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# Overview
The diagnosis of gout is based upon the identification of intracellular monosodium urate (MSU) crystals in the synovial fluid aspirate of an affected joint, under polarizing light microscopy. But when this is not possible, a clinical diagnosis can be deduced with the help of classical clinical features, including the history and physical examination, laboratory findings, and various imaging studies.

## Diagnosis of acute gout
- While the favored approach is to find MSU crystals in the synovial fluid aspirate of an affected joint, in clinical practice a crystal evaluation is routinely not done.
- When a patient is presenting with classic symptoms of rapid onset (within 24 hours), podagra, swelling, and erythema, supported by the presence of hyperuricemia, a clinical diagnosis of gout can easily be concluded. 
- When an arthrocentesis is done, synovial fluid should be examined readily under routine light and polarizing light microscopy and looked for negatively birefringent needle-shaped MSU crystals. 
- In addition, testing for cell counts with differential, gram staining and culture should also be done on the aspirate.
- The sensitivity of this technique in demonstrating negatively birefringent intra- and extracellular crystals in patients with gout flares is at least 85 percent, and the specificity for gout is 100 percent.  . The sensitivity of can be further improved by examination of the sediment in a centrifuged specimen. 
Several sets of diagnostic criteria exit (see table).
A clinical prediction rule (online link) found that the following predicted urate crystals by aspiration:
- Male
- Onset within one day
- Joint redness
- First metatarsaophalangeal joint
- Previous arthritis attack per patient
- History of hypertension or 1 or more cardiovascular diseases
- Serum uric acid level > 5.88 mg/dl
However, among patients with high scores, 20% did not have crystals. Only one of 381 patients had bacterial arthritis.
HISTORICAL PERSPECTIVE:
- There is limited historical perspective for shock.

## Definition:
Shock is defined as decrease in the oxygen delivery to the cells and tissues due to either increase in oxygen demand, decrease in oxygen consumption, inadequate oxygen utilization or a combination of these processes.

## Classification:
- Distributive shock
- Obstructive shock
- cardiogenic shock
- Hypovolemic shock

## Causes:
- Distributive shock can be from Septic Shock, Systemic inflammatory response syndrome, endocrine, toxin and drug induced, Anaphylactic shock and Neurogenic shock.
- Obstructive shock can be mechanical, pulmonary or Vascular causes.
- Cardiogenic shock can be from cardiomyopathy, Arryhthmias or mechanical.
- Hypovolemic shock can be hemorrhagic or non -hemorrhagic.

## Pathophysiology:
OVERVIEW
-  Neogi T (2011). "Clinical practice. Gout". N Engl J Med. 364 (5): 44352. doi:10.1056/NEJMcp1001124. PMID 21288096..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
-  Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G (2004). "Purine-rich foods, dairy and protein intake, and the risk of gout in men". N Engl J Med. 350 (11): 1093103. doi:10.1056/NEJMoa035700. PMID 15014182.CS1 maint: Multiple names: authors list (link)
-  Jump up to: 8.0 8.1 Malik A, Schumacher HR, Dinnella JE, Clayburne GM (2009). "Clinical diagnostic criteria for gout: comparison with the gold standard of synovial fluid crystal analysis". J Clin Rheumatol. 15 (1): 224. doi:10.1097/RHU.0b013e3181945b79. PMID 19125136.CS1 maint: Multiple names: authors list (link)
-  Jump up to: 9.0 9.1 9.2 Janssens HJ, Fransen J,  van de Lisdonk EH, van Riel PL, van Weel C, Janssen M (2010). "A  diagnostic rule for acute gouty arthritis in primary care without joint  fluid analysis". Arch Intern Med. 170 (13): 11206. doi:10.1001/archinternmed.2010.196. PMID 20625017.CS1 maint: Multiple names: authors list (link)
-  Jump up to: 10.0 10.1 10.2 Schlesinger N, Norquist JM, Watson DJ (2009). "Serum urate during acute gout". J. Rheumatol. 36 (6): 12879. doi:10.3899/jrheum.080938. PMID 19369457. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)