Angioedema — MCQs
Not typically associated with Ludwig's angina is
Laboratory evaluation of a patient with recurrent lip edema shows decreased C4 and C1 inhibitor (quantity and function) with normal C1q. Diagnosis is
A patient who experiences recurrent urticaria during exercise and heat exposure, including sunlight, most likely has:
Which condition is not associated with complement deficiency?
Acute febrile neutrophilic dermatosis is seen in-
Which ACE inhibitor is safe in renal failure?
Hereditary angioneurotic edema is due to?
Assertion: Nasal polyps are commonly associated with aspirin-exacerbated respiratory disease (AERD). Reason: Aspirin directly causes nasal polyp formation in all patients with AERD.
Which of the following are early mediators of allergic rhinitis?
Which of the following preformed toxins is involved in the mechanism of allergic rhinitis?
Angioedema Indian Medical PG Practice Questions and MCQs
Question 1: Not typically associated with Ludwig's angina is
- A. It is caused by anaerobic organisms
- B. Cellulitis in the floor of mouth
- C. Aphthous ulcer in pharynx (Correct Answer)
- D. Glottal edema, may require tracheostomy
Explanation: ***Aphthous ulcer in pharynx*** - **Aphthous ulcers** are discrete, painful oral lesions typically associated with trauma, stress, or certain systemic conditions, and are **not a feature** of the infection and inflammation seen in Ludwig's angina [1]. - Ludwig's angina is a severe **bacterial infection** of the submandibular, sublingual, and submental spaces, characterized by aggressive cellulitis rather than ulcerative lesions. *It is caused by anaerobic organisms* - **Mixed flora**, including **anaerobic bacteria** (e.g., Peptostreptococcus, Bacteroides, Fusobacterium), are commonly implicated in Ludwig's angina, often originating from odontogenic infections [2]. - The presence of anaerobes contributes to the rapid progression and extensive tissue destruction characteristic of this severe infection [2]. *Cellulitis in the floor of mouth* - Ludwig's angina is specifically defined as a **rapidly spreading cellulitis** that involves the **submandibular, sublingual, and submental spaces** of the floor of the mouth. - This cellulitis is non-suppurative but causes significant edema and induration, which can displace the tongue superiorly and posteriorly. *Glottal edema, may require tracheostomy* - The extensive edema in the floor of the mouth can extend rapidly to the **larynx**, leading to **glottal edema** and **airway obstruction**. - Due to the critical risk of airway compromise, an emergency **tracheostomy** or **cricothyrotomy** may be necessary to secure the airway in advanced cases.
Question 2: Laboratory evaluation of a patient with recurrent lip edema shows decreased C4 and C1 inhibitor (quantity and function) with normal C1q. Diagnosis is
- A. Hereditary angioedema type I (Correct Answer)
- B. Acquired angioedema type II
- C. Acquired angioedema type I
- D. Hereditary angioedema type II
Explanation: ***Hereditary angioedema type I*** - This condition is characterized by **low levels of C4 and C1 inhibitor quantity and function**, with **normal C1q** [1]. - It is caused by a genetic deficiency in the **C1 inhibitor gene (SERPING1)**, leading to overactivation of the complement system and bradykinin production [1]. *Acquired angioedema type II* - This type involves the presence of an **autoantibody** that binds to and inactivates the C1 inhibitor. - While C4 and C1 inhibitor function are decreased, C1 inhibitor quantity is usually normal, which contradicts the patient's presentation. *Acquired angioedema type I* - This form is typically associated with **lymphoproliferative disorders** or **autoimmune diseases**, leading to consumption of C1 inhibitor. - It is characterized by **low C1q levels** in addition to low C4 and C1 inhibitor quantity and function, which is not seen in this patient. *Hereditary angioedema type II* - In this rare genetic variant, the **C1 inhibitor protein is dysfunctional** but present in normal or elevated quantities. - The patient exhibits a **decreased quantity** of C1 inhibitor, ruling out Type II hereditary angioedema.
