Mast Cell Stabilizers — MCQs
Which of the following medications is known to cause dysgeusia?
Which of the following is NOT a mechanism of action of theophylline in bronchial asthma?
Choose the correct options regarding the route of administration and bioavailability. A- Intravenous =1 B- 0.75< Oral <1 C-0.75 <IM ≤ 1 D- 0.75<SC ≤ 1 IM - Intramuscular SC- Subcutaneous
A drug used to prevent niacin-induced flushing is
Which of the following is not a side effect of topical beta blockers?
Histamine in anaphylaxis is secreted by which of the following cells?
How do corticosteroids reduce symptoms of allergic rhinitis?
A 42-year-old man was seen in the clinic because of pain and redness in his finger. Last week he had injured the finger while working in his garage. On physical examination, there is erythema, swelling, and tenderness of the second digit in the right hand. Flexion and extension of the finger were normal. A clinical diagnosis of cellulitis is made and he is prescribed cephalexin. A few days later he presents to the emergency room complaining of difficulty breathing. He has angioedema due to a drug reaction to the cephalexin. Which of the following physical findings is characteristic of this syndrome?
IgE is secreted by which of the following cells?
A 68-year-old with depression and chronic pain is on amitriptyline. What side effect may arise if given oxybutynin for overactive bladder?
Mast Cell Stabilizers Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following medications is known to cause dysgeusia?
- A. Captopril (Correct Answer)
- B. Enalapril
- C. Ramipril
- D. Lisinopril
Explanation: ***Captopril*** - **Captopril**, an ACE inhibitor, is well-known for causing taste disturbances, specifically **dysgeusia** (altered taste sensation) or **ageusia** (loss of taste). - This side effect is thought to be related to its **sulfhydryl group** [1], which can chelate zinc, a metal crucial for normal taste perception. *Enalapril* - While also an ACE inhibitor, **enalapril** rarely causes taste disturbances compared to captopril. - It lacks the **sulfhydryl group** present in captopril, which is implicated in the mechanism of dysgeusia. *Ramipril* - **Ramipril** is another ACE inhibitor not commonly associated with dysgeusia. - Its chemical structure does not contain the **sulfhydryl group** that is linked to taste alterations. *Lisinopril* - **Lisinopril**, like enalapril and ramipril, is an ACE inhibitor that **seldom** causes dysgeusia. - The absence of the **sulfhydryl group** is a key differentiator from captopril regarding this specific side effect.
Question 2: Which of the following is NOT a mechanism of action of theophylline in bronchial asthma?
- A. Adenosine receptor antagonism
- B. Increased histone deacetylation
- C. Phosphodiesterase inhibition
- D. Beta-2 receptor stimulation (Correct Answer)
Explanation: ***Beta-2 receptor stimulation*** - Theophylline is a **non-selective phosphodiesterase inhibitor** and an **adenosine receptor antagonist**, but it does not directly stimulate beta-2 receptors. - **Beta-2 receptor agonists** like salbutamol or formoterol are the medications that work by stimulating these receptors to cause bronchodilation. *Phosphodiesterase inhibition* - Theophylline inhibits **phosphodiesterase enzymes**, leading to an increase in intracellular **cAMP** levels. - This increase in **cAMP** promotes bronchodilation by relaxing airway smooth muscle. *Adenosine receptor antagonism* - Theophylline acts as an antagonist at **adenosine receptors**, particularly A1 and A2B. - Antagonism of adenosine receptors can reduce bronchoconstriction and inflammatory mediator release, contributing to its anti-asthmatic effects. *Increased histone deacetylation* - Theophylline, particularly at lower concentrations, increases the activity of **histone deacetylase (HDAC)**. - This action helps to **repress inflammatory gene expression**, which is a unique anti-inflammatory mechanism separate from its bronchodilatory effects.
Question 3: Choose the correct options regarding the route of administration and bioavailability. A- Intravenous =1 B- 0.75< Oral <1 C-0.75 <IM ≤ 1 D- 0.75<SC ≤ 1 IM - Intramuscular SC- Subcutaneous
- A. A and D
- B. A and C
- C. A, C, D (Correct Answer)
- D. A, B, D
Explanation: ***A, C, D*** - Intravenous (IV) administration has **100% bioavailability** because the drug enters the systemic circulation directly, bypassing any absorption barriers. - Intramuscular (IM) and subcutaneous (SC) routes generally have **high bioavailability**, often between 75% and 100%, as drugs are absorbed directly into the bloodstream without first-pass metabolism. *A and D* - While options A and D are correct, this choice is incomplete as option C is also a correct statement regarding bioavailability. - IM administration typically results in high systemic bioavailability, similar to SC, making its exclusion here incorrect. *A and C* - While options A and C are correct, this choice is incomplete as option D is also a correct statement regarding bioavailability. - Subcutaneous administration also generally results in high bioavailability, as absorption tends to be complete. *A, B, D* - While options A and D are correct, option B is typically incorrect for oral bioavailability. - Oral bioavailability of many drugs is often less than 0.75 (75%) due to factors like **first-pass metabolism** and incomplete absorption in the gastrointestinal tract.
