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ICM > 2: Crystal Induced Arthropathies > Flashcards

2: Crystal Induced Arthropathies Flashcards

1
Q

what are four microcrystals associated with crystal induced arthropathies?

A
  • monosodium urate (MSU)
  • calcium pyrophosphate dihydrate (CPPD)
  • calcium apatite (apatite)
  • calcium oxalate (CaOx)
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2
Q

what conditions are included in a ddx for crystal induced arthropathies?

A
  • gout
  • pseudogout: acute CPP crystal arthritis
  • psoriatic arthritis
  • reactive arthritis
  • osteoarthritis
  • rheumatoid arthritis
  • septic arthritis
  • cellulitis
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3
Q

pathogenesis of gout

A

Hyperuricemia followed by extracellular deposition of uric acid crystals in synovia of joints, bursae, and/or tendons - then release of crystals into joint or bursae with accompanying inflammation (key involvement of IL-1)

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4
Q

biochem associated with gout

A
  • uric acid = end product of human purine metabolism
  • humans cannot metabolize it- must be excreted
  • serum [urate] determined by balance of urate production vs. elimination
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5
Q

definition of hyperuricemia

A

> 6.8 mg/dl (limit of its solubility in serum)

at this level, there is an accumulation of MSU at levels that drive the precipitation of urate crystals

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6
Q

some famous people with gout

A
  • King Henry VIII
  • Ben Franklin
  • Jared Leto
  • Ansel Adams
  • Maurice Cheeks
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7
Q

risk factors for gout

A
  • age
  • male; or PMS women
  • HTN (thiazide diuretic use)
  • obesity
  • hyperlipidemia
  • hyperuricemia
  • dietary excess: meat, seafood, alcohol (highest with beer)
  • dehydration
  • trauma/surgery/transplant
  • AMI/stroke
  • urate lowering therapy
  • Lesch-Nyhan syndrome (HGPRT def: orange, sandy urine; self mutilation, mental retardation)
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8
Q

causes of hyperuricemia

A
  • 90% secondary to underexcretion
  • 10% secondary to overproduction

use 24h quantitative urine uric acid to help define pathophysiology (normal = 250-750mg/24h)

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9
Q

4 causes of primary uric acid overproduction

A
  • Lesch Nyhan (NGPRT deficiency)
  • overactive PRPP
  • G6PD deficiency
  • F1P aldolase deficiency
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10
Q

many causes of secondary uric acid overproduction

A
  • myelo/lympho-proliferative disorders
  • malignancies
  • hemolytic diseases
  • psoriasis
  • obesity
  • chemotherapy (tumor lysis)
  • Down syndrome
  • Glycogen storage disease (III, V, VII)
  • excessive purine or fructose rich foods
  • pancreatic extract, Nicotinic acid, B12 deficiency
  • alcohol (mix of overproduction and underexcretion)
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11
Q

relationship b/w hyperuricemia and alcohol

A
  • alcohol needs ATP degradation to metabolize thus increased purine turnover and urate generation (overproduction)
  • binging can cause elevated lactate levels and decreased renal excretion via URAT-1 (underexcretion)
  • promotes diuresis via suppression of ADH causing dehydration, volume depletion, and urate retention (underexcretion)
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12
Q

what alcohols affect purine levels?

A

beer, ale, and distilled spirits

wine does not!

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13
Q

describe urate excretion

A

kidney:
1. glomerular filtration of all serum urate
2. PCT resorption of 99% filtered load
3. resecretion in descending of 50% resorbed load
4. resorption in ascending of 80% of resecreted load
5. excretion of about 10% of filtered load (about 600 mgms/d)

