Glucocorticoids as Anti-inflammatory Agents — MCQs
All of the following are indications for use of corticosteroids in SLE except:
Which of the following is the most potent topical corticosteroid?
Long-term steroid ingestion leads to all of the following except:
A 70-year-old woman is seen by her physician for evaluation of severe headaches. She noted these several weeks ago, and they have been getting worse. Although she has not had any visual aura but she has been intermittently losing vision in her left eye for the last few days. She denies new weakness or numbness, but she does reports jaw pain with eating. Her past medical history includes coronary artery disease requiring a bypass grafting 10 years prior, diabetes mellitus, hyperlipidaemia, and mild depression. Full review of symptoms is notable for night sweats and mild low back pain particularly prominent in the morning. Which of the following is the next most appropriate step?
Which enzyme is primarily inhibited by the drug prednisolone, leading to its anti-inflammatory effects?
A patient on long-term high-dose steroid therapy (prednisolone 20 mg/day for 6 months) is scheduled for major abdominal surgery. What is the most essential perioperative requirement?
Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
Which drug is commonly used for outpatient department (OPD) analgesia?
Which enzyme is irreversibly inhibited by aspirin?
A 50-year-old man presents with complaints of bilateral morning stiffness in his wrists and knees and painful joints on exercise. On physical examination, the joints are slightly swollen. The rest of the examination is unremarkable. His laboratory findings are also negative except for slight anemia, elevated erythrocyte sedimentation rate, and positive rheumatoid factor. The patient was started on weekly methotrexate to control the inflammation. What is the principle mechanism of action here?
Glucocorticoids as Anti-inflammatory Agents Indian Medical PG Practice Questions and MCQs
Question 1: All of the following are indications for use of corticosteroids in SLE except:
- A. Endocarditis (Correct Answer)
- B. Nephritic syndrome
- C. Pericarditis
- D. Neuropsychiatric lupus
Explanation: ***Endocarditis*** - While **Libman-Sacks endocarditis** is a known manifestation of SLE, it typically involves **non-infectious vegetations** and rarely causes significant valvular dysfunction requiring corticosteroid therapy for acute treatment. - Steroids are generally not indicated for the primary treatment of established endocarditis, whether infectious or non-infectious, unless there is a severe active inflammatory component or an autoimmune-driven valvulitis. *Nephritic syndrome* - **Lupus nephritis**, especially the proliferative forms (Class III and IV), often presents with nephritic syndrome and is a **primary indication for aggressive corticosteroid therapy** to suppress inflammation and prevent renal failure [1]. - Corticosteroids are crucial in combination with immunosuppressants to manage renal inflammation, proteinuria, and declining renal function. *Pericarditis* - **Pericarditis** in SLE can be symptomatic and is often managed with **corticosteroids** to reduce inflammation and alleviate chest pain [1]. - Severe or recurrent pericarditis may require higher doses of steroids, and tamponade is a rare but serious complication. *Neuropsychiatric lupus* - Manifestations such as **CNS vasculitis**, **seizures**, psychosis, and severe cognitive dysfunction are considered **major organ involvement** and are treated with **high-dose corticosteroids** to reduce inflammation and prevent permanent neurological damage. - Steroids are often part of the initial treatment regimen for acute and severe neuropsychiatric SLE.
Question 2: Which of the following is the most potent topical corticosteroid?
- A. Triamcinolone acetonide
- B. Hydrocortisone acetate
- C. Clobetasol propionate (Correct Answer)
- D. Betamethasone valerate
Explanation: ***Clobetasol propionate*** - **Clobetasol propionate** is recognized as one of the most potent **Class I topical corticosteroids**, used for severe inflammatory skin conditions. - Its high potency allows for effective suppression of severe inflammation and pruritus, but also carries a greater risk of **adverse effects** with prolonged use. *Triamcinolone acetonide* - **Triamcinolone acetonide** is a **medium-potency** topical corticosteroid (Class IV-V), less potent than clobetasol propionate. - It is commonly used for moderate inflammatory skin conditions, such as eczema and psoriasis, but not for severe cases requiring maximum potency. *Hydrocortisone acetate* - **Hydrocortisone acetate** is a **low-potency** topical corticosteroid (Class VII), making it the least potent option listed. - It's often used for mild inflammatory conditions, sensitive areas like the face, or for less severe conditions requiring minimal corticosteroid strength. *Betamethasone valerate* - **Betamethasone valerate** is a **medium-to-high potency** topical corticosteroid (Class III-V), placing it among stronger corticosteroids but still less potent than clobetasol propionate. - It is effective for moderate to severe inflammatory skin conditions but does not reach the highest level of potency demonstrated by clobetasol.
