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Rheumatoid and other inflammatory arthritis Flashcards

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1
Q

What is arthritis

A

Joint inflammation

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2
Q

What are the two major divisions of arthritis

A

Osteoarthritis - degenerative
Inflammatory arthritis

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3
Q

Clinical signs of joint inflammation

A

Rubor - redness
Tumour - swelling
Dolor - pain
Calor - heat

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4
Q

What are three causes of joint inflammation?

A

Infection,
Crystal Arthritis,
Immune-Mediated (autoimmune)

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5
Q

What are two types of infection causing joint inflammation?

A

Septic arthritis
TB

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6
Q

What are two types of crystal arthritis?

A

Gout - uric acid crystals
Pseudogout - CPPD (calcium pyrophosphate)

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7
Q

Which of the three types are primary inflammation?

A

Autoimmune (others are secondary to toxins)

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8
Q

Which of the three is the only non-sterile inflammation?

A

Infection (others are sterile)

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9
Q

Distinguishing features of osteoarthritis

A

Very little inflamm
Slow onset
Sterile

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10
Q

Distinguishing features of Autoimmune arthritis

A

Inflamm
Subacute onset
Sterile
^ CRP

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11
Q

Distinguishing features of Crystal arthritis

A

2º inflamm to crystals
Rapid onset
Sterile, crystals present in synovial fluid
^ CRP

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12
Q

Distinguishing features of Septic arthritis

A

2º inflamm to infection
Rapid onset
Bacteria present
^ CRP
^ WBC

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13
Q

What is the clinical presentation of septic arthritis?

A

Acute, red, hot, painful, swollen monoarthritic joint

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14
Q

What is the diagnosis for septic arthritis?

A

Joint aspiration for gram stain and culture

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15
Q

What are the common organisms that cause septic arthritis?

A

Staph aureus, strep, gonococcus

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16
Q

What is the treatment for septic arthritis?

A

Surgical lavage (wash out) and IV antibiotics

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17
Q

What is the primary site of pathology for rheumatoid arthritis?

A

Synovium

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18
Q

What is rheumatoid arthritis

A

Chronic autoimmune disease leading to synovial inflammation

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19
Q

Where is synovium found?

A

Synovial Joints, Tenosynovium (around tendons), Bursa

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20
Q

What are the key features of rheumatoid arthritis?

A

Polyarthritis, Pain, Swelling, Early Morning Stiffness, Extra-articulate manifestations

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21
Q

How can you identify RA on an x ray

A

joint erosions due to damage

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22
Q

How can you estimate the contribution of genetics vs environment in these conditions?

A

Twin studies - monozygotic/dizygotic twins
If the concordance is greater in monozygotic twins this indicates there is a greater genetic component

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23
Q

What are some environmental risk factors for rheumatoid arthritis?

A

Smoking,
Microbiome,
Poor oral health (P. gingivalis)

lead to citrullination of proteins in the lung epithelium which can increase prevalence of ACPA - anti citrullinated protein antibodies

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24
Q

What is the strongest genetic risk factor for rheumatoid arthritis?

A

HLA-DR shared epitope
polygenic, cumulative genetic burden rather than any specific locus

