Sublingual Immunotherapy — MCQs
What is an atypical side effect of montelukast?
Which condition is characterized by conjunctival injection, pharyngeal injection, polymorphic rash, and cervical lymphadenopathy?
Which is the best investigation to confirm diagnosis of anaphylaxis?
Omalizumab is indicated for which of the following conditions?
Oral cholera vaccine is effective for:
A 30-year-old shows delusions, hallucinations, and marked thought disorder. Labs reveal anti-NMDA receptor antibodies. Best initial treatment?
Which of the following are early mediators of allergic rhinitis?
Which of the following is the preformed toxin involved in the mechanism of allergic rhinitis?
Paracusis willis is a feature of which condition?
What is the full form of ARIA?
Sublingual Immunotherapy Indian Medical PG Practice Questions and MCQs
Question 1: What is an atypical side effect of montelukast?
- A. Goodpasture syndrome
- B. Membranous glomerulonephritis
- C. Bronchial asthma
- D. Churg-Strauss syndrome (Correct Answer)
Explanation: ***Churg-Strauss syndrome*** - The apparent development of **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) has been reported in patients treated with montelukast, although it is believed to be related more to the unmasking of the disease rather than a direct drug effect. - This typically occurs when **corticosteroids** are tapered or withdrawn as montelukast takes over, revealing the underlying vasculitis. *Goodpasture syndrome* - **Goodpasture syndrome** is an autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary hemorrhage, characterized by anti-glomerular basement membrane (GBM) antibodies. - There is no established association between montelukast use and the development of Goodpasture syndrome. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is a common cause of nephrotic syndrome, characterized by immune complex deposition on the glomerular basement membrane. - This condition is not typically linked to the use of montelukast. *Bronchial asthma* - **Bronchial asthma** is the condition montelukast is used to treat, acting as a leukotriene receptor antagonist to reduce inflammation and bronchoconstriction. - It is a primary indication for the drug, not a side effect.
Question 2: Which condition is characterized by conjunctival injection, pharyngeal injection, polymorphic rash, and cervical lymphadenopathy?
- A. Kawasaki syndrome (Correct Answer)
- B. Measles
- C. Scarlet fever
- D. Mumps
Explanation: ***Kawasaki syndrome*** - **Kawasaki syndrome** is characterized by a constellation of symptoms including **conjunctival injection**, **pharyngeal injection**, a **polymorphic rash**, and **cervical lymphadenopathy**, often described as the CRASH and burn criteria (Conjunctivitis, Rash, Adenopathy, Strawberry tongue, Hand/foot changes, and Fever). - It is an acute systemic vasculitis, primarily affecting young children, and without treatment, it can lead to **coronary artery aneurysms**. *Measles* - Measles is characterized by a maculopapular rash that typically starts on the face and spreads downwards (cephalocaudal), along with the presence of **Koplik spots** on the buccal mucosa. - While it presents with conjunctivitis and rash, the rash is not polymorphic in the same way as Kawasaki, and cervical lymphadenopathy is less prominent. *Scarlet fever* - **Scarlet fever** is caused by Group A Streptococcus and presents with pharyngitis, fever, and a characteristic **sandpaper-like erythematous rash** with circumoral pallor. - While it has pharyngeal involvement and rash, it lacks the **conjunctival injection** and **polymorphic nature of the rash** seen in Kawasaki syndrome. The rash is typically fine and blanching. - Cervical lymphadenopathy may be present but the overall constellation differs from Kawasaki. *Mumps* - Mumps is an acute viral infection primarily characterized by the swelling of the **parotid glands** (parotitis), often accompanied by fever, headache, and malaise. - It does not typically present with conjunctival injection, a polymorphic rash, or prominent cervical lymphadenopathy as seen in Kawasaki syndrome.
Question 3: Which is the best investigation to confirm diagnosis of anaphylaxis?
- A. IgA levels
- B. Serum tryptase (Correct Answer)
- C. IgD levels
- D. Serum precipitins
Explanation: ***Serum tryptase*** - **Serum tryptase** is released from activated mast cells and is a reliable biomarker for confirming anaphylaxis, particularly when measured within 1-3 hours of symptom onset. - Elevated levels help differentiate anaphylaxis from other conditions with similar symptoms, especially when the clinical picture is ambiguous. *IgA levels* - **IgA levels** are relevant in diagnosing conditions like selective IgA deficiency or celiac disease, but they do not play a direct role in confirming acute anaphylaxis. - They reflect long-term immune status rather than immediate hypersensitivity reactions. *IgD levels* - **IgD levels** have no established role in the diagnosis or confirmation of anaphylaxis. - Their physiological function is not fully understood, but they are not used as biomarkers for acute allergic reactions. *Serum precipitins* - **Serum precipitins** are antibodies detected in various hypersensitivity reactions, especially to inhaled antigens, and are not specific for anaphylaxis [1]. - They are primarily associated with conditions like hypersensitivity pneumonitis, reflecting different immunological mechanisms [1].
Question 4: Omalizumab is indicated for which of the following conditions?
- A. Multiple myeloma
- B. Psoriasis
- C. Bronchial asthma (Correct Answer)
- D. Rheumatoid arthritis
Explanation: ***Bronchial asthma*** - Omalizumab is an **anti-IgE antibody** that binds to circulating IgE, preventing it from binding to mast cells and basophils, thus reducing allergic reactions. - It is specifically approved for the treatment of **moderate to severe persistent asthma** in patients over 6 years old whose symptoms are inadequately controlled by inhaled corticosteroids. *Multiple myeloma* - Multiple myeloma is a **plasma cell malignancy** affecting bone marrow, for which omalizumab has no approved indication. - Treatment typically involves **chemotherapy**, proteasome inhibitors, immunomodulatory drugs, and stem cell transplantation. *Psoriasis* - Psoriasis is a **chronic inflammatory skin condition** primarily treated with agents targeting inflammatory pathways such as TNF-alpha, IL-17, or IL-23, not IgE. - Common psoriasis medications include **topical corticosteroids**, phototherapy, and systemic biologics like adalimumab or ustekinumab. *Rheumatoid arthritis* - Rheumatoid arthritis is an **autoimmune disease** causing chronic joint inflammation, primarily treated with DMARDs (disease-modifying antirheumatic drugs) and TNF inhibitors. - **IgE does not play a significant role** in the pathogenesis of rheumatoid arthritis, making omalizumab ineffective for this condition.
Question 5: Oral cholera vaccine is effective for:
- A. 6 months
- B. 12 months
- C. 3 years (Correct Answer)
- D. 2 years
Explanation: ***3 years*** - **Oral cholera vaccines** like Shanchol and Euvichol-Plus provide protection for at least **3 years** after complete 2-dose immunization. - Studies in endemic areas demonstrate sustained protection extending **up to 5 years** with Shanchol. - The **WHO recommends** OCVs as part of comprehensive cholera control strategies in endemic regions and outbreak settings. - This duration is based on field effectiveness studies and clinical trials in various populations. *2 years* - While **Dukoral** (another OCV) provides protection for approximately **2 years**, this is not the standard duration for the most widely used OCVs. - **2 years** represents the conservative lower estimate, not the established duration for Shanchol/Euvichol vaccines. - Current evidence supports longer protection than 2 years for most recipients. *12 months* - **12 months** significantly underestimates the protective duration of oral cholera vaccines. - All WHO-prequalified OCVs provide protection well beyond 1 year. - This duration might represent only the initial phase of immunity, not the full protective window. *6 months* - **6 months** is far too short and does not reflect the established efficacy of any current oral cholera vaccine. - While seroconversion occurs within weeks, the protective immunity lasts much longer. - No WHO-prequalified OCV has such a limited duration of protection.
Question 6: A 30-year-old shows delusions, hallucinations, and marked thought disorder. Labs reveal anti-NMDA receptor antibodies. Best initial treatment?
- A. Immunotherapy (Correct Answer)
- B. Benzodiazepines
- C. ECT
- D. Antipsychotics
Explanation: ***Immunotherapy*** - The presence of **anti-NMDA receptor antibodies** indicates an autoimmune etiology for the psychiatric symptoms, making **immunotherapy** (e.g., corticosteroids, IVIG, plasmapheresis) the definitive first-line treatment. - Immunotherapy aims to reduce inflammation and remove autoantibodies, thereby reversing the neurological and psychiatric manifestations. *Benzodiazepines* - While useful for acute agitation or catatonia in psychiatric disorders, **benzodiazepines** do not address the underlying autoimmune pathology of anti-NMDA receptor encephalitis. - They would provide only symptomatic relief and would not prevent disease progression or long-term neurological damage. *ECT* - **Electroconvulsive therapy (ECT)** is a treatment for severe, refractory mood disorders or catatonia, which might be present in anti-NMDA receptor encephalitis. - However, ECT is a symptomatic treatment and does not target the autoimmune cause, making it less appropriate as the **initial definitive treatment**. *Antipsychotics* - **Antipsychotics** are used to manage psychosis, delusions, and hallucinations, which are prominent in anti-NMDA receptor encephalitis. - However, they do not treat the underlying **autoimmune inflammation** and may worsen some symptoms, such as autonomic instability or seizures, in this specific condition.
Question 7: 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 8: Which of the following is the preformed toxin involved in the mechanism of allergic rhinitis?
