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clinical medicine exam 3 > lecture 1 gout, SLE > Flashcards

lecture 1 gout, SLE Flashcards

1
Q

Podagra

A

gout affecting the 1st MTP (big toe)

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2
Q

what is gout

A
  • deposition of monosodium urate crystals in joints and connective tissue
  • associated with joint pain and inflammation
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3
Q

what condition is associated with hyperuricemia

A

gout

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4
Q

complications of gout

A
  • tophi
  • uric acid nephrolithiasis
  • urate nephropathy
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5
Q

uric acid is formed from the breakdown product of what

A

purine metabolism

  • uric acid is usually secreted by the kidney
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6
Q

what serum uric acid level is classified as hyperuricemia

A

>6.8 mg/dL

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7
Q

people who have hyperuricemia can be broken down into what two categories

A
  • uric acid overproducers (5%)
  • uric acid underexcreters (95%)
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8
Q

what causes uric acid overproducers; primary hyperuricemia

A
  • idiopathic
  • genetic disorders (rare)
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9
Q

what causes uric acid overproducers; secondary hyperuricemia

A
  • increased purine consumption
  • malignancy
  • psoriasis
  • enzyme defects
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10
Q

what causes uric acid underexcreters; primary hyperuricemia

A

idiopathic

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11
Q

what causes uric acid underexcreters; secondary hyperuricemia

A
  • decreased renal function
  • metabolic acidosis
  • volume depletion (dehydration)
  • medications
  • lead nephropathy
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12
Q

triggers for acute gout attack

A
  • etoh
  • trauma
  • medications
    • loop diuretics, ASA, allopurinol
  • high purine consumption
    • red meat, organ meat, sardines, scallops, legumes
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13
Q

name the stage: elevated uric acid levels but no sx

A

stage 1

*don’t usually need treatment

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14
Q

name the stage: acute attacks of arthritis

  • periods in between acute attacks-generally completely asymptomatic
A

stage 2

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15
Q

name the stage: usually occurs after 10 years or more of acute attacks. in this period, the intercritical gout periods are no longer asymptomatic, the involved joints will develop chronic swelling and tophi

A

stage 3

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16
Q

clinical presentation

  • rapid onset (often at night)
  • pain peaks w/in 8-12 hours
  • severe pain, redness, warmth and swelling
  • usually mono-articular
    • great toe, MTP joint-most common
    • knees, ankles
  • can be self-limiting
  • often recurrent
    • tophi
A

gout

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17
Q

diagnostic studies:

  • joint erosion
  • “rat bite” appearance
    • punched out erosions
A

chronic, advanced gout

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18
Q

what is the gold standard to diagnose gout

A

arthrocentesis

  • needle aspiration of involved joint or tophaceous deposit
  • culture and gram stain
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19
Q

what findings will be present in an arthrocentesis of gout

A
  • monosodium urate crystals
    • negatively birefringent
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20
Q

whys is serum uric acid levels not the best test for gout

A

sUA may be normal during acute attack

*most accurate >2 weeks after acute gout flare subsides

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21
Q

what diagnostic study can be done to find out if a patient is an uric acid overproducer

A

check urinary uric acid over a 24 hr period

    • if >800 mg on normal diet
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22
Q

treatment for acute gout attack

A
  • anti-inflammatory: initiate within 48 hours of onset of sx
  • NSAIDS: Indomethacin 50 mg TID (or Naproxen 500mg BID)
    • discontinue NSAIDs 1-2 days after sx completely resolved
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23
Q

when would you not give Indomethacin for acute gout attack

A

hx of

  • pelvic ulcer disease
  • GI bleed
  • renal impairment
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24
Q

Treatment for acute gout attack for patients who are unable to take NSAIDs

A

colchicine

initial dose 1.2mg, then 0.6 mg 1 hr later, then 0.6 mg BID until sx free

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25
Q

Treatment for acute gout attack for patients who are unable to take NSAIDs or colchicine

A

glucocorticoids

  • oral: taper over 1-2 weeks after sx resolve
  • intra-articular: r/o septic arthritis first
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26
Q

what prophylactic therapy can you give to prevent recurrent gout?

A
  • NSAIDs
  • Colchicine
  • added to a urate-lowering agent
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27
Q

what are examples of urate lowering therapies

A
  • uricosuric agents
    • probenecid
  • xanthine oxidase inhibitors
    • allopurinol (used for long term therapy)
    • febuxostat
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28
Q

If your patient has one of the following: what treatment should you give

  • frequent and disabling attacks
  • polyarticular gouty arthritis
  • tophaceous gout
  • renal stones
  • prophylacis during cytotoxic therapy
A
  • indications for urate-lowering therapy
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29
Q

the drug probenecid (uricosuric agents) is indicated for what type of gout

A
  • underexcreters
  • enhances renal excretion of uric acids
  • requires good renal function
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30
Q

dosing for probenecid (uricosuric agents)

A

250 mg BID x 1 week (target uric acid <6 mg/dL)

*avoid in patients with hx of nephrolithiasis and use ASA

31
Q

when would you give allopurinol (xanthine oxidase inhibitor)

A
  • agent of choice for most patients with gout
    • overproducers AND underexcreters
    • decreases uric acid synthesis
32
Q

dosing for allopurinol (xanthine oxidase inhibitor)

A

start at 100mg daily for a week and gradually titrate up until target range is reached

  • 300mg/d adequately controls most
33
Q

when would you give febuxostate (xanthine oxidase inhibitor)

A

treatment of gout in patients with mild-moderate renal insufficiency

34
Q

why should urate lowering therapy never be used treat an acute gout attack

A

initiation may precipitate an acute attack

*wait at least 2 weeks before starting treatment

35
Q

when treating patients with gout, what condition should you be weary of

A

decreased renal function

  • consider rheumatology referral
36
Q

what is calcium pyrophosphate dihydrate (CPPD) deposition disease

A

pseudogout

37
Q

pseudogout is primarily found in what patient population

A

almost 50% > 84 yo

38
Q

what disease is characterized by deposition of CPP crystals

A

pseudogout

39
Q

what two diseases is pseudogout commonly associated with

A
  • hemochromatosis
  • hyperparathyroidism
40
Q

clinical presentation

  • acute, typically a monoarticular inflammatory arthritis
  • attacks may be spontaneous or provoked by trauma or surgery
  • self -limited
  • joints affected
    • knees (50%), wrists, shoulders, feet, ankles, elbows
A

pseudogout

41
Q

radiographic presentation:

  • chondrocalcinosis (cartilage calcification)
  • degenerative changes
    • subchondral cysts
    • osteophyte formation
A

pseudogout

42
Q

what diagnostic study of synovial fluid aspiration diagnoses pseudogout

A

postively birefringent CPP crystals

43
Q

treatment for acute pseudogout

A
  • NSAIDs or colchicine
  • colchicine 0.6 mg BID daily
    • recommended if > 3 attacks/year
44
Q

what is systemic lupus erythematosus (SLE)

A
  • autoimmune disorder
  • autoantibodies to nuclear antigens
  • multisystem disease
  • female > male
    • peak incidence of disease during reproductive years
45
Q

clinical presentation

  • fever, fatigue, weight changes
  • photosensitivity, alopecia, oral ulcers, rash (malar “butterfly” and discoid)
  • arthritis (symmetric, nonerosive)
  • inflammation of pericardium
  • nephritis
  • sz, psychosis
  • CAD
  • raynaud’s
A

systemic lupus erythematosus

46
Q

describe malar “butterfly” rash

A

fixed erythema over nasal bridge (spares nasolabial folds)

47
Q

what is raynaud’s phenomenon

A
  • episodic vasospastic disease
  • worse with cold and stress
  • red, white, and blue
    • 1st white (pallor)
    • 2nd blue (cyanosis)
    • 3rd red (erythema -following rewarming)
48
Q

diagnostic lab testing for systemic lupus erythematosus

A
  • ANA subtypes
    • anti-dsDNA antibodies
    • anti-sm (anti-smith) antibodies
49
Q

hydroxychloroquine (Plaquenil) is used to treat what condition

A

antimalarials

systemic lupus erythematosus

50
Q

give examples of cytotoxic/immunosuppressive agents you could use to treat systemic lupus erythematosus

