MSK Peer Teaching Flashcards
what is the role of articular cartilage
friction reduction
shock absorption
what is the role of the synovial fluid
lubrication
shock absorption
nutrient distribution (since hyaline cartilage is avascular and relies on diffusion from SF)
what is the pathophysiology of osteoarthritis
- this is non-inflammatory wear and tear resulting from loss of articular cartilage
- there is an imbalance of cartilage damage and repair
- damage
- disordered repair
- fibrillations
- osteophytes
- sclerosis
risk factors for osteoarthritis
older
female
genes
obesity
previous joint trauma
RA
gout
name a disease that reduces the risk of osteoarthritis
osteoporosis
presentation of OA
mostly knee and hip but can be anywhere
pain on movement and at rest if severe
worse at the END of the day
minimal swelling
morning stiffness lasts <30 minutes
affects the DIPs
crepitus
osteoarthritis X ray findings
- LOSS
- loss of joint space
- osteophytes
- subchondral sclerosis
- subchondral cysts
Ix for osteoarthritis
- bloods: normal
- X-Ray: Loss
treatment for osteoarthritis
- conservative
- weight loss
- exercise
- physio
- hot/cold packs
- medical
- analgesic ladder
- intra-articular steroids
- PPI if long term NSAIDs
- surgical
- osteophyte removal
- joint replacement
what is rheumatoid arthritis
it is chronic systemic inflammatory disease due to deposition of immune complexes in synovial joints which causes symetrical, deforming polyarthritis
how common is RA
common it’s ~ 0.5 - 1% of the population
rheumatoid arthritis risk factors
increasing age
female
premenopausal
smoking
stress
infection
what is the typical presentation of RA
symmetrical swollen, painful and stiff joints (hands and feet) which is worse in the morning for >1hr and in hot weather. symptoms ease off with use
name 4 deformities associated with RA
rheumatoid nodule on elbow
ulnar defiation
boutonniere
swan neck deformity
z thumb
signs of RA apart from deformities
MCP, PIP, MTP, DIP (sparingly) symmetrical swelling
muscle wasting
carpal tunnel syndrome
9 extra-articular manifestations of RA
weight loss
xeropthalmia
pulmonary fibrosis
pericarditis
sjorgen’s
raynaud’s
neuropathies
scleritis
increased CV event risk
diagnostic criteria for RA
- You need 4 of the following 7
- morning stiffness
- arthritis of 3 or more joints
- arthritis of hand joints
- symmetrical
- rheumatoid nodules
- rheumatoid factor +ve
- radiographic changes (LESS)
radiographic changes seen in RA
- LESS
- loss of joint space
- erosions (peri-articular)
- soft tissue swelling
- soft bones (osteopenia)
Investigations for RA
- rheumatoid factor (only 70% patients)
- anti-CCP (anticitrulinated protein antibody)
- very specific
- FBC
- high platelets
- high CRP
- high ESR
- X-Ray
- LESS
treatment for RA
- initially NSAIDS
- give PPI
- refer to rheumatology
- early use of DMARDs reduces joint destruction
- methotrexate
- sulfasalazine
- biologics
- rituximab
- encourage exercise and manage RF
name 6 groups involved in the RA MDT
GP
Rheumatolgy
OT
Physiotherapy
acute exacerbations of RA are treated how
with IM steroid like methylprednisolone
TNF-alpha blockers like etenercept if DMARDs aren’t working
how is the swelling different in RA and OA
in RA the swelling is usually due to joint effsions in OA it’s bony
what is osteoporosis
it is low bone mass, high bone fragility and increased fracture risk
