CRYSTAL INDUCED ARTHROPATHIES

BY: DR MEHRUNNISA UMAR ASSISSTANT PROFESOR DEPARTMENT OF MEDICINE

 Two main types of crystals:

- Sodium Urate & - Calcium pyrophosphate crystals Rarely - Crystals of cholesterol or - Calcium apatite cause acute synovitis.
Diffrentiated by their shapes and properties.

Gout
Gout is defined as a peripheral arthritis resulting from

the deposition of sodium urate crystals in one or more joints.

It is a metabolic disease. Associated with hyperuricemia. Often familial Usually monoarticular

Epidemiology
Affects less than 0.5% of the population Due to familial disposition, incidence may be as high as

80% in families affected by disorder.

Men > Women =10:1 over30 years. About 90% with Primary gout are men. In women onset is typically postmenopausal

Pathogenesis
Hyperuricemia is the major determinant for

developing gout.
Uric acid levels depends upon the balance between:

- Purine synthesis + ingestion of dietry purines & - excretion of uric acid by the kidneys.
Urate saturates in plasma at 7 mg/dL

Assuming pH, temp, Na are WNL

Uric Acid Metabolism

Synthesis:

- Last step in the purine metabolism pathway. - conversion of : Hypoxanthine Xanthine - Uric acid - Catalyzed by enzyme Xanthine Oxidase.
Excretion:

- Completely filtered by glomerulus - 98-100% reabsorbed by the proximal tubule. - 50% is secretted by the distal tubule.

Causes of Hyperuricemia
Impaired Excretion: (90%)

- Chronic renal disease

- Hypertension - Lead therapy - Hyperparathroidism - Hypothyroidism - Inc. lactic acid production-due to: - Alcohol - Exercise - Starvation - Drug therapy: - Thiazide diuretics - Low dose Aspirin

 Increased production of Uric acid (10%)

- Inc. purine synthesis due to: - Lesch Nyhan Syndrome - Phosphoribosyl pyrophosphate synthetase overactivity - G6PD deficiency (inc production +dec excretion) - Inc. turnover of purines due to: - Myeloproliferative disorders (Polycythemia Vera) - Lymphoproliferative disorders (leukemia, lymphoma) - carcinoma - Severe Psoriasis

Gout encompasses a group of disorders that occur alone or in combination and include 1) Hyperuricemia 2) Attacks of acute, typically monarticular, inflammatory arthritis 3) Tophaceous deposition of urate crystals in and around joints

4) Interstitial deposition of urate crystals in renal parenchyma

5) Urolithiasis

 Typical sequence involves progression through:

Asymptomatic hyperuricemia Acute gouty arthritis Interval or intercritical gout Chronic or tophaceous gout

Types Of Gout
Primary gout:
Overproducers: 10% Under-excretors: 90%

Secondary gout:
Excess nucleoprotein turnover (lymphoma, leukemia) Increased cell proliferation/death (psoriasis) Rare genetic disorder Lesch-Nyan Syndrome Pharmaceuticals(diuretics,low dose aspirin,cyclosporin) Alcohol

Signs and Symptoms

Acute attack:
Over hours frequently nocturnal Excruciating pain Swelling, redness and tenderness Podagra: 1st MTP classic presentation May effect knees, wrist, elbow, and rarely SI and hips.

Chronic:
Destructive tophacous arthritis Much greater chance if untreated Rarely presents as a chronic condition

Diagnosis
Based on history and physical exam Confirmed by Arthrocentesis

Urate crystals: needle-shaped negatively birefringent either free floating or within neutrophils & macrophages.

Uric acid level non specific.

30% may show normal level

24 hrs Urine collection:

<800 mg ------- Underexcertor > 800 mg ------- Overproducers

Microscopic Diagnosis

 Radiology
- Acute

Soft tissue swelling

Chronic

Chronic tophaceous gouty arthritis, extensive bony erosions are noted throughout the carpal bones Sclerosis and joint-space narrowing are seen in the first metatarsophalangeal joint, as well as in the fourth interphalangeal joint .

Treatment
Acute:
NSAIDs anti-inflammatory doses

- Naproxen -Indomethacin or - Diclofenac

Colchicine

- Started in acute attack. - Stop if no response or side effects. - Causes bone marrow suppression.
Corticosteroids

- Intramuscular or - Intra-articular depot methylprednisolone.

Treatment
Chronic: Dietry advice:
- Diet will decrease uric acid 1 mg/dL at best - Dec alcohol intake - Avoid foods rich in purines such as sea food, Spinach etc. - Weight loss Modification of medications

Avoid low dose ASA, diuretics, etc.

Treatment

Uricosuric drugs: for under-excretors

Probenicid: Sulfinpyrazone: toxic side effects Avoid with renal disease

Consider NSAIDs to avoid exacerbation of gout

Should not be started within a month of acute attack

Treatment

Indications for Allopurinol (xanthine Oxidase inhibitor)

Tophaceous deposites Uric acid consistently >9 Persistent symptoms with moderate UA levels Impaired renal function Prophylaxis for tumor-lysis syndrome

Consider NSAIDs to avoid exacerbation

Prognosis
Generally good More severe course when Symptoms present at less

than 30 yrs of age

Up to 50% progress to chronic disease if untreated. Surgical intervention may be required for tophi.

PSEUDOGOUT
Characterized by calcium pyrophosphate deposits in

hyaline and fibrocartilage.

Leads to chondrocalcinosis
Resembles Gout in presentation More common in elderly females Usually effects knee or wrist joints.

 In young people it is associated with:

- Haemochromatosis - Hyperparathyroidism - Wilsons disease - Alkaptonuria

Diagnosis
Joint Fluid Aspiration:

- Rhomboid shaped, weakly positively briefringent crystals

Radiology:

- Chondrocalcinosis on X Ray of joints.

TREATMENT
Aspiration of jointreduces pain. NSAIDs Colchicine Corticosteroidsintra articular

After exclusion of infection.

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