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X Clin Med Exam 3 > Gout, Pseudogout, Reactive Arthritis and AS > Flashcards

Gout, Pseudogout, Reactive Arthritis and AS Flashcards

1
Q

What kind of crystals are seen in gout?

A

Monosodium urate (uric acid into these crystals)

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2
Q

Cardinal feature of gout

A

Inflammatory arthritis due to hyperuricemia

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3
Q

Where does the body get uric acid from?

A

It is a breakdown product of purine metabolism and is excreted by the kidney

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4
Q

What levels constitute hyperuricemia?

A

> 7.0 mg/dL in males
6.0 mg/dL in females
Either due to being underexcreter (most common) or overproducer

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5
Q

Overproducer

A

Due to inherited enzyme defects
High cell turnover (psoriasis or myeloproliferative disease)
Increased purine consumption (in diet)

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6
Q

Underexcretors

A

Renal insufficiency
Diuretics
Volume depletion
Lead nephropathy

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7
Q

Comorbidities of gout

A

HTN, obesity, CKD, diabetes, hyperlipidemia

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8
Q

Non-modifiable risk factors of gout

A

Male sex, advanced age, ethnicity (Pacific Islanders), genetic mutations/polymorphisms

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9
Q

Modifiable risk factors of gout

A

Obesity, diets rich in meat and seafood, ETOH, fructose-rich foods/beverages, diuretic use, transplant recipient status

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10
Q

4 stages of gouty arthritis

A 
Asymptomatic hyperuricemia (15% get gout)
Acute gouty arthritis (first attack)
Intercritical gout (asymptomatic gout between attacks)
Chronic gouty arthritis (tophaceous gout-involved joints will develop chronic swelling and tophi)
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11
Q

Tophi

A

White chalky material consisting of dense concentrations of MSU crystals
Due to duration and severity of hyperuricemia
Occur on avg 10 yrs after 1st attack if untreated gout

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12
Q

Pathogenesis pathway of gout

A 
Hyperuricemia
Deposition of crystals in/around joint
Inflammatory cascade (painful joint)
Without intervention tophi may develop
Chronic gouty arthropathy (eroding bone and cartilage) without treatment
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13
Q

4 clinical manifestations of gout

A

Recurrent flares of inflammatory arthritis (gout flare)
Accumulation of urate crystals as tophaceous deposits
Chronic arthropathy
Renal complications (uric acid nephrolithiasis, urate nephropathy)

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14
Q

Presentation of acute gout attack

A 
Monoarticular most of the time (can be poly)
1st MTP joint-big toe (Podagra) is most common site
Self limiting (2 wks if untreated)
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15
Q

What triggers an acute gout flare?

A

Acute increases or decreases in urate levels
Ex: acute EtOH ingestion, food overindulgence, trauma, dehydration/starvation, meds (allopurinol or uricosuric agents usually treat gout but can also cause acute)

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16
Q

History of acute gout attack

A

Rapid onset, severe pain, pain peaks w/in 8-12 hours, redness, warmth, swelling, disability, maybe fever chills malaise

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17
Q

What will you see on the X-ray of established gout?

A

Bony erosions “punched out” with sclerotic margin and overhanging edges (rat bite erosions)
*early on there is only soft tissue swelling around joint

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18
Q

What does a duel-energy CT do?

A

ID urate deposits and tophi

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19
Q

What is seen in the ultrasound of gout?

A

Double contour sign (on artricular cartilage surfaces)

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20
Q

What must be done to diagnose gout?

A

Arthrocentesis

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21
Q

Arthrocentesis

A

Needle aspiration of the involved joint
Culture and gram stain it
Microscopic analysis shows MSU crystals and under polarized microscopy they are needle shaped and negatively bifefringent

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22
Q

When is serum uric acid the most accurate test?

A

> 2 wks after acute gout flare subsides (because might be normal level during acute attack)
Helpful to monitor effects of uric acid lowering therapy

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23
Q

What is 24 hour urinary uric acid used for?

