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Phase2a > MSK > Flashcards

MSK Flashcards

1
Q

compare inflammatory vs degenerative joint problems

A 
inflammatory 
- pain eases with use
- a lot of stiffness - >60minutes, early morning/at rest
- swelling - synovial/bone
- joints - hands and feet
- pts young psoriasis, family history 
- responds to NSAIDS
- hot and red
degenerative 
- pain increases with use - clicks/clunks
- stiffness not prolonged <30mins - morning/evening
- swelling - none/bony
- joints - CMCJ, DIPJ, knees
- Pts - older, prior occupation/sport
- doesn't respond to NSAIDS
- not inflamed
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2
Q

describe two inflammatory markers that can be used to diagnose MSK disease

A

ESR - erythrocyte sedimentation rate
- raised in infection
- increased fibrinogen = RBC’s stick together = fall faster
- false positives : age, female, obesity, racial difference, hypercholesterolaemia, high Ig, anaemia
- rises and falls slowly
CRP - C reactive protein
- produced by liver in response to IL6 from activated macrophages
- rises and falls rapidly
- binds to damaged cells activating complement
- increases phagocytosis

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3
Q

list three types of autoimmune joint paint

A
  • rheumatoid
  • spondyloarthropathy (HLA B27 associated)
  • connective tissue disorders
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4
Q

what are the features of spondyloarthropathy

A
  1. seronegativity - rheumatoid factor negative
  2. HLA B27 association - class I surface antigen on all cells, encoded by MHC on chromosome 6, human leucocyte antigen
  3. Axial arthritis - spine and SI joints
  4. asymmetrical large joint oligoarthritis
  5. enthesis - inflammation of site of insertion into tendon or ligament
  6. dactylitis - inflammation of entire digit
  7. extra articular - anterior uveitis, psoriasis, IBD, oral ulcers, aortic valve incompetence
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5
Q

describe the three theories to why HLA B27 is linked with disease

A
  • molecular mimicking theory - infection —> immune response —-> infectious agent has peptides very similar to HLA B27 molecule —-> autoimmune response
  • heavy chain homodimer hypothesis - heavy chains can form stable dimers and bind to NKreceptors + accumulate in ER, causing stress response
  • misfolding theory - unfolded HLA B27 accumulate in ER causing pro inflammatory stress response and releasing IL23
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6
Q

describe ankylosing spondylitis

A
  • a spondyloarthopathy
  • inflammatory arthritis
  • HLA B27 linked
  • axial arthritis
  • leads to new bone formation and fusion of the joints
  • men present earlier < 30 years old
  • syndesmophytes (new bone formation and vertical growth from anterior vertebral corners)
  • sacroilitis - joint fusion
  • eventually unable to look ahead whilst walking
  • inflammation — erosive damage — repair —- new bone
  • spectrum of disease
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7
Q

what are the signs of ankylosing spondylitis

A
  • gradual onset of lower back pain
  • worse during night with exercise relieving stiffness
  • pain radiates from SI joints to buttocks/hips
  • progressive loss of spinal movement
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8
Q

what are the tests for ankylosing spondylitis

A
  • MRI -active inflammation
  • X-rays - joint space decreased or increased, sclerosis, erosions, ankylosis/fusions. Vertebral syndesmophytes
  • HLA B27 positive
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9
Q

what is the management of ankylosing spondylitis

A
  • exercise
  • NSAIDS
  • TNFa blockers
  • surgery
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10
Q

what are the 5 patterns of psoriatic arthritis

A
  1. symmetrical polyarthritis
  2. DIP joints
  3. axial
  4. large joint oligoarthritis
  5. arthritis mutilans (telescoping fingers)
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11
Q

what is the management of psoriatic arthritis

A
  • NSAIDS
  • anti TNFa drugs
  • MTX, suldasalazine
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12
Q

what is reactive arthritis

A
  • sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant, usually GI or genital
    GI - salmonella, shigella
    STI - chylamidia, ureaplasma urealyticum
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13
Q

what are the signs of reactive arthitis

A
  1. arthritis
  2. conjunctivitis
  3. sterile urethritis
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14
Q

what are the tests for reactive arthritis

A
  • ESR + CRP
  • culture stool
  • sexual health review
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15
Q

