MSK Flashcards

1
Q

2 major divisions of arthritis

A

OA (degenerative)
inflammation

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2
Q

3 main causes of joint inflammation

A
  1. infection
  2. crystal arthritis
  3. immune mediated (autoimmune)
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3
Q

which one is primary joint inflammation

A

autoimmune

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4
Q

which one is secondary joint inflammation

A

infection and crystal arthritis

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5
Q

examples of infection in joint inflammation (2)

A

septic arthritis
TB

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6
Q

examples of crystals arthritis in joint inflammation (2)

A

gout
pseudogout

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7
Q

which are sterile joint inflammation

A

crystal arthritis
autommune

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8
Q

which are non sterile joint inflammation

A

septic arthritis
TB

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9
Q

speed of onset of OA

A

slow

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10
Q

speed of onset of immune mediated arthritis

A

acute

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11
Q

speed of onset of crystal arthritis and septic arthritis

A

rapid

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12
Q

which arthritis has both CRP & WCC elevated

A

septic arthritis

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13
Q

what is the key investigation of septic arthritis

A

joint aspiration and send fluid for gram stain and culture

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14
Q

management of septic arthritis

A

lavage (joint washout) and IV antibiotics

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15
Q

what are the 3 kinds of autoimmune arthritis

A
  1. lupus
  2. seronegative arthritis
  3. rheumatoid arthritis
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16
Q

where is the primary site of pathology of RA

A

synovium

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17
Q

where can synovium be found

A

synovial joints
tenosynovium surrounding tendons
bursa

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18
Q

sex bias of RA

A

F:M = 2:1

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19
Q

features of RA (4)

A

polyarthritis
chronic
pain, swelling, morning stiffness
joint erosions

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20
Q

what are detected in blood in RA

A

autoantibodies

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21
Q

what is the strongest genetic risk factor in RA

A

HLA-DR

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22
Q

what are in HLA class 1

A

HLA class A, B , C

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23
Q

what are in HLA class 2

A

HLA class D

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24
Q

where are HLA class 1 expressed on

A

all cells

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25
Q

what are associated with HLA class 1

A

CD8 killer cells

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26
Q

where are HLA class 2 expressed on

A

only on APCs eg dendritic cells, macrophages, B cells

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27
Q

what are associated with HLA class 2

A

CD4 helper cells with B cells

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28
Q

HLA class 1 associate with which disease in RA

A

ankylosing spondylitis

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29
Q

which HLA associate with ankylosing spondylitis

A

HLA-B27

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30
Q

why autoantibodies in RA but no ankylosing spondylitis

A

HLA class 2 implicates CD4 T cells and B cells

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31
Q

RA pattern of joint involvement (symmetry or not, how many joints, large or small joint)

A

symmetrical
polyarthritis
always small joints invovled

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32
Q

where do RA most commonly affect

A

hand and feet

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33
Q

common affected joints by RA

A

MCPJ
PIPJ
wrists
knees
ankles
MTPJ

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34
Q

which arthritis associate with morning stiffness

A

RA

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35
Q

which arthritis associate with worse with activities

36
Q

which joints are affected by OA

A

DIPJ
PIPJ
thumb CMCJ
MCPJ

37
Q

what are some systemic symptoms of RA

A

fatigue
fever
weight loss

38
Q

what are some organ-specific extra-articular features of RA

A

subcutaneous nodules
lung diseases (ILD, fibrosis, pleuritis)
vasculitis
neuropathies
amyloidosis
ocular inflammation (eye episcleritis)
felty’s syndrome

39
Q

where are subcutaneous nodules found in RA

A

central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissues

40
Q

what can be found in RA in blood

A

rheumatoid factors (Ab that bind to IgG)
anti CCP antibodies

41
Q

what is pannus in RA

A

synovium becomes proliferated mass of tissue due to neovascularisation, lymphangiogenesis, inflammatory cells

42
Q

what cells does healthy synovial membrane has

A

macrophage like (type A synoviocyte)
fibroblast like (type B synoviocyte)
type 1 collagen

43
Q

what are different types of RA pathogenesis (cellular and molecular pathways)

A

autoreactive B cells
autoreactive T cells
cytokines (TNF alpha, IL-6, IL-1)

