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Rheumatology Exam > Crystalline Arthritis > Flashcards

Crystalline Arthritis Flashcards

1
Q

crystalline diseases - examples

A
  1. gout
  2. calcium pyrophosphate dihydrate disease (pseudogout)
  3. basic calcium phosphate diseases
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2
Q

crystal associated with gout

A

*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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3
Q

crystal associated with calcium pyrophosphate dihydrate disease (pseudogout)

A

*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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4
Q

crystal associated with basic calcium phosphate disease

A

*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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5
Q

gout - epidemiology

A

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

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6
Q

gout - symptoms

A

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

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7
Q

gout - physical exam

A

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

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8
Q

gout - diagnosis

A

*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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9
Q

gout - pathogenesis

A

*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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10
Q

causes of hyperuricemia

A
  1. underexcretion of uric acid: renal dysfunction, medications
  2. overproduction of uric acid: Lesch-Nyhan (HGPRT deficiency), PRPP increase, increased cell turnover, tumor lysis
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11
Q

triggers of gout flares

A

*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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12
Q

gout - acute treatment

A

*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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13
Q

colchicine - MOA

A

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

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14
Q

colchicine - ADEs

A

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

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15
Q

gout - intercritical period

A

*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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16
Q

chronic gout - overview

A

*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

17
Q

diet modifications for gout

A

*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)

18
Q

uricosuric agents for gout

A

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

  1. probenecid: MOA = inhibits URAT1 in proximal tubules of nephron → more uric acid excreted (decreased reabsorption of uric acid)
  2. losartan also has uricosuric properties
19
Q

allopurinol for gout

A

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

20
Q

allopurinol - ADEs

A

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

21
Q

allopurinol - drug interactions

A
  1. theophylline
  2. warfarin
  3. azathioprine / 6-MP
22
Q

febuxostat in gout

A

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

23
Q

febuxostat - ADEs

A

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

24
Q

how to use xanthine oxidase inhibitors for gout

A

*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

25
Q

uricases

A
  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)
26
Q

monosodium urate crystal

A

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

27
Q

CPPD arthropathy - overview

A

*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

28
Q

causes of CPPD crystals

A

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

29
Q

acute, symptomatic CPPD arthropathy

A

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

30
Q

chronic, symptomatic CPPD arthropathy

A

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

31
Q

CPPD arthropathy - treatment

A

*NSAIDs
*steroids for acute attacks
*colchicine

32
Q

basic calcium phosphate deposition disease - overview

A

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

33
Q

basic calcium phosphate deposition disease - clinical presentations

A
  1. Milwaukee Shoulder Syndrome = elderly female, one-sided shoulder pain
  2. calcific periarthritis / tendinitis = younger people, esp females (ages 31-40)
34
Q

basic calcium phosphate deposition disease - Milwaukee shoulder syndrome

A

*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

35
Q

basic calcium phosphate deposition disease - calcific tendinitis

A

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

36
Q

probenecid - MOA, uses

A

*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

Rheumatology Exam (20 decks)

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