Gout ppt
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Gout is a chronic inflammatory disease in which monosodium urate crystal precipitate in joints, soft tissues and cartilage. it is due to increase uric acid level in blood. Gout characterized by red, hot, tender and pain. Presence of MSU crystals (needle shape) in aspirated synovial fluid confirm Gout.
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Gout ppt
- 1. GOUT Mohammad Reza Abdullahi Master student in Medical Science in Biochemistry International Islamic University Malaysia
- 2. Introduction • Gout is known as disease of kings • Gout is a chronic disease of deposition of monosodium urate (MSU) crystal, which form in the presence of increased urate concentration • It causes inflammation of joints and surrounding tissues • Formation of kidney stone may also be seen • It affects 1-2% of adult in developed countries • The prevalence of gout is much higher in men than in women • Uric acid level increase in half of gout patients • Uric acid is the end product of purine catabolism 2
- 3. Synthesis of purine • De novo synthesis • Salvage pathway 3
- 4. De novo synthesis of purine nucleotides: construction of the purine ring of inosinate (IMP) 4
- 5. 5
- 7. Degradation of purine nucleotide • Dietary nucleic acids will be degraded to nucleotide in the small intestine by pancreatic enzymes • Inside intestinal mucosal cell nucleotides converted to nucleosides, free base and uric acid as the end product • Purine nucleotides from de novo synthesis are primarily degraded in the liver • The free bases are send out from liver and salvaged by peripheral tissues 7
- 8. Digestion of dietary nucleic acids 8
- 10. pathophysiology • Gout is associated with increase uric acid in the plasma • Once uric acid has passed its saturation point of (6.8 mg/dL; at 37 °C, pH 7.4), it starts to precipitate out in the form of monosodium urate crystals • monosodium urate crystals deposit in joints, soft tissues and cartilage • Trigger the inflammatory response • Microcrystals tend to form in cooler areas of the body 10
- 11. Causes of hyperuricemia • Underexcretion of uric acid • More common ( ˜90%) • Decline in urinary excretion of uric acid • Overproduction of uric acid • Less common • Genetic abnormalities in enzyme related purine metabolism • Increased phosphoribosyl pyrophosphate synthetase (PRPP) • Decreased hypoxanthine-guanine phosphoribosyl transferase (HGPRT) • Increased cell turnover (cytotoxic chemotherapy, malignancies) • Increased ingestion of diets rich in purine 11
- 12. Laboratory diagnosis • Synovial fluids • Identification of MSU • Blood test • Plasma uric acid • ˃7mg in men • ˃6mg in women • WBC count • ESR 12 A) Under light microscope, B) under polarized microscope
- 13. Treatment • Anti inflammatory drugs (colchicine, prednisolone, indomethacin) • Uricosuric drugs (probenecid) • Xanthine oxidase inhibitor (allopurinol) 13
- 14. Dietary modification • Limiting food high in purine (seafood, red meat) • Limiting alcohol consumption • Maintaining adequate fluid intake 14
- 15. References • Denise R.Ferrier, Lippincott’s illustrated review Biochemistry, 6th edition, 2014 • David L.Nelson, Michael M.Cox, lehninger principles of biochemistry, 6th edition, 2013 • Richette, P., & Bardin,T. (2010). Gout. The Lancet, 375(9711), 318–328. https://doi.org/10.1016/S0140-6736(09)60883-7 • Tausche, A.-K., Jansen,T. L., Schröder, H.-E., Bornstein, S. R., Aringer, M., & Müller-Ladner, U. (2009). Gout--current diagnosis and treatment. Deutsches Ärzteblatt International, 106(34–35), 549–55. https://doi.org/10.3238/arztebl.2009.0549 15
- 16. Thank you 16
Editor's Notes
- Each addition to the purine ring is shaded to match Figure 22–34. After step 2, R symbolizes the 5-phospho-D-ribosyl group on which the purine ring is built. Formation of 5-phosphoribosylamine (step 1) is the first committed step in purine synthesis. Note that the product of step 9, AICAR, is the remnant of ATP released during histidine biosynthesis (see Fig. 22–22, step 5). Abbreviations are given for most intermediates to simplify the naming of the enzymes. Step 6a is the alternative path from AIR to CAIR occurring in higher eukaryotes.
- Both enzymes use PRPP as the source of the ribose 5-phosphate group (Figure 22.10). The release of pyrophosphate and its subsequent hydrolysis by pyrophosphatase makes these reactions irreversible. [Note : Adenosine is the only purine nucleoside to be salvaged. It is phosphorylated to AMP by adenosine kinase.
- causing the development of symptoms and clinical findings of gout.. Lower temperature allows crystallization. among cytokines, interleukins 1, 18, and 8, and of tumor necrosis factor, attracting more polymorphonuclear neutrophilic granu- locytes
- Increase availability of purine. The hyperuricemia can lead to the deposition of monosodium urate (MSU) crystals in the joints and an inflammatory response to the crystals, causing first acute and then progressing to chronic gouty arthritis. Formation of uric acid stone in kidney can also be seen.
- Colchicine suppress synthesis and secretion of chemotactic factor, NSAID inhibit synthesis of PG, probenecid increase renal excretion of UA, allopurinol is structural analogue of hypoxanthine
- Patients should maintain an adequate fl uid intake to produce an output of 2,000 mL/day—especially if patients are taking a uricosuric agent. Increased fl uid intake can also prevent the development of uric acid kidney stones