Question 3: Long-term steroid ingestion leads to all of the following except:
- A. Avascular necrosis of head of femur
- B. Growth retardation
- C. Hypoglycemia (Correct Answer)
- D. Cataract
Explanation: ***Hypoglycemia*** - Chronic steroid use primarily leads to **hyperglycemia** due to increased **gluconeogenesis** and **insulin resistance**, not hypoglycemia. - Steroids raise blood glucose levels, potentially inducing or worsening **diabetes mellitus**. *Avascular necrosis of head of femur* - Long-term steroid use is a well-established risk factor for **avascular necrosis**, particularly affecting the **femoral head**. - This occurs due to impaired blood supply to the bone, leading to its death. *Cataract* - **Posterior subcapsular cataracts** are a known ocular complication of prolonged systemic corticosteroid therapy. - The mechanism involves direct effects of steroids on lens metabolism and protein aggregation. *Growth retardation* - In children, chronic corticosteroid therapy can suppress growth, leading to **growth retardation**. - This is due to interference with **growth hormone secretion** and direct effects on bone formation.
Question 4: A 70-year-old woman is seen by her physician for evaluation of severe headaches. She noted these several weeks ago, and they have been getting worse. Although she has not had any visual aura but she has been intermittently losing vision in her left eye for the last few days. She denies new weakness or numbness, but she does reports jaw pain with eating. Her past medical history includes coronary artery disease requiring a bypass grafting 10 years prior, diabetes mellitus, hyperlipidaemia, and mild depression. Full review of symptoms is notable for night sweats and mild low back pain particularly prominent in the morning. Which of the following is the next most appropriate step?
- A. Immediate initiation of glucocorticoid (Correct Answer)
- B. Aspirin 975 mg orally daily
- C. Measurement of erythrocyte sedimentation rate
- D. Referral for temporal artery biopsy
Explanation: ### Immediate initiation of glucocorticoids - The patient's symptoms, including **severe headaches**, **transient vision loss (amaurosis fugax)**, **jaw claudication**, and **systemic symptoms** like night sweats in an elderly woman, are highly suggestive of **giant cell arteritis (GCA)**. [1] - **Prompt initiation of high-dose glucocorticoids** is crucial to prevent irreversible vision loss, which is a devastating complication of GCA. [1] *Aspirin 975 mg orally daily* - While aspirin may be considered as an adjunct in treating GCA to reduce thrombotic complications, it is **not the primary or immediate treatment** for the disease itself. - **High-dose aspirin** is typically not used for GCA and would not address the underlying inflammation causing ocular ischemia. *Measurement of erythrocyte sedimentation rate* - An **elevated ESR** is characteristic of GCA and can support the diagnosis. [1] - However, performing this test first would **delay crucial treatment** for GCA, potentially leading to permanent vision loss. [1] *Referral for temporal artery biopsy* - A **temporal artery biopsy** is the gold standard for confirming the diagnosis of GCA but should **not delay the initiation of glucocorticoids**. [1] - Treatment should begin immediately based on clinical suspicion, and the biopsy can be performed safely within **1-2 weeks of starting steroids** without significantly impacting diagnostic yield. [1]
Question 5: Which enzyme is primarily inhibited by the drug prednisolone, leading to its anti-inflammatory effects?
- A. Lipoxygenase
- B. Phosphodiesterase
- C. Phospholipase A2 (Correct Answer)
- D. Cyclooxygenase
Explanation: ***Phospholipase A2*** - Prednisolone, a corticosteroid, primarily exerts its anti-inflammatory effects by inhibiting **phospholipase A2**. - Inhibition of **phospholipase A2** prevents the release of **arachidonic acid** from cell membrane phospholipids, thereby blocking the synthesis of all downstream inflammatory mediators. *Cyclo oxygenase* - **Cyclooxygenase (COX)** enzymes are responsible for converting arachidonic acid into **prostaglandins, prostacyclins**, and **thromboxanes**. - While COX is involved in inflammation, it is primarily inhibited by **NSAIDs**, not directly by prednisolone as its initial target. *Lipoxygenase* - **Lipoxygenase (LOX)** enzymes metabolize arachidonic acid into **leukotrienes**, other potent inflammatory mediators. - While leukotrienes contribute to inflammation, prednisolone's primary mechanism of action is upstream of both COX and LOX pathways, rather than direct LOX inhibition. *Phosphodiesterase* - **Phosphodiesterases (PDEs)** are a diverse group of enzymes that break down cyclic nucleotides (cAMP and cGMP). - PDE inhibitors are used for conditions like asthma and erectile dysfunction, and their inhibition is not the primary mechanism of action for the anti-inflammatory effects of prednisolone.
