Etanercept New DMARD Inactivates TNF Use Moderate to severe RA Adverse effects

Etanercept new dmard inactivates tnf use moderate to

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Etanercept New DMARD Inactivates TNF Use Moderate to severe RA Adverse effects Infection (may be serious) Injection-site reactions Tuberculosis Heart failure Cancer Other adverse effects
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GOUT
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Gout Recurrent inflammatory disorder Seen mainly in men Hyperuricemia Uric acid level greater than 7 mg/dL in men or greater than 6 mg/dL in women Uric acid crystals deposited in joints Episodes of severe joint pain (typically in large toe) Causes Excessive production of uric acid Impaired renal excretion of uric acid
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Gout Lifestyle Drug-Induced Obesity Alcohol Increased purine intake - Red meats, fatty fish, seafood, organ meats, anchovies Kidney Disease Thiazide diuretics Low-moderate ASA Ethambutol Nicotinic acid Vitamin B12 Cyclosporine Levodopa Pyrazinamide Cytotoxic agents Ethanol
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Drug Therapy for Hyperuricemia Goals of therapy Promote dissolution of urate crystals Prevent new crystal formation Prevent disease progression Reduce the frequency of acute attacks Improve quality of life Note: Because these drugs have no analgesic or anti-inflammatory actions, they are not useful in an acute gouty attack
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Overview of Drug Therapy Short-term to relieve symptoms of attack Infrequent flare-ups (fewer than 3 times/yr) NSAIDs: first-line agents Glucocorticoids also used Long-term to lower blood levels of uric acid 3 or more times per year Uricosuric drugs
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NSAIDs Agents of first choice for gouty arthritis Better tolerated and more predictable than colchicine Relief should be within 24 hours; swelling subsides over the next few days Adverse effects GI ulceration, decreased renal function, fluid retention, increased risk of cardiovascular events
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Glucocorticoids Highly effective in relieving pain Useful for patients who are hypersensitive to, are unresponsive to, or have medical conditions that contraindicate the use of NSAIDs Avoid in patients prone to hyperglycemia
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Colchicine Anti-inflammatory agent No longer the first-line drug Now reserved for patients who are unresponsive/intolerant to safer agents Uses Treats acute gouty attack Reduces incidences of attack Aborts an impending attack
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Copyright © 2015 Wolters Kluwer • All Rights Reserved Chapter 36 Figure 36.19
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Colchicine Mechanism of action Binds to tubulin, a microtubular protein, causing its depolymerization. This disrupts cellular functions, such as the mobility of granulocytes, thus decreasing their migration into the affected area. Furthermore, colchicine blocks cell division by binding to mitotic spindles. Pharmacokinetics Administer within 36 hours of onset of attack Alleviate pain within 12 hours Substrate of CYP3A4 and pgp Adverse effects Gastrointestinal (N/V, HA, diarrhea) Myelosuppression Myopathy Alopecia
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Drug Therapy for Hyperuricemia Goals of therapy Promote dissolution of urate crystals Prevent new crystal formation
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