JAK inhibitors US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for JAK inhibitors. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
JAK inhibitors US Medical PG Question 1: A 22-year-old man comes to the physician for a follow-up evaluation for chronic lower back pain. He has back stiffness that lasts all morning and slowly improves throughout the day. He has tried multiple over-the-counter medications, including ibuprofen, without any improvement in his symptoms. Physical examination shows tenderness over the iliac crest bilaterally and limited range of motion of the lumbar spine with forward flexion. The results of HLA-B27 testing are positive. An x-ray of the lumbar spine shows fusion of the lumbar vertebrae and sacroiliac joints. The physician plans to prescribe a new medication but first orders a tuberculin skin test to assess for the risk of latent tuberculosis reactivation. Inhibition of which of the following is the most likely primary mechanism of action of this drug?
- A. mTOR kinase
- B. Calcineurin
- C. NF-κB
- D. Inosine monophosphate dehydrogenase
- E. TNF-α (Correct Answer)
JAK inhibitors Explanation: **TNF-α**
- The clinical presentation with **chronic lower back pain**, morning stiffness, **limited lumbar spine range of motion**, positive **HLA-B27**, and **fusion of lumbar vertebrae and sacroiliac joints** is highly suggestive of **ankylosing spondylitis**.
- Biologic medications, specifically **TNF-α inhibitors**, are a cornerstone of treatment for ankylosing spondylitis, especially when conventional therapies like NSAIDs fail. The mention of screening for latent tuberculosis reactivation strongly points to the use of a TNF-α inhibitor, as these drugs increase the risk of TB reactivation.
*mTOR kinase*
- **mTOR inhibitors** (e.g., sirolimus, everolimus) are primarily used as **immunosuppressants** in organ transplantation and in some cancers.
- They are not a first-line or common treatment for ankylosing spondylitis or other spondyloarthropathies.
*Calcineurin*
- **Calcineurin inhibitors** (e.g., cyclosporine, tacrolimus) are potent **immunosuppressants** used in transplant rejection prevention and some autoimmune diseases.
- While they can have immunosuppressive effects, they are not the primary target for the treatment of ankylosing spondylitis.
*NF-κB*
- **NF-κB** is a crucial transcription factor involved in inflammation and immune responses. While relevant to inflammatory conditions, directly targeting NF-κB is not the primary mechanism of action for the most effective biologic therapies used in ankylosing spondylitis.
- **Glucocorticoids** can inhibit NF-κB, but they are not the main long-term treatment for ankylosing spondylitis, and the context points to a biologic.
*Inosine monophosphate dehydrogenase*
- **Inosine monophosphate dehydrogenase (IMPDH) inhibitors** (e.g., mycophenolate mofetil) block purine synthesis, thus inhibiting lymphocyte proliferation.
- These drugs are used in **transplantation** and some **autoimmune diseases** (e.g., lupus, vasculitis) but are not typically used for ankylosing spondylitis.
JAK inhibitors US Medical PG Question 2: A 62-year-old man, a retired oil pipeline engineer, presents to his primary care physician with complaints of headaches, fatigue, and constant ringing in his ears. Recurrently he has developed pruritus, usually after a hot shower. He also noted a constant burning sensation in his fingers and toes, independent of physical activity. On examination, he has a red face and his blood pressure levels are 147/89 mm Hg. A CBC revealed that his Hb is 19.0 g/dL and Hct is 59%. Because of his condition, his physician prescribes him 81 mg of aspirin to be taken daily in addition to therapeutic phlebotomy. Which of the statements below is true about this patient’s condition?
- A. Warfarin and phlebotomy are the preferred course of treatment.
- B. The patient has a decreased risk of developing myelofibrosis.
- C. Serum erythropoietin is expected to be high.
- D. Arterial oxygen saturation is usually higher than normal values in this condition.
