Crystalline Arthritis Flashcards by Kyra Porter

crystalline diseases - examples

gout
calcium pyrophosphate dihydrate disease (pseudogout)
basic calcium phosphate diseases

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crystal associated with gout

*monosodium urate (MSU) crystal
*needle-shaped
*negatively birefringent:
-crystal is YELLOW when parallel to the compensator (yeLLow = paraLLel)
-crystal in BLUE when perpendicular
-compensator in direction of black arrow

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crystal associated with calcium pyrophosphate dihydrate disease (pseudogout)

*calcium pyrophosphate dihydrate crystal
*small, rhomboid shaped
*positively birefringent:
-crystal is blue when parallel and yellow when perpendicular (pseudogout = opposite of gout)

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crystal associated with basic calcium phosphate disease

*basic calcium phosphate crystal
*“Shiny coin”
*not seen on polarizing microscopy
*use Alizarin red (binds to calcium)
*can use scanning EM

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gout - epidemiology

*2% of all people > 45 yo
*9:1 ratio of men:women
*women with gout are postmenopausal

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gout - symptoms

*acute, severely painful joint
*most often monoarticular
*can be polyarticular as disease progresses

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gout - physical exam

*warm, swollen joint
*erythematous
*podagra (gout affecting the big toe)

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gout - diagnosis

*labs = elevated serum uric acid
*diagnosis:
-aspirate the joint
-crystal identification (monosodium urate crystal: needle-shaped, negatively birefringent; yellow when parallel light)

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gout - pathogenesis

*many things TRIGGER gout attacks
*the pathologic impetuous is the crystal itself: MSU crystals activate the NALP3 inflammasome, causing IL-1 release and inflammatory cascade

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causes of hyperuricemia

underexcretion of uric acid: renal dysfunction, medications
overproduction of uric acid: Lesch-Nyhan (HGPRT deficiency), PRPP increase, increased cell turnover, tumor lysis

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triggers of gout flares

*triggers either increase or decrease serum uric acid:
-acute illness, trauma, surgery, alcohol (beer), seafood, red meat, medications
*causes crystal precipitation

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gout - acute treatment

*self-limited: may resolve on its own, but VERY painful
*NSAIDs, indomethacin (high dose for short period of time)
*alternatives: colchicine, steroids

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colchicine - MOA

1. inhibits microtubule assembly
2. inhibits neutrophil adhesion and chemotaxis (cytoskeleton-dependent functions)
3. blocks activation of the NALP3 inflammasome

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colchicine - ADEs

*diarrhea
*nausea
*vomiting
*bone marrow suppression (esp in renal failure)
*myopathy

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gout - intercritical period

*the time between gout flares
*average time to second attack: 12-18 months
*decrease in the time between attack as the disease progresses; eventually becomes continuous

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chronic gout - overview

*more polyarticular arthritis
*less acutely painful; attacks incompletely resolve
*increasing involvement of upper extremity joints
*Tophi (skin nodules on extensor surfaces) develop - “rat bite” lesion on radiology

diet modifications for gout

*can only decrease serum uric acid by about 1 mg/dL
*avoidance is often insufficient (can avoid specific triggers for patient)
*examples that increase risk for gout flares: red meat, seafood (shelled creatures), alcohol, certain sweetened drinks (sweet tea)

uricosuric agents for gout

*uricosuric agents increase excretion of uric acid
*used for under-excretors
*must have good renal function
*contraindications: nephrolithiasis, CKD

probenecid: MOA = inhibits URAT1 in proximal tubules of nephron → more uric acid excreted (decreased reabsorption of uric acid)
losartan also has uricosuric properties

allopurinol for gout

*MOA: xanthine oxidase inhibition → decreased amount of uric acid production
*most commonly used xanthine oxidase inhibitor
*cannot use in severe CKD

allopurinol - ADEs

*rash
*hypersensitivity syndrome (HLA association)
*drug interactions

allopurinol - drug interactions

theophylline
warfarin
azathioprine / 6-MP

febuxostat in gout

*MOA: non-purine xanthine oxidase inhibitor
*primarily metabolized in liver, therefore CAN use in pts with decreased renal function

febuxostat - ADEs

*elevated LFTs
*no drug interactions (compared to allopurinol)
*expensive

how to use xanthine oxidase inhibitors for gout

*important to remember that any change (increase or decrease) in uric acid can precipitate a gout flare
*therefore, giving a xanthine oxidase inhibitor can trigger a gout flare
*so, we need to add something to prevent flares: colchicine, low dose prednisone, PRN prednisone for flares

uricases

1. rasburicase: -nonPEGylated recombinant fungal enzyme -prevents tumor lysis syndrome -short half-life, highly immunogenic 2. pegloticase: -PEGylated recombinant porcine-BABOON uricase -less immunogenicity, longer half-life -highly effective in tophi debulking -infusion reactions commonly (methotrexate may help decrease risk)

monosodium urate crystal

*associated with **gout** *under polarized light: -**needle shaped -negatively birefringent: ~yellow under parallel light** ~blue under perpendicular light

CPPD arthropathy - overview

*prevalence increases with age *most common: knee, hip, triangular fibrocartilage of the wrist *often asymptomatic, found incidentally on imaging (chondrocalcinosis) *the blue P's of CPPD: blue when parallel, positive birefringence. calcium pyrophosphate, pseudogout

causes of CPPD crystals

*increasing age *genetics ***hyperparathyroidism *hemochromatosis** *hypomagnesemia *hypothyroidism *hypophosphatasia

acute, symptomatic CPPD arthropathy

*acute attacks, inflammation in 1-2 joints *knees and wrists most common *provoked by trauma, surgery, illness, etc *chondrocalcinosis ABSENT

chronic, symptomatic CPPD arthropathy

*symmetric polyarthritis: wrists, MCPs, flexion contractures *negative RF, CCP *no erosions *often chondrocalcinosis (deposition of crystal in cartilage)

CPPD arthropathy - treatment

*NSAIDs *steroids for acute attacks *colchicine

basic calcium phosphate deposition disease - overview

*crystals are small and **non-birefringent** *deposit in tendons, discs, joint capsule, synovium, cartilage, skin, arteries, and other tissues

basic calcium phosphate deposition disease - clinical presentations

1. Milwaukee Shoulder Syndrome = elderly female, one-sided shoulder pain 2. calcific periarthritis / tendinitis = younger people, esp females (ages 31-40)

basic calcium phosphate deposition disease - Milwaukee shoulder syndrome

*elderly female with one-sided shoulder pain *radiology: -rapid glomerulohumeral joint destruction -high riding humerus (rotator cuff tear) -soft tissue calcification *synovial fluid: -**low synovial fluid WBC (<500) -BCP crystals -high collagenase**

basic calcium phosphate deposition disease - calcific tendinitis

*F > M, ages 31-40 *acute shoulder pain, may sound like inflammatory arthritis *most often in supraspinatus laterally *treatment = symptomatic, resolves without intervention typically

probenecid - MOA, uses

*MOA = **inhibits URAT1 in proximal tubules of nephron → more uric acid excreted (decreased reabsorption of uric acid)** *can be used for gout in "under-excretors"; must have good renal function

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Crystalline Arthritis Flashcards

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