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Rheumatiod Arthritis 1 (SD) Flashcards

1
Q

What type of disorder is RA?

A

chronic autoimmune inflammatory disorder

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2
Q

Where does RA occur?

A

within synovial joints

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3
Q

symptoms of RA

A

pain
swelling
stiffness
joint erosion and destruction

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4
Q

What other places does RA affect? (inflammation elsewhere)

A 
blood vessels
bone marrow
GI tract
lungs
eyes
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5
Q

What causes mortality with RA?

A

cardiovascular disease

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6
Q

When is symptom onset of RA?

A

> 25 years of age

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7
Q

male:female

A

1:2.7

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8
Q

swelling

A

synovial tissue in caps of joints becomes damaged causing tissue to thicken and swell

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9
Q

stiffness

A

inflammed joints stiffen and are difficult to move correctly
especially in mornings or after long rest
can last for hours

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10
Q

pain

A

cartilage and bone within the joints will wear down over time
muscles, ligaments and tendons weaken and no longer stabilise joints
causes intense pain and joint damage

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11
Q

redness

A

joints can be warm

may appear pink/red on the outside during flare/when inflammed

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12
Q

What are the 3 bones in the finger called?

A

distal phalanx
middle phalanx
proximal phalanx

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13
Q

What are the 3 joints in the fingers called?

A

distal interphalangeal joint - DIP
proximal interphalangeal joint - PIP
metacarpophalangeal joint - MCP

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14
Q

symptoms in early stage RA

A

ulnar deviation - hand less straight, inflammation in metacarpal region
boutonniere deformity - DIP hyperextended and PIP flexed (bend)
swan-neck deformity - DIP flexed and PIP hyperextended

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15
Q

healthy bone/joint

A

articular cartilage provides a lubricated surface for the opposing bones
synovial membrane produces/contains synovial fluid
synovial fluid provides lubrication and removes debris

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16
Q

What are autoantigens?

A

antigens produced by the body that are attacked by the immune system

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17
Q

What do autoantigens cause?

A

an immune response

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18
Q

What genes regulate the immune system?

A

human leukocyte antigen (HLA)

genes on chromosone 6

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19
Q

What are HLA genes part of?

A

MHC 1 and MHC 2 complex

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20
Q

at risk patients related to HLA genes

A

patients with alterations to HLA-DR1 and HLA-DR4 alleles at increased risk of RA

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21
Q

mutation of what is involved in activation of inflammatory cells

A

PTP2N22 mutation
-> encodes the protein tyrosine phosphatase
involved in the activation and control of inflammatory cells, including T cells

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22
Q

What is produced that is thought to be an environmental factor for RA?

A

environmental arthritogen

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23
Q

What environmental factors may cause RA?

A 
viruses
gut bacteria
smoking
gum disease
obesity
diet
citrullinated proteins
-> lead to autoantigen generation
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24
Q

What is citrullination?

A

citrullination is a post translational conversion of arginine to citrulline in proteins by an enzyme called PAD

