Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine 2.1 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is the normal response to infection?

A
  • Inflammation

- There will be acute or chronic response involving immune cells and you will eventually get resolution.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is an incorrect immune response significant?

A

-Incorrect immune response can lead to autoimmunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some examples of autoimmune disease?

A
  • Rheumatoid arthritis
  • Graves Disease
  • Diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why dont we all get autoimmune disease?

A
  • Immune system has regulatory checks

- We have a level of tolerance (controlled unresponsiveness to self) maintained by numerous control mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the symptoms of rheumatoid arthritis?

A
  • Widespread joint pain, stiffness and swelling leading to joint destruction
  • Fatigue
  • Weight loss
  • Fevers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some risk facotrs of rheumatoid arthritis?

A

-Females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is rheumatoid arthritis?

A

-Chronic inflammatory disorder of joints but can also affect the skin, lungs, blood vessels and more.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some commonly affected joints by RA?

A
  • Smaller joints; MCP, PIP, MTP

- Larger; shoulder, elbow, knees, ankles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the diagnostic tests for RA?

A
  • Blood tests; look out for increased rheumatoid factor and increased anti CCP antibody
  • Imaging; in Xray look for soft tissue sweilling, narrowed joint space, decrease in bone density, bony erosions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are possible treatments for RA?

A
  • DMARDS
  • Biologics
  • NSAIDS
  • Corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some examples of DMARDS and what do they do?

A
  • Methotrexate
  • Hyroxychloroquine
  • Sulfasazine
  • They supress inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some examples of biologics and what do they do?

A
  • Abatacept; supress T cells
  • Rituximab; supress B cells
  • Infliximab; blocks chemokines such as TNF
  • Anakinra; block IL1
  • Tocilizumab; blocks IL6
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Are single drugs better for RA treatment or combinations?

A

Combinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are biological agents?

A

-Drugs such as monoclonal antibodies, receptors or peptides, which have been developed rationally by targetting important processes in disease pathogenesis eg. cytokines, T-cells, B-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What needs to be considered when making therapeutics from immunological understanding?

A
  1. Define behaviour of molecular target
  2. Ask, does it participate in disease process
  3. Can it be effectively inhibited ex vivo or en vivo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is inhibiting TNF in RA significant?

A
  • TNF seen as major conductor of pathology in RA

- Ability to block cytokine signalling via its receptor

17
Q

What are biosimilars?

A

-Cheaper alternatives

18
Q

What is the issue with biosimilars of biologic agents?

A

-Still some uncertainities surrounding use as they are more complex than any other medicine

19
Q

What type of inhibition is more effective?

A

-Intracellular as it offers oppurtunity to inhibit multiple pathways

20
Q

What are the future of inhibitors?

A

-JAK inhibitors

21
Q

What is the genetic part of the pathophysiology of RA?

A

-There are certain susceptibility genes eg. HLA-DR1 and HLA-DR4

22
Q

What is the environmental part of pathophysiology of RA?

A
  • EG. cig smoke, pathogens

- This may lead to modifications to our own antigens eg. type II collagen, vimentin.

23
Q

What changes occur as a result of environmental and genetic triggers of RA?

A
  • Citrullination of arginine

- Due to susceptibility genes, these are no longer recognised as self antigens.

24
Q

What happens as a result of our genes not being recognised as self in RA?

A

-Antigen picked up by antigen presenting cell and taken to lymph nodes to activate CD4 cells which stimulate B cells to produce autoantibodies against self antigens.

25
Q

What happens after autoantibodies produced against self antigens?

A

-CD4 cells and autoantibodies enter circulation and go to joints.
They then secrete cytokines eg. interferon gamma and IL-17 to recruit macrophages.

26
Q

What happens when macrophages produced in joints for RA?

A
  • Produce more cytokines eg. TNF-alpha, IL-1, IL-6 which cause synovial cells to proliferate.
  • This forms a pannus (made of fibroblasts, myofibroblasts and inflammatory cells)
27
Q

What does the creation of the pannus lead to?

A

-Over time this can damage cartilage and other soft tissue.

Proteases may be secreted and destroy cartilage.

28
Q

What other things may cytokines cause in RA?

A

-More RANK-L on T cells which recruit osteoclasts

29
Q

What is an eg of an autoantibody produced in RA?

A

-Anti-CCP; targets citrullinated proteins to form immune complexes to activate complement system.

30
Q

How does RA also effect organs around the body?

A

-The cytokines escape and cause problems all over eg. artheroscleratic plagues in blood vessels.

Medicine 2.1 (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions