disease profiles MSK Flashcards
what is osteoporosis
reduced bone mineral density and increased porosity
what comes as a result of osteoporosis
increased fragility and fracture risk
normal quality of bone just not enough of it
osteoporosis
risk factors of osteoporosis
smoking, poor diet, female, inactivity, increased alcohol intake and lack of sunlight exposure
what is the intermediate stage of osteoporosis
osteopenia
what is type 1 osteoporosis
post menopausal
what is type 2 osteoporosis
osteoporosis of old age
what type of fractures dominate osteoporosis type 2
neck and vertebral fractures
how to diagnose osteoporosis
DEXA scanning
how to treat (slow process) of osteoporosis
calcium and vit D supplements
abnormal softening of bone due to deficient minerilisation of osteoid secondary to inadequate amounts of calcium and phosphorus
osteomalacia
what is an osteoid
immature bone
what is osteomalacia in children known as
rickets
what are the causes of osteomalacia and rickets
insufficinet calcium and phosphate deficiency
how can there by a lack of calcium
lack of absorption in intestine or resistance to action of vit D
how does phosphate deficiency happen
increased renal losses
what is the presentation of osteomalacia and rickets
pain, deformities from soft bone, pathological fractures, symptoms of hypocalcaemia
how to treat osteomalacia and rickets
vit D therapy with calcium and phosphate supplementation
what is hyperparathyroidism
over activity of parathyroid glands with high levels of PTH
what is primary hyperparathyroidism due to
benign adenoma, hyperplasia or rarely a malignant neoplasia
labs of someone with primary hyperparathyroidism
raised serum PTH, raised Ca, phosphate low or normla
what is secondary hyperparathyroidism due to
physiologial overproduction of PTH secondary to hypocalceamia
what is secondary hyperparathyroidism caused by
vit D deficincy or chronic kidney disease
what is tertiary hyperparathyroidism due to
people with chronic secondary who develop adenoma which continues to produce PTH despite biochemical correction
what is renal dystrophy
reduced phosphate excretion and inactive activation of Vitamin D
what does renal dystrophy lead to
secondary hyperparathyroidism with subsequent osteomalacia, sclerosis of bone and calcification of soft tissues
what is pagets disease
a chronic disorder resulting in thickened britter and misshapen bones
labs of pagets disease
serum alk phos is raised whilsy calcium and phsphorus are usually normal
how to treat pagets disease
with biphosphonates or calitonin
what is rheumatoid arthritis
symmetrical inflammatory polyarthtritis affecting mainly the peripheral joints which if untreated can potentially lead to joint damage and irreversible deformities and increased morbidity and mortality
prevalence of RA in men and women
3x more common in women
prevalence of RA in the UK
1%
what is RA mediated by
HLA -DR4
cause of RA
unknown
trigger of RA
infections, stress, cigarette smoking
severity of RA depends on
genetic factors, presence of auto antibodies
what is the main structure involved in RA
synovium
what does the synovium line
the inside of the synovial joint capsules and tendon sheaths
what joints in the spine are synovial fluid lined
C1/C2
what joints are usually affected by RA
hand joints, wrists, elbows, shoulders, TMJs, knees, hips, ankles, feet
difference between osteoarthritis and RA
osteoarthritis is when bone ends rub together and RA is when a swollen inflamed synovial membrane causes bone erosion
inflamed synovial is called
pannus
what happens when panes is in contact with bone
osteoclast is activated causing bone erosion
what is released from macrophage in RA
TNFa, IL1 and IL6
what is released from B cells in RA
RF and IL 6
what do the activation of pro inflammatory cytokines lead to in RA
- activation of synoviocytes to cause the hypertrophic synovium / pannus
- activation of osteoclasts
