Gout is an inflammatory arthritis caused by high uric acid levels in the blood (hyperuricemia) which leads to the deposition of urate crystals in the joints. It ranges from mild asymptomatic hyperuricemia to severe chronic tophaceous gout. Risk factors include family history, diet high in purines, obesity, alcohol use, and certain medications. Treatment involves lifestyle changes, medications to reduce uric acid production like allopurinol, or increase excretion like probenecid. Nonsteroidal anti-inflammatory drugs and corticosteroids are used for acute flares while long term management focuses on normalization of uric acid levels.

1. Gout
Dr. V. S. Swathi
Assistant Professor

2. Definition
 Gout is most common inflammatory
disease caused by deposition of
mono sodium urate crystals in
joints and tissues following chronic
Hyperurecemia

3. Epidemiology
 In the world, prevalence of gout
ranges from 0.1%-10%
 In India, prevalence of gout is
0.12%

4. Types
Based on progression of disease
Asymptomatic Hyperurecemia
 In this, patients will not show any symptoms
 Uric acid levels in the synovial fluid increases
 Patients are treated by non pharmacological management (life
style changes)
Acute Gout
 Uric acid crystals deposited and cause inflammation and
intense pain
 Pain subside within 3-10 days
 It is triggered by stress, alcohol, drugs, and cold weather
Interval Gout
 It is the stage between attacks of acute gout
 In this stage, deposition of urate crystals occurs continuously

5. Chronic tophaceous Gout
 It is severe condition
 Permanent damage occurs in joints
and kidneys
 Patients develops tophi in joints
and fingers
Pseudo Gout
 Here symptoms are similar to Gout
 Crystals which are deposited in
joints are calcium pyrophosphate

6. Based on Causes
 Primary Gout- It is not a
consequence of acquired disorder
 Secondary Gout- It is a
consequence of specific disorder
and specific use of drugs

7. Risk factors
 Family history
 Genitical defects in Enzymes (HPRT)
 Etiology
 Renal disease
 Obesity
 Gender-Men are having more risk than
women
 Dyslipidemia
 Glucose Intolerance
 Hypertension
 Diet
 Alcohol consumption
 Medications

8. Etiology
Primary Gout
 Rare enzyme deficiencies
 Hypoxanthine –Guanine
phosphoribosyl transferase deficiency
(HPRT)
 Phosphoribosyl pyrophosphate
synthetase superactivity
 Ribose -5-Phospahe AMPdeaminase
deficiency

9. Secondary Gout
Increased uric acid production
 Chronic haemolytic anemias
 Secondary polycythemia
 Severe exfoliative psoriasis
 Gaucher’s disease
 Cytotoxic drugs
 Glucose-6-Phosphate deficiency
 High purine diet

10. Decreased uric acid excretion
 Renal failure
 Alcohol
 Down’s Syndrome
 Myxedema
 Lead poisoning
 Beryllium poisoning
 Drugs like:
 Aspirin
 Ciclosporin
 Cytotoxic drugs
 Diuretics
 Ethambutol
 Levodopa
 Pyrizinamide
 Ribavirin
 Interferon
 Teriparatide

11. Pathogenesis

13. Clinical Presentation
In the joints of lower limbs like big toe, ankles, knees,
arms
◦ Pain
◦ Swelling
◦ Redness
◦ Warmth
 Shiny overlying skin
 Anorexia
 Nausea
 Change in mood
 Pruritis
 Tophi

16. Complications
 Secondary infections
 Chronic renal failure
 Severe degenerative arthritis
 Uric acid nephropathy
 Nerve/ Spinal cord impingement
 Joint damage
 Joint deformity
 Loss of mobility
 Osteoporosis

17. Diagnosis
 Medical history
 Medication history
 Family history
 Clinical presentation
 Physical examination
 Lab tests (Elevated ESR, WBC)
 Synovial fluid exam
 Polarised light microscopy

