Anti-inflammatory therapies US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Anti-inflammatory therapies. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Anti-inflammatory therapies US Medical PG Question 1: A 50-year-old woman presents to the clinic with joint pain that has persisted for the last 2 months. She reports having intermittently swollen, painful hands bilaterally. She adds that when she wakes up in the morning, her hands are stiff and do not loosen up until an hour later. The pain tends to improve with movement. Physical examination is significant for warm, swollen, tender proximal interphalangeal joints, metacarpophalangeal joints, and wrists bilaterally. Laboratory results are positive for rheumatoid factor (4-fold greater than the upper limit of normal (ULN)) and anti-cyclic citrullinated peptide (anti-CCP) antibodies (3-fold greater than ULN). CRP and ESR are elevated. Plain X-rays of the hand joints show periarticular osteopenia and bony erosions. She was started on the first-line drug for her condition which inhibits dihydrofolate reductase. Which medication was this patient started on?
- A. Hydroxyurea
- B. Allopurinol
- C. Methotrexate (Correct Answer)
- D. 5-fluorouracil
- E. Leflunomide
Anti-inflammatory therapies Explanation: ***Methotrexate***
- The patient's clinical presentation (symmetrical polyarthritis, morning stiffness, elevated inflammatory markers, positive **rheumatoid factor**, and **anti-CCP antibodies**) is classic for **rheumatoid arthritis (RA)**.
- **Methotrexate** is the **first-line disease-modifying anti-rheumatic drug (DMARD)** for RA and acts by inhibiting **dihydrofolate reductase**, thereby interfering with purine and pyrimidine synthesis.
*Hydroxyurea*
- **Hydroxyurea** is an antineoplastic agent that works by inhibiting **ribonucleotide reductase**, not dihydrofolate reductase.
- It is primarily used in conditions like **myeloproliferative disorders** (e.g., chronic myeloid leukemia, polycythemia vera, essential thrombocythemia) and **sickle cell disease**, not rheumatoid arthritis.
*Allopurinol*
- **Allopurinol** is a **xanthine oxidase inhibitor** used to reduce **uric acid production** in conditions like **gout and tumor lysis syndrome**.
- It is not indicated for the treatment of rheumatoid arthritis, nor does it inhibit dihydrofolate reductase.
*5-fluorouracil*
- **5-fluorouracil** is a **pyrimidine analog** that inhibits **thymidylate synthase** (after being metabolized to 5-FdUMP), primarily used in **chemotherapy for various cancers**, especially gastrointestinal malignancies.
- It does not inhibit dihydrofolate reductase and is not used to treat rheumatoid arthritis.
*Leflunomide*
- **Leflunomide** is another DMARD used for rheumatoid arthritis, but it inhibits **dihydroorotate dehydrogenase**, an enzyme involved in *de novo pyrimidine synthesis*, not dihydrofolate reductase.
- While it is a treatment for RA, it is not the medication that acts specifically by inhibiting dihydrofolate reductase.
Anti-inflammatory therapies US Medical PG Question 2: 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)
Anti-inflammatory therapies 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.
Anti-inflammatory therapies US Medical PG Question 3: A 49-year-old man being treated for Helicobacter pylori infection presents to his primary care physician complaining of lower back pain. His physician determines that a non-steroidal anti-inflammatory drug (NSAID) would be the most appropriate initial treatment. Which of the following is the most appropriate NSAID for this patient?
- A. Aspirin
- B. Ibuprofen
- C. Celecoxib (Correct Answer)
- D. Naproxen
- E. Diclofenac
Anti-inflammatory therapies Explanation: **Celecoxib**
- This patient is being treated for a *Helicobacter pylori* infection, indicating a potential risk for **gastrointestinal complications** like ulcers. **Celecoxib** is a selective **COX-2 inhibitor**, which has a lower risk of causing GI side effects compared to non-selective NSAIDs.
- Its selective inhibition of COX-2 helps reduce pain and inflammation while largely sparing the **COX-1 enzyme**, which is responsible for maintaining the **gastric mucosal lining**.
*Aspirin*
- **Aspirin** is a non-selective NSAID that inhibits both **COX-1** and **COX-2** enzymes.
- Inhibition of COX-1 can lead to a significant increase in the risk of **gastrointestinal bleeding** and **ulcer formation**, which is particularly concerning for a patient with an *H. pylori* infection.
*Ibuprofen*
- **Ibuprofen** is a non-selective NSAID that can cause **gastrointestinal irritation** and damage by inhibiting **COX-1**.