what is the pathology of RA

A 
Inflammation
- chronic inflammatory reaction 
- infiltation of lymphocytes, macrophages, plasma cells
proliferation 
- tumour like mass - pannus
- grows over articular cartilage
- cartilage destruction by released proteinases e.g MMP - matrix mellatorproteinases
- due to autoantibodies
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16
Q

what are the symptoms/signs of RA

A
  • symmetrical swollen, painful and stiff small joints of hands and feet
  • worse in morning
  • general fatigue
  • malaise
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17
Q

what are the extraarticular features of RA

A
  • Heart disease
  • pleural disease, small airways disease, diffuse fibrosing alveolitis
  • eyes - sicca (dry eyes) , scleritis (corneal ulceration)
  • skin
  • nodules (lumps on skin)
  • bursitis
  • muscle wasting
  • neuro - sensory peripheral neuropathy, entrapment neuropathy (swelling around nerves) e.g carpal tunnel
  • instability of cervical spine (spinal cord compression/nerve root compression)
  • pericarditis
  • anaemia
  • splenomegaly
  • palpable lymph nodes
  • amyloidosis
  • analgesic nephropathy
  • vasculitis
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18
Q

what are the tests for RA

A
  • Anaemia
  • increased ESR/CRP
  • Positive rhuematoid factor in 80% - antibody against Fc portion of Ig - altered immune response
  • anti CCP antibody - highly specific, relatively sensitive
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19
Q

what is the management of RA

A
  • disease modifying anti rheumatic drugs (DMARD) e.g methotrexate
  • steroids decrease symptoms and inflammation
  • NSAIDS decrease symptoms e.g diclofenac
  • physio
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20
Q

what is the pathology of vasculitis

A
  • inflammation and necrosis of blood vessel walls with subsequent impaired
  • vessel wall destruction - perforation and haemorrhage into tissues
  • endothelial injury - thrombosis and ischaemia/infarction of dependent tissues
  • infiltration of neutrophils, mononuclear cells and giant cells
    -leukocytoclasis (dissolution of leucocytes)
    -
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21
Q

give examples of large, medium and small vessel vasculitis

A 
large 
- giant cell arteritis
- takayasu's arteritis 
- isolated CNS angitis
medium 
- classical polyarteritis nodosa (PAN)
- Kawasaki disease
small/med
- wegeners granulomatosis 
- churg strauss
- microscopic polyangitis 
small vessels 
- henoch schonlein purpura
- essenial mixed cyyoglobulinaemia 
-cutaenous leucocytooclastic angitis
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22
Q

what are the symptoms of vasculitis

A

systemic - fever, malaise, weight loss, arthralgia/myalgia
skin - purpura, ulcers, livedo reticularis (pink blue mottling), digital gangrene
eyes - visual loss, scleritis, episcleritis
CV - angina/MI, HF, pericarditis
pulmonary - haemoptysis, dyspnoea
GI - pain or perforation
Renal - failure, inc BP, haematuria
Neuro - stroke, fits, confusion

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23
Q

what is ANCA and when is an ANCA result positive

A

antineutrophilic cytoplasmic antibodies

  • positive in small/med vessel vasculitis
  • specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes
  • detected with immunofluroscence microscopy
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24
Q

what is giant cell (temporal arteritis)

A
  • granulomatous arteritis of aorta and large vessels - extracranial branches of carotid arteries
  • > 50 yrs
  • ANCA negative
  • 2x more common in women
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25
Q

what are the diagnostic criteria or temporal/giant cell arteritis

A

3 or more:

  • age > 50
  • new headache
  • temporal artery tenderness on decreased pulse
  • ESR > 50mm/h
  • abnormal artery biopsies showing necrotising artertis with mononuclear infiltrate or granulomatous inflammation
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26
Q

what are the symptoms of giant cell arteritis

A
  • headache
  • jaw claudation
  • non specific malaise
  • scalp tenderness
  • acute blindness
  • symptoms of polymyalgia rhuematica
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27
Q

what are the tests of temporal arteritis

A
  • increased ESR, CRP
  • increased platelet
  • inc ALP
  • decreased Hb
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28
Q

what is the management of temporal arteritis

A
  • corticosteroids immediately
  • falling ESR/CRP guides treatment
  • prophylaxis of osteoporosis - bisphosphonate and vit D + DEXA
  • steroid sparing agents - methotrexate
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29
Q

what is granulomatosis with polyangitis ( GPA)

