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Inhibiting binding of tumor necrosis factor alpha to receptors
36%
18/50
Inhibiting dihydrofolate reductase
12%
6/50
Inhibiting microbial DNA by formation of radicals
4%
2/50
Inhibiting purine synthesis
10%
5/50
Inhibiting synthesis of inflammatory cytokine
Select Answer to see Preferred Response
This patient is exhibiting symptoms of inflammatory bowel disease (e.g., abdominal pain, fatigue, and diarrhea). Specifically, she is presenting with Crohn disease (e.g., non-bloody diarrhea, right lower quadrant pain to palpation, and skip lesions [unharmed regions between intestinal ulcers]) that is medically refractory (failed steroids, thiopurines, and methotrexate). For refractory Crohn disease, remission involves the use of biologic agents such as adalimumab that inhibit binding of tumor necrosis factor alpha to receptors. Crohn disease is a subcategory of inflammatory bowel disease (IBD) characterized by possible non-continuous involvement of any region along the gastrointestinal tract, with the distal ileum commonly affected. Ulcerative colitis, the other subcategory of IBD, has continuous lesions that always affect the rectum but are limited to the colon. Diagnosis requires colonoscopy with biopsies: Crohn disease presents with transmural inflammation and granulomas while ulcerative colitis presents with mucosal inflammation and crypt abscesses. While colectomy can be curative for ulcerative colitis, Crohn disease needs to be chronically managed. Moderate disease can be treated with steroids, thiopurines, and methotrexate. Since tumor necrosis factor plays a key role in the pathogenesis of IBD as a pro-inflammatory agent, tumor necrosis factor-alpha (TNFa) inhibitors (e.g., infliximab and adalimumab) are used to induce remission in severe Crohn disease (medically refractory). However, as external monoclonal antibodies against TNFa, these biologic agents can develop an immune response against themselves. Thus, combination therapy with an immunomodulator (e.g., azathioprine or methotrexate) is often prescribed rather than monotherapy. Incorrect Answers: Answer 2: Inhibiting dihydrofolate reductase is the mechanism of methotrexate. As an immunomodulator, methotrexate reduces immunogenicity against the anti-TNFa agent and can be used for maintenance therapy but not remission induction. Methotrexate is used to treat choriocarcinomas and trophoblastic tumors. Answer 3: Inhibiting microbial DNA by formation of radicals is the mechanism of metronidazole. Metronidazole is the choice of drug for Clostridioides difficile or Giardia infections. However, the endoscopy did not reveal yellow plaques (pseudomembranous colitis seen in C. difficile) and the patient did not report steatorrhea (seen in Giardiasis). Answer 4: Inhibiting purine synthesis is the mechanism of azathioprine. An immunomodulator, azathioprine helps reduce immunogenicity against biologic agents but is not used for induction of remission. It is often used in the management of other inflammatory diseases such as rheumatoid arthritis or lupus. Answer 5: Inhibiting synthesis of inflammatory cytokine is the mechanism of prednisone. Prednisone is the first-line therapy for Crohn disease acute exacerbation. However, it does not play a role in induction of remission or maintenance therapy. It is not used long-term due to its numerous major side effects (e.g., skin thinning, fluid retention, and osteoporosis). Bullet Summary: Medically refractory Crohn disease remission involves biologic agents that inhibit binding of tumor necrosis factor alpha to receptors.
3.5
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