Gout and pseudogout are crystal-induced arthropathies caused by the deposition of urate crystals or calcium pyrophosphate dihydrate crystals in the joints respectively. Gout results in painful flares typically affecting the big toe and is characterized by periods of acute inflammation. Pseudogout causes intermittent arthritis that may be asymptomatic and is detected by chondrocalcinosis on x-rays. Both can be diagnosed by identifying the characteristic crystals in synovial fluid under polarized microscopy. Treatment involves management of symptoms during acute flares and reducing crystal deposition long-term.

1. GOUTY ARTHRITIS
Dr YANGO M L-PGY2.
FACILITATOR –DR PETER
MASIKINI.

2. INTRODUCTION
The three most common crystal-induced arthropathies are:
1. Gout: caused by precipitation of monosodium urate
monohydrate (MSU),
2. CPPD arthropathy: Calcium pyrophosphate dehydrate,
3. Basic calcium arthropathy: basic calcium phosphate

3. COMPARISON OF
GOUT AND PSEUDO-
GOUT

4. GOUTY
Gout is an inflammatory monoarticular arthritis caused by the
crystallization of monosodium urate in joints.
A metabolic disease characterized by recurrent attack of acute
inflammatory arthritis due to deposition of urates in and around
the joint and usually elevated of uric acid in the blood,
 Is the most common crystal-induced arthropathies
The uric acid crystallizes and deposits in the joint ,tendons and
surrounding tissue
Hyperuricemia is not equal to gouty serum urate level 7mg/dl
(416micromol/l)

5. Group of conditions which may be characterized by
 An elevation of serum uric acid (usually)
 Recurrent attacks (flares) of an acute inflammatory arthritis with monosodium
urate crystals demonstrated in synovial fluid leukocytes
 Bone and joint destruction in some cases
 Aggregates of uric acid crystals (tophi) in and around joints, soft tissues, and
various organs
 Tophus in bone leading to erosions in some cases
 Kidney disease and stones

6. THE INTENSE INFLAMMATION OF ACUTE GOUTY ARTHRITIS
A: The marked swelling of the first metatarsophalangeal
joint (podagra) is demonstrated. A dusky blue hue over an
intense erythema is characteristic.
B: Ankle swelling is shown with erythema extending beyond
the area of the tibiotalarjoint.

7. EPIDEMIOLOGY
Burden of gouty increased around the world from 1990 to
2017 with total prevalence of 41.2m
and 1.3m lived with disability
Prevalence vary from country to country due to
environmental factors ,dietary and genetic influences
It Is common in male with the male to female ratio of 3:1
The rate of gouty is almost 5 times higher in persons aged
70-79 year
Jason et-al Data published in arthritis and rheumatology

8. PATHOPHYSIOLOGY:
1.) Increased production of uric acid.
Inborn errors of purine metabolism
Hypoxanthine-guanine phosphoribosyl
transferase deficiency—for example, in
Lesch–Nyhan syndrome
Phosphoribosyl pyrophosphate synthetase
overactivity
Excess cell death and rate generation e.g.
Glycogen storage disease 1,3,5 and 7,
Fructose-1-phosphate aldolase deficiency,
Myoadenylate deaminase deficiency,
Carnitine palmitoyltransferase II deficiency
(late onset).
Increased cell turnover associated with
several conditions, including cancer,
chemotherapy, chronic hemolysis, and
hematologic malignancies.
2.) Decreased excretion of uric acid
(accounts for 90% of cases)
Renal disease e.g. Medullary cystic kidney
disease, Familial juvenile hyperuricemic
nephropathy , Uric acid transportasome
mutations (GLUT-9, ABCG2, URAT1
Familial gout)
NSAIDs, diuretics
Acidosis

9. PATHOGENESIS

10. HYPERURICEMIA
Biologically significant hyperuricemia (≥6.8 mg/dL) is less
than
laboratory defined hyperuricemia (≥8.0 mg/dL)
Underexcretion
Silent
tissue
deposition
Urate
Hyperuricemia ≥6.8 mg/dL
Overproduction
Associated
cardiovascular events
and mortality
Renal
manifestations
Gout
Endogenous
purine synthesis
Dietary
purines
Tissue
nucleic acids
The Hyperuricemia Cascade

11. ETIOLOGY
Renal disease
Increased protein ingestion
Prolonged dehydration
Reduced renal excretion of urates.
All these will lead to formation Monosodium urate crystal precipitation in
tissues

12. Copyrights apply

13. GOUTY
Results in deposition of monosodium urate crystals in the joints and soft
tissues, with accompanying inflammation and degenerative consequences
Most common form of inflammatory joint disease in men aged ≥40 years
This disorder can be progressive through four stages if undertreated
1. Asymptomatic hyperuricemia
2. Acute gout
3. Intercritical gout
4. Chronic tophaceous gout

14. GOUTY ARTHRITIS
A. Acute gouty
Self limiting monoarticular, usually resolve within 2
weeks if untreated. May occur even if serum urate is
normal
LL>UL
Common affected joint 1 metatarsophalangeal joint
(podagral)
Ankle, knee, wrist, elbow, fingers joints
Extra articular olecranon bursa ,Achilles tendon
O/E erythematous ,warm, swelling over involved joint
with extreme tenderness plus /minus fever

15. COMMON SITES OF ACUTE FLARES
Midfoot
Gout can occur
in bursae, tendons,
and joints
Olecranon Bursa
Elbow
Wrist
Knee
Ankle
Subtalar
1st MTP
(eventually affected in
~90% of individuals
with gout)
Fingers

16. CHARACTERISTIC LOCATIONS OF
GOUTY TOPHI
A: At the elbow, tophi present as hard nodules along the ulnar ridge or as multiple nodules within the
olecranon bursa.
B: Ear tophi are uncommon but may be an easy source of crystal confirmation of gout when present.
C: Small subcutaneous tophi can occur along the ventral creases of fingers.
D: Tophi over the proximal interphalangeal or distal interphalangeal joints may be confused with
Bouchard or Heberden nodes, respectively.

18. B, Inter critical gouty
Asymptomatic period between attack
C ,Chronic gouty
Polyarticular arthritis with tophi formation ( collection of crystals in
soft tissues )
Tophi more likely to occur in patients with Polyarticular
presentation ,serum urate level 540umol/l and disease onset at
younger age
Sites for tophi , digit of hand and feet more common ,pinna of the
ear (classic, less common ), bursa around elbow and knees, Achilles
tendon

19. ADVANCED CHRONIC TOPHACEOUS
GOUT
Articular gout is characterized by deposits of urate
crystals (also known as tophi) on both intraarticular and
periarticular tissues.
Tophi can be seen clinically, with obvious deformity
demonstrated in hands and
foot
Tophi may be associated with bony destruction as seen
on the x-ray
on right
Urate deposits(Tophi) appears as chalky, white covering in
Images reprinted with permission. American College of Rheumatology. ACR Clinical Slide Collection on the Rheumatic
Diseases. Atlanta, Ga.: American College of Rheumatology; 1998.

20. DIFFERENTIAL DIAGNOSIS
Pseudo gouty
Rheumatoid arthritis
Septic arthritis
Reactive arthritis
Psoriatic anthropopathy
Bursitis
Calcific periathritis

21. DIAGNOSIS
 Definitive diagnosis require
direct identification of urate
crystal in the joint synovial
fluid analysis
 Needle shaped negatively
birefringent MSU by polarizing
microscope
 Hyperuricemia is the primary
risk for gout
 20% of adult population had
hyperuricemia

22. RADIOLOGY
Skeletal x ray
Acute gouty arthritis : soft tissue swelling
Chronic tophaceous gouty: tophi ,erosive bone lesion (punched out lesions),
joint space is preserved until late stage, pathognomonic in foot and big toe

24. TREATMENT:
The main goal is to:
 To reduce pain
To reduce the incidence of tissue and articular deposition of uric acid
crystals
Supportive care
Acute Cases:
Hyperuricemia is treated with aggressive diuresis with intravenous or
intrasosseous fluid therapy
Decrease protein ingestion
Prolonged SC fluid administration is often recommended

26. MANAGEMENT
Non pharmacological
Life style modification and dietary advance
 Achieve ideal body mass index
Restriction of alcohol
Restriction of consumption of high purine foods
Consumption of low fat daily products
Adequate intake of fluid of 2-3l/d

27. CHANGING TREATMENT LANDSCAPE
AFTER FOUR DECADES
Current
Allopurinol
Uricosurics
Symptomatic relief
In Development
Uricosurics
Selective xanthine
oxidase inhibitor
Pegylated uricase enzyme
IL-1 receptor antagonists
URAT1 Transporter
Inhibitor
IL-1 = Lnterleukin-1
URAT1 = urate transporter 1

28. PHARMACOLOGICAL
For asymptomatic
hyperuricemia is not
necessary except
Persistence severe
hyperuricemia
>770umol/l in male
and >600umol/l in
female
Tumor lysis
syndrome. Require
pre hydration and
allopurinol to
prevent acute urate
nephropathy
ACUTE ARTHRITIS
Initiation within 24 hours of onset
If on allopurinol continue without
interruption
For symptoms relief
Analgesic, NSAIDs, colchicine ,
glucocorticoids
NSAIDs ± PPI studies have shown
that etoxicoxib has equal efficacy to
indomethacin

30. HOPE YOU ARE GUD WITH
GOUT,RIGHT????

31. DIFFERENTIAL DIAGNOSIS
Pseudo gouty
Rheumatoid arthritis
Septic arthritis
Reactive arthritis
Psoriatic anthropopathy
Bursitis
Calcific periathritis

32. CALCIUM PYROPHOSPHATE DIHYDRATE CRYSTAL
DEPOSITION DISEASE
Clinical CPPD disease is divided into
three categories based on the etiology
of altered inorganic pyrophosphate (PPi)
metabolism.
The categories are:
1. Hereditary (familial),
2. sporadic (idiopathic),
3. and metabolic.

33. PSEUDO GOUTY
CPPD disease is characterized by acute and chronic inflammatory joint disease,
usually affecting older individuals..
A metabolic disease characterized by recurrent attack of acute inflammatory
arthritis due to deposition of Calcium deposits in and around the joint
The knee and other large joints are most commonly affected. in articular
cartilage (chondrocalcinosis) may be seen radiographically; these are not
always associated with symptoms

34. WITH PSEUDOGOUT
1.the calcification should be bilateral
2.present clinically similar to gout, you can only differentiate by
synovial fluid analysis.
3.sign and symptoms are
Painfull,sollen,warmth, joint, Swelling with effusion, Limited motion on the
affected joint
4.pseudogout are less painful compared to gout
5.only single joint is affected.
6.large joint are affected than small joints.
7.self limited if untreated.

35. PSEUDOGOUT
It is frequently asymptomatic and recognized only by the
appearance of chondrocalcinosis on radiographs.
Pseudo-osteoarthritis:
most common clinical manifestation accounting for
approximately 60% of CPPD disease is a polyarticular,
noninflammatory arthritis affecting joints not typically involved
in primary osteoarthritis, including the wrists, shoulders, and
metacarpophalangeal joints (particularly the second and third
metacarpophalangeals).

36. Pseudogout:
the acute monoarticular presentation,
occurs more often in the large joints than in small joints, with
onset usually not as abrupt as with gout,
and the attacks tend to last longer—frequently months.
CPPD crystal deposition disease can occasionally present as a
chronic polyarticular inflammatory disease that may mimic
rheumatoid arthritis or polymyalgia rheumatica.

37. THANK YOU ALL
References
Medscape
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