NR 508 Week 6 TD, Quiz and Summary

PART 1: Jonathon is a 56 year-old retired automobile mechanic who has not been to the doctor in approximately 6-7 years. He presents to your office complaining that three weeks ago he was awoken with severe pain and ...

PART 1: Jonathon is a 56 year-old retired automobile mechanic who has not been to the doctor in approximately 6-7 years. He presents to your office complaining that three weeks ago he was awoken with severe pain and inflammation in his knee, which has been consistent since that initial night. Upon physical examination of his knee, it appears swollen and erythematous with periarticular involvement. Upon physical examination and laboratory results you notice the following: Physical examination: GEN: well nourished, obese male (310 pounds) VS: BP 191/112 HR 75 RR 15 T 98.6, HT 5’8” EXT: Knee joint inflammation Laboratory (fasting): Na 139 mEq/L K 3.8 mEq/L Ca 9.1 mg/dL (9-10) Low Normal CL 102 mmol/L (98-106) HCO3 22 mEq/L BUN 10 mg/dL SCr 0.9 mg/dL Serum Uric Acid 6.5 mg/dL (4-8.5) (>6.5 hyperuricemia) Alb 4.1 g/dL (3.5-5) Cholesterol 300 mg/dL (<200) H UA: pH 6.8 (4.6-8) , uric acid 250 mg/24h (250-750) What problems can be identified in this patient? Please provide a list of differential diagnoses, as well as indication of your primary diagnosis. What is your pharmacological plan for your primary diagnosis including the medication, dose, and mechanism of action? Probs = HTN, Obesity, High Cholesterol Poss Dx = Pseudogout (calcium pyrophosphate dz), monoarthritis, septic jointPseudogout. Pseudogout, also referred to as acute calcium pyrophosphate crystal arthritis, is an inflammatory disease process that belongs to a class of diseases called calcium pyrophosphate deposition diseases (CPPDs) (Rho, Zhu, Zhang, Reginato, & Choi, 2012). The two prevalent crystal-induced arthropathies are gout and pseudogout (Rothschild, 2017). Sometimes, pseudogout and its symptoms can be indistinguishable from gout (Rothschild, 2017). Symptoms of both diseases include crippling pain in one or more joints as well as erythema, warmness, tenderness, and swelling (Rothschild, 2017). These symptoms generally effect the larger joints, such as the knees and wrists (Papadakis & McPhee, 2017). When the affected joint is examined via diagnostic imaging, chondrocalcinosis is almost always present (Papadakis & McPhee, 2017). If the patient presents with the symptoms above plus a fever, an infection of the joint should be investigated (Rothschild, 2017). There are some studies that can be useful in diagnosing, which include urine and serum uric acid levels (even though these labs are not considered diagnostic) and blood work such as a CBC to evaluate WBCs, a cholesterol panel, a renal panel, liver enzymes, and glucose levels (Rothschild, 2017). An ultrasound can be used to visualize the joint and examine for crystals, tophaceous materials, and erosions that have overhanging edges (Rothschild, 2017). However, the best way to distinguish between gout and pseudogout is to aspirate the synovial joint fluid; calcium pyrophosphate crystals indicate pseudogout while monosodium urate monohydrate crystals indicate gout (Rothschild, 2017). Gout and pseudogout are treated similarly; both aim at reducing pain and preventing flares via medications and/or decreasing urate levels (Rothschild, 2017). Before making a decision on the treatment plan, the provider needs a baseline of renal functioning, to make sure the diagnosis is not septic arthritis, and to know if the patient has a history of GI complications, especially bleeding (PDR, 2017). Once crystal deposits are confirmed, relief of pain and inflammation can be treated with NSAIDs, adrenocorticotropic hormone (ACTH), colchicine, or a combination of meds including intraarticular glucocorticoid (Rothschild, 2017). For Jonathon, he is experiencing symptoms that could be either gout or pseudogout. Based on the information given, I chose pseudogout because, even though uric acid levels are not considered a diagnostic tool, his serum and urine levels are within normal limits. Assuming he is afebrile and thepain and inflammation is not from an infection, I would aspirate some synovial fluid from his effected knee and analyze it for specific crystal formation. I would also order an ultrasound of his knee to evaluate for crystal or tophi development. Assuming the results are positive, I would make sure to have certain labs done, such as a CBC with diff, CMP, renal panel, and liver panel for baseline results. I would also inject Triamcinolone 40mg with 1 percent lidocaine into the intraarticuar knee space. I would also have him take Ibuprofen 800mg Q6H prn for pain until pain is tolerable. Colchicine 0.6mg PO QD or BID, can be effective in preventing recurrence in both diseases, therefore could be another treatment option if the above does not work (Rothschild, 2017). Triamcinolone is a corticosteroid that provides vasoconstrictive, antiinflammatory, and antipruritic properties (PDR, 2017). Corticosteroids induce lipocortins, which antagonize phospholipase A2, which in turn leads to the breakdown of leukocyte lysosomal membranes to discharge arachidonic acid (PDR, 2017). The release of arachidonic acid inhibits the release of endogenous inflammatory mediators (PDR, 2017). Ibuprofen inhibits both COX-1 and COX-2 (enzymes) by blocking arachidonate binding, which results in anti-inflammatory, analgesic, and antipyretic effects (PDR, 2017). These enzymes accelerate the conversion