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14
Q

primary causes of renal underexcretion

A
  • hereditary deficiency in urate exporter

- medullary cystic kidney disease in kids

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15
Q

secondary causes of renal underexcretion

A
  • kidney disease
  • lactic and diabetic or starvation ketoacidosis
  • dehydration: fluid loss, heart failure
  • hypoparathyroidism
  • hypothyroidism
  • sarcoidosis
  • pre-eclampsia
  • medications
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16
Q

drugs that promote hyperuricemia

A
  • diuretics: thiazide > loop
  • organic acids: low dose salicylates, nicotinic acid, pyrazinamide
  • cyclosporine
  • ethambutol
  • ethanol
  • levadopa
  • CSF?
  • lead toxicity (lead nephropathy -> saturnine gout)
  • laxative abuse (alkalosis)
  • severe salt restriction
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17
Q

presentation of acute gouty arthritis

A
  • acute inflammation with pain, redness, and swelling
  • max severity in hours, resolves in 3-10d
  • 80% monoarticular, often podagra (great toe MTP)
  • pain to even put sheet over foot
  • inflammation can spread beyond joint, giving tenosynovitis mimicking cellulitis
  • urate crystals in synovial fluid at time of inflammation
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18
Q

diagnosis of acute gouty arthritis

A
  • joint aspiration (hyperuricemia + joint effusion not enough)
  • look at fluid under polarized light
  • can mimic septic arthritis (fever, leukocytosis, high ESR)
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19
Q

what imaging can be used to tentatively diagnose gout, and what will you see?

A

US - superficial, hyperechoic, irregular band on surface of articular cartilage = “double contour sign” or “urate icing”

MRI/ CT - good for finding gouty erosions

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20
Q

most important indication for arthrocentesis

A

to check for septic arthritis

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21
Q

how can you determine if blood in aspirated synovial fluid is from hemarthrosis or from trauma from a poorly performed arthrocentesis?

A
  • trauma: blood may remain unmixed with synovial fluid, appearing as red streaks in an otherwise yellow fluid
  • hemarthrosis: synovial fluid is generally homogeneously bloody and does not form a clot
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22
Q

how to differentiate MSU from CPPD crystals with polarized microscopy

A

MSU: yellow parallel, blue perpendicular

CPPD: blue parallel, yellow perpendicular

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23
Q

how long can asymptomatic hyperuricemia last

A

up to 20 years

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24
Q

3 stages of gout

A
  • acute gout
  • intercritical gout
  • chronic tophaceous gout
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25
Q

describe the first gout attack

A
  • usually monoarticular (big toe, instep, ankle, heel, knee, wrists, fingers, elbows)
  • can get bursitis, tendinitis and tenosynovitis
  • acute w/ intense pain and limited time
  • men 40-60 y/o and women more than 60 y/o
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26
Q

describe intercritical gout

A
  • after 1st attack there is “intercritical gout period”
  • most untreated patients will have a second episode within 2 years
  • trend if untreated:
    • additional acute attacks
    • progressively shorter asymptomatic periods
    • increasingly severe, prolonged and polyarticular flares
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27
Q

describe chronic recurrent gout

A
  • polyarticular acute exacerbations
  • more commonly in upper extremities
  • bony erosions and deformities
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28
Q

tophaceous gout

A
  • solid urate deposits (tophi) in tissues

- 75% with tophi after 20 years of untreated gout

29
Q

factors that can precipitate a gout flare

A
  • trauma
  • surgery or hospital admission w/ IV fluids
  • starvation
  • dehydration
  • increased alcohol consumption (but NOT wine)
  • dietary indulgence
  • acute changes in serum uric acid level
  • stopping or starting medications for gout
30
Q

gout treatment goals

A
  • rapidly end acute flares
  • protect against future flares for lifetime
  • reduce change of crystal inflammation
  • prevent disease progression (lower serum urate to less than 6 mg/dl)
  • correct metabolic cause
31
Q

specific treatments for acute gout

A
  • rest, ice packs, elevation
  • increase water consumption
  • NSAIDs
  • colchicine
  • glucocorticoids
  • IL-1B antagonists
32
Q

does ending acute flares cure gout?

A

no- but it controls inflammation, relieves pain. but not a cure b/c crystals remain in joints

33
Q

what steps can one take after a first attack to try to slow down/prevent future attacks?