Question 3: A patient who experiences recurrent urticaria during exercise and heat exposure, including sunlight, most likely has:
- A. Chronic Spontaneous Urticaria
- B. Universal Dermographism
- C. Cholinergic Urticaria (Correct Answer)
- D. Photodermatitis
Explanation: ***Cholinergic Urticaria*** - Cholinergic urticaria is characterized by the appearance of small, itchy wheals in response to stimuli that raise the **body temperature**, such as **exercise**, **heat**, or **emotional stress**. - The symptoms resolve when the body cools down, aligning with the patient's presentation of recurrent urticaria during exercise and heat exposure. *Chronic Spontaneous Urticaria* - This condition involves daily or almost daily urticaria for **six weeks or more** without an identifiable external cause. - While it is chronic, the specific triggers of exercise and heat exposure point more directly to a physical urticaria like cholinergic urticaria. *Universal Dermographism* - **Dermographism** (or dermatographia) is a type of physical urticaria where hives appear after **firm stroking or scratching** of the skin. - Universal dermographism would imply this reaction over a large body surface area, but it is not typically triggered by systemic heat or exercise. *Photodermatitis* - **Photodermatitis** is a general term for skin inflammation caused by **exposure to light**, especially sunlight, often due to an abnormal reaction to UV radiation. - While sunlight is a trigger for this patient's symptoms, the additional triggers of exercise and general heat exposure make cholinergic urticaria a more encompassing diagnosis than photodermatitis alone.
Question 4: Which condition is not associated with complement deficiency?
- A. SLE
- B. PNH
- C. Membranous nephritis (Correct Answer)
- D. Hereditary angioedema
Explanation: Membranous nephritis - Membranous nephritis is associated with immune complex deposition rather than complement deficiencies. [1] - The disease is characterized by thickening of the glomerular basement membrane without significant complement involvement. [1] PNH - Paroxysmal nocturnal hemoglobinuria (PNH) is due to a defect in the GPI-anchor leading to complement-mediated hemolysis. - Complement activation plays a critical role in the destruction of red blood cells in this condition. Hereditary angioedema - Hereditary angioedema is caused by deficiencies in C1 inhibitor, leading to uncontrolled activation of complement. - This results in edema episodes, directly linked to complement pathway dysregulation. SLE - Systemic lupus erythematosus (SLE) involves complement consumption due to autoantibody formation against nuclear antigens. - The disease often presents with hypocomplementemia, indicating complement system involvement.
Question 5: Acute febrile neutrophilic dermatosis is seen in-
- A. Behcet's syndrome
- B. Sweet syndrome (Correct Answer)
- C. Haberman syndrome
- D. Kasabach-Merritt syndrome
Explanation: ***Sweet syndrome*** - Sweet syndrome is also known as **Acute febrile neutrophilic dermatosis**. - It presents with **fever**, painful erythematous plaques, and a prominent **neutrophilic infiltrate** in the dermis. *Behcet's syndrome* - Behcet's syndrome is characterized by **recurrent oral and genital ulcers**, uveitis, and skin lesions like **erythema nodosum** or **pathergy**. - It is a systemic vasculitis, not typically presenting as acute febrile neutrophilic dermatosis. *Haberman syndrome* - Haberman syndrome is better known as **Pityriasis lichenoides et varioliformis acuta (PLEVA)**. - It is a rare skin condition characterized by an acute eruption of **papules** and **erosions** that can resemble **chickenpox**. *Kasabach-Merritt syndrome* - This syndrome is a rare disorder involving **vascular tumors** (e.g., hemangiomas) that lead to profound **thrombocytopenia** and **consumptive coagulopathy**. - It does not present with acute febrile neutrophilic dermatosis.
Question 6: Which ACE inhibitor is safe in renal failure?
- A. Captopril
- B. Enalapril
- C. None of the options
- D. Benazepril (Correct Answer)
Explanation: ***Benazepril*** - Among the listed ACE inhibitors, benazepril has the **most favorable excretion profile** in renal failure with approximately **50% renal and 50% hepatic elimination** (dual excretion pathway). - This balanced elimination reduces the risk of drug accumulation compared to predominantly renally excreted ACE inhibitors. - While dose adjustment may still be needed in **severe renal impairment**, benazepril is considered the **safest option among those listed** for patients with renal dysfunction. - **Note:** Fosinopril (not listed here) has true 50/50 dual elimination and requires no dose adjustment in renal failure, making it the ideal choice in clinical practice. *Captopril* - This ACE inhibitor undergoes predominantly **renal excretion (95%)** as unchanged drug and metabolites. - Requires significant **dose reduction** in renal failure to prevent accumulation and adverse effects including **hyperkalemia** and **hypotension**. - Less safe than benazepril in renal impairment due to heavy dependence on renal elimination. *Enalapril* - Enalapril is a prodrug converted to **enalaprilat**, with approximately **90% renal excretion**. - Dose adjustment is mandatory based on **creatinine clearance** in patients with renal failure. - Higher risk of accumulation and toxicity compared to dual-elimination ACE inhibitors like benazepril.
