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Applied Pathophysiology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis (RA)?

A

chronic inflammatory disease with possible periods of remission

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2
Q

What is usually inflamed with RA?

A

episclera (protective lining covering sclera)
RA nodules
RA joint swelling

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3
Q

What organs could RA potentially affect?

A

eyes
lungs
heart

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4
Q

what is the prevalence of RA in Canada?

A

1 in 100

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5
Q

who is affected by RA more, men or women?

A

women 3:1 men

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6
Q

What age is RA usually diagnosed? why?

A

25-50y.o

starts earlier because it’s an immune response, not a deterioration of body with age

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7
Q

Is RA hereditary?

A

NO

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8
Q

What are 4 risk factors associated with RA?

A

genetics
smoking
infection
autoimmunity

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9
Q

how does genetics play a role in RA?

A

not hereditary, but may predispose an individual as a result of environmental triggers

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10
Q

How does smoking play a role in RA?

A

increases RA development and severity

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11
Q

how does an infection play a role in RA?

A

may activate pathways that prime the development of RA

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12
Q

how does autoimmunity play a role in RA?

A

rheumatoid factor (RF; antigen-driven auto-antibodies) is an antibody detected in the blood of several RA patients

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13
Q

What are 4 auto-immune components you can test for to determine RA? Which is the best one to use?

A

anti-cyclic citrullinated peptide (anti-CCP) - best
anti-nuclear antibody (ANA)
erythrocyte sedimentation rate (ESR)
C Reactive protein (CRP)

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14
Q

what is anti-CCP used for?

A

a marker for diagnosis and prognosis of RA

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15
Q

what is ANA used for?

A

to evaluate a person for auto-immune disorders such as lupus, Sjorgren’s syndrome, MS, Hashimoto disease, and RA
used to rule out RA

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16
Q

what is ESR?

A

reflects the degree of inflammation in the body (better than ANA)

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17
Q

what is CRP?

A

indicates the amount of inflammation in the body (better than ESR)

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18
Q

what is the synovial membrane?

A

thin layer of connective tissue between joint capsule and synovial cavity with underlying interstitum containing blood vessels

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19
Q

what is the synovial fluid?

A

ultrafiltrate of blood that diffuses across the synovial membrane and into the joint cavity

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20
Q

what are the two main components of the synovial fluid?

A

hyaluronan

lubrican

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21
Q

what is the function of hyaluronan?

A

regulates cartilage viscosity

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22
Q

what is the function of lubrican?

A

lubricates cartilage surface

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23
Q

what cell produces synovial fluid? where can this cell be found in a normal joint?

A

synoviocytes

found on inner surfase of joint capsule

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24
Q

what is a key molecule in a normal joint?

A

fibronectin

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25
Q

what is fibronectin?

A

general cell adhesion molecule that acts like glue to hold collagen together than make up the cartilage

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26
Q

what are two hallmark characteristics of RA?

A

pannus formation

inflammatory mediators present in synovial fluid but no infection

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27
Q

what is pannus formation?

A

thickened cellular membrane of fibrovascular tissue that invades the underlying cartilage bone, causing loss of bone and cartilage erosion

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28
Q

what feature of RA is caused by pannus formation?

A

joint nodules

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29
Q

what are the immune system activated cells found in the synovial fluid in RA?

A

fibroblast-like synoviocytes
macrophage-like synoviocytes
T cells
B cells

30
Q

how do inflammation mediators get into the joint?

A

enter joint via ultrafiltrate of blood that diffuses from the synovial membrane and into joint cavity

31
Q

what role do neutrophils play in RA?

A

damage hyaluronic acid and the joint

32
Q

what is the first step in RA pathophys?

A

antigen presenting cell (APC) presents and process the antigen to the T cell, causing T cell (TH1) activation and proliferation and secretion of cytokines

33
Q

What is the second step in RA pathophys?

A

Activation of T cell stimulates B cells to produce plasma cells that produce self-antibodies (RF, ACPA) and osteoclasts to destroy and remove bone

34
Q

what is the 3rd step in RA pathophys?

A

macrophages stimulated by the immune response can stimulate T cells and osteoclasts to promote inflammation

35
Q

how do macrophages contribute to RA pathophysiology?

A

major producers of proinflammatory cytokines;
can also stimulate fibroblasts which produce matrix metalloproteinases to degrade bone matrix and produce proinflammatory cytokines

36
Q

what is the 4th step in RA pathophys?

A

activated T cells and macrophages release factors that promote tissue destruction and increase blood flow, resulting in cellular invasion in synovial tissue and joint fluid

37
Q

what is the 5th step in RA pathophys?

A

once activated, RASFs produce cytokines, chemokines and matrix degrading enzymes that mediate interaction with neighbouring inflammatory/endothelial cell, resulting in progressive destruction of articular cartilage and bone

38
Q

what does T cell activation result in?

A

1) production of prostaglandins, cytotoxins, and cytokines
2) release of inflammatory cytokines, matrix metalloproteinases, osteoclasts, and B cells leading to antibody formation that are involved in the phagocytosis of bone cartilage

39
Q

what are two steps required for T cell activation?

