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Y2 LCRS > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What are the functions of bone?

A
  • STRUCTURE -> give structure and shape to the body
  • MECHANICAL -> support and site for muscle attachment
  • PROTECTIVE -> vital organs and bone marrow
  • METABOLIC -> reserve of calcium (high surface area)
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2
Q

Describe the composition of bone.

A

o INORGANIC = 65%

  • calcium hydroxyapatite (Ca10(PO4)6(OH)2)
  • store house for 99% of Ca in the body, 85% of the phosphorous and 65% Na & Mg

o ORGANIC – 35%

  • bone cells and protein matrix -> collagen, osteoid
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3
Q

Describe bone geography.

A
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4
Q

What are the 5 types of anatomical bones?

A
  • flat
  • long
  • short/cuboid
  • irregular (vertebrate)
  • sesamoid
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5
Q

What are the 3 major classifications of bone?

A
  • anatomical
  • macroscopic
  • microscopic
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6
Q

How is macroscopic bone classified?

A

o CORTICAL/COMPACT

  • long bones
  • 80% of skeleton
  • appendicular
  • 80-90% calcified
  • mainly mechanical and protective

o TRABECULAR/CANCELLOUS/SPONGY

  • vertebrae & pelvis
  • 20% of skeleton
  • axial
  • 15-25% calcified
  • mainly metabolic function
  • Large surface
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7
Q

What is the classification of bone by microanatomy?

A
  • woven -> immature
  • lamallar -> mature
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8
Q

Describe the microanatomy of cortical bone.

A
  • organised into concentric lamellae -> form in response to mechanical forces -> give bone strength in the cortical bone -> can be seen under a microscope due to its striped pattern
  • blood vessels travel through and across the bone in Haversian canals -> come into the periosteum and travel up, down and across the bone
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9
Q

What do osteoblasts do?

A
  • build bone by laying down osteoid
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10
Q

What do osteoclasts do?

A
  • multinucleate cells of macrophage family -> resorb or chew bone
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11
Q

What do osteocytes do?

A
  • osteoblast like cells -> sit in lacunae in bones -> look inert (imbedded in matrix)
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12
Q

What is RANK/RANKL?

A
  • a ligand that is responsible for laying down of new bone via differentiation of the osteoclast
  • up-regulated in response to stimuli -> infection, trauma etc
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13
Q

What is osteoprotegerin?

A
  • inhibitor of RANk/RANKL -> inhibits osteoclastogenesis
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14
Q

When does osteoprotegerin fall?

A
  • menopause -> oestrogen falls -> OPG falls -> more resorption
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15
Q

When might a bone biopsy be taken?

A
  • evaluate bone pain or tenderness
  • investigate an abnormality seen on x-ray
  • bone tumour diagnosis (benign vs. malignant)
  • determine the cause of an unexplained infection
  • evaluation of therapy
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16
Q

Name the 2 types of bone biopsy.

A
  • CLOSED -> needle (Jamshidi needle) -> core biopsy
  • OPEN -> for sclerotic or inaccessible lesions -> requires general anaesthetic
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17
Q

What is the common site for bone biopsy?

A
  • transilliac -> good site to get a sample of cortical and cancellous bone
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18
Q

What are the 3 bone labels?

A
  • H&E
  • Masson - Goldner Trichrome
  • tetracycline
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19
Q

What are the 3 main categories of metabolic bone disease?

A
  1. Related to endocrine abnormality (Vitamin D, Parathyroid hormone)
  2. Non-endocrine (e.g. age-related osteoporosis)
  3. Disuse osteopenia (results from the reduced use of bones e.g. in injury)
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20
Q

How is osteoporosis definded?

A
  • a patients with a bone mineral density T-score -2.5 or lower when using a DEXA scan
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21
Q

Describe the aetiology of osteoporosis.

A
  • primary = age-related or post-menopausal
  • secondary = drugs or systemic disease
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22
Q

What are the two classification of osteoporosis?

A
  • high and low turnover
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23
Q

What is osteomalacia?

A
  • defective mineralisation of normally synthesise bone matrix
  • can be due to vitamin D or PO4 deficiency

o called Rickets in children

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24
Q

What are the signs and symptoms of osteomalacia?

A
  • bone pain/tenderness
  • fracture and microfracture
  • proximal weakness
  • bone deformity -> e.g. tibia bowing in rickets
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25
Q

What happens in someone with hyperparathyroidism?

A

o excess PTH -> bone resorption

  • ncreased Ca and PO4 excretion in urine -> calcium hydroxyapatite is broken down into its constituents
  • hypercalcaemia
  • hypophosphatemia
  • skeletal changes of osteitis fibrosa cystica if disease is allowed to progress
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26
Q

What 4 organs are affeced by PTH?

