Disease-Modifying Antirheumatic Drugs — MCQs
A patient of RA is taking methotrexate, steroids and NSAIDs since 4 months but activity of disease progression is same. What should be the next probable step?
Drug X is useful in the treatment of rheumatoid arthritis. It is available only in the parenteral formulation and its mechanism of action is antagonism of tumor necrosis factor. Which of the following can be X?
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 which of the following conditions are Anti-TNF agents contraindicated?
In cervical cancer brachytherapy, the primary reference point for dose prescription is -
A patient with rheumatoid arthritis on Methotrexate, steroids and NSAIDs for past 4 months has had no retardation of disease progression. What is the next rational step in management?
Which of the following combinations can result in severe toxicity due to inhibition of cytochrome P450 enzymes?
Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
Which of the following drugs is not used in management of rheumatoid arthritis?
Disease-Modifying Antirheumatic Drugs Indian Medical PG Practice Questions and MCQs
Question 1: A patient of RA is taking methotrexate, steroids and NSAIDs since 4 months but activity of disease progression is same. What should be the next probable step?
- A. Continue methotrexate and steroids
- B. Stop oral methotrexate and start parenteral methotrexate
- C. Add sulfasalazine
- D. Add anti TNF alpha drugs (Correct Answer)
Explanation: ***Add anti TNF alpha drugs*** - This patient has **active rheumatoid arthritis** despite 4 months of treatment with **methotrexate**, **steroids**, and **NSAIDs**, indicating an inadequate response to conventional DMARDs [1]. - Current major rheumatology guidelines (**ACR 2021**, **EULAR 2019**) recommend escalating to **biologic DMARDs** like **anti-TNF-alpha agents** as the preferred next step for patients with persistent disease activity after 3-6 months of methotrexate therapy [1]. *Continue methotrexate and steroids* - Continuing the current regimen unchanged is not appropriate as the patient's **disease activity has not improved** over four months. - This approach would leave the patient at risk for ongoing **joint damage** and functional decline due to **uncontrolled inflammation** [2]. *Stop oral methotrexate and start parenteral methotrexate* - While changing to **parenteral methotrexate** can improve **bioavailability** and absorption, the primary issue here is the **overall lack of disease control**, not necessarily methotrexate non-response [1]. - This step alone is unlikely to provide sufficient additional benefit for a patient whose disease is still active after 4 months, especially when more potent **biologic options** are available [1]. *Add sulfasalazine* - **Sulfasalazine** is a valid conventional synthetic DMARD that can be used in **combination therapy** with methotrexate and has proven efficacy in RA treatment. - However, current major rheumatology guidelines (**ACR 2021**, **EULAR 2019**) recommend escalating to **biologic DMARDs** like **anti-TNF agents** as the preferred next step for patients with inadequate response to methotrexate after 3-6 months, especially when **disease activity remains high** as in this case [1].
Question 2: Drug X is useful in the treatment of rheumatoid arthritis. It is available only in the parenteral formulation and its mechanism of action is antagonism of tumor necrosis factor. Which of the following can be X?
- A. Cyclosporine
- B. Etanercept (Correct Answer)
- C. Phenylbutazone
- D. Penicillamine
Explanation: ***Etanercept*** - **Etanercept** is a **tumor necrosis factor (TNF)-alpha inhibitor** used in the treatment of **rheumatoid arthritis** [1], and it is administered via **subcutaneous injection** (parenteral) [1]. - Its mechanism of action involves binding to and **inactivating TNF-alpha**, a key cytokine in the inflammatory process of rheumatoid arthritis [1].*Cyclosporine* - **Cyclosporine** is an **immunosuppressant** that primarily acts by inhibiting **calcineurin**, thereby reducing T-lymphocyte activity, not directly antagonizing TNF. - While used in some autoimmune conditions, it is available in **oral and intravenous formulations** and is not primarily identified as a TNF antagonist.*Phenylbutazone* - **Phenylbutazone** is a **nonsteroidal anti-inflammatory drug (NSAID)** that inhibits **prostaglandin synthesis**, providing symptomatic relief from pain and inflammation. - It does not target TNF and is associated with significant **adverse effects**, leading to its limited use in modern medicine.*Penicillamine* - **Penicillamine** is a **disease-modifying antirheumatic drug (DMARD)** with a mechanism of action that is not fully understood, but it is thought to reduce immune complex formation and suppress T-cell activity. - It is an **oral medication** and its primary action is not TNF antagonism; its use has largely been replaced by newer, more effective DMARDs.
Question 3: 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 4: 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 5: In which of the following conditions are Anti-TNF agents contraindicated?