Question 6: A patient on long-term high-dose steroid therapy (prednisolone 20 mg/day for 6 months) is scheduled for major abdominal surgery. What is the most essential perioperative requirement?
- A. Insulin only
- B. Hydrocortisone only (Correct Answer)
- C. Both
- D. None of the options
Explanation: ***Hydrocortisone only*** - Patients on chronic **high-dose steroid therapy** (>5 mg prednisolone daily for >3 weeks) are at risk of **adrenal insufficiency** during surgical stress due to suppression of the hypothalamic-pituitary-adrenal (HPA) axis. - **Hydrocortisone stress dose** (100 mg IV at induction, followed by 50 mg every 8 hours) is the **most essential and immediate requirement** to prevent **adrenal crisis** during major surgery. - Hydrocortisone has both glucocorticoid and mineralocorticoid activity, mimicking the body's natural cortisol response to surgical stress. *Insulin only* - While steroids can cause **hyperglycemia** requiring insulin management, this is a **secondary concern** compared to preventing life-threatening **adrenal crisis**. - Insulin addresses a metabolic complication but does not protect against **inadequate cortisol response** to surgical stress. - **Without stress-dose steroids**, the patient risks hemodynamic collapse regardless of glucose control. *Both* - Although **both** medications might eventually be needed if hyperglycemia develops, the question asks for the **most essential** requirement. - **Hydrocortisone is non-negotiable** and must be given prophylactically; insulin is only needed if blood glucose is elevated. - Prioritizing both equally misses the critical time-sensitive need for **adrenal axis support**. *None of the options* - This is incorrect because patients on chronic high-dose steroids undergoing major surgery **absolutely require stress-dose steroid coverage**. - Failure to administer hydrocortisone can result in **acute adrenal crisis** with severe hypotension, shock, and potential mortality. - Modern guidelines confirm the need for perioperative steroid supplementation in high-risk patients.
Question 7: Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
- A. Acetaminophen
- B. Tramadol
- C. Aspirin
- D. Gabapentin (Correct Answer)
Explanation: ***Gabapentin*** - **Gabapentin** is a widely recommended first-line treatment for diabetic neuropathic pain due to its efficacy in modulating neuronal excitability. - It works by binding to the **α2δ subunit of voltage-gated calcium channels**, reducing calcium influx and thereby decreasing the release of excitatory neurotransmitters involved in pain signaling. *Acetaminophen* - **Acetaminophen** is primarily an analgesic and antipyretic, effective for mild to moderate non-neuropathic pain. - It has no significant efficacy against **neuropathic pain**, which involves distinct neurobiological mechanisms. *Tramadol* - **Tramadol** is an opioid analgesic with some serotonin and norepinephrine reuptake inhibition, offering moderate pain relief. - While it can be used for moderate to severe pain, it is generally considered a **second-line agent** for neuropathic pain due to its opioid nature and potential side effects. *Aspirin* - **Aspirin** is a nonsteroidal anti-inflammatory drug (NSAID) primarily used for its anti-inflammatory, analgesic, and antiplatelet effects. - It is **ineffective for neuropathic pain**, which does not typically involve peripheral inflammation as its primary mechanism.
Question 8: Which drug is commonly used for outpatient department (OPD) analgesia?
