GOUTY ARTHRITIS ASSOCIATED WITH KIDNEY FAILURE
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GOUTY ARTHRITIS ASSOCIATED WITH KIDNEY FAILURE

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THIS HAPPENSTO BE MY FIRST PRESENTATION ONLINE

THIS HAPPENSTO BE MY FIRST PRESENTATION ONLINE

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    GOUTY ARTHRITIS ASSOCIATED WITH KIDNEY FAILURE GOUTY ARTHRITIS ASSOCIATED WITH KIDNEY FAILURE Presentation Transcript

    • TERNOPIL STATE MEDICAL UNIVERSITY UKRAINEDEPARTMENT OF INTERNAL MEDICINE (HEMATOLOGY) A PRESENTATION ON GOUTYARTHRITIS ASSOCIATED WITH KIDNEY FAILURE BY DR JOSEPH UCHENNA VICTOR GROUP 5 4TH COURSE
    • GOUTY ARTHRITIS ASSOCIATED WITHKIDNEY FAILURE
    • INTRODUCTIONETIOLOGYCAUSES AND SYMPTOMSDIAGNOSISDIFFERENTIAL DIAGNOSISTREATMENTCONCLUSION
    • INTRODUCTIONGouty arthritis refers to a form of arthritis caused by deposits ofneedle-like crystals of uric acid, usually strikes a single joint,most commonly the big toe (about 75% of people are affectedat least once), however, it can also affect thefoot (instep/heel), ankles, knees, wrists, fingers, elbowsGouty arthritis is rare in children and young adults. Men aremore likely to develop gouty arthritis than women.The main cause of development of gout is deposition of uricacid crystals in the synovial fluid and synovial lining of joints.
    • Gout may occur alone (primary gout) or may be associated withother medical conditions or medications (secondary gout). Gout results when crystals of uric acid form in tissues of thebody. Gout is characterized by an overload of uric acid in thebody and recurring attacks of joint inflammation (arthritis).Chronic gout can lead not only arthritis, but hard lumps of uricacid in and around the joints, decreased kidney function, andkidney stones. Gouty arthritis is usually an extremely painfulattack with a rapid onset of joint inflammation. The inflammationis precipitated by the deposition of uric acid crystals in the liningof the joint (synovial lining) and the fluid within the joint. Intensejoint inflammation occurs when white blood cells engulf thecrystals of uric acid and release chemicals that promoteinflammation. The resulting inflammation causes pain, heat, andredness of the joint.
    • CAUSES SYMPTOM RISk FACTOR FOR (GoutyArthritis) This disease causes the inflammation, pain, redness andtenderness of the joints of big toe, ankles, knees, feet, wristsand hands. Higher levels of uric acid, obesity, exposure to leadin the environment, high intake of food containing purines,high alcohol intake and abnormal kidney function are the majorrisk factors for gout (gouty arthritis). People with impaired excretion of uric acid or increasedproduction of uric acid have high risk for development of gout.Elevated uric acid levels may be associated with obesity, age,diabetes mellitus, type IV hyperlipidaemia, hypertension andcoronary heart diseases. Besides this, certain conditions likejoint injury, dehydration, excessive dining, fever, recent surgeryand heavy alcohol intake are considered as the risk factors forgout (gouty arthritis
    • Patients with impaired renal function or kidney failure are moresusceptible to gout. Uric acid present in normal amounts getsdissolved in the blood and easily passes through the kidneys. Butdue to kidney dysfunction, there is increase in uric acid levels inthe blood which may result in formation of crystals of uric acid.These uric acid crystals get accumulated in the synovial fluid andlining and cause inflammation of joints.A person with medications like aspirin, levodopa and diuretics ismore prone to gout as these medications can interfere with theability of body to remove uric acid. Besides that, the medicationslike cyclosporine used to suppress the immune system of thebody after organ transplant, can increase the risk for developingthis disease.Intake of foods containing large amounts of uric acid such as redmeats and internal organs like kidneys and liver, anchovies andsome shellfish can lead to raised levels of uric acid anddevelopment of gout. Excessive intake of alcohol is associatedwith gout in young people.
