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 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
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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 (> 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
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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, 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
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METABOLIC ASSOCIATIONS Many reflect chance concurrence of
common age- related conditions Diabetes Uremia Pagets disease
Hypothyroidism ?Ochronosis ?Gout
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 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 (