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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
what is fibronectin?
general cell adhesion molecule that acts like glue to hold collagen together than make up the cartilage
26
what are two hallmark characteristics of RA?
pannus formation | inflammatory mediators present in synovial fluid but no infection
27
what is pannus formation?
thickened cellular membrane of fibrovascular tissue that invades the underlying cartilage bone, causing loss of bone and cartilage erosion
28
what feature of RA is caused by pannus formation?
joint nodules
29
what are the immune system activated cells found in the synovial fluid in RA?
fibroblast-like synoviocytes macrophage-like synoviocytes T cells B cells
30
how do inflammation mediators get into the joint?
enter joint via ultrafiltrate of blood that diffuses from the synovial membrane and into joint cavity
31
what role do neutrophils play in RA?
damage hyaluronic acid and the joint
32
what is the first step in RA pathophys?
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
What is the second step in RA pathophys?
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
what is the 3rd step in RA pathophys?
macrophages stimulated by the immune response can stimulate T cells and osteoclasts to promote inflammation
35
how do macrophages contribute to RA pathophysiology?
major producers of proinflammatory cytokines; can also stimulate fibroblasts which produce matrix metalloproteinases to degrade bone matrix and produce proinflammatory cytokines
36
what is the 4th step in RA pathophys?
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
what is the 5th step in RA pathophys?
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
what does T cell activation result in?
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
what are two steps required for T cell activation?
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
what is the most abundant pro-inflammatory cytokine in the synovium?
IL-6
41
what does cytokine activation lead to?
stimulation of the synthesis of acute-phase reactants from liver, osteoclasts, T-lymphoctes, and B-lymphocytes
42
What are 3 ways B cell activation affects RA?
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
What is the clinical presentation of RA?
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
what is the criteria for RA diagnosis?
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
what are the most common joints affected by RA?
``` hands (PIP joint, MCP joint, MTP joint) wrists feet shoulders neck ```
46
what are the consequences of long term RA with no exercise?
loss of range of motion atrophy of muscles weakness deformity
47
What are some things to test for that can be done to diagnose RA?
``` Iron Anti-CPP ESR - elevated ANA CRP - elevated (second best) Blood platelets RF ```
48
Why would testing for iron be useful in RA diagnosis?
absorption of iron is inversely correlated with ESR and CRP, resulting in Normocytic normochromic anemia
49
why would testing for blood platelets be useful in RA diagnosis?
thrombocytosis is common in RA, meaning there are too many platelets in the bloodstream, increasing the risk of blood clots and CV event
50
why is anti-CPP the best thing to test for?
highly specific and sensitive | may be detected up to 15 years before onset of RA symptoms
51
What are 5 non-pharm treatment options for RA patients?
``` rest occupational therapy/physical therapy assistive devices (canes, walkers, splints, etc) wt loss surgery (in severe cases) ```
52
why is rest important in RA treatment?
reduces pain
53
why is wt loss important in RA?
reduces joint stress
54
what are 3 classes of drugs that can be helpful in RA treatment?
NSAIDs Corticosteroids Disease-modifying anti-rheumatic drugs (DMARDs)
55
what are NSAIDs used for in RA?
analgesia and inflammation (no affect on disease progression) decrease prostaglandin synthesis
56
how do corticosteroids help in RA treatment?
decrease inflammation and immunosuppression
57
how do DMARDs help in RA treatment?
suppress cellular and humoral immune system responses | modify the course of the disease and improve prognosis
58
how do biologic DMARD agents work against RA? (3pts)
interfere with cytokine function inhibit the second signal or co-stimulation required for T cell activation Deplete B cell (decrease antibodies)
59
what is the difference between OA and RA in terms of joint pain?
OA - pain and swelling | RA - inflammation
60
what are two other diagnostic tests that could be used to diagose RA?
joint fluid aspiration | joint radiographs
61
how is joint fluid aspiration useful in diagnosing RA?
analysis of edematous fluid may show increased white blood cell count w/o infection
62
how are joint radiographs useful in diagnosing RA?
may show peri-articular osteoporosis, joint space narrowing, or erosiona
63
what are 5 systemic effects of RA?
1) rheumatoid nodules 2) cardiopulmonary disease 3) eye diseases 4) sjorgren's syndrome 5) rheumatoid vasculitis
64
what are rheumatoid nodules?
fibrous cells surrounding necrotic tissue centre | they are often painless and usually found on extensor surface of arm
65
what are two medical conditions that could result from cardiopulmonary disease?
pericarditis | atherosclerosis (leading cause of RA death)
66
why may you contract an eye disease from RA?
reduced tear production can result in chronic eye irritation (episcleritis)
67
what is sjorgen's syndrome?
exocrine glands that produce tears and saliva are destroyed, resulting in dry eyes(kertaoconjunctivitis sicca), dry mouth (xerostomia), and bad breath
68
what is rheumatoid vasculitis?
inflammation in other areas leads to reduced blood flow to finger tips, resulting in digital nail bed infarcts (black finger tips)
69
what are the three types of clinical courses for RA? which is most common?
cyclic type: flares with remission (most common) mild - stable and controlled severe/aggressive - poor response to treatments and can lead to early death
70
what is the role of cox-1 and cox-2 in RA and OA?
produce the prostaglandins

Applied Pathophysiology (11 decks)

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