A
  • avoid dehydration
  • modify meds
  • reduce alcohol intake
  • lose weight
  • meds to increase excretion (probenecid)
  • meds to reduce production (allopurinol, febuxostat, PEG-uricase)
  • prophylaxis against attacks with colchicine and NSAIDs
34
Q

reasons to start urate lowering therapy

A
  • recurrent attacks
  • urate nephrolithiasis
  • tophaceous gout
  • evidence of gout-induced joint damage
35
Q

how do you choose what urate lowering therapy to use

A

base choice on whether pt is an overproducer or underexcreter:
700/24h = overproducer (10%) - use xanthine oxiase inhibitor

36
Q

function of uricosuric agents

A

-increase secretion of urate into urine

37
Q

examples of uricosuric agents

A
  • probenecid
  • benzbromarone
  • losartan or fenofibrate (mild urisocurics)
38
Q

two xanthine oxidase inhibitors and their MOA

A
  • allopurinol: blocks conversion of hypoxanthine to uric acid
  • febuxostat (didn’t say MOA)
39
Q

function of urate oxidase (UO)

A

catalyzes the oxidation of uric acid to 5-hydroxyisourate, which can then be converted to more soluble and excretable allantoin

(humans have a gene for this, but its non-functional)

40
Q

calcium crystal disease involves what two crystal types

A

calcium pyrophosphate dihydrate (CPPD)

basic calcium phosphate (BCP)

41
Q

describe CPPD disease

A
  • excessive cartilage pyrophosphate production leads to CPPD crystals depositing in joint articular cartilage (hyaline), fibrocartilage (menisci), and ligaments
  • can be asymptomatic
  • acute release of CPPD crystals into joint space - phagocytosis by macrophages - release of chemotactic and inflammatory substances - activating inflammasome
  • can also cause mild chronic inflammation
42
Q

XR diagnosis for CPPD disease

A

chondrocalcinosis - calcification of the cartilage and fibrocartilage

*high res US helpful b/c XR of CPPD not always detectable

43
Q

describe the production of CPPD

A
  • extracellular ATP ‘scavenging’ by nucleoside triphosphate pyrophosphate hydrolase yields PP
  • OA cartilage matrix abnormal: favors Ca + PP deposition
44
Q

epidemiology of CPPD

A
  • both sexes equally affected

- idiopathic with aging most common

45
Q

causes of CPPD deposition

A
  • idiopathic with aging most common**
  • complication of primary osteoarthritis
  • long term consequence from trauma/menisectomy
  • familial chondrocalcinosis
  • gitelman syndrome
  • systemic metabolic disease (primary hyperparathyroidism)
46
Q

describe gitelman syndrome

A

autosomal recessive renal tubular disorder

  • mimics chronic thiazide ingestion
  • presents as older child/adult w/ hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, and normal BP
  • leg and arm cramps, weakness, polyuria, nocturia, and chondrocalcinosis
47
Q

three possible presentations of CPPD disease

A
  • asymptomatic CPPD crystal deposition
  • acute CPP crystal arthritis (pseudogout)
  • chronic CPP crystal inflammatory arthritis
48
Q

describe pseudogout

A
  • acute inflammatory mono or oligoarticular arthritis
  • typically involves larger joints (knees most)
  • lasts 1-3w
  • flares after parathyroidectomy
49
Q

describe chronic CPP crystal inflammatory arthritis

A
  • pseudo-RA
  • non-erosive, asynchronous, inflammatory arthritis with CPPD crystals in joint fluid of clinical joints, suggesting RA
  • XR changes more typical of osteoarthritis than RA
50
Q

MSU vs. CPPD crystals

A

MSU:

  • gout
  • needle-shaped, about size of PMN
  • negatively birefringent (yellow parallel)

CPPD:

  • pseudogout
  • rhomboid, smaller than PMN
  • positively birefringent (blue parallel)
51
Q

how does aspirated fluid in CPPD differ from gout

A

fluid tends to be inflammatory - typically 15,000 to 30,000 WBCs (90% neutrophils)

52
Q

XR findings of CPPD

A
  • chondrocalcinosis
  • subchondral cysts
  • beak-like projections (2nd and 3rd metacarpal heads)
53
Q

how an you diagnose CPPD when unable to prove crystals?

