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intro to rheumatology Flashcards

1
Q

what is rheumataology

A

The medical specialty dealing with diseases of the musculoskeletal system including:

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2
Q

what is a joint

A

where 2 bone meets

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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

Ligaments

A

flexible fibrous connective tissue which connect two bones

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5
Q

Structural classification:

A

Fibrous Joints
Cartilaginous Joints
Synovial Joints

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6
Q

Fibrous Joints

A

No space between the bones
Examples:
-sutures in the skull
-syndesmosis (sheet of connective tissue) in tibia and fibula joint (ankle)

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7
Q

Cartilaginous Joints

A

Joints in which the bones are connected by cartilage

E.g. joints between spinal vertebrae

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8
Q

Synovial Joints

A
  • have a space between the adjoining bones (synovial cavity)

- This space is filled with synovial fluid.

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9
Q

syndesmosis

A

sheet of connective tissue) in tibia and fibula joint (ankle)

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10
Q

Functional classification:

A

Synarthroses
Amphiarthroses
Diarthroses

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11
Q

Diarthroses

A

Allow for free movement of the joint

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12
Q

Amphiarthroses

A

Allow very limited movement

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13
Q

Synarthroses

A

Generally allow no movement

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14
Q

synovial joints allow what sort of movement/s

A

Diarthroses

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15
Q

Cartilaginous Joints

A

Synarthroses

Amphiarthroses

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16
Q

Fibrous Joints

A

Synarthroses

Amphiarthroses

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17
Q

structure of synovial joint

A

Bone
artciular cartilage
joint cavity containing the synovial fluid

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18
Q

Synovium

what type of cell

A

1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)

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19
Q

which collagen

A

Type I collagen

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20
Q

what is type A synoviocyte

A

macrophage like phagocytic cell

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21
Q

what is type B synoviocyte

A

fibroblast like cell that produces hyaluronic acid

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22
Q

Synovial fluid

function

A

lubricating fluid allows the joint to move freely

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23
Q

contains

A

Hyaluronic acid-rich viscous fluid

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24
Q

Articular cartilage

function

A

smooth lining to end of bone

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25
Q

conatins

A

Type II collagen

Proteoglycan (aggrecan)

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26
Q

Cartilage is composed of:

A

1) specialized cells (chondrocytes)
2) extracellular matrix: water, collagen and proteoglycans
(mainly aggrecan)

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27
Q

why does cartliage heal poorly after injury

A

Cartilage is avascular – it has no blood supply

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28
Q

what is Aggrecan- contains

and function

A

a proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains
-characterized by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates

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29
Q

Arthritis is

A

= disease of the joints

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30
Q

what are the 2 main diviosns

A

Osteoarthritis
(Degenerative arthritis)

Inflammatory arthritis
(main type is rheumatoid arthritis)
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31
Q

main problem in OA

A

cartlilage is worn out

bony remodelling

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32
Q

main prob with IA

A

inflammation

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33
Q

what factors increase chacnce

A
  • more prevalent as age increases,
  • previous joint trauma (e.g. footballer’s knees)
  • jobs involving heavy manual labour
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34
Q

onset of disease

A

gradual. Slowly progressive disorder

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35
Q

joints affected in the hand

A

Distal interphalangeal joints (DIP)
Proximal interphalangeal joints (PIP)
First carpometacarpal joint (CMC)

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36
Q

joints else where

A

Spine
Weight-bearing joints of lower limbs
esp. knees and hips
First metatarsophalangeal joint (MTP)

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37
Q

symptoms and sign

A 
Joint pain
(worse with activity, better with rest)
Joint crepitus
(creaking, cracking grinding sound on moving affected joint)
Joint instability (‘giving way’)
Joint enlargement
(e.g. Heberden’s nodes)
Joint stiffness after immobility (‘gelling’)
Limitation of range of motion
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38
Q

Heberden’s nodes.

A

Bony bumps on the finger joint closest to the fingernail

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39
Q

Bouchard’s nodes

A

bony bumps on the middle joint of the finger are known

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40
Q

Radiographic features of osteoarthritis:

A

Joint space narrowing
Subchondral bony sclerosis
Osteophytes
Subchondral cysts

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41
Q

what is Subchondral bony sclerosis shown on x ray

A

appears as a region of increased density on an X-ray

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42
Q

what do Osteophytes show on x ray

A

are bony lumps (bone spurs) that grow on the bones of the spine or around the joints

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43
Q

Subchondral cysts

A

is a fluid-filled space inside a joint that extends from one of the bones that forms the joint. This type of bone cyst is caused by osteoarthritis. It may require aspiration (drawing the fluid out), but the arthritis condition usually must also be addressed to prevent further cyst formation.

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44
Q

What is inflammation?

