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(msk) rheumatology Flashcards

1
Q

what is rheumatology?

A

the medical speciality dealing with diseases of the musculoskeletal system including

  • bones
  • muscles
  • tendons
  • ligaments
  • cartilage
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2
Q

what is a synovial joint?

A

a fluid-filled joint cavity contained in a fibrous capsule where two bones meet

(diarthrosis = freely mobile)

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3
Q

what is the synovium?

A

lining of the fibrous synovial capsule
(1-3 cells deep)

i.e. synovial membrane

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4
Q

which two cells types are present in the synovium?

A

type A synoviocytes
type B synoviocytes

(together with type I collagen)

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5
Q

what are type A synoviocytes?

A

macrophage-like phagocytic cells

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6
Q

what are type B synoviocytes?

A

fibroblast-like cells that produce hyaluronic acid

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7
Q

what type of collagen is present in the synovium?

A

type I collagen

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8
Q

what is the main component of synovial fluid?

A

hyaluronic acid

rich viscous fluid

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9
Q

what type of collagen is present in the articular cartilage?

A

type II collagen

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10
Q

where is the proteoglycan Aggrecan found in a synovial joint?

A

a proteoglycan found in the articular cartilage

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11
Q

what is arthritis?

A

inflammation of the joints

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12
Q

what are the three divisions of arthritis?

A

degenerative (osteoarthritis)

inflammatory (rheumatoid arthritis)

septic arthritis

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13
Q

what is inflammation?

A

a physiological response to deal with injury or infection

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14
Q

what are the manifestations of inflammation?

A 
redness (rubor)
heat (calor)
pain (dolor)
swelling (tumor)
loss of function
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15
Q

what physiological changes underlie inflammation?

A

increased blood floew

increased activation and recruitment of leukocytes to site of injury/infection

cytokine release (TNFa, IL1, IL6, IL17)

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16
Q

which cytokines are released in inflammation?

A

TNFa, IL1, IL6, IL17

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17
Q

when does crystal arthritis occur?

A

crystals deposit in the joint triggering inflammation

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18
Q

what are the two types of crystal arthritis?

A

gout

pseudogout

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19
Q

what is gout?

A

a syndrome caused by deposition of urate (uric acid) crystals in the joints
= inflammation

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20
Q

what is the biggest risk factor for gout?

A

hyperuricaemia (high uric acid levels in the blood)

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21
Q

what are the main causes of gout?

A

genetic tendency

increased consumption of purine-rich foods

kidney failure (reduced excretion)

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22
Q

what is pseudogout?

A

a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals

= inflammation

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23
Q

what are the risk factors for pseudogout?

A

background osteoarthritis

elderly patients

intercurrent infections

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24
Q

name two diseases that can be caused by the excessive deposition of MSU (monosodium urate) in tissues due to hyperuricaemia

A

1) gout arthritis

2) tophi

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25
Q

what is tophi?

A

aggregated deposits of MSU (monosodium urate) in tissue

subcutaneous deposits of MSU

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26
Q

which joint is affected most commonly in gout and what is this called?

A

the 1st metatarsophalangeal joint (‘big toe’)

= podagra

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27
Q

how does podagra present?

A 
pain
redness
swelling, tenderness
abrupt onset
usually resolves in 3-10 days
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28
Q

what is podagra?

A

gout of the 1st MTPJ ‘big toe’

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29
Q

gout causes monoarthritis most commonly - what is this?

A

arthritis affecting a singular joint

gout can cause polyarthritis but not initially

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30
Q

what are the signs of gout on an X-ray?

A

juxta-articular rat-bite erosions of the 1st MTPJ

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31
Q

how are suspected gout and pseudogout investigated?

A 
joint aspiration
(synovial fluid analysis)
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32
Q

how is acute gout managed?

A

NSAIDs
steroids
colchicine

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33
Q

how is chronic gout managed?

A

allopurinol

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34
Q

how are synovial fluid samples analysed for pathogens?

A

rapid gram stains followed by culture and antibiotic sensitivity assays

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35
Q

how are synovial fluid samples analysed for gout crystals?

A

polarising light microscopy to identify crystals

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36
Q

what kind of crystals are seen in gout on synovial fluid analysis?

A

urate crystals

needle shape

negative birefringence

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37
Q

what kind of crystals are seen in pseudogout on synovial fluid analysis?