- E. Mutation of the JAK2 gene is commonly seen in this condition. (Correct Answer)
JAK inhibitors Explanation: ***Mutation of the JAK2 gene is commonly seen in this condition.***
* The patient's symptoms (headaches, fatigue, tinnitus, pruritus after hot showers, erythromelalgia, facial plethora, hypertension, and elevated hemoglobin/hematocrit) are highly suggestive of **polycythemia vera (PV)**.
* Over 95% of patients with PV have a **JAK2 V617F mutation**, leading to constitutive activation of the JAK-STAT pathway, resulting in uncontrolled erythrocyte production.
*Warfarin and phlebotomy are the preferred course of treatment.*
* While **phlebotomy** is a cornerstone of PV management to reduce hematocrit and prevent thrombotic events, **warfarin** is generally not indicated for primary thromboprophylaxis in PV.
* **Low-dose aspirin** is preferred for reducing thrombotic risk, as indicated by the physician's prescription, along with phlebotomy.
*The patient has a decreased risk of developing myelofibrosis.*
* Polycythemia vera is a **myeloproliferative neoplasm**, and a significant percentage of patients (10-15%) will progress to **post-polycythemia vera myelofibrosis** over time.
* This progression is a natural history of the disease rather than a decreased risk, occurring as the bone marrow becomes exhausted and fibrotic.
*Serum erythropoietin is expected to be high.*
* In polycythemia vera, the **erythroid progenitors** are hypersensitive to erythropoietin (EPO), and red blood cell production occurs independently of EPO.
* Consequently, the **serum erythropoietin level is typically low or undetectable** due to feedback inhibition from the high red blood cell mass.
*Arterial oxygen saturation is usually higher than normal values in this condition.*
* Arterial oxygen saturation is generally **normal** in polycythemia vera, differentiating it from secondary polycythemia caused by hypoxemia (where oxygen saturation would be low).
* The increased red blood cell mass in PV does not inherently lead to higher-than-normal arterial oxygen saturation; it leads to increased oxygen-carrying capacity.
JAK inhibitors US Medical PG Question 3: A 46-year-old male presents to his dermatologist for routine follow-up of his psoriasis. He was last seen in the office six months prior, at which time he started undergoing ultraviolet light therapy. He reports that he initially noticed an improvement in his symptoms but the effects were transient. He has also started noticing pain and stiffness in his fingers. His past medical history is notable for obesity and diabetes mellitus. He takes metformin. His temperature is 99°F (37.2°C), blood pressure is 130/80 mmHg, pulse is 80/min, and respirations are 16/min. Multiple plaques with scaling are noted on the extensor surfaces of the upper and lower extremities. The patient’s physician suggests stopping the ultraviolet light therapy and starting an injectable medication that acts as a decoy receptor for a pro-inflammatory cytokine. Which of the following is an adverse effect associated with the use of this medication?
- A. Cushing’s syndrome
- B. Retinopathy
- C. Myelosuppression
- D. Reactivation of latent tuberculosis (Correct Answer)
- E. Nephrotoxicity
JAK inhibitors Explanation: ***Reactivation of latent tuberculosis***
- The patient's symptoms (psoriasis with associated arthralgias) suggest **psoriatic arthritis**. The physician's recommendation for an injectable medication acting as a decoy receptor for a **pro-inflammatory cytokine** refers to a **TNF-α inhibitor** (e.g., etanercept, infliximab, adalimumab).
- TNF-α inhibitors suppress the immune system, making patients susceptible to **opportunistic infections**, including the **reactivation of latent tuberculosis** (TB). Screening for latent TB is crucial before initiating these medications.
*Cushing’s syndrome*
- **Cushing's syndrome** is caused by prolonged exposure to high levels of **glucocorticoids**, either endogenous (e.g., adrenal tumors) or exogenous (e.g., long-term steroid use).
- TNF-α inhibitors do not directly cause Cushing's syndrome; they are **biologic agents** that target specific inflammatory pathways.
