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MSK > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is arthritis?

A

Inflammation of the joint

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2
Q

What is rheumatism?

A

Umbrella term for conditions causing chronic pain affecting the joints/connective issue

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3
Q

Give examples of rheumatic diseases

A 
RA
Seronegative arthritis
Gout/pseudogout 
Connective tissue dx 
Systemic vasculitis
Bone disease
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4
Q

What are the functions of the normal synovium?

A

Maintain intact tissue surface
Lubrication of cartilage
Controls synovial fluid production and composition
Nutrition of cartilage

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5
Q

What is the appearance of a rheumatic joint?

A

Bone eroded
Cartilage thinning
Synovial inflammation
Loss of joint space etc.

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6
Q

Define rheumatoid arthritis

A

Chronic autoimmune symmetrical polyarticular inflammatory joint disease and other systemic features

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7
Q

What joints does RA tend to affect?

A

MCP, PID, MTP

As disease worsens can affect large joints - shoulder, knees, ankles, elbows

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8
Q

What type of disease is RA?

A

Autoimmune

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9
Q

What is the aetiology of RA?

A

Interaction of a genetic factor with an environmental factor

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10
Q

What is the strongest genetic association with RA?

A

HLA-DR4

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11
Q

What environmental factors are most associated with RA?

A

Cigarette smoking
Pathogens (EBV, CMV, E. coli, mycoplasma, periodontal disease)
Gut microbiome

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12
Q

Repeated insults in a genetically susceptible person leads to:

A

Modification of our antigens, e.g. IgG antibodies or other proteins, e.g. type 2 collagen
E.g. via citrullination

Immune system doesn’t recognise these antigens to be self anymore

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13
Q

What is citrullination?

A

Conversion of arginine into citrulline

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14
Q

Changes to these proteins, mean the host immune system doesn’t recognise their antigens as self anymore - what does this lead to happening?

A

Antigens picked up by APC
APC cells carry antigen to lymph nodes and activate T-helper cells
T-helper cells stimulate B cells –> plasma cells –> autoantibodies

T helper cells and autoantibodies reach joint
T cells secrete cytokines, e.g. IF-gamma, IL-17 to recruit macrophages etc.
Macrophages produce TNFa and IL1 and Il6 –> stimulates synovial cells to proliferate –> pannus (made up of scar tissue, and T lymphocytes, macrophages)

Pannus damages cartilage and bone
Activated synovial cells make proteases –> breaks down protein in cartilage

Exposed bone rubs against each other

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15
Q

Explain the correlation of RANKL and RA

A

Inflammatory cytokines release in RA, cause T cells to have more of a surface protein RANKL

RANKL allows T cells to bind to RANK protein on osteoclasts –> causing them to break down more bone

Chronic inflammation –> angiogenesis –> more blood cells can make their way to the joint

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16
Q

What is rheumatoid factor?

A

IgM antibody that targets the Fc domain of altered IgG antibodies

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17
Q

What is anti-CCP?

A

Antibody that targets citrullinated proteins

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18
Q

What happens when autoantibodies meet their antigens?

A

They form immune complexes which sit in the synovial fluid and can activate the compliment system –> joint inflammation and injury

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19
Q

Why are there sometimes extraarticular manifestations in RA?

A

Inflammatory cytokines can escape from the BS and reach multiple organs
E.g. IL1 and 6 travel to the brain and act as pyrogens –> fever
In skeletal muscles, cytokine can induce protein breakdown
In the skin they lead to rheumatoid nodules

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20
Q

What is a rheumatoid nodule?

A

Round collections of macrophages and lymphocytes with a central area of necrosis

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21
Q

What are the lung manifestations in RA?

A

Fibrosis can occur, leading to reduced gas exchange

Pleural effusion

22
Q

What haematological condition is associated with RA?

A

Iron deficient anaemia

23
Q

What are flares of RA?

A

Sudden worsening of condition

Joints become swollen, red, warm and painful

24
Q

What are common hand deformities in RA?

A

Ulnar deviation
Butonniere deformity
Swan neck deformity

25
Q

Describe butonniere deformity

A

Hyperextension of DIP, flexion of PIP

26
Q

Describe swan neck deformity

A

Hyperextension of PIP, flexion of DIP

27
Q

What white blood cell does the synovial fluid contain in RA?