A
  • wegeners granulomatosis
  • necrotizing granulomatous vasculitis of arterioles, capillaries and post capillary venules
  • ANCA associated
  • 25-60 years
  • vasculature of all organ systems
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30
Q

what are the extravascular symptoms of GPA

A
  • URT - sinusitis, otitis media
  • lungs- pulmonary haemorrhage/nodules
  • kidneys - glomerulonephritis
  • skin - purpura/ulcers
  • NS - CNS vasculitis
  • pericarditis
  • synovitis
  • uveitis, scleritis
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31
Q

what is the management of GPA

A
  • High dose steroids/ cyclophosphamide/ biologics (severe)

- moderate dose steroids + methotrexate (moderate)

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32
Q

what is osteoarthritis

A
  • non inflammatory arthritis of movable joints characterised by deterioration of articular cartilage and the formation of new bone of the joint surfaces and margins
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33
Q

what are the predisposing factors of osteoarthritis

A
  1. genetic
    - dominant trait with mendelian pattern
    - hip, knee, dipj, pipj, cppd
  2. trauma
    - intraarticular
    - long bone fractures with malalignment
    - joint instability e.g torn ACL
  3. deformities
    - birth deformities, syndromes
  4. occupation
  5. obesity
  6. bone density
    - increased in patients with OA
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34
Q

What is the pathogenesis of osteoarthritis

A
  • articular cartilage failure
  • chondrocytes main cells responsible
  • proteases - mellatoproteases
  • catabolic cytokines -IL1, TNFa
  • anabolic cytokines - insulin like GF, TGFb
  • inflammation
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35
Q

what are the symptoms of osteoarthritis

A 
- not systemic unlike inflammatory conditions
pain (articular cartilage and synovium have no nerve supply, pain is from capsular stretching and vascular congestion of the bone)
- insidious and increases over months or years 
- relieved by rest 
-aggrevated by activity 
- may be referred pain 
swelling 
- may be intermittent - effusion
- continuous - capsular thickening
stiffness
- worse after periods of rest 
-muscle wasting 
- deformtiy 
- decreased ROM
- crepitus
- osteophytes palpable - heberdens nodes at DIP, bouchards at PIP
- joint instability
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36
Q

what are the differential diagnoses of osteoarthritis

A
  • rheumatoid
  • gout
  • osteonecrosis
  • neuropathic joint
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37
Q

what are the investigations for osteoarthritis

A 
xrays show
- loss of joint space
- osteophytes
- subarticular sclerosis 
- subchondrial cysts 
CT -some joints not visible
isotope bone scan - hot due to increased vascularity and new bone
blood and synovial fluid all normal
diagnostic injection to isolate joint affected 
arthroscopy
CRP may be slightly elevated
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38
Q

what is the management of osteoarthritis

A

depends on

  • joint
  • stage of disorder
  • severity of symptoms
  • age
  • functional needs

conservative/non surgical

  • goals - decreased load on joint, relieve pain, promote movement
  • lifestyle modification - diet and weight loss
  • splints and orthotics - walking stick, soft soled shoes, heel raises
  • exercise and physio to improve flexibility and strengthen muscle
  • topical products - contain capsaicin, decrease pain by depleting stores of substance P. And NSAIDS
  • Tablets - analgesics and glucosamine- constituents of proteoglycans which resists compression forces in the joint - paracetemol, NSAIDS and COX 2 inhibitors

injection

  • steroid
  • viscosupplementation agent - hyaluronic acid - cartilage matrix component

surgery

  • goals: remove pain, improve function, correct deformity
  • debridement of joint - removal of dead bone and waste products
  • realignment of osteotomies - take bit of bone below joint (tibia) and add to top of articular surface to make joint space narrower
  • joint excision
  • joint fusion (arthrodesis) e.g ankle
  • joint replacement (arthroplasty)
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39
Q

what is the pathology of systemic lupus erythematosus

A
  • multisystemic autoimmune disease
  • autoantibodies made against autoantigens such as ANA which form immune complexes
  • inadequate clearance of immune complexes results in host of immune responses which cause tissue damage
  • inflammation leading to scarring
  • can be treated with immunosuppressive drugs
  • thrombosis - phospholipid antibodies
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40
Q