*Retinopathy*
- **Retinopathy** is a condition affecting the retina, often associated with systemic diseases like **diabetes** or medications such as **hydroxychloroquine**.
- TNF-α inhibitors are not typically associated with retinopathy as a direct side effect.
*Myelosuppression*
- **Myelosuppression** (bone marrow suppression) is a common adverse effect of **chemotherapeutic agents** and some immunosuppressants (e.g., methotrexate, azathioprine).
- While TNF-α inhibitors can rarely cause hematologic abnormalities, significant myelosuppression is not a characteristic or common adverse effect compared to traditional cytotoxic drugs.
*Nephrotoxicity*
- **Nephrotoxicity** refers to kidney damage caused by drugs, such as **NSAIDs**, aminoglycosides, or certain chemotherapeutic agents.
- TNF-α inhibitors are not primarily associated with nephrotoxicity as a significant adverse effect.
JAK inhibitors US Medical PG Question 4: A 38-year-old woman comes to the physician for a follow-up examination. Two years ago, she was diagnosed with multiple sclerosis. Three weeks ago, she was admitted and treated for right lower leg weakness with high-dose methylprednisone for 5 days. She has had 4 exacerbations over the past 6 months. Current medications include interferon beta and a multivitamin. Her temperature is 37°C (98.6°F), pulse is 90/min, and blood pressure is 116/74 mm Hg. Examination shows pallor of the right optic disk. Neurologic examination shows no focal findings. She is anxious about the number of exacerbations and repeated hospitalizations. She is counseled about the second-line treatment options available to her. She consents to treatment with natalizumab. However, she has read online about its adverse effects and is concerned. This patient is at increased risk for which of the following complications?
- A. Tuberculosis
- B. Syndrome of inappropriate antidiuretic hormone
- C. Parkinsonism
- D. Progressive multifocal leukoencephalopathy (Correct Answer)
- E. Aplastic anemia
JAK inhibitors Explanation: ***Progressive multifocal leukoencephalopathy***
- **Natalizumab** is a monoclonal antibody that blocks the binding of leukocytes to endothelial cells, preventing their entry into the central nervous system. This immunosuppressive effect increases the risk of **progressive multifocal leukoencephalopathy (PML)**, especially in patients who are positive for the **JC virus**.
- PML is a serious and often fatal opportunistic infection of the brain caused by the **JC virus**, which demyelinates axons and leads to severe neurological deficits.
*Tuberculosis*
- While some immunosuppressants can reactivate **latent tuberculosis**, natalizumab is not typically associated with an increased risk of TB compared to other immunomodulatory drugs like TNF-alpha inhibitors.
- The mechanism of action of natalizumab (alpha-4 integrin blocker) does not directly impede the immune response responsible for containing mycobacterial infections to the same extent as other treatments.
*Syndrome of inappropriate antidiuretic hormone*
- **SIADH** is not a known adverse effect of natalizumab.
- SIADH is characterized by excessive secretion of **antidiuretic hormone**, leading to hyponatremia, and is often associated with certain medications (e.g., SSRIs, carbamazepine) or underlying conditions like malignancy or pulmonary disease.
*Parkinsonism*
- Parkinsonism involves symptoms like **bradykinesia**, rigidity, and tremor, and is a neurodegenerative disorder.
- There is **no evidence** suggesting a causal link between natalizumab treatment and the development of Parkinsonism.
*Aplastic anemia*
- **Aplastic anemia** is a rare but severe condition where the bone marrow fails to produce blood cells.
- This adverse effect is not associated with natalizumab; it is more commonly linked to certain **chemotherapeutic agents**, radiation, or specific antimicrobial drugs like chloramphenicol.
JAK inhibitors US Medical PG Question 5: A 53-year-old man with hyperlipidemia comes to the physician for a follow-up examination. His home medications include acetaminophen and atorvastatin. Serum studies show elevated total cholesterol and triglyceride concentrations. A drug that activates the peroxisome proliferator-activated receptor alpha is added to his existing therapy. This patient is at highest risk for developing which of the following drug-related adverse effects?