A
  • parathyroid
  • bones
  • kidneys
  • proximal small intestine
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27
Q

What are the causes of hyperparathyroidism?

A
  • primary = parathyroid adenoma (85-90%) or chief cell hyperplasia
  • secondary = chronic renal deficiency or vitamin D deficiency
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28
Q

What are the symptoms of hyperparathyroidism?

A
  • stones -> Ca oxalate renal stones
  • bones -> osteitis fibrosa cystica, bone resorption
  • abdominal groans -> acute pancreatitis
  • psychic moans -> psychosis & depression
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29
Q

What bone changes occur in hyperparathyroidism?

A
  • small Brown cell tumours (lytic lesions) -> usually on the radial side of the digits and thumbs
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30
Q

What are the 3 stages of Paget’s Disease?

A
  1. osteolytic (osteoclast pre-dominant stage)
  2. osteolytic-osteosclerotic (osteoblasts will try to build bone)
  3. quiescent osteosclerotic (there is disorganised, mineralised bone
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31
Q

When does Paget’s disease usually arise?

A
  • over the age of 40
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32
Q

What is the aetiology of Paget’s disease?

A

o aetiology is unknown but could be:

  • familial -> cases show autosomal pattern of inheritance with incomplete penetrance
  • mutation 5q35-qter -> sequestosome 1 gene (on the long arm of chromosome 5)
  • parvomyxovirus type particles have been seen on EM in Pagetic bone but has been disproven so unlikely
  • overuse or previous bone injury
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33
Q

What sites are commonly affects in Paget’s disease?

A
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34
Q

What are the symptoms of Paget’s Disease?

A
  • often asymptomatic -> found by chance

o pain

o microfractures

o nerve compression (incl. Spinal N and cord)

o skull changes may put medulla at risk

o deafness – AFFECTS region of temporal bone

o haemodynamic changes (sometimes)

o cardiac failure haemodynamic changes, cardiac failure

o hypercalcaemia

o development of sarcoma in area of involvement, 1% (osteosarcoma)

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35
Q

What is osteopenia?

A
  • a T-score of -1.5 to -2.5
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36
Q

What is the FRAX tool?

A
  • a calculation using BMD, age, weight, sex and height to generate a risk score for a particular patient -> Nogg guidelines are then referred to
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37
Q

What are the radiological signs of osteoporosis?

A
  • loss of cortical bone/thinning of cortex (white line around bones on an X-ray - prominent of vertebrate)
  • loss of trabeculae
  • insufficiency fractures
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38
Q

What are insufficiency fractures?

A
  • stress fractures due to normal stress on abnormal bones -> not limited to osteoporosis
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39
Q

What are the common sites of insufficiency fractures?

A
  • sacrum
  • underside of the femoral neck
  • vertebral bodies
  • pubic rami
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40
Q

What are the signs of insufficiency fractures on imaging?

A

o X-ray/CT scan

  • initially normal (if caught early) -> but can get periosteal reaction and callus
  • more commonly seen is increased sclerosis around fracture lines

o MRI

  • bone oedema (i.e. low signal on T1, high signal on T2 and STIR)

o Bone scan

  • increased osteoblastic activity (i.e. increased uptake)
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41
Q

Describe what is being seen on these scans.

A
  • CT scan = would expect the normal bone to have a similar sort of density -> there would be areas of increased density (SCLEROSIS).
  • MRI = same as CT
  • bone scan = increased bone turnover in the same area -> commonly seen in the pelvic area (Honda sign) -> also see areas of increased uptake due to a vertebral body fracture

o all this points to an insufficiency fracture and osteoporosis

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42
Q

What is a possible consequence of osteomalacia is it is untreated?

A
  • secondary hyperparathyroidism
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43
Q

What are the radiological signs of osteomalacia?

A
  • radiology of osteomalacia depends on AGE and CLOSURE of the growth plates
  • if the patient is an adult with a MATURE skeleton and CLOSED growth plates, they will get: looser’s zones osteopenia, codfish vertebrae and bending deformities
  • if the patient is a child (i.e. before growth plate closure), they develop rickets: radiological signs centres mainly to growth plates, changes of osteomalacia
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44
Q

What are Looser’s zones?

A

o Looser’s zones are pseudofractures at high tensile strength areas -> type of insufficiency fracture

o found at similar areas to other insufficiency fractures:

  • medial proximal femur
  • lateral scapula
  • pubic rami
  • posterior proximal ulna
  • ribs

o usually, they look less clean than normal insufficiency fractures -> look like short lucent lines with irregular sclerotic margins -> because the bones cannot heal properly

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45
Q

What can be seen on these scans?

A

o Looser’s Zones

  • short, lucent lines with very sclerotic, irregular margins
  • in right diagram, the bone is very osteopenic -> the whole femur has bent compared to normal
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46
Q

What is codfish vertebrate?

