13. Introduction to diseases of the musculoskeletal system Flashcards
tendonitis
Tendon problem.
bursitis
Inflammation of bursa. Bursae are synovial membrane lined pockets that serve to allow free movement of adjacent structures where otherwise, there could be friction.
enthesitis
Inflammation of an enthesis. Entheses are the points where tendons, ligaments or joint capsules insert into bone. The largest site is the Achilles insertion.
Osteoperosis
reduced bone density
osteomalacia
poor bone mineralisation
osteomyelitis
bone infection
osteosarcoma
an example of malignant bone tumour
myalgia
- Pain in muscles.
- Very common.
- Commonly associated with viral infections.
- Can be drug induced (eg by statins).
myositis
Inflammation of the muscles.
Far less common than myalgia and can be autoimmune
what is a joint?
A joint is formed where two or more bones meet each other
This is an example of a normal joint
Approach to a patient with a musculoskeletal disorder
Full history
& } Often enough to
Physical examination make a diagnosis
Serological tests – help to support the diagnosis
Some ways of classifying rheumatic disease
Articular or Non articular/ Periarticular
Inflammatory or non-inflammatory/degenerative/mechanical
number of joints affected - suspect infection in all acute monoarthritis
duration of onset
Periartciular joint pain
Point tenderness over the involved structure,
Pain reproduced by movement involving that structure
then think about which structure? bursa, tendon, tendon sheath, ligament, others?
articular joint pain
joint line tenderness
pain at the end range of movement in any direction
inflammatory or mechanical? any signs of inflammation? features of mechanical problems? locking, catching etc
joint inflammation nomenclature
MonoARHRITIS – arthritis affecting 1 joint
OligoARTHRITIS – arthritis affecting 4 or fewer joints (2-4)
PolyARTHRITIS – arthritis affecting 5 or more joints (>=5)
Soft tissue conditions
Problems with radiolucent moving tissues
Very common, part of everyday life
Some examples:
- tennis elbow (lateral epicondylitis) - golfers elbow (medial epicondylitis) - carpal tunnel (median nerve compression as it passes through the carpal tunnel in the wrist)
importance of rheumatic disease
Common and getting more common
Expensive
Important
Leading cause of disability
Worldwide impact of rheumatic disease
MSK disorders are the second most common cause of disability worldwide, measured by years lived with disability (YLDs)
Low back pain is the single leading cause for disability globally
Disability due to MSK disorders is estimated to have increased by 45% from 1990 to 2010, in particular OA, and is expected to continue to rise with an increasingly obese, sedentary and ageing population.
UK impact of rheumatoid disease
Third greatest impact on the health of the UK population, considering both death and disability (Lancet 9 March 2013)
– Musculoskeletal disorders account 15.6%
– Low back pain accounts for over half of this
– Ranking of major causes of death and disability
MSK disorders and work
Poor musculoskeletal health is a major barrier to workplace participation. People with musculoskeletal conditions are less likely to be employed than people in good health, and more likely to retire early.
Septic arthritis
Differential diagnosis of hot swollen joint is wide – ALWAYS consider joint aspiration and gram stain
The commonest organisms are staph and strep
Septic arthritis
Always think about it in a patient with a (usually) single, hot and swollen joint.
Mortality rates are of 11%. This increases to 50% in polyarticular disease with sepsis.
They do not have to be systemically unwell and they may be able to weight bear.
Seek senior advice. Do not delay antibiotic therapy.
Gout
Most common inflammatory arthropathy worldwide
• Serum urate levels > physiological saturation point (around 408 μmol/L)
Monosodium urate crystals form and deposit in cartilage, bone and periarticular tissues of peripheral joints
Clinical aspects of gout
Crystal deposition is often clinically silent
About 10% of people with hyperuricaemia develop clinical gout
UK GP Studies show the prevalence of gout per 1,000 has been steadily increasing from 2.6 in 1975, to 3.4 in 1987, and 9.5 in 1993
1 in 40 adults in the UK is affected by gout= 2.5% - 15 years analysis (2014)
Clinical cure is achievable with treatment which is cheap, widely available, and under-prescribed
Who gets gout?
Men aged 40 years and over
Women over 65 years.
It increases with age, affecting 15% of men aged over 75 in the United Kingdom
Epidemiological studies show that the metabolic syndrome and its components (insulin resistance, obesity, hyperlipidaemia, and hypertension) are strongly associated with gout
gout risk factors
Male sex, older age
Genetic factors (mainly reduced excretion of urate)
Chronic kidney disease (reduced excretion of urate)
Metabolic syndrome, obesity, hypertension, hyperlipidaemia, loop and thiazide diuretics (reduce urate excretion)
osteoarthritis (enhanced crystal formation)
deitary factors (increased production of uric acid)
Gout crystals
Gout is caused by negatively birefringent rods – monosodium urate
Pseudogout (CPPD) by positively birefringent rhomboids – calcium pyrophosphate
Gout management
Acute attacks:
NSAIDs e.g. naproxen, colchicine, steroids
Long-term: urate-lowering therapy e.g. allopurinol or febuxostat
Rheumatoid arthritis
Common, chronic, multisystem inflammatory condition affecting up to 0.5-1% of world population
More common in women (3:1). Peak onset is 45-65 years
Unknown cause with around 30% genetic susceptibility and the rest environmental
Main problem in rheumatoid arthritis
The main problem in inflammatory arthritis is with the SYNOVIUM whereas in osteoarthritis, the main problem is with the CARTILAGE
What is the most important environmental risk factor for rheumatoid arthritis?
