Crystal induced arthropathies Flashcards

1
Q

Uric acid solubility limit

A

6.8 mg/dL

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2
Q

Medication that predisposes to gout

A

Thiazides

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3
Q

Congenital syndrome that predisposes to gout

A

Lesch Nyhan (HGPRT deficiency)

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4
Q

Uric acid excretion

A

80% renal

20% GI

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5
Q

Key player in acute gout flare

A

IL1

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6
Q

Causes of Hyperuricemia (seondary to…)

A

10% secondary to overproduction

90% to underexcretion

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7
Q

Rreactions using HGPRT

A

Guanine to Guanylic acid

HX to Inosinic acid

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8
Q

Uric Acid Secondary overproduction

(excluding alcohol and purine foods)

A
  • Myelo/Lympho proliferative
  • Malignancy
  • Hemolytic diseases
  • Psoriasis
  • Obesity
  • Chemo
  • Down Syndrome
  • Glycogen storage disease
  • Pancreatic extract, Nicotinic acid
  • B12 deficiency
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9
Q

Why does alcohol increase risk for hyperuricemia

A

needs ATP = higher puine turnover

Lactate elevation and decreased renal excretion via URAT-1

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10
Q

Majority of renal excretion uses..

A

complex series of transport proteins

URAT

OAT

NPT

ABCG

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11
Q

Kidney excretes of about ___% of filtered urate load

A

10%

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12
Q

__% of urate is re-secreted

A

50%

80% of the resulting load is reabsorbed in the ascending limb

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13
Q

Primary causes of underexcretion

A

Deficiency of Urate transporter (exporter)

Medulary cystic kidney disease (kids)

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14
Q

Secondary renal underexcretion causes

A
  • Kidney disease
  • Lactic acidosis/ DKA
  • Dehydration
  • HypoPTH and Hypothyroidism
  • Sarcoid
  • Preeclampsia
  • SODIUM WASTING or VOLUME DEPLETION
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15
Q

Drugs that promote hyperuricemia

A
  1. Thiazides, loop diuretics
  2. Orgaic acids (salicyclate, NA, Pyrizinamide)
  3. Cylcosporine
  4. ethambutol
  5. levadopa
  6. CSF
  7. Lead Tox.
  8. Laxative abuse
  9. Severe salt restriction
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16
Q

What hppens when gout spreads beyond joint

A

Tenosynovitis mimicking cellulitis

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17
Q

Diagnosis of gout involves

A

Joint aspiration!

HU + joint effusion NOT enough for definitive

Can mimic septic arthritis

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18
Q

____ are good at finding gouty erosions

A

MRI/CT

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19
Q

Sign for gout in ultrasound

A

Double contour sign (urate icing) = irregular band on surface of articular cartilage

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20
Q

Most important indication for arthrocentesis

A

check for septic arthritis

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21
Q

WBC above ____ assume septic and give AB

A

50k

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22
Q

difference between blood from traumatic aspiration and hemarthrosis?

A

Red streaks in otherwise yellow fluid = TA

Homogenously bloody and NO clot = HA

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23
Q

Specificity for MSU visualization on polarized light

A

Near 100%

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24
Q

Three stages of gout

A

Acute

Intercritical

Chronic Tophaceous

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25
Q

Other complications for gout

A

Bursitis

Tenosynovitis

Tendinitis

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26
Q

Most untreated gout patient will have…

A

recurrence within 2 years

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27
Q

Bony erosions and deformaties occur during

A

Chronic recurrent gout

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28
Q

Defining characteristic of tophaceous gout

A

Solid urate deposits in tissues

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29
Q

Tx goal to prevent disease progression

A

Lower urate to less than 6mg/dL = deplete urate from serum

(also to correct the underlying cause)

30
Q

Tx combo for acute gout

A

NSAID + Colchicine + GC’s + IL-1b antagonist

31
Q

What dont you do during a flare?

A

Dont try to lower urate levels!

You’ll make the attack worse because crystals will get mobilized.

32
Q

Medication to increase excretion

A

Probenecid

33
Q

What to do after first attack?

A

Avoid dehydration

Modify meds (losartan)

Reduce alcohol intake

Lose weight

34
Q

Medications to reduce production

A

allopurinol

febuxostat

PEG-uricase

35
Q

Prophylaxis against attacks with…

A

Colchicine and NSAIDs

36
Q

Uricosuric agents:

Function

Examples

A

increases secretion into urine

Probenecid - Potent, limited use in CKD and nephrolithiasis

Benzbromarone = less potent but can be used in renal disease

Losartan or Fenofibrate = for mild disease with HTN or hyperlipidemia

37
Q

Allopurinol MOA

May be effective in ______

Sides?

