Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 LCRS Musculoskeletal > rheumatology and orthopaedics > Flashcards

rheumatology and orthopaedics Flashcards

rheumatoid arthritis: summarise the pathogenesis, clinical features and management of rheumatoid arthritis

1
Q

define rheumatoid arthritis

A

chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis (inflammation of synovial membrane) of synovial (diarthrodial) joints

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

3 key features of rheumatoid arthritis

A

chronic arthritis, extra-articular disease can occur, rheumatoid ‘factor’ may be detected in blood

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

rheumatoid arthritis: 4 key features of chronic arthritis

A

polyarthritis (swelling of >5 small joints of hand and wrists is common), symmetrical, early morning stiffness in and around joints (lasting several hours), joint erosions (damage)

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

rheumatoid arthritis: most common extra-articular disease, and other rare ones

A

rheumatoid nodules; rarer include vasculitis and episcleritis

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

rheumatoid arthritis: what rheumatoid ‘factor’ may be detected in blood as diagnostic test

A

IgM autoantibody against IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

rheumatoid arthritis: female:male ratio and age

A

3:1; usually 30-50yrs old (affects 1% of population)

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

rheumatoid arthritis: main genetic component (not hereditary) as affects monozygotic twins more than dizygotic

A

HLA-DRB gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

rheumatoid arthritis: HLA-DRB gene variants

A

amino acids 70-74 of DRB-chains are strongly associated with rheumatoid arthritis (encodes conserved amino acid sequence in HLA-DR antigen-binding goove - “shared epitope”)

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

rheumatoid arthritis: main environmental component

A

smoking contributes 25% of population-attributable risks and interacts with shared epitope to increase risk

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

6 commonest affected joints in rheumatoid arthritis

A

metacarpophalangeal joints, proximal interphalangeal joints, wrists, knees, ankles, metatarsophalangeal joints

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

features of symmetrical polyarthritis

A

swelling and altered biomechanics, causing a build up of callous under metatarsal heads

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

joint damage and destruction

A

swell neck deformity (hyper-extension at proximal interphalangeal joint and hyper-flexion at distal interphalangeal joint), with ulnar deviation of fingers; Boutonniere deformity affects little finger

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

what is the primary site of pathology of rheumatoid arthritis

A

synovium

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

what does the synovium affected by rheumatoid arthritis include

A

synovial joints, tenosynovium surrounding tendons (between wrist and metacarpophalangeal joints, preventing ring and little fingers fully extending), olecranon bursa

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

describe subcutaneous nodules

A

central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue (typically ulnar border of forearm)

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

what are subcutaneous nodules associated with

A

severe disease, extra-articular manifestations, rheumatoid factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is rheumatoid factor

A

antibodies (typically IgM (pentametic) antibodies) that recognise Fc portion of IgG as their target antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

prevalence of rheumatoid factor in rheumatoid arthritis

A

positive in 70% at disease, and further 10-15% become positive over first 2 years of diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what antibodies are highly specific for rheumatoid arthritis

A

antibodies to citrullinated protein antigens e.g. anti-cyclic citrullinated peptide antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what enzymes mediate citrullination of peptides (arginine -> citrulline)

A

peptidyl arginine deiminases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why do antibodies to citrullinated protein antigens develop in rheumatoid arthritis

A

as peptidyl arginine deiminases are present in high concentrations in monocytes and neutrophils, due to inflammation there is increased citrullination of autologous peptides in inflamed synovium

22
Q

what are antibodies to citrullinated protein antigens strongly associated with

A

smoking and HLA ‘shared epitope’

23
Q

what does the ‘shared epitope’ preferentially bind to

A

non-polar amino acids like citrulline (not arginine), so likely to develop with citrullinated autoantigens who have shared epitope

24
Q

3 environmental factors that cause inflammation resulting in citrullination in rheumatoid arthritis

