Complications of Immunotherapy — MCQs
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 patient comes to you with skin reactions after visiting the hair dresser. What will you do to confirm the diagnosis of contact dermatitis?
Allograft rejection is an example of which type of hypersensitivity reaction?
Skin erythema dose is:
Which condition is characterized by conjunctival injection, pharyngeal injection, polymorphic rash, and cervical lymphadenopathy?
Which of the following is false regarding transfusion-associated anaphylactic reactions?
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?
Complications of Immunotherapy Indian Medical PG Practice Questions and MCQs
Question 1: 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. Vancomycin (Correct Answer)
- C. Piperacillin
- D. Aztreonam
Explanation: ***Vancomycin*** - **Vancomycin** is a glycopeptide antibiotic with a completely different mechanism of action and chemical structure compared to penicillins, making it **safe for patients with penicillin allergy**. - It is the **first-line treatment for enterococcal endocarditis** in patients with penicillin allergy, providing excellent coverage against both *Enterococcus faecalis* and *E. faecium*. - No cross-reactivity with beta-lactam antibiotics. *Ceftriaxone* - **Ceftriaxone** is a third-generation **cephalosporin**, a beta-lactam antibiotic with structural similarity to penicillin. - There is **5-10% cross-reactivity risk** in patients with IgE-mediated penicillin allergy (rash, swelling, anaphylaxis), making it potentially unsafe in this patient. - Should be avoided in patients with a history of immediate hypersensitivity reactions to penicillin. *Piperacillin* - **Piperacillin** is a **penicillin derivative** (ureidopenicillin) and shares the same beta-lactam core structure that triggers allergic reactions. - **Absolutely contraindicated** in patients with known penicillin allergy—would almost certainly provoke an allergic reaction. - Using this drug would expose the patient to significant risk of anaphylaxis. *Aztreonam* - **Aztreonam** is a **monobactam** with minimal cross-reactivity (<1%) with penicillins and is generally **safe for penicillin-allergic patients** from an allergy perspective. - However, aztreonam has **primarily gram-negative coverage** and **poor activity against enterococci**, making it ineffective for treating enterococcal endocarditis. - While safe regarding allergy concerns, it is not the appropriate choice due to **lack of efficacy** against the causative organism.
Question 2: A patient comes to you with skin reactions after visiting the hair dresser. What will you do to confirm the diagnosis of contact dermatitis?
- A. S IgE
- B. Allergy Test
- C. Patch Test (Correct Answer)
- D. VDRL
Explanation: ***Patch Test*** - A **patch test** is the gold standard for diagnosing **allergic contact dermatitis** by directly applying suspected allergens to the skin. - This test identifies specific substances that cause a delayed hypersensitivity reaction, which is characteristic of contact dermatitis. *S IgE* - **Serum IgE** levels are primarily indicative of **Type I hypersensitivity** reactions, such as allergic rhinitis or asthma. - Contact dermatitis is a **Type IV delayed hypersensitivity reaction**, not mediated by IgE antibodies. *Allergy Test* - The term "allergy test" is broad and can refer to various methods including skin prick tests, IgE blood tests, or patch tests. - Without specifying **patch testing**, other forms of allergy tests are less appropriate for diagnosing contact dermatitis, as they target different immune mechanisms. *VDRL* - **VDRL (Venereal Disease Research Laboratory)** test is used to screen for **syphilis**, a sexually transmitted infection. - It has no relevance to the diagnosis of contact dermatitis, which is an inflammatory skin condition caused by contact with an allergen or irritant.
Question 3: Allograft rejection is an example of which type of hypersensitivity reaction?
- A. Type IV hypersensitivity (Correct Answer)
- B. Type I hypersensitivity
- C. Type II hypersensitivity
- D. Type III hypersensitivity
Explanation: ***Delayed hypersensitivity*** - Allograft rejection primarily involves **T-cell mediated mechanisms** [1][3][5], characteristic of delayed hypersensitivity reactions [1][2]. - This type of reaction occurs days to weeks after exposure, leading to lymphocyte infiltration and tissue damage [1][4]. *Immediate hypersensitivity* - This type is mediated by **IgE antibodies** and occurs rapidly (within minutes) upon exposure to the allergen. - It is exemplified by **anaphylaxis**, which is not related to the T-cell-mediated rejection seen in allografts. *Swartzmans reaction* - This is a form of **opsonization and hypersensitivity** that results in systemic reactions due to previously sensitized antigen. - Unlike allograft rejection, it is not specifically related to transplant rejection mechanisms. *GVHD* - Graft-versus-host disease (GVHD) is a complication where the **graft attacks the host's tissues** as seen in hematopoietic stem cell transplants. - While related to immune responses, it is not the same as allograft rejection, which refers to the host's rejection of the graft. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 240. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 240-241.
Question 4: Skin erythema dose is:
- A. 300-400 R
- B. 400-500 R
- C. 200-300 R (Correct Answer)
- D. 100-200 R
Explanation: ***200-300 R*** - The **skin erythema dose** refers to the amount of radiation exposure, expressed in Roentgens (R), that typically causes reddening of the skin. - This range historically served as a basic measure for assessing acute radiation effects and was an early practical limit for radiation exposure in medical imaging. *300-400 R* - While within the broader range of doses that can cause skin effects, **300-400 R** is generally considered a higher dose than the threshold for a noticeable, transient erythema. - Exposure at this level might lead to more pronounced or persistent skin reactions. *400-500 R* - Doses of **400-500 R** are significantly high and would typically cause more severe skin reactions, such as blistering or moist desquamation, rather than just transient erythema. - This level of exposure is well beyond what is considered the skin erythema dose threshold. *100-200 R* - A dose of **100-200 R** is generally considered to be below the threshold for reliably inducing noticeable skin erythema in most individuals. - While some mild, transient redness might occur in very sensitive individuals, it is not the commonly accepted range for the skin erythema dose.
Question 5: 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 6: 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 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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