1. CRYSTAL ASSOCIATED DISEASE
4/23/2017
Dr. Alka Stoelinga

2. CRYSTAL ASSOCIATED DISEASES
ASSOCIATION
COMMON
Monosodium urate monohydrate
Calcium pyrophosphate dihydrate
Basic calcium phosphates
Acute gout
Chronic tophaceous gout
Acute pseudogout
Chronic arthropathy
Chondrocalcinosis
Calcific periarthritis
Calcinosis
UNCOMMON
Cholesterol
Calcium oxalate
Extrinsic crystals/ semi-crystalline particles
Synthetic crystals
Plant thorns/ sea urchin spines
Chronic effusions in rheumatoid arthritis
Acute arthritis in Dialysis patient
Acute synovitis
Chronic monoarthritis, tenosynovitis
4/23/2017
Dr. Alka Stoelinga

3. GOUT
4/23/2017
Dr. Alka Stoelinga

4. GOUT Also known as podagra when it involves the big toe
Is medical condition usually characterized by recurrent attacks of acute inflammatory arthritis
Gout is an abnormality of uric acid metabolism that results in the deposition of Monosodium urate Monohydrate crystals
It is caused by elevated levels of uric acid in the blood which crystallize and are deposited in joints, tendons, and surrounding tissues.
The metatarsal- phalangeal joint at the base of the big toe is the most commonly affected
Results in pathological reaction in:
Joints: Gouty arthritis
Soft tissue: Tophi and Tenosynovitis
Urinary tract: Urate stones/ Urate nephropathy.
M:F=10:1
Prevalence rate increase with:
--Age
--Serum uric acid concentration
4/23/2017
Dr. Alka Stoelinga

5. Hyperuricemia is the underlying cause of gout.
Hyperuricemia is defined as
A plasma urate level
> 420 μmol/L (7.0 mg/dL) in males and
> 360 μmol/L (6.0 mg/dL) in females.
This can occur for a number of reasons, including
Diet
Genetic predisposition
Underexcretion of urate, the salts of uric acid
Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases
Overproduction is the cause in less than 10%
About 10% of people with hyperuricemia develop gout at some point in their lifetimes
The risk varies depending on the degree of hyperuricemia.
When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dL), the risk is 0.5% per year
In those with a level greater than 535 μmol/L (9 mg/dL), the risk is 4.5% per year
4/23/2017
Dr. Alka Stoelinga

6. PATHOPHYSIOLOGY
4/23/2017
Dr. Alka Stoelinga

7. Pathophysiology Disorder of purine metabolism
Final metabolite uric acid
Crystallizes in the form of monosodium urate, precipitates in joints, on tendons, and in the surrounding tissues.
These crystals then trigger a local immune-mediated inflammatory reaction with interleukin 1β
An evolutionary loss of uricase (breaks down uric acid)
Uric acid crystallizes as levels increase
Other factors triggering an acute episode of arthritis include
cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate.
Rapid changes in uric acid may occur due to a number of factors, including
trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.
4/23/2017
Dr. Alka Stoelinga

8. Types: Primary Gout: Exclusively in male
Common cause of inflammatory arthritis in men>40 years
Secondary Gout:
Due to renal impairment
Drugs
4/23/2017
Dr. Alka Stoelinga

9. Predisposing factors for Hyperuricemia:
Diminished renal excretion of uric acid
Inherited isolated renal tubular defect
Renal failure
Drugs: Diuretics, Pyrazinamide, Low dose of aspirin
Lead poisoning
Hyperparathyroidism
Myxedema
Down’s syndrome
Lactic Acidosis: Alcohol, Exercise, Starvation, Vomiting, Toxemia of pregnancy
4/23/2017
Dr. Alka Stoelinga

10. Predisposing factors for Hyperuricemia:
2. Increased production of Uric acid:
Increased turnover of Purines
--Chronic Myeloproliferative disorders e.g. Polycythaemia Vera
--Chronic Lymphoproliferative disorders e.g. CLL
--Psoriasis
Increased purine synthesis de novo
--Unidentified abnormality
--Specific enzyme defect
--HGPRT deficiency
--PRP deficiency
4/23/2017
Dr. Alka Stoelinga

11. Predisposing factors for Hyperuricemia:
MSUM crystal deposition:
Around synovial joints
Initially lower limb joints
Especially 1st Metatarsophalangeal joint
Small joints of feet and hand
Crystal induces:
Inflammation of the joints/Periarticular tissue
Pressure effect
Secondary osteoarthritis
4/23/2017
Dr. Alka Stoelinga

12. Gout with Tophi on elbow and knee.
4/23/2017
Dr. Alka Stoelinga

13. Clinical features: ACUTE GOUTY ARTHRITIS:
Peak age of onset in men is 45 years
Usually after years of sustained Hyperuricemia
Usually single joint involvement at first, common is 1st Metatarsophalangeal joint of great toe.
Other joints : Ankle, Midfoot, Knee, small joints of hands and wrist
Severe pain and extreme tenderness
The joint is red, hot, swollen with shiny overlying skin and dilated veins
Fever, malaise
Pruritis, desquamation
Initial attacks are usually self limited over 5-14 days
4/23/2017
Dr. Alka Stoelinga