- inhibition of chondrocytes
- stimulation of angiogenesis
what drugs inhibit TNFa
infliximab, etanercept, adalimumab, certolizumab, golimumab
what drugs inhibit iL1-
anakinra
what drugs inhibit the IL6 receptor
tocilizumab
presentation of RA
pain and swelling in symmetrical fashion affecting peripheral synovial joints, typically small joints of hands and feet, prolonged morning stiffness, monoarthritis (rare), tenosynovitis, trigger finger, carpal tunnel, palindromic, systemic symptoms, poor grip strength
what test can be used of the detection of synovitis in RA
squeeze test
what is tenosynovitis
inflammation of the tendon sheath
what is trigger finger
fingers lock
palindromic
episodic RA
lung manifestations of RA
Plueral effusion, rheumatoid nodules
heart manifestations of RA
pericarditis, pericardial effusions
neurological manifestations of RA
peripheral neuropathy, carpal tunnel syndrome
leg ulcers associated with RA
arterial
diagnosis of RA
mainly clinical, peripheral symmetrical polyarthtritis affecting hands and feet, raised inflammatory markers, antibody testing not always positive, imaging
autoantibodies in RA
rheumatoid factor (rheumatoid IgM), antiCCP antibodies
what autoantibody in RA is more specific
Anti CCP
what autoantibody has low sensitivity in RA
anti CCP
score for disease activity in RA
DAS 28
management of RA
early diagnosis, disease modifying anti rheumatic drugs, NSAIDs and steroids, education
what is early RA defined as
less than 2 years since symptom onset
therapeutic window of opportunity in RA
first 3 months
first line for RA
education, rest, exercise, social services, salicylates, NSAIDs
second line for RA
gold salts, hydroxychloroquine
third line for RA
MTX, penicillin amine, AZA
last line for RA
cytotoxic agents and experimental drugs
examples of DMARD
methotrexate, sufasalazine, hydrochloroquine, leflunomide, steroids
what can methotrexate cause in the lungs
pneumonitis
who to avoid methotrexate with
people with lung disease
less than 2.6 DAS28 scoring
remission
2.6-3.2 DAS28 scoring
low disease activity
3.2-5.1 DAS28 scoring
moderate disease activity
more than 5.1 DAS28 scoring
active disease
what DAS28 score qualifies for biologic therapy
3.2 inspite of 2 DMARDs
what is osteoarthritis
a chronic disease characterised by cartilage loss and accompanying periarticular damage
what are the most affected joints in osteoarthritis
knees, hands and hips
what is the pathophysiology of OA
metabolically active dynamic process that involves all joint tissues
what are the key pathological changes in OA
localised loss of hyaline cartilage and remodelling of adjacent bone with new bone formation at joint margins
what indicates a repair process of synovial joints
combination of tissue loss and new tissue synthesis
risk factors of OA
genetic, ageing, female, obesity, biomechanics
features of a OA joint
subchondral bone cyst, thickened joint capsule, episodic synovitis, fibrillated cartilage, osteophyte, degenerative cartilage loss, subchondral bone sclerosis
localised OA
can effect hips, knees, finger interphalangeal joints, facet joins of lower cervical and lower lumbar spines
generalised OA
defined as OA at either the spinal or hand joints and in atleast 2 other joint regions
what does the presence of multiple heberdens nodes indicate
a subset of OA involving DIP joints, thumb bases, first MTP joints, lower lumbar and cervical facet joints, knees and hips
joints most affected by OA
neck, lower back, hips, base of thumb, finger joints, knee, base of toe
examination features of OA
joint line tenderness, crepitus, joint effusion, bony swelling, deformity, limitation of motion
where is heberdens node found
top of fingers
where is bouchards node found
bottom of fingers
presentation of knee OA
osteophytes, effusions, crepitus, restriction in movement, genuflects varies and valgus deformities, bakers cysts
distribution of hip OA