A

high res US:

  • thin hyperechoic bands, parallel to surface of cartilage (knee)
  • ‘punctate’ pattern w/ several thin hyperechoic spots (fibrous cartilage and tendons)
  • homogenous hyperechoic nodular or oval deposits in bursae and articular recesses
54
Q

treatment of pseudogout

A
  • joint aspiration and intra-articular corticosteroid
  • NSAIDs
  • colchicine
  • systemic corticosteroid
55
Q

pseudogout prophylaxis

A
  • necessary if more than 3 episodes/year
  • low dose colchicine
  • methotrexate or hydroxychloroquine for refractory chronic inflammation/synovitis
  • IL-1B inhibitors for recurrent acute or severe attacks
56
Q

describe BCP deposition

A
  • closely tied to osteoarthritis
  • can cause chondrocalcinosis on XR
  • rarely causes acute inflammation- more of a chronic low grade destructive arthritis
57
Q

what conditions can BCP be found in?

A
  • advanced chronic renal failure (hyperphosphatemia)
  • hypercalcemic metastatic calcification
  • hyperparathyroidism
  • areas of tissue damage (dystrophic calcification)
58
Q

what is the most common BCP crystal

A

hydroxyapatite

-primary mineral in bone/teeth (apatite is)

59
Q

ID of hydroxyapatite crystals in BCP

A
  • amorphous crystals not visible with polarized light*
  • if in a clump, edge can be birefringent
  • synovial fluid crystal stain w/ alizarin red to ID crystals
  • absolute ID with EM
60
Q

what does hydroxyapatite crystals cause

A
  • cartilage and bone damage with chronic low grade inflammation
  • synovial fluid WBC counts less than 2000
61
Q

presentation of hydroxyapatite crystals

A
  • associated with periarthritis, tendon calcifications
  • knees, shoulders, hips, fingers
  • acute onset pain and swelling or chronic low grade inflammation
62
Q

what are hydroxyapatite crystals associated with?

A
  • progressive rotatoe cuff degeneration
  • elderly women: Milwaukee shoulder
    • extremely destructive chronic arthropathy
    • hemorrhagic shoulder effusions
    • synovial fluid shows BCP crystals
63
Q

treatment of BCP crystal deposition arthropathy

A
  • NSAIDs or COX2 inhibitors
  • intra-articular or periarticular corticosteroid injections
  • local irrigation
  • high frequency therapeutic US to degrade BCP crystal deposits
  • agents to lower serum [phosphate] may lead to resorption of deposits in renal failure patients receiving hemodialysis
64
Q

describe primary calcium oxalate deposition disease

A
  • rare hereditary metabolic enzyme defect
  • overproduction of oxalic acid
  • oxalate crystals in tissue, nephrocalcinosis
  • renal failure and death before age 20
65
Q

describe secondary calcium oxalate deposition disease

A
  • more common than primary
  • metabolic abnormality complicating end-stage renal disease dependent on long-term peritoneal/hemodialysis who received ascorbic acid supplements
66
Q

where do you find CaOx deposits?

A
  • bone, articular cartilage, synovium, and periarticular tissues
  • crystals may be shed, causing acute synovitis stimulating synovial cell proliferation and enzyme release, resulting in progressive articular destruction
  • deposits in fingers, wrists, elbows, knees, ankles, feet
67
Q

describe shape of CaOx crystals

A
  • variable shape and variable birefringent to polarized light
  • most easily recognizable ones are bipyramidal with strong birefringence and stain with alizarin red
68
Q

treatment of CaOx arthropathy

A
  • NSAIDs
  • colchicine
  • intra-articular glucocorticoids
  • increased frequency of dialysis (only slight improvement)
  • primary oxalosis, liver transplantation

ICM (26 decks)

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