Drugs Used in Rheumatoid Arthritis — MCQs
Which of the following drugs is not used in Rheumatoid arthritis?
Which of the following is not a first-line drug for the management of a patient with rheumatoid arthritis?
In cervical cancer brachytherapy, the primary reference point for dose prescription is -
What should be the correct treatment for a 14-year-old child with newly diagnosed Juvenile Rheumatoid Arthritis?
What is the mechanism of action of Methotrexate?
Which fully humanized antibody is used in treatment of rheumatoid arthritis?
The primary goal of glucocorticoid treatment in rheumatoid arthritis is -
Which of the following drugs is not used in management of rheumatoid arthritis?
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?
Which drug used in treatment of rheumatoid arthritis acts by inhibition of T-cell proliferation?
Drugs Used in Rheumatoid Arthritis Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following drugs is not used in Rheumatoid arthritis?
- A. Leflunomide
- B. Etanercept
- C. Febuxostat (Correct Answer)
- D. Methotrexate
Explanation: ***Febuxostat*** - **Febuxostat** is a **xanthine oxidase inhibitor** used to treat **gout** by reducing uric acid levels. - It has no role in the management of **rheumatoid arthritis**, which is an autoimmune inflammatory condition. *Leflunomide* - **Leflunomide** is a **DMARD (disease-modifying antirheumatic drug)** that works by inhibiting pyrimidine synthesis. - It is a common and effective treatment for **rheumatoid arthritis**, either as monotherapy or in combination with other DMARDs. *Etanercept* - **Etanercept** is a **TNF-alpha inhibitor**, a biologic DMARD that targets tumor necrosis factor-alpha. - It is widely used in **rheumatoid arthritis** to reduce inflammation and slow disease progression, especially in patients who do not respond to conventional DMARDs. *Methotrexate* - **Methotrexate** is considered the **first-line DMARD** for most patients with **rheumatoid arthritis**. - It works by inhibiting dihydrofolate reductase and has both anti-inflammatory and immunosuppressive effects.
Question 2: Which of the following is not a first-line drug for the management of a patient with rheumatoid arthritis?
- A. Hydroxychloroquine
- B. Sulfasalazine
- C. Azathioprine (Correct Answer)
- D. Methotrexate
Explanation: ***Azathioprine*** - While an **immunosuppressant**, azathioprine is generally reserved for patients with **refractory rheumatoid arthritis (RA)** or those who cannot tolerate or have failed first-line DMARDs. - Its use often comes with a higher risk of side effects, making it less suitable as an initial agent compared to other conventional synthetic DMARDs. *Hydroxychloroquine* - This is a **first-line DMARD** for RA, particularly in patients with **mild disease**, due to its relatively favorable safety profile. - It is often used in combination with other DMARDs like methotrexate. *Sulfasalazine* - Sulfasalazine is a common **first-line conventional synthetic DMARD** for RA, especially effective in patients with peripheral arthritis. - It is frequently used when methotrexate is contraindicated or not tolerated, or as part of combination therapy. *Methotrexate* - **Methotrexate is considered the cornerstone** and **first-line treatment** for most patients with rheumatoid arthritis due to its efficacy and tolerability [1]. - It is recommended for early initiation in newly diagnosed patients to prevent joint damage and improve outcomes [2].
Question 3: In cervical cancer brachytherapy, the primary reference point for dose prescription is -
- A. Point A (Correct Answer)
- B. Point B
- C. Side walls of pelvis
- D. Point H
Explanation: ***Point A*** - **Point A** is defined as 2 cm lateral to the central canal of the uterus and 2 cm superior to the external os, representing a dose estimation to the **parametrium** and a critical reference for tumoricidal dose. - This point serves as the **primary prescription and reporting point** for brachytherapy in cervical cancer, as it is highly correlated with treatment outcomes and complications. - Established by **ICRU Report 38** as the standard reference point for dose prescription. *Point B* - **Point B** is located 5 cm from the midline (3 cm lateral to Point A) at the level of Point A, and is primarily used to estimate the dose received by the **pelvic side wall** and regional lymphatics. - It provides an indication of dose to structures further from the applicator but is **not the primary prescription point** for the target volume in brachytherapy. *Side walls of pelvis* - The dose to the **side walls of the pelvis** is relevant for assessing potential toxicity to structures like the obturator nerve and external iliac vessels, and for ensuring adequate coverage of pelvic lymph nodes. - While critical for treatment planning, the side walls themselves are not a primary dose prescription point but rather a **region of interest** for dose constraints and coverage. *Point H* - **Point H** represents the reference point for estimating the dose to the **rectum** in brachytherapy, located at the posterior vaginal wall. - While important for assessing **rectal toxicity** and as a dose-limiting structure, Point H is used for reporting organ-at-risk doses, not for primary tumor dose prescription.
