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Flashcards in Crystal Induced Arthritis-Gout Deck (37):
1

Gout- Pathogenesis

What does that mean?
Formation of uric acid in the form of urate with elevated levels = precipitation of urate into a crystallized form
Inflammatory Response to the crystals that are formed

2

Characteristics of Gout

 Hyperuricemia (increased uric acid/urate level)


 Recurrent attacks of acute arthritis in which urate crystals are present in synovial fluid
 Tophi deposited in and around joints which can lead to joint deformity
 Renal disease involving glomerular, tubular, and interstitial tissues and blood vessels
 Uric Acid nephrolithiasis

3

What is Uric Acid?


 Breakdown product of purine metabolism. Generation of Uric Acid is dependent on intrinsic purine production and purine intake. Depletion of Uric Acid is dependent upon excretion
Purines are in DNA and RNA ( i.e.- adenine and guanine)
 Serum Urate level (Uric Acid)- Balance between production and excretion of uric acid, between 4-6.8 mg/dl

4

Uric Acid

Uric Acid in levels > 6.8 mg/dl then precipitate needle shaped crystals that can result in an inflammatory response
These increased levels can deposit crystals occultly or in the form of noticeable masses around or in the joint called Tophi
Other factors that may influence precipitation of crystals include: Lower PH, Lower Temperature, Joint space and cartilage role?, and immune response

5

Hyperuricemia- Overproduction

Primary or Secondary Overproduction


Primary= Inborn errors of metabolism
Secondary= Conditions that induce cell turnover that produces purines and purine breakdown (i.e. erythropoietic diseases like anemias, sickle cell disease and myloproliferative disorders like multiple myeloma, leukemias)

6

Hyperuricemia- Underexcretion
Most common cause of Hyperuricemia

Primary and Secondary Underexcretion


Primary= Hereditary defects in renal tubule urate excretion
Secondary= Acute and Chronic renal failure, drugs and toxins, systemic illness that alters urate handling directly or indirectly
Drugs that can effect underexcretion- Thiazide diuretics, Loop Diuretics, ETOH, ASA

7

Incidence and Prevalance

Hyperuricemia prevalance of 2.6%-47.2% which varies among populations


 Gout prevalance 1%-15.3%
 A Hyperuricemic individual may have sustained hyperuricemia for 20 years prior to first attack
 Men > women
 1st attack usually occurs between 40-60 yrs in
men, after 60 in women (postmenopausal)
 Most common site= 1st MPJ ( Podagra)

8

Risk Factors


Drugs: ASA, Thiazide or Loop Diuretic
Genetics (family hx of gout)
 Obesity
Metabolic syndrome (Insulin resistance, HTN, dyslipoproteinemia)
 CAD
 Hypothyroidism
 Diet

9

Diet

Foods that may increase likely hood of Acute Gout attack



Seafood
Red Meat (organ meat) Fructose
ETOH- Beer and ales ( dark beer)

Foods used to be concerned about
Leafy Green Veggies

10

Diet
Foods that can Decrease risk/levels of urate


Low fat diary products (yogurt) Milk
Vitamin C

11

Stages of Gout

Asymptomatic Hyperuricemia
Acute Gouty Arthritis
Intercritical Gout
Chronic Gout

12

Asymptomatic Hyperuricemia


Urate level in serum high but no acute attack of gout either in the joint or nephrolithiasis

This stage ends with the first gout attack

13

Acute Gout- Clinically


Acute/Rapid onset- 6 hours to 24 hours
Intensely painful
Usually monoarticular ( may become poly articular with increasing attacks)
Affected area hot, red, swollen, tender to palpation
Could have fever, chills, malaise
Resolving Acute attack may have sloughing skin

14

Acute Gout- General

Self limiting (d or wks)
Over time shorter interval between attacks and last longer
1st MPJ most common site then midfoot, ankles, heels, knees, wrists, finger, and elbows
Could present in a joint previously damaged ( trauma/OA)
After Surgery?

15

Intercritical Gout


Period between Acute Gout attacks
Usually suffer another attack within 6 months to 2 years after the 1st attack
Radiographic changes may occur during the intercritical period

16

Chronic Gout


 Polyarticular gout with no pain free intercritical periods
 Visible Tophi
 Needs to be differentiated between other
arthropathies
 Rate of Tophi formation correlates with degree and duration of hyperuricemia
 Severity of renal disease and use of diuretics can influence chronic gout

17


What are Tophi?