which gene is systemic lupus erythematosus associated with

A

HLA DR2, DR3

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41
Q

what are the symptoms of signs of SLE

A
  • acute cutaneous lupus: malar rash/butterfly
  • chronic cutaneous lupus: discoid rash
  • non scarring alopecia
  • oral/nasal ulcers
  • synvoitis
  • serositis a) lung b) pericarditis
  • urinalysis - proteinuria- glomerulonephritis
  • neurological - seizures, psychosis, depression
  • haemolytic anaemia
  • leucopenia
  • thrombocytopenia
  • arthritis - symmetrical, less proliferative than RA, can be deforming, non erosive
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42
Q

what is the management of SLE

A
  • Patient education and support
  • UV protection
  • assessment of lupus activity
  • screening for major organ development
  • topical - sunscreens, steroids, cytotoxic
  • NSAIDS
  • antimalarial
  • anticoagulants
  • biological - target B cells - rituximab, belimumab
  • plasmapheresis
  • stem cell transplant
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43
Q

what is raynauds phenomenon and what is it caused by

A
  • peripheral digit ischaemia
  • either primary or secondary to
  • connective tissue disorders
    systemic sclerosis, SLE, mixed connective
  • drugs
  • vascular damage
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44
Q

what does the crest acronym stand for in reference to systemic sclerosis

A 
Calcinosis 
Raynouds phenomenon
Oesophageal reflux
Sclerodactyly
Terangestasia
45
Q

what is the pathogenesis of systemic sclerosis

A
  • vasculopathy
  • excessive collagen deposition
  • inflammation
  • autoantibody production
46
Q

what is the management of systemic sclerosis

A 
Raynaud's
- physical protection
-vasodilators
Renal crisis 
- use of ACE i
early detection of pulmonary arterial hypertension 
- ECHO's and pulmonary function tests
cyclophosphamide for treatment of pulmonary fibrosis
47
Q

what are the causes of Sjogrens syndrome

A 
primary
or secondary to:
- SLE
- RA
- scleroderma
- primary biliary sclerosis
48
Q

what are the symptoms of sjogrens syndrome

A
  • dry eyes
  • dry mouth
  • -enlarged salivary gland
  • inflammatory arthritis
  • rash
  • neuropathies
  • vasculitis
  • neonatal lupus
49
Q

what are the tests for sjogrens syndrome

A
  • increased Ig
  • increased ESR
  • autoantibodies RF, ANA
50
Q

what is the management of sjogrens syndrome

A
  • tear and saliva replacement
  • immunosuppression
  • rituximab
51
Q

what is osteomyelitis and what is it caused by

A
  • bone marrow inflammation
  • bimodal age distribution
    children = acute, haematogenous osteomyelitis (80%)
    adolescents and adults get contiguous osteomyelitis - often due to direct trauma
    older people - caused by PVD, DM, arthoplasties (therefore increased incidence of chronic osteomyelitis due to increased prevalance of DM and PVD)
52
Q

what are the categories of osteomyelitis

A
  • direct inoculation of infection into the bone - trauma or surgery, polymicrobial or monomicrobial
  • contiguous spread of infection into the bone - from adjacent soft tissues and joints, DM, chronic ulcers, vascular disease, arthroplasties/prosthetic material
  • haematogenous seeding - children (long bones), monomicrobial
53
Q

what are the host and microbial factors that make osteomyelitis more likely

A
  • vascular supply - arterial disease, sickle cell, DM
  • behavioural - risk of trauma
  • pre-existing bone/joint problem - inflammatory arthritis, prosthetic material
  • immune deficiency - immunosuppressive drugs or primary

microbial

  • microbial surface components adhere to matrix molecules
    s. aureus
  • binds host proteins fibronectin, fibrinogen and collagen
  • can survive intracellularly in cultured and macrophages
  • salmonella in sickle cell
  • pseudomonas aeruginosa in IVDU
54
Q

What acute and chronic histological changes are seen in osteomyelitis

A 
acute 
- inflammatory cells
- oedema
- vascular congestion
-small vessel thrombosis
 chronic 
-necrotic bone
-new bone formation
-neutrophil exudates
- lymphocytes and histiocytes
55
Q

in osteomyelitis, what does inflammatory exudate in the marrow lead to?

