1. Dr. Müge Bıçakçıgil Kalaycı
Gout
Dr. Müge Bıçakçıgil Kalaycı

2. GOUT Common medical problem,
Affects at least 1 percent of men in Western countries,
Male: female ratio 7:1 to 9:1.

3. Uric Acid Overproduction
Secondary causes
Excessive dietary purine intake
Increased nucleotide turnover
Myeloproliferative disease
Lymphoproliferative disease
Hemolytic anemia
Psoriasis
Accelerated ATP degradation
Hereditary fructose intolerance
Glycogen storage disease
Severe muscle exertion
Ethanol abuse
Primary causes
Idiopathic
HGPRT deficiency
Increased PRPP activity

4. Uric Acid underexcretion
Renal insufficiency
Inhibition of tubular urate secretion:
Keto- and lactoacidosis
Enhanced tubular urate reabsorption:
Diuretics,
Insulin resistance,
Dehydration
Undefined mechanism:
Hypertension,
Hyperparathyroidis
Low-dose salicylates,
Pyrazinamide,
Ethambutol
Lead nephropathy

5. Clinical & Laboratory Features
GOUT
Clinical & Laboratory Features

6. Stages - Asymptomatic Hyperuricemia
In physiological terms any level above 6.8 mg/dl is hyperuricemia, since it exceeds the soluble concentration of MSU in body fluids.
Vast majority of people with hyperuricemia will never develop symptoms.

7. Stages - Acute intermittent gout
Characteristic gout attack:
rapid development of warmth, swelling, erythema and pain in the affected joint.
The initial attack
is monoarticular and
in 50% of cases involves the 1st metatarsal joint, which will finally be affected in 90% of patients.

8. Acute Podagra

9. Stages - Acute intermittent gout
Other joints: MT, ankle, heels and knees.
Systemic symptoms: Fever, chills and malaise.
Early in the disease the episodes are infrequent
Between the attacks the previously affected joints are free of pain,
despite this, MSU crystals can be identified in the synovial fluid.

10. Stages – Chronic Tophaceous Gout
Usually develops after 10 years of acute intermittent gout.
In this stage the affected joints become persistently uncomfortable and swollen.
The intensity of these symptoms is much less than the acute attacks.

11. Stages – Chronic Tophaceous Gout
Characterized by:
tophi formation and
polyarticular involvement, including the small joints of the hands .
Subcutaneous gouty tophi can be found in the fingers, wrists, ears, knees, olecranon bursa and pressure points

12. Tophi

13. Tophi

14. Provocative factors
The degree of decrease or increase in the concentration of synovial-fluid urate is more related to acute attack than the degree of hyperuricemia .
Trauma is frequently reported as an initiating event for an acute gouty attack:
the attack occurs when the joint is allowed to rest,
there is arapid efflux of water from the joint fluid and the result is sudden increase in urate concentration.

15. Provocative factors Alcohol ingestion: Drugs:
By accelerating the breakdown of intracellular ATP
Alcohol contains large quantities of guanosine.
Drugs:
thiazides,
low dose aspirin.

16. Clinical association – Renal involvement
Chronic urate nephropathy:
Deposition of MSU in the renal medulla and pyramids,
Associated with mild microalbuminuria.
Acute uric acid nephropathy:
ARF caused by hyperuricemia
in tumor lysis syndrome or post chemotherapy.
Uric acid renal stones:
10-25% of all people with gout,
the incidence correlate with the serum urate levels.

17. Radiological features
In early stages :
Soft tissue swelling around the affected joints
Preserved joint space
Later:
Bony erosions that are both atrophic and hypertrophic,
Erosions with overhanging edges

18. Radiological features

19. Laboratory Features and Diagnosis
Uric acid level in serum is of limited value in establishing the diagnosis:
The majority of hyperuricemic subjects will not develop gout.
Normal level of uric acid during gouty attack is frequent.

20. Diagnosis
Definitive diagnosis is possible only by aspiration and inspection of the synovial fluid or tophaceous material.
Crystals are needle or rod-shaped.
On compensated polarized microscopy, they appear as a bright, birefringent crystals (usually intracellular) that are yellow when parallel to the axis of slow vibration.

21. Crystals

22. Treatment treating acute arthritic inflammation and urolithiasis
The management of gout involves
treating acute arthritic inflammation and urolithiasis
lowering urate levels with the goal of preventing recurrent disease and progression.

23. Treatment of Acute Gouty Arthritis
NSAIDs are considered first-line therapy.
Selective Cox-2 inhibitors are an alternative in patients with GI contraindications.
Corticosteroids or subcutaneous injections of corticotropin are additional alternatives.
Because colchicine adverse effects can be serious, IV colchicine should not be used.

24. Long-Term or Prophylactic Therapy
NSAIDs and colchicine are frequently used as prophylaxis against recurrent acute gout, since such episodes are common during the initiation of uric acid–lowering treatment.
Allopurinol and
Probenecid - a potent uricosuric agents equally acceptable as first-line drug.

25. PSEUDOGUT- CHONDROCALCİNOSİS

26. CPPD Crystals Deposition Disease (PSEUDOGUT- CHONDROCALCİNOSİS)
Can cause monoarthritis clinically indistinguishable from gout – Pseudogout.
Rheumatic manifestation of calcium pyrophosphate crystal deposition in articular cartilage (chondrocalcinosis), synovium, and periarticular ligaments and tendons

27. Pseudogout is most common in the knee (50%) but often also the wrist, elbow, shoulder,ankle and hand.
Identification of crystals is the only means of positive diagnosis.
Increasing age is a predisposing factor; more than 80% of patients are over 60 years old.
Peak age

28. Affects one or a few joints; typically those that are weight bearing or have suffered previous injury
Slowly progressive with occasional aexacerbations , which are usualy not associated with effusion, warmth, and redness
No rest pain (unless disease is end stage ) symptoms worse with or after sustained activity
Joints show bony swelling, crepitus, and restricted movement

29. Ca pyrophosphate (pseudogout)
Rod or rhomboid-shaped
Weakly positive birefringent