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
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
3
Q
list three types of autoimmune joint paint
A
- rheumatoid
- spondyloarthropathy (HLA B27 associated)
- connective tissue disorders
4
Q
what are the features of spondyloarthropathy
A
- seronegativity - rheumatoid factor negative
- HLA B27 association - class I surface antigen on all cells, encoded by MHC on chromosome 6, human leucocyte antigen
- Axial arthritis - spine and SI joints
- asymmetrical large joint oligoarthritis
- enthesis - inflammation of site of insertion into tendon or ligament
- dactylitis - inflammation of entire digit
- extra articular - anterior uveitis, psoriasis, IBD, oral ulcers, aortic valve incompetence
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
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
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
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
9
Q
what is the management of ankylosing spondylitis
A
- exercise
- NSAIDS
- TNFa blockers
- surgery
10
Q
what are the 5 patterns of psoriatic arthritis
A
- symmetrical polyarthritis
- DIP joints
- axial
- large joint oligoarthritis
- arthritis mutilans (telescoping fingers)
11
Q
what is the management of psoriatic arthritis
A
- NSAIDS
- anti TNFa drugs
- MTX, suldasalazine
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
13
Q
what are the signs of reactive arthitis
A
- arthritis
- conjunctivitis
- sterile urethritis
14
Q
what are the tests for reactive arthritis
A
- ESR + CRP
- culture stool
- sexual health review
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
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
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
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
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
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)
-
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
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
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
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
25
what are the diagnostic criteria or temporal/giant cell arteritis
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
26
what are the symptoms of giant cell arteritis
- headache
- jaw claudation
- non specific malaise
- scalp tenderness
- acute blindness
- symptoms of polymyalgia rhuematica
27
what are the tests of temporal arteritis
- increased ESR, CRP
- increased platelet
- inc ALP
- decreased Hb
28
what is the management of temporal arteritis
- corticosteroids immediately
- falling ESR/CRP guides treatment
- prophylaxis of osteoporosis - bisphosphonate and vit D + DEXA
- steroid sparing agents - methotrexate
29
what is granulomatosis with polyangitis ( GPA)
- wegeners granulomatosis
- necrotizing granulomatous vasculitis of arterioles, capillaries and post capillary venules
- ANCA associated
- 25-60 years
- vasculature of all organ systems
30
what are the extravascular symptoms of GPA
- URT - sinusitis, otitis media
- lungs- pulmonary haemorrhage/nodules
- kidneys - glomerulonephritis
- skin - purpura/ulcers
- NS - CNS vasculitis
- pericarditis
- synovitis
- uveitis, scleritis
31
what is the management of GPA
- High dose steroids/ cyclophosphamide/ biologics (severe)
| - moderate dose steroids + methotrexate (moderate)
32
what is osteoarthritis
- non inflammatory arthritis of movable joints characterised by deterioration of articular cartilage and the formation of new bone of the joint surfaces and margins
33
what are the predisposing factors of osteoarthritis
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
34
What is the pathogenesis of osteoarthritis
- articular cartilage failure
- chondrocytes main cells responsible
- proteases - mellatoproteases
- catabolic cytokines -IL1, TNFa
- anabolic cytokines - insulin like GF, TGFb
- inflammation
35
what are the symptoms of osteoarthritis
```
- 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
```
36
what are the differential diagnoses of osteoarthritis
- rheumatoid
- gout
- osteonecrosis
- neuropathic joint
37
what are the investigations for osteoarthritis
```
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
```
38
what is the management of osteoarthritis
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)
39
what is the pathology of systemic lupus erythematosus
- 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
40
which gene is systemic lupus erythematosus associated with
HLA DR2, DR3
41
what are the symptoms of signs of SLE
- 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
42
what is the management of SLE
- 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
43
what is raynauds phenomenon and what is it caused by
- peripheral digit ischaemia
- either primary or secondary to
- connective tissue disorders
systemic sclerosis, SLE, mixed connective
- drugs
- vascular damage
44
what does the crest acronym stand for in reference to systemic sclerosis
```
Calcinosis
Raynouds phenomenon
Oesophageal reflux
Sclerodactyly
Terangestasia
```
45
what is the pathogenesis of systemic sclerosis
- vasculopathy
- excessive collagen deposition
- inflammation
- autoantibody production
46
what is the management of systemic sclerosis
```
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
what are the causes of Sjogrens syndrome
```
primary
or secondary to:
- SLE
- RA
- scleroderma
- primary biliary sclerosis
```
48
what are the symptoms of sjogrens syndrome
- dry eyes
- dry mouth
- -enlarged salivary gland
- inflammatory arthritis
- rash
- neuropathies
- vasculitis
- neonatal lupus
49
what are the tests for sjogrens syndrome
- increased Ig
- increased ESR
- autoantibodies RF, ANA
50
what is the management of sjogrens syndrome
- tear and saliva replacement
- immunosuppression
- rituximab
51
what is osteomyelitis and what is it caused by
- 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
what are the categories of osteomyelitis
- 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
what are the host and microbial factors that make osteomyelitis more likely
- 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
What acute and chronic histological changes are seen in osteomyelitis
```
acute
- inflammatory cells
- oedema
- vascular congestion
-small vessel thrombosis
chronic
-necrotic bone
-new bone formation
-neutrophil exudates
- lymphocytes and histiocytes
```
55
in osteomyelitis, what does inflammatory exudate in the marrow lead to?