A
  • bioconcave deformities of vertebral bodies
  • seen in osteoporosis and osteomalacia
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47
Q

What can be seen in this scan?

A

o codfish vertebrae

  • bodies should be much squarer
  • usually bones are also very osteopenic
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48
Q

What are the features of rickets?

A

o changes are focused around the growth plate

  • indistinct/frayed metaphyseal margin
  • widened growth plate without calcification
  • cupping/splaying metaphyses due to weight bearing
  • enlargement of anterior ribs
  • osteopenia
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49
Q

What are the main radiological differences between primary and secondary hyperparathyroidism?

A
  • primary = bone resorption
  • secondary = bone resorption and increase density
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50
Q

What is bone resorption?

A
  • where bone as been eroded away
  • often centred in spaces that are subperiosteal, subchondral and intracortical
  • if they are large, they become brown tumours.
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51
Q

Describe what can be seen in these scans.

A
  • cortical margin looks like it is harder to define on an x-ray
  • lucencies in the skull, and there is a lack of crisp cortical edges due to periosteal reactions -> lucencies are areas of intracortical resorption (can be dot like instead of large) – PEPPER POT SKULL
  • large lytic bone lesions in patients with primary hyperparathyroidism (brown tumour)
  • on the same scan, you’ll probably see bone resorption elsewhere
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52
Q

What are the radiological signs of renal osteodystrophy?

A
  • Looser’s zones
  • bending of bones
  • osteopenia
  • insufficiency fractures at end plates
  • subperiosteal erosions and brown tumours
  • sclerosis
  • soft tissue calcification
  • vertrea with increased density at endplates but reduced density in the middle -> called rugger jersey spine
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53
Q

What is renal osteodystrophy?

A
  • a specialised type of primary hyperparathyroidism which can lead to secondary hyperparathyroidism
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54
Q

What is the diagnosis of this patients?

A

o renal osteodystrophy

  • subperiosteal erosions and brown tumours are present
  • sclerosis -> vertebral endplates giving a rugger jersey spine
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55
Q

What radiological signs of Paget’s exsist?

A
  • cortical thickening
  • bone expansion
  • coarsening of trabeculae
  • osteolytic
  • osteosclerotic
  • mixed lesions and osteoporosis circumscripta
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56
Q

What can be seen in this X-ray?

A
  • patient is in the early phase of Paget’s
  • fracture at the femoral head, and loosened bones around inferior pubic ramus
  • at the same time, there is thickening of the bone cortex and trabeculae
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57
Q

What can be seen in this X-ray?

A
  • this is a patient in a late phase of Paget’s
  • left pubic ramus and left pelvic bone are very thick
  • trabeculae is a lot coarser compared with the right side.
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58
Q

Explain what disease this patient is suffering from?

A
  • Paget’s
  • cortex is very thick -> disease is also affecting the mandible
  • multiple lucencies in the skull (osteoporosis circumscripta)
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59
Q

What is a unique feature of Paget’s?

A
  • Paget’s tends to only affect one bone, and doesn’t cross the joint -> might get poly-ostotic Paget’s (multiple bones affected)
  • if a disease process affects adjacent bones -> it’s probably not Paget’s
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60
Q

What is rheumatoid arthritis?

A
  • chronic joint inflammation -> specifically inflammation of the synovium (lining of synovial joints) -> SYNOVITIS
  • if untreated it causes pain and destruction of the joint
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61
Q

What antibodies are associated with rheumatoid arthritis?

A

o autoantibodies

  • rheumatoid factor
  • anti-cyclic citrullinated peptide (CCP)
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62
Q

What is ankylosing spondylitis?

A
  • a seronegative spondyloarthropathy
  • is chronic inflammation to the enthesis (where tendons insert into bone) -> ENTHESITIS
  • if untreated it leads to pain and spinal fusion and deformities -> exaggerated thoracic kyphosis
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63
Q

What antibodies are associated with ankylosing spondylitis?

A
  • no autoantibodies -> is seronegative
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64
Q

What are seronegative spondyloarthropathies?

A

o spinal inflammation of the joints without the presense of rheumatoid factor

  • ankylosing spondylitis
  • reiters syndrome and reactive arthritis
  • arthritis associated with psoriasis (psoriatic arthritis)
  • arthritis associated with gastrointestinal inflammation (enteropathic synovitis)
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65
Q

What is systemic lupus erythematosus?

A
  • chronic tissue inflammation in the presence of antibodies directed against self antigens -> PATHOGENESIS IS DRIVEN BY AUTOANTIBODIES AND IMMUNE COMPLEXES
  • causes multi-site inflammation but particularly the to joints, skin and kidney
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66
Q

What antibodies are associated with systemic lupus erythematosus?