pain felt radiating to knee or groin, pain in hip can be radiating from lower back, hip movement restricted
distribution of spine OA
cervical - pain and restriction of movement , occipital headaches, osteophytes may impinge on nerve roots
lumbar - osteophytes can cause spinal stenosis if they encroach on the spinal canal q
diagnosis of spinal OA
clinical, imaging
what would u see on a OA x ray
marginal osteophytes, joint space narrowing, subchondral sclerosis, subchondral cysts
management of OA
education, lifestyle, physiotherapy, occupation therapy, analgesia, local intra articular steroid infections
surgical management of OA
joint replacements arthroscopic surgery to remove loose bodies
what are crystal arthropathies
a diverse group of disorders characterised by the deposition of various minerals in joints and soft tissues leading to inflammation
types of crystal arthropathies
gout monosodium urate crystals, pseudogount calcium pyrophosphate crystal deposition, hydroxyapatite - basic calcium phosphate deposition
define gout
a potentially disabling and erosive inflammatory arthritis caused by deposition of monosodium urate crystals into joints and soft tissues
prevalence of gout
2.49%
prevalence of gout in men vs women
more common in men
causes of hyperuricaemia
increased urate production and reduced urate excretion
what causes increase urate production
inherited enzyme defects, myeloproliferative / lymphoproliferative disorders, psoriasis, alcohol, high dietary purine intake
what causes reduced urate excretion
chronic renal impairment, volume depletion, hypothyroidism, diuretics, cytotoxic
how long does acute gout usually last
3 days with treatment, 10 days without
what is chronic tophaceous gout associated with
diuretics
investigations of gout
serum uric acid is raised, raised inflammatory markers, polarised microscopy synovial fluid, renal impairment, x rays
treatment of acute gout
NSAIDs, cohcicine, steroids, lifestyle modification
preventative measures for gout
Xanthine oxidase inhibitors - allopurinolm febuxostat, uricosuirc drugs - sulfinpyrzone, prodenecid, benzbromarone,
when should you start preventive treatment for gout
1 week after acute attack
WHO target for serum uric acid
300-360 mol/L
indications for prophylactic treatment of gout
one or more attacks of gout in a year inspite of lifestyle modifications, presence of gouty tophi or signs of gouty arthritis, uric acid calculi, chronic renal impairment, heart failure where unable to stop diuretics, chemo therapy patients who develop gout
who is pseudo gout most common in
elderly
what is pseudo gout also known as
calcium pyrophosphate deposition disease
treatment of pseudo gout
NSAIDS, cochincine, steroids rehydration
what is hydroxyapatite
crystal deposition in or around the joint
treatment of hyrocyapaitie
NSAIDs, intra articular steroid injection, physiotherapy, partial or total arthroplasty
what does hydroxyapatite lead to the release of
collagenases, serine proteinases and IL-1
what is soft tissue rheumatism
pain that is caused by inflammation/damage to ligaments, tendons, muscles or nerve near a joint rather than bone or cartilage
generalised soft tissue pain
fibromyalgia
what is the most common area for soft tissue pain
shoulder
investigation of soft tissue rheumatism
clinical history and examination, Xray, US, MRI, identify precipitating factors
treatment of soft tissue rheumatism
pain control, rest and ice compression, PT, steroid injections surgery
prevalence of joint hyper mobility syndrome in men and women
women more than men
genetic syndromes leading to joint hypermobility syndrome
marfans, Ehlers danlos syndrome
when does joint hyper mobility syndrome tend to present
childhood or 3rd decade
signs and symptoms of jointer hypermobility syndrome
joint pains, joint stiffness, foot and ankle pain, neck and backaches frequent sprains and dislocations, thin stretchy skin
