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rheumatology > Crystal arthropathies and OA > Flashcards

Crystal arthropathies and OA Flashcards

1
Q

epidemiology of gout?

A

common > 60 year old (male > 40)

rare in premenopausal female

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2
Q

Cause of gout

A

primary

  • idiopathic (90% - underexcretion of uric acid)
  • rare enzyme deficiencies (hypoxanthin-guanine phosphoribosyltransferase)

secondary
- excess uric acid produce/ intake
- dietary excess (shellfish, liver, kidney, anchoves, turkey, sardine, beer)
- myeloproliferative and lymphoproliferative disorders
- cytolyic therapy
- acidosis (ketosis of starvation/ diabetes)
- extreme exercise, status epilepticus
- psoriasis
decrease uric acid excretion
- renal failure, drugs (flurosemide, aspirin/ alcohol, cytotoxic drugs, thaizide diuretics)
- lead intoxication
- Down syndrome

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3
Q

what are some precipitates of acute gout?

A

change in pH, temp, initiation of antihyperuricemics, alcohol, dietary excess, dehydration, trauma, illness, sx,

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4
Q

clinical features of gout

A

single/ recurrent episodes of acute inflammatory arthritis
acute crystal arthritis
- affect small joints of the feet (eg. MTP - podagra)
- ankle, knee

gouty nephropathy

  • parenchymal crystal deposition -> acute renal failure
  • urate stone formation (radiolucent)

chronic tophaceous arthritis
- urate crystals affect articular, periarticular and non-articular cartilage

o/e: stretch over tophi will see white deposit, hard

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5
Q

diagnosis of gout

A

joint aspiration**

  • negative, brirefringent needle shaped crystals
  • > 90% crystals of monosodium urate

xray
- tophi (soft tissue swelling, punched out lesions)

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6
Q

what is the pitfall of using uric acid measurement as dx?

A

uric acid may fall and rise, and may fall > 30% during acute attack and hyperuricaemia is common may not be gout

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7
Q

pharmcotherapy for mx of gout

A

acute gout:
NSAIDs,
colchicine/ predinisolone (intra-articular/ musular -> if renal/ CVD/ GI disease/ NSAIDs CI)

chronic gout:

  • antihyperuricemic drugs (allopurinol, febuxostat): xanthine oxidase inhibitor
  • uricosuric durgs (probenecid, sulfinpyrazone): if intolerant/ failure to allopurinol (CI in renal failure)
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8
Q

what conditions are associated with gout?

A

HTN
glucose intolerance
hyperlipidaemia
obesity

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9
Q

indications for urate lowering therapy

A 
attack recur within 1 year of first attack
OR
after 1st attack:
- visible tophi
- renal impairment
- uric acid stones
- cannot stop diuretics
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10
Q

what is the aim to reduce serum urate to?

A
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11
Q

how to prevent precipitate of acute attacks after using urate lowering agents

A

use colchicine during first few months of urate lowering med

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12
Q

non-pharm mx of gout

A 
lose wt (obese)
reduce alcohol intake
reduce excessive dietary purine intake
identify and treat associated factors (hypertension, hyperlipidemia, hyperglycaemia)
withdraw drugs that can precipitate gout
reduce alcohol intake
avoid dehydration
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13
Q

renal disease secondary to hyperuricemia, what is the tx

A

low dose allopurinol and monitor Cr

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14
Q

is sx recommended for gout?

A

surgery is not recommended, as crystal impairs healing (need very good clearing), unless pending rupture

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15
Q

drugs:

allopurinol

A

moa: inhibit xanthine oxidase > reduce uric acid production by inhibiting oxidation of hypoxanthine and xanthine -> uric acid
se: maculopapular rash, abdom pain, heptotoxicity, SJS, TEN,

CI: acute gout (change in conc. of uric aicd -> worsen/ prolong attack)

Treat with colchicines/ low dose NSAIDs

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16
Q

drugs:

colchicine

A

use: relief pain in acute gout, prevent recurrent attacks, use when starting urate lowering tx to prevent acute attack
moa: inhibit microtuble polymerization and synthesis by binding to tubulin, inhibit mitosis and cell motility, ihnibit neutrophil migration, in inflamed area, reduce inflame reaction to urate crystals but no effect on urice production/ excretion
se: diarrhoea, n and vomit, rash, myopathy, hypersensitiy

renal impairment/ hepatic impairment can increase SE (reduce elimination)

Start asap (within 24 hours of onset of symptoms) in acute setting, consider if NSAIDs/ corticosteroids CI/ not appropraite

17
Q

probenecid (drugs)

A

use: LT tx of gout
moa: increase renal excretion of uric acid by block renal tubular reaborption, no analgesic/ anti-inflam effection

se: rash, nause, vomit, alopecia, urinary frequency, uric acid kidney stones (prevent via keep hydrate)
(prohibited in elite sport as it can block use of other banned substance)

regular check of FBC and renal funciton
start once attack settle (not acute as it can precipitate)

18
Q

what is pseudogout?

