MSK Flashcards
what is osteoarthritis?
it is often described as wear and tear in joints.
NOT an inflammatory condition
occurs in the synovial joints and is a result of a combination of genetic factors, overuse and injury.
there is loss of cartilage
remodelling of adjacent bone
associated inflammation
what are the risk factors for osteoarthritis?
age >50 female obesity genetic factors trauma fam history
what are the four key changes seen on an X-ray of a patient with osteoarthritis?
LOSS
L- loss of joint space
O - osteophytes forming in joint margins
S - subarticular sclerosis - increased density of the bone along the joint line
S - subchondral cysts - fluid-filled holes in bones
X-ray changes do not necessarily correlate with symptoms. Significant changes might be found incidentally on someone without symptoms. Equally, someone with severe symptoms of osteoarthritis may only have mild changes on X-ray
how does osteoarthritis present?
pain - the pain tends to be worsened by activity (pain at rest or at night is unusual)
reduced joint function
bony deformities - common in the hands and lead to enlargement of the proximal interphalangeal joints (Bouchard’s nodes) and distal interphalangeal (DIP) joints (Heberden’s nodes), as well as squaring at the base of the thumb.
limited range of movement
joint instability
they may have joint tenderness and crepitus
what joints are commonly affected in osteoarthritis?
often large weight-bearing joints - hips, knees, sacroiliac joint DIPs MCP joint at the base of the thumb wrist cervical spine
what investigations do you perform for suspected osteoarthritis?
if the patient is over 45, has typical activity-related pain and no morning stiffness NICE suggests that a diagnosis can be made without any investigations.
investigations that can be performed are
X-ray affected joints
serum CPR and ESR
how is osteoarthritis managed?
All patients should be offered help with weight loss, given advice about local muscle strengthening exercises and general aerobic fitness
1st line - topical analgesia e.g capsaicin topical, methylsalicylate, diclofenac topical (topical analgesia is usually only offered for knee and hand
2nd line - paracetamol plus topical analgesia
3rd line - NSAIDs can be added and also consider prescribing PPI to protect their stomach (omeprazole)
4th line - opioid - consider opiates such as codeine and morphine - should be used cautiously
other options:
- Intra-articular steroid injections
- Joint replacement
what is another name for joint replacement?
arthroplasty
after hip replacement how long should LMWH be given for?
4 weeks as there is an increased risk of thromboembolism.
what is a baker’s cyst?
aka popliteal cyst - not true cysts but rather distension of the gastrocnemius-semimembranosus bursa
primary: no underlying pathology - typically seen in children
secondary - underlying condition such as OA - typically seen in adults
they present as swellings in the popliteal fossa behind the knee. Rupture may occur resulting in simial symptoms to DVT i.e. pain, redness and swelling in the calf however the majority of ruptures are asymptomatic
what is cervical spondylosis?
cervical spndylosis is and extremely common condition that results from OA
peresents as neck pain although referred pain may mimic headaches
complications include radiculopathy and myelopathy
what is rheumatoid arthritis?
it is an autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa.
It is an inflammatory arthritis - a symmetrical poly-arthritis
what are the genetic associations of rheumatoid arthritis?
HLA DR4
HLA DR1
What are the antibodies involved in rheumatoid arthritis?
Rheumatoid factor - a circulating antibody, usually, IgM, which reacts with the Fc portion of the patients own IgG.
RF is positive in 70-80% of patients with RA - high titre levels are associated with severe progressive disease (but not a marker of disease activity.
Anti-cyclic citrullinated peptide antibody - may be detectable up to 10 years before the development of RA - it may therefore play a key role in the future of RA, allowing early detection of patients suitable for aggressive anti-TNF therapy.
how can RF be detected?
rose-waaler test: sheep red cell agglutination
latex agglutination test
what conditions other that RA are associated with positive RF?
Sjogren's syndrome Felty's syndrome infective endocarditis SLE systemic sclerosis 30% of the general population will have positive RF
how does RA present?
swollen, painful joints in the hands and feet (typically the MCP and PIP in the hands and MTP in the feet)
stiffness worse in the morning
gradually gets worse with larger joints becoming involved (knees, shoulders, elbows, ankles)
presentation will usually develop over a few months
positive squeeze test - discomfort on squeezing across the metacarpal or metatarsal joints
what is the difference between pain on OA and RA?