Question 4: What should be the correct treatment for a 14-year-old child with newly diagnosed Juvenile Rheumatoid Arthritis?
- A. DMARDs with a short course of steroids (Correct Answer)
- B. Only NSAIDs
- C. DMARDs after initial treatment with NSAIDs
- D. Monotherapy with TNF inhibitors
- E. Long-term high-dose corticosteroid therapy
Explanation: ***DMARDs with a short course of steroids*** - For **newly diagnosed rheumatoid arthritis** in children (juvenile idiopathic arthritis), the primary goal is to **control inflammation** and prevent joint damage with **disease-modifying antirheumatic drugs (DMARDs)**. - A **short course of corticosteroids** is often used as a **bridging therapy** to rapidly reduce inflammation while the DMARDs take effect. - This approach ensures **early aggressive treatment** to prevent joint damage while minimizing long-term steroid exposure. *Incorrect: Only NSAIDs* - **NSAIDs** alone provide **symptomatic relief** but do not alter the course of the disease or prevent joint damage in rheumatoid arthritis. - Relying solely on NSAIDs can lead to **progressive joint erosion** and functional impairment. *Incorrect: DMARDs after initial treatment with NSAIDs* - While NSAIDs can be used for initial symptom control, delaying **DMARD initiation** is generally not recommended as it allows for continued joint inflammation and potential damage. - Early and aggressive treatment with DMARDs is crucial for **optimizing long-term outcomes** and preserving joint function. *Incorrect: Monotherapy with TNF inhibitors* - **TNF inhibitors** are potent **biologic DMARDs** and are typically considered for patients who have **failed conventional DMARDs** (e.g., methotrexate). - They are not usually the **first-line monotherapy** for treatment-naive rheumatoid arthritis due to their cost, potential side effects, and the availability of other effective options. *Incorrect: Long-term high-dose corticosteroid therapy* - **Prolonged corticosteroid use** at high doses is associated with significant side effects including growth suppression, osteoporosis, increased infection risk, and cushingoid features. - While steroids are useful as **bridging therapy** for a short duration, long-term high-dose use is avoided in pediatric patients whenever possible.
Question 5: What is the mechanism of action of Methotrexate?
- A. Inhibition of Dihydrofolate reductase (Correct Answer)
- B. Inhibits pyrimidine synthesis
- C. Inhibits cell replication by acting on G phase of cell cycle
- D. Inhibits Thymidylate synthase
- E. Inhibits RNA polymerase
Explanation: ***Inhibition of Dihydrofolate reductase*** - **Methotrexate** is a **folate analog** that competitively inhibits **dihydrofolate reductase (DHFR)**, an enzyme essential for converting **dihydrofolate** to **tetrahydrofolate**. - This inhibition blocks the synthesis of **purines** and **pyrimidines**, thereby preventing DNA and RNA synthesis and ultimately inhibiting cell proliferation. *Inhibits pyrimidine synthesis* - While methotrexate ultimately inhibits pyrimidine synthesis by depleting tetrahydrofolate, its direct mechanism is not the inhibition of the pyrimidine synthesis pathway enzymes themselves. - Its primary action is upstream, by inhibiting DHFR. *Inhibits cell replication by acting on G phase of cell cycle* - Methotrexate primarily inhibits cells in the **S-phase** of the cell cycle, as it interferes with DNA synthesis. - It does not specifically target the G phase; rather, it affects cells that are actively attempting to replicate their DNA. *Inhibits Thymidylate synthase* - **Thymidylate synthase** is inhibited by drugs like **5-fluorouracil**, which directly blocks the conversion of **deoxyuridine monophosphate (dUMP)** to **deoxythymidine monophosphate (dTMP)**. - Methotrexate's effect on thymidylate synthesis is indirect, mediated by the depletion of the cofactor **N5,N10-methylene-tetrahydrofolate** due to DHFR inhibition. *Inhibits RNA polymerase* - **RNA polymerase** inhibition is the mechanism of drugs like **rifampin** (bacterial RNA polymerase) and **α-amanitin** (eukaryotic RNA polymerase). - Methotrexate does not directly inhibit RNA polymerase; its effects on RNA synthesis are secondary to depletion of nucleotide precursors through DHFR inhibition.
Question 6: Which fully humanized antibody is used in treatment of rheumatoid arthritis?
