1 / 51

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) .

dara
Télécharger la présentation

Metabolic conditions and the musculoskeletal system

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related