what causes osteoporosis
it is due to increased resorption and inadequate formation
or it can be caused by inadequate peak bone mass
osteoporosis risk factors
elderly
female
family history
smoking
low BMI
alcohol excess
those with low calcium i.e. lactose intolerant
what sort of drugs might cause osteoporosis
cortico steroids
hormone therapy e.g. androgen deprivation therapy in prostate cancer
what other diseases can predispose to Osteoporosis
- joint diseases
- RA
- SLE
- hyperparathyroidism & pseudohyperparathyroidism (high bone turnover)
- high cortisol e.g. cushing’s (causes high resorption and low osteoblast activity)
- low oestrogen or testosterone (e.g. menopause)
- renal disease (low vit D)
what is the difference between primary and secondary osteoporosis
primary is basically old age + menopause because oestrogen protects bones
secondary is due to other disease or drugs
causes of secondary osteoporosis
- SHATTERRED
- Steroid use
- Hyperthyroid/hyperparathyroid
- Alcohol/smoking
- Thin (low BMI)
- Testosterone low
- Early menopause
- Renal/liver disease
- Relatives (FH)
- Erosive bone disease (RA or Myeloma)
- Dietary calcium low
diagnosis of osteoporosis
- DEXA BMD scan T score:
- -2.5 SDs = OP
- between -1 and -2.5 SDs = osteopenia
- more than -1 = normal
- bloods will be normal
1st, 2nd and 3rd line treatments for osteoporosis
- 1st: bisphosphonates = alendronate
- 2nd: another bisphosphonate = risendronate
- 3rd: strontium ranelate
what antibody might be present in antiphospholipid syndrome
anti-cardiolipin antibody
primary prevention of osteoporosis
Adcal D3 (vitD with calcium)
calcium rich diet (dairy, sardines, white beans)
HRT
if they’re on corticosteroids consider prophylactic bisphosphonates
regular weight bearing exercise
reduce smoking and alcohol consumption
how do bisphosphinates work
bind calcium
is absorbed by osteoclasts
stimulate osteoclast apoptosis
reduce bone resorption
what is SLE
- systemic lupus erythematosus
- a multi-systemic disease in which autoantibodies are produced by B cells
- these target a variety of autoantigens leading to formation of immune complexes at various sites
- this activates complement system and an influx of neutrophils causing inflammation in those tissues
what are the risk factors for SLE
women in 90% cases
peak onset 20-40yrs
afro-carribeans 10x more likely than caucasians
hereditary
triggers for SLE
UV light
EBV
drugs e.g. isoniazid
presentation of SLE
- typically relapsing remitting
- very non specific symptoms
- fatigue
- myalgia and arthralgia
- skin problems
- fever
- lymhadenopathy
- weight loss
diagnostic criteria of SLE
- 4 of the following 11 are required
- MD SOAP BRAIN
- Malar rash (30%)
- Discoid rash
- Serositis
- Oral ulcers
- Arthritis
- Photosensitivity
- Blood (all low - anaemia and leukopenia)
- Renal disorder (proteinuria)
- ANA +VE (90%)
- Immunological disorder (anti-dsDNA)
- Neurological symptoms (seizures)
- MD SOAP BRAIN
Ix for SLE
screen for ANA (sensitive but not specific)
anti-dsDNA (specific but not sensitive)
inflammatory markers (ESR high but CRP may be normal)
two other conditions that SLE is associated with
raynaud’s
anti-phospholipid syndrome
4 complications of SLE
migraine
IHD
stroke
non-infective endocarditis
what is antiphospholipid syndrome
it occurs secondarily to SLE and is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies.
