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354: Pathobiology > 7. Rheumatoid Arthritis > Flashcards

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
Q

how long does RA take to develop

A

typically over several months
but in 15% of cases it can happen within 1 week

26
Q

what gene is associated with 30% of the risk of RA

A

HLA-DRB1

27
Q

what is the role of HLA-DRB1

A

encodes part of the HLA complex which is involved in distinguishing self from non-self

28
Q

name a polymorphism that can act as a risk factor for several autoimmune diseases

A

PTPN22

29
Q

name 2 environmental risk factors for RA

A

higher BMI - over 25 increases the risk by 15%

smoking

30
Q

how much increased is the risk for RA in males who smoke compared to females

A

males who smoke 2X increased risk
females = 1.3X increased risk

31
Q

what does the scientific community postulate to be a trigger of RA

A

both viral and bacterial infections

32
Q

what is a medical mystery in RA

A

some people get spontaneously better!!

33
Q

what does SADMD stand for

A

slow acting disease-modifying drugs

34
Q

give an example of SADMD

A

gold injections

35
Q

give an example of an immunosuppressant

A

methotrexate

36
Q

what is the risk of methotrexate

A

it is not targeted immune suppression - can lead patients vulnerable to infection and can increase the risk of tumour growth

37
Q

describe the use of corticosteroids in RA

A

effective short term relief from symptoms
potent anti-inflammatory drugs
effectiveness is short term!!

38
Q

what is the problem with corticosteroids

A

they are addictive and effectiveness is short term

39
Q

how does infliximab work?

A
  • 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

354: Pathobiology (10 decks)

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