A
  • increased intramedullary pressure
  • extension of exudate into the bone cortex
  • rupture through periosteum
  • interruption of periosteal blood supply causing necrosis
  • leaves pieces of separated dead bone “sequestra”
  • New bone forms here “involucrum”
56
Q

what are the signs and symptoms of osteomyelitis

A 
symptoms 
- onset: several days 
- dull pain at site of OM
- maybe aggravated by movement 
-chronic ulcers
-non healing fractures
signs 
- local - tenderness, warmth, erythema, swelling
- systemic - fever, rigors, sweats, malaise

OM in sites like hip, vertebrae (lumbar > thoracic > cervical)

  • in vertebrae can lead to abscesses
  • can also present as septic arthritis - when infection breaks through cortex resulting in discharge of pus into the joint
  • more common in infants due to patent transphyseal blood vessels and immature growth plate
57
Q

what are the tests for osteomyelitis

A
  • acute - increased WCC
  • chronic - can be normal WCC
  • ESR/CRP raised
  • imaging
    plain X-ray shows - cortical erosion, periosteal reaction, sequestra, soft tissue swelling, sclerosis
    MRI - marrow oedema from 3-5 days
  • bone biopsy - histology showing inflammation and osteonecrosis
  • positive blood cultures
58
Q

what are the differential diagnoses of osteomyelitis

A
  • soft tissue infection
  • avascular necrosis
  • gout
  • fracture
  • bursitis
  • malignancy
  • charcot joint
59
Q

what is the treatment of osteomyelitis

A
  • surgical - debridement (removal of damaged tissue), hardware placement or removal
  • antimicrobial therapy - s.aureus/strep/emterococci, pseudomonas - flucloxacillin IV
60
Q

give examples of things that increase urate

A
  • increased intake
  • increased cell turnover (production)
  • increased cell damage (surgery)
  • increased cell death ( chemo)
  • inborn errors of metabolism (Lesch Nyan syndrome)
  • reduced excretion (90% of cases) - renal - diuretics
  • drugs, genetics, fructose, increased insulin levels (lower rate excretion)
  • increased risk with alcohol, red meat, seafood, fructose intake
61
Q

which molecule causes gout

A

monosodium urate crystals

62
Q

what is the pathology of acute gout

A
  • change in blood/tissue balance
  • urate crystals trigger intracellular inflammation
  • self limiting - monocyte/macrophage maturation then producing anti-inflammatory cytokines
63
Q

what is the treatment of gout

A
  • colchicine 500micrograms for acute attack
  • NSAIDS
  • steroids - IM, oral, IA
  • Ice
  • Vit C
  • lifestyle changes
  • stop diuretics
  • aim urate < 300micromol/L
  • allopurinol 100mg/day - wait 3 weeks and increase by 100 if not < 300micromol/L and as prophylaxis
  • in renal impairment 1.5mg per unit eGFR
64
Q

what are the differential diagnoses of gout

A
  • septic arthritis
  • RA
  • CPPD
  • haemarthrosis
65
Q

how is gout diagnosed

A
  • polarised light microscopy shows negatively birefringent needle shaped urate crystals
  • serum urate raised
66
Q

what is osteoporosis

A
  • reduced bone mass causing pathological fracture
67
Q

what things contribute to fracture probability

A
  • trauma - likelihood of falling
  • bone strength
    BMD - peak bone mass, rate of bone loss
    bone size
    Bone quality - mineralisation, architecture, bone turnover
68
Q

what is the bone remodelling cycle

A

Quiescence
resorption
formation
quiescence

69
Q

what are the features of post menopausal osteoporosis

A
  • loss of restraining effects of oestrogen on bone turnover
  • preventable by oestrogen replacement
  • characterised by - high bone turnover resorption by osteoclasts > formation by osteoblasts, cancellous bone loss, microarchitechtural disruption
70
Q

what changes happen to trabecular architecture with aging

A
  • decrease in thickness, more pronounced for non load bearing horizontal trabeculae
  • decrease in connections between horizontal trabeculae
  • decrease in strength and increased susceptibility to fracture
71
Q

