Topical Corticosteroids — MCQs
Which of the following is a contraindication to topical steroids?
All of the following are topical steroids EXCEPT ?
Which of the following is not a side effect of topical beta blockers?
Which of the following statements about Ciclesonide is incorrect?
What is the primary mechanism by which steroids exert their anti-inflammatory action?
Hydrocortisone Acetate is injected in a painful arthritic TMJ to?
Anti-inflammatory action of steroids is due to
Dapsone is NOT used in:
Which of the following statement is correct regarding the given DRC? (AllMS Nov 2016)
Which of the following is an example of topical administration producing only local effects (not systemic)?
Topical Corticosteroids Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is a contraindication to topical steroids?
- A. Dendritic ulcer (Correct Answer)
- B. Herpetic stromal keratitis without epithelial defect
- C. Elevated intraocular pressure
- D. Non-infectious anterior uveitis
Explanation: ***Dendritic ulcer*** - A **dendritic ulcer** is characteristic of **herpes simplex keratitis**, which is an active viral infection of the cornea. - **Topical steroids** are contraindicated because they can suppress the immune response, leading to viral replication, corneal melt, and potentially severe vision loss or perforation. *Herpetic stromal keratitis without epithelial defect* - In cases of **stromal keratitis**, where the infection is deeper and an intact epithelium is present, topical steroids may be used cautiously in conjunction with antiviral agents to reduce inflammation and scarring. - The primary concern with steroids in herpes simplex keratitis is activating viral replication in the presence of an **epithelial defect**, which is not present here. *Elevated intraocular pressure* - **Elevated intraocular pressure** is a known side effect of topical steroid use, especially with prolonged administration, but it is not an absolute contraindication in itself. - It necessitates careful monitoring and may require concurrent glaucoma treatment, but the primary condition needing steroids may still warrant their use. *Non-infectious anterior uveitis* - **Topical corticosteroids** are the **mainstay of treatment** for non-infectious anterior uveitis to reduce inflammation and prevent complications such as synechiae and vision loss. - The benefits of controlling inflammation in uveitis generally outweigh the risks associated with judicious steroid use.
Question 2: All of the following are topical steroids EXCEPT ?
- A. Fluticasone propionate
- B. Prednisolone (Correct Answer)
- C. Betamethasone valerate
- D. Hydrocortisone valerate
Explanation: ***Prednisolone*** - **Prednisolone** is an **oral/systemic corticosteroid** primarily used for systemic therapy, not as a topical dermatological preparation. - While prednisolone eye drops and ear drops exist, it is NOT a standard topical corticosteroid for skin disorders. - Its high systemic absorption potential makes it unsuitable for dermatological topical applications. *Fluticasone propionate* - **Fluticasone propionate** is a **highly potent synthetic topical corticosteroid** commonly used in dermatology. - Available as creams and ointments for inflammatory skin conditions like eczema, psoriasis, and atopic dermatitis. - Also formulated as nasal spray for allergic rhinitis. *Betamethasone valerate* - **Betamethasone valerate** is a **potent topical corticosteroid** widely used in dermatology. - Available in various formulations (cream, ointment, lotion) for treating inflammatory skin conditions. - Classified as a mid-to-high potency topical steroid, effective for conditions like eczema, psoriasis, and contact dermatitis. *Hydrocortisone valerate* - **Hydrocortisone valerate** is a **moderate-potency topical corticosteroid** derived from hydrocortisone. - Frequently used in dermatological preparations to treat inflammatory skin conditions like dermatitis and eczema. - Safer for prolonged use and application on sensitive areas compared to more potent steroids.
Question 3: 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 4: Which of the following statements about Ciclesonide is incorrect?
- A. Oral candidiasis is common with its use. (Correct Answer)
- B. It is a prodrug activated by bronchial esterase.
- C. It has comparable efficacy to other inhalational corticosteroids.
- D. It has fewer side effects than other inhalational corticosteroids.
- E. It has low systemic bioavailability due to extensive first-pass metabolism.
Explanation: ***Oral candidiasis is common with its use.*** * Ciclesonide is a **prodrug** that is activated in the lungs, which minimizes systemic exposure and reduces the risk of local side effects like **oral candidiasis**. * Therefore, oral candidiasis is **less common** with ciclesonide compared to other inhaled corticosteroids that deliver the active drug directly to the oral cavity. *It is a prodrug activated by bronchial esterase.* * Ciclesonide is indeed a **prodrug** that is converted into its active metabolite, **des-ciclesonide**, by **esterases** primarily found in the lungs. * This specific activation mechanism helps ensure that the drug's therapeutic effects are localized to the airways while minimizing systemic exposure. *It has comparable efficacy to other inhalational corticosteroids.* * Studies have shown that ciclesonide provides **comparable efficacy** to other established inhaled corticosteroids in controlling asthma symptoms and improving lung function. * Its potent anti-inflammatory effects are effective in reducing airway hyperresponsiveness and inflammation. *It has fewer side effects than other inhalational corticosteroids.* * Because ciclesonide is a prodrug activated in the lungs and has a **high protein binding capacity**, it has a reduced likelihood of systemic side effects. * This contributes to a **favorable safety profile**, with a lower incidence of both local and systemic adverse drug reactions compared to some other inhaled corticosteroids. *It has low systemic bioavailability due to extensive first-pass metabolism.* * Ciclesonide has **very low systemic bioavailability** (<1%) when administered via inhalation. * The active metabolite des-ciclesonide that does reach systemic circulation undergoes **extensive first-pass metabolism** in the liver, further reducing systemic exposure. * This pharmacokinetic property contributes to its excellent safety profile and minimal systemic adverse effects.
