Gout pathophysiology: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 76: Line 76:
Image:ChronicGout.jpg|Gout with tophi on elbow and knee.
Image:ChronicGout.jpg|Gout with tophi on elbow and knee.
Image:Gout (no birefringence).jpg|Gout (Needles, no birefringence, monosodium urate) <ref>http://picasaweb.google.com/mcmumbi/USMLEIIImages</ref>
Image:Gout (no birefringence).jpg|Gout (Needles, no birefringence, monosodium urate) <ref>http://picasaweb.google.com/mcmumbi/USMLEIIImages</ref>
</gallery>
</div>
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
[[Image:Gout case 1.jpg|left|thumb|400px|This is a gross photograph of an index finger from a patient with gout. The finger has been sectioned longitudinally to demonstrate the distal interphalangeal joint. Note the white chalky material within and adjacent to the joint (arrows). ]]
<br clear="left"/>
[[Image:Gout case 2.jpg|left|thumb|400px|This is a gross photograph of the elbow of this patient. The subcutaneous nodules (arrows) on this arm are tophi caused by gout. ]]
<br clear="left"/>
[[Image:Gout case 3.jpg|left|thumb|400px|This is a low-power photomicrograph of the tophus removed from the elbow of this patient. Note the fibrous connective tissue (1) and the large foci containing the urate crystals (2) surrounded by the intense chronic inflammatory reaction. ]]
<br clear="left"/>
[[Image:Gout case 4.jpg|left|thumb|400px|This higher-power photomicrograph of the tophus demonstrates the collections of urate crystals (1) and the inflammatory cells at the edge of these foci (2). ]]
<br clear="left"/>
[[Image:Gout case 5.jpg|left|thumb|400px|This is a higher-power photomicrograph of the edge of the tophus. Most of the urate crystals dissolve away during processing. The inflammatory cells at the edge of these foci are clearly visible (arrow). ]]
<br clear="left"/>
[[Image:Gout case 6.jpg|left|thumb|400px|This is a high-power photomicrograph of the edge of the tophus. The character of the intense chronic inflammatory cell reaction is evident and note the presence of giant cells within this inflammatory cell reaction (arrows). ]]
<br clear="left"/>
[[Image:Gout case 7.jpg|left|thumb|400px|This is a photomicrograph of a tophus that was fixed in alcohol prior to histologic processing. The alcohol fixation preserves the water soluble urate crystals within the tissue. Note the urate crystals visible in this photomicrograph (arrows). Also note the chronic inflammatory reaction in the background. ]]
<br clear="left"/>
[[Image:Gout case 8.jpg|left|thumb|400px|This is a gross photograph of a tophus on the great toe of another patient with gout (arrow). The healed surgical incision and the size of this tophus indicate that this was a long-standing problem for this patient. ]]
<br clear="left"/>
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0001.jpg|Kidney: Uric Acid Deposition: Gross, an excellent example of gouty nephropathy with deposits and excavation in pyramids
Image:Gout 0002.jpg|Kidney: Papillary Necrosis: Gross, yellow foci in pyramids, a gout kidney
Image:Gout 0003.jpg|Skin: Tophus: Micro med mag H&E uric acid deposits with giant cells. Easily recognizable as gout or uric acid tophus
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0004.jpg|Bone, synovium: Gout: Gross natural color opened joint with extensive white deposits of uric acid