14. Precipitating factors: Dietary excess Alcohol Starvation Diuretics
Interictal period:
More than 50% of patients experience recurrent arthritis within 1 year of first attack, subsequently frequency increases, attacks will be more prolonged and severe and involve multiple joints.
Precipitating factors:
Dietary excess
Alcohol
Starvation
Diuretics
Trauma, unusual physical exercise
Systemic infection
4/23/2017
Dr. Alka Stoelinga

15. Acute gouty arthritis on the big toe of an elderly man.
4/23/2017
Dr. Alka Stoelinga

16. CHRONIC TOPHACEOUS GOUT:
Recurrent attacks are followed by chronic gout in which there is progressive cartilage and bone erosions in association with deposition of Tophi and secondary degenerative changes
They appear years after initial attack
Tophi is firm, painless, irregular nodules, due to deposition of large MSUM crystals
Found around extensor surfaces of joints and their presence cause immobility of joints and severe joint deformities
Usual sites: Fingers, hand, forearm, elbow, Achilles tendon, cartilage of ear.
May ulcerate, discharge of white gritty material
4/23/2017
Dr. Alka Stoelinga

17. Severe gout in the fingers resulting in large, hard deposits of crystals of uric acid. These deposits are called Tophi
4/23/2017
Dr. Alka Stoelinga

18. 4/23/2017
Dr. Alka Stoelinga

19. OTHER MANIFESTATIONS: Synovitis Deformity of joints
Urolithiasis: Uric acid Calculi
Chronic urate nephropathy
4/23/2017
Dr. Alka Stoelinga

20. INVESTIGATIONS: 1. Synovial fluid examination
A definitive diagnosis of gout is based upon the identification of monosodium urate (MSU) crystals in synovial fluid or a tophus
Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence.
The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.
Increased cells: Neutrophils
Turbid
2. Blood tests
Hyperuricemia is a classic feature of gout
However, Gout occurs nearly half of the time without hyperuricemia, and most people with raised uric acid levels never develop gout.
Other blood tests commonly performed are
White blood cell count
Electrolytes
Renal function test
Liver function test
Erythrocyte sedimentation rate (ESR).
Both the white blood cells and ESR may be elevated due to gout in the absence of infection
3. Joint X-ray/ KUB
4. Dual-energy CT scanning (DECT)
4/23/2017
Dr. Alka Stoelinga

21. Using a sterile syringe and needle, fluid is withdrawn from the inflamed joint and then analyzed for uric acid crystals
4/23/2017
Dr. Alka Stoelinga

22. Fluid obtained from crystal deposits in a patient with gout
4/23/2017
Dr. Alka Stoelinga

23. A purulent knee aspirate from a person with presumed gout
4/23/2017
Dr. Alka Stoelinga

24. Needle-shaped urate crystals diagnostic of gout from an acutely inflamed joint (left) as seen under polarized microscopy and unpolarized microscopy (right)
4/23/2017
Dr. Alka Stoelinga

25. Gouty Tophi
4/23/2017
Dr. Alka Stoelinga

26. MANAGEMENT Treatment of Acute attack: NSAIDS Indomethacin and Naproxen
Colchicine
Joint aspiration
Intra-articular steroids
Analgesics: Opioids may be required for pain and aspirin should be avoided
Bed rest for 24 hours
4/23/2017
Dr. Alka Stoelinga

27. Long term therapy:
Long term therapy should be started when acute attack has settled.
Indications of Hypourecemic drug:
Recurrent attack of acute gout
Presence of Tophi
Increased uric acid level
Evidence of bone or joint damage
Associated with renal disease
4/23/2017
Dr. Alka Stoelinga

28. --Indicated In overproduction of uric acids Xanthine oxidase inhibitor
Drug therapy:
Allopurinol:
--Indicated In overproduction of uric acids
Xanthine oxidase inhibitor
Can precipitate acute attack
Start with low dose/combine with Colchicine
Not to be used during acute attack
2. Uricosurics:
--Indicated in undersecretors of uric acid
--when increased frequency or severity of acute Gout.
Probenecid
Sulfinpyrazone
4/23/2017
Dr. Alka Stoelinga

29. 4/23/2017
Dr. Alka Stoelinga

30. LIFE STYLE MODIFICATION: Weight reduction Reduction of alcohol intake
Avoidance of foods containing high levels of Purine E.g. Meat, organ meat, seafood, beans, spinach, alcohol
Adequate fluid intake
Withdrawal of drugs such as Diuretics and salicyclates.
4/23/2017
Dr. Alka Stoelinga

31. Relationship of Hyperuricemia with other diseases:
Patients with Hyperurecemia and Gout have and increased incidence of:
Hypertension
Renal disease (Nephrosclerosis, Tophi, Pyelonephritis)
Diabetes mellitus
Hypertriglyceridemia
Atherosclerosis
4/23/2017
Dr. Alka Stoelinga

32. 4/23/2017
Dr. Alka Stoelinga