< aues in the joints There are two main categories of DMARDs, non-biologic and biologic. What is a main difference betwe

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< aues in the joints There are two main categories of DMARDs, non-biologic and biologic. What is a main difference between these two categories of DMARDs? TAMM O Bologe DMARDs target the CO2 pathway a similar way to NSAIDs, white-bigc DSARD that specific immune ces for destruction. ON biolog DMARDs tend to suppress general cytokine activation and immune cell chemot, whi belogic DMARDS target specific cytokines or cells of the immune system to reduce inflammation in the joints O Both types of DMARDs work by destroying all immune cells to suppress the immune and wo progression of RA O Non-biologic DMARDS target the CO2 pathway activation in a different way to NSAID), witbloe DMARDS Garget Lipoeggenase pathway activation 1 Why would you suggest trying a non-biologic DMARD like Methotrexate or Sulfasalazine for treatment of RA before a biologic DMARD like Rituximab? O Because non bislag DMARDS have sa few side effects they are not only effective but much safer than biologic O Because biologic OMARDs are newer they are not well tested for use in dimic making them more risky than nan biologies O Because we must consider not only the benefit to the patients health, but ase the cost of the medication and patient adherence, as non bonge DMARDs are far more affordable O The mechanisms of action are not fully understood for biologics but are fully understood for big making the sale. O All of the above are good reasons to preserbe a nen bolig DMARD 100 Che 43/FM LE
1 pts DMARDS may provide an alternative treatment option for Sonia if she is unable to tolerate NSAIDs or get relief from her symptoms with these drugs. Which of the following is an example of a DMARD that could potentially be used as an alternative treatment for Sonia and why would this DMARD help? O Methotrexate-inhibits cytokines and phagocytic cell chemotaxis, which reduces the progression of RA. O Sulfasalazine - increases production of inflammatory cytokines and increases the proliferative response of lymphocytes to kill off the RA factors, which slows the rate of bony damage in RA. O Adalimumab (Humira) - inhibits the pro-inflammatory interleukin cytokines, which slows the inflammatory response and reduces the progression of joint damage. O All of the above options are viable for Sonia's treatment and should be offered to her. 1 pts DMARDS (Disease Modifying Anti Rheumatic Drugs) are often prescribed for cases of chronic inflammation associated with RA because:
r Féplacé adrenaline, so when you withdraw them they can lead to adrenal fatigue. O All of the above are correct. Sonja Googled her condition and asked if she could be placed on corticosteroids long term as she is in so much pain throughout all of her body's joints. Why or why not would long term systemic administration of corticosteroids be advisable? O A. Only the joints in her hands will ever be affected by RA, the other joint pain must be from another condition, so there's no need to treat the rest of her body with a systemic corticosteroid. O B. Many joints are involved so administration of corticosteroids will treat them all simultaneously without any side effects, so administration is advisable. O C. The risks of side effects for systemic treatment are low and systemic administration would be advisable to help her in this situation. O D. Systemic treatment has too many risks long term, specifically in patients with known gastrointestinal issues, so would not be advisable. OE. B and C are correct. 13pts What are some of the risks of systemic corticosteroid use? Hint: check out your Lehne's Pharmacology for nursing care textbook for help with this question. 1 pts
ponents that are triggering the inflammation and can prevent 1 pts the disease progression long term. Which of the following enzymes are inhibited by corticosteroids? O Lipoxygenase only O COX-1 only COX-2 only Phospholipase How, therefore, is inflammation regulated by corticosteroids? O COX-2 is directly inhibited by the corticosteroids. O The COX-2 prostacyclin is not produced, so inflammation is not triggered. The arachidonic acid is not produced, so it cannot be processed by COX-2 to up-regulate inflammation. O The COX-1 prostaglandin is not produced, so inflammation is not triggered. 1 pts Corticosteroids are sometimes used to control a flare of inflammation in chronic conditions such as RA They must be carefully evaluated for use in a 1 1 pts