Image:Gout 0005.jpg|Bone, synovium: Gout: Gross natural color close-up of extensive uric acid deposits
Image:Gout 0006.jpg|Bone, synovium: Gout: Gross natural color section through sternum and clavicle showing very well uric acid deposits in the periarticular tissue
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0007.jpg|Bone: Gout: Gross close-up of elbow with enlargement of proximal radius due to gout
Image:Gout 0008.jpg|Hand: Gout: Gross view of both hand with enlarged joints
Image:Gout 0009.jpg|Kidney: Gout: Gross natural color close-up view of uric acid deposit in medullary pyramid
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0010.jpg|Hand: Gout: Gross natural color
Image:Gout 0011.jpg|Urinary Tract: Staghorn calculi in renal pelvis, Gout
Image:Gout 0012.jpg|Bones-Joints: Gout
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0013.jpg|Bones-Joints: Gout
Image:Gout 0014.jpg|Bones-Joints: Gout
Image:Gout 0015.jpg|Bones-Joints: Gout
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0016.jpg|Bones-Joints: Gout
Image:Gout 0017.jpg|Bones-Joints: Gout
Image:Gout 0018.jpg|Bones-Joints: Gout
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0019.jpg|Bones-Joints: Gout
Image:Gout 0020.jpg|Bones-Joints: Gout
Image:Gout 0021.jpg|Bones-Joints: Gout
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0022.jpg|Bones-Joints: Gout, alcohol fixed tissues, monosodium urate crystals
Image:Gout 0023.jpg|Bones-Joints: Gout, alcohol fixed tissues, monosodium urate crystals
Image:Gout 0024.jpg|Bones-Joints: Gout, alcohol fixed tissues, monosodium urate crystals
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0025.jpg|Bones-Joints: Gout
Image:Gout 0026.jpg|Bones-Joints: Gout
Image:Gout 0027.jpg|Gout; Bursa of Knee
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0028.jpg|Joint: Uric Acid Crystals in Acute Gout
Image:Gout 0029.jpg|Joint: Gout
Image:Gout 0030.jpg|Knee Joint: Gout. Heavy Deposition of Urate Crystals in Articular Cartilage
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0031.jpg|Kidney: Uric Acid Deposition: Gross, infant kidney with excellent uric acid streaks
Image:Gout 0032.jpg|Kidney: Uric Acid Deposition: Gross good example uric acid streaks in medulla (very ischemic kidney)
Image:Gout 0033.jpg|Kidney: Uric Acid Nephropathy: Gross, natural color, an excellent view of hydronephrosis with inflamed pelvis and multiple calculi with deposits in medullary pyramids
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0034.jpg|Kidney: Uric Acid Deposition: Gross natural color close-up and excellent view of opaque material in medullary pyramid of adult kidney
Image:Gout 0035.jpg|Kidney: Uric Acid Infarcts: Gross natural color opened kidney showing marked ischemia with dark red medullary pyramids which contrast sharply with the uric acid deposits
Image:Gout 0036.jpg|Kidney: Uric Acid Infarcts: Gross natural color typical lesion well shown
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0037.jpg|Kidney: Uric Acid In Medulla: Gross natural color cut surface of kidney uric acid easily seen
Image:Gout 0038.jpg|Kidney: Uric Acid Infarcts: Gross natural color close-up outstanding photo of the uric acid streaks in medullary pyramids
Image:Gout 0039.jpg|Skin: Tophus: Micro med mag H&E easily recognized uric acid deposit lesion from elbow
</gallery>
</gallery>
</div>
</div>