A

CPPD crystals (calcium pyrophosphate dihydrate)

brick ‘rhomboid’ shape

positive birefringence

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38
Q

name some immune-mediated inflammatory joint diseases

A

rheumatoid arthritis
psoriatic arthritis
reactive arthritis
SLE

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39
Q

what is the most common immune-mediated inflammatory arthritis?

A

rheumatoid arthritis

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40
Q

what is rheumatoid arthritis?

A

chronic autoimmune disease characterised by
1) pain
2) stiffness
3) symmetrical synovitis of synovial joints
(inflammation of the synovial membrane)

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41
Q

is rheumatoid arthritis a polyarthritis or a monoarthritis?

A

polyarthritis
= affects multiple joints
(mainly small joints of the hands and wrist)

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42
Q

which joints are affected most in rheumatoid arthritis?

A

mainly small joints of the hands and wrist

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43
Q

what are the key features of rheumatoid arthritis?

A

pain
stiffness (early morning)
symmetrical synovitis
polyarthritis

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44
Q

what happens if rheumatoid arthritis is left untreated?

A

can lead to joint damage and joint erosions on radiographs

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45
Q

which rheumatoid antibody is often detected in the blood?

A

rheumatoid factor (anti-IgG antibody)

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46
Q

which joints are most commonly affected in RA?

A

UL = wrist, MCPJs, PIPJs

LL = knee, ankle, MTPJs

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47
Q

what is the primary site of pathology in RA?

A

synovium

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48
Q

besides the synovial joints, where can synovitis occur in RA?

A

1) tenosynovium surrounding tendons (i.e. synovial sheaths associated with tendons - extensors, flexors)
2) bursae (e.g. olecranon bursitis)

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49
Q

what is tenosynovitis and why is it important in RA?

A

inflammation of a tendon and its respective synovial sheath
= can occur due to synovitis in RA

e.g. extensor tenosynovitis

50
Q

what are the common extra-articular manifestations of RA?

A

fever
weight loss
subcutaneous nodules

51
Q

what are the rare extra-articular manifestations of RA?

A 
vasculitis
episcleritis
neuropathies
amyloidosis
lung disease
Felty's sundrome
52
Q

what is Felty’s syndrome?

A

a rare extra-articular manifestation of RA

= triad of spenlomegaly, leukopenia and RA

53
Q

where do subcutaneous nodules form most commonly in RA?

A

elbow

extensor surfaces of hand

54
Q

what are subcutaneous nodules in RA?

A

central fibrinoid necrosis w a peripheral layers of connective tissue and histiocytes

55
Q

how common are subcutaneous nodules in RA and what are they indicative of?

A

approx 30% of RA patients

= indicate severe disease

56
Q

why two antibodies are primarily found in RA patients?

A

1) rheumatoid factor (anti-IgG)

2) anti-CCP antibody

57
Q

what is rheumatoid factor?

A

RF = pentameric IgM antibodies that bind to the Fc portion of the circulating IgG antibodies

58
Q

how many RA patients have RF and how are these patients described?

A

approx 70% of patients have RF at disease onset
= said to be ‘seropositive’

(further 10-15% become seropositive over the next 2 years following diagnosis)

59
Q

what are anti-CCP antibodies?

A

antibodies to citrullinated peptides

= highly specific for RA

60
Q

which enzyme mediates the citrullination of peptides?

A

peptidyl arginine deaminases (PADs)

= convert arginine to citrulline

61
Q

what are the three steps to managing RA effectively?

A

1) recognise symptoms early
2) initiate treatment early (joint destruction = inflammation x time)
3) choose aggressive treatment to suppress inflammation

62
Q

which group of drugs is used to treat RA?

A

DMARDs

disease-modifying anti-rheumatic drugs

63
Q

what is the first-line treatment for RA?

A

methotrexate in combination hydroxychloriquine or sulfasalazine

64
Q

what is the second-line treatment for RA?

A

biologics

Janus Kinase inhibitors (Tofacitinib & Baricitinib)

steroid therapy (prednisolone)

= multi-disciplinary approach

65
Q

why is prednisolone avoided in RA treatment?

A

avoid long-term use because of systemic side-effects

can inject to site of arthritis to avoid systemic side effects

66
Q

what is ankylosing spondylitis?

A

inflammatory arthritis of the joints of the spine

seronegative spondyloarthropathy = causes ankylosing

67
Q

what is an early sign of ankylosing spondylitis?

