rheumatology/MSK Flashcards
MSK complaint epidemiology
1/4 GP consultations
more common cause of severe long term pain and disability
prevalence increases with age
inflammatory vs. degenerative: stiffness
inflammatory- early morning/at rest, usually >60mins
degenerative- morning/evening, <30 mins
inflammatory vs. degenerative: presentation
inflammatory: swelling= synovial joints, can be bony, hot/red
degenerative- no swelling
inflammatory vs. degenerative: patient demographics
inflammatory: young, psoriasis, family history
degenerative- older, prior occupation/sport
inflammatory vs. degenerative: NSAIDS
inflammatory: responds
degenerative- no response
bone pain- patterns of pain
pain at rest and night
usually tumour/infection/fracture
inflammatory arthritis patterns of pain
pain and stiffness in morning/at rest
inflammatory/infection
osteoarthritis patterns of pain
pain on use/at end of day
neuralgic patterns of pain
pain and paraesthesia in dermatomal distribution, worsened by specific activity
root or peripheral nerve compression
joint distribution in rheumatoid arthritis
bilateral
symmetrical
hands and feet
joint distribution in osteoarthritis
1st metacarpal joint (base of thumb) distal interphalangeal joint hips knees large toe
joint distribution in psoriatic arthritis
joints
enthesitis
dactylitis- sausage digit
rheumatoid arthritis presentation
symmetrical polyarthritis deformity erosion of bone on x-ray bone nodules
osteoarthritis presentation
bouchard’s nodes- proximal interphalangeal joints
heberden’s nodes- distal interphalangeal joints
bowed legs
connective tissue disease presentation
non-erosive arthritis butterfly rash photosensitivity mouth ulcers raynaud's- circulatory changes in response to temperature changes
inflammatory markers
erythrocyte sedimentation rate
C reactive protein
erythrocyte sedimentation rate
rises with infection/inflammation
fibrinogen=RBCs stick together=fall faster so ESR rises
inflammatory markers: C reactive protein
acute phase protein
released in inflammation/infection
produced in liver in response to IL-6
auto-antibodies in inflammatory joint pain
immunoglobulins that bind to self-antigens
rheumatoid arthritis
systemic lupus erythematosus
systemic lupus erythematosus auto-antibodies
ANA- anti nuclear antibody, binds to antigens with cell nucleus, most people test positive
rheumatoid arthritis auto-antibodies
RF- IgM or IgG
CCP
seronegative spondyloarthropathies
umbrella term for inflammatory disease that involve joints and entheses
axial inflammation, asymmetrical peripheral arthritis, no RF, association with HLA-B27
seronegative spondyloarthropathies: conditions
ankylosing spondylitis acute anterior uveitis psoriatic arthritis enteropathic arthritis (crohn's/UC) JIA undifferentiated SpA reactive arthritis
seronegative spondyloarthropathies: HLA-B27
class I surface antigen (on all cells except RBCs)
immunity and self-recognition
either HLA +ve or -ve
main theory is infection triggers immune response and infectious agent has peptides similar to HLA so auto-immune response against it
seronegative spondyloarthropathies: SPINEACHE
Sause digit (dactylitis) Psoriasis Inflammatory back pain NSAID=good response Enthesitis Arthritis Crohn's/colitis/elevated CRP HLA-B27 Eye (uveitis)
ankylosing spondylitis
chronic inflammatory disorder of the spine, ribs and sacroiliac joints
ankylosis= abnormal stiffening and immobility of a joint due to new bone formation
ankylosing spondylitis: epidemiology
more common and severe in males
presents at 16 y/o, <30 y/o
88% are HLA-B27 +ve
ankylosing spondylitis: risk factors
HLA-B27
klebsiella
salmonella
shigella
ankylosing spondylitis: pathophysiology
local erosion of bone and its attachments
syndesmophyte: new bone formation and vertical growth from anterior vertebral corners
sacroilitis: sclerosis, loss of joint space, joint fusion
ankylosing spondylitis: typical patient
man, <30 y/o
gradual onset of lower back pain
worse at night with morning spinal stiffness
relieved by exercise
ankylosing spondylitis: presentations
episodic inflammation of sacroiliac joint in late teens
pain radiates from sacroiliac to hips and improves through the day
