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Year 2 MIS > Rheumatoid Arthritis- A Clinical Perspective > Flashcards

Rheumatoid Arthritis- A Clinical Perspective Flashcards

1
Q

Does RA affect men or women more?

A
  • women

- 3:1

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2
Q

What % of RA has been associated with genetic susceptabilty?

1 - 5%
2 - 20%
3 - 30%
4 - 50%

A

3 - 30%

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3
Q

RA is a breakdown in immunological tolerance. What does immunological tolerance mean?

A
  • bodies ability not to have an immune response against things that it should not have a response to (our own cells for example)
  • breakdown in immune tolerance means the immune system could react against self antigens
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4
Q

What are cytokines?

1 - signalling proteins
2 - immune cells
3 - growth factors

A

1 - signalling proteins

- able to activate immune system

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5
Q

Cytokines are cell signalling proteins that are able to activate the immune system. There are pro and anti-inflammatory cytokines. What happens if the balance between pro and anti-inflammatory cytokines is not balanced?

A
  • pro-inflammatory cytokines can dominate

- in RA pro-inflammatory cytokines can dominate causing information

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6
Q

Cytokines are cell signalling proteins that are able to activate the immune system. There are pro and anti-inflammatory cytokines. In RA what are the key pro-inflammatory interleukins that we need to be aware of?

1 - IL-6, IL-1, IL-4 and TGF-B
2 - IL-1. TNF-a, IL-13, IL-6
3 - IL-6, IL-1, IL-4 and TGF-B
4 - IL-6, IL-1, TNF-a and IL-17

A

4 - IL-6, IL-1, TNF-a and IL-17

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7
Q

What is the innate immune system?

A
  • 1st line non-specific immune system

- the skin is an example of this

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8
Q

The innate immune system is the 1st line defence. In RA what is the cell of the innate immune system that has been identified as a key effector?

1 - platelet
2 - mast cell
3 - macrophage
4 - natural killer cell

A

3 - macrophage

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9
Q

The innate immune system is the 1st line defence. In RA what is the cell of the innate immune system that has been identified as a key effector?

1 - platelet
2 - mast cell
3 - macrophage
4 - natural killer cell

A

3 - macrophage

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10
Q

The innate immune system is the 1st line defence. In RA macrophages are a cell of the innate immune system that has been identified as a key effector. Macrophages are able to phagocytose antigens and trigger an immune response through antigen presentation. What pro-inflammatory cytokines are macrophages able to produce?

1 - IL-1, IL-6 and TNF-a
2 - IL-6, TNF-a and TGF-B
3 - IL-1, IL14 and TNF-a
4 - IL-6, IL-14 and TNF-a

A

1 - IL-1, IL-6 and TNF-a

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11
Q

A number of therapies in RA target macrophage number. What does the level of macrophage relate to in terms of treatments?

1 - disease severity
2 - treatment response
3 - prescience of disease but not severity

A

2- treatment response

- this drives clinical outcomes

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12
Q

What are the 2 key cells of the adaptive/specific immune system?

A
  • T and B cells
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13
Q

T cells are part of the adaptive/specific immune system. What type of T cell has been identified to be raised within synovium and able to activate osteoclasts, favouring cartilage reabsorption?

1 - Th-17
2 - Th- 4
3 - Th-10
4 - Th- 2

A

1 - Th-17

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14
Q

Which cell of the immune system is able to produce antibodies?

1 - monocytes
2 - T cells
3 - macrophages
4 - B cells

A

4 - B cells

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15
Q

Erythrocyte sedimentation rate (ESR) is a blood test performed to detect the presence of inflammation. What is the ESR test?

A
  • time taken for RBCs to fall to the bottom of a tube
  • normally this is slow
  • a faster ESR indicates inflammation as inflammatory markers bind to RBCs
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16
Q

Erythrocyte sedimentation rate (ESR) is a blood test performed to detect the presence of inflammation. ESR is the time taken for RBCs to fall to the bottom of a tube forming a sediment, which is normally. A faster ESR indicates inflammation, why is this?

A
  • RBCs contain certain proteins (such as fibrinogen or immunoglobulins, which are increased in inflammation)
  • RBCs are therefore heavier and fall faster
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17
Q

What is C reactive protein?

1 - protein signalling molecule
2 - inflammation inducing protein
3 - pattern recognition receptor (opsonin)
4 - pattern associated molecular receptor

A

3 - pattern recognition receptor (opsonin)

  • specifically it is classed as a pentraxin produced by hepatocytes during inflammation
  • released by the liver in response to IL-6
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18
Q

C reactive protein (CRP) are pentraxins which are classed as opsonins released by the liver in response to IL-6 and inflammation. What is the function of CRP?

A
  • binds to pathogens and dying/dead cells

- accentuates phagocytosis and activates the complement pathway

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19
Q

C reactive protein (CRP) are pentraxins which are classed as opsonins released by the liver in response to IL-6 and inflammation. CRP is able to bind pathogens and dying/dead cells, accentuating phagocytosis and activating the complement pathway. How does it bind to phagocytic cells and the complement system?