A 
chronic sacroillitis
(inflammation of sacroiliac joints)

= hallmark feature

68
Q

is RF present in ankylosing spondylitis?

A

no!

ankylosing spondylitis is a seronegative spondyloarthropathy
= no RF antibody

69
Q

which group of patients is most affected by ankylosing spondylitis?

A

males

20-30 years old

70
Q

what causes ankylosing spondylitis?

A

no specific cause but increase genetic risk

= people who have a gene called HLA-B27 are at a greatly increased risk of developing ankylosing spondylitis

71
Q

what does seronegative mean?

A

lack of rheumatoid factor (RF) and anti-CCP antibodies in teh blood

72
Q

how does ankylosing spondylitis present?

A

leads to spinal fusion reducing the flexibility of the spine

= causing hunched back

73
Q

ankylosing spondylitis is a seronegative spondyloarthropathy - what does this mean?

A

ankylosing = bony fusion of the spine + stiffness

spondyloarthropathy = forms of arthritis that usually strike the bones in your spine and nearby, peripheral joints

74
Q

what are the primary sites of pathology in ankylosing spondylitis?

A

joints of the spine

sacroiliac joints (causing chronic sacroillitis)

75
Q

name other common spondyloarthropathies

A

reactive arthritis, psoriatic arthritis

76
Q

which clinical symptoms must you have alongside a seropositive test (RF, anti-CCP present) result to be diagnosed with rheumatoid arthritis?

A

pain and swelling in the joints

polyarthritis (involves many joints)

morning stiffness in the joints

X-ray evidence of the characteristic bone damage of RA (soft tissue swelling, bony erosions, peri-articular osteopenia)

77
Q

what are the symptoms of ankylosing spondylitis?

A
  • lower back pain + stiffness (early morning, improves with exercise)
  • reduced spinal movements
  • peripheral arthritis
  • plantar fasciitis, achilles tendonitis
  • fatigue
78
Q

what is the classic clinical presentation of patients with ankylosing spondylitis?

A

flexed neck

loss of lumbar lordosis

flexion of the hip and the knees

(45+, back pain for >3 months)

79
Q

what makes the stiffness of ankylosing spondylitis characteristic to the condition?

A

usually early morning stiffness that improves on exercise

80
Q

define extra-articular manifestations

A

symptoms outside of or other than a joint

81
Q

what are the key features of an ankylosing spondylitis blood test?

A

normocytic anaemia

raised CRP + ESR

positive for HLA-B27 gene

82
Q

which imaging modality is most commonly used to investigate ankylosing spondylitis?

A

MRI (but can also use X-ray)

83
Q

what are the key features of an MRI that shows ankylosing spondylitis?

A
  • shiny corner sign (i.e. Romanus lesion)
  • squaring of the vertebral bodies
  • bamboo spine (fusion of the joints)
  • bone marrow oedema (fluid fills bone marrow)
  • erosion, sclerosis, narrowing of the sacroiliac joint
84
Q

how is ankylosing spondylitis managed?

A

physiotherapy, exercise regimes

NSAIDs, DMARDs (for peripheral joints)

85
Q

why does psoriatic arthritis occur?

A

psoriasis occurs = formation of red, scaly plaques on extensor surfaces (knees, elbows)

= approx 10% of psoriasis cases have associated inflammation of the joints

86
Q

what are the two similarities between ankylosing spondylitis and psoriatic arthritis?

A
  • both seronegative (lack of RF in the blood)

- can cause inflammation of the sacroiliac joints

87
Q

what is the most common clinical presentation of psoriatic arthritis?

A

asymmetrical arthritis

bony erosions occur at ICPs, while MCPs are left unaffected

classic ‘pencil in cup’ sign

88
Q

what are the less common manifestations of psoriatic arthritis?

A
  • symmetrical arthritis
  • sacroiliac and spinal inflammation
  • oligoarthritis
  • arthritis mutilans
89
Q

what is arthritis mutilans?

A

bones around joint get completely dissolved

= telescoping of the digits
= shortened fingers, excess skin

(possible manifestation of psoriatic arthritis)

90
Q

how is psoriatic arthritis investigated?

A

blood tests

  • raised ESR + CRP
  • lack of RF factor

imaging

  • X-ray = ‘pencil in cup’ deformity
  • MRI = sacroiliitis and enthesitis
91
Q

how is psoriatic arthritis managed?

