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SHRUTI
PUROHIT
FINAL YEAR
 Defination
 Pathogenesis
 Stages Of Gout
 Risk Factors
 Clinical Features
 Differential Diagnosis
 Invetigation
 Treatment
 A Metabolic Disease Characterised By Recurrent
Attack Of Acute Inflammatory Arthritis Caused By
Elevated Levels Of Uric Acid In The Blood.
(Hyperuricemia)
 Most Common Rheumatic Disease Of Adulthood.
 The Uric Acid Crystallizes & Deposits In Joints,
Tendons, & Surrounding Tissues As Tophi.
 Podagra Is A Painful Condition Of The Big Toe
Caused By Gout.
 Mainly Affect Big Toe, Also Affects Knees, Ankle,
Wrists, Fingers, Elbow, Toes Of Feet.
 2/3 of urate formed each day is excreted
by the kidneys & 1/3 from GI tract.
 Normal adult excrete 500-700mg of uric
acid/day.
 The Purine That A Person Eats & Also
Produced Naturally In Body, Are Metabolized
By The Body.
 Liver Is The Major Site Which Breaks Down The
Purines & Produces A Waste Product Called
Uric Acid.
 The Uric Acid Is Released Into The
Bloodstream & Eventually Filtered By The
Kidneys & Excreted In The Urine.
 If Too Much Uric Acid Builds Up Can Form Into
Crystals That Deposit In Your Jts. & Cause
Pain & Inflammation.
 Elevated Uric Acid Can Occur From Over
Production Or Under Excretion Of Uric Acid
 Over Production: (PRIMARY GOUT) 10-20%
• Less Common
• Genetic Abnormalities In Enzymes Related
Purine Metabolism
• ↓ Hypoxanthine-guanine Phosphorebosyl
Transferase(hgprt)
• ↑ Phosophoribosyl Pyrophosphate
Synthetase(prpp)
 Under Excretion: (SECONDARY
GOUT) 80-90%
• More Common
• ↓ GFR
• Decline In Urinary Excretion Of Uric Acid
 Can Determine By Measuring Urine Uric Acid
• >600mg/24hr Over Production
• <600mg/24hr Under Excretion
4 stages:
 Asymptomatic
Hyperuricemia
 Acute Gout
 Intercritical Gout
 Chronic Tophaceous
Gout
 Serum Uate Abnormally High Without
Sign & Symptoms.
 Male > 7mg/Dl
 Female > 6mg/D
 Not Life Threatening & Readily
Treatable.
 Routine Prophylactic Rx Is Not
Required.
 The Intervals Between Attacks Of
Gouty Arthritis Are Reffered To As
Intercritical Periods.
 Intercritical Gout Simply Has Gout That
Has Caused Attacks Of Inflammation
In A Jts. In The Past But It Is Not Active
At The Time Evaluating The Pt.
 Acute, Self Limiting, Monoarticular
 Painful, Red, Hot, Swollen Accompained By
Fever, Raised ESR
 Usually Resolved Within 2 Weeks If Untreated.
But Recurrent Attacks Are Followed By
Progressive Cartilage & Bone Erosion,
Deposition Of Tophi, Secondary OA, &
Disability Associated With Permanent Restriction
Of Jt. Fun.
 May Occur Even If Serum Urate Is Normal
 Ll>Ul
 Also Present As Tenocynovitis, Bursitis, Cellulitis
 Polyarticular Arthritis + Tophi Formation.
 Articular Topheceous Gout May Results In
Destructive Arthropathy & Secondary OA.
 Serum Urate Level > 7mg/Dl.
 Disease Onset At Younger Age ≤ 40yrs.
 Sites Of Tophi:
 Digits Of Hands & Feet
 Helix Of Ear
 Bursa Around Elbow & Knee
 Achilles Tendon
o age (>35yr)
o sex (m>f=3:1)
o obessity
o high blood pressure
o injury
o recent surgery
o foods / drinks
o medications(diuretics, levo-dopa,
salicylates, nicotinic acid, cyclosporine)
o genetics (SLC2A9 , SLC22A12, ABCG2)
o medical
conditions(hypothyrodism, dm, pso-
riasis, heart failure, renal transplant, chronic
renal insufficiency, coronary heart disease)
o high protein diet
o life style
o Sever Pain At Joint
o Redness & Inflammation
o Fever
o Less Flexibility
o Nodules
o Itchy & Peeling Skin Later
Pseudogout (Deposition Of Calcium
Pyrophosphate Dyhydrate)
Septic Arthritis
Rheumatoid Arthritis
Trauma
Psoriatic Arthritis
Bursitis, Cellulitis, Tenosynovitis
Lab. Diagnosis
• Evidence Of Monosodium Urate Crystals By Jt.
