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Metabolic conditions and the musculoskeletal system
Johan van Rensburg
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CRYSTAL-INDUCED ARTHRITIS
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TYPES Monosodium urate monohydrate Calcium pyrophosphate
Calcium hydroxyapatite Cholesterol
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URIC ACID POOL Endogenous Exogenous Excretion Kidneys (2/3)
Intestines (1/3) Serum urate: 0, ,55mmol/l Urine urate excretion: 1, ,4mmol/24 hours
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MECHANISM OF HYPERURICAEMIA
Overproduction Underexcretion
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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
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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
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PATHOGENESIS Crystallisation in joint Crystal absorbed by PMN
Secretion lysozyme enzymes Severe synovitis
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ACUTE GOUTY ARTHRITIS INCIDENCE Mostly men > 40yrs
Sometimes postmenopausal women (Often on Diuretics)
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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
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ACUTE GOUTY ARTHRITIS
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PERCIPITATING CAUSES ACUTE GOUTY ARTHRITIS
Trauma and surgery Medication Alcohol Diet
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ACUTE GOUTY ARTHRITIS
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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)
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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
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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)
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Prevention ?
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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
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CHRONIC TOPHACEOUS GOUT
Deposition of uric acid crystals in the tissues (tophi) After repeated attacks after 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
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TOPHI
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GOUTY TOPHUS
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INDICATIONS FOR LONG-TERM PROPHYLACTIC THERAPY
If conservative measures do not have the desired effect and the levels still remain high (> 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
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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
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CPPD
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DEFINITION Arthropathy and other locomotor disease associated with CPPD crystal deposition Sporadic, familial, and metabolic disease-associated forms recognized
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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)
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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
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METABOLIC ASSOCIATIONS
Many reflect chance concurrence of common age-related conditions Diabetes Uremia Paget’s disease Hypothyroidism Ochronosis Gout
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STRONGEST EVIDENCE Hyperparathyroidism Hemochromatosis
Hypophosphatasia Hypomagnesemia Wilson’s disease
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COMMON PRESENTATIONS Acute synovitis Chronic arthritis
Incidental finding
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DISTRIBUTION Any joint may be involved Knee commonest site Followed by
wrist shoulder ankle elbow
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INVESTIGATIONS Fluid and tissue analysis Plain radiographs
Other investigations may be undertaken to exclude alternative or coexisting arthropathy
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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
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RADIOGRAPHIC Calcification Structural changes
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CALCIFICATION Fibrocartilage Also in hyaline cartilage
knee menisci wrist triangular cartilage symphysis pubis Also in hyaline cartilage Capsular and synovial calcification is less common metacarpophalangeal joints and knee
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ACHILLIS CALCIFICATION
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PATELLOFEMORAL
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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)
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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
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BLANKET SCREEN Serum calcium Alkaline phosphatase Magnesium Ferritin
Liver function
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TREATMENT Colchichine IAI/draining Saline levage Ytrium Surgery
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