DMARDs and biologic therapies US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for DMARDs and biologic therapies. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
DMARDs and biologic therapies US Medical PG Question 1: Two separate investigators have conducted cohort studies to calculate the risk of lymphoma in rheumatoid arthritis patients taking anti-TNF alpha medications. They each followed patients with rheumatoid arthritis for a number of years and tracked the number of patients who were diagnosed with lymphoma. The results of the two studies are summarized in the table.
Number of patients Follow-up period Number of new cases of lymphoma
Study 1 3000 10 years 30
Study 2 300 30 years 9
Based on these results, which of the following statements about the risk of lymphoma is most accurate?
- A. The risk is higher in study 1, with an incidence rate of 30 cases per 10 person-years
- B. The risks are equivalent, with a prevalence of 39 cases per 3300 persons
- C. The risks are equivalent, with an incidence rate of 1 case per 1000 person-years (Correct Answer)
- D. The risk is higher in study 1, with a prevalence of 30 cases per 3000 patients
- E. The risk is higher in study 2, with a cumulative incidence of 9 cases per 300 patients
DMARDs and biologic therapies Explanation: **The risks are equivalent, with an incidence rate of 1 case per 1000 person-years**
- To calculate the **incidence rate**, divide the number of new cases by the total person-time at risk.
- For Study 1: 30 cases / (3000 persons × 10 years) = 30 / 30,000 = 0.001 cases per person-year, or **1 case per 1000 person-years**.
- For Study 2: 9 cases / (300 persons × 30 years) = 9 / 9,000 = 0.001 cases per person-year, or **1 case per 1000 person-years**.
- Both studies yield the same incidence rate, indicating equivalent risk.
*The risk is higher in study 1, with an incidence rate of 30 cases per 10 person-years*
- The calculation "30 cases per 10 person-years" incorrectly uses the follow-up period instead of the total person-time at risk across all participants.
- This calculation does not accurately reflect the **incidence rate** as it doesn't account for the number of individuals in the study.
*The risks are equivalent, with a prevalence of 39 cases per 3300 persons*
- **Prevalence** refers to existing cases at a specific point in time, not new cases over a period.
- This calculation incorrectly combines data from two separate studies as if it were a single point prevalence, which is methodologically incorrect.
*The risk is higher in study 1, with a prevalence of 30 cases per 3000 patients*
- This statement uses a calculation that resembles **cumulative incidence** (new cases divided by initial population) for Study 1, but incorrectly labels it as prevalence.
- A cumulative incidence of 30/3000 = 0.01 (or 1%) for Study 1 does not account for the duration of follow-up, making direct comparison with Study 2 (which has a 30-year follow-up) inappropriate.
*The risk is higher in study 2, with a cumulative incidence of 9 cases per 300 patients*
- Study 2 has a **cumulative incidence** of 9/300 = 0.03 (or 3%) over 30 years.
- Comparing cumulative incidence directly between studies with different follow-up durations (10 years vs. 30 years) is not appropriate for assessing the underlying risk rate, as it does not account for the time component.
DMARDs and biologic therapies US Medical PG Question 2: A 33-year-old woman with a history of multiple sclerosis is brought to the physician because of dizziness, urinary incontinence, loss of vision in her right eye, and numbness and weakness of the left leg. She has had recurrent episodes of neurological symptoms despite several changes in her medication regimen. An MRI of the brain shows several new enhancing lesions in the periventricular white matter and the brainstem. Treatment with a drug that binds to CD52 is initiated. Which of the following agents was most likely prescribed?
- A. Alemtuzumab (Correct Answer)
- B. Eculizumab
- C. Abciximab
- D. Rituximab
- E. Bevacizumab
DMARDs and biologic therapies Explanation: ***Alemtuzumab***
- **Alemtuzumab** is a monoclonal antibody that targets **CD52**, a glycoprotein found on the surface of mature lymphocytes (T and B cells), monocytes, and macrophages, leading to their depletion.
- It is used in **highly active relapsing-remitting multiple sclerosis (RRMS)**, especially when other disease-modifying therapies have failed, which aligns with the patient's history of recurrent neurological symptoms and new enhancing lesions.
*Eculizumab*
- **Eculizumab** targets the **C5 complement protein** and is used for conditions like **paroxysmal nocturnal hemoglobinuria** and **atypical hemolytic uremic syndrome**, not multiple sclerosis.
- It works by inhibiting the complement cascade, which is not the primary mechanism of action for MS treatment involving lymphocyte depletion.
