Mainly for postgraduate level.

1. GOUT
A N U J A M A R Y S A B U
I V t h S E M E S T E R

2. • Disorder characterized by ↑ levels of uric acid –end product
of purine catabolism in blood – Hyperuricemia.
• Can be because of overproduction & under excretion of UA.
• Hyperuricemia leads to the deposition of monosodium urate
crystals in the joints.
• Inflammatory response to crystals → acute & progressing
to chronic gouty arthritis.
• Nodular masses of mono.sodi.urate crystals (tophi) –in soft
tissues – tophaceous gout →chronic tophaceous gout
• Formation of UA in kidney –Urolithiasis.

3. UROLITHIASIS

4. Hyperuricemia Gout ,
Gout preceded by Hyperuricemia

5. CATABOLISM OF PURINE

9. FATE OF URIC ACID

10. HYPERURICEMIC CASCADE

11. HISTORY
• 5th century BC : Hippocrates referred it as ‘unwalkable
disease’.
• The word ‘gout’ is derived from the latin word ‘gutta’.
• Earlier it was known as ‘The Disease Of Kings’

12. PATHOGENESIS
• Hyperuricemia leads to deposition of urate crystals &
subsequent inflammation.
1. Urate crystals begin precipitating at serum uric acid levels
of about6.8mg/dL.
2. Abrupt release of urate crystals into joint space may cause
acute inflammatory reaction (gouty arthritis).
3. Local factors influencing gout development in presence of
hyperuricemia include :
a. Trauma
b. Irritation
c. Reudced temparature

13. CAUSES
The proteins that we consume in our diet get digested & undergo
various steps of degradation in our body
Normal
metabolism Purines Diet
/proteins
Uric
acid
Rise in
levels
Formation
of crystals
Crystal
s
collect
in joint
Elimination from
the body:
urine/faeces
Gout
Rapid pain,
swelling &
redness of joint

14. BIOCHEMICAL CHANGES
• Changes in kinetics of PRPP synthetase.
• Glucose-6-phosphatase deficiency.
• HGPRTase absence & deficiency.
• Secondary to cancer, chemotherapy & radiotherapy.
• Conditions of increased cell proliferation.

15. RISK FACTORS

17. Uncontrolled Hyperuricemia
1 2 3 4

18. COMMON SITES OF ACUTE FLARES

19. CLASSIFICATION OF GOUT
PRIMARY
GOUT
SECONDAR
Y GOUT

20. 1.PRIMARY GOUT
• This is due to some metabolic defect that results in
increased synthesis of purine nucleotides via De Novo
synthesis pathway such as:
1. Increased PRPP synthetase activity.
2. HGPRT ase deficiency
3. G-6-P deficiency
2.SECONDARY GOUT
• It is secondary due to some diseases other than a
metabolic disorder like kidney disease & increased
breakdown of nucleic acids. E.g.-radiation/chemotherapy
or skin diseases.

21. SYMPTOMS
•Sudden, intense pain in a joint, typically the big toe or ankle,
sometimes the knee, hand or wrist.
•Swelling, inflammation and a feeling that the joint is very hot.
•Extreme tenderness of the joint to even the lightest touch.
•Red or purple skin around the joint
•In extreme cases alternating chills and fever.
•With recurring attacks soft fleshy growths may appear, called
tophi, which are accumulations of uric acid crystals.

22. DIAGNOSIS
• Specific investigations for confirmation:
1. Serum uric acid
2. Joint aspiration & crystal identification
• To detect medical conditions a/w gout or hyperuricemia
1. FBC
2. Serum Creatinine /urea
3. Serum blood glucose
4. Fasting lipid profile
5. 24 hrs urinary urate excretion
• To detect complications
1. Renal imaging
2. Skeletal x-rays

23. 1.JOINT ASPIRATION & CRYSTAL IDENTIFICATION

24. 2.BIOCHEMICAL TESTS FOR URATE STONE

25. 3.24 HRS URINARY EXCRETION OF URATE
• 24 hr urinary excretion of uric acid >1100 mg.
• Serum urate concentration >13 mg/dL.
• Having both the values above the indicated values gives the
patient 5o% probability for developing urate kidney stones.

26. 4.RENAL IMAGING & SKELETAL X-RAYS

27. TREATMENTS
1.Reduce dietary intake & restrict alcohol

28. 2.Using drugs

29. THANK YOU