Last updated: February 22, 2019
Topic: HealthDisease
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A 50 year-old Asiatic male presented for an rating of rapid oncoming of hurting and puffiness in his right toe. The patient reported that he had two similar old episodes with the same symptoms enduring four to five yearss and was treated by exigency doctors.

The patientaa‚¬a„?s past medical history is important for high blood pressure and treated with Hydrochlorothiazide.

The reappraisal of systems was negative for concern, febrility, icinesss, ortalgia, roseola, sore pharynx, cough, rhinorrhea, vision alterations, weight loss, or alteration in appetency. Physical Examination

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General visual aspect: The patient is a 50 year-old pleasant gentleman who appears to be in no evident hurt. Critical Signs: blood force per unit area 140/80, bosom rate 76, Temperature 38 and 98 % on room air. HEENT: Extraocular musculuss are integral. Students are equal, unit of ammunition, and reactive to light and adjustment. Neck: Supple. No jugular vena dilatation noted. No carotid bruits noted. Lungs: Clear to auscultation bilaterally. No wheezes. No hang-up. No rhonchi. Cardiovascular: regular rate and beat. No S3. No S4. PMI is nondisplaced. Extremities: right MTP is ruddy, hot and conceited. Neurologic: The patient is watchful and orientated x3. No focal neurologic shortages noted.


Gout is preponderantly a disease of work forces & gt ; 40 old ages of age. Work forces have higher serum urate degrees than adult females do, which increase their hazard of developing urarthritis. In adult females, urarthritis normally involves the upper appendages. Women seldom have gouty arthritis onslaughts before climacteric ( Baker & A ; Schumacher, 2010 ) . Gout is the most common inflammatory arthritis upset in the United States and about 3 to 5 million people are affected by it ( Hilaire & A ; Wozniak, 2010 ) . The prevalence of urarthritis and hyperurecimia has been increasing over the past few decennaries in response to a figure of factors. These factors include, but are non limited, to high-purine diet, intoxicant usage, fleshiness, diabetes, and kidney disease.


The exact cause of urarthritis is still unknown to day of the month. However, the pathophysiology of urarthritis is believed to be associated with purine metamorphosis and kidney map. Purines are biologically synthesized into purine bases, which can be used in the synthesis of nucleic acids. The terminal merchandise of uric metamorphosis is uric acid. Certain persons with urarthritis tend to hold an increased in purine synthesis doing an overrun of uric acid, while others break down bases at an alarmed rate that besides doing an overrun of uric acid. An increased in production of uric acid is besides caused by a lack of the enzyme hypoxanthine-guanine phophoribosyn-transferase ( HGPRT ) ( McCance & A ; Huether, 2010 ) .

Uric acid is eliminated from the organic structure through the kidneys. In primary urarthritis, the kidneys excrete the uric acid easy due to either by a lessening in glomerular filtration of urate or an acceleration in urate resorption ( McCance & A ; Huether, 2010 ) . On the other manus, secondary urarthritis is caused by certain medicines and medical jobs. Medicines that are known to be associated with urarthritis are water pills, Aspirin, niacin, Levodopa, and cyclosporine. Medical conditions related to urarthritis are high blood pressure, pre-eclampsia, diabetes, thyrotoxicosis, hypothyroidim, fleshiness, and sarcoidosis ( Teng, Nair & A ; Saag, 2006 ) .

Urine flow is besides affected when monosodium crystals deposited in nephritic interstitial tissues. There are no clear replies that can explicate precisely how crystals of monosodium urate stoping up in articulations and bring oning gouty arthritis. However, several mechanisms that may be involved include lower organic structure temperature, decreased albumen or glycosaminoglycan degrees, alterations in ion concentration and injury that promotes urate crystal precipitation ( McCance & A ; Huether, 2010 ) . The present of monododium urate crystals triggers the acute inflammatory response. The compliment system so activates cytokines to bring forth other substances called chemo attractants that will pull neutrophils out of the circulation to be phagocytizing the crystals. Several other inflammatory go-betweens are released during this procedure. These factors include chemotactic factors, lysosomal enzymes, eicosanoids, prostaglandin E ( PGE2 ) , IL-1 and IL-6, reactive O species, and collagenase. Tissue harm begins to take topographic point when urate crystals react with neutrophils and monocytes in the joint fluid ( McCance & A ; Huether, 2010 ) .