19. Diagnostic criteria
According to American college of Rheumatology
 Presence of characteristic urate crystals in the joint fluid/
 Presence of tophi which contain urate crystals by chemicals or
polarised light microscopy/
 Presence of six or more of the following:
◦ Asymptomatic swelling with in a joint on radiography
◦ Attack of mono articular arthritis
◦ Culture of joint fluid negative for microbes during attack of joint
inflammation
◦ Development of maximal inflammation with in one day
◦ Hyperurecemia
◦ Joint redness
◦ More than one attack of acute arthritis
◦ Pain/ redness in the first metatarsophalangeal joint
◦ Subcortical cyst without erosions on radiography
◦ Suspected tophi
◦ Unilateral attack involving first metatarsophalangeal joint
◦ Unilateral attack involving tarsal joint

20. Non Pharmacological
Treatment
 Avoid purine rich food like meat, sea foods, and
sweet soft drinks
 Avoid alcohol consumption
 Exercise in interval attacks
 Rest in acute attacks
 Avoid medications which decrease uric acid
excretion
 Topical ice application
 Patient counselling
 Hydration
 Surgery
◦ Tophi removal
◦ Joint fusion
◦ Joint replacement

21. Treatment Algorithm
Acute attack
 Rest for 1-3 days and Topical ice application
 Review medication and life style
 Resolve pain with NSAIDs/ Colchicine/
Corticosteroid
Chronic attack
 Uricostatic agents-Allopurinol/ Febuxostat
 Uricosuric agents-Probenacid/ Sulfinpyrazone
 Uricolytic agents- Rasburicase/ PEG-Uricase

22. Drugs used in treatment of Gout
Drug Category Mode of
Action
Dose Adverse Effects
Diclofenac NSAID Inhibit COX
enzyme and
release of
Prostaglandins
100mg-OD-PO  Abdominal Cramps
 Constipation
 Diarrhea
 Dyspepsia
 Edema
Prednisolone Corticosteroid Inhibit
inflammation by
suppressing
migration of
PMNs and
stabilizing
lysosomes at
cellular level
30mg-OD-PO for 5
days and slowly
discontinue the drug
by tappering
 Acne
 Diabetes
 Hypertension
 Edema
 Weight gain
Methyl
Prednisolone
Corticosteroid Inhibit
inflammation by
suppressing
migration of
PMNs and
stabilizing
lysosomes at
cellular level
80mg-OD-IA  Acne
 Diabetes
 Hypertension
 Edema
 Weight gain

23. Allopurinol Xanthine
Oxidase
Inhibitor
Inhibit uric
acid
production
100-900mg/day-
PO
 Rash
 Fever
 Nephrotoxicity
 Hepatotoxicity
 Vasculitis
Febuxostat Xanthine
Oxidase
Inhibitor
Inhibit uric
acid
production
80-120mg/day-
PO
 Respiratory infection
 Diarrhea
 Headache
 Hepatotoxicity
 Arthralgia
Probenacid Uricosuric
agent
Increases uric
acid excretion
0.5-2g/day-PO  Head ache
 Loss of Appetite
 Anemia
 Renal calculi
 Leukopenia
Sulfinpyrazone Uricosuric
agent
Increases uric
acid excretion
200-800mg/day-
PO
 Unusual bleeding
 Hepatotoxicity
 Nephrotoxicity
 GI ulceration
 Fluid retention

24. Rasburicase Uricolytic
agent
It coverts
insoluble uric
acid in to
soluble
allontoin
0.2mg/kg for 5-
7 days
 Fever
 Rash
 Diarrhea
 Head ache
 Hypersensitivity
Colchicine Uricosuric
agent
It prevents
activation,
degranulation
and migration
of neutrophils
and increases
uric acid
excretion
1-1.8mg-OD-
PO
 GI disturbances
 Bone marrow
suppression
 Neuropathy
 Myopathy
 Hepatotoxicity
Anakinra Immunomod
ulator
Inhibits
Interleukin
actions by
binding to IL-
1 receptor
100mg/day-SC  Injection site reactions
 Arthralgia
 Pyrexia
 Nasopharyngitis
 Neutropenia

25. Resources
 https://www.ncbi.nlm.nih.gov/pmc/artic
les/PMC6322774/
 https://www.sciencedirect.com/science
/article/pii/S0041134518302343?via%
3Dihub
 https://www.ncbi.nlm.nih.gov/pmc/artic
les/PMC6254413/
 https://www.ncbi.nlm.nih.gov/pmc/artic
les/PMC6196879/