progressive loss of spinal movement
asymmetrical joint pain
ankylosing spondylitis: spinal abnormalities
loss of lumbar lordosis and increased kyphosis (curvature of C spine/ upper T)
limitation of lumbar spine mobility in sagital and frontal planes
ankylosing spondylitis: enthesitis
inflammation at site of insertion of a tendon or ligament into bone
ankylosing spondylitis: investigations
blood: ESR raised, CRP raised (can be normal), normocytic anaemia, HLA
Xray- can be normal, erosion, blurring of vertebral rims, new bone formation, fusion of sacroiliac joints
MRI- shows early sacrolitis
ankylosing spondylitis: treatment
treat quickly to prevent irreversible syndesmophyte formation morning exercise to maintain posture NSAIDS methotrexate steroid injections surgery
psoriatic arthritis: epidemiology
can occur without psoriasis
occurs in 10-40% of those with psoriasis and can present before skin changes
psoriatic arthritis: risk factors
family history of psoriasis
psoriatic arthritis: 5 patterns of disease
asymmetrical oligoarthritis symmetrical seronegative polyarthritis spondylitis distal interphalangeal arthritis arthritis mutilans
psoriatic arthritis: spondylitis
unilateral or bilateral sacrolitis and early cervial spine involvement
similar to AS but only 50% are HLA-b27 +ve
psoriatic arthritis: distal interphalangeal arthritis
DIPJs involvement only
often adjacent with nail dystrophy, reflecting enthesitis extending into nail root
dactylitis- an entire digit is swollen
psoriatic arthritis: arthritis mutilans
5% of those with PA
causes periarticular osteolysis (bone resorption) and shortening (telescope fingers)
psoriatic arthritis: hidden sites
behind/inside ear
scalp
pitting nails
umbilicus
psoriatic arthritis: diagnosis
xray- it is erosive but central in the joint, pencil in cup deformity
psoriatic arthritis: treatment
similar to rheumatoid arthritis NSAIDS DMARDS methotrexate and ciclosporin anti-tnf alpha
reactive arthritis
sterile inflammation of synovial membrane, tendons and fascia
triggered by infection at distant site (GI/GU)
typically lower limb
reactive arthritis: epidemiology
males HLA-B27 positive (30-50 fold increased risk)
reactive arthritis: causes
GI infections (salmonella, shigella) STIs
reactive arthritis: pathophysiology
bacterial antigens or bacterial DNA found in inflamed synovium of affected joints
persistent antigenic material is driving inflammatory response
reactive arthritis: classic triad
arthritis, 2 days- 2 weeks post infection
conjunctivitis
urethritis
reactive arthritis: skin lesions
circinate balantis- ulceration of glans of uncircumcised penis, in circumcised it is raised, red and scaly
keratoderma blennorrhagica- skin of feet and hands, similar to pustular psoriasis
reactive arthritis: investigations
ESR and CRP raised culture stool if diarrhoea sexual health review aspirate spinal fluid xray
reactive arthritis: treatment
NSAIDS for joint inflammation
treat infection
screen sexual partners
relapse- methotrexate
rheumatoid arthritis: epidemiology
1% of population affected
peak prevalence 30-50 y/o
not seen as much in elderly compared to OA
more common in females
rheumatoid arthritis: risk factors
female
family history
smoking
rheumatoid arthritis: inflammation
chronic inflammatory reaction
infiltration of lymphocytes, macrophages and plasma cells
rheumatoid arthritis: proliferation
tumour like mass- pannus
grows over articular cartilage
rheumatoid arthritis: bone loss
focal erosion
periarticular osteoporosis
generalised osteoporosis in skeleton
rheumatoid arthritis: cartilage loss
joint space narrows due to loss of cartilage
TNF and IL-1 release proteinases with damages cartilage
rheumatoid arthritis: clinical manifestations
symmetrical, swollen painful, stiff joints
usually warm
morning stiffness >30 mins
hand deformities
rheumatoid arthritis: soft tissue manifestations
nodules
bursitis
tenosynovitis
muscle wasting
rheumatoid arthritis: lung manifestations
pleural effusions
pneumoconiosis
rheumatoid arthritis: cardiac manifestations
rare
pericarditis
raynaud’s
rheumatoid arthritis: eye manifestations
dry eyes, episcleritis
scleritis
