Crystal Induced Arthritis-Gout Flashcards
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
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
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
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
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)
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
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)
Risk Factors
Drugs: ASA, Thiazide or Loop Diuretic
Genetics (family hx of gout)
Obesity
Metabolic syndrome (Insulin resistance, HTN, dyslipoproteinemia)
CAD
Hypothyroidism
Diet
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
Diet
Foods that can Decrease risk/levels of urate
Low fat diary products (yogurt) Milk
Vitamin C
Stages of Gout
Asymptomatic Hyperuricemia
Acute Gouty Arthritis
Intercritical Gout
Chronic Gout
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
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
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?
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
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
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
Differential Diagnoses of Gout
Other crystal induced arthropathies
Septic arthritis
Trauma
Reactive arthritis
If chronic gout, other inflammatory arthropathies such as RA
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
Joint Aspiration-
Needle shaped crystals
Radiographic Changes
Early stage/Acute stages:
Periarticular soft tissue swelling
No Osseous changes
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
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
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