- A. Diclofenac
- B. Ibuprofen
- C. Paracetamol (Correct Answer)
- D. Tramadol
Explanation: ***Paracetamol*** - It is a widely used and generally **safe analgesic** and antipyretic often prescribed for mild to moderate pain in an outpatient setting. - Its favorable side effect profile and availability as an **over-the-counter (OTC)** medication make it a first-choice drug for many common pain conditions. *Diclofenac* - While it is an effective NSAID used for pain and inflammation, its use can be associated with **gastrointestinal side effects** like ulcers and bleeding, as well as cardiovascular risks. - It is often reserved for more significant inflammatory pain or when other analgesics are insufficient, and may require more careful monitoring in an outpatient setting. *Ibuprofen* - Similar to diclofenac, Ibuprofen is an **NSAID** which is effective for pain and inflammation. However, it also carries risks of **gastrointestinal irritation** and renal side effects, especially with prolonged use or in certain patient populations. - While available OTC, its use for routine outpatient analgesia may be less preferred than paracetamol in some cases due to its GI and renal side effect profile. *Tramadol* - Tramadol is a **central acting opioid analgesic** with a higher potential for side effects such as nausea, dizziness, constipation, and the risk of dependence or abuse. - It is typically reserved for moderate to severe pain that is not adequately managed by non-opioid analgesics, and its prescription often involves more stringent monitoring than paracetamol.
Question 9: Which enzyme is irreversibly inhibited by aspirin?
- A. Lipooxygenase
- B. Cyclooxygenase (Correct Answer)
- C. Thromboxane synthase
- D. Phospholipase
Explanation: ***Cyclooxygenase*** - **Aspirin** irreversibly inhibits **cyclooxygenase (COX-1 and COX-2)** by acetylating a serine residue in the enzyme's active site. - This irreversible inhibition prevents the production of **prostaglandins, thromboxane**, and **prostacyclin**, thereby reducing inflammation, pain, fever, and platelet aggregation. *Lipooxygenase* - **Lipooxygenase** is involved in the synthesis of **leukotrienes**, which are mediators of inflammation and allergic responses. - Aspirin does not directly inhibit lipooxygenase; rather, it primarily targets the COX pathway. *Thromboxane synthase* - **Thromboxane synthase** is an enzyme downstream of COX, responsible for converting prostaglandin H2 into **thromboxane A2**. - While aspirin's effect on platelet aggregation is due to reduced thromboxane A2 synthesis via COX inhibition, it does not directly inhibit thromboxane synthase itself. *Phospholipase* - **Phospholipase A2** is responsible for releasing **arachidonic acid** from cell membrane phospholipids, which is the initial step in both the cyclooxygenase and lipooxygenase pathways. - Aspirin does not directly inhibit phospholipase A2; its action occurs later in the cascade.
Question 10: A 50-year-old man presents with complaints of bilateral morning stiffness in his wrists and knees and painful joints on exercise. On physical examination, the joints are slightly swollen. The rest of the examination is unremarkable. His laboratory findings are also negative except for slight anemia, elevated erythrocyte sedimentation rate, and positive rheumatoid factor. The patient was started on weekly methotrexate to control the inflammation. What is the principle mechanism of action here?
- A. Inhibition of assembly of microtubules in neutrophils impairing chemotaxis
- B. Increased extracellular levels of adenosine (Correct Answer)
- C. Inhibition of cyclooxygenase enzyme
- D. Inhibition of Dihydrofolate reductase enzyme
Explanation: ***Increased extracellular levels of adenosine*** - Methotrexate, at the low doses used for rheumatoid arthritis, primarily acts by inhibiting **aminoimidazole carboxamide ribonucleotide (AICAR) transformylase**, leading to a buildup of AICAR. - This accumulation inhibits **adenosine deaminase** and **AMP deaminase**, increasing extracellular adenosine, which is an anti-inflammatory mediator. *Inhibition of assembly of microtubules in neutrophils impairing chemotaxis* - This mechanism is characteristic of **colchicine**, used in treating gout, not methotrexate in rheumatoid arthritis. - Colchicine prevents neutrophil migration and activity by disrupting **microtubule polymerization**. *Inhibition of cyclooxygenase enzyme* - This is the primary mechanism of action for **NSAIDs (Nonsteroidal Anti-inflammatory Drugs)**, which reduce inflammation and pain by blocking prostaglandin synthesis. - Methotrexate's anti-inflammatory effects are not mediated through direct cyclooxygenase inhibition. *Inhibition of Dihydrofolate reductase enzyme* - While methotrexate does inhibit **dihydrofolate reductase (DHFR)**, this mechanism is primarily responsible for its cytotoxic effects in **cancer chemotherapy** at much higher doses. - At the low doses used in rheumatoid arthritis, the primary anti-inflammatory mechanism is related to adenosine.
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