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Clin Med Exam 3 > Gout > Flashcards

Gout Flashcards

1
Q

Monosodium urate crystal deposition disease

A

Gout

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2
Q

What is gout?

A

Inflammatory artheritis; HYPERURICEMIA

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3
Q

How does gout occur?

A

Uric acid precipitats into monosodium urate (MSU crystals) –> crystal deposit in and around joints, bones and soft tissues –> pain and inflammation

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4
Q

Where does uric acid come from

A

breakdown of purine metabolism; excreted by the kidney

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5
Q

Hyperuricemia

A

sUA > 7 mg/dL in males

sUA >6 mg/dL in females

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6
Q

Causes of hyperuricemia

A
  1. Uric acid “underexcreters” (most common)
  2. uric acid “overproducers”
  3. combo of two mechanisms
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7
Q

Overproducers of uric acid

A

inherited enzyme defect; high cell turnover (psoriasis, myeloproliferative disease), increased purine consumption

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8
Q

Underexcretors

A

renal insufficiency, diuretics, volume depletion, lead nephropathy

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9
Q

Prevalence of gout

A

M>F, age 30-60 YO (post-menopausal for women)

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10
Q

Comorbid conditions with gout

A

HTN, obesity, CKD, diabetes, hyperlipidemia

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11
Q

Risk factors for hyperuricemia

A

Non-modifiable: male, advanced age, pacific islanders, genetic mutation
Modifiable: obesity, diets rich in meat/seafood, EtOH, fructose rich foods, diuretic use, transplant recipient status

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12
Q

States of gouty arthritis

A
  1. Asymptomatic hyperuricemia: may take 20 years before first gout flair
  2. Acute gouty arthritis: first attack
  3. Intercritical gout: asymptomatic interval between gout attacks (>80% have another attack w/i 2 years)
  4. Chronic gouty arthritis (tophaceous gout): involved joints will develop chronic swelling AND TOPHI
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13
Q

Tophi

A

white chalky material consisting of dense concentration of MSU crystals; function of the duration and severity of hyperuricemia; usually occur 10 years after 1st attack if left untreated; occurs at joints, bone, cartilage, skin

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14
Q

Sx of Gout

A

recurrent flares of inflammatory arthritis, accumulation of urate crystals as tophi, chronic arthropathy, renal complications (uric acid nephrolithiasis, urate nephropathy)

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15
Q

Acute gout attack

A

usually monoarticular, 1st MTP joint (“Podagra”), often recurrent, self-limited x 2 weeks

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16
Q

Triggers of gout flare

A

acute increases OR decreases in urate levels (EtOH, food high in purines, starvation, dehydration, trauma, meds (thiazide, diuretics, low-dose aspirin, niacin, cyclosporin A, allopurinol)

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17
Q

Sx of acute attack

A

rapid onset (usually at night)
SEVERE pain (peaks at 8-12 hours)
Redness, warmth, swelling & disability
Fever, chills, malaise
monoarticular/polyarticular
Signs of inflammation: may resemble cellultic, swelling, warmth, erythema, tenderness

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18
Q

Imaging for gout

A

radiography: early (swelling), established disease (bony erosions “punched out” w/ sclerotic margin, overhanging edges)
MRI
U/S
Dual-energy CT (DECT) - identify urate deposits and tophi

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19
Q

Double contour sign in U/S

A

represents crystal deposition on the articular cartilage surface

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20
Q

Dx of gout

A
  • Arthrocentesis (definitive dx); , needle aspriation of involved joint, C&S, microscopic analysis;
  • MONOSODIUM URATE CYRSTALS: seen under microscopy, needle shaped, NEGATIVE BIREFRINGENT
  • Serum Uric Acid (sUA): may be normal in acute attack, most accurate >2 wks after acute subsides, helpful to monitor effects of uric acid lowering therapy
  • 24h Urinary Uric Acid: IF uricosuric therapy is being considered; uric acid <800 mg = underexcretor (Candidate for uricosuric therapy)
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21
Q

Helpful to monitor effects of uric acid therapy

A

Serum uric acid (sUA)

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22
Q

Helpful to determine if candidate for uricosuric therapy

A

24 h Urinary Uric acid <800 mg

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23
Q

Baseline recommendations for gout

A

weight loss, smoking cessation, hydration; consider secondary causes of hyperuricemia, conisder elimination of nonessential prescription druts that may induce; evaluate severity

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24
Q

Asymptomatic hyperuricemia tx or not tx

A

Asymptomatic:
no treatment: no prior gout, no tophi, no nephrolithiasis
Treat: uric acid excretion >1100 mg/d, acute overproduction

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25
Q

Tx for acute attack

A

treat pain and inflammation (NSAIDs, Glucocorticoids, or Colchicine)

