Gout is a metabolic disorder caused by hyperuricemia, or high levels of uric acid in the blood. It most commonly affects middle-aged men and causes sudden, severe pain and inflammation in joints like the big toe. Acute gout occurs when uric acid crystals form in a joint, while chronic gout results in long-term joint damage. Treatment involves medications like NSAIDs, colchicine, corticosteroids, and allopurinol to reduce pain and prevent further attacks by lowering uric acid levels. Lifestyle changes like diet modification and exercise can also help prevent gout flares.

1. BY,
VISHWANATH GOUDA
1st M. Pharm
Dept. of Pharmacy Practice
NGSMIPS, Nitte University
Mangaluru, 57018

2. INTRODUCTION
 Gout is the most common inflammatory joint disease.
 The prevalence of gout has increased over recent decades.
 One of the oldest recognised disease and was identified in 2460BC.
 Gout is normally the result of an Interaction between genetics and
environmental risk factor.

3. DEFINATION
 Gout is a metabolic disorder characterized by hyperuricemia which occurs due
to defective purine metabolism.
 Hyperuricemia can lead to deposition of sodium urate crystals in the tissues
especially in joints and kidney.
TYPES
 Acute
it manifests as sudden onset of severe inflammation in a small joint due to
precipitation of urate crystals in joint spaces.
 Chronic
When pain and stiffness persist in a joint between attacks, gout become chronic

4. EPIDEMIOLOGY
 Gout is one of the oldest disease and was identified by Egyptians.
 Gout is a condition that most frequently affects middle aged men with only
approximately 5% of the cases occurring in women.
 Most women with gout have a family history of disease, studies in men have
failed to detect a significant genetic component.
 Disease of the ‘KINGS’ Rich foods have a higher concentration of protein.
This could cause major problems for a person afflicted with gout

5. ETIOLOGY
Gout occurs due to defective purine metabolism in which uric acid is the end
product. The main cause of hyperuricemia occurs due to following reasons.
 Over production of uric acid.
*Excessive turn over of nucleoproteins
*Excessive dietary purines
*Excessive synthesis of uric acid due to rare
enzyme mutation defects.
 Under excretion of uric acid
*Defect in renal excretion
*Inborn errors of metabolism

6. PATHOPHYSIOLOGY

7. CLINICAL PRESENTATION
 SYMPTOMS
• Severe pain, swelling and warmth in the affected joints.
• The attack is usually monarticular and the most common sites are the
metatarsophalangeal and knee joints.
 SIGNS
• Affected joints are warm, red and swollen
• Mild fever may be present
• Tophi may be present in chronic, severe disease

8. Acute Gout:
 Acute gout is a painful condition that typically affects only one or a few joints.
 The big toe, knee, or ankle joints are most often affected.
 Throbbing, crushing, or excruciating pain
 Joint appears warm and red. Fever may be there.
 The attack may go away in a few days, but may return from time to time.
 Additional attacks often last longer.

12. Chronic Gout
 Signs and symptoms include:
 Joint damage
 Loss of motion in the joints
 Joint pain and other) symptoms most of the time, throughout the day
 Skin over the deposits develops sores ((ulcers)) exuding a white pus ((chalky))
 Joint stiffness ((limited motion of the affect joint))
 Articular cartilage may be destroyed resulting in joint deformities
 Patients may develop large Subcutaneous Tophi ((Porous Stones)) in pinna of
external ear, eyelids, nose, around joints, fingers, knees, at the tips of the
elbows, tendons, cartilages, soft tissues as flexors in the forearms and rarely in
the vocal cord and around the spine

13. Gouty Nephropathy
 The precipitation of uric acid in the renal medulla with formation of
characteristic tophi was believed to evoke an inflammatory response leading to
fibrosis, a loss of nephrons, and ultimately to the piece de resistance, chronic
irreversible renal failure

14. DIAGNOSIS
Physical examination and medical history
Examination and analysis of synovial fluid

15. TREATMENT
 NON-PHARMACOLOGICAL THERAPY
 Local ice application is the most effective therapy.

16. PHARMACOLOGICAL THERAPY
For acute
gout
NSAIDs
Colchicine
Corticosteroids
For chronic
gout
Uricosurics
• Probenecid
• Sulfinpyrazoe
Synthesis
inhibitors
Allopurinol
Febuxostat

19. NSAIDS:
• Inhibits pain & inflammation.
• Inhibits urate crystal phagocytosis by decreasing the migration of
granulocytes into the inflammatory area.
 Indomethacin : 50mg three times daily
Std dose : 50mg
 Etodolac : 300mg twice daily
Std dose : 300-500mg twice daily
 Ibuprofen : 400mg three times daily
Std dose : 400-800mg three to four times daily.

20. CORTICOSTEROIDS
 corticosteroids are equivalent to NSAIDs in the treatment of acute gout flares
 They can be used either systemically or by intraarticular injection
 If only one or two joints are involved, either intraarticular or oral
corticosteroids are recommended. If an attack is polyarticular, systemic
therapy is necessary.
 Prednisone : 0.5mg/kg daily for 5-10days
 Intramuscular : Triamcinolone acetonide 60mg IM once ; methylprednisolone
100mg IM once.
 Intraarticular : triamcinolone acetonide 10mg large joints and 5mg small
joints
 Corticotropin : 40units IM or SC every 72 hrs.

21. COLCHICINE:
• Produces its anti-inflammatory effects by binding to the intracellular
protein tubulin, preventing its polymerization leading to the inhibition of
leukocyte migration into affected area.
• Inhibits the synthesis & release of leukotrienes.
 Oral colchicine (Colcrys) : 1.2mg initially, followed by 0.6 mg 1 hour later

22. URICOSURIC AGENTS:
• Probenecid
• They are weak organic acids .
• Sulfinpyrazone is a metabolite of phenylbutazone.
• Increase the excretion of Uric acid.
Probenecid : 250mg twice daily for one week.
std dose : 500-250mg/day

23. XANTHINE OXIDASE INHIBITORS
 Allopurinol/ Febuxstat:
• Inhibits synthesis of uric acid by inhibiting xanthine oxidase enzyme
 Uric acid is produced by Xanthine and Hypoxanthine by Xanthine Oxidase
Inhibitor.
 Uric Acid is more toxic than either xanthine or hypoxanthine.
Allopurinol : 100mg daily
Std dose : 100-800mg/daily
Febuxostat : 40mg daily
Std dose : 40-80mg daily

28. • Interaction with warfarin
• Contraindicated in:
• Renal disease
• PUD
• GI bleeders
NSAIDS
• Not as effective “late” in flare
• Contraindicated in dialysis patients
• Cautious use in :
• Renal or liver dysfunction
• Active infection
• Age > 70
Colchicine
• Worse glycemic control
• May need to use mod-high
doses
Corticosteroids

29. PREVENTION
 Avoiding excessive intake of purine-rich foods
 Maintain a healthy body weight by Exercise
 Restrict your intake of alcohol, especially beer ((high in Guanosine))
 Avoid foods rich in fructose and sucrose which result in hyperuricemia
 Avoid diuretic foods or drugs which increase urination
 Avoid diet low in potassium ((good sources are tomatoes, potatoes, bananas,
soybeans, brown rice)) since a deficiency increases blood urate
 Avoid consuming too much acid-containing substances
 Maintain an adequate intake of Vitamin C, since it has been demonstrated to
increase excretion of uric acid
 Drink plenty of water to dilute and assist urate excretion
 Avoid prolonged exposure to low temperature

30. Reference
 Dipiro JT, , Talbert RL, Yee GC, Matzke GR, et al. Pharmacotherapy ; A
Pathophysiologic approach. 9th edition.USA. M CGraw Hill publication2014. chapter74
Gout and Hyperuricemia, P: 1505-1520
 Walker R and Whittlesea C. Clinical pharmacy and therapeutics. In Cockwell P,
Strringer S and Marriott J; editor. Gout and hyperurecemia. Gret Britain;
Churchhill livingstone; 5th edition; 848-857.