Gout Year 4 Internal Medicine Notes OmpathStudy

Gout Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / IMED 4.3 / NGUGI -- Slide 1 Gout Dennis Tonui Ivy Chepchirchir Slide 2 Introduction Gout is an inflammatory crystal arthropathy caused by the precipitation and deposition of uric acid crystals in synovial fluid and tissues. The term "gout" was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word gutta, meaning "a drop" (of liquid) Gout has been known since antiquity. Historically, it was referred to as "the king of diseases and the disease of kings" or "rich man's disease". Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women. Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679. Slide 3 Epidemiology Commonly affects men than women 3:1 Has 2 peaks of incidences{at 30-39 yrs and at 60 yrs of age) Gout affects around 1–2% of people in the Western world at some point in their lifetimes and is becoming more common. Some studies found that attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature Slide 4 Etiology Hyperuricemia -can be idiopathic(primary) or secondary\nPrimary hyperuricemia idiopathic extracellular supersaturation of uric acid Secondary hyperuricemia can be due to decreased uric acid excretion or can be due to increased uric acid production Slide 5 Etiology cont… Decreased uric acid excretion Medications eg pyrazinamide, niacin, aspirin, loop diuretics, thiazides chronic renal insufficiency ketoacidosis, lactic acidosis postmenopause Slide 6 Etiology cont… Increased uric acid production High cell turnover eg tumor lysis syndrome, hemolytic anemia, psoriasis, radiation Enzyme defects eg Lesch Nyhan syndrome, von Gierke disease Diet rich in protein and esp. purine ( eg red meat, sea food) Obesity Hypertension Hypercholesterolemia, hypertriglyceridemia Sleep apnea Slide 7 Etiology cont… Combined decreased excretion and overproduction High alcohol consumption Slide 8 Pathophysiology Precipitation of uric acid crystals in synovial fluid and tissues and is typically associated with hyperuricemia but can also occur if uric acid levels are normal Uric acid is an end product of purine metabolism that is excreted by the kidneys Uric acid has somewhat poor water solubility Triggers of urate crystal deposition include elevated uric acid levels, acidosis and low temperatures Slide 10 Pathophys cont… Crystalline arthritis: supersaturation of uric acid in extracellular fluid intraarticular uric acid precipitation phagocytosis by PMNs release of inflammatory mediators and enzymes local joint inflammation Chronic effects: repeated attacks aggregation of urate crystals and giant cells (tophi) deformities and arthritis Slide 11 CLINICAL FEATURES Asymptomatic stage: associated with hyperuricemia with no symptoms and may last more than 10 years Acute gouty arthritis: triggers include trauma, surgery, sudden increase in uric acid, dehydration and diuresis Most common manifestations of acute gouty arthritis include\nacute severe pain with overlying erythema, decreased range of motion, swelling and warmth possibly fever,\nsymptoms more likely to occur at night waking the patient, and peak 12-24 hrs Slide 12 Clinical features cont… Location of acute gouty arthritis Usually monoarthritis during first attacks Peripheral small joints in the lower extremeties are especially affected Podagra: MTP joint inflammation of the big toe(most common site) Gonagra: inflammation of the knee Chiragra: inflammation of finger joints Slide 14 Clinical features cont… Intercritical stage: asymptomatic and may last upto several years Chronic gouty arthritis: uncommon in these times Progressive joint destruction Tophi formation(multiple painless hard nodules): bone tophi(urate crystal deposition in bones), soft tissue tophi( external ear, subcutis, tendon sheaths, synovial bursae) Renal manifestations: uric acid nephrolithiasis, uric acid nephropathy Slide 15 Gouty Tophi Slide 16 diagnostics Approach Acute gout(gout flare):\nAssess the clinical probability of septic arthritis: if relatively high, perform arthrocentesis for synovial fluid analysis Assess the clinical probability of acute gout; if relatively low, arthrocentesis with synovial fluid analysis is recommended; if high, diagnostic tests are not routinely required Chronic gout: a combo of hx, examination and imaging findings( eg tophi) and evidence of MSU crystals on aspirate of tophi or synovial fluid analysis confirms dx of chronic gout Slide 17 Diagnostics cont… Arthrocentesis and synovial fluid analysis: Gold standard for diagnosing gout but should only be performed if polarized light microscopy is available and providers are trained in the procedure Xtic findings: Polarized light microscopy: Needle shaped monosodium urate crystals that are