RA - worse at rest but improves with activity
OA - worse with activity and improves with rest
what the extra-articular manifestations of RA?
ocular manifestations - keratoconjunctivitis, episcleritis, scleritis, corneal ulcerations, keratitis
respiratory manifestations - pulmonary fibrosis, pulmonary effusion, pulmonary nodules, bronchiolitis obliterans
Felty’s syndrome - RA, neutropenia and splenomegaly)
secondary sjogren’s syndrome - aka sicca syndrome
CV disease as RA increases risk of atherosclerosis
what are poor prognostic features of RA?
anti-ccp antibodies RF positive poor functional status at presentation HLA DR4 x-ray - early erosions extra-articular features insidious onset
what deformities occur in RA?
ulnar deviation
Boutonniere’s deformity
swan neck deformity
bakers cysts in the back of the knee
what investigations would you perform for rheumatoid arthritis?
NICE have stated that clinical diagnosis is more
RF and anti CCP antibody
X-ray of the hands and feet
inflammatory markers - CRP and ESR
USS of the joints can be used to evaluate and confirm synovitis - it is particularly useful where the findings of the clinical examination are unclear.
what x-ray changes would you see in RA?
joint destruction and deformity
soft tissue swelling
periarticular osteopenia
boney erosions
what are the NICE guidelines for referral for RA??
NICE recommend referral for any adult with persistent synovitis, even if they have negative rheumatoid factor, anti-ccp antibodies and inflammatory markers - the referral should be urgent if it involves the small joints of the hands or feet, multiple joints or symptoms that have be present for more than 3 months.
what are the different diagnostic criteria for RA?
diagnostic criteria come from the American college of rheumatology (ACR)/ European league against Rheumatism (ELAR)
patients are scored based on
- the joints that are involved (more and smaller joints are scored higher)
- serology (rheumatoid factor and anti-CCP)
- inflammatory markers (ESR and CRP)
- duration of symptoms (more or less than 6 weeks)
scores are added up and a score greater than or equal to 6 indicates diagnosis of rheumatoid arthritis
what score is useful for monitoring disease activity and response to treatment in RA?
the DAS28 score the DAS28 score is the disease activity score - it is based on the assessment for 28 joints and points are given for - swollen joints - tender joints - ESR/CRP result
what is first and second line management of RA?
first line is mono-therapy with a DMARD
methotrexate, leflunomide or sulfasalazine
hydroxychloroquine can be considered in mild disease as it is considered the mildest anti-rheumatic drug
often a short course of prednisolone is started in combination
second line is 2 of these used in combination
what is third and fourth line management of RA?
third line - methotrexate plus a biological therapy - usually a TNF inhibitor
forth line is methotrexate plus rituximab
**remember TNF inhibitors all lead to immunosuppression so patients are prone to serious infection - they can also lead to reactivation of dormant infections such as TB and hep B.
how does methotrexate work and the side effects?
methotrexate works by interfering with the metabolism of folate and suppressing certain components of the immune system. It is taken by injection or tablet once a week. Folic acid 5mg is also prescribed once a week to be taken on a different day to methotrexate.
side effects:
- mouth ulcers and mucositis
- liver toxicity
- pulmonary fibrosis
- bone marrow suppression and leukopenia (low white blood cells)
- it is teratogenic - need to be avoided prior to conception in mothers and fathersm
how do anti TNF drugs work?
what are some side effects of anti TNF drugs?
what are some examples of anti TNF drugs?
tumour necrosis factor is a cytokine involved in stimulating inflammation. Blocking TNF reduces inflammation.
side effects - vulnerability to severe infections and sepsis, reactivation of TB and hep B
examples
- adalimumab
- infliximab
- golimumab
- certolizumab pegol
- etanercept
adalimumab, infliximab, golimumab and certolizumab pegol are monoclonal antibodies to TNF. Etanercept is a protein that binds TNF to the Fc portion of IgG and thereby reduces its activity
what is Rituximab? and what are the notable side effects?