what are the signs of Antiphospholipid syndrome
- CLOT
- Coagulation defects
- Levido reticularis (pink-blue mottling)
- Obstetric: recurrent miscarriages
- Thrombocytopaenia
- Also there will be anti-cardiolipin antibody present
what is the treatment for anti-phosopholipid syndrome
- manage CVS risk factors
- smoking
- weight
- diet
- exercise
- DM
- HTN
- hyperlipidaemia
- warfarin or LMWH if trying to conceive
- aspirin
what is sjorgen’s syndrome
it’s a chronic inflammatory autoimmune disease
it is either primary fibrosis of exocrine glands or it is secondary to another connective tissue disorder such as SLE, RA or systemic sclerosis
what are the clinical features of sjorgen’s syndrome
- dry eyes and mouth, aka sicca complex
- parotid swelling i.e. englarged salivary glands
- other glands and affected too causing dyspareunia and dry cough etc
- arthralgia
Ix of Sjorgen’s syndrome
Schirmer’s test - measures conjunctival dryness
treatment for Sjorgen’s syndrome
- Sicca: treat with artificial tears and artificial saliva
- NSAIDs for arthralgia
What is crest syndrome and what are the clinical features
- it is systemic sclerosis that is limited rather than diffuse
- SKIN INVOLVEMENT IS LIMITED TO THE HANDS, FACE AND THE FEET
- CREST
- Calcinosis - calcium deposits in skin
- Raynaud’s phenomenon
- Eosphageal dysfunction - acid reflux or decrease in motility
- Sclerodactyly - thickening and tightening of skin on hands
- Telangiectasias - dilation of capillaries showing red marks on surface of skin
- Also
- beak like nose
- microstomia
- potentially fatal pulmonary hypertension
what is diffuse systemic sclerosis
it is where crest syndrome is diffuse
all organs have fibrosis
anti-topoisomerase and anti-ro antibodies
there is poor prognosis
treatment for crest syndrome and systemic sclerosis
there is no cure
treat the organs involved
for raynaud’s give CCBs e.g. nifedipine
for pulmonary HTN give prostaglandins e.g. iloprost
what is ankylosing spondylitis
it is a chronic inflammatory disease of the spine and sacro-iliac joints
what HLA haplotype is ankylosing spondylitis associated with?
HLA-B27
pathophysiology of ankylosing spondylitis
enthesitis
excessive and erosive repair phase follows
this leads to formation of syndesmophytes
these then fuse (ankylosis)
this prevents flexion and rotation
bamboo spine = end stage
ankylosing spondylitis associated features
- SPINEACHE
- Sausage digit
- Psoriasis
- Inflammatory back pain
- NSAID good response
- Enthesitis
- Arthritis (asymmetrical, large joint oligoarthritis)
- Crohns, UC and high CRP
- HLA-B27
- Eye: anterior uveitis
typical ankylosing spondylitis patient
man
16-30
gradual onset back/buttock pain
axial involvement
relieved by exercise
radiates to hip/buttocks
decreased chest expansion
kyphosis
hips and knees flexed
question mark posture
what is enthesitis
inflammation of the entheses, the sites where tendons or ligaments insert into the bone
what is kyphosis
Kyphosis (from Greek κυφός kyphos, a hump) is an abnormally excessive convex curvature of the spine as it occurs in the thoracic and sacral regions.
what is a differential for ankylosing spondylitis and how would you differentiate
- mechanical back pain
- can differentiate because in AS
- onset of pain is gradual
- wakes patients from sleep
- pain is relieved by exercise
what is the major investigation for ankylosing spondylitis
sacroiliitis is the first visible sign on x ray/MRI
enthesitis also visible
if advanced: syndesmophytes and bamboo spine
diagnosis of ankylosing spondylitis
sacroiliitis on x ray/mri with at least one of the spineache features
why do you get anaemia in chronic disease
- In chronic infection, chronic immune activation, and malignancy
- These conditions all produce massive elevation of Interleukin-6,