A

Neutrophils (esp during acute flares)

28
Q

What two antibodies are associated with RA?

A

anti-CCP, RF

29
Q

How does prognosis differ based on presence of anti-CCP?

A

Worse prognosis with anti-CCP antibodies

30
Q

What medicines are used to treat RA?

A

NSAIDs - acute flares
DMARDs (disease modifying antirheumatic drugs)
Biologics
Corticosteroids (IA, IM, oral)

31
Q

What are the effect of DMARDs?

A

Slow disease activity and retard disease progression

32
Q

What DMARDs do we currently use?

A

Methotrexate - gold standard
Sulfasalazine
Hydrochloroquine
Leflumomide

33
Q

What did DMARDs did we used to use?

A

Gold salts
Penicillamine
Others

34
Q

What is the therapeutic regime for RA?

A

Early, aggressive treatment –> optimal outcomes

Effective suppression of inflammation will improve symptoms, prevent joint damage and disability

35
Q

What is good about methotrexate?

A

Effective, well tolerated, cheap
Cornerstone of combination treatment (DMARD and biologic)
Toxicity predictable and monitorable

36
Q

In what ways are biologics better than DMARDs?

A

They work rapidly and are generally well tolerated

37
Q

In what ways are biologics worse than DMARDs?

A

They are large complexes so must be given parenterally
Important toxicities, e.g. infection, TB, cold, flu
High cost
Better when co-prescribed with methotrexate
Risk of malignancy?

38
Q

What are current biologics?

A 
TNFa inhibitors 
IL-1 inhibitors (anakinra) 
Anti B cell therapies (rituximab) 
Anti T cell therapies (abatacept) 
IL-6 inhibitors 
Others
39
Q

When do we give corticosteroids to people with RA?

A

Rarely - to put them in clinical remission during acute situation

Longer you are on them –> less effective they are and the more SEs you get (e.g. cataracts, infections)

40
Q

What is the classification we use for RA?

A

2010 EULAR/ACR

41
Q

Who should be tested for RA according tot he 2010 EULAR/ACR?

A

Those with:

  1. at least 1 joint with definitive clinical synovitis (swelling)
  2. synovitis not better explained by another disease
42
Q

A score of what on the 2010 EULAR/ACR is considered as definite RA?

A

6 or more out of 10

43
Q

What is the EULAR/ACR 2010 classification of RA?

A

A. JOINT INVOLVEMENT
1 large joint - 0
2-10 large joints - 1
1-3 small joints (w/w.o. large joint involvement - 2
4-10 small joints (w/w.o. large joint involvement - 3
>10 joints (at least 1 small joint) - 5

B. SEROLOGY
negative RF and ACPA - 0
Low-positive RF or ACPA - 2
High positive RF or ACPA - 3

C. ACUTE PHASE REACTANTS
Normal CRP/ESR - 0
Abnormal CRP/ESR - 1

D. DURATION OF SYMPTOMS
<6 weeks - 0
6 weeks+ - 1

44
Q

What is the prevalence of RA?

A

1%

45
Q

In which gender is RA more common?

A

Females (3x more common)

46
Q

What investigations can you use for RA?

A

RF, antiCCP, ACPA
XRay
USS may show effusions, pannus formation

47
Q

What are the symptoms of RA?

A 
Pain 
Stiffness 
Immobility
Poor function 
Systemic symptoms
48
Q

What are the signs of RA?

A 
Swelling
Tenderness
Limited RoM 
Redness
Heat
49
Q

What are the non-specific systemic features of RA?

A

Fatigue/lassitude, wt loss, anaemia

50
Q

What are the specific systemic features of RA?

A

Eyes, lungs, nerves, skin and kidneys

Long term - CVS (increased risk of atheroma), and malignancy

51
Q

How do you measure the severity of RA?

A

Disease activity score (DAS)
<2.4 clinical remission
>5.1 indicates eligibility for biologic therapy

52
Q

What is the prognosis for RA?

A

75% cases diagnosed during working life
33% stopped working within 2 years of diagnosis
50% unable to work due to disability in 10 years
40 sick days p/a

MSK (27 decks)

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