Rituximab is monoclonal antibody that targets CD20 protein on the surface of B cells. this causes destruction of B cells. It is used for immunosuppression for autoimmune conditions such as rheumatoid arthritis and cancers relating to B cells
side effects
- vulnerability to severe infection and sepsis
- night sweats
- thrombocytopenia
- peripheral neuropathy
- liver and lung toxicity
what are the side effects of sulfasalazine ?
rashes
oligospermia
Heinz body anaemia
bone marrow suppression
what are the side effects of leflunomide?
liver impairment
interstitial lung disease
hypertension
peripheral neuropathy
what are the side effects of hydroxychloroquine?
reduced visual acuity
nightmares
what is osteoporosis?
a complex skeletal diseases characterised by low bone density and micro-architectural defects in bone tissue resulting in increased bone fragility and susceptibility to fracture.
It is defined as bone mineral density of less than -2.5 standard deviations from the mean of a young adult
what are major risk factors for osteoporosis?
corticosteroid use smoking alcohol low body mass index family history
others:
age, female, post-menopausal, diabetes, vitamin D deficiency, low physical activity, hypothyroidism, CKD
What investigations would you perform for osteoporosis?
Dual-energy X-ray absorptiometry (DEXA) - work out a T score by measuring bone density at the hip
- t score is the number of standard deviations from the mean bone density of a 30 year old adult. Z score represents the the number of standard deviations the patients bone density fall below the mean for their age.
- DEXA scan be performed about every 2 years after diagnosis of osteoporosis
FRAX - fracture risk assessment tool - this gives a prediction of the risk of a fragility fracture over the net 10 years.
how is BMD classified depending on T score
More than -1 SD- BMD Normal
-1 to -2.5 SD- BMD = Osteopenia
Less than -2.5 S- BMD = Osteoporosis
Less than -2.5 plus a fracture - Severe Osteoporosis
how is osteoporosis managed?
lifestyle changes: activity and exercise, maintain adequate health weight, adequate vitamin D, avoid falls, stop smoking, reduce alcohol
Bisphosphonates are first line (alendronate, Risedronate, zolendronic)
If at risk of fractures - calcium with vitamin D (colecalciferol)
what are the side effects of bisphosphonates?
Reflux and oesophageal erosions. Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this.
Atypical fractures (e.g. atypical femoral fractures)
Osteonecrosis of the jaw
Osteonecrosis of the external auditory canal
if bisphosphonates are contraindicated in someone with osteoporosis what other options do you have?
Denoxumab is a monoclonal antibody that works by blocking the activity of osteoclasts.
Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction.
Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus.
Hormone replacement therapy should be considered in women that go through the menopause early.
what medications other than glucocorticoids may worsen osteoporosis?
SSRIs antiepileptics PPI glitazones long term herparin therapy aromatase inhibitors e.g. anastrozole
who should be assessed for osteoporosis?
They advise that all women aged >= 65 years and all men aged >= 75 years should be assessed. Younger patients should be assessed in the presence of risk factors, such as:
previous fragility fracture
current use or frequent recent use of oral or systemic glucocorticoid
history of falls
family history of hip fracture
other causes of secondary osteoporosis
low body mass index (BMI) (less than 18.5 kg/m²)
smoking
alcohol intake of more than 14 units per week for women and more than 14 units per week for men.
what methods are used to assess risk of osteoporosis?
NICE recommend using a clinical prediction tool such as FRAX or QFracture to assess a patients 10 year risk of developing a fracture. This is analogous to the cardiovascular risk tools such as QRISK.
FRAX
estimates the 10-year risk of fragility fracture
valid for patients aged 40-90 years
based on international data so use not limited to UK patients
assesses the following factors: age, sex, weight, height, previous fracture, parental fracture, current smoking, glucocorticoids, rheumatoid arthritis, secondary osteoporosis, alcohol intake
bone mineral density (BMD) is optional, but clearly improves the accuracy of the results. NICE recommend arranging a DEXA scan if FRAX (without BMD) shows an intermediate result
QFracture
estimates the 10-year risk of fragility fracture
developed in 2009 based on UK primary care dataset
can be used for patients aged 30-99 years (this is stated on the QFracture website, but other sources give a figure of 30-85 years)
includes a larger group of risk factors e.g. cardiovascular disease, history of falls, chronic liver disease, rheumatoid arthritis, type 2 diabetes and tricyclic antidepressants
when would you use a DEXA rather than one of the clinical prediction tools for osteoporosis?