- This stimulates hepcidin production and release from the liver
- This reduces the iron carrier protein ferroportin so that access of iron to the circulation is reduced
first, second and third line treatments for Ankylosing Spondylitis
- 1st line: exercise and physio
- 2nd line: NSAIDs
- 3rd line: anti-TNF alpha e.g. etanercept
- these stop syndesmophytes forming
- once they’re formed, nothing will reverse/stop the progress
ANKYLOSING SPONDYLITIS DOES NOT RESPOND TO DMARDS
How much of the population have psoriasis
2-3%
how many of the patients with psoriasis have psoriatic arthritis
10-40%
psoriatic arthritis is associated with which HLA type
HLA B27
how does psoriatic arthritis present
- arthritis in:
- DIPJ
- Spine - sacroilliac joint (asymetrically)
- skin - psoriatic plaques
- sausage digit (‘dactylitis’)
- nail involvement in 80%
- onycholysis
- hyperkeratosis
- pitting
Ix for psoriatic arthritis
- bloods:
- anaemia
- high ESR
- Rh F -ve
- X ray
- erosive changes (pencil in cup deformity of fingers)
management of psoriatic arthritis
- NSAIDs
- DMARDs
- methotrexate
- sulfasalazine
- ciclosporin
- exercise
what is reactive arthritis
- it is typically an oligoarthritis of lower limbs caused by sterile inflammation of synovial membranes that follows an infection that is typically GI or STI
- shigella
- chlamydia
- gonorrhoea
- salmonella
- campylobacter
which HLA type is reactive arthritis typically associated with
HLA B27
what is the triad of symptoms associated with reactive artheritis and what is it called
- Reiter’s triad
- can’t see - conjunctivitis
- can’t pee - urethritis
- can’t climb a tree - arthritis
Ix for reactive arthritis
- bloods:
- high ESR and CRP
- stool culture if diarrhoea
- STI screen
- joint aspirate
- if it’s not sterile it’s septic arthritis
- X-ray
what is vasculitis
it is an inflammatory disorder of the blood vessel walls which can affect any organ causing destruction or stenosis of a vessel
management of reactive arthritis
treat cause of infection
rest and splint the joint
NSAIDs
consider the use of methotrexate and sulfasalazine as steroid sparing agents
what are two types of ANCA +ve vasculitis
Wegener’s
Churg-Strauss syndrome
what are two types of ANCA -ve vasculitis
Henoch Schonlein purpura
Goodpastures (anti-glomerular basement membrane antibodies)
in whom is Giant Cell Arteritis more common in
women and those over 50
presentation of Giant Cell Arteritis
headache
scalp tenderness (pain combing hair)
jaw claudication
acute visual changes (amaurosis fugax)
diagnosis of giant cell arteritis
- 3 of the following:
- Age >50 y/o
- New headache
- Temporal artery tenderness
- ESR >50
- Abnormal artery biopsy
Ix for giant cell arteritis
temporal artery biopsy
ESR
Treatment of Giant cell arteritis
steroids: prednisolone
visual changes: urgent IV methyprednisolone and refer to opthalmologist
what is polymyalgia rheumatica
autoinflammatory process that affects joints and muscles
often coexists with GCA
causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips.
what is the presentation of polymyalgia rheumatica
symmetrical aching and tenderness
morning stiffness in shoulders and proximal limb muscles
what is the Ix for polymyalgia rheumatica
high crp and esr
normal creatinine kinase
high alkaline phosphatase
what is the treatment for polymyalgia rheumatica
steroids like prednisolone
what is wegener’s vasculitis aka
granulomatosis with polyangiitis
what is granulomatosis polyangiitis and what tissues does it normally affect
- aka wegener’s vasculitis
- normally affects the arterioles and capillaries
what is the presentation of wegener’s vasculitis
- upper resp tract
- sinusitis
- nasal crusting
- lungs
- pulmonary nodules
- Kidney
- glomerulonephritis, destruction of basement membrane
Ix for wegener’s vasculitis
high ESR
CXR nodules
c-ANCA positive
management of granulomatosis polyangiitis
high dose steroids
cyclophosphamide
what does ANCA stand for
Antineutrophil cytoplasmic antibodies
is gout more common in men or women and what is the typical age of presentation
men 40-60
what are the crystals that cause gout
monosodium urate crystals
what dietary factor causes gout, what metabolises this and what is it turned into and where is this excreted
- purines from the diet
- turned to uric acid
- catalysed by xanthine oxidase
- excreted by the kidneys
what causes gout
- high purine diet
- alcohol
- red meat
- seafood
- fructose
- genetics
- renal disease
- diuretics
- high insulin levels
investigations for gout
- polarised light microscopy
- NEGATIVELY birefringent NEEDLE shaped monosodium urate crystals
- high serum urate but it may be normal
- JOINT ASPIRATE FOR ANY RED HOT JOINT
- R/O septic arthritis
acute treatment for gout
- NSAIDs
- Colchicine if NSAIDs contraindicated
why might NSAIDs be contraindicated
peptic ulcer
diabetes
renal disease
gout prevention: lifestyle
- lifestyle
- calorie restriction
- modify diet
- weight loss
- reduce alcohol consumption
- dairy is protective
medical prevention of gout
- allopurinol
- it’s a xanthine oxidase inhibitor
- YOU MUST NOT USE IN AN ACUTE ATTACK AS IT’S PARIDOXICALLY PROLONGS THE PAIN
What is the crystal in pseudogout
calcium pyrophosphate crystals
what are the risk factors for pseudogout
old age (70s) (older than for gout)
hyperparathyroidism
haemochromatosis
hyperphosphataemia
diabetes
Investigations for pseudogout
aspirate joint to R/O septic arthritis
polarised light microscopy shows POSITIVELY birefringent RHOMBOID shaped crystals
X-Ray shows chondrocalcinosis
what are the symptoms of pseudogout
acute pain in joint - sudden onset
typically larger joints e.g. knee
treatment for acute attacks of gout
rest
ice packs
intra-articular steroids
NSAIDs ± Colchicine may prevent the acute attacks
treatment for chronic pseudogout
methotrexate of sulfasalazine if inflammatory changes continue
what is fibromyalgia
it is a non-specific muscular disorder with unknown cause
pain with no signs of inflammation
rfs for fibromyalgia
female (10x more common)
middle age
low household income
divorced
fibromyalgia is associated with
IBS
chronic headache
depression
chronic fatigue
presentation of fibromyalgia
- widespread symptoms that have lasted >3 months
- pain worse with stress or cold weather
- morning stiffness >1hr
- non-restorative sleep
- headache and diffuse abdo pain
- neurocognitive features
- mood disorder, poor sleep, poor concentration etc
Ix and Dx of fibromyalgia
all Ix normally normal
diagnosis is based on pain in >11/18 palpitation sites
management of fibromyalgia
- reassure that there’s no serious pathology
- non pharma: CBT, exercise and education
- manage pain: with analgesia and acupuncture
- improve sleep: amitriptyline
- this is an antidepressant
red flags for lower back pain
- TUNAFISH
- Trauma, TB
- Unexplained loss of weight/night sweats
- Neurological deficits (e.g. incontinence)
- Age <20 or >55
- Fever
- IVDU
- Steroid use or immunocompromised
- History of cancer
risk factors for lower back pain (lumbago)
manual labour work
low socioeconomic status
poor working conditions
older age
smoking
when would you Ix lower back pain
only if it is chronic i.e. >12 weeks
what are the Ix for lower back pain
if young then CRP and ESR to check for tumour, myeloma or infection
only X ray if there are red flags
Tx for lower back pain and prognosis
90% will resolve within 6 weeks
continue normal activity - don’t rest
lifestyle
analgeisic ladder and diazepam if insufficient
physio
acupuncture
CBT
lifestyle advice –> better lifting, heat pads, slouching etc
mechanical vs inflammatory back pain table
major cause of inflammatory back pain?