- A. Reddish-brown discoloration of urine (Correct Answer)
- B. Bleeding from minor trauma
- C. Waxing and waning confusion
- D. Acutely swollen and painful joint
- E. Pruritus and flushing of the skin
JAK inhibitors Explanation: ***Reddish-brown discoloration of urine***
- This patient is likely being treated with a **fibrate**, a PPAR-alpha agonist, in addition to **atorvastatin** due to persistently elevated triglycerides.
- The combination of a fibrate and a statin increases the risk of **rhabdomyolysis**, which can cause **myoglobinuria**, leading to reddish-brown urine and potential **acute kidney injury**.
*Bleeding from minor trauma*
- This adverse effect is more characteristic of **anticoagulants** (e.g., warfarin, direct oral anticoagulants) or **antiplatelet agents** (e.g., aspirin, clopidogrel).
- Fibrates and statins do not typically cause significant bleeding diathesis.
*Waxing and waning confusion*
- This can be a symptom of various conditions, including **hepatic encephalopathy**, severe electrolyte imbalances, or delirium; it is not a common adverse effect of fibrates or statins.
- While statins can rarely cause cognitive side effects, **confusion** of this nature is not a hallmark.
*Acutely swollen and painful joint*
- This symptom strongly suggests an acute **arthritic flare**, particularly **gout**, caused by hyperuricemia.
- While some medications can induce gout (e.g., diuretics), neither fibrates nor statins are commonly associated with this adverse effect.
*Pruritus and flushing of the skin*
- These are characteristic side effects of **niacin (nicotinic acid)**, another lipid-lowering agent.
- Niacin causes prostaglandin-mediated vasodilation, leading to intense **flushing and itching**, which can be severe enough to cause medication non-adherence.
JAK inhibitors US Medical PG Question 6: A 49-year-old woman presents to her primary care doctor in late December with malaise. She reports worsening fatigue, myalgias, headache, and malaise that started 1 day ago. She works as a lunch lady at an elementary school. Her past medical history is notable for a distal radius fracture after a fall 2 years ago, but she is otherwise healthy and takes no medications. She does not smoke or drink alcohol. She is married and has 3 adult children who are healthy. Her temperature is 102.9°F (39.4°C), blood pressure is 101/61 mmHg, pulse is 112/min, and respirations are 21/min. On exam, she appears lethargic and uncomfortable but is able to answer questions appropriately. Breath sounds are normal bilaterally. She is started on intravenous fluids and a pharmacologic agent for treatment. Which of the following is the most likely mechanism of action of the drug being used to treat this patient?
- A. Neuraminidase inhibitor (Correct Answer)
- B. Reverse transcriptase inhibitor
- C. RNA-dependent polymerase inhibitor
- D. DNA polymerase inhibitor
- E. Protease inhibitor
JAK inhibitors Explanation: ***Neuraminidase inhibitor***
- The patient's symptoms (malaise, fatigue, myalgias, headache, fever) with rapid onset in **late December**, especially given her exposure to children in an elementary school, are highly suggestive of **influenza**.
- **Neuraminidase inhibitors** (e.g., oseltamivir, zanamivir) are the primary antiviral treatment for influenza, preventing the release of new viral particles from infected cells.
*Reverse transcriptase inhibitor*
- **Reverse transcriptase inhibitors** are primarily used in the treatment of **HIV infection**, which typically presents with a different constellation of symptoms and has a chronic rather than acute course.
- This class of drugs targets the enzyme **reverse transcriptase**, which is not central to the influenza virus replication cycle.
*RNA-dependent polymerase inhibitor*
- While **baloxavir marboxil** (an RNA polymerase inhibitor) is FDA-approved for influenza treatment, **neuraminidase inhibitors** remain the most commonly used first-line agents.
