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BROOKLYN 3 STUDENTS Adam ROSCOE Samuel THOMAS. Fri 30 th Aug 2013 Session 2 / Talk 5 11:25 – 11:35. ABSTRACT

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Fri 30thAug 2013

Session 2 / Talk 5

11:25 – 11:35


A short presentation on Gouty arthritis, to help further our understanding of a common indication seen on Xray requests. In our presentation we are going to cover the basics of Gout, including a definition, pathological classification, history and nature of this joint pathology, and also clinical management of patients suffering from Gout.

Gout is a type of arthritis that results from an inflammatory response to a build up of uric acid in the vascular system progressing to erosion of the articulating surfaces of bones. It is an inherited metabolic disease and is classed either as an acute or chronic condition.

Gout is more prevalent in males and can be influenced by diet and lifestyle. The pathogenesis of Gout involves the metabolism of Purines, a type of nucleic acid found in beer, fish, and mushrooms. This results in a waste product called Uric acid, which if not regulated by the Kidney, will crystallize and lead to bone erosion. Clinicians suspecting Gouty arthritis in their patient are likely to consider the patient’s history, and send for tests such as Xray or synovial joint aspirations.

  • Definition of Gout
  • Pathological classification
  • History of Gout
  • Gout Aetiology & Pathogenesis
  • Clinical management of Gout patients
  • Gout is a type of arthritis
  • Gout results from an inflammatory response to build up of Uric acid in blood
  • Progresses to Urate crystals in joints
  • Urate crystals erode articulating surfaces of bone
pathological classification
Pathological Classification
  • An inherited metabolic disease
  • Acute of Chronic
pathological classification1
Pathological Classification
  • Acute Gout

  • Chronic Gout

history of gout
History of Gout

gout topography
Gout topography
  • More likely to suffer Gout
  • Most often affects
  • Less likely to suffer Gout
radiographic appearance
Radiographic appearance
  • Gout appears as radiolucent bone erosions around joints
  • Soft tissue swelling and inflammation present

radiographic appearance1
Radiographic appearance

  • Gout results from a build up of Uric acid
  • Uric acid results from metabolism of Purines
  • High blood uric acid levels can be due to a Purine-rich diet or kidney insufficiency
  • The nephron
  • Higher incidence of Gout in males as Oestrogen assists renal clearance of uric acid
  • Excess uric acid levels decrease solubility
  • This leads to crystalization
  • Urate deposits are covered with proteins as part of immune response forming Tophi
  • Tophi are the cause of bone erosion

gout management
Gout management
  • Treatment is in two stages
          • Minimization of the acute inflammation
          • Prevention of future attacks
  • Acute attacks are managed with drugs. They last 1-2 weeks
  • Chronic conditions are treated by lowering uric acid levels through exercise, weight loss, diet changes
clinical tests
Clinical tests
  • Patient history & physical examination
  • Arthrocentesis test
  • Blood/Urine analysis
  • X-ray studies
clinical tests patient history
Clinical tests: Patient history

Focus will be on

  • Family history
  • Recent trauma
  • Patient’s lifestyle & diet
clinical tests arthrocentesis
Clinical tests: Arthrocentesis
  • Test involves aspirating synovial fluid from affected joint
  • Fluid is examined for urate crystals
  • Performed when diagnosing chronic Gout
clinical tests blood urine
Clinical tests: Blood/Urine
  • Performed to assess uric acid levels when Gout diagnosis is unclear
clinical tests xray
Clinical tests: Xray
  • Performed mainly in later stages of Gout
case study
Case study
  • Patient had pain, swelling, deformities of 1st MTP joints.
  • Swelling around 3rd MCP joint in both hands
  • MRT contact with Gout patients is usually in later stages of disease
  • Be mindful positioning as the patient may be in pain

Anton, F., Garcia, J., Ramos, T., Gonzalez, P., Ordas, J. (1986). Sex Differences in Uric Acid Metabolism in Adults. Metabolism: Clinical and Experimetal, 35(4), 343-8. Retrieved from

Dalbeth, N. (2006). The Pathway from Gout to Bone Erosion. Retrieved from

Doherty, M. (2009). New Insights into the Epidemiology of Gout. Oxford Rheumatology Journal, 48:ii2–ii8. doi:10.1093

Eustice, C. (2012). Cut Back Purine-Rich Foods with Gout. Retrieved from

Gout. (2012). Retrieved from

Gout: Exams and Tests. (2010). Retrieved from

Kowalczyk, N., Mace, J. (2009). Radiographic Pathology for Technologists (5th ed.) St. Louis, Missouri: Mosby Elsevier

Mandell, B. (2008). Clincal Manifestations of Hyperuricemia and Gout. Cleveland Clinical Journal of Medicine, 75(5). Retrieved from

Manno, R. (2012). Clinical Features of Gout. Retrieved from

Marieb, E., Hoehn, K. (2007). Human Anatomy & Physiology (7th ed.). San Francisco, CA: Pearson Benjamin Cummings


Nuki, G., Simkin, P., (2006). A Concise History of Gout and Hyperuricemia and their Treatment. Journal of Arthritis Research and Therapy 2006, 8(1), doi:10.1186/ar1906

Stoppler, M. (2012). Gout. Retrieved from

Taylor, K. (2012). Uric Acid Crystals. Retrieved from

Teitel, A. (2011). Gout. Retrieved from

Zare, F., Magnusson, M., Bregstrom, T., Brisslert, M., Josefsson, E., Karlsson, A., Tarkowski, A. (2006). Uric Acid, a nucleic acid degredation product, down-regulates dsRNA-triggered arthritis. Journal of Leukocyte Biology, 79(3), 482-4. Retrieved from

acknowledgments of support
Acknowledgments of Support
  • Rouse Educational Trust
  • Pauline Hext