before starting treatments that may have a rapid adverse effect on bone density (for example, sex hormone deprivation for treatment for breast or prostate cancer).
in people aged under 40 years who have a major risk factor, such as history of multiple fragility fracture, major osteoporotic fracture, or current or recent use of high-dose oral or high-dose systemic glucocorticoids (more than 7.5 mg prednisolone or equivalent per day for 3 months or longer).
what are signs of osteoporotic vertebral fractures?
Loss of height: vertebral osteoporotic fractures of lead to compression of the spinal vertebrae hence a reduction in overall length of the spine and thus the patient becomes shorter
Kyphosis (curvature of the spine)
Localised tenderness on palpation of spinous processes at the fracture site
what are bisphosphonates used for?
prevention and treatment of osteoporosis
hypercalcaemia
Paget’s disease
pain from bone metatases
what is SLE?
it is a chronic multi-system disorder that most commonly affects woman during their reproductive years. It is more common in asians and black africans.
It is an inflammatory autoimmune connective tissue disease.
It is “systemic” because it affects multiple organs and systems and “erythematosus” refers to the typical red malar rash that occurs across the face.
what is the basic pathophysiology in SLE?
SLE is characterised by anti-nuclear antibodies. These are antibodies to proteins within the persons own cell nucleus. This causes the immune system to target theses proteins. When the immune system is activated by these antibodies targeting proteins in the cell nucleus it generates an inflammatory response.
The immune system dysregulation leads to immune complex formation
Immune complex deposition can affect any organ including the skin, joints, kidneys and brain.
It is a type 3 hypersensitivity reaction
associated with HLA B8, DR2 and DR£
It often takes a relapsing-remitting course, with flares and periods where symptoms are improved. The result of chronic inflammation means patients with lupus often have shortened life expectancy. Cardiovascular disease and infection are leading causes of death.
what causes SLE?
Not really known but the interaction of an environmental agent in a genetically susceptible host is thought to be fundamental. The strong female preponderance also suggests a role for hormonal factors.
It is thought that drugs can be causative agents - procainamide, minocycline, terbinafine, sulfasalazine, isoniazid, phenytoin, carbamazepine.
how does SLE present?
General Features - fatigue, features, mouth ulcers, lymphadenopathy
skin - malar rash (most commonly erythema over the cheeks and bridge of nose), photosensitive rash (rash occurring after sun exposure - it can be painful and pruritic and usually lasts a few days), discoid rash (scaly, erythematous, well demarcated rash in sun-exposed areas), raynaud’s phenomenon, livedo reticularis, non-scarring alopecia.
MSK - arthralgia, non erosive arthritis (usually symmetrical, smaller joints, pol
CV - pericarditis, myocarditis
Resp - pleurisy, fibrosing alveolitis
Renal - proteinuria, glomerulonephritis
Neuropsychiatric - anxiety and depression, psychosis, seizures
what investigations would you perform for SLE?
> Autoantibodies - anti-nuclear antibodies (ANA) (however other things can cause this to be positive e.g. autoimmune hepatitis), anti-double stranded DNA (anti-dsDNA) is also specific to SLE. Anti-smith, anti Ro and anti La may also be positive. 20% of patients will also be RF positive.
FBC - normocytic anaemia of chronic disease
ESR and CRP - raised with active inflammation
complement levels - C3 and C4 are low during active disease.
Immunoglobulins - may be raised due to activation of B cells with inflammation
Urinalysis - if there is renal involvement there may be haematuria, casts (red cell, granular, tubular or mixed) or proteinuria
renal biopsy to look for lupus nephritis
U&E’s - elevated urea and creatinine if there is renal manifestations
CXR - if there are cardiopulmonary manifestations there may be evidence of pleural effusion, infiltrates, cardiomegaly.
ECG - may exclude other causes of chest pain
** you can use the SLICC criteria or the ACR criteria for establishing diagnosis
