Case Study of diagnosis and treatment of Gout

Case Study of diagnosis and treatment of urarthritisA 50 year-old male presented for an evaluation of rapid onset of pain and gibbousness in his c everyplace toe. The diligent reported that he had two similar previous episodes with the same symptoms lasting quaternion to volt days and was treated by emergency physicians.The longanimouss past medical history is operative for hypertension and treated with Hydrochlorothiazide.The review of systems was negative for headache, fever, chills, rash, earache, sore throat, cough, rhinorrhea, vision changes, weight loss, or change in appetite or disposition. The patient was afebrile, and this blood squelch was slightly elevated.PHYSICAL EXAMINATION General The patient is a pleasant male who appears to be in no app bent distress. Vital Signs blood pressure 123/48, heart rate 76, Temperature 38.3 and 98% on room air. HEENT Extraocular muscles are intact. Pupils are equal, round, and reactive to light and accommodation. tell apart Supple. No jugular vein distention noted. No carotid bruits noted. Lungs Clear to auscultation bilaterally. No wheezes, rubs or rhonchi. boldness Regular rate and rhythm. Normal S1, S2. A 2/6 to 3/6 systolic exclusion murmur at the right upper sternal border. PMI is nondisplaced. Abdomen Notable for laparoscopy surgical wound. Positive catgut sounds. Extremities MTP is red, hot and swollen. Neurologic The patient is alert and oriented x3. No focal neurologic deficits noted.PathophysiologyGout is an seditious disease characterized by the deposition of uric acid crystals in and around crossroadss, subcutaneous tissues, and kidneys. Although men and women are equally affected by gout, men are six times more likely to pick out serum concentrations above 7 mg per dL. Gout typically occurs during middle age and is uncommon originally the age 30 years old. Women rarely clear gouty arthritis antiaircraft guns before menopa enforce 1.Clinical introGout attacks are usually associated with p recipitated events. Patients usually present with rapid onset of severe pain, bump, redness, and warmth in one or tow joints. This pain and inflammation are caused by inflammatory response. knifelike attack untreated attacks usually last two to 21 days depending on cases. There are four clinical introduces of gout according to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). The first stage is cognise as asymptomatic hyperurecemia. During this stage, the patients can have an elevation of uric acid in the blood moreover they do not have any symptoms yet. After more and more urate deposits around a joint and if any trauma triggers the release of crystal into the joint space, patients will suffer exquisite attacks of gout. This second stage is known as sagacious gouty arthritis. The third stage, known as detachment or intercritical gout, involves the separation between subtile flare gout attacks with persist crystals in the joints. When cryst als deposits continue to accumulate, patients are likely to rear chronically stiff and swollen joints. This stage is called chronic tophceous gout. Some permanent damage to affected joints and sometimes to kidneys can be seen. This advanced stage is relatively uncommon if patients receive proper treatment.Differential diagnosisGout in the elderly is often polyarticular and involves upper extremity joints (especially proximal interphalangeal joints and distal interphalangeal joints). Women present 70% of the time with polyarticular disease rather than the classic monoarticular arthritis seen in men. Gout can be mistaken for rheumatoid arthritis because tophi may resemble rheumatoid nodules and rheumatoid factors often become weakly positive as populate age. It may be difficult to differentiate cellulitis or septic arthritis from gout, particularly when a fever, leukocytosis, redness, or sloughing is present. The term pseudogout, for calcium pyrophosphate deposition disease, beli es the difficulty in clinically differentiating it from gout. For definitive diagnosis, joint precarious moldiness be aspirated for culture and a search for urate crystals.Diagnostic TestThe gold standard diagnostic stress for gout is an arthrocentesis. The American College of Rheumatology has established 12 clinical criteria, 6 of which a patient must have for diagnosis.* Maximum joint inflammation within 1 day* More than one attack over time* Monoarticular arthritis (although gout can be polyarticular)* Redness of joint* Great metatarsophalangeal pain or swelling* Unilateral great metatarsophalangeal involvement* Unilateral tarsal involvement* Suspected tophus* Hyperuricemia* Asymmetrical swelling within the joint on x-ray* Subcortical cysts without erosion on x-ray* Joint fluid culture negative for organisms during attackTreatment and ManagementThe gold of treating gout is to background or authorise the urate crystals from the joints and other structures associated with them. Several aspects must be taken into consideration and each treatment regiment is vary from patients to patients. The three main objectives that FNP take into consideration are treatment for the acute attacks, prophylaxis against recurrent attacks, and management of hyperurecemia. symptomless hyperurecemia urate-lowering drugs is not recommended to treat patients with asymptomatic hyperurecemia. If hyperurecemia is identified, underlying causes such as obesity, hypercholesterolemia, alcohol consumption, and hypertension should be addressed.Acute gout NSAIDs are being used as first-line therapy. Indomethacin (Indocin), ibuprofen (Motrin), naproxen (Naprosyn), sulindac (Clinoril), piroxicam (Feldene) are also effective against gout.Corticosteroidsintra-articular, intravenous, intramuscular or oral corticosteroids are effective in acute gout. When one or two joints are involved, intra-articular injection of corticosteroid can be used.Intramuscular triamcinolone acetonide is as effectiv e as indomethacin in relieving acute gouty arthritis. Triamcinolone acetonide is especially reusable in patients with contraindication to NSAIDs.Oral prednisone is an option when repeat dosing is anticipate. Prenisone, 0.5 mg per kg on day 1 and tapered by 5 mg each day is effective.Cochicine is also effective treatment for acute gout. However, majority of patients experience gastrointestinal side effects, including nausea, vomiting, and diarrhea.Patient EducationIf they are obese, they should be advised to bring forth a concerted program of supervised weight reduction (see Chapter 233), but to avoid starvation or very low calorie diets that may only exacerbate the risk of gout. Drinkers should be warned against binges. Maintenance of goodish hydration needs to be stressed to those at risk for nephrolithiasis. On the other hand, patients will find it cheering to know that severe dietary restrictions are unnecessary. Fasting should be avoided because it may precipitate an attack. The importance of treating an acute attack at the first sign on of illness also needs to be stressed. For the patient with interval gout, a discussion of the risks and benefits of prophylactic therapy and the importance of compliance is indicated. Those taking allopurinol should be warned of the risk of a hypersensitivity reaction and advised to cease intake immediately and call the physician at the first sign of a rash, fever, or other manifestation. Pain management is the primary concern during acute phase of and attack. The patient should be advised to take analgesic medications as schedule. The joint should be rested as overmuch as possible in a position of comfort. Ice, not heat, may help with reducing discomfort. destructionGout is one of the most causes of acute monoarticular arthritis. Primary gout runs in families and follows multifactorial inheritance. The expanded use of agents that decrease uric acid excretion has significantly increased the incidence of secondary gou t. The Fremingham Study suggested that well-nigh half of new cases were associated with thiazide use.The FNP should be able to properly diagnose acute gout, treat it, prevent recurrence, and minimize the chances for the development of chronic gouty arthritis. Patients who present with asymptomatic hyperuricemia should be further investigated to prevent complications from this disorder.