A

o autoantibodies

  • anti-nuclear antibodies
  • anti-double stranded DNA antibodies
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67
Q

What HLA molecule is associated with a higher genetic risk of rheumatoid arthritis?

68
Q

What HLA molecule is associated with a higher genetic risk of systemic lupus erythematosus?

69
Q

What HLA molecule is associated with a higher genetic risk of ankylosing spondylitis?

70
Q

What class are HLA-A/B/C molecules?

A
  • MHC Class I molecules
71
Q

What class are HLA-DR molecules?

A
  • MHC Class II molecules
72
Q

Where are MHC Class I molecules found and what is there role?

A

expressed on = all nucleated cells

  • antigen they present = endogenous -> e.g. viral particles, tumour antigens, self-peptides
  • recognised by = CD8+ T cells
  • response = cell killing/death
73
Q

Where are MHC Class II molecules found and what is there role?

A

expressed on = antigen presenting cells -> e.g. B cells, dendretic cells

  • antigen they present = exogenous -> e.g. bacterial particles, self-peptides
  • recognised by = CD4+ T cells
  • response = antigbody response
74
Q

Name 4 rheumatoid disease which are do not have an associations with any autoantibodies.

A
  • ankylosing spondylitis
  • osteoarthritis
  • reactive arthritis
  • gout
75
Q

Describe the 2 main autoantibodies associated with SLE.

A

o anti-nuclear antibodies -> seen in all SLE cases but isn’t specific for SLE

o anti-double stranded DNA antibodies -> specific for SLE but isn’t always seen -> its serum levels correlates with the disease activity

76
Q

What is the current theory on SLE pathogenesis?

77
Q

In sympatomatic lupus, what immune elements would be high and what would be low?

A
  • low = complement levels
  • high = serum levels of anti-ds-DNA antibodies
78
Q

What are the functions of TNF-alpha?

A
  • activate osteoclasts -> bone erosion
  • activate synoviocytes -> joint inflammation and swelling (due to increased production of synovial fluid)
  • activate chondrocytes -> cartilage degradation
79
Q

What is the clinical use for anti-TNF-alpha?

A
  • rheumatoid arthritis -> has had a a massively positive effect
80
Q

What is the general treatment for SLE?

A
  • treatment paradigm for lupus is to attack the tissue inflammation -> target B cells to have an affect on B cell hyper-reactivity is key feature of SLE
81
Q

Name 2 drugs used to dampen B cell hyperactivity in SLE.

A
  • rituximab -> a chimeric anti-CD20 antibody used to deplete B cells
  • belimumab -> a monoclonal antibody against a B cell survival factor call BLYS
82
Q

What painkillers are used commonly used in rheumatology?

A
  • NSAIDs -> reduce pain, swelling/inflammation but don’t actually prevent joint damage
83
Q

Define rheumatoid arthritis.

A
  • chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis (inflammation of the synovial membrane) of synovial (diarthrodial) joints.
84
Q

What are the key features of rheumatoid arthritis?

A

o polyarthritis -> swelling of the small joints of the hand and wrists is common

o symmetrical

o early morning stiffness in and around joints is common

o may lead to joint damage and destruction: ‘joint erosions’ on radiographs

o extra-articular disease can occur -> rheumatoid nodules or others which are rarer e.g. vasculitis, episcleritis -> because of rheumatoid factor (autoantibody) forming immune complexes

85
Q

What is rheumatoid factor?

A
  • IgM autoantibody against the Fc portion of IgG -> hence also called rheumatoid antibody
  • can be detected in the blood -> isn’t a test as 1/3 of rheumatoid arthritis is negative
86
Q

Is rheumatoid arthritis more common in men or females?

A
  • females by 3:1
87
Q

What is the big environmental factor for rheumatoid arthritis?

A
  • smoking -> contributes to 25%
88
Q

What joints are most commonly affected in rheumatoid arthritis?

A
  • metacarpophalangeal joint (MCP)
  • proximal interphalangeal joint (PIP)
  • wrists
  • knees
  • ankles
  • metatarsophalangeal joint (MTP)
89
Q

What deformities will occur in severe rheumatoid arthritis?

A
  • swan-neck deformity -> hyperextension at the PIP and hyperflexion at the DIP
  • Boutonniere deformity -> hyperflexion at the PIP (boutonniere means ‘button-like’)
90
Q

Define dactylitis.

A
  • swelling of an entire digit
91
Q

Is dactylitis a sign of rheumatoid arthritis?

A
  • no -> rheumatoid arthritis is just swelling of the joints
92
Q

What is tenosynovium and how is it linked to rheumatoid arthritis?