1 - Fc receptors
2 - Fab regions of antibodies
3 - hinge junction of antibodies
4 - Fab receptors

A

1 - Fc receptors

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20
Q

What are autoantibodies?

A
  • antibodies that target our own cells
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21
Q

What are the 2 autoantibodies that can be measured to detect the risk of RA?

1 - RF and anti Cyclic citrullinated peptide (anti-CCP)
2 - IL-6 and Cyclic citrullinated peptide (anti-CCP)
3 - RF and CRP
4 - RF and FGF-B

A

1 - RF and Cyclic citrullinated peptide (anti-CCP)

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22
Q

Rheumatoid factor (RF) is an autoantibody, antibodies that target our own cells in the body. RF are able to bind with what portion of other antibodies, mainly IgG and IgM?

1 - hinge region
2 - Fc portion
3 - Fab portion
4 - antigen binding site

A

2 - Fc portion

- fab région wil bind with antigens

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23
Q

When RF autoantibodies are present they bind with the Fc portion of IgG and IgM antibodies and form what?

1 - antigen-immunoglobulin complex
2 - immune complexes
3 - B cell activated complexes
4 - T cell activated complexes

A

2 - immune complexes

- these can then go on to clump together and damage tissue

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24
Q

What % of patients with RA have elevated levels of RF?

1 - 10%
2 - 40%
3 - 60%
4 - 100%

A

3 - 60%

25
Q

What is the specificity, the ability of a test to correctly identify people without the disease of RF in RA and is RF specific to RA?

1 - 100%
2 - 86%
3 - 55%
4 - 45%

A

2 - 86%

- can be present in other autoimmune diseases and healthy patients, so not specific to RA

26
Q

Peptides and proteins can undergo citrullination, which is a normal function in the human body. However, when this becomes pathological the proteins may be folded incorrectly and the bodies antibodies then target these proteins. In RA what test is performed to detect if there are autoantibodies present that target the abnormal citrulline proteins?

A
  • anti-citrullinated peptide antibodies (ACPA)
27
Q

What does seronegative and seropositive relate to?

A
  • seropositive = RF and/or anti CCP is present with symptoms

- seronegative = RF and/or anti CCP is not present with symptoms

28
Q

Do patients that are seronegative or seropositive tend to have a more severe form of RA?

A
  • seropositive
29
Q

In RA what is the specificity of anti-citrullinated peptide antibodies (ACPA)?

1 - 50%
2 - 98%
3 - 65%
4 - 86%

A

2 - 98%

- able to accurately identify people without a disease

30
Q

Do patients with anti-citrullinated peptide antibodies (ACPA), seronegative or RF have a more aggressive form of RA prognosis?

A
  • ACPA
31
Q

If a patient has elevated anti-citrullinated peptide antibodies (ACPA) does it mean that they will go on to develop RA?

A
  • no

- requires other factors, potentially pre-existing joint damage

32
Q

In rheumatoid arthritis what is the first component in joints that are affected?

1 - Cartilage
2 - Bone
3 - Synovium (inner surface of synovial joints)
4 - menisci

A

3 - Synovium

- RA is a synovium based disease

33
Q

Is RA or osteoarthritis a cartilage based disease?

A
  • osteoarthritis
34
Q

Which population has the highest incidence of RA?

1 - North Americans
2 - British white
3 - USA native Americans
4 - Spanish

A

3 - USA native Americans

35
Q

What is the % risk of developing RA in monozygotic twins?

1 - 12-15%
2 - 20-25%
3 - 35-45%
4 - 100%

A

1 - 12-15%

36
Q

Although women are more likely to develop RA (3:1), men with a low level of what hormone have an increased risk of developing RA?

1 - thyroid stimulating hormone
2 - testosterone
3 - estrogen
4 - cortisol

A

2 - testosterone

37
Q

What can often happen to women with RA during pregnancy?

1 - RA symptoms become worse
2 - nothing happens to RA
3 - remission of RA
4 - develop osteoarthritis alongside RA

A

3 - remission of RA

38
Q

In women with early menopause, does their risk of RA increase of decrease?

A
  • increases

- linked with hormones

39
Q

In women using oral contraception, does their risk of RA increase of decrease?

A
  • decreases
40
Q

What is one of the most common modifiable risk factors that we know has a direct link with RA?

1 - oral contraception
2 - beer
3 - smoking
4 - exercise

A

3 - smoking

- HLA-DR4 alleles with encodes the MHC-II molecules

41
Q

What age does RA generally peak in?

1 - 20-30 y/o
2 - 40-60 y/o
3 - 65-76 y/o
4 - >75 y/o

A

2 - 40-60 y/o

42
Q

In RA what joints are affected in the hand?

