51
Metabolic conditions and the musculoskeletal system Johan van Rensburg

Johan van Rensburg. CRYSTAL-INDUCED ARTHRITIS TYPES Monosodium urate monohydrate Calcium pyrophosphate Calcium hydroxyapatite Cholesterol

Embed Size (px)

Citation preview

  • Slide 1
  • Johan van Rensburg
  • Slide 2
  • CRYSTAL-INDUCED ARTHRITIS
  • Slide 3
  • TYPES Monosodium urate monohydrate Calcium pyrophosphate Calcium hydroxyapatite Cholesterol
  • Slide 4
  • URIC ACID POOL Endogenous Exogenous Serum urate: 0,12 - 0,55mmol/l Urine urate excretion: 1,5 - 4,4mmol/24 hours Serum urate: 0,12 - 0,55mmol/l Urine urate excretion: 1,5 - 4,4mmol/24 hours Intestines (1/3) Excretion Kidneys (2/3)
  • Slide 5
  • MECHANISM OF HYPERURICAEMIA Overproduction Underexcretion
  • Slide 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
  • Slide 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
  • Slide 8
  • PATHOGENESIS Crystallisation in joint Crystal absorbed by PMN Secretion lysozyme enzymes Severe synovitis
  • Slide 9
  • Slide 10
  • ACUTE GOUTY ARTHRITIS INCIDENCE Mostly men > 40yrs Sometimes postmenopausal women (Often on Diuretics)
  • Slide 11
  • 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
  • Slide 12
  • ACUTE GOUTY ARTHRITIS
  • Slide 13
  • PERCIPITATING CAUSES ACUTE GOUTY ARTHRITIS Trauma and surgery Medication Alcohol Diet
  • Slide 14
  • ACUTE GOUTY ARTHRITIS
  • Slide 15
  • 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)
  • Slide 16
  • Slide 17
  • 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
  • Slide 18
  • 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)
  • Slide 19
  • Prevention ?
  • Slide 20
  • 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
  • Slide 21
  • 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
  • Slide 22
  • TOPHI
  • Slide 23
  • Slide 24
  • GOUTY TOPHUS
  • Slide 25
  • 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
  • Slide 26
  • MEDICINES FOR LONG-TERM PROPHYLAXIS Allopurinol 300mg/day Uricosurics medicines Probenecid 250mg bd Must not 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
  • Slide 27
  • CPPD
  • Slide 28
  • DEFINITION Arthropathy and other locomotor disease associated with CPPD crystal deposition Sporadic, familial, and metabolic disease-associated forms recognized
  • Slide 29
  • 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)
  • Slide 30
  • EPIDEMIOLOGY Female preponderance Rare under age 50, 1015% in those aged 6575 3060% in those over 85 years Framingham study showed an overall prevalence rate of 8 27% in those >85 years
  • Slide 31
  • METABOLIC ASSOCIATIONS Many reflect chance concurrence of common age- related conditions Diabetes Uremia Pagets disease Hypothyroidism ?Ochronosis ?Gout
  • Slide 32
  • STRONGEST EVIDENCE Hyperparathyroidism Hemochromatosis Hypophosphatasia Hypomagnesemia Wilsons disease
  • Slide 33
  • COMMON PRESENTATIONS Acute synovitis Chronic arthritis Incidental finding
  • Slide 34
  • DISTRIBUTION Any joint may be involved Knee commonest site Followed by wrist shoulder ankle elbow
  • Slide 35
  • Slide 36
  • INVESTIGATIONS Fluid and tissue analysis Plain radiographs Other investigations may be undertaken to exclude alternative or coexisting arthropathy
  • Slide 37
  • 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
  • Slide 38
  • Slide 39
  • Slide 40
  • RADIOGRAPHIC Calcification Structural changes
  • Slide 41
  • CALCIFICATION Fibrocartilage knee menisci wrist triangular cartilage symphysis pubis Also in hyaline cartilage Capsular and synovial calcification is less common metacarpophalangeal joints and knee
  • Slide 42
  • Slide 43
  • Slide 44
  • ACHILLIS CALCIFICATION
  • Slide 45
  • PATELLOFEMORAL
  • Slide 46
  • Slide 47
  • 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)
  • Slide 48
  • SCREENING Predisposing Metabolic Disease Unrewarding Warranted in the following circumstances early onset arthritis (