemic manifestation. *Epinephrine is the drug of choice* - **Epinephrine** is indeed the **first-line treatment** for acute anaphylaxis, regardless of its cause, including transfusion-associated reactions [2]. - It acts rapidly to counteract the systemic effects of histamine and other mediators by acting on α and β adrenergic receptors [3]. *Washed blood products prevent it* - **Washing blood products** (e.g., packed red blood cells or platelets) is an effective strategy to **remove plasma proteins**, including IgA. - This is particularly crucial for patients with a known **IgA deficiency and anti-IgA antibodies** to prevent severe anaphylactic reactions.
Question 6: A 60-year-old man presents with foul breath and regurgitates food eaten 3 days ago. What is the most likely diagnosis?
- A. Achalasia cardia
- B. Carcinoma esophagus
- C. Loss of tone of upper esophageal sphincter
- D. Zenker's Diverticulum (Correct Answer)
Explanation: ***Zenker's Diverticulum*** - This condition presents with a classic triad of **dysphagia**, **regurgitation of undigested food**, and **foul breath (halitosis)** due to food retention in the diverticulum. - The regurgitation of food eaten several days ago is highly characteristic, indicating significant pooling and decomposition within the **pharyngeal pouch**. *Achalasia cardia* - Characterized by **dysphagia for both solids and liquids** and regurgitation, but the regurgitated food is typically fresh or only recently ingested, not from several days prior. - The primary pathology is the **failure of the lower esophageal sphincter (LES) to relax** and loss of peristalsis in the esophageal body. *Carcinoma esophagus* - Often presents with **progressive dysphagia** (first for solids, then for liquids) and significant **weight loss**. - While regurgitation can occur, it's usually of recently ingested food and rarely associated with the severe halitosis from long-standing food decomposition seen in Zenker's. *Loss of tone of upper esophageal sphincter* - This condition would more likely lead to **regurgitation of stomach contents** into the pharynx, rather than the retention of food in a pouch. - It could contribute to **reflux symptoms** but does not explain the formation of a diverticulum or the prolonged food retention leading to foul breath.
Question 7: A 45-year-old patient with a known allergy to penicillin presents with an enterococcal endocarditis. The physician needs to prescribe an antibiotic but wants to ensure it is safe for a penicillin allergy. The patient has had previous allergic reactions to penicillin including rash & swelling. Which of the following drugs can be used safely in a patient allergic to penicillin?
- A. Ceftriaxone
- B. Piperacillin
- C. Vancomycin (Correct Answer)
- D. Aztreonam
Explanation: ***Vancomycin***- **Vancomycin** is a glycopeptide antibiotic that is **structurally unrelated to penicillin**, with no cross-reactivity in penicillin-allergic patients [2].- It has **excellent activity against Enterococcus species** and is the **preferred alternative for enterococcal endocarditis** in patients with penicillin allergy [1, 2].- Vancomycin provides reliable bactericidal activity against enterococci and is guideline-recommended for this indication in penicillin-allergic patients [1].*Aztreonam*- **Aztreonam** is a monobactam antibiotic with minimal cross-reactivity to penicillin allergies due to its unique beta-lactam structure.- However, aztreonam has **NO activity against Gram-positive organisms**, including Enterococcus species.- It would be **completely ineffective** for treating enterococcal endocarditis despite being safe in penicillin allergy.*Ceftriaxone*- **Ceftriaxone** is a third-generation cephalosporin that shares the beta-lactam ring structure with penicillins.- There is approximately **1-3% cross-reactivity risk** in patients with non-severe penicillin allergy, and up to 10% in those with severe reactions [1].- Given this patient's history of rash and swelling, ceftriaxone carries **unacceptable cross-reactivity risk** [1].*Piperacillin*- **Piperacillin** is an extended-spectrum penicillin antibiotic, belonging to the same drug class as penicillin [1].- It is **absolutely contraindicated** in penicillin-allergic patients due to identical allergenic epitopes [1].- Administration would carry a **high risk of severe allergic reaction**, including potential anaphylaxis [1].
Question 8: Drug of choice for Enterococcus infection in a patient allergic to penicillin?
