Gout Flashcards

(94 cards)

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
Tx for acute attack
treat pain and inflammation (NSAIDs, Glucocorticoids, or Colchicine)
26
DOC for acute attack
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
27
Glucocorticoids for gout
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)
28
Colchicine for gout
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
29
Urate Lowering Therapy (ULT)
``` lowers uric acid; treat those with ESTABLISHED dx AND: tophi frequent (>2/yr) acute attacks CKD state >2 previous nephrolithiasis ```
30
Types of urate lowering therapy
1. xanthine oxidase inhibitors (XOI) 2. Uriosuric Agents 3. Recombinant Uricase
31
Xanthine Oxidase Inhibitors
decrease uric acid synthesis
32
Ex. of XOI
Allopurinol, Febuxostat
33
Allopurinol
XOI; agent of choice for most patients; for overproducers AND underexcretors; 100 mg/day then reduce when CrCl <20
34
Side effects of allopurinol
rash, hypersensitivity, SEVERE CUTANEOUS ADVERSE RXN, (avoid in individuals who are HLA positive)
35
Febuoxostate
more expensive than allopurinol, initial dose 40 mg/day, reduce when CrCl <40; monitor LFTs, not good in those with high CV risk
36
Uricosuric agents
probenecid, lesinurad*
37
Probenecid
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
38
ULT
urate-lowering therapy
39
ULT not used for
acute gout attack
40
Initiation of ULT
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
Treat to target for uric acid
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
Pseudogout crystals
calcium pyrophosphate crystal deposition (CPPD)
43
Gout crystals
monosodium urate crystals
44
CPPD
calcium crystals located near surface of chondrocytes; especially in advanced age; no sex predominance
45
Etiology of CPPD
joint trauma, familial chondrocalcinosis, hemachromatosis, hyperparathyroidism
46
Joints affected in CPPD
KNEE, wrists, shoulders, ankles, feet and elbows; trauma, surgery or severe medical illness provoke attack
47
Radiography for CPPD
chondrocalcinosis (cartilage calcification)
48
Dx studies for CPPD
synovial fluid aspiration (POSITVE biferingenet CPP crystals, rhomboid-shaped)
49
Positive birefringent crystals
CPPD (pseudogout)
50
Negative birefringent
gout
51
Tx of CPPD
NSAIDS, steroid injection, colchicine, oral steroid, supportive
52
Prophylaxis for CPPD
colchicine 0.6 mg BID; recommended if >3 attacks/year; may be problematic in elderly (adjust for renal dosing)
53
Spondyloarthropathies (SpA)
reactive arthritis; ankylosing spondylitis
54
Classifications of SpA
1. Axial - ankylosing spondylitis | 2. Peripheral - RA, psoraitic arthritis, arthritis associated w/ IBD, undifferentiated SpA
55
Shared features of SpA
inflammatory back pain, enthesitis, asymmetric oligoarthritis, dactylitis, uveitis, strong association with HLA, negative RF
56
Axial clinical Sx
Si joints, spine
57
Peripheral Sx of SpA
peripheral arthritis, enthesitis, dactylitis
58
Enthesitis
inflammation of the entheses - site of insertion of ligaments, tendons, joint capsule or fascia to bone
59
Sx of enthesitis
"heel pain," swelling of heels (achilles or plantar fascia insertion), pain, swelling, local tenderness
60
can't see, can't pee, can't climb a tree
Reactive Arthritis (RA)
61
RA
acute inflammatory arthritis triggered by GI or GU infection
62
Precedd by GI/GU infection
RA
63
Prevalence of RA
young adults, M=F, genetic predisposition HLA-B27
64
Sx of RA
acute onset, ASYMMETRICAL OLIGOARTHRITIS (usually LE), occurs 1-4 weeks follwing infection; associated sx: peripheral arthritis, enthesitis, dactylitis, low back pain
65
Extraarticular manifestations of RA
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
Dx of RA
antecedent/concomittant infection; elevated ESR or CRP, POSITIVE HLA ANTIGEN, synovial fluid analysis (inflammatory, negative for crystals); imaging (enthesitis or arthritis)
67
Tx for RA
``` refer to rheumatology, initial tx: NSAIDs 2nd line: glucocorticoids 3rd choice: DMARDs (sulfasalazine or methotrexate); Uveitis- refer to opthamology ```
68
Ankylosing Spondylitis (AS)
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
Cause of AS
unknown; strong HLA component
70
Sx of AS
inflammatory back pain peripheral enthesitis and arthritis constitutional sx extra-articular manifestations
71
Disease pathology of AS
enthesitis with chronic inflammation --> structural damage --> new bone formation (ossification) --> ankylosis (fusion)
72
AS progression
begins in SI joints as it progresses, moves proximally Eventual ossification leading to syndesmophytes Condition progresses to characteristic "bamoo spine" (fusion)
73
Bamboo spine
AS
74
Hx of AS
``` 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
Worse in morning or with inactivitiy
AS
76
PE of AS
``` limited spinal mobility postural abnormalities (hyperkyphosis) loss of lumbar lordosis tenderness over SI joint ```
77
Modified Schober test
measures lumbar flexion; used to dx AS
78
Extra sx of AS
``` uveitis (refer to optha) IBD Psoriasis Restrictive disease pattern (pulmonary) CV disease Psych: pain, fatigue, sleep distrubance ```
79
Uveitis
RA, AS
80
Urethritis
RA
81
Complications of AS
``` osteopenia/osteoporosis Neuro compromise (spinal cord injury) ```
82
Labs for AS
``` No dx labs: CBC (anemia?) Elevated ESR and/or CRP negative RF and anti-CCP positive HLA-B27 (87%) ```
83
Imaging for AS
x-ray, MRI Radiographic eval of pelvis/SI Hallmark: SACROILITIS
84
Sacroilitis
AS
85
Bamboo spine
late hallmark in AS
86
Dx of AS
back pain >3 mo, less than <45 YO PLUSSSS: | sacroiliatis or HLA (+) + two other features
87
Positive response to NSAIDs
AS
88
Tx for AS
NSAIDs (1st line) refer to rheumatology NSAID-resistant disease: sulfasalazine (peripheral joint involvement), TNF inhibitors, IL inhibitors
89
Non pharm tx for AS
PT, surgical correction & stabilization; Supportive: smoking cessation EXERCISE (essential)
90
Who is most as risk for AS
young males
91
usually follow diarrheal illness or STI
RA (young adults)
92
Can't see, can't pee, can't climb tree
conjunctivitis, urethritis, oligoarthritis (RA)
93
Mucocutaneous lesions
RA
94
NSAIDS for tx
AS, RA, ACPP, Gout