what scoring system is used for hypermobility syndrome
beighton score
what score on the Brighton score constitutes a diagnosis
> 4/9
treatment of joint hypermobility syndrome
patient education, physiotherapy, analgesiA
what are connective tissue diseases
conditions associated with spontaenous overactivity of the immune system
what is present in connective tissue disease
auto antibodies
types of CTD
SLE, sjogrens syndrome, systemic scleoriss, dermatomyositis, polymyositis, anti phospholipid syndrome
what is SLE
an auto immune condition that can affect most organ systems
pathophysiology of SLE
immune system attcks cells causing inflammation and tissue damage
ratio of female to male prevelance of SLE
9:1
when does SLE present
at child bearing women
pathogenesis of SLE
defective apoptosis leading to cell contents float about for longer than normal allowing the immune system to start to develop a reaction against them so the cell contents are seen as antigens (autoantigens), immune cells trigger a response which means over time there are antbodies against these antigens which then start to recognise antigens within normal cells and attack them this causes immune complexes to form and they get deposited in skin, blood vessel walls of kidneys and that deposition activates the complement cascade causing focused inflammation in certain areas causing necrosis and fibrosis causing organ damage
SLE score
EULAR/ACR
what must be positive in SLE
ANA
what score constitutes SLE
10
skin manidestatins of SLE
discoid lupus, cutaneous lupus, alopecia, oral ulceration, buttterly facial rash
types of arthritis in SLE
synovitis, jaccouds arthropathy
x ray of jaccouds athropathy
normal
neorological manifestations of SLE
delirium, psychosis, seizure, headache, cranial nerve disorders
serositis in SLE
pleurisy, pericarditis, pericardial effusions
heamotological manifestations of SLE
leukpenia, thrombocytopenia, haemolytic anaemia, lymphadenopathy
renal manifestatiosn of SLE
proteinuria, biopsy proven nephritus, red cell casts
what is specific in SLE
dsDNA
what is highly specific for lupus
anti Sm
management of lupus (mild)
sun protection, vaccinations, lifestyle, HCQ, short courses of steroids, MTX/AZA
treatment for patients with anti phosphilipd syndrome
antiplatelets and anti coagulants
management of moderate lupus
HCQ,MTX/AZA, GC.PO/IV
treatment of severe lupus
cyclic phosphilide
how to monotor lupus
SLEDAI score
symptoms of sjogrens
drye eyes, gritty feeling, dry mouth, dry throat, vagina dryness, bilateral parotid gland enlargement, joint pains, fatigue,, unexplained increase in dental caries
immunology of sjogrens
anti Ro, anti La
what does sjogrens put people at risk of
lymphoma
what is systemic scleorisis
a multisystem autoimmune disease characterised by vasculopathy, autoimmunity and fibrosis
sympyoms of systemic scleorisis
raynauds, skin thickenng, difficulty swallowing, GORD, telangiectasia, calcinosis, +/- SOB, digital ulcers or ischeamia, skin tightness/loss of dexterity of hands
diffuse cutaneous systemic sclerosis
skin involvement above and below elbows and knees
limited systemic sclerosis
skin involvement on extermities below the elbows and knees - sparing the torsu
key antibodies in systemic sclerosis
anti centromere - limited , anti STL70 - diffuse, anti RNA polymerase 3
facial changes in systemic sclerosis
small mouth with puckering, beaked nose, tigh skin - no wrinkles and telangiasia
GI complications of systemic sclorisis
dysphagia, GORD, GAVE, small intestinal bacterial overgrowth, malabsorption, fluctuating bowel habiy, faecal incontinance
cardio plmonary complications of systemic sclerosis
interstitial lung disease, pulmonary arterial hypertension, myocardial disease
renal complications of systemic sclerosis
sclerodrma renal crisis, non specific progressive renal dysfunction
what is raynauds phenomenon
blanching, acrocyanosis, reactive hypereamia
