l13:Intro to msk diseases Flashcards
what are the bursae
-they are synovial membrane lined pockets that serve to allow free movement of adjacent structures where otherwise there could be friction
describe what occurs in 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.
define the conditions:
1-osteoporosis
2-osteomalacia
3-osteomyelitis
4-osteosarcoma
Osteoporosis – Reduced bone density
Osteomalacia – Poor bone mineralisation
Osteomyelitis – Bone infection
Osteosarcoma – An example of malignant bone tumour
what is myalgia commonly associated with
- Commonly associated with viral infections.
- Can be drug induced (eg by statins).
define a joint
A joint is formed where two or more bones meet each other
This is an example of a normal joint
how can rheumatic disease be classified
Articular
Non articular/ Periarticular
Inflammatory
Non inflammatory/ degenerative / mechanical
Number of joints affected - Suspect infection in all acute monoarthritis
Duration of onset
how is joint pain classified
Periarticular: (point tenderness over the involved structure, pain reproduced by movement involving that structure )
Articular: Joint line tenderness, pain at the end range of movement of any direction
which structure: Bursa, tendon, tendon sheath, ligament sheath, others
inflammatory or mechanical
define the terms monoarthritis, oligoarthritis, polyarthritis
MonoARHRITIS – arthritis affecting 1 joint
OligoARTHRITIS – arthritis affecting 4 or fewer joints (2-4)
PolyARTHRITIS – arthritis affecting 5 or more joints (>=5)
You are asked to review a patient presenting with thenar eminence atrophy. Which nerve do you think is affected?
Ulnar nerve
median
which epicondyle is tennis elbow
Lateral epicondyle
give aeitiology of 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)
background of rheumatic disease
- very common and getting more common
- expensive
leading cause of disability
background on MSK disorders
• 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.
what are the secondary effects of MSK on work
22.4%?30.8 million days of work lost in a year
look at slide 24 for statistics on MSK
how was it
what is a MSK differential for a 2 day history of a painful swollen right knee
1) Posttraumatic hemarthrosis
2) Gout
3) Septic arthritis
what tests can be done for septic arthritis
consider joint aspiration and gram stain
what are the organisms responsible for septic arthritis
-The commonest organisms are staph and strep
-
what is the pathophysiology of gout
Most common inflammatory arthropathy worldwide
Serum urate levels > physiological saturation point (around 408 μmol/L)
Monosodium urate. form and
crystals deposit
cartilage, bone, and periarticular tissues of peripheral joints
what is the common joint for gout to occur
first metatarsophalangeal joint
give a background of gout disease
- 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)
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
what are the risk factors for gout
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 excretion of urate)
Osteoarthritis (enhanced crystal formation)
Dietary factors (increased production of uric acid)
What crystals are you expecting to find in the knee fluid aspirated from our previous patient if you suspect clinically that he has gout?
monosodium urate
describe the gout crystal formation
Gout is caused by negatively birefringent rods – monosodium urate
what is psuedogout
Pseudogout (CPPD) by positively birefringent rhomboids – calcium pyrophosphate
how do you manage acute gout attacks
– NSAIDs e.g. naproxen
– Colchicine
– Steroids
how do you manage gout long term
Urate-lowering therapy e.g. allopurinol or febuxostat
describe rheumatoid arthritis
-Common, chronic, multisystem inflammatory condition affecting up to 0.5-1% of the 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
what is the first component affected in rheumatoid arthritis
the synovium
what is affected in osteoarthritis
cartilage
what is the most important environmental factor for rheumatoid arthritis
Smoking
what is the process smoking causes in rheumatoid
Citrilidation happens to porteins in the lung, they aren’t recognised by innate immune system, apc presents to T cells taken to B cells which produced antibodies- APA
Triggers disease
describe the phases and classification of rheumatoid disease
(induction of autoimmunity )
Phase A/B- genetic and environmental
Phase C- systemic autoimmunity
( Maturation of the antibody response)
Phase D- Symptoms
Phase R- Unclassified arthritis
Phase F- no additional changes- rheumatoid
describe the pathology behind rheumatoid arthritis
- Early lymphocyte invasion of the synovium
- Acute inflammatory reaction - swelling and increased vascular permeability
- Synovial proliferation
- pannus formation
- cartilage destruction and bone erosion
what ..articular and joints are involved in rheumatoid
Polyarticular symmetrical disease
In particular metacarpal phalangeal joints
what are the symptoms and signs
-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
what are the extra-articular manifestations of RA
- Nodules (20%)
- Bursitis / Tenosynovitis
- Eyes: dry eyes (secondary Sjogren’s syndrome) / Scleritis / Scleromalacia
- Splenomegaly (Felty’s)
- • Anaemia of chronic disease
- Lung fibrosis /effusion /Nodules (Caplan’s)
- Pericarditis
- Neurological: Atlanto-axial subluxation / Carpal tunnel syndrome / Mononeuritis multiplex
- Renal amyloidosis (AA)
- Leg ulcers / Pyoderma gangenosum
- Vasculitis
- Increased risk of cardiovascular disease
what RA investigations can be done
- • ESR and CRP
- FBC: Anaemia of chronic disease (normochromic normocytic)
• Rheumatoid factor positive
– IgM antibody against the FC portion of human IgG antibodies :
1-can be falsely elevated by illness
2– normal raised levels in 1 in 20 of population
Anti CCP antibodies - cyclic citrullinated peptide antibodies:– Antigen present on inflamed synovium
– 98% specific for diagnosis of RA
X-Rays : normal in early disease.. erosions / peri-articular osteoporosis and reduced joint space / cysts
look at slide 48
how was it
describe the management of RA (1)
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 a problem. The main routes are IM or PO though in severe disease we may give IV steroid.
what medication do u use to manage RA
DMARDs – Disease Modifying Anti-Rheumatic Drugs
- 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)
what is the multidisciplinary team that works on RA
– Nurse specialist (education and disease monitoring)
– Physiotherapy (improve strength and stamina)
– Occupational Therapy (work, home environments)
– Podiatry
study slide 52
how was it
describe 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
(Distal and proximal interphalangeal joint and the 1st metacarpal joint)
what is the pathophysiology of osteoarthritis
- • 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
what are the 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
Is there a clinical correlation between the radiological changes and the symptoms in osteoarthritis?
no
OA investigations
- Blood tests not helpful
- A clinical diagnosis
- X-rays do not correlate well with symptoms
study slide 60
how was it
describe SLE
- 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
study slide 64
how was it
what are the systemic effects of SLE
splenomegaly
glomerulonephritis
malar rash and discoid rash
lung inflammation
renal failure
atherosclerosis
pulm fibrosis
stroke
neurological damage affective disorder
Pain cycanosis warm up-red and painful
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;
SLE treatment
MTX
CS
IV MP and CYC