rheumatoid arthritis: neurological manifestations
peripheral sensory neuropathies
compression/entrapment neuropathies
cord compression
rheumatoid arthritis: kidney manifestations
amyloidosis
nephrotic syndrom
CKD
rheumatoid arthritis: skin manifestations
subcut nodules
vasculitis
rheumatoid arthritis: haematological manifestations
lymph nodes palpable
spleen enlargement
anaemia
rheumatoid arthritis: blood tests
normochromic normocytic anaemia
ESR/CRP raised
RF factor
anti CCP
rheumatoid arthritis: radiology
xray
MRI
rheumatoid arthritis: anti-CCP
marker of disease
presents early in disease
those who are positive have worse prognosis
rheumatoid arthritis: treatment
no cure lifestyle modification pain management corticosteroids DMARDS
DMARDS
inhibit inflammatory cytokines
this suppresses immune system so risk of infection
take 6 weeks to start working
regular blood tests required
methotrexate
gold standard drug
contraindicated in pregnancy due to reducing folate
nausea, mouth ulcers, diarrhoea, neutropenia, renal impairment
biological therapy
expensive TNF-alpha blockers (infliximab) B-cell inhibitor (rituximab) interleukin blockers T cell activation blockers
vasculitis
inflammation and necrosis of blood vessel wall with subsequent impaired blood flow
vasculitis damage
vessel wall destruction- aneurysm, rupture, stenosis
endothelial injury- thrombosis, ischaemia, infarction
vasculitis classification
by blood vessel involved size of vessel presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA) target oran primary vs. secondary
vasculitis histology
vessel wall infiltration
neutrophils, mononuclear cells and or giant cells
fibrinoid necrosis
leukocytoclasis (dissolution of leukocytes)
infective conditions associated with vasculitis
subacute infective endocarditis
non infective conditions associated with vasculitis
SLE scleroderma polymyositis inflammatory bowel diseases RA
primary large vessel vasculitis
giant cell (temporal) arteritis takayasu's arteritis
giant cell arteritis
inflammatory granulomatous arteries of large cerebral arteries as well as other large vessels such as aorta
giant cell arteritis: epidemiology
primarily in those >50
incidence increases with age
more common in females
giant cell arteritis: risk factors
over 50
female
RA, SLE, scleroderma
giant cell arteritis: pathophysiology
arteries inflamed and thicker
obstruction in blood flow
particularly cerebral and ophthalmic arteries
giant cell arteritis: presentation
headaches tenderness of scalp claudication of jaw sudden painless vision loss (emergency) malaise weak pulses
giant cell arteritis: signs
temporal arteries- palpable, tender, reduced pulsation
giant cell arteritis: differential diagnosis
migraine
tension headache
trigeminal neuralgia
giant cell arteritis: investigations
3 or more of: >50, new headache, temporal artery tenderness, ESR raised, abnormal artery biopsy
giant cell arteritis: temporal artery biopsy
definitive diagnostic test should be done before taking high dose corticosteroids lesions are patchy so large biopsy inflammatory infiltrates present breaking up of internal elastic lamina
giant cell arteritis: treatment
high dose corticosteroids
bone protection, bisphosphantes, ca2+ and vit d
monitor treatment progress
primary small vessel vasculitis
granulomatosis with polyangiitis
eosinophilic granulomatosis with polyangiitis
microscopic polyangiitis
granulomatosis with polyangiitis
necrotising granulomatous vasculitis of arterioles, capillaries and post capillary venules
associated with ANCAs
granulomatosis with polyangiitis: epidemiology
age 25-60 y/o
prevalence 5-7/100,000
granulomatosis with polyangiitis: vasculature affected
all organ systems but limited if no renal involvement
resp tract (sinusitis, nasal bleeding, pulmonary haemorrhage)
kidneys (glomerulonephritis)
skin (purpura/ulcers)
granulomatosis with polyangiitis: eye disease
scleritis
granulomatous orbital disease
marked bilateral periorbital oedema
granulomatosis with polyangiitis: investigations
bloods- ESR, CRP, anaemic, renal impairment, ANCA
granulomatosis with polyangiitis: treatment
untreated mortality= 90% at 2 years
severe= high dose steroids
non-end organ threatening= moderate dose steroids and methotrexate
osteoarthritis
cartilage loss with periarticular bone response
non-inflammatory degenerative arthritis
osteoarthritis: epidemiology
most common type of arthritis all tissues of joint involved increases with age majority= primary, no obvious cause secondary= obesity or occupational after age of 55 more common in females
osteoarthritis: risk factors
hypermobile joints insufficient joint repaire diabetes increasing age female obesity manual labour/farming trauma
osteoarthritis: pathophysiology
balance between cartilage degradation and production is lost
focal erosion of cartilade occurs and surface becomes fibrillated and fissured
ulceration exposes underlying bone to increased stress- microfractures
osteoarthritis: main pathological features
loss of cartilage
disordered bone repair
osteoarthritis: presentation
joint pain worse on movement stiff after rest distal interphalangeal joints muscle wasting nodes
osteoarthritis: investigations
deformity and bone enlargement of joints
CRP may be elevated
RF and antinuclear antibodies are negative
MRI to see cartilage injury
osteoarthritis Xray- LOSS
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
non- pharmacological treatment of osteoarthritis
exercise to improve muscle strength lose weight local heat or ice packs bracing devices walking aids phsyio
pharmacological treatment of osteoarthritis
paracetamol before NSAIDs
weak opioids
corticosteroid injections
surgical treatment of osteoarthritis
arthroscopy
arthroplasty
osteotomy
fusion
inherited connective tissue diseases
Marfan
Ehlers-danlos
auto-immune connective tissue diseases
systemic lupus erythematosus
systemic sclerosis
primary sjogren’s
polymyositis
systemic lupus erythematosus
inflammatory, multisystem autoimmune disorder with arthralgia and rashes
systemic lupus erythematosus: epidemiology
more common in females
peak age of onset is 20-40 years
more common in African-Caribbean’s and asians
systemic lupus erythematosus: risk factors
cause unknown
family history
UV light triggers flare ups
systemic lupus erythematosus: pathophysiology
cell apoptosis- cell remnants appear on cell surface as blebs (self antigens)
removal of blebs by phagocytosis is inefficient so transferred to lymph tissues to be taken up by APCs
the blebs are presented to B/T cells so autoantibodies produced
systemic lupus erythematosus: joint presentation
90% of cases
similar to RA
systemic lupus erythematosus: skin presentation
85% of cases erythemia in butterfly distribution vasculitis on fingertips and nails photosensitive rash alopecia raynaud's
systemic lupus erythematosus: lung presentation
50% of cases
recurrent pleural effusions and pleurisy
pulmonary fibrosis rarely
systemic lupus erythematosus: cardiac presentation
25% of cases
pericarditis and pericardial effusions
systemic lupus erythematosus: CNS presentation
60% cases depression epilepsy migraines psychosis
systemic lupus erythematosus: eye presentation
15% cases
retinal vasculitis
systemic lupus erythematosus: kidney + GI presentation
kidney= 30% of cases, glomerulonephritis with persistent proteinuria GI= mouth ulcers
systemic lupus erythematosus: tests
ESR raised, CRP normal
leukopenia, lymphopenia, thrombocytopenia
anaemia
systemic lupus erythematosus: autoantibodies
anti-nuclear antibodies, 95% +ve
raised anti-double strand DNA antibody is specific but positive in 60%
RF +ve 40%
systemic lupus erythematosus: treatment
reduce sunlight exposure reduce CVD risk factors NSAIDS topical corticosteroids for rashes treat anaemia immunosuppressants
systemic lupus erythematosus: treating severe
immunosuppressants
high dose oral corticosteroids
treat renal or cerebral disease and anaemia
systemic sclerosis
multisystem disease with involvement of skin and Raynaud’s (100% of cases)
distinct from localised sclerosis that do not involve internal organ disease
systemic sclerosis: epidemiology
highest case of mortality of any autoimmune rheumatic disease
occurs worldwide
more common in females
peak incidence 30-50 y/o
systemic sclerosis: risk factors
exposure to vinyl chloride, silica dust, adulterated rapeseed oil
bleomycin
genetic