44
Q

treatment for autoreactive B cells RA

45
Q

treatment for autoreactive T cells RA

46
Q

treatment for cytokine related RA

A

anti-TNF alpha, anti IL-6 receptor

47
Q

which cytokine is dominant pro-inflammatory cytokine in rheumatoid synovium

48
Q

pathogenesis of TNF-alpha RA

A

inflammtory cell recruitment, angiogenesis, lymphangiogenesis, –> pannus formation
matrix matalloproteases –> cartilage loss
osteoclast activation –> bone loss (osteopenia, erosions)

49
Q

blood test findings in RA

A

increase ESR, CRP
autoantibodies

50
Q

what does ACPA do in RA

A

causes chronic joint destruction and systemic inflammation

51
Q

Xray features in RA (3)

A

soft tissue swelling
peri-articular oeteopenia
bony erosions

52
Q

which is better scan for RA

53
Q

USS features of RA

A

synovial thickening (synovial hypertrophy)
increased blood flow (doppler signal)
can detect erosion not found on RA

54
Q

why not MRI for RA

A

expensive
time consuming

55
Q

why need aggressive pharmacological treatment for RA

A

suppress inflammation

56
Q

pharmacological treatment for RA

A

glococorticoid (steroids)
DMARDs(disease modifying anti-rheumatic drug)

57
Q

first line pharmacological treatment for RA

A

combine DMARD therapy (methotrexate+hydroxychloroquine +/or sulfasalazine) and IM or oral steroid short course

58
Q

second line pharmacological treatment for RA

A

biological therapies eg anti-TNF alpha blockade

59
Q

methods to administer steroid in RA (4)

A

oral prednisolone
IM methyl prednisolone
IV
Intra - articular (IA)

60
Q

steroid side effects

A

cushing’s syndrome

61
Q

what is the scoring system for RA

A

DAS28 score

62
Q

components of DAS28 scoring in RA

A

number of tender joints
number of swollen joints
patient visual analogue score (VAS)
ESR/ CRP

63
Q

what are some biological therapies targeting cytokines in RA

A

inhibit TNF-alpha and IL-6

64
Q

antibodies to inhibit TNF-alpha

A

infliximab
adalimumab
golimumab
cetrolizumab

65
Q

antibodies to inhibit IL-6 receptor

A

tocilizumab
sarilumab

66
Q

biological therapies targeting lymphocytes

A

B cell depletion
block T cell co-stimulating

67
Q

example of biological therapies to target B cell depletion

A

Rituximab (IV infusion)

68
Q

example of biological therapies to target blocking T cell co-stimulation

69
Q

what is seronegative inflammatory arthritis

A

RF CCP antibodies not present in blood
but are immune mediated

70
Q

examples of seronegative inflammatory arthritis (3)

A

psoriatic arthritis
reactive arthritis
ankylosing spondylitis

71
Q

what is psoriatic arthritis

A

immune mediated disease affecting skin

72
Q

where does psoriatic arthritis mainly affect

A

skin
extensor surfaces (elbow, knees)
some also has joint inflammation

73
Q

dominant pathogenic pathway in psoriatic arthritis

74
Q

what are some clinical signs of psoriatic arthritis

A

nail pitting
onycholysis (nail separate from nail bed)

75
Q

which joints do psoriatic arthritis affect

A

IPJs
tendon insertions (enthesitis), can hv sausage finger

76
Q

is psoriatic arthritis symmetrical

A

can be both
asymmetric in IPJ
symmetric in small joints

77
Q

what are some manifestations of psoriatic arthritis

A

spinal and sacroiliac joint inflammation
oligoarthritis of alrge koints
arthritis mutilans
symmentric involvement of small joints

78
Q

what is reactive inflammation

A

sterile inflammation followed by infection elsewhere in body

79
Q

what are some common infections causing reactive

A

urogenital infections
gastrointestinal infection (eg salmonella)

80
Q

extra-articular manifestations in reactive arthritis

A

enthesitis (tendon inflammation)
skin inflammation
eye inflammation

81
Q

reactive arthritis can be first manifestation of which disease

A

HIV
Hepatitis C infection

82
Q

is septic arthritis same as reactive arthritis

83
Q

difference between septic arthritis and reactive arthritis in terms of synovial fluid culture

A

septic: positive
reactive: sterile

84
Q

difference between septic arthritis and reactive arthritis in terms of antibiotic therapy

A

septic: yes, IV
reactive: no (but yes for treating underlying infection of STI)

85
Q

difference between septic arthritis and reactive arthritis in terms of joint lavage

A

septic: yes
reactive: no