- Its use would increase the risk of worsening the patient's existing **gastrointestinal vulnerability** due to the *H. pylori* infection.
*Naproxen*
- **Naproxen** is another non-selective NSAID with a relatively long half-life, making its **gastrointestinal side effects** potentially more prolonged and severe than some other non-selective NSAIDs.
- It carries a **higher risk for GI bleeding** and ulcers compared to selective COX-2 inhibitors, especially in patients with pre-existing GI issues.
*Diclofenac*
- **Diclofenac** is a non-selective NSAID that carries a risk of **gastrointestinal adverse events**, although some studies suggest it might have a slightly better GI safety profile than other non-selective NSAIDs at lower doses.
- However, in a patient with *H. pylori*, it still poses a significant risk for **ulcers** and bleeding compared to a COX-2 selective inhibitor.
Anti-inflammatory therapies US Medical PG Question 4: A 61-year-old woman comes to the physician because of a 6-month history of left knee pain and stiffness. Examination of the left knee shows tenderness to palpation along the joint line; there is crepitus with full flexion and extension. An x-ray of the knee shows osteophytes with joint-space narrowing. Arthrocentesis of the knee joint yields clear fluid with a leukocyte count of 120/mm3. Treatment with ibuprofen during the next week significantly improves her condition. The beneficial effect of this drug is most likely due to inhibition of which of the following?
- A. Conversion of hypoxanthine to urate
- B. Conversion of phospholipids to arachidonic acid
- C. Conversion of prostaglandin H2 to thromboxane A2
- D. Conversion of arachidonic acid to prostaglandin G2 (Correct Answer)
- E. Conversion of dihydroorotate to orotate
Anti-inflammatory therapies Explanation: ***Conversion of arachidonic acid to prostaglandin G2***
- This patient presents with symptoms and signs consistent with **osteoarthritis**, characterized by joint pain, stiffness, crepitus, and radiographic findings like **osteophytes** and **joint-space narrowing**.
- **Ibuprofen is a non-selective NSAID** that inhibits **cyclooxygenase (COX-1 and COX-2) enzymes**, which catalyze the conversion of **arachidonic acid to prostaglandin G2 (PGG2)**, the first committed step in prostaglandin synthesis.
- By blocking prostaglandin production, ibuprofen reduces inflammation and pain associated with osteoarthritis.
*Conversion of hypoxanthine to urate*
- This process is catalyzed by **xanthine oxidase** and is inhibited by medications like **allopurinol**, used in the treatment of **gout** to reduce uric acid levels.
- Gout typically presents with acute, severe joint pain with signs of inflammation and monosodium urate crystals on joint aspiration, which are not characteristic of this patient's presentation.
*Conversion of phospholipids to arachidonic acid*
- This step is catalyzed by **phospholipase A2**, which is inhibited by **glucocorticoids** (via lipocortin induction).
- While glucocorticoids have potent anti-inflammatory effects by working upstream of the arachidonic acid cascade, ibuprofen has a different mechanism targeting the COX enzymes downstream.
*Conversion of prostaglandin H2 to thromboxane A2*
- This reaction is catalyzed by **thromboxane synthase**, primarily important in platelet aggregation and vasoconstriction.
- NSAIDs like ibuprofen do not specifically inhibit thromboxane synthase; rather, they inhibit COX enzymes upstream, which reduces production of both prostaglandins and thromboxanes.
- Low-dose aspirin preferentially inhibits COX-1 in platelets, reducing thromboxane A2 for cardioprotection, but this is not ibuprofen's primary therapeutic mechanism in osteoarthritis.
*Conversion of dihydroorotate to orotate*
- This is a step in **pyrimidine synthesis**, inhibited by **leflunomide**, a disease-modifying antirheumatic drug (DMARD) used in rheumatoid arthritis.
- This mechanism is unrelated to the action of NSAIDs or the treatment of osteoarthritis.
Anti-inflammatory therapies US Medical PG Question 5: 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
Anti-inflammatory therapies 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.
Anti-inflammatory therapies US Medical PG Question 6: A 59-year-old male with a 1-year history of bilateral knee arthritis presents with epigastric pain that intensifies with meals. He has been self-medicating with aspirin, taking up to 2,000 mg per day for the past six months. Which of the following medications, if taken instead of aspirin, could have minimized his risk of experiencing this epigastric pain?