*Abciximab*
- **Abciximab** is a **glycoprotein IIb/IIIa inhibitor** that prevents platelet aggregation and is used as an antiplatelet agent in acute coronary syndromes and percutaneous coronary intervention.
- Its mechanism of action and primary indication are unrelated to the immunological processes involved in multiple sclerosis.
*Rituximab*
- **Rituximab** targets **CD20** on B cells and is used in conditions like **non-Hodgkin lymphoma**, **chronic lymphocytic leukemia**, and certain autoimmune diseases like **rheumatoid arthritis** and **vasculitis**.
- While it's a B-cell depleting agent and has shown efficacy in MS, the question specifically asks for a drug that binds to **CD52**, not CD20.
*Bevacizumab*
- **Bevacizumab** is an anti-VEGF antibody that inhibits **angiogenesis** and is primarily used in the treatment of various cancers, such as colorectal, lung, and renal cell carcinoma.
- Its mechanism of action involving inhibition of vascular endothelial growth factor (VEGF) is not indicated for the management of multiple sclerosis.
DMARDs and biologic therapies US Medical PG Question 3: A 34-year-old male comes to his family physician with complaints of joint pain that has been present for over 7 weeks. Prior to the onset of his arthritis, he recalls having a gastrointestinal infection which caused mild diarrhea and abdominal cramps. He recovered well and had no issues until his joint pain started. A prescription for naproxen was previously prescribed but he still does not feel well. He has no significant past medical or family history. On physical examination, his blood pressure is 120/78 mm Hg, respirations are 17/min, pulse is 64/min, and temperature is 36.7°C (98.0°F). Which of the following therapies is likely to be most beneficial in treating this patient’s condition?
- A. Ketoprofen
- B. Ceftriaxone
- C. Sulfasalazine (Correct Answer)
- D. Methotrexate
- E. Diclofenac
DMARDs and biologic therapies Explanation: ***Sulfasalazine***
- This patient presents with symptoms highly suggestive of **reactive arthritis**, characterized by **post-infectious arthritis** (following gastrointestinal infection and inadequate response to NSAIDs like naproxen).
- **Sulfasalazine** is an effective **disease-modifying antirheumatic drug (DMARD)** often used in reactive arthritis, particularly when NSAIDs are insufficient.
*Ketoprofen*
- Ketoprofen is another **NSAID**, similar to the naproxen that the patient has already tried and found ineffective.
- While NSAIDs are first-line for symptomatic relief, continuing with another NSAID when the first one failed is unlikely to provide sustained benefit, indicating the need for a **DMARD**.
*Ceftriaxone*
- Ceftriaxone is an **antibiotic** used to treat active bacterial infections.
- Reactive arthritis is a **sterile arthritis** that occurs *after* an infection has resolved, so antibiotics are not indicated and will not treat the joint inflammation.
*Methotrexate*
- Methotrexate is a potent **DMARD** used for various inflammatory arthritides.
- While effective, **sulfasalazine** is generally preferred as an initial DMARD for reactive arthritis, especially in cases where peripheral arthritis predominates, before escalating to more potent agents like methotrexate.
*Diclofenac*
- Diclofenac is also an **NSAID**, falling into the same class of medication as naproxen and ketoprofen.
- As the patient's symptoms persisted despite a trial of naproxen, another NSAID is unlikely to be a more beneficial long-term solution.
DMARDs and biologic therapies US Medical PG Question 4: A 49-year-old woman comes to the physician because of a 4-month history of fatigue and recurrent pain in both of her wrists and her fingers. During this time, she has also had stiffness of her joints for about 80 minutes after waking up in the morning. Examination shows swelling and tenderness of the wrists and metacarpophalangeal joints bilaterally. Her serum erythrocyte sedimentation rate is 42 mm/h and rheumatoid factor is positive. Treatment is begun with a drug that results in decreased synthesis of deoxythymidine monophosphate. This mechanism is most similar to the mechanism of action of which of the following drugs?