what tests can be used to diagnose osteoporosis

A
  • xray
  • DEXA - dual energy X-ray absorptiometry
    T score > O BMD better than reference (peak bone mass)
    0 to -1 - BMD in top 84% - not osteoporotic
    -1 to -2.5 - osteopenia
    -2.5 or below - osteoporosis
72
Q

what are the causes and risk factors for osteoporosis

A

inflammatory disease
- cytokines increase bone resorption e.g RA, IBD, connective tissue diseases
endocrine disease
- thyroid and parathyroid hormone increase bone turnover e.g hyperthyroidism and primary hyperparathyroidism
- cortisol increases bone resorption and induced osteoblast apoptosis e.g cushings syndrome
- oestrogen and testosterone control bone turnover e.g early menopause, male hypogonadism, anorexia/athletes
reduced skeletal loading increased resorption
- immobility
- low body weight

other risks 
Steroid use of >5mg prednisolone
Hyperthyroidism 
Alcohol and tobacco
Thin BMI <18.5 
Testosterone decrease
Early menopause
Renal or liver failure
Erosive/inflammatory bone disease
Dietary calcium decrease/malabsorption 
family history
previous fracture
medications 
- steroids 
-depo provera
- aromatase inhibitors
-GnRH analogues
-- androgen deprivation
73
Q

what is the management of osteoporosis

A
  • 10 year fracture probability calculated using FRAX - get a % based on risk factors
  • antiresorptive treatment -decrease osteoclast activity and therefore bone turnover - bisphosphonates such as alendronate PO, zoledronate IV
    Denosumab - monoclonal antibody to RANK ligand - no activation of osteoclast
    HRT
  • anabolic increase osteoblast activity and bone formation e.g teraparitide
- HRT (oestrogen)
benefits 
- decrease fracture his by about 50%
- stop bone loss, bone density may increase by up to 10%
- prevents hot flushes and other menopausal symptoms
-decreased risk of colon cancer
risks
-breast cancer
- stroke
-CV disease
- vaginal bleeding
74
Q

what is osteomalacia

A
  • normal amount of bone but decreased mineral content

- excessed uncalcified osteoid and cartilage

75
Q

what are the signs and symptoms of rickets

A
  • growth retardation
  • hypotonia
  • walks bow legged, knock kneed
  • features of low calcium
76
Q

what are the signs and symptoms of osteomalacia

A
  • bone pain and tenderness
  • fractures
  • proximal myopathy
  • due to decreased phosphate and vit D deficiency
77
Q

what are the cause of osteomalacia

A
  • vit d deficiency
  • renal osteodystrophy - 1,25 dihydroxycholecalciferol deficiency
  • drug induced
  • vit d resistance
  • liver disease
  • tumour induced
78
Q

what are the tests for osteomalacia

A
  • low calcium and phosphate
  • inc ALP
  • decreased Vit D
  • Biopsy shows incomplete mineralisation
  • X-ray shows loss of cortical bone
79
Q

what is the treatment of osteomalacia

A
  • vit D

- monitor Calcium

80
Q

what is Paget’s disease

A
  • increased bone turnover due to increased osteoblasts and osteoclasts
  • bone enlargement, deformity `(shown on X-ray) and weakness
  • deep boring pain
81
Q

what are the complications of pagets disease

A
  • pathological fractures
  • nerve compression due to bone overgrowth
  • increased Calcium
  • osteoarthritis
82
Q

what is the treatment of pagets disease

A
  • analgesia

- alendronic acid

83
Q

what are the red flags for MSK malignancy

A
  • rest pain
  • night pain
  • generally unwell
  • weight loss
  • lump present
  • loss of function
  • neurological symptoms
84
Q

what are the tests for MSK malignancy

A
  • blood tests - FBC, U+E, Calcium, ALK phos
  • plain xray - definition (less defined =malignant), density, zone of transition/distance between bone and tumour(wider = malignant), codmans triangle (periosteum lifted off bone by tumour), sunburst appearance (calcification of vessels around tumour), onion skin appearance - lifted off periosteum - then calcified
  • CT skin - assess bone quality, staging and metastases
  • MRI - soft tissue extent of tumour, skin lesions - islands of tumour
  • bone scan - skeletal metastases
  • US
  • biopsy
85
Q

describe the Enneking system for grading tumours of the MSK system

A

G0 - histologically benign - well differentiated, low mitotic count
G1 - low grade malignant - moderate differentiation, local spread only
G2 - not differentiated, frequent mitoses, high risk of metastases

