Rheumatology Part 1 (Gout)- Paulson (Exam 2) Flashcards

1
Q

Gout definition?

A

Recurring attacks of acute arthritis Chronic deforming arthritis

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2
Q

Gout epidemiology/RF?

A
  • Men>women
  • Pacific islanders
  • Alcohol consumption, esp beer
  • Red meat, seafood, fructose
  • Obesity
  • Meds: thiazide & loop diuretics, low dose ASA
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3
Q

Gout pathophys:

A
  • Hyperuricemia needed (but doesn’t always mean gout)
  • Serum urate levels > 6.8mg/dL
  • Monosodium urate (MSU) level has to be high enough for crystals to precipitate (causes inflammation in joints)
  • Resolution of acute inflammation is mediated by immune mechanisms (even w/o tx)
  • Over time, chronic inflammatory process, leads to tophi (deposits of MSU) formation, erosion of bone, joint injury
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4
Q

Gout uric acid balance: Underexcreters v overproducers

A

Underexcreters (majority):

  • Renal insufficiency
  • Meds: diuretics (loop/thiazide), ASA, levodopa, ethambutol, pyrazinamide)
  • Acidosis (dka, ketogenic diet, lactic acidosis)
  • Volume depletion/dehydration
  • Lead exposure

Overproducers (minority):

  • Inherited defect of metabolism
    • Lesch-Nyhan syndrome
    • Kelley-Seegmiller syndrome
  • Myeloproliferative and lymphoproliferative disorders, polycythemia, carcinoma
  • Chronic hemolytic anemias
  • Transient hyperuricemia associated with ATP consumption
    • strenuous exercise, status epilepticus, MI, sepsis
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5
Q

3 stages of gout?

A
  1. Acute gouty arthritis 2. Intercritical (interval) gout 3. Chronic articular and tophaceous (MSU crystals) gout
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6
Q

Acute gouty arthritis sx?

A
  • “My big toe hurts”
  • Sudden onset, often at night
  • Severly painful and tender, swollen joint, red, warm
  • May complain of fever
  • Reaches maximal severity in about 12-24hrs
  • May have hx of similar attacks prior
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7
Q

Seen on acute gouty arthritis exam?

A
  • Swollen, very tender, red, warm overlying skin
  • May see desquamation
  • May see tophi
  • MTP of great toe is classic sign “podagra”
    • usually monoarticular and in the lower extremity
    • polyarticular is possible
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8
Q

What is tophi?

A
  • Irregular, asymmetric, macroscopic deposits of urate
  • Pathognomonic for gout
  • Common sites include external ear, hands, olecranon, feet, knee, achilles tendon, forearm
  • Usually painless but can become acutely inflamed Usually develop after years
  • Maintain state of inflammation
    • promote tissue and joint destruction around them
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9
Q

Gout renal manifestations?

A
  • Uric acid nephrolithiasis (kidney stones)
  • Chronic urate nephropathy
    • _​_MSU crystals are deposited in the renal medulla and pyramids
  • Uric acid nephropathy
    • ARF (acute renal failure) when large amounts of uric acid crystals precipitate in the collecting ducts and ureters
      • usually seen as part of tumor lysis syndrome
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10
Q

Gout diagnosis?

A
  • Aspirate of synovial fluid showing monosodium urate (MSU) crystals
    • “negatively birefringent”, needle-like, when viewed with polarized light microscopy
  • US: hyperchoic linear density (double contour sign) over the joint cartilage or deposits that look like tophi
  • Radiographs: “rat bite” lesions later in disease process (if next to a tophus=gout)
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11
Q

What labs would you order for suspected gout?

A
  • Serum uric acid (can be normal or low, though)
  • Peripheral WBC can be high
  • ESR/CRP can be elevated
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12
Q

How many criteria needed to make clinical dx?

A

>6 Or MSU crystals in joint fluid or tophus

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13
Q

Gout tx?

A
  • If asymptomatic hyperuricemia: don’t treat
  • Lifestyle mods:
    • lose wt
    • reduce etoh
    • reduce purine-rich food consumption
    • drink lots of water
  • Avoid hyperuricemic meds, if possible
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14
Q

Tx of acute gout attack?

A
  • Goal is to relieve pt’s pain
  • Start tx asap
  • Urate-lowering meds (allopurinol) : don’t help in acute attacks so don’t start one
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15
Q

Gout tx contraindications for NSAIDs

A

CKD with CrCl< 60, active ulcer, NSAID allergy, concurrent use of anticoagulant, CV disease (esp uncontrolled CHF or HTN)

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16
Q

3 types of Gout meds for acute attack?

A

NSAIDs 1st choice

  • naproxen (Aleve)
  • indomethacin
  • Discontinue 1-2 days after complete clinical resolution. (Typical course might be 5-7 days)

Colchicine:

  • good for pts w/ nsaid intolerance
  • commonly causes diarrhea and abd cramping
  • possible reversible peripheral neuropathy
  • Contraindications: severe hepatic or renal impairment with colchicine use in past 2 wks, concomitant use of a mod-strong inhibitor of P-gp and/or CYP3A4 inhibitor (antifungals, antivirals, some antiarrhythmics)

Corticosteroids:

  • good for people who can’t take nsaids or colchicine
    • intra-articular injection: triamcinolone
    • oral prednisone
    • IV methylprednisolone
    • IM triamcinolone
  • Caution for pts with CHF, glucose intolerance, poor control of HTN
17
Q

How do we prevent gout?