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26
Q

DOC for acute attack

A

NSAIDs (indomethacin or Naproxen); initiate w/i 48 ours of onset of sx;
Naproxen 500 mg bid or indomethacin 25-50 mg q 8 hrs; reduce dose after significant reduction in sx; discontinue NSAIDs 2-3 days after sx revolve

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27
Q

Glucocorticoids for gout

A

oral, IV, IM or intraarticular (exclude infection);

oral: 20-40 mg q daily or BID (may taper over 7-10 days once resolution of attack begin)

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28
Q

Colchicine for gout

A

Most effective if started w/i 36 hours of onset; start 1.2 mg then 0.6 mg 1 hr later, then 0.6 mg daily or BID; discontinue 2-3 days after sx completely resolve

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29
Q

Urate Lowering Therapy (ULT)

A 
lowers uric acid; treat those with ESTABLISHED dx AND:
tophi
frequent (>2/yr) acute attacks
CKD state >2
previous nephrolithiasis
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30
Q

Types of urate lowering therapy

A
  1. xanthine oxidase inhibitors (XOI)
  2. Uriosuric Agents
  3. Recombinant Uricase
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31
Q

Xanthine Oxidase Inhibitors

A

decrease uric acid synthesis

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32
Q

Ex. of XOI

A

Allopurinol, Febuxostat

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33
Q

Allopurinol

A

XOI; agent of choice for most patients; for overproducers AND underexcretors; 100 mg/day then reduce when CrCl <20

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34
Q

Side effects of allopurinol

A

rash, hypersensitivity, SEVERE CUTANEOUS ADVERSE RXN, (avoid in individuals who are HLA positive)

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35
Q

Febuoxostate

A

more expensive than allopurinol, initial dose 40 mg/day, reduce when CrCl <40; monitor LFTs, not good in those with high CV risk

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36
Q

Uricosuric agents

A

probenecid, lesinurad*

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37
Q

Probenecid

A

Uricosuric agent; for UNDEREXCRETORS; enhances renal excretion; starting dose 250 mg bid; requires good renal function (avoid when GFR <50);
side effect: GI, rash; avoid in pt’s with hx of nephrolithiasis

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38
Q

ULT

A

urate-lowering therapy

39
Q

ULT not used for

A

acute gout attack

40
Q

Initiation of ULT

A

2 weeks after acute gout attack; anti-inflammatory prophylaxis (low dose colchicine or NSAID therapy) - continue for 6 months after starting ULT or if ongoing sx

41
Q

Treat to target for uric acid

A

maintain sUA of 6 mg/dL or less; 5.0 mg/dL for tophi gout; measure sUA 2-4 weeks after dose adjustment, confirm 3 mo later; once at goal measure W 6 for 1 year, than annually

42
Q

Pseudogout crystals

A

calcium pyrophosphate crystal deposition (CPPD)

43
Q

Gout crystals

A

monosodium urate crystals

44
Q

CPPD

A

calcium crystals located near surface of chondrocytes; especially in advanced age; no sex predominance

45
Q

Etiology of CPPD

A

joint trauma, familial chondrocalcinosis, hemachromatosis, hyperparathyroidism

46
Q

Joints affected in CPPD

A

KNEE, wrists, shoulders, ankles, feet and elbows; trauma, surgery or severe medical illness provoke attack

47
Q

Radiography for CPPD

A

chondrocalcinosis (cartilage calcification)

48
Q

Dx studies for CPPD

A

synovial fluid aspiration (POSITVE biferingenet CPP crystals, rhomboid-shaped)

49
Q

Positive birefringent crystals

A

CPPD (pseudogout)

50
Q

Negative birefringent

A

gout

51
Q

Tx of CPPD

A

NSAIDS, steroid injection, colchicine, oral steroid, supportive

52
Q

Prophylaxis for CPPD

A

colchicine 0.6 mg BID; recommended if >3 attacks/year; may be problematic in elderly (adjust for renal dosing)

53
Q

Spondyloarthropathies (SpA)

A

reactive arthritis; ankylosing spondylitis

54
Q

Classifications of SpA

A
  1. Axial - ankylosing spondylitis

2. Peripheral - RA, psoraitic arthritis, arthritis associated w/ IBD, undifferentiated SpA

55
Q

Shared features of SpA

A

inflammatory back pain, enthesitis, asymmetric oligoarthritis, dactylitis, uveitis, strong association with HLA, negative RF

56
Q

Axial clinical Sx

A

Si joints, spine

57
Q

Peripheral Sx of SpA

A

peripheral arthritis, enthesitis, dactylitis

58
Q

Enthesitis

A

inflammation of the entheses - site of insertion of ligaments, tendons, joint capsule or fascia to bone

