Gout, pseudogout... Flashcards

1
Q

etiology of gout

A

monosodium urate cystals precipitate within join and surrounding tissue space –> inflammatory needle like pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

patient presents with severe pain in great toe MTP. You notice redness and swelling. You predict this patient is suffering from gout..What is your next step

A

GOLD STANDARD: arthrocentesis (send fluid for culture and gram stain to r/o infection)

  • for gout = negatively birefringent monosodium urate crystals
  • 24 hour urinary uric acid secretion: overproducers >800 mg/dl, underexcreters ,700 mg/dl (not best for dx)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what would radiographic evidence of gout consist of

A

joint erotion, rat bite appearance, punched out erosions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List the stages of a gout attack

A

stage 1: asymptomatic hyperuricemia
stage 2: acute gouty arhritis triggered by acute change in uric acid
stage 3: intercritical gout/intermittent attacks
Stage 4: chronic tophaceous gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Types of gout…

A
  1. Primary Hyperuricemia = idiopathic overproduction uric acid
  2. Secondary hyperuricemia: either
    a) overproduction of uric acid due to enzyme defect, malignancy, obesity, psoriasis, drugs etc
    b) under excretion of uric acid (90%) due to renal insufficiency, diuretics, lead nephropathy, acidosis (DM, EtOH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

treatment for stage 1 (acute stage) of gout attack

A

first line = NSAIDS specifically INDOMETHACIN (indomethacin also used for ankylosing spondylosis); may do intra articular steroid injection if r/o infection, oral steroids
*second line = COLCHICINE: back!, use at lower dose during acute attack, can be used for prevention as well to reduce inflammation and pain (not helpful for decreasing uric acid or bone damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

tx for stage 2/3 (prophylaxis to prevent flares and lowering excess uric acid stores)

A

overproducers = ALLOPURINOL (watch hypersensitivity)

  • under excretors: PROBENECID
  • new med: FEBUXOSTATE (good for over producers if impaired renal function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

risks for gout

A

obesity, HTN, DM, family hx, alcohol/yeast, hospitalization, transplants, acidotic state, post menopause, high purine diet (organ meats, anchovies, mushrooms, spinach, asparagus, cauliflower, beans, seafood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what lab result differentiates Pseudogout from gout

A

synovial fluid aspiration in PSEUDO reveals POSITIVELY birefringent crystal, gout reveals NEG birefringent crystals

*note: no specific serum study for pseudogout, dx based on fluid analysis and xray revealing chondrocalcinosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the etiology of pseudogout

A

SYNOVITIS due to build up of calcium pyrophosphate dihydrate crustals (CPPD) –> chondrocalcinosis (cystal deposits into synovial tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

A patient has acute onset of erythema pain and swelling in LARGE joints (wrist, hips, shoulders, ankles, elbows). Primary Dx and why

A

Pseudogout bc in large joints (gout is more in a single smaller joint ie MCP)
**50% pseudogout cases affect Knees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What other diseases are associated with pseudogout

A

hyperparathyroidism, hypothyroidism, hypophosphatemia, hypomagnesemia, OA, joint trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

xray reveals evidence of calcium deposition (see punctate and linear radiodensities in cartilage, ligaments, joints) and osteophytes. Pt has positively birefringent crystals in synovial fluid and an elevated WBW. Dx?

A

Dx: pseudogout
tx :treat underlying cause, reduce pain (joint aspiration), intra articular steroid, NSAIDS, colcincine, joint immobilization, ice pack
PROPHYLAXIS = colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pt has complaints of fever, fatigue, joint pain, head ache and rash. What studies might you order

A

ESR, ANA (subtypes: anti-dsDNA, anti-smith Ab) antiphopholipid Ab

OTher:
*checking for SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lab results reveal +ANA. What diseases are consistent with this result

A

95% of SLE cases, 70% scleroderma, 30-40% RA, 60% sjogren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pt has +ANA, what other lab results would help dx this patient with SLE

A

+anti-dsDNA and +anti-smith (subtypes of ANA), +antiphospolipid Ab (thrombocytopenia)

  • urinalysis with microscopy revealing pro/cell casts bc glomeruli damage,
  • depressed complement levels (due to SLE immune complexes)
17
Q

Name the eleven dx guidelines for SLE. How many will confirm dx?

A
  • need 4/11
    1. Malar (butterfly) rash)
    2. +ANA
    3. +anti-sm, anti-dsDNA, antiphospholipid Ab
    4. discoid rash
    5. photosensitivity rash
    6. mucosal ulcers
    7. polyarthritis
    8. serositis
    9. renal disorders
    10. neuro disorders/HA/seizures
    11. Hematologic disorders
18
Q

tx for SLE

A
NSAIDS
antimalarials (hydroxycloroquine (plaquenil))
corticosteroids (topical, intradermal)
decrease sun exposure
immunosuppressive meds (methotrexate)
19
Q

Tx for Lupus nephritis

A

cyclphosphamide, methylprednisolone

20
Q

tx for CNS involvement SLE

A

antipsychotics, anticonvulsants

21
Q

tx thrombocytopenia SLE

A

corticosteroids, danazol

22
Q

tx if +antiphospholipid Ab

A

warfarin, heparin

23
Q

other extra manifestations of SLE

A

non specific fever, fatigue, wt. loss, anemia, visual changes (retinal vasculitis), raynauds phenom, recurrent miscarriages, hair loss, edema, effusions

24
Q

Prognosis SLE

A

dep on severity (worse with Renal and CNS)
*infectious disease responsible for 29% death
10 yr survival in more than 90%

25
Q

etiology of SLE

A

autoantibodies to nuclear and cytoplasmic antigens destroy cells resulting in tissue damage

*antibody, antigen complexes deposited in tissue, small vessel walls, and basement membrane resulting in inflammation

26
Q

Pt has positive anti-histone antibodies but is negative for anti-dsDNA and anti-Sm. They complain of arthralgia, myalgia, malaise, and a rash. They take procainamide x 2 mth. Dx and tx?

A

drug induced SLE

tx: d/c drug, administer steroids

27
Q

Pt indicates dry mouth and decreased tears in addition to fingers that freq turn white, myalgia, joint pain and hx of chrons. Primary dx? what labs would confirm dx?

A

Dx: sjogerns
Labs: +Rf, +ANA, CBC anemia of chronic disease

28
Q

you determine pt has Sjogrens based off sx and labs indicating +Rf, +ANA, CBC anemia of chronic disease. How would you differentiate bw primary sjogren and sjogren related to SLE/RA

A

of the +ANA, anti SSA or SSB would indicate PRIMARY

anti SSC would indigate sjogren related to SLE/RA