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Crystal Associated Joint Diseases

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    CRYSTAL ASSOCIATED JOINT DISEASESCRYSTAL ASSOCIATED JOINT DISEASES

    As the name indicates, this group of disorders results As the name indicates, this group of disorders resultsfrom deposition of different crystals in the synoviumfrom deposition of different crystals in the synoviumand Synovial Fluid.and Synovial Fluid.

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    CRY STAL DEPOSITIONCRY STAL DEPOSITION

    Excess production of crystals.Excess production of crystals.Decrease elimination of crystals.Decrease elimination of crystals.Both.Both.

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    CRY STALSCRY STALS

    Hard particulate irregular structures. When they Hard particulate irregular structures. When they shed into the synovial fluid, they causeshed into the synovial fluid, they cause

    mechanical damage, which further activates themechanical damage, which further activates theinflammatory response.inflammatory response.

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    CRY STAL DISEASESCRY STAL DISEASES

    COMMON:COMMON: Acute gout ( Acute gout (Monosodium UrateMonosodium Urate). ).

    Chronic tophaceous gout (Manosodium Urate).Chronic tophaceous gout (Manosodium Urate). Acute pseudo gout ( Acute pseudo gout ( Calcium PyrophosphateCalcium PyrophosphateDihydrateDihydrate). ).Chronic pyrophosphate arthropathy ( Chronic pyrophosphate arthropathy ( CalciumCalciumPyrophosphate DehydratePyrophosphate Dehydrate). ).Chondrocalcinosis ( Chondrocalcinosis ( Calcium PyrophosphateCalcium PyrophosphateDihydrateDihydrate). ).

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    UNCOMMON:UNCOMMON: )Chronic calcific periarthritis (BasicCalcium )Chronic calcific periarthritis (BasicCalciumPhosphate).Phosphate).

    )Calcinosis (BasicCalcium Phosphate). )Calcinosis (BasicCalcium Phosphate). )Chronic effusion in rheumatoid arthritis )Chronic effusion in rheumatoid arthritis

    ( Cholesterol).( Cholesterol). ) Acute arthritis in dialysis patients ( Calcium ) Acute arthritis in dialysis patients ( CalciumOxalate).Oxalate).

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    G OUTG OUT

    CLINI C AL PR ESENTATIONCLINI C AL PR ESENTATIONInflammatory arthritis.Inflammatory arthritis.

    Bursitis.Bursitis. Tenosynovitis. Tenosynovitis.Cellulitis.Cellulitis.Nodular TophaiNodular Tophai

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    Incidence 1% world population.Incidence 1% world population.

    Incidence 1% world population.Incidence 1% world population.M:F: 10 : 1M:F: 10 : 1

    Type: Type: Primary:Primary: Disease of male gender.Disease of male gender.Secondary:Secondary: Both Sexes.Both Sexes.

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    AETIOLO G Y AND PATHO G ENES AETIOLO G Y AND PATHO G ENES

    When there is hyperuricemia due to imbalance When there is hyperuricemia due to imbalancein the production and elimination of uric acid.in the production and elimination of uric acid.

    As shown. As shown.

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    INCR EASED P R ODU C TION:INCR EASED P R ODU C TION:

    CML.CML.CLL.CLL.

    Polycythemia.Polycythemia.Psoriasis.Psoriasis.Chemotheaphy.Chemotheaphy.Unidentified abnormalities ( Common).Unidentified abnormalities ( Common).Specific enzyme defect: G o PD, HypoxanthineSpecific enzyme defect: G o PD, Hypoxanthine G uannine Phosphoridbosyl Deficiency.G uannine Phosphoridbosyl Deficiency.

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    DE CR EASED ELIMINATION:DE CR EASED ELIMINATION:

    1.1. CR F.CR F.2.2. R enal Tubular Defects. (Under Secretors)R enal Tubular Defects. (Under Secretors)3.3. Drugs: Thiazide Diuretics, Loop Diuretics.Drugs: Thiazide Diuretics, Loop Diuretics.

    Low Dose Asprin, Cyclosporin.Low Dose Asprin, Cyclosporin.Pyrazinamide, Lead Toxicity.Pyrazinamide, Lead Toxicity.Lactic Acidosis.Lactic Acidosis.

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    R ISK FA C TO R S:R ISK FA C TO R S:

    Obesity.Obesity.High alcohol consumption.High alcohol consumption.

    Type IV Hyperlipidemia. Type IV Hyperlipidemia.