- In this clinical scenario without specific contraindications to neuraminidase inhibitors, oseltamivir or zanamivir would be the most likely agents prescribed.
*DNA polymerase inhibitor*
- **DNA polymerase inhibitors** are primarily used to treat **DNA viral infections** such as herpes viruses (e.g., acyclovir for HSV/VZV) or cytomegalovirus (e.g., ganciclovir).
- Influenza is an **RNA virus** and therefore does not have a DNA polymerase for replication.
*Protease inhibitor*
- **Protease inhibitors** are a class of antiviral drugs predominantly used in the treatment of **HIV** and **Hepatitis C virus** infections.
- Influenza viruses do not have a protease target that is typically inhibited by these drugs for therapeutic purposes.
JAK inhibitors US Medical PG Question 7: A 29-year-old female presents to her gynecologist complaining of a painful rash around her genitals. She has multiple sexual partners and uses condoms intermittently. Her last STD screen one year ago was negative. On examination, she has bilateral erosive vesicles on her labia majora and painful inguinal lymphadenopathy. She is started on an oral medication that requires a specific thymidine kinase for activation. Which of the following adverse effects is associated with this drug?
- A. Photosensitivity
- B. Deafness
- C. Renal failure (Correct Answer)
- D. Gingival hyperplasia
- E. Pulmonary fibrosis
JAK inhibitors Explanation: ***Renal failure***
- The patient's symptoms (painful genital rash, erosive vesicles, inguinal lymphadenopathy) are highly suggestive of **herpes simplex virus (HSV) infection**, likely genital herpes.
- The drug described is an antiviral agent like **acyclovir, valacyclovir, or famciclovir**, which require **viral thymidine kinase** for activation and are known to cause **renal impairment** (nephrotoxicity) as an adverse effect, especially with high doses or in dehydrated patients due to crystal nephropathy.
*Photosensitivity*
- **Photosensitivity** is a common side effect of some antibiotics (e.g., tetracyclines, sulfonamides), diuretics (e.g., thiazides), and antifungals, but it is **not a prominent adverse effect of acyclovir or its derivatives**.
- While theoretical, it is not a clinically significant or frequently observed adverse effect associated with the class of antiviral drugs used for HSV.
*Deafness*
- **Ototoxicity**, leading to deafness or hearing loss, is a well-known adverse effect of certain classes of drugs, such as **aminoglycoside antibiotics** (e.g., gentamicin) and **loop diuretics** (e.g., furosemide).
- It is **not an adverse effect** associated with antiviral medications like acyclovir.
*Gingival hyperplasia*
- **Gingival hyperplasia** (overgrowth of gum tissue) is a recognized side effect of specific medications including **phenytoin** (an anticonvulsant), **cyclosporine** (an immunosuppressant), and **calcium channel blockers** (e.g., nifedipine, amlodipine).
- This adverse effect is **not associated with antiviral drugs** used to treat herpes simplex.
*Pulmonary fibrosis*
- **Pulmonary fibrosis** is a serious adverse effect linked to various drugs like **amiodarone** (an antiarrhythmic), **bleomycin** (a chemotherapeutic agent), **methotrexate** (an immunosuppressant/chemotherapeutic), and **nitrofurantoin** (an antibiotic).
- **Antiviral medications for HSV** do not typically cause pulmonary fibrosis.
JAK inhibitors US Medical PG Question 8: A 61-year-old woman presents to her primary care physician complaining of left-sided facial pain that started yesterday. She describes the pain as stinging, burning, and constant. It does not worsen with jaw movement or chewing. Her past medical history includes hyperlipidemia and multiple sclerosis (MS), and she had chickenpox as a child but received a shingles vaccination last year. Medications include simvastatin and glatiramer acetate. The patient’s last MS flare was 5 weeks ago, at which time she received a prednisone burst with taper. At this visit, her temperature is 99.9 °F (37.7°C), blood pressure is 139/87 mmHg, pulse is 82/min, and respirations are 14/min. On exam, there is no rash or skin change on either side of the patient’s face. Gentle palpation of the left cheek and mandible produce significant pain, but there is full range of motion in the jaw. Which of the following medications is the most likely to prevent long-term persistence of this patient’s pain?