Hazard Factors

A major hazard factor for urarthritis is usage of thiazide diuretic. Patients who are treated for high blood force per unit area with a cringle or thiazide water pill over a period of clip frequently have hyperuricemia and can take to farther addition in gout onslaught ( Hunter, York, Chaisson, Woods, Niu & A ; Zhang, 2006 ) . Diuretics play an of import function in gouty arthritis by diminishing uric acerb elimination and by increasing volume depletion ( Gurwitz, Kalish, Bohn et al. , 1997 ) . Several dietetic factors besides play an of import function in increasing the hazard of urarthritis. These factors include, but are non limited to, meat and seafood ingestion, sugar sweetened soft drinks, intoxicant and ingestion of nutrients high in fructose. Certain medicine conditions such as hypertriglyceridemia, high blood pressure, nephritic inadequacy, hypercholesteremia, hyperuricemia, fleshiness, diabetes, and early menopause contribute to a higher hazard of incident urarthritis ( Singh, Reddy & A ; Kundukulam, 2011 ) .

Clinical Presentation

Gouty arthritis normally occurs in a peripheral articulation. The primary symptom that patients ever ailment of is terrible hurting. Approximately half of the initial onslaught occurs in the metatarsophalangeal articulation of the great toe. The other half is normally involved with the heel, mortise joint, carpus, cubitus, or instep of the pes. Within a few hours the affected articulation becomes inflamed and highly stamp and may be swollen. Systemic marks of redness such as leucocytosis, febrility, elevated deposit rate and lymphangitis sometimes present. There are four clinical phases of urarthritis harmonizing to the National Institute of Arthritis and Musculoskeletal and Skin Diseases ( NIAMS ) . The first phase is known as symptomless hyperurecemia. During this phase, the patients can hold an lift of uric acid in the blood but they do non attest any symptoms yet. After more and more urate sedimentations around a joint and if any injury triggers the release of crystal into the joint infinite, patients will endure acute onslaughts of urarthritis. This 2nd phase is known as acute gouty arthritis. The 3rd phase, known as interval or intercritical urarthritis, involves the interval between ague flair urarthritis onslaughts with persist crystals in the articulations. When crystals sedimentations continue to roll up, patients are likely to develop inveterate stiff and conceited articulations. This phase is called chronic tophceous urarthritis. Some lasting harm to affected articulations and sometimes to kidneys can be seen. This advanced phase is comparatively uncommon if patients receive proper intervention.

Differential Diagnosis

Gout can be mistaken for rheumatoid arthritis because chalkstone may resemble rheumatoid nodules and arthritic factors frequently become decrepit positive as people age. It is still ill-defined why certain persons with hyperuricemia are susceptible to develop chalkstones while others are non. The presence of urate crystals in the aspirate of a nodule will distinguish urarthritis from arthritic arthritis. Radiographs can besides be used to corroborate the diagnosing ( Mandell, 2008 ) . It may be hard to distinguish cellulitis or infected arthritis from urarthritis, peculiarly when a febrility, leucocytosis, or inflammation is present. The term Pseudogout, Ca pyrophosphates dehydrate deposition disease, can be hard in clinically distinguishing from urarthritis. To corroborate the diagnosing, joint aspiration is performed for civilization and a hunt for urate crystals ( Winstock, Neides & A ; Miriam, 2009 ) . Careful survey of crystals obtained from the joint aspiration will find the difference between the two conditions.

Diagnostic Trial

The gilded criterion diagnostic trial for urarthritis is join aspiration ( Winstock, Neides & A ; Miriam, 2009 ) . This process should take topographic point after an acute onslaught has lessened to avoid patient uncomfortableness. The present of monosodium urate crystals suggests the diagnosing of urarthritis. The white blood cell count may be elevated within the synovial fluid ( 10, 000 to 60, 000 ) with neutrophils predominating. The American College of Rheumatology has established 12 clinical standards for the instance of urarthritis. Patients must hold at least six of the following symptoms to corroborate the diagnosing.