Question 5: What is the primary mechanism by which steroids exert their anti-inflammatory action?
- A. Phospholipase A2 (Correct Answer)
- B. Myeloperoxidase
- C. Cyclooxygenase
- D. Lipoxygenase
Explanation: ***Phospholipase A2*** - Steroids exert their primary anti-inflammatory action by inducing the synthesis of **lipocortin-1 (annexin-1)**, which then inhibits **phospholipase A2 (PLA2)**, an enzyme crucial for the release of **arachidonic acid** from cell membrane phospholipids. - By blocking PLA2, steroids prevent the formation of all subsequent inflammatory mediators derived from arachidonic acid, including **prostaglandins**, **leukotrienes**, and **thromboxanes**. - This represents the most **upstream** mechanism of steroid anti-inflammatory action, affecting multiple downstream pathways simultaneously. *Cyclooxygenase* - **Cyclooxygenase (COX)** enzymes, specifically COX-1 and COX-2, are responsible for converting arachidonic acid into **prostaglandins** and **thromboxanes**. - While steroids ultimately reduce COX activity by limiting substrate availability, their direct and primary inhibition is not on COX itself but at an earlier step in the inflammatory cascade. *Lipoxygenase* - The **lipoxygenase (LOX)** pathway converts arachidonic acid into **leukotrienes**, which are potent mediators of inflammation, particularly in asthma and allergic reactions. - Steroids do inhibit the formation of leukotrienes indirectly by blocking their precursor, arachidonic acid, but their direct target is not LOX itself. *Myeloperoxidase* - **Myeloperoxidase** is an enzyme found primarily in **neutrophils** and macrophages, playing a role in oxidative stress and microbial killing by producing hypochlorous acid (bleach). - While steroids can modulate immune cell function, their direct anti-inflammatory mechanism is not through the inhibition of myeloperoxidase activity.
Question 6: Hydrocortisone Acetate is injected in a painful arthritic TMJ to?
- A. Lubricate the synovial joint
- B. Decrease the inflammatory response (Correct Answer)
- C. Anaesthetize the nerve supply
- D. Increase the blood supply
Explanation: ***Decrease the inflammatory response*** - **Hydrocortisone Acetate** is a **corticosteroid**, well-known for its potent anti-inflammatory properties. - Injecting it directly into an arthritic temporomandibular joint (TMJ) helps to reduce local inflammation, thereby alleviating pain and improving joint function. *Lubricate the synovial joint* - While lubrication is important for joint function, **hydrocortisone acetate** does not act as a lubricant like hyaluronic acid. - Its primary mechanism is based on immune modulation and anti-inflammatory effects, not physical lubrication. *Anaesthetize the nerve supply* - **Hydrocortisone acetate** is not a local anesthetic; it does not directly block nerve impulses to provide immediate pain relief through numbness. - Although it reduces pain, this is secondary to its anti-inflammatory action rather than direct neural blockade. *Increase the blood supply* - **Corticosteroids** generally have vasoconstrictive properties, meaning they can *decrease* blood flow rather than increasing it, especially at the site of inflammation. - Increasing blood supply is not a therapeutic goal in managing acute inflammation in an arthritic joint.
Question 7: Anti-inflammatory action of steroids is due to
- A. Inhibition of lipoxygenase
- B. Inhibition of phospholipase A2 (Correct Answer)
- C. Inhibition of cyclooxygenase
- D. Increased activity of lipoprotein lipase
Explanation: ***Inhibition of phospholipase A2*** - Steroids exert their potent anti-inflammatory effects primarily by inducing the synthesis of **lipocortin-1 (annexin-1)**, which then inhibits **phospholipase A2 (PLA2)** activity. - This inhibition of PLA2 prevents the release of **arachidonic acid** from cell membrane phospholipids, thereby blocking the entire cascade of downstream inflammatory mediators, including prostaglandins, thromboxanes, and leukotrienes. *Inhibition of lipoxygenase* - While leukotrienes (products of the lipoxygenase pathway) are inflammatory mediators, steroids achieve their effect upstream by blocking the precursor (arachidonic acid) rather than directly inhibiting **lipoxygenase**. - **Zileuton** is an example of a drug that directly inhibits lipoxygenase. *Inhibition of cyclooxygenase* - Steroids do not directly inhibit **cyclooxygenase (COX) enzymes**; this is the primary mechanism of action for **NSAIDs (Nonsteroidal Anti-inflammatory Drugs)** like ibuprofen and aspirin. - By inhibiting COX, NSAIDs primarily block the synthesis of prostaglandins and thromboxanes, but not leukotrienes. *Increased activity of lipoprotein lipase* - Increased activity of **lipoprotein lipase (LPL)** by steroids is related to their metabolic effects, such as promoting fat deposition and contributing to steroid-induced dyslipidemia, rather than their anti-inflammatory action. - LPL's role is in the metabolism of triglycerides in lipoproteins, which is distinct from the inflammatory cascade.