- A. Trimethoprim (Correct Answer)
- B. Gentamicin
- C. Sulfamethoxazole
- D. Doxycycline
- E. Azithromycin
DMARDs and biologic therapies Explanation: ***Trimethoprim***
- The patient has **rheumatoid arthritis** being treated with **methotrexate**, which inhibits **dihydrofolate reductase** leading to decreased **deoxythymidine monophosphate (dTMP)** synthesis
- **Trimethoprim** also inhibits **dihydrofolate reductase** in bacteria, targeting the same enzyme in the folate metabolism pathway as methotrexate
- This makes their mechanisms of action most similar among the options provided
*Gentamicin*
- Aminoglycoside antibiotic that inhibits bacterial protein synthesis by irreversibly binding to the **30S ribosomal subunit**
- Mechanism is entirely different from inhibition of dTMP synthesis
*Sulfamethoxazole*
- Sulfonamide antibiotic that inhibits bacterial **dihydropteroate synthase** by competing with para-aminobenzoic acid (PABA)
- While it targets the folate pathway, it acts **earlier** in the pathway than trimethoprim or methotrexate (before dihydrofolate reductase)
*Doxycycline*
- Tetracycline antibiotic that inhibits bacterial protein synthesis by reversibly binding to the **30S ribosomal subunit**
- Does not involve the folate pathway or dTMP synthesis
*Azithromycin*
- Macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**
- Unrelated to dTMP synthesis or folate metabolism
DMARDs and biologic 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
DMARDs and biologic 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.
DMARDs and biologic therapies US Medical PG Question 6: A 28-year-old woman with a history of migraines presents to your office due to sudden loss of vision in her left eye and difficulty speaking. Two weeks ago she experienced muscle aches, fever, and cough. Her muscle aches are improving but she continues to have a cough. She also feels as though she has been more tired than usual. She had a similar episode of vision loss 2 years ago and had an MRI at that time. She has a family history of migraines and takes propranolol daily. On swinging light test there is decreased constriction of the left pupil relative to the right pupil. You repeat the MRI and note enhancing lesions in the left optic nerve. Which of the following is used to prevent progression of this condition?
- A. Dexamethasone
- B. Infliximab
- C. Methotrexate
- D. Adalimumab
- E. Natalizumab (Correct Answer)
DMARDs and biologic therapies Explanation: ***Natalizumab***
- This patient's presentation with recurrent optic neuritis, fatigue, and enhancing lesions on MRI, combined with a history of similar episodes, strongly suggests **multiple sclerosis (MS)**. Natalizumab is a **monoclonal antibody** that blocks the migration of lymphocytes across the blood-brain barrier, effectively preventing disease progression in MS.
- It is a **highly effective disease-modifying therapy** for relapsing-remitting MS (RRMS) and is often used in patients who have failed other first-line treatments due to its efficacy in reducing relapse rates and preventing new lesions.
*Dexamethasone*
- While **corticosteroids** like dexamethasone are used to treat **acute exacerbations** or relapses in MS by reducing inflammation, they do not prevent long-term disease progression.
- Its primary role is to **shorten the duration and severity of an acute attack**, rather than to modify the underlying disease course.
*Infliximab*
- Infliximab is an **anti-TNF-α biologic agent** primarily used in the treatment of **inflammatory bowel disease** (Crohn's disease, ulcerative colitis), rheumatoid arthritis, and other autoimmune conditions.
- It is **contraindicated in MS** as it has been shown to worsen the disease and even induce demyelination in some patients.
*Methotrexate*
- Methotrexate is an **immunosuppressant** and **chemotherapeutic agent** used in conditions like rheumatoid arthritis, psoriasis, and certain cancers.
- It is **not a primary treatment for MS** and has limited to no role in preventing its progression.
*Adalimumab*
- Adalimumab is another **anti-TNF-α agent** similar to infliximab, used for conditions such as rheumatoid arthritis, psoriatic arthritis, and inflammatory bowel disease.
- Like infliximab, **TNF-α blockers are generally avoided in MS** due to concerns about exacerbating the disease.
DMARDs and biologic therapies US Medical PG Question 7: A 68-year-old woman comes to the physician for a follow-up examination. Three months ago, she underwent heart transplantation for restrictive cardiomyopathy and was started on transplant rejection prophylaxis. Her pulse is 76/min and blood pressure is 148/82 mm Hg. Physical examination shows enlargement of the gum tissue. There is a well-healed scar on her chest. Serum studies show hyperlipidemia. The physician recommends removing a drug that decreases T cell activation by inhibiting the transcription of interleukin-2 from the patient's treatment regimen and replacing it with a different medication. Which of the following drugs is the most likely cause of the adverse effects seen in this patient?
- A. Mycophenolate mofetil
- B. Azathioprine
- C. Tacrolimus
- D. Cyclosporine (Correct Answer)
- E. Prednisolone
DMARDs and biologic therapies Explanation: ***Cyclosporine***
- The patient's symptoms of **gingival hyperplasia**, **hypertension**, and **hyperlipidemia** are classic side effects associated with cyclosporine.
- Cyclosporine is a calcineurin inhibitor that **decreases T-cell activation** by inhibiting IL-2 transcription, matching the drug description.
