Pathophysiology of Allergic Rhinitis — MCQs
Which drug does not cause rhinitis?
Which of the following statements about vasomotor rhinitis is false?
Partial and full closure of nasal passages is characteristically seen in:
Which of the following is a secondary mediator of anaphylaxis?
All of the following are true about nasal myiasis except which of the following?
Which interleukin is primarily responsible for inducing IgE production from B cells?
What is the most likely finding in the CT image of the left maxillary sinus in a patient with a history of allergic rhinitis?
In which condition is Young's operation performed?
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?
Pathophysiology of Allergic Rhinitis Indian Medical PG Practice Questions and MCQs
Question 1: Which drug does not cause rhinitis?
- A. ACE inhibitors
- B. Glucocorticoid (Correct Answer)
- C. Reserpine
- D. Prazosin
Explanation: ***Glucocorticoid*** - **Glucocorticoids** are the **first-line treatment** for allergic rhinitis, not a cause of rhinitis. - They work by reducing **inflammation** and **immune responses** in the nasal mucosa [1], [2]. - Intranasal corticosteroids effectively **prevent and treat** rhinitis symptoms [1]. *ACE inhibitors* - **ACE inhibitors** primarily cause a persistent, **dry cough** (10-20% of patients) due to accumulation of **bradykinin**. - Nasal congestion is **not a typical side effect**, though the bradykinin-mediated effects primarily manifest as cough rather than rhinitis. - The hallmark adverse effect is **cough**, not rhinitis. *Reserpine* - **Reserpine** causes **nasal congestion** and rhinitis as a well-documented side effect. - Mechanism: depletion of **norepinephrine** and catecholamines leads to increased **parasympathetic tone**. - This results in **vasodilation** and increased secretions in the nasal passages. *Prazosin* - **Prazosin**, an **alpha-1 adrenergic blocker**, commonly causes **nasal congestion** and rhinitis. - Mechanism: blocking alpha-1 receptors in nasal vasculature causes **vasodilation** and increased blood flow to the nasal mucosa. - This side effect is seen with all **alpha-blockers** and is well-documented.
Question 2: Which of the following statements about vasomotor rhinitis is false?
- A. It is an infective condition (Correct Answer)
- B. It primarily presents with nasal congestion and rhinorrhea
- C. It involves autonomic dysfunction of nasal blood vessels
- D. It is triggered by non-allergic stimuli like weather changes and strong odors
Explanation: ***It is an infective condition*** - **Vasomotor rhinitis** is a **non-allergic, non-infectious** condition of the nasal passages. - Its pathophysiology involves **autonomic nervous system dysfunction** affecting nasal blood vessels, not microbial infection. *It primarily presents with nasal congestion and rhinorrhea* - This statement is **true** because classic symptoms of vasomotor rhinitis include persistent or intermittent **nasal congestion** and **rhinorrhea** (runny nose). - These symptoms result from the dysregulation of the autonomic control over nasal vasculature and glands. *It involves autonomic dysfunction of nasal blood vessels* - This statement is **true** and describes the core mechanism of vasomotor rhinitis, where the **parasympathetic nervous system** is relatively overactive, leading to vasodilation and increased glandular secretions. - This dysfunction causes the characteristic symptoms without an allergic or infectious trigger. *It is triggered by non-allergic stimuli like weather changes and strong odors* - This statement is **true** as patients with vasomotor rhinitis often report symptoms triggered by **environmental irritants** such as strong perfumes, temperature changes, humidity fluctuations, or even emotional stress. - These triggers differentiate it clinically from allergic rhinitis.