    • Certain medical conditions like rapid weight loss, chronic kidneydisease, high blood pressure, hypothyroidism, surgery andconditions like multiple myeloma, psoriasis, tumors or hemolyticanemia are also significant risk factors for gout (gouty arthritis).People with Lesch-Nyhan syndrome or Kelley-Seegmillersyndrome may have deficiency of enzyme that controls the uricacid levels. Such people have a greater risk of developing goutyarthritis.In addition to that, heredity, age and gender significantlycontribute in development of gout. Usually, men are commonlyaffected by gout than women. Men in the middle age with highblood pressure, obesity, heavy alcohol intake and unhealthycholesterol levels are more susceptible to this disorder.
    • DIAGNOSIS Joint aspiration: This is the most important diagnostictest. It is the ultimate method of being certain of adiagnosis of gouty arthritis, as opposed to other causessuch as an infection in the joint. Blood tests:Your doctor may obtain a blood sample to look at yourcell counts, uric acid levels, kidney function, etc. Radiographs:X-rays are primarily used to assess underlying jointdamage, especially in those who have had multipleepisodes of gouty arthritis.
    • DIFFERENTIAL DIAGNOSISDiagnostic ConsiderationsThe history and physical examination alone cannot reliablydetermine the cause of new-onset acute monoarticular arthritis.Septic arthritis, gout, and pseudogout can present in very similarways.Certain clinical presentations are so characteristic of gout thatattempts have been made to accurately diagnose or exclude goutwithout joint aspiration. Male sexPrevious arthritis attackOnset within 1 dayJoint rednessFirst metatarsophalangeal joint involvementHypertension or one or more cardiovascular diseasesA serum uric acid level of more than 5.88 mg/dL
    • Arthritis as a Manifestation of Systemic DiseaseBursitisCellulitisChondrocalcinosisHyperparathyroidismNephrolithiasisParonychiaRheumatoid ArthritisSeptic ArthritisTenosynovitis
    • TREATMENTNonsteroidal anti-inflammatory drugs (NSAIDs)Examples include indomethacin(Indocin), ibuprofen (Advil),andnaproxen (Aleve). Newer drugs such ascelecoxib (Celebrex)can also be used. Aspirin should not be used for this condition.High doses of anti-inflammatory medications are needed tocontrol the inflammation and can be tapered off within a coupleof weeks.
    • Colchicine (Colcry)This medication is given in two different ways, either to treat theacute attack of arthritis or to prevent recurring attacksTo treat the hot, swollen joint, colchicine is given rapidly(generally, two tablets at once followed by another tablet anhour later).To help prevent an attack from coming back, colchicine can begiven once or twice a day. While the chronic use of colchicinecan reduce the attacks of gout, it does not prevent theaccumulation of uric acid that can lead to joint damage evenwithout attacks of hot, swollen joints.Tell your doctor if you have any problems with your kidney orliver function.
    • CorticosteroidsCorticosteroids such as prednisone (Meticorten, Sterapred,Sterapred DS) are generally given when your doctor feels this isa safer approach than using NSAIDs.When given by mouth, high-dose corticosteroids are usedinitially and tapered off within a couple of weeks. It is importantto take these medications as prescribed to avoid problems.Some complications with the short-term use of corticosteroidsinclude altered mood, elevated blood pressure, and problemswith control of glucose in patients with diabetesCorticosteroids can also be injected into the swollen joint.Resting the joint temporarily, after it is injected with steroids,can be helpful.Occasionally, corticosteroids or a relatedcompound, corticotropin(ACTH), can also be injected into themuscle or given intravenously.
    • CONCLUSION In this study a high prevalence of CKD was observed among gout patients. Serum uric acid goal attainment was low among patients treated with allopurinol, and poorest among those with CKD. The findings suggest that poor outcomes among gout patients with CKD are partly due to clinicians reluctance to prescribe higher doses of allopurinol to patients with impaired renal function. The benefits and risks of allopurinol treatment must be weighed carefully in patientswith CKD, and alternate treatment approaches are needed to improve the prognosis of these patients. Future research should address at least three additional issues: (1) the role of non-oxypurinol metabolites of allopurinol in efficacy and toxicity, (2) more sophisticated pharmacogenomics-based studies of allopurinol dosing in the presence of CKD, and (3) development of urate-lowering drugsthat are not renally cleared. Additionally, our results suggest a need to raise awareness among physicians regarding the importance of titrating therapy to reach uric acid goals.