* Hyperuricemia

* Redness of articulation

* Suspected chalkstone

* Unilateral tarsal engagement

* Joint fluid civilization negative for beings during onslaught

* Maximum joint redness within one twenty-four hours

* More than one onslaught over clip

* Monoarticular arthritis ( although urarthritis can be polyarticular )

* Great metatarsophalangeal hurting or puffiness

* Unilateral great metatarsophalangeal engagement

* Asymmetrical puffiness within the joint on X ray

* Subcortical cysts without eroding on X ray

Treatment and Management

The end of handling urarthritis is to minimise or extinguish the urate crystals from the articulations and other constructions associated with them. Several facets must be taken into consideration and each intervention regiment is varied from patients to patients. The three chief aims that FNP take into consideration are intervention for the ague onslaughts, prophylaxis against recurrent onslaughts, and direction of hyperurecemia.

Urate-lowering drugs is non recommended to handle patients with symptomless hyperurecemia. If hyperurecemia is identified, underlying causes such as fleshiness, intoxicant ingestion, hypercholesteremia, and high blood pressure should be addressed. There are no high-quality randomized, placebo-controlled tests of nonsteoidal anti-inflammatory drugs ( NSAIDs ) and cox-2 inhibitors for handling acute gouty arthritis. However, they are recommended as first-line therapy for patients with acute urarthritis. If the intervention is indicated within 24 hours of the oncoming of symptoms, naproxen 500 mg twice daily or indomethacin 50 milligram three times day-to-day is preferred for acute gouty redness. If patients experience several onslaughts per twenty-four hours, anti-inflammatory agents with fewer gastroduodenal side effects such as Relafen or selective COX-2 inhibitor can be used. Aspirin is non recommended to handle acute urarthritis onslaughts because of self-contradictory effects of salicylates on serum urate.

Corticosteroids can be used when there is monarthric urarthritis involved. Patients with monarthric grout normally respond good when giving intra-articular injection. Systemic corticoids such as Prednisone in a dose of 20 to 30 milligrams should be used merely when NSAIDs and colchicine are contraindicated or non effectual ( Pittman & A ; Bross, 1999 ) .

Cochicine is besides an effectual intervention for ague urarthritis. Oral colchicine is appropriate for patients who can non digest NSAIDs and have contraindications to glucocorticoid. Colchicine works best when it is given within the first 12 to 36 hours of an onslaught. It works by suppressing the phagocytosis of uric acid and barricading the release of chemotactic factor. It has anti-inflammatory activity but no analgetic activity ( Pittman & A ; Bross, 1999 ) . However, bulk of patients experience GI side effects, including diarrhoea, sickness, and emesis.


It is really of import to follow up patients after the intervention of an ague urarthritis onslaughts. The patients should return for a follow-up visit within one month to be evaluated for therapy to take down serum uric acid degrees. Initially, FNPs should measure their patients every one to two months to set the dosage of uric acid-lower agents to accomplish the curative degree of 5-6 mg/gL. After the curative degree is achieved and maintained, patients can be seen every 6-12 months. Patient Education

Certain heredity conditions can do patients more susceptible to gout. Patients who are corpulent should be advised to get down a strict plan of supervised weight decrease but to avoid famishment that may merely worsen the hazard of urarthritis. Care of good hydration demands to be addressed to those who are at hazard for kidney rocks. Alcohol ingestion such as beer and difficult spirits can potentially increase the hazard of incident urarthritis. Dietary factors that increased the hazard of urarthritis include seafood, meat, sugar sweetened soft drinks, and ingestion of nutrients that are high in fructose ( Singh, Reddy, & A ; Kundukulam, 2011 ) .

The most of import of handling an acute onslaught at the first mark of illness demand to be addressed. Patients who are taking Allopurinol should be educated about the hazard of hypersentivity reaction and advised to halt taking the medicine instantly and name the doctor at the first mark of a roseola, febrility, or other serious manifestation. Pain direction is the primary concern during ague onslaughts. The patient should be instructed to take analgetic medicine as directed. The articulation should be rested every bit much as possible in a place of comfort during onslaughts. Ice battalion may assist relieving uncomfortableness. The patient should non use an ice battalion no more than 15 proceedingss at a clip to forestall nervus and tissue harm.


Gout is one of the most causes of acute monoarticular arthritis. Primary urarthritis tallies in households and follows multifactorial heritage. The expanded usage of agents that decrease uric acerb elimination like Hydrochlorothiazide has significantly increased the incidence of secondary urarthritis. The FNP should be able to decently name ague urarthritis, dainty it, prevent return, and minimise the opportunities for the development of chronic gouty arthritis. Patients who present with symptomless hyperuricemia should be farther investigated to forestall serious complications from this upset.