A
  • tenosynovium wraps around tendons to allow them to move freely
  • if you ask a patient with extensor tenosynovitis to raise fingers à you will see the swelling being pulled back -> confirms that the synovitis is around the tendons and not the joints
  • tenosynovitis can damage the tendons and impair their function
93
Q

What are sometimes found at the ulnar border in patients with rheumatoid arthritis?

A
  • rheumatoid factor can produce immune complexes that can deposit in any tissue -> have a tendency to deposit in subcutaneous tissue and cause extra-articular manifestations -> commonly along the ulnar border of the forearm
  • these extra-articular manifestations are relatively rare
  • rheumatoid nodules are clinically relevant because if rheumatoid nodules are present, the patient is always rheumatoid factor positive
94
Q

What extra-articular features are still common and which are uncommon?

A

o common -> fever (due to abnormal production of cytokines), weight loss and subcutaneous nodules

o uncommon -> vasculitis, ocular inflammation, neuropathies, amyloidosis, lung disease (nodules, fibrosis, pleuritic) and Felty’s syndrome (triad of splenomegaly, leukopenia and rheumatoid arthritis)

  • a less common due to the better health of general population -> less smokers mainly
95
Q

What is Felty’s syndrome?

A
  • triad of splenomegaly, leukopenia and rheumatoid arthritis
96
Q

What are the radiographic signs of rheumatoid arthritis?

A
  • early -> juxta-articular osteopenia (bones look a little less dense around the joints)
  • later -> joint erosions at margins of the joint
  • later still -> joint deformity and destruction
97
Q

Describe the synovial joint.

A
  • the synovium is normally a single type-1 collagen cell lining (can be 1-3 cells deep)
  • are macrophages and fibroblasts (which produce synovial fluid) within the synovial lining
  • synovial fluid is viscous because it contains a lot of hyaluronic acid
  • articular cartilage is made up of type 2 collagen -> main proteoglycan in articular cartilage is aggrecan
98
Q

What is the general management of rheumatoid arthritis?

A
  • treatment goal is to prevent joint damage
  • a multi-disciplinary approach involving physiotherapists, occupational therapists, surgery etc
99
Q

What are the DMARDs?

A
  • disease-modifying anti-rheumatoid drugs
  • often reffered to as steroid sparing agents -> are safer and more effective in the long-term than steroid
100
Q

When are DMARDs started?

A
  • early on in disease -> joint damage = inflammation x time
  • won’t to prevent joint damage
101
Q

What biological therapies can be used in rheumatoid arthritis?

A
  • inhibition of tumour necrosis factor-alpha (‘anti-TNF’) -> infliximab (an antibody)
  • B cell depletion -> rituximab
  • modulation of T cell co-stimulation
  • inhibition of interleukin-6 -> tocilizumab
102
Q

What are the downsides to biological therapy?

A

o increased infection risk -> TNF-alpha is important in granuloma formation -> increased susceptibility to mycobacterial infection e.g. tuberculosis

  • all patients must be screened for tuberculosis before starting treatment -> may use prophylactic antibiotics in those at high risk

o B cell depletion therapy can be associated with hepatitis B reactivation, progressive multifocal leukoencephalopathy (PML) and JC virus -> patients scanned for hepatitis B before treatment

o very expensive

103
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
104
Q

What helps distinguish reactive arthritis from rheumatoid arthritis?

A
  • extra-articular manifestations - particularly:
  • enthesopathy (overlap between reactive arthritis and seronegative spondyloarthropathies)
  • skin inflammation
  • eye inflammation
105
Q

Reactive arthritis is often the first manifestation of what disease?

A
  • HIV and hepatitis C
106
Q

Is there a genetic component to reactive arthritis?

A
  • yes -> genetic predisposition could be HLA-B27, and environmental trigger could be salmonella infection
107
Q

How long does it take for symptoms of reactive arthritis to appear?

A
  • 1-4 weeks after infection
108
Q

What are the symptoms of reactive arthritis?

A

o ARTHRITIS -> asymmetrical, oligoarthritis (<5 joints), lower limbs are typically affected

o ENTHESITIS -> are manifestations involving inflammation of the enthesis:

  • heel pain (Achilles tendonitis)
  • swollen fingers (dactylitis)
  • painful feet (metatarsalgia due to plantar fasciitis)

o SPONDYLITIS -> predilection for spinal inflammation:

  • sacroiliitis (inflammation of the sacro-iliac joints)
  • spondylitis (inflammation of the spine)
109
Q

What are the extra-articular features of reactive arthritis?

A
  • ocular -> sterile conjunctivitis
  • genito-urinary -> sterile urethritis
  • skin -> circinate balanitis AND psoriasis-like rash on hands and feet
110
Q

Fill in this table.

111
Q

How is the diagnosis for reactive arthritis established?