-> Peptidyl Arginine Deminiase

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25
citrullination of proteins in RA
- this becomes disregulated in RA - lead to alterations of proteins in the synovium - the protein AA sequence is changed - the immune system thinks this protein is not normal, thinks it's a foreign protein - the immune system attacks these protiens - it can lead to autoantigens being formed which are then no longer recognised as self antigens by the immune system - anti-citrullinated protein antibodies (ACPA) are produced that attact these proteins
26
How does periodontal infection/gum disease cause RA?
gum disease releases PAD enzymes at sites of infection this causes citrullination of bacterial and human proteins activates ACPA production
27
How does smoking cause RA?
PAD is released from inflammation, apoptosis and necrosis in the lungs citrullination of proteins ACPA production
28
What is MHC?
major histocompatibility complex
29
What does MHC complex do?
binds antigens presents antigens to T cells to activate the immune response (destroyed)
30
What does MHC contain that can cause RA?
HLA complex HLA-DRbeta1 contains a binding site of the arthritogen that initiates the inflammatory synovitis - alterations in genetics that cause RA
31
What is synovitis?
inflammation of the synovial joint/fluid
32
example of an auto-antigen
citrullinated protein
33
What is activated when an auto-antigen is detected?
``` T helper cells activated they activate B cells B cells produce antibodies fibroblast like synoviocytes activated macrophages activated ```
34
Why do auto-antigens activate the cells of an immune response?
it thinks it's a foreign body doen't know it's our own cells it it attacking it
35
How does destruction occur?
- T helper cells activate fibroblast like synoviocytes and macrophages - these activate osteoclasts, pannus, somatic mutations, proteases
36
What are osteoclasts?
cells that break down bone
37
What are cytokines?
small secreted proteins relesaed by cells that have a specific effect on the interaction and communications between cells (cause a biological effect)
38
What do cytokines bind to?
cytokine receptors
39
What do cytokines regulate?
innate and adaptive immune system | process of inflammation
40
Why do we block cytokines in RA?
to block the immune response/inflammation/RA
41
autocrine cytokines
feed back onto themselves
42
paracrine cytokines
affect nearby cells and activate them
43
endocrine cytokines
released into the bloodstream, circulate and activate cells elsewhere
44
main cytokines for RA
interleukins: IL-1, IL-6 interferons: INF-gamma tumour necrosis factors: TNF-alpha
45
antigen presentation
1. antigen binds to APC (antigen presenting cell) 2. APCs couple to T cells 3. T cells release cytokines IFN gamma, IFN17 4. T cells recruit macrophages and B cells 5. macrophages release cytokines TNF-alpha, IL1, IL6 6. T cells, macrophages, B cells attack the invader/bacteria and destroy it 7. synovial cells release MMPs and RANKL
46
What does an RA joint look like?
- synovial membrane is inflammed - thick pannus - bone and cartilage is eroded - macrophages release cytokines (TNF alpha, IL1, IL6) - increased fibroblast like synoviocytes - macrophage like synovicytes (MLS) line the membrane
47
another name for APC
dendritic cell
48
What is a the pannus?
``` inflammed synovial membrane contains: - osteoclasts - macrophages - T cells - dendritic cells (APC) - B cells - leukocytes - plasma cells ```
49
What does IL-1 induce?
inflammation
50
What does IL-6 stimulate?
osteoclast stimulation
51
Where are fibroblast like synoviocytes located?
they line the RA joint
52
Where are macrophage like synoviocytes located?
the line the membrane
53
What do macrophage like synoviocytes (MLS) do?
proliferate in response to cytokines | produce RANKL
54
What stimulates the release of fibroblast like synoviocytes (FLS)?
IL-1 TNF (from macrophages)
55
What doe FLS (fibroblast like synoviocytes) release?
cytoines | RANKL
56
What does RANKL do?
stimulates osteoclasts which degrade bone
57
What can the pannus lead to?
scar tissue cartilage damage bone erosion
58
diagosis of RA
- FH - pain Hx and examination of joints - blood tests - scans: x-rays, ultrasound, MRI (determines if RA is the cause of erosion)
59
What blood tests are done to diagnose RA?
positive Rheumatoid Factor (RF) positive anti-cyclic citrullinated peptide (anti-CCP) high erythrocyte sedimentation rate (ESR) positive c-reactive protein (CRP)
60
How does RA decrease life expectancy?
decreases life expectancy by 3-7 years
61
other problems caused by RA
heart disease infection GI bleeding
62
factors for poor prognosis
``` causasians women patients with subcutaneous nodules advanced age at onet inflammation >20 joints early erosion smoking high ESR high levels of RF high anticyclic cirtullinated protein ```
63
What causes other problems like CV/CNS/liver with RA
IL-6 that goes into the bloodstream
64
CNS affects of RA
depression | fatigue
65
CV affects of RA
accelerated CVD | increased myocardial electric instability
66
affects on adipose tissue of RA
insulin resistance
67
affects RA can have on the liver
anaemia

PHA223 (43 decks)

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