7. Rheumatoid Arthritis Flashcards

1
Q

what key feature distinguishes RA from OA

A

RA is an autoimmune disease

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2
Q

how is inflammation in the joints presented in RA

A

symmetrical in presentation and develops simultaneously

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3
Q

name 3 similarities between RA and OA

A
  • both located in joints
  • no cure for either
  • not fatal conditions but can decrease quality of life
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4
Q

what is the difference between RA and OA in terms of the area it affects

A

OA primarily affects cartilage
RA primarily affects the lining of the joint (synovial membrane)

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5
Q

which has a shorter timescale: RA or OA

A

RA

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6
Q

how long does RA take to develop

A

a few months, but can be within a week in 15% of cases

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7
Q

name 4 symptoms of RA

A

symmetrical joint swelling
morning stiffness
fatigue
Raynaud’s phenomenon

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8
Q

describe 3 methods of how RA is diagnosed

A

observation of symptoms

detection of rheumatoid factor

X-ray

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9
Q

at what stage would an Xray only provide a diagnosis

A

at late stages - where there is joint erosion

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10
Q

what is rheumatoid factor

A

a group of autoantibodies to the Fc portion of IgG

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11
Q

what joint is affected the most in RA

A

finger joints

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12
Q

name two joints on the fingers affected by RA

A

proximal interphalangeal joint

distal interphalangeal joint

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13
Q

what are synoviocytes

A

fibroblast like cells

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14
Q

what is the role of synoviocytes

A

cells responsible for the production of synovial fluid components, absorption from the joint cavity and for blood/synovial fluid exchange

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15
Q

describe the positioning of normal synoviocytes

A

line the fluid filled synovial membrane

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16
Q

what causes the abnormal proliferation of synoviocytes

A

inflammatory processes

17
Q

what does the extensive growth of synoviocytes result in

A

uncontrolled growth = vascularisation and extensive angiogenesis

18
Q

describe what happens to the synovial lining when cells start to grow

A

it eventually connects with the cartilage on the surface of the tibial plaque and causes damage to the cartilage

19
Q

what facilitates bone erosion

A

imbalance of osteoclasts and osteoblasts prevents the normal turnover of bone = destruction

20
Q

what aggrecan damaging protein is also elevated in RA, what does this do?

A

matrix metalloproteinase

  • breaks down aggrecan, no water can be held in the cartilage = cartilage damage
21
Q

which is more common: OA or RA

A

OA - less than 1% of the population suffer with RA

22
Q

is RA sex biased?

A

yes - women are 2-3x more likely to suffer RA

23
Q

name some ethnic groups with a lower prevalence of RA

A

Chinese and japanese

24
Q

what is the typical age of onset for RA

A

40-60 years old

25
how long does RA take to develop
typically over several months but in 15% of cases it can happen within 1 week
26
what gene is associated with 30% of the risk of RA
HLA-DRB1
27
what is the role of HLA-DRB1
encodes part of the HLA complex which is involved in distinguishing self from non-self
28
name a polymorphism that can act as a risk factor for several autoimmune diseases
PTPN22
29
name 2 environmental risk factors for RA
higher BMI - over 25 increases the risk by 15% smoking
30
how much increased is the risk for RA in males who smoke compared to females
males who smoke 2X increased risk females = 1.3X increased risk
31
what does the scientific community postulate to be a trigger of RA
both viral and bacterial infections
32
what is a medical mystery in RA
some people get spontaneously better!!
33
what does SADMD stand for
slow acting disease-modifying drugs
34
give an example of SADMD
gold injections
35
give an example of an immunosuppressant
methotrexate
36
what is the risk of methotrexate
it is not targeted immune suppression - can lead patients vulnerable to infection and can increase the risk of tumour growth
37
describe the use of corticosteroids in RA
effective short term relief from symptoms potent anti-inflammatory drugs effectiveness is short term!!
38
what is the problem with corticosteroids
they are addictive and effectiveness is short term
39
how does infliximab work?
- soluble TNF alpha is prevented from binding and creating a pro-inflammatory cascade - transmembrane TNF alpha is marked for cell lysis via complement cascade - increases IL-10 to create an anti-inflammatory microenvironment