Aspiration For Definitive Diagnosis
Synovial Fluid Analysis- Arthrocentesis
• Blood Test- Check Serum Uric Acid Level
• Urine Test
Most Uric Acid Disolves In Blood & Travels To The Kidneys, Where It
Passes Out In Urine.
If Body Produces Too Much Uric Acid Or Dosen’t Remove Enough Of
It, Person Can Get Sick
 REDIOGRAPHIC DIAGNOSIS
 PHARMECOLOGICAL
Rx
• NSAIDs
• Colchicine
• Corticosteroids
• Uricosurics
• Allopurinol
• Xanthine Oxidase
 Other
• Wt.Loss
• Exercise
• Diet(purine Contain
Diet ×)
 Surgical
• Removal Of Tophi
• Joint Fusion
• Joint Replacement

PHYSIOTHERAPY
 Pain control
 Barce
 Cryotherapy
 Ultrasound(1MHZ,1-
2W/Cm², 3-5min)
TREATMENT
 Rom
 Strenghtening
Ex.
 A Seronegative Arthritis Found In Pts. With
Psoriasis.
 It Is A Chronic Disease Charecterized By A
Form Of Inflammation Of The Skin & Jts.
 Classified With Hla-b27 Genetic Factor
Associated Spondyloarthritis.
 Immunologic Factor & Environmental Factor
Also Progress The Disease.
 Males & Femaes Are Equally Affected
 Peak Age Of Onset Between 30-55yrs.
 Family history.
 trauma, viral, bacterial
infection.
Signs & symptoms
 Painful,Tendor,Swolloen Jts.
 Hot red jts.-knee, ankle, feet
 Fatigue, morning stiffness
 Pitted nails, LBP
 Gouty Arthritis
 Ankylosing Spondyosis
 Rheumatoid Arthritis
INVESTIGATIONS
 Not Specific Diagnostic Test.
 Elevation Of Esr.
 Base On Clinical & Rdiological Basis.
New Bone Formation In Distal Jts.
 Lysis Of Terminal Phalanges.
“ Pencil In Cup” Like Appearance.
 Nsaids
 Corticosteroids
 DMARDS- Methotrexate,cyclosporine
 Coordinate B/W Rheumatology &
Dermatology
 Modalities- Heat, Cold
 Orthotics
 Active & Passive Exercise
 Streatching
 Strengthening
Gout

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Gout

  • 2.  Defination  Pathogenesis  Stages Of Gout  Risk Factors  Clinical Features  Differential Diagnosis  Invetigation  Treatment
  • 3.  A Metabolic Disease Characterised By Recurrent Attack Of Acute Inflammatory Arthritis Caused By Elevated Levels Of Uric Acid In The Blood. (Hyperuricemia)  Most Common Rheumatic Disease Of Adulthood.  The Uric Acid Crystallizes & Deposits In Joints, Tendons, & Surrounding Tissues As Tophi.  Podagra Is A Painful Condition Of The Big Toe Caused By Gout.  Mainly Affect Big Toe, Also Affects Knees, Ankle, Wrists, Fingers, Elbow, Toes Of Feet.
  • 4.
  • 5.  2/3 of urate formed each day is excreted by the kidneys & 1/3 from GI tract.  Normal adult excrete 500-700mg of uric acid/day.  The Purine That A Person Eats & Also Produced Naturally In Body, Are Metabolized By The Body.  Liver Is The Major Site Which Breaks Down The Purines & Produces A Waste Product Called Uric Acid.
  • 6.  The Uric Acid Is Released Into The Bloodstream & Eventually Filtered By The Kidneys & Excreted In The Urine.  If Too Much Uric Acid Builds Up Can Form Into Crystals That Deposit In Your Jts. & Cause Pain & Inflammation.
  • 7.
  • 8.  Elevated Uric Acid Can Occur From Over Production Or Under Excretion Of Uric Acid  Over Production: (PRIMARY GOUT) 10-20% • Less Common • Genetic Abnormalities In Enzymes Related Purine Metabolism • ↓ Hypoxanthine-guanine Phosphorebosyl Transferase(hgprt) • ↑ Phosophoribosyl Pyrophosphate Synthetase(prpp)
  • 9.  Under Excretion: (SECONDARY GOUT) 80-90% • More Common • ↓ GFR • Decline In Urinary Excretion Of Uric Acid  Can Determine By Measuring Urine Uric Acid • >600mg/24hr Over Production • <600mg/24hr Under Excretion
  • 10. 4 stages:  Asymptomatic Hyperuricemia  Acute Gout  Intercritical Gout  Chronic Tophaceous Gout
  • 11.  Serum Uate Abnormally High Without Sign & Symptoms.  Male > 7mg/Dl  Female > 6mg/D  Not Life Threatening & Readily Treatable.  Routine Prophylactic Rx Is Not Required.
  • 12.  The Intervals Between Attacks Of Gouty Arthritis Are Reffered To As Intercritical Periods.  Intercritical Gout Simply Has Gout That Has Caused Attacks Of Inflammation In A Jts. In The Past But It Is Not Active At The Time Evaluating The Pt.
  • 13.  Acute, Self Limiting, Monoarticular  Painful, Red, Hot, Swollen Accompained By Fever, Raised ESR  Usually Resolved Within 2 Weeks If Untreated. But Recurrent Attacks Are Followed By Progressive Cartilage & Bone Erosion, Deposition Of Tophi, Secondary OA, & Disability Associated With Permanent Restriction Of Jt. Fun.  May Occur Even If Serum Urate Is Normal  Ll>Ul  Also Present As Tenocynovitis, Bursitis, Cellulitis
  • 14.  Polyarticular Arthritis + Tophi Formation.  Articular Topheceous Gout May Results In Destructive Arthropathy & Secondary OA.  Serum Urate Level > 7mg/Dl.  Disease Onset At Younger Age ≤ 40yrs.  Sites Of Tophi:  Digits Of Hands & Feet  Helix Of Ear  Bursa Around Elbow & Knee  Achilles Tendon
  • 15. o age (>35yr) o sex (m>f=3:1) o obessity o high blood pressure o injury o recent surgery o foods / drinks o medications(diuretics, levo-dopa, salicylates, nicotinic acid, cyclosporine) o genetics (SLC2A9 , SLC22A12, ABCG2) o medical conditions(hypothyrodism, dm, pso- riasis, heart failure, renal transplant, chronic renal insufficiency, coronary heart disease) o high protein diet o life style
  • 16. o Sever Pain At Joint o Redness & Inflammation o Fever o Less Flexibility o Nodules o Itchy & Peeling Skin Later
  • 17. Pseudogout (Deposition Of Calcium Pyrophosphate Dyhydrate) Septic Arthritis Rheumatoid Arthritis Trauma Psoriatic Arthritis Bursitis, Cellulitis, Tenosynovitis
  • 18. Lab. Diagnosis • Evidence Of Monosodium Urate Crystals By Jt. Aspiration For Definitive Diagnosis Synovial Fluid Analysis- Arthrocentesis • Blood Test- Check Serum Uric Acid Level • Urine Test Most Uric Acid Disolves In Blood & Travels To The Kidneys, Where It Passes Out In Urine. If Body Produces Too Much Uric Acid Or Dosen’t Remove Enough Of It, Person Can Get Sick
  • 19.
  • 21.  PHARMECOLOGICAL Rx • NSAIDs • Colchicine • Corticosteroids • Uricosurics • Allopurinol • Xanthine Oxidase  Other • Wt.Loss • Exercise • Diet(purine Contain Diet ×)  Surgical • Removal Of Tophi • Joint Fusion • Joint Replacement
  • 22.
  • 23.  PHYSIOTHERAPY  Pain control  Barce  Cryotherapy  Ultrasound(1MHZ,1- 2W/Cm², 3-5min) TREATMENT  Rom  Strenghtening Ex.
  • 24.
  • 25.  A Seronegative Arthritis Found In Pts. With Psoriasis.  It Is A Chronic Disease Charecterized By A Form Of Inflammation Of The Skin & Jts.  Classified With Hla-b27 Genetic Factor Associated Spondyloarthritis.  Immunologic Factor & Environmental Factor Also Progress The Disease.  Males & Femaes Are Equally Affected  Peak Age Of Onset Between 30-55yrs.
  • 26.  Family history.  trauma, viral, bacterial infection. Signs & symptoms  Painful,Tendor,Swolloen Jts.  Hot red jts.-knee, ankle, feet  Fatigue, morning stiffness  Pitted nails, LBP
  • 27.  Gouty Arthritis  Ankylosing Spondyosis  Rheumatoid Arthritis INVESTIGATIONS  Not Specific Diagnostic Test.  Elevation Of Esr.  Base On Clinical & Rdiological Basis.
  • 28. New Bone Formation In Distal Jts.  Lysis Of Terminal Phalanges. “ Pencil In Cup” Like Appearance.
  • 29.  Nsaids  Corticosteroids  DMARDS- Methotrexate,cyclosporine  Coordinate B/W Rheumatology & Dermatology
  • 30.  Modalities- Heat, Cold  Orthotics  Active & Passive Exercise  Streatching  Strengthening