Revision as of 17:09, 21 August 2012

Gout Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Differentiating Gout from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Gout pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Gout pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Gout pathophysiology

CDC on Gout pathophysiology

Gout pathophysiology in the news

Blogs on Gout pathophysiology

Directions to Hospitals Treating Gout

Risk calculators and risk factors for Gout pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Uric acid is more likely to form into crystals when there is a hyperuricaemia, although it is 10 times more common without clinical gout than with it[1]

Purines can be generated by the body via breakdown of cells in normal cellular turnover, or can be ingested in purine-rich foods such as seafood. the kidneys are responsible for approximately one-third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.

There are also different racial propensities to develop gout. Gout is high among the peoples of the Pacific Islands, and the Māori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid.[2] In the United States, gout is twice as prevalent in African American males as it is in Caucasians.[3]

A seasonal link also may exist, with significantly higher incidence of acute gout attacks occurring in the spring.[4] [5]

Hyperuricemia is considered an aspect of metabolic syndrome, although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among obese individuals.

Gout is a form of arthritis that affects mostly men between the ages of 40 and 50. The high levels of uric acid in the blood are caused by protein rich foods. Alcohol intake often causes acute attacks of gout and hereditary factors may contribute to the elevation of uric acid. Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.[6] It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout,[7][8] which condition is then known as saturnine gout, because of its association with alcohol and excess.[9]

Gout also can develop as co-morbidity of other diseases, including polycythaemia, leukaemia, intake of cytotoxics, obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. This form of gout is often called secondary gout. Diuretics (particularly thiazide diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this conclusion.[10]

(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, CA)







Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

This is a gross photograph of an index finger from a patient with gout. The finger has been sectioned longitudinally to demonstrate the distal interphalangeal joint. Note the white chalky material within and adjacent to the joint (arrows).


This is a gross photograph of the elbow of this patient. The subcutaneous nodules (arrows) on this arm are tophi caused by gout.


This is a low-power photomicrograph of the tophus removed from the elbow of this patient. Note the fibrous connective tissue (1) and the large foci containing the urate crystals (2) surrounded by the intense chronic inflammatory reaction.


This higher-power photomicrograph of the tophus demonstrates the collections of urate crystals (1) and the inflammatory cells at the edge of these foci (2).


This is a higher-power photomicrograph of the edge of the tophus. Most of the urate crystals dissolve away during processing. The inflammatory cells at the edge of these foci are clearly visible (arrow).


This is a high-power photomicrograph of the edge of the tophus. The character of the intense chronic inflammatory cell reaction is evident and note the presence of giant cells within this inflammatory cell reaction (arrows).


This is a photomicrograph of a tophus that was fixed in alcohol prior to histologic processing. The alcohol fixation preserves the water soluble urate crystals within the tissue. Note the urate crystals visible in this photomicrograph (arrows). Also note the chronic inflammatory reaction in the background.


This is a gross photograph of a tophus on the great toe of another patient with gout (arrow). The healed surgical incision and the size of this tophus indicate that this was a long-standing problem for this patient.


Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology













References

  1. Virsaladze D, Tetradze L, Djavashvili L, Esakia N, Tananashvili D. (2007). "Levels of uric Acid in serum in patients with metabolic syndrome". Georgian Med News. 146: 34&ndash, 7. PMID 17595458.
  2. Roberts-Thomson R, Roberts-Thomson P (1999). "Rheumatic disease and the Australian aborigine". Ann Rheum Dis. 58 (5): 266&ndasgh, 70. PMID 10225809.
  3. Rheumatology Therapeutics Medical Center. "What Are the Risk Factors for Gout?". Retrieved 2007-01-26.
  4. Schlesinger N, Gowin KM, Baker DG, Beutler AM, Hoffman BI, Schumacher HR Jr. "Acute gouty arthritis is seasonal". Retrieved 2007-09-27.
  5. Gallerani M, Govoni M, Mucinelli M, Bigoni M, Trotta F, Manfredini R. "Seasonal variation in the onset of acute microcrystalline arthritis". Retrieved 2007-09-27.
  6. Robert S. Ivker, D.O. ; et al. (1999). The Complete Self-Care guide to Holistic Medicine. pp. 186&ndash, 8. ISBN0-87477-986-J.
  7. Lin JL, Huang PT. (1994). "Body lead stores and urate excretion in men with chronic renal disease". J Rheumatol. 21 (4): 705&ndash, 9. PMID 8035397.
  8. Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. (2000). "Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the Normative Aging Study". J Rheumatol. 27 (7): 1708&ndash, 12. PMID 10914856.
  9. Ball GV. (1971). "Two epidemics of gout". Bull Hist Med. 45 (5): 401&ndash, 8. PMID 4947583.
  10. Janssens H, van de Lisdonk E, Janssen M, van den Hoogen H, Verbeek A (2006). "Gout, not induced by diuretics? A case-control study from primary care". Ann Rheum Dis. 65 (8): 1080&ndash, 3. doi:10.1136/ard.2005.040360. PMID 16291814.
  11. http://picasaweb.google.com/mcmumbi/USMLEIIImages

Template:WH Template:WS