A

XO inhibitor

underexcretors

Toxic epidermal necrolysis, vasculitis, BM supression

38
Q

Interaction with allopurinol

A

thiazide use or allergy to Pen

39
Q

Febuxostat MOA

A

blocks XO

no dose adjustment for renal patients

40
Q

Uricase enzymes function

A

Catalyzes the oxidation of uric acid o 5OH isourate

–> converted to allantoin (excreted)

*humans have a NONFUNTIONAL gene for uricase (because uric acid is a powerful antioxidant)

41
Q

Uricase enzymes examples:

A

Pegloticase = recombinant porcine uricase, modified by covalent linkage to PEG

**reserved for refractory tophaceous gout

**prophylaxis with colchicine NSAIDs or CS for first 6 months

Rasburicase = nonPegylated recombinant uricase = for BRIEF cuorses and prevention of neuropathy

42
Q

CPPD etiology

A

Excessive cartilage pyrophosphate production leads to CPPD crystals deposit in

  • Joint hylaine cartilage
  • fibrocartilage
  • ligaments
43
Q

Acute release of CPPD crystals into joint space causes _______________ >> _____________

A

phagocytosis by MQ

Release of chemotactic substances and activation of inflammasome

44
Q

CPPD can cause _____

A

chondrocalcinosis

45
Q

CPPD doesnt always have radiographic evidence, so ___ is helpful

A

US

46
Q

Extracellular …….. yields PP

A

EC ATP scavenging by nucleoside triphosphate pyrophosphate hydrolase yields PP

47
Q

CPPD prevalenece

A

equal in gender, increases with age

48
Q

CPPD a complication of ____

A

primary OA

49
Q

Other diseases that predispose to CPPD

A

Familial chondrocalcinosis

Gitelman syndrome

50
Q

Explain Gitelman

A

Mimics thiazide

presents with Hypokalemia, Met. Acidosis, hypoMagnesemia, Hypocalciuria, and normal BP

51
Q

What systemic metabolic disease associates with CPPD

A

Primary Hyperparathyroidism

52
Q

pseudogout typically affects

A

larger joints (knee)

53
Q

pseudogout flares following…

A

parathyroidectomy

(low calcium = partial dissolution of crystals = release into joint fluid)

54
Q

Pseudogout aka

A

acute CPP crystal arthritis

55
Q

Chronic CPP inflammatory arthritis aka

A

pseudo-RA

56
Q

In pseudo-RA, Radiographic changes are…

A

more typical of OA than RA

57
Q

CPPD crystals are ___ refringent and ____ whe parallel to the light

A

Positive

Blue

58
Q

CPPD aspirate tends to be

A

inflammatory

(90% PMN with 15-30k cells)

59
Q

X ray findings of CPPD

A
  • Beak like projections at 2nd/3rd Metacarpal heads
  • Subchondral cysts
  • chondrocalcinosis
60
Q
A
61
Q

CPPD deposits present with…

A
  • Hyperechoic bands parallel to cartilage surface of knee
  • Punctate pattern with hyperechoic spots
  • Homogenous hyperechoic nodular or oval deposits in bursae
62
Q

Treatment of pseudogout involving more than one joint

A

intraarticular glucocorticoids

63
Q

Indications for pseudogout prophylaxis

A

if more than 3 per year = low dose colchicine

Refractory or chronic = MTX or hydroxychloroquine

Reurrent acute or severe = IL-1b inhibitor

64
Q

Other deposition closely tied to OA

A

Hydroxyaapatite (Basic Ca Phosphate) crystals

65
Q

Elderly women get this with Hydroxyapatite deposition disease

A

Milwaukee shoulder

extremely destructive, hemorrhagic ffusions, synovial fluid has BCP crystals

66
Q

BCP Tx

A
  • NSAID or COX2 inhibitors
  • Intra-articular injections
  • Local irrigation
  • ULTRASOUND to degrade crystals

*Agents to lower phosphate levels = resorption of deposits in RF patients

67
Q

Calcium Oxalate Deposition Disease:

Primary and secondary disease =

Ascorbate metabolism and clearance =

A

Primary = enyme defect, overproduction of oxalic acid = nephrocalcinosis

Secondary = MORE COMMON, metabolic abnormality complicating end-stage renal disease

*Ascorbate is metabolozed to oxalate… inadequately cleared in uremia and by dialysis patients

68
Q

CaOx induced synovial effusions are usually ____

A

Noninflammatory

69
Q

Shape of CaOx

A

Bipyramidal

Stain with ALIZARIN RED

70
Q

CaOx therapy

A

NSAIDs

Colchicine

IA GC’s

LIVER TRANSPLANT in primary oxalosis