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Gout - Coggle Diagram
Gout
Risk Factors
Diet
Eating a diet rich in meat and seafood and drinking beverages sweetened with fruit sugar (fructose) increase levels of uric acid, which increase your risk of gout. Alcohol consumption, especially of beer, also increases the risk of gout.)
Obesity
If you're overweight, your body produces more uric acid and your kidneys have a more difficult time eliminating uric acid.
Medical Conditions
Certain diseases and conditions increase your risk of gout. These include untreated high blood pressure and chronic conditions such as diabetes, metabolic syndrome, and heart and kidney diseases.
Family History of Gout
If other members of your family have had gout, you're more likely to develop the disease.
Age and Sex
Gout occurs more often in men, primarily because women tend to have lower uric acid levels. After menopause, however, women's uric acid levels approach those of men. Men are also more likely to develop gout earlier, usually between the ages of 30 and 50, whereas women generally develop signs and symptoms after menopause.
Singh, Jasvinder A, et al. “Risk Factors for Gout and Prevention: a Systematic Review of the Literature.” Current Opinion in Rheumatology, U.S. National Library of Medicine, Mar. 2011, www.ncbi.nlm.nih.gov/pmc/articles/PMC4104583/.
Diagnostics
Joint Fluid Test
Fluid is drawn from affected joint and looked under microscope to see if urate crystals are present.
X-Ray Imaging
X-rays of joints can rule out other causes of joint inflammation, determining if gout could be a cause.
Blood Test
Blood test can be given to see uric acid and creatinine levels. Normal uric acid levels are less than 6mg/dL and normal creatinine levels are 0.7-1.2mg/dL.
Ultrasound
Musculoskeletal ultrasound can detect urate crystals in a joint which are present in gout.
Dual Energy CT Scan
This type of imaging can detect the presence of urate crystals in a joint, even when it is not acutely inflamed.
Mayo Clinic. “Gout.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 6 Mar. 2021, www.mayoclinic.org/diseases-conditions/gout/diagnosis-treatment/drc-20372903.
Clinical Manifestations
Intense joint pain typically in joints of big toe, ankles, feet, or knees.
Limited mobility/range of motion
Inflammation, lumps, redness, and swelling
Recurrent flare of inflammatory arthritis (gout flare)
Chronic inflammation of one or more joints (arthropathy)
Mayo Clinic. “Gout.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 6 Mar. 2021, www.mayoclinic.org/diseases-conditions/gout/symptoms-causes/syc-20372897.
Pathogenesis
When tissues become saturated, the urate salts precipitate, forming monosodium urate crystals.
Deposition of these crystals is most commonly in synovial areas, bone, skin, cartilage, tendon, ligament, and kidney, but involvement of a range of other musculoskeletal and non-musculoskeletal tissues also occurs.
An elevated serum urate level, together with local factors, can result in the deposition of urate crystals into the joints. Once crystals are deposited into a joint, they can be released into the joint space and initiate an inflammatory cascade causing acute gouty arthritis
The four phases of gout include asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout.
Gout is a type of inflammatory arthritis that is triggered by the crystallization of uric acid within the joints and is often associated with hyperuricemia.
Acute gout is typically intermittent, constituting one of the most painful conditions experienced by humans.
Chronic tophaceous gout usually develops after years of acute intermittent gout, although tophi occasionally can be part of the initial presentation. In addition to the morbidity that is attributable to gout itself, the disease is associated with such conditions as the insulin resistance syndrome, hypertension, nephropathy, and disorders associated with increased cell turnover
In some patients, advanced gout may occur with structural joint damage. Joint damage in gout is mediated both by direct effects of monosodium (MSU) crystals on joint tissue and by indirect effects of joint inflammation. In addition to their central role in pathogenesis of gout, MSU crystals have a physiological role, particularly as an adjuvant or ‘danger signal’ in immune surveillance.
An elevated serum urate level, together with local factors, can result in the deposition of urate crystals into the joints. Once crystals are deposited into a joint, they can be released into the joint space and initiate an inflammatory cascade causing acute gouty arthritis. These acute flares resolve, but the crystals remain in the joint.
HR;, Schumacher. “The Pathogenesis of Gout.” Cleveland Clinic Journal of Medicine, U.S. National Library of Medicine, 2008, pubmed.ncbi.nlm.nih.gov/18822468/.
Incidence and Prevalence
It affects about 8.3 million people, or 4% of the population.
In the United States in 2015–16, the overall prevalence of gout in adults was 3.9%, corresponding to a total affected population of 9.2 million.
Risk of getting gout increases with age.
Prevalence is approximately 20% in patients with a family history of gout.
Roddy, Edward, and Hyon K Choi. “Epidemiology of Gout.” Rheumatic Diseases Clinics of North America, U.S. National Library of Medicine, May 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4119792/.
Treatments
Gout medications can be used to treat acute attacks and prevent future attacks. Medications can also reduce your risk of complications from gout, such as the development of tophi from urate crystal deposits.
Colchicine
Your doctor may recommend colchicine, a type of pain reliever that effectively reduces gout pain. The drug's effectiveness may be offset, however, by side effects such as nausea, vomiting and diarrhea, especially if taken in large doses.
Examples: Colcrys, Mitigare
Corticosteroids
Corticosteroid medications, such as the drug prednisone, may control gout inflammation and pain. Corticosteroids may be in pill form, or they can be injected into your joint.
Examples: bethamethasone (Celestone), prednisone (Prednisone Intensol), prednisolone (Orapred, Prelone), Triamcinolone
Corticosteroids are generally used only in people with gout who can't take either NSAIDs or colchicine. Side effects of corticosteroids may include mood changes, increased blood sugar levels and elevated blood pressure.
Nonsteroidal anti-inflammatory drugs (NSAIDs).
NSAIDs include over-the-counter options such as ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve), as well as more-powerful prescription NSAIDs such as indomethacin (Indocin) or celecoxib (Celebrex).
Mayo Clinic. “Gout.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 6 Mar. 2021, www.mayoclinic.org/diseases-conditions/gout/diagnosis-treatment/drc-20372903.