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PSYCH > Introduction to Rheumatology > Flashcards

Introduction to Rheumatology Flashcards

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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 allows 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

Bone, joint cavity containing synovial fluid and Articular cartilage

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17
Q

What is the synovium?

A

A 1-3 cell deep lining containing macrophage-like phagocytic cells and fibroblast-like cells that produce hyaluronic acid

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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
  1. Chondrocytes

2. ECM: Water, collage and proteoglycans (mainly aggrecan)

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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

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28
Q

What is aggrecan?

A

A proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains

Characterised by its ability to interact with hyaluronan to form larger proteoglycan aggregates

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29
Q

What are the two major divisions of arthritis?

A

Osteoarthritis and Inflammatory arthritis (RA)

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30
Q

What are the pathological changes associated with OA?

A

Cartilage worn out, and attempts made at bony remodelling

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31
Q

Describe the onset of OA?

A

Gradual, slowly progressing disorder

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32
Q

How does age affect OA?

A

Increases as age increase

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33
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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34
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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35
Q

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

A

Knees, Hips

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36
Q

Signs and Symptoms of OA? PRICES

A 
Pain
Range of motion is limited
Instability
Crepitus
Enlargement of joint
Stiffness
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37
Q

What is crepitus of a joint?

A

`Creaking, cracking grinding when moving the affected joint

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38
Q

what are heberen’s nodes?

A

Osteophyctes at the DIP Joints

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39
Q

What are bouchards nodes?

A

Osteophytes at the PIP joints

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40
Q

What are the radiological features of OA? JOSS

A

Joint Space Narrowing
Osteophytes
Subchondral bony sclerosis
Subchondral cysts

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41
Q

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

A

Increased white appearance

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42
Q

What are osteopytes?

A

Bony spurs

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43
Q

What are the 5 manifestations of inflammation?

A 
Rubor - red
Dolor - pain
Calor - heat
Tumour - swelling
Loss of function
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44
Q

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

A

Increased blood flow
Migration of white blood cells into tissues
Activations of leucocytes
Cytokine production

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45
Q

What cytokines are produced during an inflammation reaction?

A

TNF-Alpha, IL1, IL6 and IL17

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46
Q

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

A

Septic arthritis

Tuberculosis

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47
Q

What are the two types of crystal arthritis?

A

Gout

Pseudogout

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48
Q

What is an example of immune-mediated joint inflammation?

A

RA

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49
Q

What causes septic arthiritis?

A

bacterial infection of a joint, usually spread by blood

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50
Q

What are risk factors of septic arthritis?

A

Immunosuppressed, pre-existing joint damage and intravenous drug use

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51
Q

How many joints are usually affected in septic arthritis?

A

One joint

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52
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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53
Q

What are the four hallmarks associated with septic arthritis?

A

Pain, redness, hot, swelling, and fever

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54
Q

What is a lavage?

A

A surgical wash out

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55
Q

What are common organisms that are involved septic arthritis?

A

Staph aureus, Streptococci, Gonococcus

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56
Q

In what was is gonococcal septic arthritis an exception?

A

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

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57
Q

What are the crystals found in gout made of?

A

Urate (uric acid) crystals

58
Q

What is the main risk factor for gout?

A

Hyperuricaemia - high levels of uric acid

59
Q

What are the causes of hyperuricaemia?

A

Genetics
Increased intake of purine-rich food
reduced excretion due to kidney failure

60
Q

What are the crystals in pseudogout made of?

A

Deposition of calcium pyrophosphate dihydrate (CPPD)

61
Q

What are the risk factors for pseudogout

A

Elderly, history of osteoarthritis and intercurrent infection

62
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

63
Q

What are the crystal deposits found in gout called?

A

Tophi

64
Q

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

A

Metatarsophalangeal - bone in toe

65
Q

What is podagra?

A

Gout of the big toe

66
Q

What feature is seen on X-rays in gout?

A

Rat bit erosions

67
Q

How is the diagnosis of crystal out made?

A

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

68
Q

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

A

Needle shaped crystals with negative birefringence

69
Q

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

A

Rhomboid shaped crystals with positive birefringence

70
Q

What is RA?

A

Rheumatoid arthritis is a chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis of synovial joints

71
Q

What is synovitis?

A

Inflammation of the synovial joints

72
Q

What are the key features of rheumatoid arthritis?

A

There is swelling of the small joints in the hands and wrists, symmetrical and early morning stiffness is also seen

73
Q

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

A

Joint erosions

74
Q

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

A

Rheumatoid factor - this is an autoantibody against IgG

75
Q

What is the pattern of joint involvement in RA?

A

Symmetrical and affects multiple joints - polyarthritis

76
Q

What are the most commonly affected joints with RA?

A 
Metacarpophalangeal MCP
PIP
Wrists
Kness
Ankles
Metatarsophalangeal MTP
77
Q

In RA, where is the primary site of pathology?

