The Cause And Effects Of Gout Biology Essay

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A 50 year-old Asian male presented for an evaluation of rapid onset of pain and swelling in his right toe. The patient reported that he had two similar previous episodes with the same symptoms lasting four to five days and was treated by emergency physicians.

The patient’s past medical history is significant for hypertension and treated with Hydrochlorothiazide.

The review of systems was negative for headache, fever, chills, ortalgia, rash, sore throat, cough, rhinorrhea, vision changes, weight loss, or change in appetite. Physical Examination

General appearance: The patient is a 50 year-old pleasant gentleman who appears to be in no apparent distress. Vital Signs: blood pressure 140/80, heart rate 76, Temperature 38 and 98% on room air. HEENT: Extraocular muscles are intact. Pupils are equal, round, and reactive to light and accommodation. Neck: Supple. No jugular vein distention noted. No carotid bruits noted. Lungs: Clear to auscultation bilaterally. No wheezes. No rubs. No rhonchi. Cardiovascular: regular rate and rhythm. No S3. No S4. PMI is nondisplaced. Extremities: right MTP is red, hot and swollen. Neurologic: The patient is alert and oriented x3. No focal neurologic deficits noted.

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Epidemiology

Gout is predominantly a disease of men >40 years of age. Men have higher serum urate levels than women do, which increase their risk of developing gout. In women, gout usually involves the upper extremities. Women rarely have gouty arthritis attacks before menopause (Baker & Schumacher, 2010). Gout is the most common inflammatory arthritis disorder in the United States and approximately 3 to 5 million people are affected by it (Hilaire & Wozniak, 2010). The prevalence of gout and hyperurecimia has been increasing over the past few decades in response to a number of factors. These factors include, but are not limited, to high-purine diet, alcohol use, obesity, diabetes, and kidney disease.

Pathophysiology

The exact cause of gout is still unknown to date. However, the pathophysiology of gout is believed to be associated with purine metabolism and kidney function. Purines are biologically synthesized into purine nucleotides, which can be used in the synthesis of nucleic acids. The end product of uric metabolism is uric acid. Certain individuals with gout tend to have an increased in purine synthesis causing an overproduction of uric acid, while others break down nucleotides at an alarmed rate that also causing an overproduction of uric acid. An increased in production of uric acid is also caused by a deficiency of the enzyme hypoxanthine-guanine phophoribosyn-transferase (HGPRT) (McCance & Huether, 2010).

Uric acid is eliminated from the body through the kidneys. In primary gout, the kidneys excrete the uric acid slowly due to either by a decrease in glomerular filtration of urate or an acceleration in urate reabsorption (McCance & Huether, 2010). On the other hand, secondary gout is caused by certain medications and medical problems. Medications that are known to be associated with gout are diuretics, Aspirin, niacin, Levodopa, and cyclosporine. Medical conditions related to gout are hypertension, preeclampsia, diabetes, hyperthyroidism, hypothyroidim, obesity, and sarcoidosis (Teng, Nair & Saag, 2006).

Urine flow is also affected when monosodium crystals deposited in renal interstitial tissues. There are no clear answers that can explain exactly how crystals of monosodium urate ending up in joints and inducing gouty arthritis. However, several mechanisms that may be involved include lower body temperature, decreased albumin or glycosaminoglycan levels, changes in ion concentration and trauma that promotes urate crystal precipitation (McCance & Huether, 2010). The present of monododium urate crystals triggers the acute inflammatory response. The compliment system then activates cytokines to produce other substances called chemo attractants that will draw neutrophils out of the circulation to be phagocytizing the crystals. Several other inflammatory mediators are released during this process. These factors include chemotactic factors, lysosomal enzymes, eicosanoids, prostaglandin E (PGE2), IL-1 and IL-6, reactive oxygen species, and collagenase. Tissue damage begins to take place when urate crystals react with neutrophils and monocytes in the joint fluid (McCance & Huether, 2010).

Risk Factors

A major risk factor for gout is use of thiazide diuretic. Patients who are treated for high blood pressure with a loop or thiazide diuretic over a period of time often have hyperuricemia and can lead to further increase in gout attack (Hunter, York, Chaisson, Woods, Niu & Zhang, 2006). Diuretics play an important role in gouty arthritis by decreasing uric acid excretion and by increasing volume depletion (Gurwitz, Kalish, Bohn et al., 1997). Several dietary factors also play an important role in increasing the risk of gout. These factors include, but are not limited to, meat and seafood consumption, sugar sweetened soft drinks, alcohol and consumption of foods high in fructose. Certain medication conditions such as hypertriglyceridemia, hypertension, renal insufficiency, hypercholesterolemia, hyperuricemia, obesity, diabetes, and early menopause contribute to a higher risk of incident gout (Singh, Reddy & Kundukulam, 2011).