- 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
what are the signs and symptoms of osteomyelitis
```
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
what are the tests for osteomyelitis
- 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
what are the differential diagnoses of osteomyelitis
- soft tissue infection
- avascular necrosis
- gout
- fracture
- bursitis
- malignancy
- charcot joint
59
what is the treatment of osteomyelitis
- surgical - debridement (removal of damaged tissue), hardware placement or removal
- antimicrobial therapy - s.aureus/strep/emterococci, pseudomonas - flucloxacillin IV
60
give examples of things that increase urate
- 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
which molecule causes gout
monosodium urate crystals
62
what is the pathology of acute gout
- change in blood/tissue balance
- urate crystals trigger intracellular inflammation
- self limiting - monocyte/macrophage maturation then producing anti-inflammatory cytokines
63
what is the treatment of gout
- 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
what are the differential diagnoses of gout
- septic arthritis
- RA
- CPPD
- haemarthrosis
65
how is gout diagnosed
- polarised light microscopy shows negatively birefringent needle shaped urate crystals
- serum urate raised
66
what is osteoporosis
- reduced bone mass causing pathological fracture
67
what things contribute to fracture probability
- trauma - likelihood of falling
- bone strength
BMD - peak bone mass, rate of bone loss
bone size
Bone quality - mineralisation, architecture, bone turnover
68
what is the bone remodelling cycle
Quiescence
resorption
formation
quiescence
69
what are the features of post menopausal osteoporosis
- 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
what changes happen to trabecular architecture with aging
- 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
what tests can be used to diagnose osteoporosis
- 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
what are the causes and risk factors for osteoporosis
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
what is the management of osteoporosis
- 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
what is osteomalacia
- normal amount of bone but decreased mineral content
| - excessed uncalcified osteoid and cartilage
75
what are the signs and symptoms of rickets
- growth retardation
- hypotonia
- walks bow legged, knock kneed
- features of low calcium
76
what are the signs and symptoms of osteomalacia
- bone pain and tenderness
- fractures
- proximal myopathy
- due to decreased phosphate and vit D deficiency
77
what are the cause of osteomalacia
- vit d deficiency
- renal osteodystrophy - 1,25 dihydroxycholecalciferol deficiency
- drug induced
- vit d resistance
- liver disease
- tumour induced
78
what are the tests for osteomalacia
- low calcium and phosphate
- inc ALP
- decreased Vit D
- Biopsy shows incomplete mineralisation
- X-ray shows loss of cortical bone
79
what is the treatment of osteomalacia
- vit D
| - monitor Calcium
80
what is Paget's disease
- increased bone turnover due to increased osteoblasts and osteoclasts
- bone enlargement, deformity `(shown on X-ray) and weakness
- deep boring pain
81
what are the complications of pagets disease
- pathological fractures
- nerve compression due to bone overgrowth
- increased Calcium
- osteoarthritis
82
what is the treatment of pagets disease
- analgesia
| - alendronic acid
83
what are the red flags for MSK malignancy
- rest pain
- night pain
- generally unwell
- weight loss
- lump present
- loss of function
- neurological symptoms
84
what are the tests for MSK malignancy
- 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
describe the Enneking system for grading tumours of the MSK system
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
describe osteoid osteomas/osteoblastoma
- 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
describe osteosarcomas
- 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
what is the management of msk tumours
- 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
what is fibromyalgia
- chronic symptoms of fatigue and widespread pain
| - caused by aberrant peripheral and central pain processing
90
what are the risk factors for fibromyalgia
- middle aged
- female
- low educated
- low social class
- low household income
- divorced
91
what is the management of fibromyalgia
- pacing of activity - long term graded exercise therapy
- cognitive behaviour therapy
- amitriptyline at night
92
what are the features of fibromyalgia
allodynia - pain in response to none painful stimuli
| hyper asthenia - exaggerated response to midly painful stimulus
93
what are the symptoms of degenerative disc disease
- pain in lower back
| - can radiate to hips and legs
94
what molecule causes pseudogout
positively birefringent rhomboid shaped calcium pyrophosphate crystals
95
what are the risk factors for septic arthritis
- >80
- existing joint disease, especially RA
- IVDU
- immunosuppressed
- diabetes mellitus
- chronic renal failure
- recent joint surgery
- prostethic joint
96
what are the investigations for septic arthritis
- synovial fluid aspiration microscopy and culture
- blood culture
- CRP and X-rays may be normal
97
what is the treatment of septic arthritis
- empirical IV antibiotics until sensitivities are knows
- flucloxicillin or clindamycin if allergic to penicillin (s.aureus)
- vancomycin (MRSA) plus cephalosporin
98
which organisms most commonly cause septic arthritis
- staph aureus
- streptococci
- neisseria gonococcus
- gram -ve bacilli
99
what is the treatment of reactive arthritis
- chylamydia - doxycycline
| - gonorrhea - ceftriaxone
100
What is seen on ESR/CRP measurements if a patient has SLE
- raised ESR and normal CRP
101
which autoantibody is positive in SLE
- antiDsDNA
102
describe antiphospholipid syndrome and its features
- 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
what is the diagnostic criteria of ankylosing spondylitis
- sacroilitis on XRAY or MRI
| + 1 or more spineache feature
104
what is the treatment of reactive arthritis
- chlamydia - doxycycline
| - n.gonorrhoea - ceftriaxone
105
what is a swan neck deformity
- hyperextension of PIP
- flexion of DIP
- seen in RA
106
what is a boutonniere deformity
hyperextension of DIP
flexion of PIP
seen in RA
107
give 5 hand signs of rheumatoid arthritis
- swan neck deformity
- boutonniere deformity
- z thumb
- ulnar deviation
- DIP sparing
- swollen symmetrical PIP, MCP joints
108
what is seen on an xray for RA
Loss of joint space
Erosions (periarticular)
Soft bones (osteopenia)
Soft tissue swelling