A

o clinical diagnosis -> investigations to exclude other causes of arthritis e.g. septic arthritis

  • these include:

o microbiological analysis -> microbial cultures and serology e.g. HIV, hepatitis C

o immunological tests -> rheumatoid factor should be negative in reactive arthritis

o synovial fluid examination -> especially if only single joint affected

112
Q

How is septic arthritis different from reactive arthritis?

A
  • has a positive synovial fluid culture
113
Q

How is reactive arthritis treated?

A

o articular -> NSAIDs, intra-articular corticosteroid therapy

o extra-articular -> typically self-limiting, hence symptomatic therapy -> e.g. topical steroids & keratolytic agents in keratoderma

o refractory disease -> oral glucocorticoids or steroid-sparing agents e.g. sulphasalazine

114
Q

What is osteoarthritis?

A
  • chronic slowly progressive disorder, primarily due to failure of articular cartilage that typically affecting joints of the hand (especially those involved in pinch grip), spine and weight-bearing joints (hips and knees) -> often due to the wear and tear of age
115
Q

Which joints are most commonly effected in osteoarthritis?

A

o joints of the hand -> distal interphalangeal joints, proximal interphalangeal joints and first carpometacarpal joint

o spine

o weight-bearing joints of lower limbs -> especially the knees and hips and also the first metatarsophalangeal joint

116
Q

What are the names of the bony outgrowth in osteoarthritis?

A
  • Heberden’s nodes -> bony, prominent swelling around the distal interphalangeal joints
  • Bouchard’s nodes -> bony swellings around the proximal interphalangeal joints
117
Q

What are the symptoms of osteoarthritis?

A
  • joint pain -> worse with activity, better with rest (loss of articular cartilage -> mechanical failure of joints)
  • joint crepitus -> creaking, cracking, grinding sound on moving affected joint
  • joint instability
  • joint enlargement -> e.g. Heberden’s nodes
  • joint stiffness after immobility (‘gelling’)
  • limitation of motion
118
Q

What are the radiological features of osteoarthritis?

A
  • joint space narrowing -> represents the loss of articular cartilage
  • subchondral bony sclerosis (underlying bone reacting to damaged articular cartilage)
  • osteophytes (Heberden’s and Bouchard’s nodes)
  • subchondral cysts
119
Q

Fill in the table.

120
Q

What causes osteoarthritis?

A
  • DEFECTIVE and IRREVERSIBLE articular cartilage and DAMAGE to underlying bone
  • develops due to either excessive loading on the joints or abnormal joint components
  • is a very multifactorial condition -> are some rare metabolic and endocrine factors -> the vast majority of patients have an obvious cause of osteoarthritis: lifestyle activity, or aging
121
Q

What does the viscousity of synovial fluid depend on?

A
  • hyaluronic acid contained within it
122
Q

What is the main proteoglycan in articular cartilage?

A
  • aggrecan -> makes up articular cartilage with type 2 collagen
123
Q

What are the cartilage changes in osteoarthritis?

A
  • reduced proteoglycan
  • reduced collagen
  • chondrocyte changes -> e.g. apoptosis
  • changes are often localised
124
Q

What changes to the bone occur in osteoarthritis?

A

o changes in denuded sub-articular bone

  • proliferation of superficial osteoblasts results in production of sclerotic bone e.g. subchondral sclerosis
  • focal stress on sclerotic bone can result in focal superficial necrosis

o new bone formation at the joint margins (termed osteophytes) -> Heberdens and Bouchards nodes

125
Q

What is the current management plan for osteoarthritis?

A

o CURRENTLY NO DISEASE MODIFYING TREATMENTS

  • education
  • physical therapy -> physiotherapy, hydrotherapy (optimizing physical strength of patient)
  • occupational therapy
  • weight loss where appropriate
  • exercise
  • analgesia -> paracetamol, NSAIDs, intra-articular corticosteroid injection
  • joint replacement if it comes to it -> has been a MAJOR success
126
Q

What is SLE?

A
  • a chronic autoimmune disease characterised by relapse and remitting -> affects multiple organ systems including the heart, lungs, kidneys, skin and feotus
127
Q

What are the risk factors for SLE?

A
  • sex = M:F ratio is 1:9
  • age = seen at 15-40 years -> rare to present after menopause
  • race = predominantly affects Afro-Caribbeans, Asians and Chinese
  • genetics = multiple genes implicated
128
Q

Describe the pathogenesis of SLE.

A
  1. abnormal clearance of apoptotic cell material due to genetic predisposition (HLA-DR3) and an environmental trigger (UV-light, EBV etc.)
  2. dendretic cell uptake of autoantigens and activation of B cells
  3. B cell Ig class switching -> IgG autoantiboides
  4. immune complexes form -> complement activation cytokine generation
  5. CLINICAL DISEASE ONSET -> IRREVERSIBLE TISSUE DAMAGE
129
Q

What is the general presentation of SLE patient?