A

DMARDs (methotrexate)

avoid oral steroids = cause pustular psoriasis

92
Q

what classic feature is visible on an X-ray for psoriatic arthritis?

A

‘pencil in cup’ deformity

93
Q

what is seen on a psoriatic arthritis MRI?

A

sacroiliitis and enthesitis

94
Q

why are oral steroids avoided in psoriatic arthritis?

A

cause pustular psoriasis

95
Q

what is reactive arthritis?

A

sterile inflammation of the joints secondary to an infection elsewhere in the body

primary infection is most commonly:

1) urogenital = chlamydia
2) gastrointestinal = salmonella, campylobacter
3) can also be due to HIV/Hep C

96
Q

what possible pathogens cause reactive arthritis?

A

urogenital
- Chlamydia trachomatis

gastrointestinal

  • Salmonella
  • Shigella
  • Campylobacter

HIV
hepatitis C

97
Q

what are the extra-articular manifestations of reactive arthritis?

A

skin inflammation
eye inflammation
tendon inflammation (enthesitis)

98
Q

what causes reactive arthritis?

A

genetic predisposition (HLA-B27) + environmental trigger (infection)

99
Q

how is reactive arthritis treated?

A

condition is usually self-limiting

can treat with DMARDs or NSAIDs

100
Q

how is reactive arthritis different to septic arthritis?

A

septic = inflammation due to infection in the joint

reactive = inflammation due to infection elsewhere

101
Q

SLE is a multi-system inflammatory disease - which parts of the body are affected?

A

kidney, lungs, skin, haematological features

102
Q

what are antinuclear antibodies?

A

antibodies produced against nuclear components of the cell

= high sensitivity for SLE, but low specificity

103
Q

what does a negative ANA indicate?

A

excludes the diagnosis of SLE

104
Q

what does a positive ANA indicate and what is tested subsequently?

A

indicates SLE, only in the presence of other appropriate clinical signs

= anti-dsDNA tested for subsequently

105
Q

what does anti-dsDNA indicate?

A

highly specific for SLE and can be used to monitor SLE progression

106
Q

briefly explain the pathogenesis of rheumatoid arthritis

A

proliferation of the cells in the synovium to form an abnormal mass = pannus

due to

1) neurovascularisation
2) lymphangiogenesis
3) immune cell infiltrate

107
Q

what is the term used to describe the structure that forms as a result of synovium proliferation in rheumatoid arthritis?

A

pannus

108
Q

what is a pannus?

A

an abnormal proliferated mass (extra growth) that forms due to uncontrolled proliferation in the synovium

= leads to rheumatoid arthritis

109
Q

within the inflammatory cell infiltrate, what causes cell recruitment, activation and effector functions?

A

inflammatory cytokine release

110
Q

which type of cytokines are most active in rheumatoid arthritis: pro-inflammatory or anti-inflammatory?

A

pro-inflammatory

111
Q

name the dominant pro-inflammatory cytokine in rheumatoid arthritis

A

TNFa

112
Q

which three cell types does TNFa mainly affect in rheumatoid arthritis?

A

osteoclasts
synoviocytes
chondrocytes

113
Q

how does TNFa affect osteoclasts?

A

activates osteoclasts
= increased bone resorption
= bone erosion

114
Q

how does TNFa affect synoviocytes?

A

activates synoviocytes
= increased joint inflammation
= increased pain and swelling

115
Q

how does TNFa affect chondrocytes?

A

= increased cartilage degradation

= joint space narrowing

116
Q

which cells produce TNFa in rheumatoid arthritis?

A

activated macrophages within the rheumatoid synovium

117
Q

what is anti-TNFa?

A

monoclonal antibody that binds to and inactivates the inflammatory cytokine, TNFa

118
Q

what are biological therapies?

A

proteins (usually antibodies) that specifically target another protein such as an inflammatory cytokine

119
Q

what four biological therapies are available to treat rheumatoid arthritis?

A

1) inhibition of TNFa = influximab
2) B cell depletion (inactivating CD20) = rituximab
3) modulating T cell co-stimulation = abatacept
4) inhibition of IL-6 signalling = tocilizumab

120
Q

which normal structural feature becomes pathological in rheumatoid arthritis?

A

synovium (i.e. synovial membrane)

121
Q

in rheumatoid arthritis, which cells are found in the immune cell infiltrate preceding pannus formation?

A

activated T and B cells

activated macrophages

mast cells

plasma cells

brs (phase 1b) (71 decks)

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