A

If uricosuric therapy is being considered, then <800 mg is underexcretory and candidate for uricosuric therapy

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24
Q

Treatment vs no treatment for asymptomatic hyperuricemia

A

No treatment: no prior gouty arthritis, no tophaceous deposits, no nephrolithiasis
Treatment: urid acid excretion > 1100 mg/d, acute overproduction

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25
Tx for acute gout attack
Treat pain and inflammation with NSAIDs, glucocorticoids or colchicine Others: ice, ACTH, IL-1 inhibitors, Chinese herbs Do not discontinue ULT
26
When are NSAIDs contraindicated to treat acute gout?
Chronic kidney disease, active duodenal or gastric ulcer, cardiovascular disease (not controlled), allergy, tx with anticoagulants *most effected within 48 hours of onset of sx
27
Reasons to not use glucocorticoids or colchicine to treat gout
Glucocorticoids can increase blood sugar | Colchicine can be toxic when the patient has decreased renal function
28
When do you use urate lower therapy?
``` Treat those with an established dx of gout and: Tophi (clinical exam or imaging) Frequent (>2/yr) acute attacks Chronic kidney disease stage > 2 Previous nephrolithiasis ```
29
Xanthine oxidase inhibitors in urate lowering therapy
Allopurinol (zyloprim) or Febuxostat (Uloric)
30
Uricosuric agents in urate lowering therapy
Probenecid Lesinurad (in combo with XOI) Others (Losartan, Fenofibrate)
31
Recombinant uricase in urate lowering therapy
Pegloticase (Krsyexxa) by IV and used by the rheumatologist | For refractory gout
32
What do xanthine oxidase inhibitors do?
Decrease urid acid synthesis
33
Allopurinol
``` DOC for most patients (overproducers and underexcretors) Side effects (rash, hypersensitivity, severe cutaneous adverse rxns like SJS or TENS) *avoid in individuals who are HLA-B 5801 positive ```
34
Probenecid
Primarily used for underexcretors Enhances renal excretion of uric acids Avoid in pts with hx of nephrolithiasis and take ASA (large doses) Requires good renal function
35
When do you initiate urate lowering therapy?
Wait until after acute gout flare has resolved (at least 2 weeks) Must do anti-inflammatory prophylaxis of low dose Colchicine or NSAIDs for if have an acute flare (must continue for 6 moths after start ULT)
36
Whats the target level for ULT?
sUA of 6 mg/dL or less (5 for tophaceous gout) *adjust dose if not at goal Measure 2-4 wks after adjustment and confirm at 3 months Then measure every 6 months for a year Then annually
37
When to refer for a gout patient?
Unclear etiology of hyperuricemia Difficulty reaching target serum uric acid level Multiple and/or serious adverse effects from ULT
38
What crystals are seen in pseudogout?
Calcium pyrophosphate crystals
39
Where does CPPD start?
Formation is initiated in cartilage located near surface of chondrocytes
40
Avg age of diagnosis of CPPD
72
41
What metaboic/endocrine disorders are associated with CPPD?
Hemochromatosis, hyperparathyroidism, hypomagnesemia, hypophosphatasia *also associated with joint trauma or familial chondrocalcinosis
42
Acute attacks of pseudogout
Self-limited severe acute inflammation Knee affected in over 50% (other joints also seen) Trauma, surgery of severe medical illness often provoke acute attacks
43
Chondrocalcinosis
Cartilage calcification Seen with radiographic evidence of CPP crystal deposts Punctate and linear radiodensities
44
Synovial fluid aspiration in pseudogout
Positively bifefringent CPP crystals (P, P) | *diagnose with synovial fluid analysis and/or radiographic findings
45
Acute tx for pseudogout
NSAIDs, intraarticular glucocorticoid injection (after ruling out septic joint), colchicine, oral glucocorticoids, support
46
Tx for chronic prophylaxis of pseudogout
Colchicine .6 mg twice daily (or another NSAID) Recommended if >3 attacks per year Adjust for renal dosing!
47
2 classifications of spondyloarthritis (SpA)