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    CLINI C AL FEATU R ESCLINI C AL FEATU R ES

    ACUTE GOUT ACUTE GOUT1.1. Any joint. Any joint.2.2. First metatarso phalangeal joint.First metatarso phalangeal joint.3.3. The axial skeleton rarely involved. The axial skeleton rarely involved.4.4. Very acute onset. Very acute onset.5.5. Severe pain and tenderness.Severe pain and tenderness.6.6. Signs of acute inflammation.Signs of acute inflammation.7.7. Self limiting in 5Self limiting in 5 14 days.14 days.8.8. Constitutional symptoms.Constitutional symptoms.9.9. Petite attacks.Petite attacks.10.10. C luster attacks.C luster attacks.

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    CHR ONI C G OUTCHR ONI C G OUT

    Tophi at different sites. Tophi at different sites. Whitish appearance. Whitish appearance.Ulceration and secondary infection can occur.Ulceration and secondary infection can occur.Chalky white material.Chalky white material.

    There may be arthritic features. There may be arthritic features.

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    INVESTI G ATIONSINVESTI G ATIONS

    FBC .FBC .ESR; CR P.ESR; CR P.

    Joint aspirate. Joint aspirate.Polarized microscopy.Polarized microscopy.Serum uric acid: Normal or R aised.Serum uric acid: Normal or R aised.24 hours uric acid excretion (On Low Purine Diet).24 hours uric acid excretion (On Low Purine Diet).R enal function.R enal function.Fasting lipid profile.Fasting lipid profile.R adiological features in chronic diseases.R adiological features in chronic diseases.

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    MANAG EMENT:MANAG EMENT:

    Acute G out: Acute G out:NSAIDS (Not Salicylic Acid).NSAIDS (Not Salicylic Acid).C

    olchicine (Potent Inhibitor of Neutrophils).C

    olchicine (Potent Inhibitor of Neutrophils). Joint aspiration. Joint aspiration.Intra articular injection of steroids.Intra articular injection of steroids.Splinting.Splinting.

    Avoid precipitating factors. Avoid precipitating factors.

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    LON G TER M MANAG EMENTLON G TER M MANAG EMENT1.1. Counselling.Counselling.2.2. Correct predisposing factors.Correct predisposing factors.3.3. Life style modification.Life style modification.

    4.4. Low purine diet.Low purine diet.5.5. Hypourecemic Drugs: Allopurinol (Xanthine oxidaseHypourecemic Drugs: Allopurinol (Xanthine oxidase

    inhibitor).inhibitor).(Purines Hypoxanthine Xanthine Uric Acid).(Purines Hypoxanthine Xanthine Uric Acid).

    Dose is 100Dose is 100 300 mg / day:300 mg / day:Small dose in penal failure.Small dose in penal failure.

    Can precipitate acute goutCan precipitate acute gout..

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    C ALCIUM P YR OPHOSPHATEC ALCIUM P YR OPHOSPHATEDIH Y DR ATE CRY STAL DEPOSITIONDIH Y DR ATE CRY STAL DEPOSITION Aetiology: Sporadic, Familial; Metabolic Aetiology: Sporadic, Familial; MetabolicDiseases.Diseases.Majority cases occur after the age of 50 years.Majority cases occur after the age of 50 years.

    There is reduction in the proteoglycans There is reduction in the proteoglycans(inhibitor of crystal deposition).(inhibitor of crystal deposition).

    There is increased chondrocyte metabolism There is increased chondrocyte metabolism(pyrophosphate crystals).(pyrophosphate crystals).

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    METABOLI C C AUSES OF CPPDMETABOLI C C AUSES OF CPPD

    Haemochromatosis.Haemochromatosis.Hyper parathyroid.Hyper parathyroid.

    Hyphosphatisia.Hyphosphatisia.Hypomagnesemia.Hypomagnesemia.

    Wilsons disease. Wilsons disease.

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    CLINI C AL PR ESENTATION OF CPPDCLINI C AL PR ESENTATION OF CPPD

    Like acute gout.Like acute gout.Like osteoarthritis.Like osteoarthritis.

    An incidental finding. An incidental finding.

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    INVESTI G ATIONINVESTI G ATION

    FBC .FBC .ESR .ESR .

    CR P.CR P. Joint aspirate for polarized microscopy. Joint aspirate for polarized microscopy.R adiological:Chondrocalcinosis.R adiological:Chondrocalcinosis.

    Screening for the above metabolic disease inScreening for the above metabolic disease inselected cases.selected cases.

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    MANAG EMENMANAG EMEN

    As in acute gout. As in acute gout. As in osteoarthritis. As in osteoarthritis.


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