- A. Histamine (Correct Answer)
- B. Leukotriene
- C. TXA2
- D. PGD2
Explanation: ### Explanation The pathophysiology of Allergic Rhinitis is a **Type I Hypersensitivity reaction** mediated by IgE. When an allergen cross-links IgE antibodies on the surface of mast cells, it triggers **degranulation**, leading to the release of two types of inflammatory mediators: **1. Why Histamine is Correct:** Histamine is a **preformed mediator** stored in the granules of mast cells and basophils. Upon activation, it is released immediately (within minutes), causing the "Early Phase" response characterized by sneezing, itching, and rhinorrhea. Because it is synthesized and stored *before* the allergic trigger occurs, it is classified as a preformed toxin/mediator. **2. Why the Other Options are Incorrect:** * **Leukotrienes (B), TXA2 (C), and PGD2 (D):** These are **newly synthesized mediators** (lipid-derived). They are not stored in granules but are produced *de novo* from arachidonic acid via the cyclooxygenase (COX) or lipoxygenase (LOX) pathways only after the mast cell is activated. These mediators typically contribute to the "Late Phase" response, leading to nasal congestion and sustained inflammation. ### NEET-PG High-Yield Pearls: * **Early Phase (Minutes):** Primarily mediated by **Histamine**. Clinical features: Sneezing, itching, watery rhinorrhea. * **Late Phase (4–8 hours):** Mediated by **Leukotrienes (LTC4, LTD4, LTE4)**, Cytokines, and PGD2. Clinical feature: Nasal congestion (due to cellular infiltration, mainly eosinophils). * **Gold Standard Investigation:** Skin Prick Test (detects specific IgE). * **Drug of Choice:** Intranasal Corticosteroids (act on both early and late phases). * **Mast Cell Stabilizer:** Sodium Cromoglycate (prevents degranulation; used prophylactically).
Question 9: Paracusis willis is a feature of which condition?
- A. Tympanosclerosis
- B. Otosclerosis (Correct Answer)
- C. Meniere's disease
- D. Presbyacusis
Explanation: **Explanation:** **Paracusis Willis** is a clinical phenomenon where a patient with hearing loss paradoxically hears better in a noisy environment than in a quiet one. **Why Otosclerosis is correct:** Otosclerosis is a condition characterized by the fixation of the stapes footplate, leading to **conductive hearing loss (CHL)**. In a noisy environment, normal-hearing individuals naturally raise their voice volume (the Lombard effect) to overcome background noise. A patient with Otosclerosis has a "conductive barrier" that filters out the low-frequency background noise, but because their inner ear and nerve function are intact, they can clearly perceive the loud, raised voices of others. This makes their hearing appear improved in noisy settings. **Why other options are incorrect:** * **Tympanosclerosis:** While this causes CHL due to hyalinization of the tympanic membrane, Paracusis Willis is classically described and most significantly associated with the stapes fixation found in Otosclerosis. * **Meniere’s Disease:** This is a sensory-neural hearing loss (SNHL) condition. Patients typically suffer from **loudness recruitment**, making noisy environments distressing rather than helpful. * **Presbyacusis:** This is age-related SNHL. These patients struggle significantly in noise due to poor speech discrimination and the loss of high-frequency clarity. **Clinical Pearls for NEET-PG:** * **Schwartz Sign:** A flamingo-pink flush seen on the promontory through the TM (indicates active otosclerosis/otospongiosis). * **Carhart’s Notch:** A characteristic dip in the bone conduction threshold at **2000 Hz**. * **Gelle’s Test:** Negative in Otosclerosis (indicates an immobile ossicular chain). * **Treatment of Choice:** Stapedotomy (using a Teflon piston).
Question 10: What is the full form of ARIA?
- A. Allergic rhinitis and its impact on asthma (Correct Answer)
- B. Allergic rhinitis induced asthma
- C. Antibody response in allergic rhinitis
- D. Antibody response in asthma
Explanation: **Explanation:** **1. Why Option A is Correct:** ARIA stands for **Allergic Rhinitis and its Impact on Asthma**. It is a global initiative launched by the World Health Organization (WHO) in 1999 (published in 2001) to provide evidence-based guidelines for the management of allergic rhinitis. The core medical concept behind ARIA is the **"United Airway Disease"** hypothesis, which posits that the upper and lower airways are a single functional unit. Inflammation in the nasal mucosa (allergic rhinitis) often coexists with and exacerbates inflammation in the bronchial tree (asthma). **2. Why Other Options are Incorrect:** * **Option B:** While allergic rhinitis is a major risk factor for developing asthma, ARIA is the name of the *guideline/initiative*, not a description of the pathophysiology of "induced" asthma. * **Options C & D:** These are distractors. While ARIA guidelines discuss IgE-mediated antibody responses, the acronym itself does not stand for "Antibody Response." **3. High-Yield Clinical Pearls for NEET-PG:** * **Classification:** ARIA replaced the old "seasonal/perennial" classification with a more clinical approach based on duration and severity: * **Intermittent:** Symptoms < 4 days/week OR < 4 consecutive weeks. * **Persistent:** Symptoms > 4 days/week AND > 4 consecutive weeks. * **Severity:** Categorized as **Mild** (normal sleep/daily activities) or **Moderate-Severe** (disturbed sleep/impairment of daily activities). * **Treatment Strategy:** Intranasal corticosteroids (INCS) are the first-line treatment for moderate-to-severe persistent rhinitis. * **The Link:** Approximately 80% of asthmatics have co-existing allergic rhinitis, and up to 40% of patients with allergic rhinitis have asthma. Treatment of the nose often improves asthma control.
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