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25
Implications of HLA class 1 genetic association
e.g. HLA-B27 in AnkS, implicates CD8 cells in pathogenesis It is expressed on all cells and presented to CD8 cells
26
Implications of HLA class 2 genetic association
e.g. HLA-DR4 in RA implicates CD4 T cells and B cells Only expressed on APCs which are presented to CD4 cells B cells activated by CD4 .: pathogenesis causes prod of autoantibodies
27
What is the pattern of joint involvement for rheumatoid arthritis?
Symmetrical, polyarthritis, small jts: hands/wrists/feet
28
Rheumatoid vs Osteoarthritis
RA - prolonged morning and inactivity stiffness. - affects PIPJs, MCPJs, wrist OA - pain worse with activity - affects PIPJs, DIPJs , thumb CMCJs
29
Common extra articular features of RA due to systemic inflammation
Fever Fatigue Weight loss
30
extra articular features of RA due to organ specific inflammation
subcutaneous nodules, lung fibrosis/ lung disease episcleritis, vasculitis leading to digital ischaemia
31
What is Felty's syndrome
extra-articular presentation of RA triad incl: splenomegaly, leukopenia, RA
32
Describe the subcutaneous nodules in rheumatoid arthritis
Central area of fibrinoid necrosis surrounded by histiocytes (macrophage-like) and connective tissue present on the hand/ulna
33
What is the pathogenesis of rheumatoid arthritis?
Synovium becomes proliferated mass of tissue (pannus) due to neovascularisation, lymphangiogenesis, pro-inflammatory cytokines (TNF-alpha) ## Footnote synovial inflamm due to autoreactive T/B cells (HLA-DR4) cause compliment activation and raised pro-inflamm cytokines (TNF-a)
34
cellular causes of RA
autoreactive T/B cells cytokine imbalance, more pro-inflammatory cytokines
35
What are some of the roles of TNF-alpha?
pro-inflamm cytokine Leukocyte accumulation, Osteoclast activation - bone absorption Chondrocytes activation (cartilage destruction MMP prod)
36
How does TNF-a cause pannus formation
Inflamm cell recruitment angiogenesis lymphangiogenesis
37
How does TNF-a cause cartilage loss
Matrix metalloprotease
38
How does TNF-a cause bone loss
Osteoclast activation leads to osteopenia, erosions
39
RA bloods presentation
^ESR, ^CRP ^Platelets RF - rheumatoid factor (not a standalone indicator) Anti-CCP, specific and associated with aggressive disease
40
What are the three methods of imaging in rheumatoid arthritis?
X-Rays, USS, MRI
41
What features can X-Rays pick up?
Soft tissue swelling, peri-articular osteopenia - dark areas around jts bony erosions
42
What can ultrasound see?
Synovitis - synovial hypertrophy, increased blood flow using doppler, erosions (more detail)
43
What are the disadvantages of MRIs?
Expensive and time-consuming
44
What is the treatment objective for rheumatoid arthritis?
Prevent joint damage
45
How can we prevent joint damage in RA
Early diagnosis, prompt aggressive pharmacological treatment, MDT input (physio, OT)
46
What is the first line treatment regime for rheumatoid arthritis?
IM or oral glucocorticoids (steroids), DMARD therapy (disease-modifying anti-rheumatic drugs)
47
What are some examples of DMARDs?
Methotrexate, Hydroxychloroquine
47
What is the second line treatment for rheumatoid arthritis?
if the disease is still active Biological therapies, targeting sp molecules Janus Kinase (JAK) inhibitors
47
What are DMARDs
disease-modifying anti-rheumatic drugs Immunomodulatory drugs that halt or slow the disease process
47
What are NSAIDs
Non-steroid anti inflammatory drugs e.g. ibuprofen, naproxen Provide partial symptom relief but do not prevent disease progression
47
What is the mechanism of glucocorticoids?
Bind to glucocorticoid receptor in cytoplasm, complex acts as transcription factor
47
Methods of steroid admin
oral intramuscular intravenous intra-articular
48
Side effects of glucocorticoids
Cushing's disease T2DM Weight gain Infection risk
48
What do biological therapies usually target?
Inflammatory cytokines
48
How do you measure progression of disease
DAS28, swollen/tender jts If not suppressed rq treatment escalation
48
What are four different biological therapies?
Inhibition of TNF-alpha, IL 6 inhibition B cell depletion, T cell modulation,
48
What are examples of an anti-TNF drug?
Infliximab, Adalimumab
49
What is an example of an IL-6 inhibitor?
Tocilizumab
49
What is an example of a b cell depletion drug?
Rituximab
50
What antibody does rituximab target?
CD20
51
What is an example of a T cell modulator drug?
Abatacept CTLA4-Ig
52
What are four examples of seronegative arthritis?
Psoriatic arthritis, reactive arthritis, ankylosing spondylitis, IBD-associated
53
What is seronegative arthritis
Immune mediated but w/o antibodies in the blood
54
What are the clinical features of psoriatic arthritis?
Scaly red plaques on elbows and knees, (extensor surfaces) joint inflammation, asymmetrical arthritis affecting mainly IPJs enthesitis
55
What is the main pathogenic pathway in psoriatic arthritis?
IL-17, IL-23
56
Nail changes in psoriatic arthritis
Pitting Onycholysis
57
What is reactive arthritis?
Sterile inflammation from infections elsewhere in body (urogenital, gastrointestinal) may be the first manifestation of HIV/Hep C
58
What are the extra-articular manifestations of reactive arthritis?
Enthesitis, Skin inflammation, eye inflammation
59
What is a genetic predisposition to reactive arthritis?
HLA-B27
60
What is an environmental trigger for reactive arthritis?
Salmonella infection
61
Septic arthritis vs Reactive arthritis
SA - positive culture RA - negative culture AB therapy No AB joint lavage No lavage

MSK (7 decks)

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