smoking
rheumatoid arhritis pathophysiology
Early lymphocyte invasion of synovium Acute inflammatory reaction - swelling and increased vascular permeability synovial proliferation pannus formation cartilage destruction and bone erosion
Symptoms and signs of rheumatoid arthritis
Onset varies, can be acute or chronic
Symmetrical pain and boggy swelling of the small joints of the hands and feet (MCP, PIP, wrist, MTP, subtalar, NOT the DIPs)
early morning stiffness > 1 hour
malaise and fatigue are common
systemically unwell
examination - look for pain, swelling and restriction of movement
also really important to examine other organ systems as RA is a systemic disease
Extra-articular manifestations of RA
nodules (20%) bursitis/tenosynovitis eyes: dry eyes (secondary Sjogren's)/scleritis/scleromalacia splenomegaly (Feity's) Anaemia of chronic disease Lung fibrosis/effusion/nodules (Caplan's) pericarditis neurological: atlanto-axial sublucation/carpal tunnel syndrome/mononeuritis multiplex renal amyloidosis (RA) leg ulcers/pyoderma gangenosum vasculitis increased risk of CVD
RA investigations
ESR and CRP
FBC: anaemia of chronic disease (normochromic normocytic)
rheumatoid factor positive - IgM antibody against Fc portion of human IgG antibodies (but this can be falsely elevated by illness and are normally raised in 1/20 of population)
Anti CCP antibodies - cyclic citrullinated peptide antibodies (antigen present on inflamed synovium - 98% specific for RA diagnosis)
X-rays: normal in early disease… erosions/peri-articular osteoperosis and reduced joint space/cysts
RA principles of management
Early and aggressive treatment to reduce inflammation and joint damage
->
Non-steroidal anti-inflammatory drugs for short periods
->
Corticosteroids: intra-articular joint injections if only 1 or 2 troublesome. Systemic if many joints are problem - main routes are IM or PO though in severe disease maybe IV
RA drugs
DMARDs (disease modifying anti-rheumatoid drugs)
biologic agents
Synthetic DMARDs
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Biologic agents
Anti TNF agents ( Etanercept, Adalimumab, Infliximab)
Anti B-cell (Rituximab)
Anti Interleukin-6 receptor blocker (Tociluzumab)
Anti T-cell – selective co-stimulation modulator- CTLA4-Ig (Abatacept)
Janus kinase inhibitor (JAK 2) (Tofacinitib, Baricitinib)
Multidisciplinary aspects of RA management
Multidisciplinary team input
– Nurse specialist (education and disease monitoring)
– Physiotherapy (improve strength and stamina)
– Occupational Therapy (work, home environments)
– Podiatry
Osteoarthritis
Common, degenerative disease of which the prevalence increases with age
Affects 70% of over 65 years olds
Most commonly clinically affects the knees, hips and small joints of the hands (DIP, PIP, 1st CMCJ)
Characterised by joint pain and very variable degrees of functional limitation
Osteoarthritis pathophysiology
Metabolically active, dynamic process involving all joint tissues (cartilage, bone, synovium, capsule, ligaments/muscles)
->
Focal destruction of articular cartilage
->
Remodelling of adjacent bone = hypertrophic reaction at joint margins (osteophytes)
->
Remodelling and repair process (efficient but SLOW)
->
Secondary synovial inflammation and crystal deposition
Clinical features of osteoarthritis
Age > 50 years Morning stiffness < 30 minutes Persistent joint pain aggravated on use Crepitus NO INFLAMMATION Bony enlargement and/or tenderness
Osteoarthritis investigations
A clinical diagnosis
Blood tests not helpful
X-rays do not correlate well with symptoms
OA management
physiotherapy, weight loss if overweight/obese, education and advice
NSAIDS, paracetamol
opioids, capsaicin, intra-articular corticosteroid injections, local heat and cold, joint arthoplasty, supports and braces, shock-absorbing shoes, manual therapy (manipulation and stretching)
Systemic lupus erythmatosus
Chronic, relapsing, remitting disease
Broad spectrum of clinical features involving almost all organs and tissues
Prevalence in the UK: 97 per 100,000
F:M= 10-20:1
Peak onset between 15- 40 years
More common and severe in those of Afro-Caribbean, India, Hispanic and Chinese origin living in USA and Europe> Caucasians
PATHOPHYSIOLOGY
UV light results in cell death (apoptosis) but cells not cleared quick enough, there is abnormal immune response and autoantibodies are formed, leads to inflammation systematically leading to damage
Classification criteria for SLE
4 of 17 factors have to apply (at least 1 clinical) or biopsy-proven nephritis compatible with SLE in presence of ANA antibodies or anti-dsDNA antibodies
SLE investigations
Urinalysis - urinary protein:creatinine ratio full blood count urea and electrolytes ESR CRP liver function test antibodies: ANA, ENA, Anti-dsDNA, lupus anticoagulant, anti C1q C3, C4