Question 3: Partial and full closure of nasal passages is characteristically seen in:
- A. Allergic rhinitis
- B. Atrophic rhinitis
- C. Occupational rhinitis
- D. Vasomotor rhinitis (Correct Answer)
Explanation: ***Vasomotor rhinitis*** - This condition is characterized by **vascular dysregulation** in the nasal mucosa, leading to episodic **swelling** and **congestion** that can result in partial or full nasal closure without an identifiable allergic or infectious cause. - Symptoms are often triggered by **non-specific irritants** like temperature changes, strong odors, or emotional stress, causing the nasal blood vessels to dilate excessively. *Allergic rhinitis* - While it causes nasal congestion and obstruction, the primary mechanism is an **IgE-mediated inflammatory response** to specific allergens, leading to mucosal edema and increased mucus production. - The closure is typically accompanied by other allergic symptoms such as **sneezing**, **itching**, and **rhinorrhea**, which differentiates it from vasomotor rhinitis. *Atrophic rhinitis* - This condition involves **progressive atrophy** of the nasal mucosa, turbinates, and underlying bone, resulting in an abnormally wide nasal passage rather than obstruction. - Patients typically experience **paradoxical nasal obstruction** due to altered airflow dynamics and crusting, alongside a characteristic foul odor. *Occupational rhinitis* - This type of rhinitis is caused by **exposure to specific agents** in the workplace, leading to inflammation and nasal obstruction, often accompanied by sneezing and rhinorrhea. - Symptom onset is directly linked to **workplace exposure** and improves away from the occupational environment, which is not suggested by the general term "partial and full closure."
Question 4: Which of the following is a secondary mediator of anaphylaxis?
- A. Leukotriene B4 (Correct Answer)
- B. Protease
- C. Histamine
- D. Eosinophilic chemotactic factor
Explanation: ***Leukotriene B4*** - **Leukotrienes** are synthesized from **arachidonic acid** via the 5-lipoxygenase pathway during an anaphylactic reaction, making them **secondary mediators**. - **Leukotriene B4** is a potent **chemoattractant for neutrophils** and contributes to the inflammatory response in anaphylaxis. - Note: The **cysteinyl leukotrienes (LTC4, LTD4, LTE4)** are the primary leukotrienes responsible for **bronchoconstriction** and increased vascular permeability in anaphylaxis. *Protease* - **Proteases**, such as **tryptase**, are **preformed mediators** stored in mast cell granules and are rapidly released upon activation. - They are considered **primary mediators** due to their immediate release following mast cell degranulation. *Histamine* - **Histamine** is a classic **preformed mediator** stored in mast cell granules and is one of the first substances released during anaphylaxis. - Its rapid release causes immediate effects such as **vasodilation**, **bronchoconstriction**, and increased vascular permeability. *Eosinophilic chemotactic factor* - **Eosinophilic chemotactic factor (ECF-A)** is a **preformed mediator** stored in mast cell granules. - While it attracts eosinophils, it is released immediately from granules upon mast cell activation, classifying it as a **primary mediator**.
Question 5: All of the following are true about nasal myiasis except which of the following?
- A. Common in vasomotor rhinitis
- B. Nasal myiasis can cause intense nasal irritation.
- C. Meningitis may occur in severe nasal myiasis.
- D. Nasal myiasis is typically asymptomatic (Correct Answer)
Explanation: ***Nasal myiasis is typically asymptomatic*** - This statement is **INCORRECT** and is the correct answer to this "except" question. - **Nasal myiasis** is characterized by infestation of the nasal cavity with **fly larvae (maggots)**, which typically causes **significant symptoms** rather than being asymptomatic. - Patients usually experience **nasal obstruction**, **epistaxis (nosebleeds)**, **foul-smelling nasal discharge**, **intense irritation**, and a sensation of movement in the nose due to the feeding and movement of the larvae. - The condition is rarely asymptomatic and usually prompts patients to seek medical attention due to the distressing symptoms. *Common in vasomotor rhinitis* - This statement is **INCORRECT** as a factual claim about myiasis. Nasal myiasis is **NOT** commonly associated with vasomotor rhinitis. - Nasal myiasis is more commonly associated with **atrophic rhinitis**, **ozena**, neglected nasal wounds, poor hygiene, open mouth breathing during sleep, and immunosuppression. - **Vasomotor rhinitis** is a non-allergic condition characterized by fluctuating nasal congestion, rhinorrhea, and sneezing, without any direct association with parasitic infestations. - However, this option may cause confusion as it could also be considered false. The most clearly false statement is that myiasis is "typically asymptomatic." *Nasal myiasis can cause intense nasal irritation* - This statement is **TRUE**. The presence and movement of **maggots** within the nasal cavity leads to severe **irritation**, pain, and a foreign body sensation. - The feeding activity of the larvae causes **tissue destruction**, mucosal damage, and secondary bacterial infections, intensifying discomfort. - Patients often describe a crawling sensation and severe itching in the nasal cavity. *Meningitis may occur in severe nasal myiasis* - This statement is **TRUE**. In advanced or neglected cases, the **larvae** can erode through the nasal structures, sinuses, and skull base, potentially breaching the **meninges**. - This invasion can result in serious intracranial complications such as **meningitis**, **brain abscess**, **cavernous sinus thrombosis**, or other central nervous system infections. - These complications are life-threatening and require urgent surgical debridement and antimicrobial therapy.