how to treat rynauds
nifedipine - first line, PDE-5 inhibitor- sildenafil, proyacyclin infisiom - iloprots, endothelin recepyor antagonst - basentan
pulmonary hypertension classified by
> 25mmhg at rest by right heart catheterisation
symtoms of pulmonary hypertension
SOB on exertion
treatment for pulmonary hypertension
PDE5 inhibitor, ERA, eproprotinol infusions, oxgen
examples of PDE5 inibitor
sildenafil
example of ERA
bosentan
treatment of interstitial lung disease
MYCOPHEMOLATE, rarely cyclophosphamide, rituximab, nintedanib
what is systemic sclerosis renal disease assoiated with
anti RNA polymerase 111 antibody
what puts people at risk of enal disease
steroids
how to treat renal crisis
ace inhibitors
treatment of skin fibrosis
methotrexate, mycophenolate
what is spndyloarthropathy
family of inflammatory arthritides characterised by involvement of both spine and joints, principally in genetically predisposed individuals
genetic predisposition of spondyloarthropathies
HLA-B27
what is HLA-B27 associated with
ankylosing sponylitis, reactive arthritis, crohns disease, uveitis
spondyloarthrtitis sub groups
ankylosing spondylitis, psoriatic arthritis, reactive arthritis, enteropathic arthritic
mechanical back pain
worsened by activity, typically worst at end of the day, better with rest
inflammatory back pain
worse with rest, better with activity, significant early morning stiffness
what is enthesitis
inflammation at isertion of tendons into bones
what is anklylosing sponylitis
chronic systemic inflammatory disorder that primarily affects the spine
when does ankylosing spondylitis present
late adolescence or early childhood
who is ankylosing spondylitis more common in
men
sacrolitis on imaging
active acute inflammation on MRI suggestive of sacroilitis associated with SpA
clinical features of ankylosing spondylitis
back pain, enthesitis, peripheral arthritis, uveitis, cardiovascular involvement, enetric mucosal inflammation, neurological involvement, amyloidosis
diagosis of ankylosing spondylitis
history, examination, bloods, x ray
examination of ankylosing spondylitis
tragus/occiput to wall, chest expansion, modified schober test
bloods for ankylosing spondylitis
inflammatory parameters, HLAB27
x rays for ankylosing spondylitis
sacroiliitis, syndesmophytes, bamboo spine
difference between AS and OS on imaging
bone density is normal in early AS but reduced in late disease, shiny corners in AS and bamboo spine but in OA there is normal bne density and reduced joint space
what is psoriasitic arthritis
inflammatory arthritis asscoated with psoriasis
clinical features of psoriasitic arthritis
nail pitting, onycholysis, dactylitis, enthesitis, extra articular features
bloods of psoriasitic arthtritis
raised inflammatory parameters, negative RF
xray findings of psoriasitic arthritis
marginal erosions and whiskering, pencil in cut deformity, osteolysis, enthesitis
what is reactive arthritis
infection induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorganisms cannot be cultures
when do symptoms of reactive arthritis occur
1-4 weeks after infection
common infections for reactive arthritis
urogenital eg chlamydia, enterogenic eg salmonella, shigella and yersinia
who does reactive arthritis typically affect
young adults
HLA B27 in reactive arthritis
positive
what is reiters syndrome
triad and a form of reactive arthritis
what is the triad of reiters syndrome
urethritis, conjutivitis, arthritis
clinical features of reither syndrome
general symptoms, asymmetrical monarthritis or oligoarthritis, enthesitis, mucocutaneous lesions, ocular lesions and visceral manifestations
bloods of reiters syndrme
inflammatory parameters, FBC, U +Es, HLA B27
what is enteropathic arthritis associated with
IBS
clinical symptoms of enteropathic arthritis
loose watery stool with mucous and blood, weeightloos and low grade fever, eveitis, pyoderma gangrenosum, enthesitis and oral apthous ulcers
management of spondyloarthropathies
NSAIDs, corticosteorids, topical steroid eyedrops, MTX, anti TNF
when can you ise secukinumab
only for PsA and AS
what is secunumab
anti IL 17
what is SLE
a chronic auto immune disease
what does SLE incidence increase with
high oestrogen exposue
pathogenesis of SLE
developmemnt of autoantibodies as a result of a defect in apoptosis that causes increased cell death and a disturbance of immine tolerance
what does increased apoptosis release
nuclear material
what produces autoantibodies inSLE
B cell adn T cells
epidemiology of SLE
high prevelance in back people in the uS but not black people in africa
prognosis of SLE
10 year survival of >90%
presentation of SLE
fever, fatigue, weight loss, athralgia, myalgia, inflammatory arthrtitis, avascular necrosis, jacouds arthritis
what is jaccouds arthritis
lateral shift on metacarpal = parangeal joint
skin manifestations of SLE
malar rash, photosensitiviy, discoid lupus, alopecia, subacute cutaenous lupus, oral/nasal ulceration (painless), reynaids phenomenon
what is raynauds phenominon
white/blue extremities in cold
renal manifestation of SLE
lupus nephritis
respiratory manifestation of SLE
pleurisy, pleural effusion, pnuemonitis, PE, pH and ILD
haemolytic manifestations of SLE
leukopenia, lymphopenia, anaemia, thrombocytopenia
neuropsychiatric manifestations of SLE
seizures, psychosis, headache, aseptic meningitis
cardiac manifestations of SLE
pericarditis, pericardial effusion, PH, sterile endocardiris, and accelerated ischeamic heart disease
neurological manifestations of SLE
migraines, seizures, cranial or peripheral neuropathy, mononeuritis complex
GI manifestations of SLE
autoimmune hepatitis, pancreatitis, mesenteric vasculitis
serositis
inflammation of serous membranes
investigations of SLE
immunology, FBC, urinalysis, imaging
ANA positive in what % of SLE patients
> 95%
is ANA specific to SLE
no also in RA, HIV and hepC
what antibody is specific to SLE
anti-dsDNA
what antibody is spefic to SLE but has low sensitivity
anti-sm
what is low when SLE is activity
C3/4 levels
what may FBC of SLE show
anaemia, leucopenia, thrombocytopenia
what may urinalysis show
glomerulonephritis
if glomerulonephritis is positive what should you do
kidney biopsy
management of SLE - non pharmacological
Counselling, regular monitoring, avoid sun,
what does every lupus get
hydrochloroquine
how to treat skin disease and arthralgia in SLE
hydrochloroquine, topical steroids and NSAIDs
how to treat inflammatory arthritis or evidnee of some types of organ involvement in SLE
immunosuppresion, moderate corticosteroids
how to treat severe organ disease in SLE
Iv steroids, cyclophosphamide
how to treat unresponsive SLE
Iv immunoglobin and rituximab
mild SLE management
HCQ, topical steroids NSAIDs
moderate SLE management
oral steroids, azatioprine/methotrexate
severe SLE management
IV steroids cyclophosphamide rituximab
what is sjogrens syndrome
autoimmune condition characterised by lymphocyte infiltrates in exocrine organs
presentations of sjogrens syndrome
dryness of eyes and mouth, arthralgia, fatigue and vagina dryness and parotid gland swelling
what does sjorgens syndrome put people at risk of
lymphoma
what can sjorgens syndrome be secondary to
RA or SLE
diagnosis of sjorgens syndrome
confirmation of ocular dryness (schirmers test)< +anti-ro and anti-la antibodies and typical features on a lip gland biopsy
management of sjorgens syndrome
symptomatic, lubricating eye drops, saliva replacement, dental care, HCQ for athragia and faatigue, immunosuppression in organ involvement
what is systemic sclerosis
systemic connective tissue disease
what constitutes systemic sclerosis
vasomotor disturbances (raynauds), fibrosis and subsequent atrophy of the skin and subcutaneous tissue, excessive collagen deposition causes skin and internal oragn chnages
