L13 Introduction to diseases of the MSK system Flashcards
Prefix - problems with bones
Osteo
Prefix - problems with muscle
My/Myo
Prefix - problems with joints
Arth
Prefix - describes cartilage
Chond
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
Osteoporosis
- 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
- Formed where two or more bones meet each other
Approach to a patient with MSK disorder
- Full history
- Physical examination
- Serological tests - help to support the diagnosis
Some ways of classifying rheumatic disease
- Articular vs non articular/periarticular
- Inflammatory vs non- inflammatory/degenerative/mechanical
- Duration of onset
What should be suspected in acute monoarthritis
- Infection
Periarticular vs articular joint pain
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 in any direction
Structures affected by periarticular joint pain
- Bursa
- Tendon
- Tendon sheath
- Ligament
- others
What to look for if articular joint pain
- Any signs of inflammation
- Features of mechanical problem (locking, catching etc)
Joint inflammation nomenclature
- Monoarthritis - 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
Examples of soft tissue conditions
- 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
- Leading cause of disability
Septic arthritis - differential diagnosis
- Differential diagnosis of hot swollen joint is wide
- Always consider joint aspiration and gram stain
What can increase the possibility of a diagnosis being septic arthritis
- Always think about it in a patient with a (usually) single, hot and swollen joint
- They do not have to be systemically unwell and they may be able to weight bear
Most common organisms - septic arthritis
- Staph and strep
Gout
- Most common inflammatory arthropathy worldwide
- Serum urate levels > physiological saturation point (around 408 micromol/L)
- Form and deposit cartilage, bone, and periarticular tissues of peripheral joints
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 UK
Conditions associated with gout
- Metabolic syndrome and its components (insulin resistance, obesity, hyperlipidaemia, and hypertension)
Risk factors for gout
- Male sex
- Older age
- Genetic factors (mainly reduced excretion of urate)
- Chronic kidney disease(reduced excretion of urate)
- Loop and thiazide diuretics(reduce excretion of urate)
- Osteoarthritis(enhanced crystal formation)
- Dietary factors(increased production of uric acid)
Crystals in gout
- Gout is caused by negatively birefringent rods (monosodium urate)
- Pseudogout (CPPD) by positively birefringent rhomboids - calcium pyrophosphate
Management of gout
Acute attacks:
- NSAIDs eg naproxen
- Colchicine
- Steroids
Long term:
- Urate-lowering therapy eg, allopurinol or febuxostat
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
Main problem in inflammatory arthritis vs osteoarthritis
- The main problem in inflammatory arthritis is with the synovium whereas in osteoarthritis, the main problem is with the cartilage
Classification and disease duration - ‘Normal’
Phase A/B - Genetic and environmental risk factors
Phase C - Systemic autoimmunity
Induction of autoimmunity
Classification and disease duration - ‘symptoms’
- symptoms
- Phase D
- Maturation of the antibody response
0-3 months from symptom onset
Classification and disease duration - Swelling
- Unclassified arthritis
- Swelling
- Phase E
3-6 months from time of onset
Classification and disease duration - Fulfilment of classification criteria
- Rheumatoid arthritis
- Phase F
- No additional changes
6-9 months from time of onset
Rheumatoid arthritis pathophysiology
- Early lymphocyte invasion of the 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 hr
- 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/tensosynovitis
- 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
- Leg ulcers/pyoderma gangenosum
- Vasculitis
- Increased risk of cardiovascular disease
RA investigations
- ESR and CRP
- FBC - Anaemia of chronic disease (normochronic normocytic)
- Rheumatoid factor positive - IgM antibody against the Fc portion of human IgG antibodies (can be falsely elevated by illness, 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
RA principles of management 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
RA principles of management 2
- 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)
RA principles of management 3
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 year 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 and SLOW)
- Secondary synovial inflammation and crystal deposition
Clinical features of osteoarthritis
- Age > 50 years
- Morning stiffness < 30 mins
- Persistent joint pain aggravated on use
- Crepitus
- No inflammation
- Bony enlargement and/or tenderness
OA investigations
- Blood tests not helpful
- A clinical diagnosis
- X-rays do not correlate well with symptoms
RA vs OA
Synovial disease - cartilage disease
Both bilateral and symmetrical
MCPs and PIPs - DIPs and 1st CMCJs(humb bases)
Stiffness in the morning > 30 mins - Can be stiff in morning but less significant
Better after some activity (less stiff) - Worse on exertion and at the end of the day
Raised inflammatory markers common - inflammatory markers not raised
Extra-articular features may be present - is a joint disease
Auto-immune - cause unknown but described to patients as ‘wear and tear’
Both have family history
Systemic lupus erythematosus (SLE)
- Chronic, relapsing, remitting disease
- Broad spectrum of clinical features involving almost all organs and tissues
- Prevalence in the UK: 97 per 100,000
- Peak onset between 15-40 years
- More common and severe in those of afro-caribbean, India, hispanic and chinese origin living in the USA and Europe > caucasians
SLE pathophysiology
- Genes C1q, C2, C4 HLA-D2,3, 8. MBL. FcR 2A, 3A, 2B, IL-10, MCP-1, PTPN22. Environment, UV light, gender and infection.
- Abnormal immune response
- Autoantibodies Immune Complexes
- Inflammation - Rash, nephritis, arthritis, leukopenia, CNS dz, carditis, clotting
–chronic inflammation and oxidation–>
- Damage - Renal failure, atherosclerosis, pulm fibrosis, stroke and damage from Rx
SLE - 2012 SLICC classification criteria
1) Acute cutaneous LE - malar rash, photosensitivity - positive ANA
2) Chronic cutaneous LE - dicoid rash - Anti - dsDNA
3) Oral or nasal ulcers - antiphospholipid antibodies
4) Nonscarring alopecia - low C3, C4, CH50
5) Non-erosive arthritis(jaccoud arthropathy) - direct coomb’s test
6) Serositis
7) Renal disorder - 4/17 (at least 1 clinical)
8) Neruological disorder
Haematological disorder:
9) Haemolytic anaemia
10) