Gout is a metabolic disorder manifesting in primary or secondary forms characterized by hyperuricemia & joint lesions .
A metabolic disease characterized by recurrent attack of acute inflammatory arthritis caused by elevated levels of uric acid in the blood (hyperuricemia).
Gout: Very painful form of arthritis characterized by the formation of uric acid crystals and severe inflammation.
Gout is a metabolic disorder of purine metabolism, characterized by intermittent attacks of acute pain, swelling and inflammation. • It always preceded by hyperuricemia
Gout is a metabolic disorder manifesting in primary or secondary forms characterized by hyperuricemia & joint lesions .
A metabolic disease characterized by recurrent attack of acute inflammatory arthritis caused by elevated levels of uric acid in the blood (hyperuricemia).
Gout: Very painful form of arthritis characterized by the formation of uric acid crystals and severe inflammation.
Gout is a metabolic disorder of purine metabolism, characterized by intermittent attacks of acute pain, swelling and inflammation. • It always preceded by hyperuricemia
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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
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
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.
17.
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.
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
23.
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
25.
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
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.