A
  • Adress preventative issues during the intercritical period
  • Goal is to achieve a serum urate level <6mg/dL
    • Slowly (not > 1-2mg/dL/month)
  • use low-dose prophylactic colchicine (or low-dose NSAID) when initiating antihyperuricemic therapy to reduce risk for acute flare
18
Q

Meds for chronic gout?

A

Xanthine Oxidase Inhibitors (XOI) - reduce production of uric acid

  • Allopurinol OR Febuxostat
    • Give prophylactic colchicine when initiating
19
Q

Uricosuric meds?

A
  • Block tubular reabsorption of urate and increases the rate that uric acid is renally excreted
    • Pt must have nl renal function
  • Probenecid
  • Do not give to a pt with G6PD (increases risk of hemolysis)
20
Q

Uricase med for gout?

A
  • Enzyme present in other mammals that breaks urate down to allantoin, which is more easily excreted
  • For pts who have been refractory to all other therapies
  • Pegloticase: given IV q 2 weeks
  • Don’t give to people with G6PD
21
Q

Gout prognosis/referral?

A
  • Acute attack will self-resolve even w/o tx
  • Over time attacks become more frequent and longer
  • W/ urate lowering meds (XO allopurinol or uricase Pegloticase), much less chronic gouty arthritis, tophi, and deformity
  • Can refer to rheumatology
22
Q

How is pseudogout different from gout?

A
  • Gout is urate crystal (needle-like) deposition in joints, while pseudogout is calcium pyrophospate dihydrate (CPPD) crystal (rhomboids) deposition, which can mimic gout.
  • Gout usually effects the great toe, while CPPD or pseudogout usually effects larger joints such as the knee.
23
Q

What is a sign of CPPD pseudogout seen on plain film radiographs?

A

Chondrocalcinosis: which look like white deposits in the joint space.

24
Q

What does the typical CPPD pseudogout pt look like?

A
  • Older adults (rare before 55)
  • Around 50% of those >85 are affected
  • Joint trauma
  • Familial chondrocalcinosis
  • Hemochromatosis
25
Q

How would you describe an acute CPPD pseudogout attack?

A
  • Self-limited, sudden attack of pain, redness, warmth, disability, and swelling (can be one or several joints)
  • Knee is most commonly affected with pseudogout (great toe for gout)
    • Others: wrists, shoulders, elbows, ankles Possible chills/fever
  • Can be provoked by surgery (parathyroidectomy), trauma, or major illness
  • May have associated f/c
26
Q

Chronic CPP crystal inflammatory arthritis is also known as, and can mimic sxs of what autoimmune disease?

A
  • “pseudo RA”
  • Similar sx to RA, involving multiple joints in a symmetric pattern (bilat)
    • usually affects joints unaffected by OA: MCP, wrists, elbows, glenohumeral joints
27
Q

Pseudogout can also mimic OA, called “pseudo-OA”. Which joint is the most common and what do you see on clinical examination?

A
  • Knee most common for pseudo-OA (also hips, shoulder, spine, etc)
  • Clinical exam is like that of OA: tenderness of joints, bony enlargement, crepitus, restriction of motion
28
Q

Pseudo-neuropathic disease is another mimicking diesease of pseudogout. What does it mimic?

A
  • Charcot joint/foot: joint degenerates and collapses from CPP crystal deposition
  • Resembles neuropathic arthropathy but w/o neurologic impairment
29
Q

How is a dx of pseudogout vs gout made?

A
  • Pseudogout: “weakly positively birefringent RHOMBOID crystals”
  • Gout: “negatively birefringent, needle-like, when viewed with polarized light microscopy”
30
Q

How do you treat an acute pseudogout attack?

A
  • Aspirate the joint then intraarticular glucocorticoid (triamcinolone) injection
  • Nsaids: indomethacin, naproxen, salicylates
  • Colchicine
  • System corticosteroids
31
Q

How do you treat pseudo OA?

A

Same way as OA Nsaids, steroid injections into joint, joint replacement

32
Q

What prophylactic meds would you give for pseudogout? For pseudo-RA?

A

Pseudogout:

  • Colchicine
  • Nsaid

Pseudo-RA:

  • nsaids (naproxen, indomethacin)
  • Alternative: colchicine, hydroxycholorquine, low-dose glucocorticoids ie: prednisone
33
Q

If the 24 hr urine uric acid test shows <800 mg/d, this means the pt is an undersecreter of uric acid and you should prescribe which class of medication?

A

Uricosuric agent (Probenecid) or XOI (Allopurinol or Febuxostat)

34
Q

The 24 hr urine uric acid test comes back >800 mg/d, which means your pt is an overproducer of uric acid and you should prescribe which class of medication?

A

XOI (Allopurinol or Febuxostat)