- A. Naproxen
- B. Celecoxib (Correct Answer)
- C. Indomethacin
- D. Ibuprofen
- E. Ketorolac
Anti-inflammatory therapies Explanation: ***Celecoxib***
- **Celecoxib** is a selective **COX-2 inhibitor**, which preferentially inhibits the COX-2 enzyme responsible for inflammation and pain, while largely sparing COX-1.
- Sparing **COX-1** reduces the inhibition of **prostaglandins** that protect the gastric mucosa, thereby lowering the risk of GI side effects like epigastric pain and ulcers compared to non-selective NSAIDs.
*Naproxen*
- **Naproxen** is a **non-selective NSAID** that inhibits both COX-1 and COX-2 enzymes.
- Inhibition of **COX-1** interferes with the production of protective prostaglandins in the stomach, increasing the risk of gastrointestinal adverse effects such as epigastric pain, ulcers, and bleeding, similar to aspirin.
*Indomethacin*
- **Indomethacin** is a potent **non-selective NSAID** with significant inhibition of both COX-1 and COX-2.
- Its strong **COX-1 inhibition** makes it particularly prone to causing gastrointestinal side effects including severe epigastric pain, nausea, and dyspepsia.
*Ibuprofen*
- **Ibuprofen** is a **non-selective NSAID** commonly used for pain and inflammation that inhibits both COX-1 and COX-2 enzymes.
- Although generally better tolerated than indomethacin or high-dose aspirin, it still carries a dose-dependent risk of **GI adverse effects** due to COX-1 inhibition.
*Ketorolac*
- **Ketorolac** is a potent **non-selective NSAID** primarily used for short-term management of acute moderate to severe pain.
- It has a high risk of **gastrointestinal complications**, including gastric ulcers and bleeding, making it unsuitable for long-term use and not a safer alternative to aspirin in terms of GI risk.
Anti-inflammatory therapies US Medical PG Question 7: A 64-year-old woman is brought to the emergency department because of a 1-week history of progressive shortness of breath, lower extremity edema, and a 4-kg (9-lb) weight gain. She has ischemic cardiomyopathy and rheumatoid arthritis. Her respirations are 27/min. Examination shows pitting edema of the lower extremities and crackles over both lower lung fields. Therapy is initiated with intravenous furosemide. After 2 hours, urine output is minimal. Concomitant treatment with which of the following drugs is most likely to have contributed to treatment failure?
- A. Sulfasalazine
- B. Digoxin
- C. Prednisone
- D. Infliximab
- E. Diclofenac (Correct Answer)
Anti-inflammatory therapies Explanation: ***Diclofenac***
- **NSAIDs** like diclofenac can cause **sodium and water retention** and reduce the effectiveness of loop diuretics like furosemide by inhibiting prostaglandin synthesis in the kidneys.
- This patient's symptoms of **heart failure exacerbation** (shortness of breath, edema, weight gain, crackles) and minimal urine output despite furosemide suggest drug-induced diuretic resistance.
*Sulfasalazine*
- This drug is used for **rheumatoid arthritis** and inflammatory bowel disease, but it does not typically interfere with diuretic action or cause fluid retention.
- Its mechanism involves anti-inflammatory properties, not directly affecting renal hemodynamics or diuretic efficacy.
*Digoxin*
- Digoxin is used to improve **cardiac contractility** and does not directly cause fluid retention or diminish the effects of loop diuretics.
- While it has a narrow therapeutic index, it does not antagonize furosemide's action.
*Prednisone*
- Prednisone is a **corticosteroid** that can cause **fluid retention** due to its mineralocorticoid effects, but it is not known to directly inhibit the action of loop diuretics to this extent.
- Its use in rheumatoid arthritis would primarily suppress inflammation, not directly cause diuretic resistance in acute heart failure.
*Infliximab*
- Infliximab is a **TNF-alpha inhibitor** used in rheumatoid arthritis; it can rarely exacerbate heart failure by its mechanism of action but does not directly interfere with the efficacy of loop diuretics.
- It does not cause fluid retention through renal mechanisms or reduce the renal response to furosemide.
Anti-inflammatory therapies US Medical PG Question 8: A 23-year-old woman comes to the office because of a 2-day history of right knee pain. She says, "I can't run anymore because my knee hurts." The pain is localized "somewhere under the kneecap" and is achy, rated 5/10, but increases to 8/10 with prolonged sitting. She reports an occasional "popping" sound and sensation when she rises from a seated position. She has no history of trauma to the knee. She had a right clavicular fracture 2 years ago that was treated with a shoulder sling. She takes a daily multivitamin and has no known drug allergies. She does not smoke and drinks up to three glasses of wine weekly.
Vital signs: Temperature 37°C (98.6°F), pulse 65/min, respirations 15/min, blood pressure 108/62 mm Hg. Height 173 cm (5 ft 8 in), weight 54 kg (119 lb), BMI 18 kg/m².
Physical examination shows no acute distress. Pulmonary examination shows lungs clear to auscultation. Cardiac examination shows regular rate and rhythm with normal S1 and S2; no murmurs, rubs, or gallops. The abdomen is thin with no tenderness, guarding, masses, bruits, or hepatosplenomegaly. Extremities show no joint erythema, edema, or warmth; dorsalis pedis, radial, and femoral pulses are intact. Musculoskeletal examination shows diffuse tenderness to palpation over the right anterior knee, worse with full extension of the knee; no associated effusion or erythema; full, symmetric strength of quadriceps, hip abductors, and hip external rotators; crepitus with knee range of motion; and antalgic gait. Neurologic examination shows the patient is alert and oriented with cranial nerves grossly intact and no focal neurologic deficits.
Which of the following is the most appropriate next step in management?
- A. Physical therapy (Correct Answer)
- B. Pain control and rest
- C. Synovial fluid analysis
- D. Intraarticular steroid injection
- E. Arthroscopy of the knee
Anti-inflammatory therapies Explanation: ***Physical therapy***
- This patient presents with symptoms highly suggestive of **patellofemoral pain syndrome (PFPS)**, including anterior knee pain, pain worse with prolonged sitting and activity, and crepitus. **Physical therapy** focusing on quadriceps strengthening, hip abductor strengthening, and core stability is the cornerstone of PFPS management.
- PFPS is often related to **biomechanical imbalances** and muscle weakness (e.g., weak vastus medialis obliquus or hip abductors), which can be effectively addressed through a structured physical therapy program.
*Pain control and rest*
- While **rest** can temporarily alleviate symptoms, it does not address the underlying biomechanical issues contributing to PFPS and can lead to **deconditioning**, potentially worsening the condition in the long term.
- **Pain control**, often with NSAIDs, can be used adjunctively, but it is not the primary or sole management strategy for PFPS as it also does not address the root cause.
*Synovial fluid analysis*
- **Synovial fluid analysis** is indicated for suspected inflammatory or infectious arthritis, which is not suggested by this patient's presentation of an atraumatic, "achy" pain without signs of inflammation (e.g., warmth, effusion, erythema).
- The patient's symptoms are more consistent with a **mechanical issue** rather than an intra-articular pathology requiring fluid analysis.
*Intraarticular steroid injection*
- **Intraarticular steroid injections** are generally not recommended for PFPS as the condition is typically not inflammatory within the joint space itself, but rather an issue of patellar tracking or soft tissue irritation.
- Steroid injections carry risks and provide only **temporary symptom relief** for inflammatory conditions, and their efficacy in PFPS is limited.
*Arthroscopy of the knee*
- **Arthroscopy** is an invasive surgical procedure and is typically reserved for cases where conservative management has failed, or when there is suspicion of a specific intra-articular lesion like a meniscal tear or loose body, which are not indicated here.
- This patient's symptoms are classic for PFPS, which is a **non-surgical condition** in the first line of management.
Anti-inflammatory therapies US Medical PG Question 9: A 36-year-old woman presents with thyroid swelling. She has been healthy until now and follows all the healthcare precautions except for missing a flu shot this year. On physical examination, the thyroid gland is diffusely enlarged and tender to palpation. Laboratory findings show a decreased serum TSH level and elevated erythrocyte sedimentation rate. Which of the following histopathologic findings would most likely be found in the thyroid gland of this patient?
- A. Extensive fibrosis of the stroma
- B. Mixed cellular infiltration with multinuclear giant cells (Correct Answer)
- C. Lymphocytic infiltration with germinal centers
- D. Orphan Annie nuclei with psammoma bodies
- E. Sheets of polygonal cells in amyloid stroma
Anti-inflammatory therapies Explanation: ***Mixed cellular infiltration with multinuclear giant cells***
- The patient's symptoms of a **diffusely enlarged and tender thyroid**, suppressed **TSH**, elevated **ESR**, and a recent viral illness (missing flu shot) are classic for **subacute granulomatous (De Quervain's) thyroiditis**.