*Mycophenolate mofetil*
- Mycophenolate mofetil is an **antiproliferative agent** that inhibits purine synthesis, primarily affecting lymphocytes.
- Its common side effects are mainly **hematologic** (leukopenia, anemia) and **gastrointestinal** (diarrhea, nausea), not gingival hyperplasia or hypertension.
*Azathioprine*
- Azathioprine is a **purine analog** that impairs DNA synthesis and inhibits lymphocyte proliferation.
- Key side effects include **myelosuppression** (leukopenia, thrombocytopenia) and **hepatotoxicity**, which are not present here.
*Tacrolimus*
- Tacrolimus is also a **calcineurin inhibitor** that inhibits IL-2 transcription, similar to cyclosporine.
- While it can cause **hypertension** and **hyperlipidemia**, it is less commonly associated with **gingival hyperplasia** than cyclosporine.
*Prednisolone*
- Prednisolone is a **corticosteroid** used for immunosuppression, acting broadly on the immune system.
- Common side effects include **hyperglycemia**, **osteoporosis**, and **cataracts**, not specific gingival overgrowth.
DMARDs and biologic therapies US Medical PG Question 8: A 53-year-old woman presents to her primary care physician with complaints of pain and swelling in her hands and fingers. She states that she has had these symptoms since she was in her 20s, but they have recently become more severe. She states that her wedding ring no longer fits, due to increased swelling of her fingers. She is a 30-pack-year smoker with a body mass index (BMI) of 31 kg/m2. The vital signs include: blood pressure 122/78 mm Hg, heart rate 72/min, and respiratory rate 15/min. On physical exam, a mild systolic murmur is heard over the apex, and her lungs are clear bilaterally. There is swelling of all the digits bilaterally, and a yellow-white plaque is noted beneath 3 of her nail beds. When asked about the plaques, she states that she was given itraconazole for them about 3 weeks ago; however, the plaques did not resolve. When asked further about joint pain, she notes that she has had shoulder and knee pain for the last several years, although she has not sought medical care for this. Which of the following is the best initial step in this patient’s therapeutic management?
- A. Administer methotrexate
- B. Administer indomethacin
- C. Administer indomethacin and methotrexate (Correct Answer)
- D. Administer sulfasalazine
- E. Administer indomethacin and sulfasalazine
DMARDs and biologic therapies Explanation: ***Administer indomethacin and methotrexate***
- This patient presents with symptoms highly suggestive of **psoriatic arthritis**, including typical joint pain distribution (hands, fingers, shoulders, knees), **dactylitis** (swelling of all digits causing the wedding ring to no longer fit), and **nail lesions** (yellow-white plaques unresponsive to antifungals).
- Given the patient's severe and chronic symptoms, a **combination of a non-steroidal anti-inflammatory drug (NSAID) like indomethacin for symptomatic relief and a disease-modifying anti-rheumatic drug (DMARD) like methotrexate** is the most appropriate initial therapy to control inflammation and prevent joint damage.
*Administer methotrexate*
- While **methotrexate** is a cornerstone DMARD for psoriatic arthritis, it takes several weeks to exert its full therapeutic effects.
- Administering methotrexate alone would not provide immediate relief for the patient's significant pain and swelling.
*Administer indomethacin*
- **Indomethacin**, an NSAID, would provide symptomatic relief from pain and inflammation.
- However, NSAIDs alone do not modify the disease course or prevent joint damage in psoriatic arthritis; therefore, it is an insufficient long-term monotherapy.
*Administer sulfasalazine*
- **Sulfasalazine** is an alternative DMARD used in psoriatic arthritis, often considered for patients who cannot tolerate methotrexate or for milder forms, especially with peripheral arthritis.
- However, for a patient with severe, chronic, and potentially erosive disease suggested by long-standing symptoms and diffuse dactylitis, **methotrexate is generally preferred due to its stronger efficacy profile** as an initial DMARD for psoriatic arthritis if no contraindications exist.
*Administer indomethacin and sulfasalazine*
- This combination provides short-term symptomatic relief (indomethacin) and long-term disease modification (sulfasalazine).
- While a valid option, **methotrexate is generally considered the first-line DMARD for psoriatic arthritis**, especially in severe cases, due to its greater efficacy in controlling both skin and joint manifestations compared to sulfasalazine.