A

o can be vague initially -> malaise, fatigue, fever, weight loss

  • lymphadenopathy is a feature of early, active SLE
  • more specific features are butterfly rash (malar rash), alopecia, arthralgia, Raynaud’s syndrome
130
Q

What is the diagnostic criteria for SLE?

A

o if a patient has 4 or more of these 11 it points towards lupus

  • S-serositis
  • O-oral ulcers
  • A-arthritis
  • P-photosensitivity
  • B-Blood (all low)
  • R-Renal proteinuria
  • I-Immunological -> ANA, anti-dsDNA
  • N-neurological-seizures/psychosis
  • M-Malar rash
  • D-discoid rash
131
Q

Dose the presence of ANA mean a patient has lupus?

A
  • no -> 5% of teh population has it
  • can just be a marker for infection or another autoimmune disease
132
Q

How is a diagnosis of SLE made after being suspect?

A
  1. antinuclear antibodies in the blood -> non-specific, so a positive ANA test is NOT necessarily diagnostic of SLE -> use an indirect immunofluorescence test -> antibodies in serum will bind nuclear antigens and give a pattern of staining -> homogenous pattern suggests SLE
  2. in order to direct our diagnosis towards SLE, we need to look for more specific anti-nuclear antibodies-> anti-dsDNA antibodies and Sm, anti-Sm antibody, anti-Ro and/or La antibodies
  3. Useful Laboratory Tests -> increased complement consumption/a reduction in the circulating amount of C3 and C4
    - > anti-cardiolipin antibodies, lupus anticoagulant, beta-1 glycoprotein
    - > haematology -> lymphopaenia, anaemia (commonly normochromic), keukopenia and thrombocytopenia
    - > renal -> proteinuria (using a dipstick sample) and haematuria
133
Q

What antibody in lupus can cause feotal heart block?

A
  • anti-Ro antibodies -> can cross the placenta
134
Q

How is the severtiy of SLE assessed?

A
  1. identify pattern of organ involvement
  2. monitor function of affected organ
  3. identify pattern of autoantibodies expressed
135
Q

How can SLE be group in term of severity?

A

o MILD = joint +/- skin involvement

o MODERATE = inflammation of other organs too

o SEVERE = severe inflammation in vital organs -> severe nephritis, CNS disease, pulmonary disease, cardiac involvement, AIHA, thrombocytopenia, TTP

136
Q

What is the treatment for mild SLE?

A
  • paracetamol or NSAIDs
  • hydroxychloroquine if arthtopathy/arthrtitis is a bit worse
  • topical corticosteroid cream for rashes
137
Q

What indicates that SLE is moving from mild to moderate and then to severe?

A
  • failure of the treatment plan for the lesser severity of the disease
  • progression to more serious symptoms
138
Q

What is the treatment for moderate SLE?

A
  • first line treatment of MODERATE SLE is CORTICOSTEROIDS -> start at a HIGH initial dose to suppress disease activity (0.5-1.5 mg/kg/day) -> then give intravenous methylprednisolone (3 x 0.5-1g per 24 hours)
  • reduce the dose SLOWLY over 2-3 months, to 10mg/day, and then to 1mg per month
139
Q

What is the treatment for severe SLE?

A
  • azathioprine -> immunomodulatory therapy (2.5 mg/kg/day)
  • FBC & biochemistry monitoring (predominant side effects are on the bone marrow)
  • cyclophosphamide is given in severe organ involvement, intravenously pulsed or oral administration -> causes bone marrow suppression, a risk of infertility, and cystitis (acrolein)
140
Q

What is the prgonosis of SLE?

A
  • 85% 15 year survival in patients without nephritis
  • 60% 15 year survival in patients WITH nephritis
  • prognosis tends to be worse if black, male and low socio-economic status
141
Q

What are the 3 main categories of SLE treatment?

A
  • symptomatic
  • immune-modulating
  • immunosuppresive
142
Q

What are the 3 major biomarkers of disease activity?

A
  1. complement factors -> C3 and C4
  2. ESR
  3. anti-dsDNA antibodies
143
Q

What questions are asked in the GALS examination before the actuall examination begins?

A
  • Have you any pain or stiffness in your muscles, joints or back?
  • Can you dress yourself completely without any difficulty?
  • Can you walk up and down stairs without any difficulty?
144
Q

What does GALS stand for?

A
  • G = gait
  • A = arms
  • L = legs
  • S = spine
145
Q

How is gait examined?

A

o observe patient walking, turning and walking back

  • smoothness and symmetry of leg, pelvis and arm movements
  • normal stride length
  • ability to turn quickly
146
Q

How is the spine examined, focusing on the GALS examination?