- A. Streptomycin
- B. Cephalosporin
- C. Vancomycin (Correct Answer)
- D. Rifampicin
Explanation: ***Vancomycin*** - **Vancomycin** is a glycopeptide antibiotic that is effective against **Gram-positive bacteria**, including *Enterococcus*, especially in patients with a **penicillin allergy**. - It inhibits **cell wall synthesis** by binding to the D-Ala-D-Ala terminus of peptidoglycan precursors, a different mechanism from penicillins. *Streptomycin* - **Streptomycin** is an aminoglycoside that inhibits **protein synthesis** and is primarily used in **combination therapy** for serious *Enterococcal* infections, but typically alongside a cell-wall active agent (like penicillin or vancomycin) for synergistic killing in endocarditis or other severe infections. - It is not usually recommended as a **monotherapy** for *Enterococcus*, especially in the context of penicillin allergy, as it doesn't provide bactericidal activity on its own against all enterococcal strains. *Cephalosporin* - **Cephalosporins** are **not active** against *Enterococcus spp.* as these bacteria intrinsically lack the **penicillin-binding proteins (PBPs)** that cephalosporins target effectively. - This **intrinsic resistance** makes cephalosporins an inappropriate choice for treating *Enterococcal* infections, regardless of penicillin allergy status. *Rifampicin* - **Rifampicin** is an antibiotic primarily used for **Mycobacterial infections** (e.g., tuberculosis) and some **Staphylococcal infections**, often in combination to prevent resistance. - It has **poor activity** against *Enterococcus* and is not a recommended treatment for *Enterococcal* infections.
Question 9: Which of the following are early mediators of allergic rhinitis?
- A. Leukotrienes
- B. Interleukin-4
- C. Interleukin-5
- D. Platelet-activating factor and bradykinin (Correct Answer)
Explanation: ### Explanation Allergic rhinitis is a Type I hypersensitivity reaction occurring in two distinct phases: the **Early Phase** (within minutes) and the **Late Phase** (4–8 hours later). **Why Option D is Correct:** The early phase is triggered when an allergen cross-links IgE antibodies on the surface of **mast cells**, leading to immediate degranulation. This releases **pre-formed mediators** and rapidly synthesized lipid mediators. * **Histamine** is the primary mediator. * **Platelet-activating factor (PAF), Bradykinin, and Prostaglandin D2** are also released during this immediate window, causing vasodilation, increased vascular permeability (edema), and stimulation of sensory nerves (itching/sneezing). **Why Other Options are Incorrect:** * **A. Leukotrienes:** While Cysteinyl Leukotrienes (CysLTs) are produced during the early phase, they are most characteristic of the transition to and maintenance of the **Late Phase** response, contributing significantly to prolonged nasal congestion. * **B & C. Interleukin-4 and Interleukin-5:** These are **cytokines** produced by Th2 lymphocytes. They are involved in the **Late Phase** response. IL-4 promotes IgE isotype switching, while IL-5 is the primary factor for **eosinophil** recruitment and activation. **NEET-PG High-Yield Pearls:** 1. **Early Phase (Minutes):** Mediated by Mast cells. Key symptoms: Sneezing, itching, rhinorrhea. Key mediator: Histamine. 2. **Late Phase (Hours):** Mediated by Eosinophils, Basophils, and Th2 cells. Key symptom: Nasal congestion. 3. **Gold Standard Diagnosis:** Skin Prick Test (detects specific IgE). 4. **Pharmacology Link:** Antihistamines work best on early-phase symptoms (itch/sneeze), while Intranasal Steroids are the most effective treatment for late-phase symptoms (congestion) because they inhibit cytokine release.
Question 10: Which of the following preformed toxins is involved in the mechanism of allergic rhinitis?
- A. Histamine (Correct Answer)
- B. Leukotriene
- C. TXA2
- D. PGD2
Explanation: Allergic rhinitis is a **Type I Hypersensitivity reaction** mediated by IgE antibodies. When an allergen cross-links IgE on the surface of mast cells, it triggers **degranulation**, releasing two types of chemical mediators: **Preformed mediators** (stored in granules) and **Newly synthesized mediators** (produced after activation). ### Why Histamine is Correct **Histamine** is the primary **preformed mediator** stored in the granules of mast cells and basophils. Upon degranulation, it is released immediately (within minutes), causing the "Early Phase" symptoms of allergic rhinitis: vasodilation, increased capillary permeability (edema/nasal block), and stimulation of sensory nerves (itching/sneezing). ### Why Other Options are Incorrect * **Leukotrienes (B):** These are **newly synthesized** mediators derived from arachidonic acid via the lipoxygenase pathway. While potent (causing mucus secretion and congestion), they are produced *after* mast cell activation and are not pre-stored. * **TXA2 (Thromboxane A2) (C):** This is a product of the cyclooxygenase pathway primarily involved in platelet aggregation and vasoconstriction; it plays a minimal role in the pathophysiology of allergic rhinitis. * **PGD2 (Prostaglandin D2) (D):** Like leukotrienes, PGD2 is a **newly synthesized** mediator produced via the cyclooxygenase pathway. It contributes to late-phase inflammation but is not preformed. ### NEET-PG High-Yield Pearls * **Early Phase Response:** Mediated by **Histamine** (Preformed). Occurs within minutes. * **Late Phase Response:** Mediated by **Leukotrienes, PGD2, and Cytokines**. Occurs 4–8 hours later; characterized by eosinophil infiltration. * **Drug of Choice:** Intranasal corticosteroids are the most effective maintenance therapy for allergic rhinitis. * **Gold Standard Test:** Skin Prick Test (SPT) is used to identify specific allergens.
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