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C. Year 3: SBOM > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Rheumatoid arthritis (RA) is a common chronic inflammatory autoimmune disease characterised by an inflammation of the synovial joints leading to joint and periarticular tissue destruction. Does RA affect men or women more?

A
  • women
  • 3:1
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2
Q

Rheumatoid arthritis (RA) is a common chronic inflammatory autoimmune disease characterised by an inflammation of the synovial joints leading to joint and periarticular tissue destruction. 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?

1 - body produces immune response against self antigens
2 - bodies ability not to initiate an immune response against self-antigens
3 - bodies produces abnormal antibodies causing excessive secretion of IgE
4 - all of the above

A
  • 2 - bodies ability not to initiate an immune response against self-antigens
  • 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. 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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6
Q

Cytokines are cell signalling proteins that are able to activate the immune system. There are pro and anti-inflammatory cytokines. If there is an imbalance between pro and anti-inflammatory cytokines, is this good or bad?

A
  • bad
  • pro-inflammatory cytokines can dominate
  • in RA pro-inflammatory cytokines can dominate causing information
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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 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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10
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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11
Q

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

1 - T cells and macrophages
2 - T and B cells
3 - NK and neutrophils
3 - B cells and macrophages

A

2 - T and B cells

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12
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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13
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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14
Q

Erythrocyte sedimentation rate (ESR) is the time it takes for RBCs to fall to the bottom of a sample tube. ESR can be used to detect the presence of inflammation. If inflammation is high would we expect the ESR to be high or low?

A
  • low, which means RBCs fall quickly
  • a faster ESR indicates inflammation as inflammatory markers bind to RBCs and make cells heavier
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15
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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16
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?

1 - binds to pathogens and dying/dead cells
2 - accentuates phagocytosis
3 - activates the complement pathway
4 - all of the above

A

4 - all of the above

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17
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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18
Q

What are autoantibodies?

A
  • antibodies that target our own cells
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19
Q

Auto-antibodies are antibodies that react against self antigens due to a breakdown in immunological tolerance. 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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20
Q

Rheumatoid factor (RF) is an autoantibody, antibodies that target our own cells in the body. RF is 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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21
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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22
Q

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

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

A

3 - 60%

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23
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

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24
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
25
Q

Seronegative and positive relate to:

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

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

A
  • seropositive
26
Q

Τype II collagen and vimentin can get modified through a process called citrullination. Here the amino acid arginine found in these proteins is converted into another amino acid, citrulline. However, when this becomes pathological the proteins may be folded incorrectly and the bodies antibodies then target these abnormall folded proteins. In RA what test is performed to detect if there are autoantibodies present that target the abnormal citrulline proteins?

1 - argine levels
2 - RF antibodies
3 - anti-citrullinated peptide antibodies (ACPA)
4 - citrulline levels

A

3 - anti-citrullinated peptide antibodies (ACPA)

27
Q

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

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

A

2 - 98%
- ability of test to correctly identify those patients without RA

28
Q

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

A
  • ACPA
29
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
30
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

31
Q

Is RA or osteoarthritis a cartilage based disease?

A
  • osteoarthritis
32
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

33
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%

34
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

35
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

36
Q

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

A
  • increases
  • linked with hormones
37
Q

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

A
  • decreases
  • due to elevated hormones
38
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
- HLA-DR1 is also associated with RA

39
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

40
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

41
Q

In RA how long does morning stiffness generally last for?

1 - >1 hours
2 - >2 hours
3 - >5 hours
4 - >10 hours

A

1 - >1 hours
- RA joints are worse when they have been inactive and remain stiffer for longer
- <30 minutes means it is an inflammatory disease, such as osteoarthritis

42
Q

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

1 - swelling
2 - pain
3 - redness
4 - heat
5 - all of the above

A

5 - all of the above

43
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
44
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
45
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

> 1 joint affected and what score is used as to identify a patient who may have RA?

  • 0 - 2
  • 2 - 4
  • 4 - 6
  • > 6
A
  • > 6
46
Q

When looking at the affected joints in RA, are these unilateral of symmetrical?

A
  • symmetrical
  • joints on both sides are the equally affected
47
Q

In the foot which joint it typically affected?

1 - metatarsophalangeal joints
2 - subtalar joint
3 - tarsometatarsal joint
4 - tibiotalar joint

A

1 - metatarsophalangeal joints

48
Q

Patients with RA can experience extra-articular problems, one of which is nodules composed of macrophages and lymphocytes with a centre of necrosis. Where do these nodules NOT commonly occur?

1 - skin (elbows)
2 - lungs
3 - breast
4 - cardiac

A

3 - breast

49
Q

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

1 - just to be safe
2 - baseline measures to assess safety of RA medication
3 - assess for risk of hypersensitivity from medications
4 - all of ther above

A

2 - baseline measures to assess safety of RA medication
- medication can affect bone marrow, eGFR and the liver
- need to know baseline of patient and if it is safe to begin

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
- immunosuppressant

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

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

1 - bone marrow suppression
2 - increased risk of infection
3 - liver dysfunction
4 - all of the above

A

4 - all of the above

59
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)

C. Year 3: SBOM (39 decks)

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