Question 4: A drug used to prevent niacin-induced flushing is
- A. Dexamethasone
- B. Aspirin (Correct Answer)
- C. Paracetamol
- D. Cetirizine
Explanation: ***Aspirin*** - Niacin-induced flushing is mediated by **prostaglandins**, primarily prostaglandin D2 (PGD2), which cause vasodilation. - **Aspirin**, being a non-steroidal anti-inflammatory drug (NSAID) and a cyclooxygenase (COX) inhibitor, blocks the synthesis of prostaglandins, thereby reducing flushing. *Cetirizine* - Cetirizine is a **second-generation H1 antihistamine** primarily used to treat allergic symptoms like rhinitis or urticaria. - It does not significantly affect prostaglandin pathways implicated in niacin-induced flushing. *Dexamethasone* - Dexamethasone is a **corticosteroid** with potent anti-inflammatory and immunosuppressive effects. - While it can broadly reduce inflammation, it is not the primary or most appropriate treatment for niacin-induced flushing, which is better managed with prostaglandin inhibitors. *Paracetamol* - Paracetamol (acetaminophen) is an **analgesic and antipyretic** that works primarily by inhibiting prostaglandin synthesis in the central nervous system. - It has minimal anti-inflammatory effects and does not effectively reduce peripheral prostaglandin production responsible for niacin flush.
Question 5: Which of the following is not a side effect of topical beta blockers?
- A. Heterochromia iridis (Correct Answer)
- B. Asthma
- C. Hypoglycemia
- D. Bradycardia
Explanation: ***Heterochromia iridis*** - **Heterochromia iridis** (different colored irises) is a well-known side effect of **prostaglandin analogs** (e.g., latanoprost, bimatoprost), not topical beta blockers. - This change in eye color occurs due to increased **melanin production** in melanocytes. *Asthma* - Topical beta blockers can be absorbed systemically and block **beta-2 receptors** in the lungs, leading to **bronchoconstriction** and exacerbating **asthma**. - This side effect is particularly concerning in patients with a history of **reactive airway disease**. *Hypoglycemia* - Topical beta blockers are listed as a concern for **hypoglycemia risk** because they **mask the adrenergic symptoms of hypoglycemia** (tremor, palpitations, tachycardia). - While they don't directly cause hypoglycemia, masking these warning symptoms can lead to **delayed recognition and treatment**, particularly dangerous in **diabetic patients on insulin or sulfonylureas**. *Bradycardia* - Systemic absorption of topical beta blockers can lead to a decrease in **heart rate** (bradycardia) by blocking **beta-1 receptors** in the heart. - This effect is a significant concern for patients with pre-existing **cardiac conduction disorders** or those taking other medications that lower heart rate.
Question 6: Histamine in anaphylaxis is secreted by which of the following cells?
- A. Mast cells (Correct Answer)
- B. B-cells
- C. Basophils
- D. Macrophages
Explanation: ***Mast cells*** - Mast cells are the primary cells responsible for the secretion of **histamine** during anaphylaxis, leading to rapid allergic responses [2][4]. - They are located in **tissues** and are involved in **immediate hypersensitivity reactions** by releasing various mediators upon activation [1][2]. *Basophils* - While basophils do contain **histamine**, they play a lesser role in acute anaphylaxis as compared to mast cells [1]. - Basophils are more associated with chronic allergic reactions rather than the **immediate release** observed in anaphylaxis [1]. *Macrophages* - Macrophages are primarily involved in **phagocytosis** and immune response but do not secrete significant amounts of histamine. - They release cytokines and other mediators but are not key players in **histamine-dependent** anaphylactic reactions. *B-cells* - B-cells are crucial for the production of **antibodies** but do not secrete histamine at all. - They are involved in **adaptive immunity** and do not play a direct role in **anaphylaxis** mechanisms [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.
Question 7: How do corticosteroids reduce symptoms of allergic rhinitis?
- A. inhibit histamine release from mast cells.
- B. decrease prostaglandin production.
- C. block leukotriene receptors.
- D. reduce inflammation by inhibiting phospholipase A2. (Correct Answer)
Explanation: ***reduce inflammation by inhibiting phospholipase A2*** - Corticosteroids exert their anti-inflammatory effects by inhibiting **phospholipase A2**, an enzyme crucial for releasing arachidonic acid from cell membranes. - This inhibition in turn prevents the synthesis of various inflammatory mediators, including **prostaglandins** and **leukotrienes**, thereby reducing the symptoms of allergic rhinitis. *inhibit histamine release from mast cells.* - While corticosteroids can stabilize mast cell membranes over time, their primary mechanism of action in allergic rhinitis is not the direct, immediate inhibition of **histamine release**. - **Antihistamines** are specifically designed to block the effects of histamine or reduce its release. *decrease prostaglandin production.* - Corticosteroids do decrease **prostaglandin production**, but this is a *downstream effect* of their inhibition of phospholipase A2, which is the more direct and overarching mechanism. - Non-steroidal anti-inflammatory drugs (NSAIDs) primarily inhibit **cyclooxygenase (COX) enzymes** to reduce prostaglandin synthesis. *block leukotriene receptors.* - Blocking **leukotriene receptors** is the mechanism of action for **leukotriene receptor antagonists** (e.g., montelukast), not corticosteroids. - Corticosteroids reduce the *production* of leukotrienes by inhibiting phospholipase A2, rather than directly blocking their receptors.
Question 8: A 42-year-old man was seen in the clinic because of pain and redness in his finger. Last week he had injured the finger while working in his garage. On physical examination, there is erythema, swelling, and tenderness of the second digit in the right hand. Flexion and extension of the finger were normal. A clinical diagnosis of cellulitis is made and he is prescribed cephalexin. A few days later he presents to the emergency room complaining of difficulty breathing. He has angioedema due to a drug reaction to the cephalexin. Which of the following physical findings is characteristic of this syndrome?
- A. Invariably severe itching
- B. Prolonged nature of the edema
- C. Fluid extravasation from subcutaneous and intradermal postcapillary venules
- D. Involvement of lips, tongue, eyelids, genitalia, and dorsum of hands or feet (Correct Answer)
Explanation: ***Involvement of lips, tongue, eyelids, genitalia, and dorsum of hands or feet*** - **Angioedema** is characterized by episodic, localized swelling of the deeper dermal and subcutaneous tissues, often affecting the **lips, tongue, eyelids, genitalia, and dorsum of hands or feet** [1]. - This distribution is due to the **loose connective tissue** in these areas, which allows for significant fluid accumulation. *Invariably severe itching* - While angioedema can sometimes be accompanied by itching, **severe itching (pruritus)** is more characteristic of **urticaria** (hives), which involves the superficial dermis [1]. - In many cases of angioedema, particularly **bradykinin-mediated types**, itching is absent or minimal. *Prolonged nature of the edema* - The edema in **angioedema** typically resolves within **24 to 72 hours**, not weeks or months, differentiating it from other chronic inflammatory conditions. - Its self-limiting nature is a key diagnostic feature, although recurrence is common. *Fluid extravasation from subcutaneous and intradermal postcapillary venules* - **Fluid extravasation** from postcapillary venules occurs in both urticaria and angioedema. However, in angioedema, the fluid extravasation occurs at the level of the **deep dermis and subcutaneous tissue**, leading to deeper swelling. - In **urticaria**, the extravasation is more superficial, affecting the **epidermis and superficial dermis**, resulting in itchy wheals.
Question 9: IgE is secreted by which of the following cells?
- A. Mast cell
- B. Basophils
- C. Eosinophils
- D. Plasma cells (Correct Answer)
Explanation: ***Plasma cells*** - Plasma cells are **terminally differentiated B lymphocytes** that are specialized in producing and secreting large quantities of antibodies, including **IgE**. - While other cells like mast cells and basophils have receptors for IgE and play roles in IgE-mediated reactions, they do not synthesize **IgE** themselves. *Mast cell* - Mast cells are key players in allergic reactions and express **FcεRI receptors** that bind to IgE antibodies. - Upon binding the antigen, they degranulate, releasing **histamine** and other mediators, but they do not produce IgE. *Basophils* - Basophils also express **FcεRI receptors** for IgE and are involved in allergic responses, releasing inflammatory mediators. - Similar to mast cells, they do not synthesize IgE, but rather bind pre-formed **IgE** antibodies. *Eosinophils* - Eosinophils are involved in allergic reactions and defense against **parasitic infections**, and their granules contain toxic proteins. - They can be activated by IgE-mediated mechanisms but are not producers of **IgE** antibodies.
Question 10: A 68-year-old with depression and chronic pain is on amitriptyline. What side effect may arise if given oxybutynin for overactive bladder?
- A. Severe dry mouth (Correct Answer)
- B. Bradycardia
- C. Increased sweating
- D. Urinary incontinence
Explanation: ***Severe dry mouth*** - Both **amitriptyline** (a tricyclic antidepressant) and **oxybutynin** (an anticholinergic for overactive bladder) have significant anticholinergic effects. - The combination of these two drugs can lead to an additive effect, causing pronounced anticholinergic side effects such as **severe dry mouth**, blurred vision, constipation, and cognitive impairment. *Bradycardia* - **Anticholinergic drugs** typically cause **tachycardia** (increased heart rate) by blocking the parasympathetic nervous system's muscarinic receptors on the heart, rather than bradycardia. - While amitriptyline can affect cardiac conduction, severe bradycardia is not a typical **additive anticholinergic side effect** in this context. *Increased sweating* - **Anticholinergic drugs** like amitriptyline and oxybutynin inhibit the activity of sweat glands, which are primarily innervated by cholinergic nerves. - Therefore, the combination of these drugs would likely lead to **decreased sweating** (anhidrosis) rather than increased sweating. *Urinary incontinence* - **Oxybutynin** is prescribed specifically to treat **overactive bladder** and reduce urinary incontinence by relaxing the detrusor muscle. - Therefore, it would improve rather than worsen urinary incontinence; however, it can cause **urinary retention** due to its anticholinergic effect, especially in older male patients.
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