 Deposits of Urate crystals
 Formed by inability to eliminate urate until the urate pool expands and crystals are formed
 Tophi can appear in cartilage, synovial membranes, tendons, soft tissues, as well other places
 Locations can include fingers, hands, knees, feet, ulnar surfaces of forearm, ear, Achilles tendon

18

Differential Diagnoses of Gout


 Other crystal induced arthropathies
 Septic arthritis
 Trauma
 Reactive arthritis
 If chronic gout, other inflammatory arthropathies such as RA

19

How to Diagnose Gout


 Joint aspiration: under polarized light will see needle shaped crystals with negative birefringence
 Radiographs
 Ultrasound
 Labs- Uric Acid, CBC, RF

*** cbc- check septic

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Joint Aspiration-

Needle shaped crystals

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Radiographic Changes

 Early stage/Acute stages:


Periarticular soft tissue swelling
No Osseous changes

22

Radiographic Changes

 Chronic/late stages:


 Assymetric soft tissue swelling Tophi
 Erosions with over hanging Margins ( Martel’s sign). ** rat bite
 Joint space preservation (until severe late stage)
 The erosions tophi cause may be intra-articular or extra-articular which can then result in significant boney destruction (joints are gone)
 Tophi may calcify

23

Treatment- Acute Gout


 Early treatment within 24 hrs of attack preferred

 Colchicine (Colcrys)- dosing 1.2mg, then 1 hour later 0.6mg for a total 1.8 mg
*** 2.6 mg pills -> 1.2->0.6

 NSAIDs- Indomethacin 50 mg initially followed by 50 mg every 8 hours with a max dose of 200mg in 1st 24 hours, or 50 mg TID until pain tolerated, or 75 mg po one to two times per day

24

Treatment- Acute Gout (cont.)


 Corticosteroids- Intra articular injections to single joint or bursa, Oral Medrol Dose Pack, IM or IV
** usually intra articular, oral

 Adrenocorticotropic Hormone (ACTH)- IM, ? Patients that cannot take orals?

 May use a combination depending of severity and number of joints involved.

 Tibial nerve block with local anesthetic- sympathetic response

25

Treatment- Prophylactic Gout tx



Used in conjunction with urate lowering agents
Colchicine- dosing 0.6 mg 1 to 2 tabs daily
If unable to tolerate colchicine, then may use a lower dose of Indomethacin or another NSAID
Use only until hyperuricemia maintained and no attacks for 3-6 months

26

Treatment- Gout

Hyperuricemia Contol
Xanthine Oxidase Inhibitors- i.e. Allopurinol
Uricosuric Agents- i.e. Probenecid and Sulfinpyrazone
Uricases- i.e. Krystexxa/Pegloticase (severe tophaceous gout/may reduce tophi)

27

CPPD

Calcium Pyrophosphate Dihydrate crystal deposition disease


 Inflammatory Arthritis
 Crystals of calcium salt called Pyrophosphate
 Cause Unknown
 Potentially related to overproduction of extracellular pyrophosphate in abnormal cartilage
 most common calcium containing crystals
 Use to be known as “Pseudogout”

28

Chondrocalcinosis


Seen radiographically in CPPD
Chondrocalcinosis is CPPD crystal deposition in articular cartilage or fibrocartilage

29

Risk Factors


 Increased age ( 3% in the 60’s and 50% in the 90’s)
 Genetics (CPPD

30

CPPD Crystals


 Can be found in:
 Cartilage
 Synovial Fluid
 Ligaments, Tendons, and Periarticular soft tissue (less likely)
 Enthesophytes

31

Differential Diagnoses


 Gout
 Septic Arthritis
 OA
 RA
 Neuropathic Arthropathies- charcot

32

Diagnosis



 Synovial Fluid analysis: Detects CPPD crystals
 Rhomboidal shaped and weakly birefringes
**** needle shape- gout
 Radiographs
 TSH
 Total iron binding/Iron
 Calcium
 Phosphorus
 Magnesium
 Labs to rule out other differential diagnoses

33

Clinical Symptoms



 Vary Widely
 Can be asymptomatic
 Recurrent acute inflammatory monoarticular arthritis
 Recurrent hemiarthrosis
 Chronic degenerative arthritis
 Fever or systemic symptoms
 Carpal tunnel
 Tumoral or Pseudo Tophaceous CPPD crystal depostition

34

Clinical symptoms- cont.

McCarty's patterns of CPPD



 Pseudo Gout
 Pseudo OA
 Pseudo RA
 Pseudo Neuropathic Arthritis


 CPPD may mimic any of these other arthropathies and therefore have symptoms like any of these

35

Radiographic Changes


Chondrocalcinosis
 On Radiographs of the foot changes may be subtle
 CT may pick up better changes
 Screening other susceptible joints
 CPPD likes bigger joints such as the knee, but also shoulder, elbow, wrist

36

Treatment


 No treatment to dissolve the crystals
 For Acute symptoms
 NSAIDs
 Joint Aspiration with corticosteroid injection
 Prophylaxis for further attacks
 Colchicine?
 Severe Attack
 Methotrexate?
 Hydroxychloroquine (Plaquenil)

37

Gout

Gout is a disease of both metabolism and
inflammation