A

Inflammation = a physiological response to deal with injury or infection
However, excessive/inappropriate inflammatory reactions can damage the host tissues

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45
Q

signs of inflammation

A
  1. RED (rubor)
  2. PAIN (dolor)
  3. HOT (calor)
  4. SWELLING (tumor)
  5. LOSS OF FUNCTION
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46
Q

Physiological, cellular and molecular changes:

A

Increased blood flow
-Migration of white blood cells (leucocytes) into the tissues
-Activation/differentiation of leucocytes
-Cytokine production
E.g. TNF-alpha, IL1, IL6, IL17

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47
Q

Causes of joint inflammation

A

1 ) Infection

2) Crystal arthritis
3) Immune-mediated (“autoimmune”)

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48
Q

example of infection as a cause for joint inflammation

A

Septic arthritis

Tuberculosis

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49
Q

Crystal arthritis

A

Gout

Pseudogout

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50
Q

Immune-mediated (“autoimmune”)

A

Rheumatoid arthritis
Psoriatic arthritis
Reactive arthritis
Systemic lupus erythematosus (SLE)

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51
Q

what causes Septic arthritis

A

Bacterial infection of a joint (usually caused by spread from the blood)

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52
Q

risk factors

A

immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

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53
Q

why is it bad

A

-> Untreated, septic arthritis can rapidly destroy a joint

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54
Q

does it affect both joints

A

Usually only 1 joint is affected* (monoarthritis)

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55
Q

signs/symptoms

A

Consider septic arthritis in any patient with an acute painful, red, hot, swelling of a joint, especially if there is fever

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56
Q

how to formely diagnose

A

Diagnosis is by joint aspiration. Send sample for urgent Gram stain and culture

57
Q

common microorganisms

A

Staphylococcus aureus, Streptococci, Gonococcus*

58
Q

how to treat

A

Treatment is with surgical wash-out (‘lavage’) and intravenous antibiotics

59
Q

exception to 1 joint rule

A

It often affects multiple joints (polyarthritis)

-It is less likely to cause joint destruction

60
Q

what are the 2 forms of Crystal arthritis

A

Gout

Pseudogout

61
Q

what is gout

A

Gout is a syndrome caused by deposition of urate (uric acid) crystals -> inflammation

62
Q

does high levesl of gout ensure you have artittis

A

nope, High uric acid levels (hyperuricaemia) = risk factor for gout

63
Q

Causes of hyperuricaemia:

A

Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure
beer drinkers

64
Q

what is Pseudogout

A

Pseudogout is a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation

65
Q

risk factors

A

: background osteoarthritis, elderly patients, intercurrent infection

66
Q

clinical features of gout

A

presents as an acute monoarthritis of rapid onset

67
Q

which joint is first affected

A

metatarsophalangeal joint is the most commonly affected joint (podagra

68
Q

what is tophi

A

Crystal deposits (tophi) may develop around hands, feet, elbows, and ears.

69
Q

when gout has been chrinic causes

A

erosions- looks like rat butes in x ray

70
Q

a great way to identify whether pseudo or gout

A

The diagnosis of crystal arthritis is made by aspirating fluid from the affected joint and examining it under a microscope using polarized light
(synovial fluid anaylsis under polarised light)

71
Q

how is gout shown

A

needle shaped crystals with negative birefringence

72
Q

Pseudogout

A

rhomboid shaped crystals with positive birefringence

73
Q

most common cause of . Immune-mediated inflammatory joint disease

A

is rheumatoid arthritis (RA)

74
Q

what does it do

A

= chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis
(inflammation of the synovial membrane) of synovial (diarthrodial) joints

75
Q

key features

A

Chronic arthritis
Polyarthritis - swelling of the small joints of the hand and wrists is common
Symmetrical
Early morning stiffness in and around joints
May lead to joint damage and destruction - ‘joint erosions’ on radiographs

76
Q

Extra-articular disease can occur like

A

Rheumatoid nodules

Others rare e.g. vasculitis, episcleritis

77
Q

what may be detected in the blood

A

Autoantibody against IgG - should really call this rheumatoid ‘antibody’

78
Q

what does Symmetrical mean in terms of ra

A

effects left and right sides of the body equaly

79
Q

define polyarthritis

A

Affects multiple joints

80
Q

what is the primary site of pathology

A

synovium

81
Q

why does ra have extra articular features

A

becuase it is an utoimmune disease

82
Q

common extra articular features

A

Fever, weight loss

Subcutaneous nodules

83
Q

uncommon features

A

Ocular inflammation e.g. episcleritis
Neuropathies
Amyloidosis
Lung disease – nodules, fibrosis, pleuritis
Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis

84
Q

what do Subcutaneous nodules contain

A

Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

85
Q

what (factor) is it associated

A

Rheumatoid factor

86
Q

what is the main problem in ra

A

synovial membrane is abnormal in ra and is inflammed

the synovial becomes a proliferated mass of tissue (pannus)

87
Q

why a pannus

A 
Neovascularisation
Lymphangiogenesis
inflammatory cells:
activated B and T cells
plasma cells
mast cells
activated macrophages
88
Q

what is Neovascularisation

A

Neovascularization is the natural formation of new blood vessels

89
Q

Lymphangiogenesis

A

s the formation of lymphatic vessels from pre-existing lymphatic vessels

90
Q

why is there inflammation

A

an excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)

91
Q

a dominant pro inflamm cytokine

A

tnf alpha

92
Q

does it only affect 1 system

A

no Its pleotropic actions are detrimental in this setting:

93
Q

affect in osteoclast

A

bone resoption and erosion

94
Q

affect in synoviocytes

A

joint inflammation and pain joint swelling

95
Q

chondrocytes

A

cartilage degradation

joint space narrowing

96
Q

how to combact tnf alpha

A

TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

97
Q

what are the Two types of antibodies are found in the blood of RA patients:

A
  1. Rheumatoid factor

2. Antibodies to citrullinated protein antigens (ACPA)

98
Q

what is rf

A

Antibodies that recognize the Fc portion of IgG as their target antigen
typically IgM antibodies i.e. IgM anti-IgG antibody !

99
Q

what is Citrullination

A

ARGININE — CITRULLINE

100
Q

WHAT ENZYME

A

Peptidyl arginine deiminases (PADs)

101
Q

treatment goal for ra

A

: prevent joint damage

becuase once its damaged there is no going back

102
Q

what is the drug class used

A

Disease-modifying anti-rheumatic drugs (‘DMARDs’)

103
Q

what is DMARDs

A

= drugs that control the disease process

104
Q

what is the first line treatment

A

methotrexate in combination with hydroxychloroquine or sulfasalazine

105
Q

2nd line

A

Biological therapies offer potent and targeted treatment strategies

106
Q

what are biological therapies for ra

A

Biological therapies are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

107
Q

what are the 4 biological therapies

A
  1. Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
  2. B cell depletion
  3. Modulation of T cell co-stimulation
  4. Inhibition of interleukin-6 signalling
108
Q

what is b cell depletion

A

antibody against the B cell antigen, CD20

causes near complete depletion of b cell in peripheral blood

109
Q

what is Modulation of T cell co-stimulation

A

Abatacept - fusion protein - extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, and CH3 domains) of human immunoglobulin G1

110
Q

what is Inhibition of interleukin-6 signalling

A

antibody against interleukin-6 receptor

111
Q

what is a limitation to part mouse part human antibody

A

overtime you can develop antibodies against the mouse part, rendering the antibody inneffective

112
Q

ra vs oa in age of onset

A

ra : 30-50

oa: 50+

113
Q

speed

A

ra: rapid
oa: slow

114
Q

joint pattern

A

ra: bilateral symmetrical
oa: asymmetrcial

115
Q

movement

A

ra: often better after moveement
oa: worse

116
Q

am stiffness

A

ra: more than an hour
oa: uncommon rarely more than 30

117
Q

systemic symptoms

A

ra: common
oa: not present

118
Q

joint swelling

A

ra: effusion, red, warm
oa: bony

119
Q

serology

A

ra: rf+
oa: ra-

120
Q

x ray findings that are common

A

both have joint space narrowing

121
Q

what can you see in ra and cant see in oa

A

Osteopenia

bony errosions

122
Q

what u see in oa not in ra

A

Subchondral sclerosis

Osteophytes

123
Q

what is Psoriatic arthritis and how doe sit show

A

Psoriasis is an autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees)

124
Q

does it have the rf

A

no

125
Q

is it symmetrical or asymmetrical

A

a

126
Q

other possible signs

A

Symmetrical involvement of small joints (rheumatoid pattern)

  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
127
Q

what is -Arthritis mutilans

A

An extremely severe form of chronic rheumatoid or psoriatic arthritis characterized by resorption of bones and the consequent collapse of soft tissue. When this affects the hands, it can cause a phenomenon sometimes referred to as ‘telescoping fingers. ‘- - - - - - short fingers excess skin

128
Q

what is Reactive arthritis

A

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

129
Q

what extra articular manifestation occur

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

130
Q

does it have a genetic component and an enviromental component

A

Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)

131
Q

what is sterile inflammation

A

inflammation without pathogens

132
Q

would you wash the joint in septic a or reaxtive a

A

septic (for larger joints) not reactive

133
Q

what is Lupus

A

a multi-system autoimmune disease

134
Q

Systemic Lupus Erythematous (SLE) as well as an inflmmatory joint disease is a…

A

Multi-site inflammation: can affect any almost any organ.

Often joints, skin, kidneys, haematology. Also: lungs, CNS involvement

135
Q

what sort of antibodies do you have if you have sle

A

autoantibodies

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

136
Q

clinical test for sle

A
  1. Antinuclear antibodies (ANA):

2. Anti-double stranded DNA antibodies (anti-dsDNA Abs):

137
Q

what is ana/Antinuclear antibodies

e.g. what is a positive result and negative

A

High sensitivity for SLE but not specific.

A negative test rules out SLE, but a positive test does not mean SLE.

138
Q

is sle more prevalent in males or females

A

female

139
Q

how old

A

15 to 40

nuero (36 decks)

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