86
Q

describe osteoid osteomas/osteoblastoma

A
  • osteoblastoma = osteoid osteoma > 2cm - treat with excision as pain not self limiting
  • osteoid osteoma found in young pts, with localised pain and self limiting, high levels of prostaglandins E2 produced
87
Q

describe osteosarcomas

A
  • malignant
  • spindle cell neoplasms that produce osteoid
  • intramedullary = high grade and most common - found in children and young adults
  • associated with P53 gene mutation
  • most common around one
  • treat with multi agent chemo and limb salvage surgery/amputation
  • 20% have pulmonary metastases at presentation
88
Q

what is the management of msk tumours

A
  • MDT
  • histological tests to show sensitivity of tumour to chemo - chemo/radio therapy - adjuvant post surgery or neo adjuvant pre surgery
  • surgery - limb sparing or limb sacrificing
89
Q

what is fibromyalgia

A
  • chronic symptoms of fatigue and widespread pain

- caused by aberrant peripheral and central pain processing

90
Q

what are the risk factors for fibromyalgia

A
  • middle aged
  • female
  • low educated
  • low social class
  • low household income
  • divorced
91
Q

what is the management of fibromyalgia

A
  • pacing of activity - long term graded exercise therapy
  • cognitive behaviour therapy
  • amitriptyline at night
92
Q

what are the features of fibromyalgia

A

allodynia - pain in response to none painful stimuli

hyper asthenia - exaggerated response to midly painful stimulus

93
Q

what are the symptoms of degenerative disc disease

A
  • pain in lower back

- can radiate to hips and legs

94
Q

what molecule causes pseudogout

A

positively birefringent rhomboid shaped calcium pyrophosphate crystals

95
Q

what are the risk factors for septic arthritis

A
  • > 80
  • existing joint disease, especially RA
  • IVDU
  • immunosuppressed
  • diabetes mellitus
  • chronic renal failure
  • recent joint surgery
  • prostethic joint
96
Q

what are the investigations for septic arthritis

A
  • synovial fluid aspiration microscopy and culture
  • blood culture
  • CRP and X-rays may be normal
97
Q

what is the treatment of septic arthritis

A
  • empirical IV antibiotics until sensitivities are knows
  • flucloxicillin or clindamycin if allergic to penicillin (s.aureus)
  • vancomycin (MRSA) plus cephalosporin
98
Q

which organisms most commonly cause septic arthritis

A
  • staph aureus
  • streptococci
  • neisseria gonococcus
  • gram -ve bacilli
99
Q

what is the treatment of reactive arthritis

A
  • chylamydia - doxycycline

- gonorrhea - ceftriaxone

100
Q

What is seen on ESR/CRP measurements if a patient has SLE

A
  • raised ESR and normal CRP
101
Q

which autoantibody is positive in SLE

A
  • antiDsDNA
102
Q

describe antiphospholipid syndrome and its features

A
  • a side efFect of SLE - Increase in coagulation
  • Coagulation defect
  • Levido reticularis
  • Obstettric: recurrent miscarriages
  • Thrombocytopenia
  • Anti cardiolipin antibody = for antiphospholipid syndrome
  • TX – manage CV risks, warfarin or LMWH if trying to conceive
103
Q

what is the diagnostic criteria of ankylosing spondylitis

A
  • sacroilitis on XRAY or MRI

+ 1 or more spineache feature

104
Q

what is the treatment of reactive arthritis

A
  • chlamydia - doxycycline

- n.gonorrhoea - ceftriaxone

105
Q

what is a swan neck deformity

A
  • hyperextension of PIP
  • flexion of DIP
  • seen in RA
106
Q

what is a boutonniere deformity

A

hyperextension of DIP
flexion of PIP
seen in RA

107
Q

give 5 hand signs of rheumatoid arthritis

A
  • swan neck deformity
  • boutonniere deformity
  • z thumb
  • ulnar deviation
  • DIP sparing
  • swollen symmetrical PIP, MCP joints
108
Q

what is seen on an xray for RA

A

Loss of joint space
Erosions (periarticular)
Soft bones (osteopenia)
Soft tissue swelling

Phase2a (10 decks)

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