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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
Q

Tx for acute gout attack

A

Treat pain and inflammation with NSAIDs, glucocorticoids or colchicine
Others: ice, ACTH, IL-1 inhibitors, Chinese herbs
Do not discontinue ULT

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26
Q

When are NSAIDs contraindicated to treat acute gout?

A

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

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27
Q

Reasons to not use glucocorticoids or colchicine to treat gout

A

Glucocorticoids can increase blood sugar

Colchicine can be toxic when the patient has decreased renal function

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28
Q

When do you use urate lower therapy?

A 
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
Q

Xanthine oxidase inhibitors in urate lowering therapy

A

Allopurinol (zyloprim) or Febuxostat (Uloric)

30
Q

Uricosuric agents in urate lowering therapy

A

Probenecid
Lesinurad (in combo with XOI)
Others (Losartan, Fenofibrate)

31
Q

Recombinant uricase in urate lowering therapy

A

Pegloticase (Krsyexxa) by IV and used by the rheumatologist

For refractory gout

32
Q

What do xanthine oxidase inhibitors do?

A

Decrease urid acid synthesis

33
Q

Allopurinol

A 
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
Q

Probenecid

A

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
Q

When do you initiate urate lowering therapy?

A

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
Q

Whats the target level for ULT?

A

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
Q

When to refer for a gout patient?

A

Unclear etiology of hyperuricemia
Difficulty reaching target serum uric acid level
Multiple and/or serious adverse effects from ULT

38
Q

What crystals are seen in pseudogout?

A

Calcium pyrophosphate crystals

39
Q

Where does CPPD start?

A

Formation is initiated in cartilage located near surface of chondrocytes

40
Q

Avg age of diagnosis of CPPD

A

72

41
Q

What metaboic/endocrine disorders are associated with CPPD?

A

Hemochromatosis, hyperparathyroidism, hypomagnesemia, hypophosphatasia
*also associated with joint trauma or familial chondrocalcinosis

42
Q

Acute attacks of pseudogout

A

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
Q

Chondrocalcinosis

A

Cartilage calcification
Seen with radiographic evidence of CPP crystal deposts
Punctate and linear radiodensities

44
Q

Synovial fluid aspiration in pseudogout

A

Positively bifefringent CPP crystals (P, P)

*diagnose with synovial fluid analysis and/or radiographic findings

45
Q

Acute tx for pseudogout

A

NSAIDs, intraarticular glucocorticoid injection (after ruling out septic joint), colchicine, oral glucocorticoids, support

46
Q

Tx for chronic prophylaxis of pseudogout

A

Colchicine .6 mg twice daily (or another NSAID)
Recommended if >3 attacks per year
Adjust for renal dosing!

47
Q

2 classifications of spondyloarthritis (SpA)

A

*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
Q

Shared clinical features of SpA

A

Inflammatory back pain, enthesitis, asymmetric oligoarthritis, dactylitis (sausage digits), uveitis, strong association with HLA-B27, seronegative (negative RF)

49
Q

Clinical manifestations of SpA

A

Either axial (sacroilitis or spondylitis) or peripheral symptoms (peripheral arthritis, enthesitis, dactylitis)

50
Q

Enthesitis

A

Inflammation around the entheses (site of insertion of ligaments, tendons, joint capsule, or fascia to bone)

51
Q

Clinical manifestation of enthesitis

A

“Heel pain”
Swelling at the heels (because of insertion of achilles or plantar fascia into the calcaneus)
Pain, swelling and local tenderness

52
Q

Saying for reactive arthitis

A

Can’t see (conjunctivitis/uveitis), can’t pee (urethritis), can’t climb a tree (arthritis in knee)

53
Q

What is reactive arthritis?

A

Acute inflammatory arthritis triggered by a preceding GI or GU infection (autoimmune)
GI: shigella, salmonella, yersinia, campylobacter
GU: chlamydia trachomatis

54
Q

Genetic predisposition for reactive arthritis or ankylosing spondylitis

A

HLA-B27

55
Q

Clinical presentation of reactive arthritis

A

Acute onset
Typically present with asymmetrical oligoarthritis** (predominantly lower extremity)
Usually 1-4 wks following inciting infection (diarrheal illness or urethritis)

56
Q

Associated/peripheral MSK s/sx in reactive arthritis

A

Peripheral arthritis, enthesitis, dactylitis, inflammatory low back pain in spine or SI joints

57
Q

Extra articular manifestations in reactive arthritis

A

Conjunctivitis/uveitis, urethritis, nail changes, circinate balanitis (nonpainful penis ulcers), oral ulcers, keratoderma blennorrhagicum (thickened pustules)

58
Q

Diagnostic evaluation of reactive arthritis

A

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
Q

Tx for reactive arthritis

A 
Initial therapy (NSAIDs)- mainstay of therapy
Refer if uveitis
60
Q

What is ankylosing spondylitis?

A

Chronic inflammatory disease of the axial skeleton (particularly SI and spinal facet joints)

61
Q

Manifestation of ankylosing spondylitis

A

Back pain and progressive stiffness of the spine (seen more in whites and males)
*young males!

62
Q

Progression of ankylosing spondylitis

A

Enthesitis with chronic inflammation
Structural damage
New bone formation (ossification)
Ankylosis (fusion)

63
Q

How does ankylosing spondylitis initially present and how is it seen later?

A

Initially is SI joints
Moves proximally
Annulus fibrosus undergoes ossification to form syndesmophytes
Progresses to bamboo spine appearance in late advanced disease

64
Q

History seen with ankylosing spondylitis

A

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
Q

PE findings for ankylosing spondylitis

A

Hyperkyphosis
Limited spinal mobility
Loss of lumbar lordosis
Tenderness over insertion sites (SI joints)
*modified Schober test is flexing forward

66
Q

Extraarticular manifestations and comorbities with AS

A 
Acute anterior uveitis (30%)- immediate referral
IBD
Psoriasis
Restrictive disease pattern
Cardiovascular disease
Pain, fatigue, sleep disturbance
67
Q

Lab studies seen in AS

A

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
Q

Hallmark imaging study for AS

A

Radiographic sacroiliitis

69
Q

Pharmacologic tx of AS

A

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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