- A. Anakinra
- B. Infliximab
- C. Leflunomide
- D. Adalimumab (Correct Answer)
Explanation: ***Adalimumab*** - **Adalimumab** is a **fully human monoclonal antibody** that targets **tumor necrosis factor-alpha (TNF-α)**, making it suitable for treating autoimmune conditions like rheumatoid arthritis without causing significant immunogenic reactions. - Its humanized structure minimizes the risk of developing **anti-drug antibodies**, improving long-term efficacy and safety. *Anakinra* - **Anakinra** is a **recombinant human interleukin-1 (IL-1) receptor antagonist**, not a fully humanized antibody. - While used in rheumatoid arthritis, its mechanism of action and structural classification differ from a fully humanized antibody. *Infliximab* - **Infliximab** is a **chimeric monoclonal antibody** (mouse-human), meaning it contains both mouse and human protein components. - It targets **TNF-α** but is not fully humanized, increasing the potential for immunogenicity compared to fully human antibodies. *Leflunomide* - **Leflunomide** is a **pyrimidine synthesis inhibitor**, functioning as an immunosuppressant rather than an antibody. - It works by inhibiting dihydroorotate dehydrogenase, which reduces lymphoid proliferation, making it a **disease-modifying antirheumatic drug (DMARD)**, not a biologic agent.
Question 7: The primary goal of glucocorticoid treatment in rheumatoid arthritis is -
- A. Suppression of inflammation and improvement in functional capacity (Correct Answer)
- B. Prevention of suppression of the hypothalamic pituitary-adrenal axis
- C. Development of a sense of well-being in the patient
- D. Reversal of the degenerative process
Explanation: ***Suppression of inflammation and improvement in functional capacity*** - **Glucocorticoids** are potent anti-inflammatory agents that rapidly reduce pain, swelling, and stiffness in **rheumatoid arthritis (RA)**. - This reduction in inflammation directly leads to improved **joint function** and overall quality of life for the patient. *Prevention of suppression of the hypothalamic pituitary-adrenal axis* - **Suppression of the HPA axis** is an *undesirable side effect* of chronic glucocorticoid use, not a primary goal of treatment. - While clinicians try to minimize this, it is a complication to manage, not an intended therapeutic effect. *Development of a sense of well-being in the patient* - While patients often experience an improved sense of well-being due to rapid symptom relief, this is a **secondary outcome** of effective inflammation control. - The direct objective of the medication is physiological—targeting the inflammatory process. *Reversal of the degenerative process* - Glucocorticoids do not reverse the **structural damage** or **degenerative changes** to joints that occur in chronic RA. - Their main role is to control the inflammatory component, which helps prevent further damage but does not repair existing erosion.
Question 8: Which of the following drugs is not used in management of rheumatoid arthritis?
- A. Etanercept
- B. Leflunomide
- C. Febuxostat (Correct Answer)
- D. Methotrexate
Explanation: ***Febuxostat*** - **Febuxostat** is a **xanthine oxidase inhibitor** used to treat **hyperuricemia** and **gout**, not rheumatoid arthritis. - Its mechanism of action involves reducing the production of **uric acid**, which is not directly involved in the pathophysiology of rheumatoid arthritis. *Etanercept* - **Etanercept** is a **biologic disease-modifying antirheumatic drug (DMARD)** that acts as a **TNF-alpha inhibitor**. - It is effectively used in treating **moderate to severe rheumatoid arthritis** by reducing inflammation and preventing joint damage. *Leflunomide* - **Leflunomide** is a **synthetic DMARD** that inhibits **pyrimidine synthesis**, thereby reducing lymphocyte proliferation. - It is a cornerstone treatment for **rheumatoid arthritis**, often used when methotrexate is not tolerated or insufficient. *Methotrexate* - **Methotrexate** is considered the **first-line synthetic DMARD** for most patients with rheumatoid arthritis. - It works by inhibiting **dihydrofolate reductase**, leading to anti-inflammatory and immunosuppressive effects.
Question 9: 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.
Question 10: Which drug used in treatment of rheumatoid arthritis acts by inhibition of T-cell proliferation?
- A. Anakinra
- B. Leflunomide (Correct Answer)
- C. Infliximab
- D. Etanercept
Explanation: ***Leflunomide*** - **Leflunomide** is a **pyrimidine synthesis inhibitor** that works by inhibiting the enzyme **dihydroorotate dehydrogenase** [1]. - This inhibition leads to a decrease in **de novo pyrimidine synthesis**, which is essential for **T-cell proliferation**, thereby exerting its immunomodulatory effects in **rheumatoid arthritis** [1], [2]. *Anakinra* - **Anakinra** is an **interleukin-1 receptor antagonist** that blocks the activity of **IL-1**, a pro-inflammatory cytokine. - It does not primarily act by inhibiting **T-cell proliferation**, but rather by modulating the inflammatory response. *Infliximab* - **Infliximab** is a **monoclonal antibody** that targets and neutralizes **tumor necrosis factor-alpha (TNF-α)**, a key cytokine in inflammation. - Its mechanism of action is primarily related to blocking **TNF-α activity**, not directly inhibiting **T-cell proliferation**. *Etanercept* - **Etanercept** is a **fusion protein** that acts as a **TNF-α receptor decoy**, binding to **TNF-α** and preventing it from interacting with its natural receptors. - Similar to infliximab, its main action is to inhibit **TNF-α**, rather than directly inhibiting **T-cell proliferation**.
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