what causes death in systemic sclerosis
renal and lung changes
what % of petinets with systemic sclerosis have pulmonary hypertesion
12%
major features of systemic sclerosis
centrally located skin sclerosis that affects the arms, face or neck
minor features of systemic sclerosis
includes sclerodactyl and atrophy of the fingertips and bilateral lung fibrosis
diagnosis of systemic sclerosis
1 major and 2 minor features
organ involvement in systemic sclerosis
pulmonary hypertension, pulmonary fibrosis and accelerated hypersion causing renal crisis, gut involvement may cause dysphagia, malabsorption and bacterial overgrowth of small bowel inflammatory arthritus and myositis
limited systemic sclerosis
skin affected confined ti face, hands, forearms and feet
antibody in systemic sclerosis limited
anti centromere
antibody in diffuse systemic sclerosis
anti - acl- 70
what is diffuse systemic sclerosis
organ involvement, rapid skin changes, may involve trunk
investigations of systemic sclerosis
anti centromere and anti scl-70, organ screening
management of raynauds
raynauds - CCB
management of renal crisis
ACEi
management of GI symptoms in systemic sclerosis
PPI
management of interstitial lung disease
immunosuppression, usually cyclophophamide
what is MCTD
raynauds, arthraligia, myositis, slcerodactyl, PH and ILD
what is MCTD associated with
anti RNP antibodies
managements of MCTD
regular echos, screen of ILD
whats is anti phosphilipd syndrome
recurrent venous or arterial thrombosis and / or fetal loss, may not have associated disease but often occurs in conjunction with SLE
presentation of APS
increased frequency of stroke or MI, multiorgan infarctions, migraines
invesitations of APS
thrombocytopenia and prolongaton of APTT, lupus anticoagulant, ant cardioliin antibodies and anti beta 2 glycoprotein may be positive
management of APS
anticoagulation - LMWH in pregnancy as warfarin is teratogenic
acute attack of crystal arthropathies duration
upto 2 weeks
cause of gout is
monosodium urate
how many people have gout in the world
1-2%
what gender is gout more common in
men
when does prevelance of gout increase
with age
what is hyperuricemia
serum uric acid >7mg/dL
diagnosis of gout
radiograohic identification of crystals and hyperuricemia
when should you meaure serum urate
2 weeks after attack
how can hyperuricaemia occur
renal underxcretion or excessive intake of alcohol, red meat and seafood
where can uric acid crytals precipitate
in joints which can be triggered by dehydration traima or surgery
what can renal underexcretion be exacerbated by
diuretics or renal failure
most affected joints in gout
1st MTP, ankle and knee are most affected joints
clinical presentation of gout
rapid onset, red, hot joint, severe pain - mimics spetic arthritis symptoms last for 7-10 days
what is gouty tophi
painless accumulations of uric acid which can occur in soft tissue and occasuonally erput through skin
what. ischronic polyarticular gout
chronic joint inflammation, usually after having recureent acut attacks >10 years. Often diuretic associated. may get acute attacks can alos cause erosive arthritis
investigations of gout
inflammatory markers raised, WCC may be raised, X ray, joint aspirate with polarised microscopu
what should you see in gout joint aspirate and polarised microscopy
needle shaped crystals yellow to blue
management of acute gout
NSAIDs, colchoncne or corticosterods
lifestyle modifications in gout
less red meat, beans, shellfish, reduve alcohol,wgt loss, fluids
how should you treat people who suffer from recuurent attacks of gout
urate lowering therapy - allopurinal
when to start allopurinal in gout
AFTER FLARE HAS CLEARED
what is pseudogot caused by
CPPD
who mainly gets pseudogout
elderly
what is pseudogout related to
OA
what does pseudogout tend to affect
knee wrist and ankle
crystals seen in pseudogout
rhomboid / envelop shaped crystals
treatment of pseudogout