Question 8: Dapsone is NOT used in:
- A. Dermatitis herpetiformis
- B. Alopecia areata (Correct Answer)
- C. Pneumocystis jirovecii pneumonia prophylaxis
- D. Leprosy
Explanation: ***Alopecia areata*** - **Dapsone** is an **antibiotic** with anti-inflammatory and immunomodulatory properties and is not indicated for the treatment of **alopecia areata**. - Treatment for **alopecia areata** typically involves **corticosteroids** (topical, intralesional, or systemic) or other immunosuppressants. *Dermatitis herpetiformis* - **Dapsone** is the **first-line treatment** for **dermatitis herpetiformis** due to its rapid antipruritic effect, often providing relief within 24-48 hours. - It works by reducing the inflammation and formation of the characteristic **subepidermal blisters** seen in this condition. *Pneumocystis jirovecii pneumonia prophylaxis* - **Dapsone** is an effective **alternative agent** for prophylaxis against **Pneumocystis jirovecii pneumonia (PCP)**, especially in patients who cannot tolerate trimethoprim-sulfamethoxazole. - It is often used in combination with **pyrimethamine** for toxoplasmosis prophylaxis in HIV-infected patients. *Leprosy* - **Dapsone** is a crucial component of **multidrug therapy (MDT)** for both paucibacillary and multibacillary forms of **leprosy**. - It acts as a **bacteriostatic agent** against Mycobacterium leprae and has been a cornerstone of leprosy treatment for decades.
Question 9: Which of the following statement is correct regarding the given DRC? (AllMS Nov 2016)
- A. C is non-competitive antagonist
- B. B is more potent than A
- C. A is more efficacious than B
- D. A and B are full agonists (Correct Answer)
Explanation: ***A and B are full agonists*** - Both Drug A and Drug B reach the **maximum biological effect**, indicated as 100 on the y-axis, meaning they are capable of producing the full response. - A full agonist is a substance that binds to a receptor and produces the **maximum possible biological response**. *C is non-competitive antagonist* - Drug C *does* produce a biological effect, albeit a lower one, making it a **partial agonist**, not an antagonist. - A non-competitive antagonist would **reduce the maximum effect** of the agonist and shift the curve downwards, which is not what is observed here for C. *B is more potent than A* - Drug A achieves 50% of its maximal effect at a **lower concentration** than Drug B (i.e., further to the left on the x-axis). - Therefore, Drug A is **more potent** than Drug B, as potency is inversely related to the concentration required for a given effect. *A is more efficacious than B* - Both Drug A and Drug B reach the **same maximum biological effect** (100 on the y-axis), indicating they have equal efficacy. - Efficacy refers to the **maximum effect** a drug can produce, regardless of the dose.
Question 10: Which of the following is an example of topical administration producing only local effects (not systemic)?
- A. Topical corticosteroid cream (Correct Answer)
- B. Sublingual nitroglycerin
- C. Transdermal patch
- D. Rectal diazepam
Explanation: ***Topical corticosteroid cream*** - When applied to the skin for conditions like dermatitis, topical corticosteroids primarily exert their effects at the site of application, reducing **local inflammation** and itching. - While systemic absorption can occur with potent steroids over large areas, typical use aims for **localized action** without significant systemic effects. *Sublingual nitroglycerin* - This route is designed for **rapid systemic absorption** through the oral mucosa, bypassing first-pass metabolism to quickly treat angina. - The goal is a **widespread vasodilatory effect** throughout the body, not a local one within the mouth. *Transdermal patch* - Transdermal patches, such as those for nicotine or fentanyl, are specifically designed to deliver medication **systemically** through the skin into the bloodstream over a prolonged period. - They provide a **sustained release** and systemic therapeutic effect throughout the body. *Rectal diazepam* - Administered rectally, diazepam is absorbed into the systemic circulation to produce **CNS effects** such as sedation, anxiolysis, or anticonvulsant activity. - Although the administration is local, the intended clinical effect is **systemic** and widespread throughout the body.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free