ankylosing spondylitis
5 causes of mechanical back pain
degenerative discs
osteoarthritis
muscular imbalance
disc herniation
vertibral fracture
what is the most common causative organism in septic arthritis
staph aureus
name 4 organisms that can cause septic arthritis and some examples of situations in which they are more common
- staph aureus (most common)
- N. gonorrhoea (if young and sexually active)
- Staph epidermidis (joint replacement)
- E.coli (if immunocompromised)
presentation of septic arthritis
- any red hot swollen joint is septic arthritis until proven otherwise
- knee in 50% cases
- 90% monoarthritis
- fever
risk factors for septic arthritis
- any pre-existing joint disease
- DM
- recent joint surgery
- immunosuppression
- penetrating trauma
- skin breaks or ulcers
- elderly >80
management of septic arthritis
- urgent aspiration for M, C &S
- they must have been off abx at this point
- then empiricle Abx followed by abx for known organism
- rest
- analgesia
- stop immunosuppressive drugs
three causes of osteomyelitis
haematogenous origin (80%) e.g. from a boil
direct innoculation to bone (trauma/surgery)
contigous spread of infection to bone from adjacent tissues
what is the major causative organism in osteomyelitis and what is another one in a specific situation
staph aureus in 90% cases
salmonella in sickle cell anaemia
what are the risk factors for osteomyelitis
- the same as for septic arthritis
- pre-existing joint disease
- DM
- recent surgery
- immunosuppression
- penetrating trauma
- skin breaks/ulcers
- elderly >80yrs
osteomyelitis presentation
fever and dull, localised bone pain
made worse on movement
overlying tenderness and erythema
commonly occurs in the metaphysis of long bones in children
Ix for osteomyelitis
- bloods: wcc, CRP, ESR
- imaging: X-ray or MRI
- Bone biopsy is diagnostic
management of osteomyelitis
surgical drainage of abscess
debridement of dead bone
IV Abx
what does osteomyelitis lead to if untreated
bone death
name three types of primary bone tumour
osteosarcoma
ewings sarcoma
chondrosarcoma
who is affected by osteosarcoma and where in the body mostly
kids, and adults <20yrs
in the knees and humerus
pagets is a RF
who gets ewing’s sarcoma and where in the body is it
<25yrs old
mostly hips and long bones
symptoms of primar bone malignancy
bone pain that is nocturnal
local red and swelling - maybe painful or painless
fatigue, weight loss and anaemia
unexplained bone fractures
Ix for bone tumours
x ray
mri
biopsy
treatment for bone tumours
- chemo ± radiotherapy
- useful in ewing’s but not chondrosarcoma
- surgery
- bisphosphonates
- decrease pain and fracture rates
pathology of myeloma
- increased RANKL causes increased osteoclast activity
- CRAB
- high ca2+
- renal failure
- anaemia
- bone lytic lesion (i.e. pepper pot skull)
- bone marrow infiltration –> fatigue, infection and bruising/bleeding
who should you screen for myeloma
all patients over 50 with new back pain
screen with serum electropheresis and ESR
investigation of myeloma
serum electrophoresis - single Ig band
bence jones protein in urine
bone marrow aspirate
x ray - pepper pot skull
management of myeloma
analgesia - avoid NSAIDs (renal failure)
bisphosphinates
EPO transfusions for anaemia
chemotherapy
they don’t tend to transplant for myeloma
what is RF and where would you find it
rheumatoid factor seen in rheumatoid arthritis and other autoimmune conditions with low specificity
what is anti-ccp and where would you find it
anti cyclic citrullinated peptide
it’s seenin RA with good specificity
what are ANA antibodies, what is an example and when would you find it
anti nuclear antibodies
an example is anti-dsDNA antibody
found in SLE
what are ANA antibodies, what is an example and when would you find it
anti nuclear antibodies
an example is anti-dsDNA antibody
found in SLE
when is anti-ro found
sjorgen’s
c-ANCA what is it and when would you find it
it is cytoplasmic anti neutrophil cytoplasmic antibodies
found in wegener’s
what is p-ANCA and when is it found
perinuclear anti-neutrophil cytoplasmic antibodies,
found in churg-strauss
when is anti-centromere/anti-topoisomerase antibody found?
in CREST or systemic sclerosis
what is anti-GBM and when is it found?
it is anti glomerular basement membrane antibody and it is found in goodpasture’s
what are the two antibodies associated with coeliac
anti-endomysial antibodies of the immunoglobulin A (Anti-EMA)
Anti-transglutaminase antibodies (Anti-tTG)
what is bence jones protein
A Bence Jones protein is a monoclonal globulinprotein or immunoglobulin light chain found in the urine.
Detection of Bence Jones protein may be suggestive of multiple myeloma
which hand joint is more affected in OA than in RA
DIP
in which condition would you see hebarden’s nodes and bouchard’s nodes and which one is which
osteoarthritis (RA much more rarely)
outer hebredes
what are the antibodies present in diffuse systemic sclerosis
anti-topoisomerase and anti-ro antibodies