*family of inflammatory rheumatic diseases that cause arthritis Predominantly axial disease (ankylosing spondylitis) Predominantly peripheral disease (reactive arthritis, PsA, arthritis associated with IBD, undifferentiated SpA)
48
Shared clinical features of SpA
Inflammatory back pain, enthesitis, asymmetric oligoarthritis, dactylitis (sausage digits), uveitis, strong association with HLA-B27, seronegative (negative RF)
49
Clinical manifestations of SpA
Either axial (sacroilitis or spondylitis) or peripheral symptoms (peripheral arthritis, enthesitis, dactylitis)
50
Enthesitis
Inflammation around the entheses (site of insertion of ligaments, tendons, joint capsule, or fascia to bone)
51
Clinical manifestation of enthesitis
"Heel pain" Swelling at the heels (because of insertion of achilles or plantar fascia into the calcaneus) Pain, swelling and local tenderness
52
Saying for reactive arthitis
Can't see (conjunctivitis/uveitis), can't pee (urethritis), can't climb a tree (arthritis in knee)
53
What is reactive arthritis?
Acute inflammatory arthritis triggered by a preceding GI or GU infection (autoimmune) GI: shigella, salmonella, yersinia, campylobacter GU: chlamydia trachomatis
54
Genetic predisposition for reactive arthritis or ankylosing spondylitis
HLA-B27
55
Clinical presentation of reactive arthritis
Acute onset Typically present with asymmetrical oligoarthritis** (predominantly lower extremity) Usually 1-4 wks following inciting infection (diarrheal illness or urethritis)
56
Associated/peripheral MSK s/sx in reactive arthritis
Peripheral arthritis, enthesitis, dactylitis, inflammatory low back pain in spine or SI joints
57
Extra articular manifestations in reactive arthritis
Conjunctivitis/uveitis, urethritis, nail changes, circinate balanitis (nonpainful penis ulcers), oral ulcers, keratoderma blennorrhagicum (thickened pustules)
58
Diagnostic evaluation of reactive arthritis
Evidence or antecedent or concomitant infection Elevated ESR or CRP maybe Positive HLA-B27 in 30-50% Negative for crystals or infection in synovial fluid analysis Maybe imaging with enthesitis or arthritis
59
Tx for reactive arthritis
``` Initial therapy (NSAIDs)- mainstay of therapy Refer if uveitis ```
60
What is ankylosing spondylitis?
Chronic inflammatory disease of the axial skeleton (particularly SI and spinal facet joints)
61
Manifestation of ankylosing spondylitis
Back pain and progressive stiffness of the spine (seen more in whites and males) *young males!
62
Progression of ankylosing spondylitis
Enthesitis with chronic inflammation Structural damage New bone formation (ossification) Ankylosis (fusion)
63
How does ankylosing spondylitis initially present and how is it seen later?
Initially is SI joints Moves proximally Annulus fibrosus undergoes ossification to form syndesmophytes Progresses to bamboo spine appearance in late advanced disease
64
History seen with ankylosing spondylitis
Insidious (slow) onset of low back pain in SI joints Pain and stiffness Often radiates into buttocks Symptoms longer than 3 months Symptoms worse in morning or with inactivity Onset before age of 40
65
PE findings for ankylosing spondylitis
Hyperkyphosis Limited spinal mobility Loss of lumbar lordosis Tenderness over insertion sites (SI joints) *modified Schober test is flexing forward
66
Extraarticular manifestations and comorbities with AS
``` Acute anterior uveitis (30%)- immediate referral IBD Psoriasis Restrictive disease pattern Cardiovascular disease Pain, fatigue, sleep disturbance ```
67
Lab studies seen in AS
CBC that may show normocytic-normochromic anemia (seen in chronic disease) Elevated ESR and/or CRP Negative RF and anti-CCP antibodies Positive HLA-B27 (85%)
68
Hallmark imaging study for AS
Radiographic sacroiliitis
69
Pharmacologic tx of AS
First line: NSAIDs (indomethacin/naproxen) | NSAID resistant disease (sulfasalazine for peripheral joint involvement) or TNF/IL inhibitors

X Clin Med Exam 3 (8 decks)

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