A

smoking, changes in microbiota, chronic infections

25
Q

3 common extra-articular features of rheumatoid arthritis

A

fever, weight loss, subcutaneous nodules

26
Q

6 uncommon extra-articular features of rheumatoid arthritis

A

vasculitis (if untreated causes digital ischaemia), ocular inflammation (e.g. episcleritis), neuropathies, amyloidosis, lung disease (nodules, fibrosis (can be caused by methotrexate used to treat), pleuritis), Felly’s syndrome (splenomegaly, leukopenia and rheumatoid arthritis)

27
Q

early radiographic abnormalities of rheumatoid arthritis

A

normal, with early sign of juxta-articular osteopenia (thinning bone appearing more translucent around bone due to matrix mettaloproteinases)

28
Q

late radiographic abnormalities of rheumatoid arthritis

A

joint erosions at margins of joint

29
Q

later radiographic abnormalities of rheumatoid arthritis

A

joint deformity and destruction

30
Q

pathology of rheumatoid arthritis

A

synovitis, bone erosion, pannus (inflammatory tissue), cartilage degradation

31
Q

3 contents of synovial joint

A

synovium (consists of synoviocytes), synovial fluid, articular cartilage (T2 collagen and aggrecan)

32
Q

what happens to carpal bones in rheumatoid arthritis

A

carpal bones much closer together

33
Q

what does the synovium become in rheumatoid arthritis

A

proliferated mass of tissue (pannus)

34
Q

why does the synovium become a pannus in rheumatoid arthritis

A

neovascularisation, lymphangiogenesis, inflammatory cells

35
Q

what inflammatory cells can cause pannus in rheumatoid arthritis

A

activated B and T cells, plasma cells, mast cells, activated macrophages

36
Q

what is recruitment, activation and effector functions of inflammatory cells in rheumatoid arthritis mediated by

A

cytokine network (in rheumatoid arthritis, shifted to pro-inflammatory)

37
Q

what is the dominant pro-inflammatory cytokine in rheumatoid synovium

A

TNF-a

38
Q

functions of TNF-a

A

proinflammatory, osteoclast activation, angiogenesis, leukocyte accumulation, chemokine release, endothelial cell activation, PGE2 production

39
Q

how is TNF-a inhibited

A

paraenteral administration of antibodies or fusion proteins

40
Q

what inflammatory interleukins are blocked to treat rheumatoid arthritis

A

IL-6 and IL-1 (IL-1 not as effective)

41
Q

how else can rheumatoid arthritis be treated using antibodies besides cytokine blockade

A

depletion of B cells by paraenteral administration of an antibody against B cell surface antigen CD20 (e.g. rituximab)

42
Q

what is the treatment goal of rheumatoid arthritis

A

prevent joint damage and induce remission (not cure)

43
Q

multi-disciplinary approach to preventing joint damage in rheumatoid arthritis

A

physiotherapy, occupational therapy, hydrotherapy, surgery, medication (DMARDs to treat early and aggresively)

44
Q

what are DMARDs

A

disease-modifying anti-rheumatic drugs (give steroids initially, but then this as steroid-sparing agents)

45
Q

what do DMARD drugs do

A

reduce amount of inflammation in synovium, and slow or prevent structural joint damage, inducing remission

46
Q

examples of DMARD drugs

A

methotrexate (first line with another drug), sulphasalazine, hydroxychloroquine, Janus Kinase inhibitors (end in -ib)

47
Q

what must be monitored in patient taking DMARD due to adverse effects

A

have significant adverse effects and therefore require regular blood test monitoring

48
Q

4 biological therapies for rheumatoid arthritis

A

inhibition of TNF-a (antibodies or etanercept), B cell depletion (e.g. rituximab), modulation of T cell co-stimulation (e.g. abatacept), inhibition of IL-6

49
Q

side effects of biological therapy (monoclonal antibodies)

A

antibody therapy is very expensive (give DMARDs for 6 months and then give biological therapy if hasn’t worked), and side effects for all include increased infection risk

50
Q

what can anti-TNFa antibodies reactivate when treating rheumatoid arthritis

A

reactivates TB, so give prophylactic TB therapy as well

51
Q

what can rituximab cause when treating rheumatoid arthritis

A

progressive multifocal leukoencephalopathy (PML) - viral disease of white matter of brain

Y2 LCRS Musculoskeletal (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions