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BRS 5 Musculoskeletal > Introduction to Rheumatology > Flashcards

Introduction to Rheumatology Flashcards

1
Q

What is rheumatology?

A

A medical speciality dealing with diseases of the musculoskeletal system

Joints
Tendons
Ligaments
Muscles
Bones
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2
Q

What is a joint?

A

Where two bones meet

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3
Q

What is a tendon?

A

Cords of strong fibrous collagen tissue attaching MUSCLE TO BONE

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4
Q

What is a ligament?

A

Flexible fibrous connective tissue which connects BONE TO BONE

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5
Q

What is a fibrous joint?

A

A joint where there is no space between the bones

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6
Q

What is an example of a fibrous joint?

A

Bones of the skull

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7
Q

What is a cartilaginous joint?

A

Joints in which the bones are connected by cartilage eg spinal vertabrae

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8
Q

What are synovial joints, and an example?

A

Joints where there is space between the adjoining bones - known as the synovial cavity

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9
Q

What fills the synovial cavity?

A

Synovial Fluid

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10
Q

What are the three types of functional classifications of bones?

A

Synarthroses
Amphiarthroses
Diarthroses

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11
Q

What is meant by Synarthroses?

A

Joints with generally no movement

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12
Q

What is meant by amphiarthroses?

A

Joints which allow very limited movement

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13
Q

What is meant by diarthroses?

A

Joints which allow free movement of the joint

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14
Q

Which structural classification of joints correspond with diarthroses?

A

Synovial joints

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15
Q

Which functional classification of joints are both fibrous and cartilaginous joints associated with?

A

Synarthroses and Amphiarthroses

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16
Q

What are the three main components of the synovial joint?

A

Synovium
Joint cavity with synovial fluid
Articular cartilage

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17
Q

What is the synovium?

A

A 1-3 cell deep lining containing type A and type B synoviocytes

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18
Q

What are type A synoviocytes?

A

Macrophage-like phagocytic cells

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19
Q

What are type B synoviocytes?

A

Fibroblast like cells that produce hyaluronic acid

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20
Q

What is synovial fluid?

A

Hyaluronic acid-rich fluid which lubricates the joint and allows it to move smoothly

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21
Q

In what part of the synovial joint is type 1 collagen found?

A

Synovium

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22
Q

In which part of the synovial joint is type 2 cartilage found?

A

Articular cartilage

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23
Q

What is the articular cartilage made of?

A

Proteoglycans (aggrecans) and Type 2 collagen

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24
Q

What are the specialised cells found in cartilage called?

A

Chondrocytes

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25
Q

What is cartilage composed of?

A
  • Chondrocytes
  • ECM (water, collagen and proteoglycans)
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26
Q

Does cartilage have a blood supply?

A

NO

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27
Q

Why does cartilage heal poorly after injury?

A

It has no blood supply (avascular)

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28
Q

Label this diagram

A
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29
Q

What is aggrecan?

A
  • A proteoglycan with many chondroitin sulfate and keratin sulfate chains
  • Interacts with hyaluronan to form larger proteoglycan aggregates
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30
Q

What are the two major divisions of arthritis?

A

Osteoarthritis and Inflammatory arthritis (RA)

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31
Q

What are the pathological changes associated with OA?

A

Cartilage is worn out and attempts are made at bony remodelling, leading to spurs (bony projections)

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32
Q

What is OA?

A
  • Long-term chronic disease
  • Articular cartilage in joints deteriorates
  • Results in bones rubbing together, creating stiffness, pain and impaired movement
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33
Q

When does inflammation occur in OA?

A

Late in disease (whereas RA starts with inflammation)

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34
Q

Describe the onset of OA?

A

Gradual, slowly progressing disorder

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35
Q

How does age affect OA?

A

Increases as age increase

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36
Q

What are the three joint most commonly affected with OA?

A

Joints of hands
Spine
Weight-bearing joints of lower limbs

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37
Q

Which joints of the hands are most commonly affected with OA?

A

DIP - Distal interphalangeal joints (First joint in finger)
PIP - Proximal Interphalangeal Joints (Second joint in finger)
CMC - First Carpometacarpal joint (Thumb joint)

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38
Q

Which weight-bearing joints of the lower limbs are most commonly affected with OA?

A

Knees, Hips

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39
Q

Signs and Symptoms of OA? PRICES

A 
Pain
Range of motion is limited
Instability
Crepitus
Enlargement of joint
Stiffness
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40
Q

What is crepitus of a joint?

A

Creaking, cracking and grinding when moving the affected joint

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41
Q

What are heberen’s nodes?

A

Osteophytes at the DIP Joints

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42
Q

What are bouchards nodes?

A

Osteophytes at the PIP joints

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43
Q

What are the radiological features of OA? JOSS

A

Joint space narrowing
Osteophytes
Subchondral bony sclerosis
Subchondral cysts

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44
Q

How will subchondral bony sclerosis appear on an X-Ray?

A

Increased white appearance

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45
Q

What are osteophytes?

A

Bony spurs

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46
Q

What are the 5 manifestations of inflammation?

A 
Rubor - red
Dolor - pain
Calor - heat
Tumour - swelling
Loss of function
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47
Q

What are the physiological, cellular and molecular changes that occur during inflammation? IMAC

A

Increased blood flow
Migration of white blood cells into tissues
Activation of leukocytes
Cytokine production

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48
Q

What cytokines are produced during an inflammation reaction?

A

TNF-Alpha, IL1, IL6 and IL17

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49
Q

What are the two infection-related causes of joint inflammation?

A

Septic arthritis and tuberculosis

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50
Q

What are the two types of crystal arthritis?

A

Gout and pseudogout

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51
Q

What is an example of immune-mediated joint inflammation?

A

RA

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52
Q

What causes septic arthiritis?

A

Bacterial infection of a joint, usually spread by blood

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53
Q

What are risk factors for septic arthritis?

A

Immunosuppressed, pre-existing joint damage and intravenous drug use

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54
Q

How many joints are usually affected in septic arthritis?

A

One joint

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55
Q

How is septic arthritis diagnosed?

A
  • Through joint aspiration - aspirate pus out the joint, and send to lab for culturing
  • Once bacteria is known then treat with antibiotics
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56
Q

What are the 5 hallmarks associated with septic arthritis?

A

Pain, redness, hot, swelling, and fever

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57
Q

What is a lavage?

A

A surgical wash out

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58
Q

What are common organisms that are involved septic arthritis?

A

Staph aureus, Streptococci, Gonococcus

59
Q

Why is gonococcal septic arthritis an exception?

A

It often affects multiple joints (polyarthritis), and is less likely to cause joint destruction

60
Q

What are the crystals found in gout made of?

A

Urate (uric acid) crystals

61
Q

What is the main risk factor for gout?

A

Hyperuricaemia (high levels of uric acid)

62
Q

What are the causes of hyperuricaemia?

A

Genetics
Increased intake of purine-rich food
Kidney failure (thus reduced excretion)

63
Q

What are the crystals in pseudogout made of?

A

Deposition of calcium pyrophosphate dihydrate (CPPD)

64
Q

What are the risk factors for pseudogout?

A

Age, history of osteoarthritis and intercurrent infection

65
Q

Why are beer drinkers highly vulnerable to gout?

A

Beer contains high levels of purine, which gets broken down into uric acid, resulting in more deposition at the joints

66
Q

What are the crystal deposits found in gout called?

A

Tophi

67
Q

What is the most common joint to become affected with gout?

A

First metatarsophalangeal joint of the toe

68
Q

What is podagra?

A

Gout of the big toe

69
Q

What feature is seen on X-rays in gout?

A

Juxta-articular rat bite erosions of the metatarsophalangeal joint

70
Q

How is the diagnosis of crystal gout made?

A

Through aspirating fluid from the affected joint and examining it under a microscope using polarised light

71
Q

What is seen in synovial fluid analysis which would indicate a positive test result for gout?

A

Needle shaped crystals with negative birefringence

72
Q

What is seen in synovial fluid analysis which would indicate a positive test result for pseudogout?

A

Rhomboid shaped crystals with positive birefringence

73
Q

What is RA?

A

Chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis of synovial joints

74
Q

What is synovitis?

A

Inflammation of the synovial joints

75
Q

What are the key features of rheumatoid arthritis?

A
  • Swelling of the small joints in the hands and wrists
  • Symmetrical
  • Early morning stiffness
76
Q

What feature is seen on radiographs when a patient has RA?

A

Joint erosions

77
Q

What may be detected in the blood of patients with RA?

A

Rheumatoid factor (autoantibody against IgG)

78
Q

What is the pattern of joint involvement in RA?

A

Symmetrical and affects multiple joints - polyarthritis

79
Q

What are the most commonly affected joints with RA?

A 
Metacarpophalangeal MCP
PIP
Wrists
Kness
Ankles
Metatarsophalangeal MTP
80
Q

In RA, where is the primary site of pathology?

A

The synovium, which includes the synovial joint, tenosynovium surrounding tendons, and the bursa

81
Q

What clinical feature of patients is consistent with extensor tenosynovitis

A

incomplete extension of the little and ring finger

82
Q

What is a bursa?

A

A bursa is a closed, fluid-filled sac that works as a cushion and gliding surface to reduce friction between tissues of the body.

83
Q

What are some common extra-articular features of RA?

A

Fever, weight loss, subcutaneous nodules

84
Q

What is vasculitis?

A

Blood vessel inflammation

85
Q

What is episcleritis?

A

Inflammation of the eye

86
Q

What is amyloidosis?

A

Build up of an abnormal protein called amyloid

87
Q

What is Felty’s Syndrome?

A

Triad of splenomegaly, leukopenia and RA

88
Q

Where are RA nodules most commonly found?

A

Distal to the elbow and in the hands

89
Q

What are RA nodules?

A

They are a central area of fibrinoid necrosis surrounded by histiocytes and a peripheral layer of connective tissue

90
Q

In RA, the synovium becomes a proliferated mass of tissue. What causes this?

A

Neovascularisation (new blood vessels)
Lymphaniogenesis (new lymph vessels)
An infiltrate of inflammatory cells

91
Q

What inflammatory cells are present in the synovium during RA?

A

Activated B and T cells, Plasma cells, Mast cells and macrophages

92
Q

What controls the requirement of inflammatory cells during RA?

A

An extensive cytokine imbalance where there are more pro-inflammatory cytokines than anti-inflammatory ones

93
Q

What is the dominant pro-inflammatory cytokine in RA?

A

Tumour necrosis factor alpha - TNFa

94
Q

What produces the cytokine TNFa seen in RA?

A

The activated macrophages in the rheumatoid synovium

95
Q

What affect does TNFa have on osteoclasts?

A

Activates them, leading to more bone resorption and thus bone erosion

96
Q

What affect does TNFa have on synoviocytes?

A

Triggers joint inflammation which leads to pain in the joints and swelling

97
Q

What effect does TNFa have on chondrocytes?

A

Leads to cartilage degradation, thus resulting in joint space narrowing

98
Q

How is inhibition of TNFa achieved?

A

Through parenteral administration of either antibodies or fusion proteins

99
Q

What are the 2 types of autoantibodies that are found in blood of patients with rheumatoid arthritis?

A

Rheumatoid factor
Antibodies to citrullinated protein antigens (ACPA)

100
Q

What are rheumatoid factor antibodies?

A
  • Antibodies that recognise the Fc portion of IgG as their target antigen
  • Typically IgM antibodies i.e. IgM anti-IgG antibody.
101
Q

Citrullination is mediated by enzymes termed…

A

Peptidyl arginine deaminases (PADs)

102
Q

What do peptidyl arginine deaminases convert arginine into?

A

Citrulline

103
Q

What is the overall treatment goal for rheumatoid arthritis and what does this goal therefore require?

A
  • Treatment goal is to prevent joint damage
  • This requires early recognition of symptoms and referral from GP to a rheumatologist, prompt initiation of treatment (joint destruction gets worse with time) and AGGRESSIVE treatment to suppress inflammation.
104
Q

What are DMARDs?

A

Disease-modifying anti-rheumatic drugs

105
Q

What is the 1st line treatment of RA?

A

Methotrexate in combination with with hydroxychloroquine or sulfasalzine

106
Q

What are the 2nd line treatments of RA?

A

Biological therapies

107
Q

Why should the long term use of prednisolone (glucocorticoid therapy) be avoided?

A

There can be severe side effects

108
Q

What are biological therapies?

A

Antibodies that target a specific protein such as an inflammatory cytokine

109
Q

What biological therapies are used to inhibit TNF?

A

Antibodies (infliximab and others)

Fusion proteins (etanercept)

110
Q

What biologicals are used for B-cell depletion?

A

Rituximab – an antibody against the B-cell antigen CD20

111
Q

What fusion protein is used as a biological to modulate T cell co-stimulation?

A

Abatacept which combines with the CTLA-4 receptor linked to the modified Fc of human immunoglobulin G1

112
Q

Which two drugs are used as biologicals to inhibit IL-6 signalling?

A

Tocilizumab (RoActemra) - Antibody against IL-6 receptor
Sarilumab (Kevzara) - Ab against IL-6 receptor.

113
Q

What MDT approaches are important in the management of rheumatoid arthritis?

A

Physiotherapy, OT, hydrotherapy, (surgery → barely needed)

114
Q

Why might treatment with infliximab and rituximab be rejected by a patient?

A
  • Both have Fab regions which have a mouse sequence hence they are chimeric (human/mouse) antibodies.
  • Patient likely to develop antibodies to this mouse component, thus the effect of drugs on TNF and CD20 respectively will wear off.
115
Q

What is the difference in joint pattern between RA and OA?

A 
RA = symmetrical
OA = asymmetric
116
Q

What is the difference in the speed of onset between RA and OA?

A

RA is rapid, OA is slower

117
Q

What is the difference in the hand joints affected between RA and OA?

A 
RA = PIP and MCP
OA = DIP and Thumb CMC
118
Q

What is the difference in the swelling of the joint between RA and OA?

A 
RA = effusion, red, warm
OA = bony
119
Q

What happens to ESR/CRP in RA?

ESR is erythrocyte sedimentation rate
CRP is c-reative protein

A

Elevated

120
Q

Are osteophytes found in OA or RA?

A

OA

121
Q

Is osteopenia common in RA or OA?

A

RA

122
Q

Are bony erosions present in RA or OA?

A

RA

123
Q

Where do bony erosions initially occur in RA?

A

At the margins of the joint where the synovium is in direct contact with the blood

124
Q

What is the difference between the causes of joint space narrowing in rheumatoid and osteoarthritis?

A

In OA this is the primary abnormality whereas in RA it is caused by secondary damage due to synovitis

125
Q

What is psoriatic arthritis?

A

Autoimmune disease affecting skin (scaly red plaques on extensor surfaces)

126
Q

Are rheumatoid factors present in patients with psoriatic arthritis?

A

No - they are seronegative

127
Q

What is the classical clinical presentation of psoriatic arthritis?

A

Classically asymmetrical arthritis affecting IP (interphalangeal) joints

128
Q

What else can psoriatic arthritis manifest as other than the classical presentation?

A

Symmetrical involvement of small joints (rheumatoid pattern)
Spine and sacroiliac joint inflammation
Oligoarthritis of large joints (inflammation of 2-4 joints)
Arthritis mutilans

129
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infections, especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. salmonella, Shigella, Campylobacter infections)

130
Q

What are the important extra-articular manifestations of reactive arthritis?

A
  • Enthesitis (another form of tendon inflammation)
  • Skin inflammation
  • Eye inflammation
131
Q

Reactive arthritis may be the first manifestation of what 2 infections?

A

HIV and Hep-C infection

132
Q

How long do symptoms follow for reactive arthritis after infection?

A

1-4 weeks

133
Q

What are the key differences between septic and reactive arthritis?

A
  • Septic – positive synovial fluid; reactive – sterile
  • Antibody therapy used in septic, not reactive
  • Joint drainage/lavage can be used in septic, not reactive
134
Q

What is SLE?

A

Systemic lupus erythematous

135
Q

What is the pathophysiology of SLE?

A

Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)

136
Q

How can anti-nuclear antibodies be used in the diagnosis of SLE?

A
  • Antinuclear antibodies (ANA) have high sensitivity for SLE but are not specific.
  • Negative test rules out SLE, but positive doesn’t mean patient has SLE
137
Q

A patient has a negative Anti-Nuclear Antibody test. Does this patient have SLE?

A

No

138
Q

What are the two clinical tests for SLE?

A

Anti-nuclear antibodies (ANA)
Anti-double stranded DNA antibodies

139
Q

Which test for SLE has a higher specificity?

A

Anti-double stranded DNA antibodies

140
Q

Which sex does SLE affect mre commonly?

A

Females (9:1)

141
Q

In which ethnic populations is there an increased prevalence of SLE?

A

African and Asian ancestry populations

142
Q

What does SLE present as clinically?

A

Malar / Butterfly rash

143
Q

What is arthritis mutilans?

A

Bones around the joints get completely dissolved, causing telescoping of the digits, resulting in shortening of the fingers and excess skin

144
Q

What does the yellow arrow point at and what is the clinical significance of this?

A

Rheumatoid nodule
Invariably associated with rheumatoid factor, thus confirms diagnosis of rheumatoid arthritis

BRS 5 Musculoskeletal (13 decks)

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