1 - PIP and DIP
2 - DIP and MCP
3 - wrist and PIP
4 - PIP and MCP

PIP = proximal interphalangeal joints
DIP = distal interphalangeal joints
MCP = metacarpophalangeal joints
A

4 - PIP and MCP

43
Q

In RA how long does morning stiffness generally last for?

A
  • > 1 hour

- >1 hour means it is an inflammatory disease

44
Q

What can be seen and felt at the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands in RA?

A
  • swelling
  • pain
  • redness
  • heat
45
Q

A swan neck deformity is common in RA, the the fingers resemble a swans neck. There is hyperextension of the proximal interphalangeal joint and flexion of the distal interphalengeal joint. Why does this occur in RA?

A
  • extensor tendons and ligaments are damaged due to damage at the PIP and MCP joints
  • PIP and DIP do opposite functions
46
Q

A Boutonniere deformity is common in RA, which is where there is flexion of the proximal interphalangeal joint and hyperextension of the distal interphalengeal joint. Why does this occur?

A
  • extensor tendons and ligaments are damaged due to damage at the PIP and MCP joints
  • PIP and DIP do opposite functions
47
Q

We know that in RA patients can present with Boutonniere and swan neck deformities. This is where PIP and DIP, which generally do the same movements controlled by the lumbricals, do opposite movements in these deformities, where DIP does flexion, the PIP will hyperextend and vice versa. What does the mnemonic below mean in relation to these deformities relative to the PIP joint?

  • Boy Friend = BF
  • Sing Hallelujah = SH
A
  • BF = Boutonniere and Flexion of PIP (DIP will hyperextend)

- SH = Swan and Hyperextension of PIP (DIP will flex)

48
Q

The ACR/EULAR classification system uses the following to identify if a patient does or does not have RA:

  • joint distribution
  • serology (blood markers)
  • symptom duration
  • acute phase reactant

What score is used as to identify a patient who may have RA?

  • 0 - 2
  • 2 - 4
  • 4 - 6
  • > 6
A
  • > 6
49
Q

If a patient presents with symptoms that suggest a patient has RA, what blood tests that should be performed?

1 - RF, FBC, ESR, CRP and anti-CCP
2 - FBC, CK, ESR, CRP and anti-CCP
3 - RF, IL-6, ESR and anti-CCP
4 - RF, FBC, ESR, CK and anti-CCP

A

1 - RF, FBC, ESR, CRP and anti-CCP

50
Q

If a patient presents with symptoms that suggest they have RA and they are started on medication, why would a FBC, kidney and liver function be performed straight away?

A
  • need to know baseline and if safe to begin

- medication can affect bone marrow, eGFR and the liver

51
Q

If a patient presents with symptoms that suggesting that they have RA, blood tests will be performed including RF, FBC, liver and kidney function, ESR, CRP and anti-CCP. What imaging modality can be useful as well?

1 - MRI
2 - CT-scan
3 - X-ray
4 - PET-scan

A

3 - X-ray and/or MRI

- look at joint space and bone deformities

52
Q

In RA bone can be eroded if treatment is delayed or is ineffective. Can this bone be regained?

A
  • no

- loss of bone affects function

53
Q

Is X-ray always useful when diagnosing RA?

A
  • no
  • early on the scan may appear normal
  • useful if disease pathology is present
54
Q

What is generally the 1st line treatment for RA?

1 - Disease-modifying anti-rheumatic drugs (DMARDs) - Methotrexate
2 - non-steroidal drugs
3 - aspirin
4 - corticosteroids

A

1 - Disease-modifying anti-rheumatic drugs (DMARDs) - Methotrexate

55
Q

If a patient has RA and is already on disease-modifying anti-rheumatic drugs (DMARDs), namely Methotrexate. What drugs can be given to help with flare ups?

1 - paracetamol
2 - non-steroidal drugs
3 - aspirin
4 - corticosteroids

A

2 - non-steroidal drugs for short periods

56
Q

The 1st line treatments for RA are disease-modifying anti-rheumatic drugs (DMARDs). What is the core drug from this list that we need to know?

1 - methotrexate
2 - sulfasalazine
3 - hydroxychloroquine
4 - leflunomide

A

1 - methotrexate

57
Q

The 1st line treatments for RA are disease-modifying anti-rheumatic drugs (DMARDs). The core drug is methotrexate, but other drugs include sulfasalazine, hydroxychloroquineand leflunomide. If DMARDs are not successful patients can be prescribed Biologic Agents, such as anti-B, anti-T and anti-TNF-a. How many DMARDs do patients need to have tried prior to being prescribed Biologic Agents?

1 - can go straight to Biologic Agents
2 - >4 drugs
3 - >3 drugs
4 - >2 drugs

A

4 - >2 drugs

58
Q

What are the major side effects of Disease Modifying Anti-Rheumatic Drugs?

A
  • bone marrow suppression
  • increased risk of infection
  • liver dysfunction

Year 2 MIS (48 decks)

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