- A. RA with Hepatitis B (Correct Answer)
- B. RA with HCV
- C. RA with pulmonary fibrosis
- D. RA with HIV
Explanation: ***RA with Hepatitis B*** - **Anti-TNF agents** can cause reactivation of **latent Hepatitis B virus (HBV)** infection, leading to severe hepatitis and liver failure [1]. Therefore, screening for HBV is crucial before initiating these medications [1]. - Patients with active or chronic HBV infection often require **antiviral therapy** before or concurrently with anti-TNF treatment to prevent reactivation. *RA with HIV* - While caution is advised, **anti-TNF agents** can be used in patients with **well-controlled HIV infection** on antiretroviral therapy, often with close monitoring for infections. - The risk of opportunistic infections is carefully balanced against the benefits of controlling rheumatoid arthritis and preventing joint damage [1]. *RA with HCV* - **Anti-TNF agents** are generally considered safe for patients with **Hepatitis C virus (HCV)** infection, especially if the HCV is stable or being treated. - There is no strong evidence to suggest that anti-TNF therapy commonly causes HCV reactivation or worsening of liver disease. *RA with pulmonary fibrosis* - The use of **anti-TNF agents** in patients with established **pulmonary fibrosis** is generally not contraindicated, though careful monitoring for worsening respiratory symptoms is important. - Some anti-TNF agents have been associated with **interstitial lung disease**, but this is typically a new onset condition rather than exacerbation of pre-existing fibrosis.
Question 6: 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 7: A patient with rheumatoid arthritis on Methotrexate, steroids and NSAIDs for past 4 months has had no retardation of disease progression. What is the next rational step in management?
- A. Continue Methotrexate and steroids at higher dose
- B. Stop oral Methotrexate and start parenteral Methotrexate
- C. Add Sulfasalazine (Correct Answer)
- D. Start treatment with anti-TNF alpha drugs
Explanation: Focus on **Add Sulfasalazine**: - Since the patient has not responded to **Methotrexate** alone, adding a second conventional synthetic **disease-modifying antirheumatic drug (DMARD)** like **Sulfasalazine** is a common and appropriate step in a **treat-to-target strategy** for rheumatoid arthritis [1]. - This approach aims to achieve **disease remission** or **low disease activity** by combining therapies to enhance efficacy. *Continue Methotrexate and steroids at higher dose* - Increasing the dose of **Methotrexate** might be considered if the current dose is sub-optimal, but after 4 months with no improvement, simply continuing current medications at higher doses without adding another agent is less likely to significantly alter **disease progression** [1]. - Prolonged higher-dose **steroids** carry significant risks and are generally used for symptom control, not primary disease modification. *Stop oral Methotrexate and start parenteral Methotrexate* - Switching to **parenteral Methotrexate** is considered if **oral Methotrexate** absorption is an issue or if the patient experiences gastrointestinal side effects [1]. - While parenteral administration can improve bioavailability, it doesn't represent a change in therapeutic strategy for **uncontrolled disease activity**. *Start treatment with anti-TNF alpha drugs* - **Biologic DMARDs** like **anti-TNF alpha drugs** are typically reserved for patients who have failed **two or more conventional synthetic DMARDs**, including **Methotrexate**, or in cases of severe, rapidly progressing disease [2]. - While effective, they are more expensive and have different side effect profiles, making them a later-line treatment in the management algorithm [2].
Question 8: Which of the following combinations can result in severe toxicity due to inhibition of cytochrome P450 enzymes?
- A. Amiodarone + Atorvastatin
- B. Carbamazepine + Atorvastatin
- C. Atorvastatin + Itraconazole (Correct Answer)
- D. Phenytoin + Atorvastatin
Explanation: ***Atorvastatin + Itraconazole*** - **Itraconazole** is a potent inhibitor of **CYP3A4**, the primary enzyme responsible for atorvastatin's metabolism. - Co-administration leads to significantly increased **atorvastatin plasma concentrations**, raising the risk of severe side effects like **rhabdomyolysis** and **hepatotoxicity**. *Amiodarone + Atorvastatin* - **Amiodarone** is a moderate **CYP3A4 inhibitor** and can increase atorvastatin levels, but the inhibition is **less potent** than itraconazole. - While this combination does carry a risk and requires dose adjustment, the interaction is **less severe** compared to the potent inhibition seen with itraconazole. - The direct CYP inhibition leading to severe atorvastatin toxicity is less pronounced than with itraconazole. *Carbamazepine + Atorvastatin* - **Carbamazepine** is a potent **CYP3A4 inducer**, meaning it would increase the metabolism of atorvastatin, potentially *decreasing* its efficacy rather than causing toxicity through inhibition. - This interaction would typically lead to subtherapeutic atorvastatin levels, rather than severe toxicity. *Phenytoin + Atorvastatin* - **Phenytoin** is also a potent **CYP3A4 inducer**, similar to carbamazepine. - Concurrent use would likely lead to enhanced metabolism and **reduced efficacy of atorvastatin**, not increased toxicity due to enzyme inhibition.
Question 9: 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 10: 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.
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