- A. Carbamazepine
- B. Topical corticosteroids
- C. Oral acyclovir (Correct Answer)
- D. Amitriptyline
- E. Gabapentin
JAK inhibitors Explanation: ***Oral acyclovir***
- The patient's symptoms (stinging, burning, constant facial pain, history of chickenpox, recent MS flare, and prednisone use) are highly suggestive of a **herpes zoster (shingles) reactivation**, despite prior vaccination. Early antiviral therapy, such as oral acyclovir, is crucial to reduce the duration and severity of the acute pain and, more importantly, to prevent **postherpetic neuralgia (PHN)**.
- Starting acyclovir within 72 hours of symptom onset significantly decreases the risk of developing long-term pain complications like PHN by inhibiting viral replication and reducing nerve damage.
*Carbamazepine*
- This medication is a first-line treatment for **trigeminal neuralgia**, characterized by brief, excruciating, shock-like pain triggered by specific stimuli, which differs from the patient's constant burning pain.
- While it can manage neuropathic pain, it does not address the underlying viral cause of herpes zoster and will not prevent PHN.
*Topical corticosteroids*
- Topical corticosteroids are primarily used to reduce **inflammation and itching** associated with skin rashes, such as those that may occur with herpes zoster.
- They do not possess antiviral properties and therefore will not *prevent* the long-term neurological complication of PHN.
*Amitriptyline*
- Amitriptyline, a tricyclic antidepressant, is a common treatment for **postherpetic neuralgia** once it has already developed, as well as other neuropathic pain conditions.
- However, it is not used to prevent the development of PHN in the acute phase of a herpes zoster infection; early antiviral treatment is the preventative strategy.
*Gabapentin*
- Gabapentin is an effective medication for established **neuropathic pain**, including postherpetic neuralgia.
- Similar to amitriptyline, gabapentin treats the *symptoms* of PHN once it is present but does not prevent its occurrence when used during the acute viral stage.
JAK inhibitors US Medical PG Question 9: A 25-year-old man presents to the emergency department with pain in his leg. He states that the pain was sudden and that his leg feels very tender. This has happened before, but symptoms resolved a few days later with acetaminophen. His temperature is 98.5°F (36.9°C), blood pressure is 129/88 mmHg, pulse is 90/min, respirations are 12/min, and oxygen saturation is 98% on room air. Physical exam reveals clear breath sounds bilaterally and a normal S1 and S2. The patient’s right leg is red, inflamed, and tender to palpation inferior to the popliteal fossa. Which of the following is the best treatment for this patient?
- A. Heparin (Correct Answer)
- B. Aspirin
- C. Ibuprofen and rest
- D. Clindamycin
- E. Warfarin
JAK inhibitors Explanation: ***Heparin***
- The sudden onset of leg pain, tenderness, and inflammation, especially with a history of recurrent episodes, is highly suggestive of a **deep vein thrombosis (DVT)**. The location inferior to the popliteal fossa is a common site for calf vein DVTs.
- **Heparin** (either unfractionated or low molecular weight) is the first-line treatment for acute DVT to prevent clot propagation, pulmonary embolism, and post-thrombotic syndrome.
*Aspirin*
- **Aspirin** is an antiplatelet agent used for arterial thrombosis and cardiovascular event prevention, not effective for treating acute venous thromboembolism like DVT.
- Its mechanism primarily involves inhibiting cyclooxygenase to reduce thromboxane A2, which is less relevant in the coagulation cascade implicated in DVT.