59
Q

Sx of enthesitis

A

“heel pain,” swelling of heels (achilles or plantar fascia insertion), pain, swelling, local tenderness

60
Q

can’t see, can’t pee, can’t climb a tree

A

Reactive Arthritis (RA)

61
Q

RA

A

acute inflammatory arthritis triggered by GI or GU infection

62
Q

Precedd by GI/GU infection

A

RA

63
Q

Prevalence of RA

A

young adults, M=F, genetic predisposition HLA-B27

64
Q

Sx of RA

A

acute onset, ASYMMETRICAL OLIGOARTHRITIS (usually LE), occurs 1-4 weeks follwing infection;
associated sx: peripheral arthritis, enthesitis, dactylitis, low back pain

65
Q

Extraarticular manifestations of RA

A

conjunctivitis/uveitis (can’t see)
urethritis (can’t pee)
peripheral arthritis (can’t climb a tree);
also: nail changes, cricinate balanitis, oral ulcers, keratoderma

66
Q

Dx of RA

A

antecedent/concomittant infection; elevated ESR or CRP, POSITIVE HLA ANTIGEN, synovial fluid analysis (inflammatory, negative for crystals); imaging (enthesitis or arthritis)

67
Q

Tx for RA

A 
refer to rheumatology, 
initial tx: NSAIDs
2nd line: glucocorticoids
3rd choice: DMARDs (sulfasalazine or methotrexate); 
Uveitis- refer to opthamology
68
Q

Ankylosing Spondylitis (AS)

A

chronic inflammatory disease of AXIAL skeleton; usually SI and spinal joints (also hips, shoulders, peripheral joints, entheses);
back pain and PROGRESSIVE STIFFNESS of spine
white>nonwhites; M>F; yound adults (20-30)

69
Q

Cause of AS

A

unknown; strong HLA component

70
Q

Sx of AS

A

inflammatory back pain
peripheral enthesitis and arthritis
constitutional sx
extra-articular manifestations

71
Q

Disease pathology of AS

A

enthesitis with chronic inflammation –> structural damage –> new bone formation (ossification) –> ankylosis (fusion)

72
Q

AS progression

A

begins in SI joints
as it progresses, moves proximally
Eventual ossification leading to syndesmophytes
Condition progresses to characteristic “bamoo spine” (fusion)

73
Q

Bamboo spine

A

AS

74
Q

Hx of AS

A 
INFLAMMATORY BACK PAIN (low/SI joints, insidious, pain and stiffness, intermittent, radiates to butt)
Systemic: fatigue
before age 40
Sx >3 months
WORSE IN MORNING OR INACTIVITY
Sx improve with exercise
good response to NSAIDS
75
Q

Worse in morning or with inactivitiy

A

AS

76
Q

PE of AS

A 
limited spinal mobility
postural abnormalities (hyperkyphosis)
loss of lumbar lordosis
tenderness over SI joint
77
Q

Modified Schober test

A

measures lumbar flexion; used to dx AS

78
Q

Extra sx of AS

A 
uveitis (refer to optha)
IBD
Psoriasis
Restrictive disease pattern (pulmonary)
CV disease
Psych: pain, fatigue, sleep distrubance
79
Q

Uveitis

A

RA, AS

80
Q

Urethritis

A

RA

81
Q

Complications of AS

A 
osteopenia/osteoporosis
Neuro compromise (spinal cord injury)
82
Q

Labs for AS

A 
No dx labs:
CBC (anemia?)
Elevated ESR and/or CRP
negative RF and anti-CCP
positive HLA-B27 (87%)
83
Q

Imaging for AS

A

x-ray, MRI
Radiographic eval of pelvis/SI
Hallmark: SACROILITIS

84
Q

Sacroilitis

A

AS

85
Q

Bamboo spine

A

late hallmark in AS

86
Q

Dx of AS

A

back pain >3 mo, less than <45 YO PLUSSSS:

sacroiliatis or HLA (+) + two other features

87
Q

Positive response to NSAIDs

A

AS

88
Q

Tx for AS

A

NSAIDs (1st line)
refer to rheumatology
NSAID-resistant disease: sulfasalazine (peripheral joint involvement), TNF inhibitors, IL inhibitors

89
Q

Non pharm tx for AS

A

PT, surgical correction & stabilization;
Supportive:
smoking cessation
EXERCISE (essential)

90
Q

Who is most as risk for AS

A

young males

91
Q

usually follow diarrheal illness or STI

A

RA (young adults)

92
Q

Can’t see, can’t pee, can’t climb tree

A

conjunctivitis, urethritis, oligoarthritis (RA)

93
Q

Mucocutaneous lesions

A

RA

94
Q

NSAIDS for tx

A

AS, RA, ACPP, Gout

Clin Med Exam 3 (7 decks)

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