A

The synovium

78
Q

What clinical feature of patients is consistent with extensor tenosynovitis

A

incomplete extension of the little and ring finger

79
Q

What clinical feature of patients is consistent with extensor tenosynovitis

A

incomplete extension of the little and ring finger

80
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.

81
Q

What are some common extra-articular features of RA?

A

Fever, weight loss, subcutaneous nodules

82
Q

What is vasculitis?

A

Blood vessel inflammation

83
Q

What is episcleritis?

A

Inflammation of the eye

84
Q

What is amyloidosis?

A

Build up of an abnormal protein called amyloid

85
Q

What is Felty’s Syndrome?

A

Triad of splenomegaly, leukopenia and RA

86
Q

Where are RA nodules most commonly found?

A

Distal to the elbow and in the hands

87
Q

what are RA nodules

A

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

88
Q

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

A

Neovascularisation
Lymphaniogenesis
An infiltrate of inflammatory cells

89
Q

What inflammatory cells are present in the synovium during RA?

A

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

90
Q

What controls the requirement of inflammatory cells during RA?

A

An extensive cytokine imbalance - more pro-inflammatory cytokines than anti-inflammatory

91
Q

What is the dominant pro-inflammatory cytokine in RA?

A

Tumour necrosis factor alpha - TNFa

92
Q

What produces the cytokine TNFa seen in RA?

A

The activated macrophages in the rheumatoid synovium

93
Q

What affect does TNFa have on osteoclasts?

A

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

94
Q

What affect does TNFa have on synoviocytes?

A

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

95
Q

What effect does TNFa have on chondrocytes?

A

Leads to cartilage degradation, thus resulting in joint space narrowing

96
Q

How is inhibition of TNFa achieved?

A

Through parenteral administration of either antibodies or fusion proteins.

97
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)

98
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.

99
Q

Citrullination is mediated by enzymes termed…

A

peptidyl arginine deaminase (PADs).

100
Q

What does peptidyl arginine deaminase convert arginine into?

A

citrulline

101
Q

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

A

Treatment goal - 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.

102
Q

What are DMARDS?

A

Disease-modifying anti-rheumatic drugs

103
Q

What is the 1st line treatment of RA?

A

Methotrexate in combination with with hydroxychloroquine or sulfasalzine.

104
Q

What is the 2nd line treatment of RA?

A

Biological therapies.

New therapies include Janus Kinase inhibitors: Tofacitinib and Baricitinib

105
Q

Why should the long term use of prednisolone be avoided?

A

There can be severe side effects

106
Q

What are biological therapies?

A

Antibodies that target a specific protein such as an inflammatory cytokine

107
Q

WHat biologicals are used to inhibit TNF?

A

Antibodies (infliximab and others)

Fusion proteins (etanercept)

108
Q

What Biologicals are used for B-cell depletion?

A

Rituximab - Ab agains the B-cell antigen CD20.

109
Q

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

A

Abatacept

110
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.

111
Q

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

A

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

112
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 → Effect of drugs on TNF and CD20 respectively will wear off.

113
Q

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

A 
RA = symmetrical
OA = asymmetric
114
Q

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

A

RA is rapid, OA is slower

115
Q

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

A 
RA = PIP and MCP
OA = DIP and Thumb CMC
116
Q

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

A 
RA = effusion, red, warm
OA = bony
117
Q

What happens to ESR/CRP in RA?

A

Elevated

118
Q

Are osteophytes found in OA or RA?

A

OA

119
Q

Is osteopenia common in RA or OA?

A

RA

120
Q

Are bony erosions present in RA or OA?

A

RA

121
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

122
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.

123
Q

What is psoriatic arthritis?

A

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

124
Q

Are rheumatoid factors present in patients with psoriatic arthritis?

A

No - they are seronegative

125
Q
  • What is the classical clinical presentation of psoriatic arthritis?
A

Classically asymmetrical arthritis affecting IPJs

126
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

Arthritis mutilans

127
Q

What is reactive arthritis?

A

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

128
Q

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

A

Enthesitis (another form of tendon inflammation)

Skin inflammation

Eye inflammation

129
Q

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

A

HIV and Hep-C infection

130
Q

How long do symptoms follow for reactive arthritis after infection?

A

1-4 weeks

131
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 SA, not Reactive

132
Q

What is SLE?

A

Systemic lupus erythematous

133
Q

What is the pathophysiology of SLE?

A

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

134
Q

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

A

Antinuclear antibodies (ANA) - high sensitivity for SLE but not specific. Negative test rules out SLE, but positive doesn’t mean patient has SLE.

135
Q

Negative Anti-Nuclear Antibody test. Does this patient have SLE?

A

No

136
Q

What are the two clinical tests for SLE?

A

ANA

Anti0double stranded DNA antibodies

137
Q

Which test for SLE has a higher specificity?

A

Anti-double stranded DNA antibodies

138
Q

Which sex does SLE affect mre commonly?

A

Females (9:1)

139
Q

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

A

African and Asian ancestry populations.

140
Q

What does SLE present as clinically?

A

Malar / Butterfly rash

141
Q

What is arthritis mutilans

A

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

PSYCH (78 decks)

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