*Ibuprofen and rest*
- **Ibuprofen** is an NSAID that can reduce pain and inflammation but does not address the underlying **thrombotic process** and will not prevent complications like pulmonary embolism.
- While rest might alleviate discomfort, it is not a primary treatment for DVT and prolonged immobility can actually worsen venous stasis.
*Clindamycin*
- **Clindamycin** is an antibiotic used to treat bacterial infections; it has no role in the management of DVT, which is a vascular condition.
- There are no signs of infection in the patient's presentation that would warrant antibiotic therapy.
*Warfarin*
- **Warfarin** is an oral anticoagulant used for long-term management of DVT and other thrombotic conditions, but it has a **delayed onset of action** (several days) due to its mechanism of inhibiting vitamin K-dependent clotting factors.
- It is typically initiated concurrently with a rapid-acting anticoagulant like heparin, which provides immediate anticoagulation until warfarin reaches therapeutic levels.
JAK inhibitors US Medical PG Question 10: A 40-year-old woman presents to her primary care physician with a 2-month history of joint pain and morning stiffness that improves through the course of the day. Her left knee also sometimes bothers her. She has taken ibuprofen and Tylenol without relief, and the pain is starting to upset her daily routine. On physical examination, the joints of her fingers and wrists are swollen and tender to touch. Her left knee also feels warm. The strength in both hands is reduced but the sensation is intact. On auscultation, the heart sounds are regular and the lungs are clear. Laboratory findings are presented below:
Hemoglobin 12.7 g/dL
Hematocrit 37.5%
Leukocyte count 5,500/mm3
Mean corpuscular volume 82.2 μm3
Platelet count 190,000/mm3
Erythrocyte sedimentation rate 45 mm/h
C-reactive protein 14 mg/dL
Anti-citrullinated protein antibody 43 (normal reference values: < 20)
Which of the following is the most appropriate treatment for this patient?
- A. Methotrexate (Correct Answer)
- B. Hydroxychloroquine
- C. Infliximab
- D. Etanercept
- E. Ibuprofen
JAK inhibitors Explanation: ***Methotrexate***
- This patient presents with **symmetrical polyarthritis** (fingers, wrists, knee), **morning stiffness**, elevated **ESR and CRP**, and a **positive anti-citrullinated protein antibody**, all highly suggestive of **rheumatoid arthritis (RA)**.
- **Methotrexate** is considered the **first-line disease-modifying antirheumatic drug (DMARD)** for RA due to its efficacy in reducing joint inflammation and preventing joint damage.
*Hydroxychloroquine*
- While used in RA, **hydroxychloroquine** is generally reserved for **mild RA** or for patients who cannot tolerate methotrexate, and it is less effective for moderate to severe disease.
- This patient's symptoms are beginning to upset her daily routine, indicating more than mild disease, and she has **high inflammatory markers** (ESR 45, CRP 14) and a **positive anti-CCP antibody**, suggesting a more aggressive course.
*Infliximab*
- **Infliximab** is a biologic DMARD (TNF-alpha inhibitor) used for RA, but it is typically reserved for patients with a **suboptimal response to methotrexate** or other conventional DMARDs.
- It is not usually prescribed as a first-line treatment due to its higher cost and potential side effects compared to methotrexate.
*Etanercept*
- **Etanercept** is another biologic DMARD (TNF-alpha inhibitor) used for RA that is also typically reserved for patients who have had an **inadequate response to methotrexate** or other non-biologic DMARDs.
- Like infliximab, it is not a first-line agent, and initial management begins with conventional DMARDs.
*Ibuprofen*
- **Ibuprofen** is a **nonsteroidal anti-inflammatory drug (NSAID)** that provides symptomatic relief from pain and inflammation but does **not modify the disease course** or prevent joint damage in RA.
- The patient has already tried ibuprofen without relief, and NSAIDs are used as adjuncts to DMARDs, not as monotherapy for chronic inflammatory conditions like RA.
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