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Clinical Presentation

Gouty arthritis usually occurs in a peripheral joint. The primary symptom that patients always complaint of is severe pain. Approximately half of the initial attack occurs in the metatarsophalangeal joint of the great toe. The other half is usually involved with the heel, ankle, wrist, elbow, or instep of the foot. Within a few hours the affected joint becomes inflamed and extremely tender and may be swollen. Systemic signs of inflammation such as leukocytosis, fever, elevated sedimentation rate and lymphangitis sometimes present. There are four clinical stages of gout according to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). The first stage is known as asymptomatic hyperurecemia. During this stage, the patients can have an elevation of uric acid in the blood but they do not manifest 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 acute attacks of gout. This second stage is known as acute gouty arthritis. The third stage, known as interval or intercritical gout, involves the interval between acute flare gout attacks with persist crystals in the joints. When crystals deposits continue to accumulate, patients are likely to develop 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 Diagnosis

Gout can be mistaken for rheumatoid arthritis because tophi may resemble rheumatoid nodules and rheumatoid factors often become weakly positive as people age. It is still unclear why certain individuals with hyperuricemia are susceptible to develop tophi while others are not. The presence of urate crystals in the aspirate of a nodule will differentiate gout from rheumatoid arthritis. Radiographs can also be used to confirm the diagnosis (Mandell, 2008). It may be difficult to differentiate cellulitis or septic arthritis from gout, particularly when a fever, leukocytosis, or redness is present. The term Pseudogout, calcium pyrophosphates dehydrate deposition disease, can be difficult in clinically differentiating from gout. To confirm the diagnosis, joint aspiration is performed for culture and a search for urate crystals (Winstock, Neides & Miriam, 2009). Careful study of crystals obtained from the joint aspiration will determine the difference between the two conditions.

Diagnostic Test

The gold standard diagnostic test for gout is join aspiration (Winstock, Neides & Miriam, 2009). This procedure should take place after an acute attack has lessened to avoid patient discomfort. The present of monosodium urate crystals suggests the diagnosis of gout. 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 criteria for the case of gout. Patients must have at least six of the following symptoms to confirm the diagnosis.

* Hyperuricemia

* Redness of joint

* Suspected tophus

* Unilateral tarsal involvement

* Joint fluid culture negative for organisms during attack

* Maximum joint inflammation within one day

* More than one attack over time

* Monoarticular arthritis (although gout can be polyarticular)

* Great metatarsophalangeal pain or swelling

* Unilateral great metatarsophalangeal involvement

* Asymmetrical swelling within the joint on x-ray

* Subcortical cysts without erosion on x-ray

Treatment and Management

The goal of treating gout is to minimize or eliminate the urate crystals from the joints and other structures associated with them. Several aspects must be taken into consideration and each treatment regiment is varied 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.

Urate-lowering drugs is not recommended to treat patients with asymptomatic hyperurecemia. If hyperurecemia is identified, underlying causes such as obesity, alcohol consumption, hypercholesterolemia, and hypertension should be addressed. There are no high-quality randomized, placebo-controlled trials of nonsteoidal anti-inflammatory drugs (NSAIDs) and cox-2 inhibitors for treating acute gouty arthritis. However, they are recommended as first-line therapy for patients with acute gout. If the treatment is indicated within 24 hours of the onset of symptoms, naproxen 500 mg twice daily or indomethacin 50 mg three times daily is preferred for acute gouty inflammation. If patients experience several attacks per day, anti-inflammatory agents with fewer gastroduodenal side effects such as nabumetone or selective COX-2 inhibitor can be used. Aspirin is not recommended to treat acute gout attacks because of paradoxical effects of salicylates on serum urate.

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Corticosteroids can be used when there is monarthric gout involved. Patients with monarthric grout usually respond well when giving intra-articular injection. Systemic corticosteroids such as Prednisone in a dosage of 20 to 30 mg should be used only when NSAIDs and colchicine are contraindicated or not effective (Pittman & Bross, 1999).

Cochicine is also an effective treatment for acute gout. Oral colchicine is appropriate for patients who cannot tolerate NSAIDs and have contraindications to glucocorticoid. Colchicine works best when it is given within the first 12 to 36 hours of an attack. It works by inhibiting the phagocytosis of uric acid and blocking the release of chemotactic factor. It has anti-inflammatory activity but no analgesic activity (Pittman & Bross, 1999). However, majority of patients experience gastrointestinal side effects, including diarrhea, nausea, and vomiting.

Follow-up

It is very important to follow up patients after the treatment of an acute gout attacks. The patients should return for a follow-up visit within one month to be evaluated for therapy to lower serum uric acid levels. Initially, FNPs should assess their patients every one to two months to adjust the dose of uric acid-lower agents to achieve the therapeutic level of 5-6 mg/gL. After the therapeutic level is achieved and maintained, patients can be seen every 6-12 months. Patient Education

Certain heredity conditions can make patients more susceptible to gout. Patients who are obese should be advised to begin a rigorous program of supervised weight reduction but to avoid starvation that may only exacerbate the risk of gout. Maintenance of good hydration needs to be addressed to those who are at risk for kidney stones. Alcohol consumption such as beer and hard liquor can potentially increase the risk of incident gout. Dietary factors that increased the risk of gout include seafood, meat, sugar sweetened soft drinks, and consumption of foods that are high in fructose (Singh, Reddy, & Kundukulam, 2011).

The most important of treating an acute attack at the first sign of illness need to be addressed. Patients who are taking Allopurinol should be educated about the risk of hypersentivity reaction and advised to stop taking the medication immediately and call the physician at the first sign of a rash, fever, or other serious manifestation. Pain management is the primary concern during acute attacks. The patient should be instructed to take analgesic medication as directed. The join should be rested as much as possible in a position of comfort during attacks. Ice pack may help alleviating discomfort. The patient should not apply an ice pack no more than 15 minutes at a time to prevent nerve and tissue damage.

Conclusion

Gout 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 like Hydrochlorothiazide has significantly increased the incidence of secondary gout. 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 serious complications from this disorder.