NSAIDs, colchincine, corticosteroids, rehydration
what is hydroxyapatite
crystal deposiy in shoulder, acute and rapid deterioration
who gets hydroapatite
females 50-60 years old
what is hydroxyapatite also known as
milwaukee shoulder
what are inflammatory myopathies
polymyositis and dermatomyositis
prevelnace of muscle disease by gender
2x more common in females
peak age for inflammatory myopathies
40-50 years
what does inflammatory myopathies come with
increased incidence of malignancy
increase in malignancy in dermatomyositis
15%
increase in malignancy in polymyositis
9%
pathophysiology of inflammatory myopathies
muscle fibre necrosis, degneration, regeneration, inflammatory cell infitrate
clinical features of inflammatory myopathies
muscle weakness (neck, shoulder, hips), worsening onset, usually symmetrical and proximal muscles, often difficulty doing specific tasks myalgia
signs of demratomyositis
gottrons sign, heliostrope rash, shawl sign
what is gottrons sign
pink rash over MCPJ
what is shawl sign
rash accross back of shoulders
other manifestations of inflammatory myoapthies
ILD, resp muscle weakness, dysphagia, myocarditis, also fever weight loss, raynauds, non erosive, polyarthritis
what to ask about in patients with inflammatory myopaties
diabetes, thyroid disease, steroids, statins, alcohol and illicit drugs
diagnosis of inflammatory myopathies
confrontational testing, isotonic testing, blood test, auto antibodies, EMG, muscle biopsy, MRI
auto antibodies in inflammatory myopathies
ANA, anti jo 1
treatment of inflammatory myopathies
high dose steroid to suppress initially and then decease dose, 20 mg of prednisolone + methotrexate or azathioprine
who is body myositis more common in
men and older people
what muscles does inclusion body myositis effect
distal muscles
what des polymyalgia rheumatica present as
ache in shoulder and hip girdle, morning stiddness, symmetrical, fatigue, anorexia, weight loss, fever, reduced movement, muscle strength is normal
who does polymyalgia present in
over 50s
incidence of polymyalgia
1%
what is polymyalgia associated iwth
temporal arteritis/giant cell arteritis
what is termpal arteritis /giant cell arteritis
granulomas arteis of large vessels
presentation of temporal/giant cell arthritis
headaches, scalp tenderness, jaw claudication, visual loss and tender enlarged non pulstile temporal arteries
diagnosis of polymyaligia rheumatica
exclude other diagnosis, raised ESR, plasma viscosity, CRP, temperoal artery biopsy
treatment of polymyalgia rheumatica
treat with low dose steroids, gradually reduce over 18 months to 2 years
what is fibromyalgia
oversensitised pain stimulus
prevelance of fibromyalgia
2.5%
who does fibromyalgia present in
women 22-50
presentation of fibromyalgia
pain in neck, shoulders, lower back, chest wall, pins and needles, ibs, poor concentration and memroy
examination of fibromyalgia
excessive tenderness on palpation of soft tissues
treatment of firbomyalgia
pain control - atypical analgesia - amitriptyline, gabapentin, pregbalin, graded excersise programme, cbt
what. is vasculitis
presence of leukocytes / immune complexes in vessel wall damaging structure
how to classify vasculiti
by size of vessel or ANCA +
example of ANCA + vasculitis
wegeners, microscopic polyangitis, churg strauss
presentation of vasculitis
myalgia, arthralgia, fever, wgt loss, skin infarct, bloody nasal discharge, ulcers, paranasl sinus involvement, gangrene, subglottic stenosis, conductive deafness, sensorineural, hearing loss, pulse loss, valve disease, pericarditis, cardiomyopathy, congestive HF, peritonitis, bloody diarrhoea, ischeamic abdominal pain
test for vasculitis
ANCA
score for vasculitis
BVAS
untreated vasculitis prognosis
fatal
prognosis of treated vasculitis
5 yr survival is 90%
least common small cell
microscopic polyangitis
what does small cell microscopic polyangitis affect
kidneys