A
  • Is para-spinal and shoulder girdle muscle bulk symmetrical?
  • Is the spine straight?
  • Are the iliac crests level?
  • Is the gluteal muscle bulk normal?
  • Are the popliteal swellings?
  • Are the Achilles tendons normal?
  • Are there signs of fibromyalgia?
  • Are spinal curvatures normal?
  • Is lumbar spine and hip flexion normal?
  • Is cervical spine normal?
147
Q

How are arms examined in the GALS examination?

A
  • Look for normal girdle muscle bulk and symmetry
  • Look to see if there is full extension at the elbows
  • Are shoulder joints normal?
  • Examine hands palms down with fingers straight
  • Observe supination, pronation, grip and finger movements
  • Test for synovitis at the metacarpo-phalangeal joints (MCP joints)
148
Q

How are the legs examined in GALS examination?

A
  • Look for knee or foot deformity
  • Assess flexion of hip and knee
  • Look for knee swellings
  • Test for synovitis at the metatarso-phalangeal joints (MTP joints)
  • Inspect soles of the feet for rashes and/or callosities
149
Q

Whta happens after the GALS screen?

A
  • locomotor examination -> detailed examination of any abnormal joints identified in the GALS screen
150
Q

What is the difference between arthritis and arthralgia?

A
  • arthritis = inflammation of a joint
  • arthralgia = pain within a joint without demonstartable inflammation by physical examination
151
Q

What are the 5 signs of inflammation?

A
  • tumor = swelling
  • calor - warmth
  • rubor = redness
  • dolor = tenderness
  • functio laesa = loss of function
152
Q

Describe gout.

A
  • a disease in which tissue deposition of monosodium urate (MSU) crystals occurs as a result of hyperuricaemia and leads to one or more of -> gouty arthritis or tophi (aggregated deposits of MSU in subcutaneous tissue – this is RARE)
  • > gouty arthritis commonly affects the metatarsophalangeal joint of the big toe (‘1st MTP joint’) podagra
  • symptoms are an abrupt onset, extreme pain, joint redness, warm, swollen and tender
  • will resolves spontaneously over 3-10 days
153
Q

What is enthesopathy?

A
  • pathology at the enthesis -> site where ligament or tendon inserts into bone
  • includes plantar fasciitis AND Achilles tendinitis
154
Q

How are abnormal joints examined?

A
  • inspection -> swelling, redness, deformity
  • palpation -> warmth, crepitus, tenderness
  • movement -> active, passive, against resistance
  • function -> loss of function
155
Q

What are the signs of irreversible joint damage?

A
  • joint deformity -> mal-alignment of two articulating bones
  • crepitus -> audible (crunching sound) and palpable sensation resulting from movement of one roughened surface on another -> classic feature of osteoarthritis e.g. patello-femoral crepitus on flexing the knee
  • loss of joint range or abnormal movement
156
Q

Define dislocation.

A
  • articulating surfaces which are displaced and no longer in contact
157
Q

Define sublaxation.

A
  • partial dislocation -> not a complete loss of contact
158
Q

Define varus deformity.

A
  • lower limb deformity whereby distal part is directed towards the midline -> e.g. varus knee with medial compartment osteoarthritis
159
Q

Define valgus deformity.

A
  • lower limb deformity whereby distal part is directed away from the midline -> e.g. hallux valgus
160
Q

What are the usualy causes of a mechanical defect of a joint?

A
  • inflmmation, degenerative arthritis, trauma
  • often causes painful restriction
161
Q

Describe the patterns of arthritis.

A

o number of joints involved -> polyarthritis = > 4 joints, ligoarthritis = 2-4 joints, monoarthritis = single affected joint

o is involvement is symmetrical

o size of the involved joints

o is there axial/spinal involvement

162
Q

What does bilateral and symmetrical involvement of large and small joints typically suggest?

A
  • rheumatoid arthritis
163
Q

What does lower limb asymmetrical oligo-arthritis and axial involvement typically suggest?

A
  • reactive arthritis
164
Q

What does exclusive inflammation of the first metatarsophalangeal joint suggest?

165
Q

How can the neutrophil content of synovial fluid be an important diagnostic marker?

166
Q

What is Sjogren’s syndrome?

A
  • a connective tissue disease in which there is destruction of exocrine glands (autoimmune exocrinopathy), lymphocytic infiltration of exocrine glands and sometimes other organs (extra-glandular involvement)
  • typically diagnosed in middle-aged female (F:M = 9:1)
  • symtpoms include dry eyes, dry mouth and parotid gland enlargement
167
Q

What is systemic sclerosis?

A
  • a disorder that attacks the skin and causes dermal fibrosis (VERY RARE)
  • thickened skin with Raynaud’s phenomenon
  • dermal fibrosis, cutaneous calcinosis and telangiectasia

Y2 LCRS (8 decks)

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