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Metabolic conditions and the musculoskeletal system

Metabolic conditions and the musculoskeletal system. Johan van Rensburg. CRYSTAL-INDUCED ARTHRITIS. TYPES. Monosodium urate monohydrate Calcium pyrophosphate Calcium hydroxyapatite Cholesterol. URIC ACID POOL. Endogenous. Exogenous. Excretion. Kidneys (2/3). Intestines (1/3) .

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Metabolic conditions and the musculoskeletal system

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  1. Metabolic conditions and the musculoskeletal system Johan van Rensburg

  2. CRYSTAL-INDUCED ARTHRITIS

  3. TYPES • Monosodium urate monohydrate • Calcium pyrophosphate • Calcium hydroxyapatite • Cholesterol

  4. URIC ACID POOL Endogenous Exogenous Excretion Kidneys (2/3) Intestines(1/3) Serum urate: 0,12 - 0,55mmol/l Urine urate excretion: 1,5 - 4,4mmol/24 hours

  5. MECHANISM OF HYPERURICAEMIA • Overproduction • Underexcretion

  6. HYPERURICAEMIA AND GOUT • (MONOSODIUM URATE) • disorder of purine metabolism • characterised • hyperuricaemia • deposition of uric acid or urate crystals in the tissues • manifests as • acute attacks of gouty arthritis • tophi • kidney stones • urate-nephropathy

  7. PATHOGENESIS • Hyperuricaemia causes gout, but is not synonomous with gout • Factors promoting crystallisation (0.55mmol/l) • the level of saturation • solubility • pH and temperature of the limb

  8. PATHOGENESIS Crystallisationinjoint CrystalabsorbedbyPMN Secretion lysozyme enzymes Severe synovitis

  9. ACUTE GOUTY ARTHRITIS • INCIDENCE • Mostly men > 40yrs • Sometimes postmenopausal women • (Often on Diuretics)

  10. CLINIAL PICTURE ACUTE GOUTY ARTHRITIS • Goes to bed healthy • Wakes up sudden monoarthritis ( 85% Podagra) • (heel, instep, knee, wrist and hands and elbow -olecranon bursitis) • Rigors with severe pain • Night spent in torture • Joint is red (“ripe tomato”),warm and very tender. • After attack skin around the joint often peels off • Acute attacks usually pass completely until the next attack Uncontrolled hyperuricaemia may lead to polyarticular gout

  11. ACUTE GOUTY ARTHRITIS

  12. PERCIPITATING CAUSES ACUTE GOUTY ARTHRITIS • Trauma and surgery • Medication • Alcohol • Diet

  13. ACUTE GOUTY ARTHRITIS

  14. DIAGNOSIS OF GOUT • Family history, as well as a typical history of attacks • Typical clinical picture and tophi • Elevated serum urate - (may be normal during attacks) • Urate crystals in aspiration fluid (as well as tophi) • X rays: Punched-out erosions (Rat bitten)

  15. TREATMENT • Exclude precipitating causes • A low purine diet and avoidance of alcohol are recommended • Foods with a very high purine content: anchovy, sardines, liver and kidneys. Most meats, fish and chicken products also have a high purine content. • Treatment of acute attacks • Long-term preventive treatment • Treatment of associated conditions such as • obesity • hypertension • hyperlipaemia • kidney failure

  16. RX ACUTE ATTACK • Avoid initiation of prophylactics with an acute attack • Prophylactic therapy is not discontinued if a patient is already on therapy • NSAIDS ( not used in kidney failure) • Colchicine • Corticosteroids (in resistant cases)

  17. Prevention ?

  18. Progression in the disease • Asymptomatic hyperuricaemia • continues until possible first attack • Acute gouty arthritis • Interval hyperuricaemia • periods between attacks • Chronic tophaceous gout • Complications • kidney stones and nephropathy

