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Musculoskeletal- > Crystal Arthopathy > Flashcards

Crystal Arthopathy Flashcards

1
Q

What are crystal arthopathy diseases characterised by?

A

Characterised by deposition of mineralised material within joints and peri-articular tissue

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2
Q

What are some common crystal arthopathy diseases?

A
  • Monosodium urate (gout)
  • Calcium pyrophosphate dehydrate (CPPD, also called pseudogout)
  • Basic calcium phosphate hydro-apatit (BCP, also called calcific periarthritis/tendonitis)
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3
Q

What crystals cause gout?

A

Monosodium urate

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4
Q

What crystals cause pseudogout?

A

Calcium pyrophosphate dehydrate

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5
Q

What crystals cause calcific periarthritis/tendonitis?

A

Basic calcium phosphate hydro-apatit

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6
Q

Where does most of the urate in the body come from?

A

2/3 of urate in body comes from breakdown of purines produced within body (breakdown of DNA and RNA), remainder comes from breakdown of purines in food and drinks

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7
Q

Where is most uric acid excreted?

A

70% of uric acid is excreted in kidney, and 30% in biliary tract

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8
Q

What can hyperuricaemia occur due to?

A

Hyperuricaemia can occur due to overproduction or under excretion:

  • Overproduction
    • Malignancy such as lymphoproliferative
  • Severe exfoliative psoriasis
  • Drugs
    • Such as ethanol, cytotoxic drugs
  • Inborn errors of metabolism
  • HGPRT deficiency
    • Known as Lesch Nyan syndrome
    • X-linked recessive
    • Intellectual disability, aggressive and impulsive behaviour, gout, renal disease
    • Under excretion (commonest cause)
      • Renal impairment
      • Hypertension
      • Hypothyroidism
      • Drugs
        • Such as alcohol, low dose aspirin, diuretics, cyclosporine
      • Exercise, starvation, dehydration
      • Lead poisoning
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9
Q

Is overproduction or underexcretion the more common cause of hyperuricaemia?

A

Under excretion

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10
Q

What are some causes of overproduction of uric acid?

A
  • Malignancy such as lymphoproliferative
  • Severe exfoliative psoriasis
  • Drugs
    • Such as ethanol, cytotoxic drugs
  • Inborn errors of metabolism
  • HGPRT deficiency
    • Known as Lesch Nyan syndrome
    • X-linked recessive
    • Intellectual disability, aggressive and impulsive behaviour, gout, renal disease
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11
Q

What is Lesch Nyan Syndrome?

A
  • HGPRT deficiency
  • X-linked recessive
  • intellectual disability
  • aggressive and impulsive behaviour
  • self-mutilation
  • gout
  • renal disease
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12
Q

What are some causes of underexcretion of uric acid?

A
  • Renal impairment
  • Hypertension
  • Hypothyroidism
  • Drugs
    • Such as alcohol, low dose aspirin, diuretics, cyclosporine
  • Exercise, starvation, dehydration
  • Lead poisoning
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13
Q

Are more woman or men affected by gout?

A

M>F (as oestrogen helps excretion of uric acid in kidney)

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14
Q

What are some lifestyle risk factors for gout?

A
  • Diet high in meat/fish
  • Alcohol drinking
  • Lots of sports
  • Dehydration
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15
Q

What is the clinical presentation of gout?

A
  • Gout episodes classically occur at the first MTP joint
  • Red
  • Hot
  • Erythema
  • Pain
  • Often the foot
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16
Q

What is the gold standard to diagnose Gout?

A

Gout is diagnosed clinically or by aspiration of fluid from the joint.

  • Excluding septic arthritis is essential as this is a potential joint and life-threatening diagnosis.
17
Q

What is a Tophi?

A

A massive accumulations of uric acid

18
Q

What is the mangement of gout?

A
  • Acute flair
    • NSAIDs
    • Colchicine
    • Steroids
  • Long term
    • Think does it need to be treated?
    • 1st attack not treated unless
      • Single attack of polyarticular gout
      • Tophaceous gout
      • Urate calculi
      • Renal insufficiency
    • Treat if 2nd attack within 1 year
    • Prophylactically prior to treating certain malignancies
    • Do not treat asymptomatic hyperuricaemia
  • Address cardiovascular and lifestyle risk factors
19
Q

How can you prophylactically lower uric acid?

A
  • Xanthine oxidase inhibitor (first line)
    • Such as allopurinol
  • Or febuxostat
    • For those unable to tolerate allopurinol
    • Avoid in patients with cardiac history
  • Uricosuric agents
    • Such as sulphinpyrazone
  • Canakinumab
20
Q

What are the rules for lowering uric acid levels?

A
  • Wait for acute attack to settle before lowering urate levels
  • Use prophylactic NSAIDs or low dose colchicine/steroids until urate level normal as the above treatments could trigger flair
  • Then adjust allopurinol dose according to renal function, starting low and working up
21
Q

Where does gout most commonly affect?

A

Feet, ears and elbows (DIP joints)

22
Q

Where does pseudogout most commonly affect?

23
Q

Does pseudogout affect more males or females?

A

Usually affects older females, with erratic flares of joint swelling

24
Q

What is the aetiology of pseudogout?

A
  • Idiopathic
  • Familial
  • Metabolic
25
Q

What are some triggers of pseudogout?

A
  • Trauma
  • Intercurrent illness
26
Q

What are some clinical features of pseudogout?

A
  • Chondrocalcinosis (depositions of CPPD crystals into fibrous or hyaline cartilage) on x-ray
  • Can see pyrophosphate crystals on aspiration
27
Q

What is chondrocalcinosis?

A

(depositions of CPPD crystals into fibrous or hyaline cartilage)

28
Q

What is the management of pseudogout?

A
  • NSAIDs
  • I/A steroids
  • There are no prophylactic therapies
29
Q

What is polymyalgia rheumatica?

A

Inflammatory condition in elderly with close relation to giant cell arthritis

30
Q

Does polymyalgia rheumatica affect more males or females, and what age group?

A
  • F > M
  • Rare <50 years, usually >70 years
31
Q

What are clinical features of polymyalgia rheumatica?

A
  • Sudden onset of shoulder with or without pelvic girdle stiffness
  • Anaemia
  • Arthralgia
  • Systemic features
    • Malaise
    • Weight loss
    • Fever
    • Depression
32
Q

What is the diagnosis of polymyalgia rheumatica?

A
  • compatible history
  • Age>50
  • ESR>50
  • dramatic steroid response
  • no specific test
33
Q

What is the differential diagnosis for polymyalgia rheumatica?

A
  • Myalgic onset inflammatory joint disease
  • Underlying malignancy
  • Inflammatory muscle disease
  • Hypo/hyperthyroidism
  • Bilateral shoulder capsulitis
  • Fibromyalgia
34
Q

What is the treatment for polymyalgia rheumatica?

A
  • Prednisolone 15mg per day initialy
    • 18-24 month course
  • Bone prophylaxis
35
Q

What is Lesch Nyan Syndrome?

A
  • HGPRT deficiency
  • X-linked recessive
  • intellectual disability

In the absence of HPRT, these purine bases cannot be salvaged; instead, they are degraded and excreted as uric acid. In addition to the failure of purine recycling, the synthetic rate for purines is accelerated, presumably to compensate for purines lost by the failure of the salvage process. The failure of recycling together with the increased synthesis of purines is the basis for the overproduction of uric acid

Musculoskeletal- (41 decks)

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