A
  • methotrexate
  • azathioprine
51
Q

pharmacologic treatment for systemic lupus erythematosus

A
  • NSAIDs
  • antimalarials
  • corticosteroids (systemic)
52
Q

with drug induced systemic lupus erythematosus, all patients will present with what diagnostic test

A
  • positive antihistone antibody
53
Q

what is Sjogren’s syndrome

A

*think dry

  • chronic, systemic autoimmune disorder
  • diminished exocrine gland function
54
Q

what is the sicca complex that is associated with Sjogren’s syndrome

A

dry eyes and mouth

55
Q

keratoconjunctivitis sicca

A

dry eyes; deficiency in tear production

56
Q

xerostomia

A

dry mouth

57
Q

clinical presentation

  • fatigue
  • keratoconjunctivitis sicca
  • xerostomia
  • parotidis
  • dryness of nose, throat, larynx, bronchi, vagina, and skin
  • arthritis
  • raynauds
A

Sjogren’s syndrome

58
Q

diagnostic evaluation for Sjogren’s syndrome

A
  • ANA
    • anti-Ro/SSA
    • anti-La/SSB
  • schirmer’s test: test for tear production
59
Q

treatment for dry eyes associated with Sjogren’s syndrome

A
  • artificial tears
  • cyclosporine drops (restasis)
60
Q

treatment for xerostomia associated with Sjogren’s syndrome

A
  • saliva substitute (biotene OTC)
  • water
61
Q

what is systemic sclerosis

A
  • autoimmune multisystem disorder
  • diffuse fibrosis of skin and internal organs
62
Q

limited cutaneous systemic sclerosis is associated with CREST syndrome. What is CREST stand for

A
  • Calcinosis cutis
  • Raynaud’s phenomenon
  • Esophageal dysmotility
  • Sclerodactyly: diffusely puffy hands
  • Telangiectasia

*limited to fingers, distal forearm, face and neck

63
Q

clinical presentation

  • rapid development of symmetric skin thickening
    • trunk and proximal extremities
  • likely to develop internal organ damage
    • ischemic injury or fibrosis
  • arthritis
  • pulmonary HTN, fibrosis
  • pericarditis, cardiomyopathy
  • renal failure
A

diffuse cutaneous systemic sclerosis

64
Q

diagnostic lab findings for systemic sclerosis

A
  • scleroderma antibody (anti-SCL-70)
  • anti-centromere antibodies (ACA): specific for limited SSc
65
Q

treatment for cutaneous systemic sclerosis

A
  • symptomatic and supportive
66
Q

treatment for raynauds

A

nifedipine (calcium channel blocker)

67
Q

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

A

reactive arthritis

68
Q

what is reactive arthritis

A
  • inflammatory arthritis caused by GI or GU infection
  • occurs predominantly in those HLA-B27
69
Q

clinical presentation

  • acute, asymmetric oligoarthritis
  • often affects lower extremities
  • occurs 1-4 weeks after GI or GU infection
  • conjunctivitis (can’t see)
  • urethritis (can’t pee)
  • keratoderma blennorrhagicum: hyperkeratotic skin lesion on palms and soles
A

reactive arthritis

70
Q

when do reactive arthritis symptoms usually resolve

A

6-12 months

71
Q

genital pathogen that causes reactive arthritis

A

chlamydia trachomatis

72
Q

diagnostic confirmation of reactive arthritis

A

HLA-B27 antigen

73
Q

treatment for reactive arthritis

A
  1. NSAIDs
    1. indomethacin 25-50 mg TID
  2. intra-articular/systemic glucocorticoids
    1. if inadequate response to NSAIDs
  3. sulfasalzine, methotrexate
    1. if inadequate response to NSAIDs and steroids

clinical medicine exam 3 (7 decks)

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