A

1) presentation of APC to the T cell receptor

2) CD28 (on T cell) binds to CD80/CD86 (on APC), ie the “on” switch

40
Q

what is the most abundant pro-inflammatory cytokine in the synovium?

A

IL-6

41
Q

what does cytokine activation lead to?

A

stimulation of the synthesis of acute-phase reactants from liver, osteoclasts, T-lymphoctes, and B-lymphocytes

42
Q

What are 3 ways B cell activation affects RA?

A

1) produces auto-antibodies (RF, anti-CCP, ANA)
2) stimulate cytotoxin and free radical release, resulting in synovial/bone damage
3) activate T cells (+ive feedback loop) to promote pro-inflammatory cytokine release

43
Q

What is the clinical presentation of RA?

A

1) Progressive symptoms
2) pain/stiffness beginning in 1-2 joints (hot, swollen joints), spreading to 5+ joints
3) pain persisting for more than 1hr after waking
4) systemic: fatigue, weakness, low-grade fever, loss of appetite, depression

44
Q

what is the criteria for RA diagnosis?

A

need 4 or more of the following for over 6 weeks:

1) morning joint stiffness lasting longer than an hour
2) soft tissue swelling of 3 or more joints
3) symmetric presentation (of peripheral joints)
4) subcutaneous nodules
5) +ive for RF and/or anti-CCP
6) radiologic evidence

45
Q

what are the most common joints affected by RA?

A 
hands (PIP joint, MCP joint, MTP joint)
wrists
feet
shoulders
neck
46
Q

what are the consequences of long term RA with no exercise?

A

loss of range of motion
atrophy of muscles
weakness
deformity

47
Q

What are some things to test for that can be done to diagnose RA?

A 
Iron
Anti-CPP
ESR - elevated
ANA
CRP - elevated (second best)
Blood platelets
RF
48
Q

Why would testing for iron be useful in RA diagnosis?

A

absorption of iron is inversely correlated with ESR and CRP, resulting in Normocytic normochromic anemia

49
Q

why would testing for blood platelets be useful in RA diagnosis?

A

thrombocytosis is common in RA, meaning there are too many platelets in the bloodstream, increasing the risk of blood clots and CV event

50
Q

why is anti-CPP the best thing to test for?

A

highly specific and sensitive

may be detected up to 15 years before onset of RA symptoms

51
Q

What are 5 non-pharm treatment options for RA patients?

A 
rest
occupational therapy/physical therapy
assistive devices (canes, walkers, splints, etc)
wt loss
surgery (in severe cases)
52
Q

why is rest important in RA treatment?

A

reduces pain

53
Q

why is wt loss important in RA?

A

reduces joint stress

54
Q

what are 3 classes of drugs that can be helpful in RA treatment?

A

NSAIDs
Corticosteroids
Disease-modifying anti-rheumatic drugs (DMARDs)

55
Q

what are NSAIDs used for in RA?

A

analgesia and inflammation (no affect on disease progression)
decrease prostaglandin synthesis

56
Q

how do corticosteroids help in RA treatment?

A

decrease inflammation and immunosuppression

57
Q

how do DMARDs help in RA treatment?

A

suppress cellular and humoral immune system responses

modify the course of the disease and improve prognosis

58
Q

how do biologic DMARD agents work against RA? (3pts)

A

interfere with cytokine function
inhibit the second signal or co-stimulation required for T cell activation
Deplete B cell (decrease antibodies)

59
Q

what is the difference between OA and RA in terms of joint pain?

A

OA - pain and swelling

RA - inflammation

60
Q

what are two other diagnostic tests that could be used to diagose RA?

A

joint fluid aspiration

joint radiographs

61
Q

how is joint fluid aspiration useful in diagnosing RA?

A

analysis of edematous fluid may show increased white blood cell count w/o infection

62
Q

how are joint radiographs useful in diagnosing RA?

A

may show peri-articular osteoporosis, joint space narrowing, or erosiona

63
Q

what are 5 systemic effects of RA?

A

1) rheumatoid nodules
2) cardiopulmonary disease
3) eye diseases
4) sjorgren’s syndrome
5) rheumatoid vasculitis

64
Q

what are rheumatoid nodules?

A

fibrous cells surrounding necrotic tissue centre

they are often painless and usually found on extensor surface of arm

65
Q

what are two medical conditions that could result from cardiopulmonary disease?

A

pericarditis

atherosclerosis (leading cause of RA death)

66
Q

why may you contract an eye disease from RA?

A

reduced tear production can result in chronic eye irritation (episcleritis)

67
Q

what is sjorgen’s syndrome?

A

exocrine glands that produce tears and saliva are destroyed, resulting in dry eyes(kertaoconjunctivitis sicca), dry mouth (xerostomia), and bad breath

68
Q

what is rheumatoid vasculitis?

A

inflammation in other areas leads to reduced blood flow to finger tips, resulting in digital nail bed infarcts (black finger tips)

69
Q

what are the three types of clinical courses for RA? which is most common?

A

cyclic type: flares with remission (most common)
mild - stable and controlled
severe/aggressive - poor response to treatments and can lead to early death

70
Q

what is the role of cox-1 and cox-2 in RA and OA?

A

produce the prostaglandins

Applied Pathophysiology (11 decks)

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