- Histopathologically, this condition is characterized by a **disruptive inflammatory infiltrate** with **multinucleated giant cells** engulfing colloid, surrounded by granulomatous inflammation.
*Extensive fibrosis of the stroma*
- This finding is characteristic of **Riedel's thyroiditis**, a rare form of chronic thyroiditis.
- Riedel's thyroiditis typically presents as a **hard, fixed, and painless goiter**, often leading to compressive symptoms, which does not match this patient's tender goiter.
*Lymphocytic infiltration with germinal centers*
- This pattern is typical of **Hashimoto's thyroiditis**, an **autoimmune thyroid disease**.
- Hashimoto's usually presents with a **painless goiter** and often leads to **hypothyroidism**, not the tender, hyperthyroid-like state seen here.
*Orphan Annie nuclei with psammoma bodies*
- These are hallmark features associated with **papillary thyroid carcinoma**.
- This patient's acute presentation with **tenderness, inflammation**, and temporary hyperthyroidism is inconsistent with a malignant thyroid neoplasm.
*Sheets of polygonal cells in amyloid stroma*
- This describes the histopathology of **medullary thyroid carcinoma**.
- Medullary thyroid carcinoma arises from parafollicular C-cells and is characterized by the production of **calcitonin** and often has a genetic predisposition, which is not suggested by the patient's presentation.
Anti-inflammatory therapies US Medical PG Question 10: A 33-year-old Caucasian female presents to her primary care provider for skin problems and difficulty breathing. She has not sought medical care in over 10 years due to anxiety around physicians. However, she has experienced gradual onset of diffuse pruritus, skin induration, and limited finger mobility over the past 5 years that has negatively impacted her work as an accountant. More recently, she has developed exertional shortness of breath and is concerned that it may impact her ability to care for her 3-year-old son. She reports no prior medical conditions and takes fish oil. She smokes 1 pack of cigarettes per day and drinks socially. Her temperature is 98.6°F (37°C), blood pressure is 145/85 mmHg, pulse is 85/min, and respirations are 22/min. On exam, she appears anxious with minimally increased work of breathing. Dry rales are heard at her lung bases bilaterally. Her fingers appear shiny and do not have wrinkles on the skin folds. A normal S1 and S2 are heard on cardiac auscultation. This patient’s lung disease is caused by increased secretion of which of the following substances within the lungs?
- A. Interleukin 1
- B. Tumor necrosis factor alpha
- C. Interleukin 2
- D. Transforming growth factor beta (Correct Answer)
- E. Interferon gamma
Anti-inflammatory therapies Explanation: ***Transforming growth factor beta***
- The patient's symptoms of **diffuse pruritus, skin induration, limited finger mobility**, exertional shortness of breath, and **shiny fingers without wrinkles** are highly suggestive of **systemic sclerosis (scleroderma)**.
- The lung disease in scleroderma, often **interstitial lung disease (ILD)**, is characterized by **fibrosis driven by excessive collagen deposition**, a process significantly mediated by **transforming growth factor beta (TGF-β)**.
*Interleukin 1*
- **Interleukin-1 (IL-1)** is a pro-inflammatory cytokine primarily involved in acute inflammation and fever, not directly implicated as the primary driver of fibrosis in scleroderma-associated lung disease.
- While IL-1 can contribute to inflammation in various autoimmune diseases, it does not directly stimulate the **fibrotic pathways** in the same manner as TGF-β.
*Tumor necrosis factor alpha*
- **Tumor necrosis factor-alpha (TNF-α)** is a prominent pro-inflammatory cytokine involved in many autoimmune and inflammatory conditions, including rheumatoid arthritis.
- Although it plays a role in the inflammatory process, TNF-α is not considered the primary mediator responsible for the **fibrotic changes** seen in systemic sclerosis.
*Interleukin 2*
- **Interleukin-2 (IL-2)** is crucial for the proliferation and differentiation of T cells, particularly regulatory T cells, and is primarily involved in immune regulation and response to infection.
- Its direct role in the **pathogenesis of fibrosis** in the context of scleroderma-associated lung disease is not as central as that of TGF-β.
*Interferon gamma*
- **Interferon-gamma (IFN-γ)** is a cytokine predominantly associated with anti-viral responses and the activation of macrophages and natural killer cells in cell-mediated immunity.
- While it has immunomodulatory effects, IFN-γ is generally considered to have **anti-fibrotic properties** in some contexts, rather than promoting fibrosis in scleroderma.
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