DMARDs and biologic therapies US Medical PG Question 9: A 53-year-old woman presents to her primary care provider complaining of fatigue for the last several months. She reports feeling tired all day, regardless of her quality or quantity of sleep. On further questioning, she has also noted constipation and a 4.5 kg (10 lb) weight gain. She denies shortness of breath, chest pain, lightheadedness, or blood in her stool. At the doctor’s office, the vital signs include: pulse 58/min, blood pressure 104/68 mm Hg, and oxygen saturation 98% on room air. The physical exam shows only slightly dry skin. The complete blood count (CBC) is within normal limits. Which of the following best describes the pathogenesis of this patient's condition?
- A. Chronic blood loss
- B. Bone marrow failure
- C. Autoimmune attack on endocrine tissue (Correct Answer)
- D. Nutritional deficiency
- E. Iatrogenesis
DMARDs and biologic therapies Explanation: ***Autoimmune attack on endocrine tissue***
- The patient's symptoms of **fatigue**, **constipation**, **weight gain**, **bradycardia**, and dry skin are classic signs of **hypothyroidism**.
- The most common cause of hypothyroidism in developed countries is **Hashimoto's thyroiditis**, an **autoimmune disease** where the immune system attacks the thyroid gland (endocrine tissue).
*Chronic blood loss*
- This typically leads to **iron deficiency anemia**, which would likely manifest as a **low hemoglobin** or hematocrit on the CBC.
- While fatigue can be a symptom, constipation and weight gain are not typical presentations of chronic blood loss, and the CBC is within normal limits.
*Bone marrow failure*
- Bone marrow failure would result in **pancytopenia** (low red blood cells, white blood cells, and platelets), which would be evident on the CBC.
- The patient's CBC is normal, ruling out this condition as the primary cause of her symptoms.
*Nutritional deficiency*
- While certain nutritional deficiencies (e.g., **Vitamin B12 deficiency**) can cause fatigue and constipation, they do not typically cause weight gain or bradycardia.
- The patient's symptom constellation points more specifically to an endocrine disorder.
*Iatrogenesis*
- Iatrogenic causes refer to conditions resulting from medical intervention or treatment.
- There is no information in the vignette to suggest any recent medical procedures or medications that would account for this specific constellation of symptoms.
DMARDs and biologic therapies US Medical PG Question 10: A 42-year-old woman presents complaining of pain in her hands. She reports that the pain is in both hands, and that it is usually worse in the morning. She reports that her hands are also stiff in the morning, but that this gradually improves throughout the morning. She notes, however, that her symptoms seem to be getting worse over the last three months. What is the most likely pathogenesis of her disease process?
- A. Production of antibodies against smooth muscle
- B. Anti-neutrophil cytoplasmic antibody production
- C. Production of antibodies against antibodies (Correct Answer)
- D. Type 1 hypersensitivity reaction
- E. Repetitive microtrauma
DMARDs and biologic therapies Explanation: ***Production of antibodies against antibodies***
- The patient's symptoms of **bilateral hand pain and morning stiffness** improving with activity, worsening over three months, are classic for **Rheumatoid Arthritis (RA)**.
- RA is characterized by the production of **rheumatoid factor (RF)**, an antibody (typically IgM) directed against the Fc portion of IgG, which is essentially an antibody against an antibody.
*Production of antibodies against smooth muscle*
- This describes the presence of **anti-smooth muscle antibodies (ASMA)**, which are characteristic of **Autoimmune Hepatitis type 1**.
- Autoimmune hepatitis primarily affects the liver, leading to symptoms like fatigue, jaundice, and elevated liver enzymes, not primarily joint pain.
*Anti-neutrophil cytoplasmic antibody production*
- This refers to **ANCA (anti-neutrophil cytoplasmic antibodies)**, which are associated with various forms of **vasculitis**, such as Granulomatosis with Polyangiitis (Wegener's), Microscopic Polyangiitis, and Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss).
- While vasculitis can cause systemic symptoms, the patient's presentation of symmetric, inflammatory arthritis is not typical for primary ANCA-associated vasculitis.
*Type 1 hypersensitivity reaction*
- A **type I hypersensitivity reaction** involves IgE-mediated mast cell degranulation, leading to immediate allergic reactions like asthma, anaphylaxis, or hives.
- This mechanism is completely unrelated to the pathogenesis of an autoimmune, chronic inflammatory arthritis like Rheumatoid Arthritis.
*Repetitive microtrauma*
- Repetitive microtrauma is more consistent with **osteoarthritis** or **occupational overuse injuries**.
- Osteoarthritis typically presents with pain that worsens with activity and improves with rest, **morning stiffness lasting less than 30 minutes**, and often affects weight-bearing joints or specific joints due to trauma or wear and tear, rather than the inflammatory pattern described.
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