A

acute inflammatory arthritis due to phagocytosis of IgG coated calcium pyrophosphate dihydrate (CPPD) crystals by neutrophils -> inflame mediators within joint space

19
Q

cause of pseudogout

A

commonly idiopathic, age related, metabolic disorder (hypercalcaemia, hypomagnesaemia)
hyperparathyroidism, Wilson’s disease, bartter syndrome, haemochromatosis (excess iron), hypophosphatasia (low ALP), ochronosis (accumulation of homogentistic acid in CT -> blueblack)

20
Q

dx of pseudogout

A

jt aspiration

  • positive birefringent brick shape crystals
  • crystals present in 60% of patients

xray:
- chondrocalcinosis in 75% (rediodensities in fibrocartiliaginous structure eg. knee menisci/ linear radiodensities in hyaline artiuclar cartilage

21
Q

risk factors for pseudogout

A

advance OA, old age, neuropathic jts

22
Q

clinical picture of psuedogout

A

slower onset then gout and last up to 3 weeks, self limited
commonly polyarticular

asymptomatic: radiological chondorcalcinosis (30% in > 80s)
acute monoarthritis: knee/ elbow/ shoulder
inflammatory polyarthritis: mimic RA (10%)

often affect:
knee, polyarticular wrist, hand (MCP), foot (1st MCP), hip

23
Q

tx of pseudogout

A 
asymptomatic does not need
treat underlying metabolic disorders
acute: NSADs, colchicine/ corticosteroids
prophylaxis: colchicine, NSAIDs
chronic: mtx or hydroxychloroquine
24
Q

what is OA

A

deterioration of articular cartilage due to local biomechanical factors and release of proteolytic and collagenolytic enzyme with secondary changes

25
Q

what are the causes of OA?

A

primary:
- idiopathic (most common)
secondary
- post trauma/ mechanical
- post inflame (RA), post infectious
- hereditable (scliosis)
- endocrine (acromegaly, hyperparathyroidism, hypothyroidism)
- metabolic (gout, pseudogout, hemochromatosis, Wilson’s disease, ochronosis)
- neuropathic (aka charcot joints) -> loss of propriocpetive disease eg. DM, syphilis
- avascular necrosis (fracture, steroids, alcohol, gout, sickle cell)
- other (congenital)

26
Q

risk factor for OA

A

advance age (70% in 70 years old), obesity (knee), female, trauma, genetic

27
Q

sign and symptoms of OA

A

localized to affected joint
pain progressive, intermitent flares and remission; joint pain with motion, relieved with rest

joint line tenderness, stress pain, bony enlargement in affected joints, malalignment/ deformity, limited ROM, crepitus on ROM, inflammation, periarticular muscle atrophy

joint lock due to joint mouse (bone/ cartliage fragment), joint instability/ buckling

28
Q

dx of OA

A

can be clinically dx if:

  • > 45 years old
  • activity related joint pain
  • morning joint stiffness that lasts
29
Q

common site of involvement in OA

A

hand:

  • DIP: distal interphalangeal joints (heberden’s nodes)
  • PIP (bouchard’s nodes)
  • 1st CMC: carpometacarpal jts at base of thumb (thumb squaring)

hip,
- groin pain +/- dull or sharp pain in trochanteric area
internal rotation and abduction lost first

knee,
- medial > lateral
1st MTP,

spine:
L-spin (L4-5/ L5-S1)
C spine (common in lower C5/6)
reactive growth -> neurological impingment (sciatica, neurogenic claudication), spondylolitsthesis

asymmetrical involvement

30
Q

investigations, esp hallmark of xray

A

blood:
normal CBC, ESR
-ve ANA and RF

xray

  • narrow of jt space
  • subcondral sclerosis
  • subchondral cysts
  • osteophytes

synovial fluid : non-inflammatory

31
Q

treatment for OA

A

non-pharm:

  • weight loss if obese
  • rest/ low impact exercise
  • exercise: muscle strengthen, aeroibc fitness
  • education: advice and access to info
  • physio: heat/cold/ exercise
  • OT: aids, splints, crane, walker, brace

pharmacological:
- oral:
acetaminophen= act on hypothalmus -> anti pyresis + black pain + decrease prostaglandin (se: hepatoxic, nephrotoxic, angiodema, dizzy, rash)
NSAIDs
glucosamine +/- chondroitin (vitamin): breakdown product of dimethyl sulfoxide (n&v, headache, bloat, insomnia)

sx:
- joint debridement, osteotomy, total/ partial jt replacement, fusion

32
Q

indication of sx

A

persistent severe pain/ stiffness not amenable via medical

loss of jt function

33
Q

what is gout?

A

hyperuricaemia, dearangement in purine metabolism, monosodium urate crystal deposit in tissue (tophi) and synovium (microtophil)

rheumatology (10 decks)

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