Question 7: Hereditary angioneurotic edema is due to?
- A. Deficiency of C1 inhibitor (Correct Answer)
- B. Deficiency of NADPH oxidase
- C. Deficiency of MPO
- D. Deficiency of properdin
Explanation: ***Deficiency of C1 inhibitor*** - **Hereditary angioedema (HAE)** is caused by a genetic deficiency or dysfunction of the **C1 esterase inhibitor (C1-INH)** protein. - C1-INH normally regulates the **complement system**, kinin system (mediating **bradykinin** release), and coagulation pathways, and its deficiency leads to uncontrolled activation and excessive bradykinin production, causing angioedema. *Deficiency of NADPH oxidase* - A deficiency in **NADPH oxidase** is associated with **Chronic Granulomatous Disease (CGD)**, a primary immunodeficiency characterized by recurrent bacterial and fungal infections due to impaired phagocytic oxidative burst. - It does not cause angioedema, which involves fluid extravasation rather than impaired microbial killing. *Deficiency of MPO* - **Myeloperoxidase (MPO) deficiency** typically leads to mild to moderate impairment in the killing of certain microorganisms by phagocytes but is often asymptomatic or causes only recurrent candidal infections. - It is not linked to the pathogenesis of angioedema, which involves dysregulation of vasoactive peptides. *Deficiency of properdin* - A deficiency in **properdin** affects the **alternative pathway of the complement system**, increasing susceptibility to **Neisseria infections**. - While properdin is part of the complement system, its deficiency does not directly lead to the uncontrolled production of bradykinin, which is the primary mediator in angioedema due to C1-INH deficiency.
Question 8: Assertion: Nasal polyps are commonly associated with aspirin-exacerbated respiratory disease (AERD). Reason: Aspirin directly causes nasal polyp formation in all patients with AERD.
- A. Both Assertion and Reason are true, and Reason is the correct explanation for Assertion.
- B. Both Assertion and Reason are false.
- C. Assertion is true, but Reason is false. (Correct Answer)
- D. Both Assertion and Reason are true, but Reason is not the correct explanation for Assertion.
Explanation: ***Assertion is true, but Reason is false.*** - The **assertion is correct** because nasal polyps are a hallmark feature of **aspirin-exacerbated respiratory disease (AERD)**, also known as **Samter's Triad** (asthma, aspirin sensitivity, chronic rhinosinusitis with nasal polyposis). - The **reason is false** because aspirin does not directly *cause* nasal polyp formation. Instead, aspirin triggers a severe inflammatory reaction in predisposed individuals through **COX-1 inhibition**, leading to an imbalance in **eicosanoid metabolism** with overproduction of **pro-inflammatory leukotrienes (LTC4, LTD4, LTE4)**. - Nasal polyps in AERD result from **chronic eosinophilic inflammation** and underlying mucosal disease, not direct causation by aspirin. *Both Assertion and Reason are true, and Reason is the correct explanation for Assertion.* - This is incorrect because the reason is fundamentally false. - Aspirin does not directly cause polyp formation; it exacerbates pre-existing inflammatory conditions in susceptible individuals. *Both Assertion and Reason are true, but Reason is not the correct explanation for Assertion.* - This is incorrect because the reason itself is false, not merely an incorrect explanation. - The pathophysiology involves aspirin triggering inflammation in predisposed patients, not causing the polyps directly. *Both Assertion and Reason are false.* - This is incorrect because the assertion is medically accurate. - Nasal polyps are indeed commonly associated with AERD and represent one component of the classic **Samter's Triad**.
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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