systemic sclerosis: pathophysiology
widespread vascular damage
continued vascular damage and increased vascular permeability
uncontrolled and irreversible proliferation of connective tissue and thickening of vascular walls with narrowing of the lumen
systemic sclerosis: limited cutaneous scleroderma
70% cases
skin involvement limited to hands, face, feet and forearms
tight over fingers and produces flexion deformities
GI involvement is common with oesophageal dysmotility
systemic sclerosis: diffuse cutaneous scleroderma
30% cases
skin changes develop more rapidly
early involvement of other organs (GI, renal, lung, cardiac)
systemic sclerosis: blood tests
normochromic normocytic anaemia
microangiopathic haemolytic anaemia
urea and creatine rise
systemic sclerosis: autoantibodies
limited= speckled or anti-centromere antibodies, 70% cases
diffuse= anti-RNA polymerase 20%, anti-topoisomerase-1 antibodies, 30% cases
RF +ve in 30%
systemic sclerosis: imaging
CXR to exclude other pathology
hand xr- calcium deposits
barium swallow- confirms impaired oesophagus
high res CT- fibrotic lung
systemic sclerosis: treatment
no cure treat raynaud's lansoprazole for oesophageal involvement nutritional supplements prevention of renal crisis- ACE inhibitors, ramipril immunosuppressants
Sjogren’s syndrome
chronic inflammatory autoimmune disorder
characterised by immunologically mediated destruction of epithelial exocrine glands
primary Sjogren’s syndrome: epidemiology
dry eyes in absence of other autoimmune disease
more common in females
onset in 40s/50s
secondary Sjogren’s syndrome: epidemiology
associated with connective tissue disease
Sjogren’s syndrome: pathophysiology
lymphocytic infiltration and fibrosis of exocrine glands, especially lacrimal and salivary glands
Sjogren’s syndrome: presentations
dry eyes dry mouth salivary and parotid gland enlargement dryness of skin and vagina fatigue
Sjogren’s syndrome: systemic presentation
arthralgia raynaud's other autoimmune diseases renal tubular defects vasculitis
Sjogren’s syndrome: investigations
schirmer tear test
rose bengal staining
raised Ig levels, RF +ve, ANA in 80%, anti-Ro Ab in 60-90%
Sjogren’s syndrome: treatment
artificial tears and saliva replacement
NSAIDS
polymyositis/dermatomyositis
PM rare muscle disorder of unknown aetiology, inflammation and necrosis of skeletal muscle fibres
when skin is involved it is DM
polymyositis/dermatomyositis: epidemiology
rare
adults and children
more common in females
polymyositis: presentation
symmetrical progressive muscle weakness and wasting affecting proximal muscles of shoulder and pelvic girdle
difficulty squatting, going upstairs and standing from sitting involvement of resp and laryngeal muscles- dysphagia and resp failure
dermatomyositis: presentation
heliotrope (purple) skin, discolouration of eyelids and plaques on knuckles
arthralgia, dysphagia from oesophageal muscle involvement
increased incidence of underlying malignancy
polymyositis/dermatomyositis: investigations
muscle biopsy
muscle enzymes
ESR not usually raised
polymyositis/dermatomyositis: serum antibodies
ANA positive in DM
RF +ve in 50%
myositis-specific antibodies
polymyositis/dermatomyositis: treatment
bed rest with exercise
oral prednisolone for at least 1 month after it is enzymatically inactive
hydroxychloroquine or topicals to help with skin
relapse: oral- methotrexate, ciclosporin
Raynaud’s
intermittent spasm of arteries supplying fingers and toes
no underlying cause- raynaud’s disease
underlying cause- phenomenon
Raynaud’s: epidemiology
5% of population
more common in females
Raynaud’s: risk factor
the cold
smoking can aggravate symptoms
Raynaud’s: pathophysiology
peripheral digit ischaemia due to vasospasm
usually bilateral and fingers affected more than toes
Raynaud’s: presentation
skin pallor followed by cyanosis, then redness due to hyperaemia (white, blue then red)
duration is variable
numbness, burning and pain
Raynaud’s: when it can exhibited
connective tissue disorders (SLE, systemic sclerosis, RA)
vibrational tools
beta blockers, smoking
Raynaud’s: treatment
avoid cold by wearing gloves
stop smoking and beta blockers
vasodilators