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Patho > RA > Flashcards

RA Flashcards

0
Q

What are the causes of RA?

A
  1. Genetics (non-modifiable)
  2. Smoking (modifiable)
  3. Infection
    • infection may activate inflammation pathway that “prime” the development of RA
  4. Autoimmunity
    • RF found in the blood
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1
Q

Why is mortality 30% higher in RA?

A

because of systemic effects

  • heart
  • eyes
  • lungs
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2
Q

What does anti-CCP tell us about RA?

A
  • It is an important marker for the diagnosis and prognosis of RA
  • just as sensitive, but more specific that RF
  • important in early detection, even prior to RA (family marker)
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3
Q

What does ANA stand for?

What is it used for?

A
  • antinuclear antibody
  • used as a general test to evaluate a patient for autoimmune disorders
  • used to rule out other autoimmune disorders
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4
Q

What is ESR and CRP used for?

Which is better?

A
  • detects the degree of inflammation in the body

- CRP has better indication of the actual amount of inflammation

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5
Q

What is the synovial membrane?

A
  • thin layer of connective tissue (1-3 cell layers thick)

- found between the joint capsule and synovial cavity

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6
Q

What is synovial fluid?

What is it composed of?

A
  • ultrafiltrate of blood that crosses the synovial membrane into the joint cavity

Composed of:
Hyaluronan - regulates cartilage viscosity
Lubrican - lubricates surface of cartilage

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7
Q

What is fibronectin?

A
  • it is the glue that holds the collagen cells together in the cartilage
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8
Q

What cells produced synovial fluid (hyaluronan and lubrican)?

A

synoviocytes

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9
Q

What is pannus formation?

A
  • growth of fibrous tissue in the joint

- causes loss of bone and erodes cartilage

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10
Q

What is present in the synovial fluid in RA patients?

A
  • activated inflammatory immune system activated cells
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11
Q

What are inflammatory immune system activated cells?

A

fibroblast-like synoviocytes
macrophage-like synoviocyes
macrophages
B and T cells

  • all mediators of inflammation
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12
Q

What are osteoclasts?

A
  • cells that promote the breakdown of bone

- stimulated by immune response

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13
Q

Fibroblasts are stimulated by the immune system.

What do they cause?

A
  • pannus formation (leading to loss of cartilage and bone)
  • matrix metalloproteinases (degradation of bone matrix)
  • pro-inflammatory cytokines
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14
Q

What does the activation of T cells cause in RA?

A
  • productions of PGs, cytokines and cytotoxins
  • release of cytokines, matrix metalloproteinases (bone degradation), osteoclasts and B cells (Abs –> cartilage phagocytosis)
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15
Q

What is IL-6?

How does it contribute to RA?

A
  • IL-6 is the most abundant cytokine in the synovium of RA pts

Causes:

  • stimulation of liver reactants, osteoclast, B cells, T cells
  • correlated with increased disease activity
  • anemia of chronic disease
16
Q

What are the 3 ways B cells affect RA?

A
  1. Activated ABs
    - RF
    - anti-CCP
    - ANA
  2. Stimulate cytotoxin and free radical release
    - damages synovium and bone
    - phagocytosis of cartilage and bone –> more inflammation
  3. Activates T cells
    - positive feedback loop between humoral and cellular immune responses
    - releases pro-inflammatory cytokines (IL-1, IL-6, TNF alpha)
17
Q

Describe the clinical symptoms of RA?

A
  • symptoms progress over months
  • pain/stiffness usually presents in 1-2 joints (eventually moves to 5+)
  • symmetrical, hot swollen joints
  • subcutaneous nodules
  • pain >1 hour after waking (lasts all day)
  • systemic complaints (fatigue, weakness, low fever, low appetite, depression)
18
Q

Which joints are the most affected in RA?

A
  • hands (PIPs and DIPs)
  • wrists (MCP)
  • shoulders
  • neck
  • feet
19
Q

If you did a blood platelet test in a RA pt, what would you find?

A
  • thrombocytosis (too many platelets)

- risk of blood clots/CV event

20
Q

What could a joint radiograph show in a RA pt?

A
  • peri-articular osteoporosis
  • joint space narrowing
  • erosions
21
Q

What are the 5 extra-articular effects of RA?

A
  1. rheumatoid nodules
  2. cardiopulmonary disease
    • pericarditis
    • atherosclerosis…from chronic inflammation
  3. eye diseases
    • episcleritis
  4. sjogren’s syndrome
    • dry eyes and mouth
  5. rheumatoid vasculitis
    • digital finger infarction (black finger)
22
Q

75-80% of pts with RA have a _____________ disease course

A

cyclic-type

23
Q

why are steroids dangerous for RA patients?

A
  • they deplete bone of their calcium

- make patient’s bone weak and brittle

24
Q

What are the 3 mechanisms in which biologic DMARDS work?

A
  1. interfere with cytokine function
  2. inhibit T cell activation
  3. deplete B cells –> reduce self-ABs
25
Q

What are the 2 steps required for T cell activation?

A
  1. presentation of APC (antigen-presenting cell) to T cell receptor
  2. co-stimulation of these cells acts as T cell “on switch”

Patho (15 decks)

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