  19. CHRONIC TOPHACEOUS GOUT • Deposition of uric acid crystals in the tissues (tophi) • After repeated attacks after 11 - 12 years • The tophi occur in • The auricles - helix • Tendons (hands, achilles tendon and feet) • Bursae - especially olecranon bursa • The tophi may ulcerate with secretion of pasty material

  20. TOPHI

  21. GOUTY TOPHUS

  22. INDICATIONS FOR LONG-TERM PROPHYLACTIC THERAPY • If conservative measures do not have the desired effect and the levels still remain high (> 0.55 - 0.6 mmol/l) with repeated attacks • (If less than 1 attack per year is experienced, treatment is not necessary) • Positive family history of gout and kidney stones with very high urate levels • Chronic tophaceous gout • Kidney stones or nephropathy

  23. MEDICINES FOR LONG-TERM PROPHYLAXIS • Allopurinol 300mg/day • Uricosurics medicines • Probenecid250mg bd • Mustnot be used if there is kidney failure or kidney stones • To avoid kidney stones a high fluid intake (2l/day) must be maintained and in addition the urine can be alkalised with something like “citrosoda” • Colchicine 0.5mg should be added once or twice daily for the first few months in order to prevent recurrent attacks

  24. CPPD

  25. DEFINITION • Arthropathy and other locomotor disease associated with CPPD crystal deposition • Sporadic, familial, and metabolic disease-associated forms recognized

  26. CLINICAL FEATURES • Predominantly a disease of the elderly • Acute self-limiting synovitis (‘pseudogout’) • Chronic arthropathy showing strong association/overlap with OA • Target joints – knees, wrists (shoulders, hips)

  27. EPIDEMIOLOGY • Female preponderance • Rare under age 50, • 10–15% in those aged 65–75 • 30–60% in those over 85 years • Framingham study • showed an overall prevalence rate of 8 • 27% in those >85 years

  28. METABOLIC ASSOCIATIONS • Many reflect chance concurrence of common age-related conditions • Diabetes • Uremia • Paget’s disease • Hypothyroidism • Ochronosis • Gout

  29. STRONGEST EVIDENCE • Hyperparathyroidism • Hemochromatosis • Hypophosphatasia • Hypomagnesemia • Wilson’s disease

  30. COMMON PRESENTATIONS • Acute synovitis • Chronic arthritis • Incidental finding

  31. DISTRIBUTION • Any joint may be involved • Knee commonest site • Followed by • wrist • shoulder • ankle • elbow

  32. INVESTIGATIONS • Fluid and tissue analysis • Plain radiographs • Other investigations may be undertaken to exclude alternative or coexisting arthropathy

  33. CPPD Crystal Identification • Aspirated fluid turbid / blood-stained • Greatly elevated cell count (usually >90% neutrophils). • CPPD crystals poorly visualized LM • Polarized light microscopy • Morphology (usually rhomboids or rods) • Weak positive birefringence • May often be missed

  34. RADIOGRAPHIC • Calcification • Structural changes

  35. CALCIFICATION • Fibrocartilage • knee menisci • wrist triangular cartilage • symphysis pubis • Also in hyaline cartilage • Capsular and synovial calcification is less common • metacarpophalangeal joints and knee

  36. ACHILLIS CALCIFICATION

  37. PATELLOFEMORAL

  38. Additional Investigations • Aspirated fluid • Gram stain and culture • Moderate acute phase response • Elevation • plasma viscosity • ESR • acute phase reactants (e.g. C reactive protein) • peripheral white cell count (neutrophils)

  39. SCREENING • Predisposing Metabolic Disease • Unrewarding • Warranted in the following circumstances • early onset arthritis (<55 yrs) • florid polyarticular • recurrent acute attacks • additional clinical or radiographic clues

  40. BLANKET SCREEN • Serum calcium • Alkaline phosphatase • Magnesium • Ferritin • Liver function

  41. TREATMENT • Colchichine • IAI/draining • Saline levage • Ytrium • Surgery

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