Question 6: Which interleukin is primarily responsible for inducing IgE production from B cells?
- A. IL-1 and IL-3
- B. IL-3
- C. IL-1
- D. IL-4 (Correct Answer)
Explanation: ***IL-4*** - **IL-4** is the primary cytokine responsible for promoting B cell differentiation into **plasma cells** that produce **IgE antibodies**. - It plays a crucial role in the development of **allergic reactions** by stimulating IgE class switching. *IL-1* - **IL-1** is a pro-inflammatory cytokine primarily involved in the **innate immune response**, fever, and acute phase reactions. - It does not directly induce IgE production but can modulate immune responses in a broader context. *IL-3* - **IL-3** is a cytokine that primarily supports the growth and differentiation of **hematopoietic stem cells** in the bone marrow. - It is crucial for the development of various blood cell lineages but is not directly involved in IgE class switching. *IL-1 and IL-3* - While both **IL-1** and **IL-3** have important roles in immunity and hematopoiesis, neither directly induces **IgE production** from B cells. - **IL-4** is the specific and most significant interleukin for this function.
Question 7: What is the most likely finding in the CT image of the left maxillary sinus in a patient with a history of allergic rhinitis?
- A. Ground-glass opacity (Correct Answer)
- B. Honeycomb appearance
- C. Onion peel appearance
- D. Double density
Explanation: ***Ground-glass opacity*** - This image shows diffuse opacification of the left maxillary sinus with a characteristic **ground-glass appearance**, which is often associated with allergic fungal rhinosinusitis (AFRS), a condition that can complicate allergic rhinitis. - The patient's history of **allergic rhinitis** makes AFRS a strong consideration, and the CT finding of ground-glass opacity within the sinus lumen is a classic imaging feature of this condition, representing fungal elements and mucin. *Honeycomb appearance* - A **honeycomb appearance** on CT is typically seen in the lungs and indicates **pulmonary fibrosis**, characterized by clustered cystic airspaces with thickened walls. - This finding is not associated with paranasal sinus pathology, especially not with allergic rhinitis or its common complications. *Onion peel appearance* - The **onion peel appearance** on imaging refers to periosteal reaction with multiple concentric layers of new bone formation. - This is a hallmark feature of conditions like **Ewing sarcoma** and chronic osteomyelitis, primarily affecting bone, not the soft tissue or mucosal lining of a sinus in the context of allergic rhinitis. *Double density* - **Double density** is a term primarily used in echocardiography to describe specific findings related to left atrial enlargement, or occasionally in chest radiography where it might represent superimposed densities. - This term does not describe a finding relevant to paranasal sinus pathology on CT imaging.
Question 8: In which condition is Young's operation performed?
- A. Allergic rhinitis
- B. Vasomotor rhinitis
- C. Lupus vulgaris
- D. Atrophic rhinitis (Correct Answer)
Explanation: ***Atrophic rhinitis*** - **Young's operation** is a surgical procedure specifically designed to treat severe cases of **atrophic rhinitis**, aiming to narrow the nasal cavity and promote mucosal regeneration. - Involves **closing the nostrils temporarily** for several months to allow healing and reduce crusting and foul odor associated with the condition. *Allergic rhinitis* - This condition is managed primarily with **antihistamines**, **nasal corticosteroids**, and allergen avoidance, not surgical methods like Young's operation. - It is an **inflammatory response** to allergens, causing sneezing, itching, and rhinorrhea, which is distinct from the mucosal atrophy seen in atrophic rhinitis. *Vasomotor rhinitis* - Vasomotor rhinitis is characterized by **non-allergic triggers** like temperature changes or irritants, leading to nasal congestion and rhinorrhea. - Treatment typically involves **topical nasal sprays** (e.g., ipratropium bromide) or lifestyle modifications, not **Young's operation**. *Lupus vulgaris* - Lupus vulgaris is a form of **cutaneous tuberculosis** affecting the skin, primarily treated with **anti-tubercular drugs**, not a nasal surgical procedure. - It presents as chronic, progressive skin lesions and is unrelated to nasal cavity disorders.
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 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).
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free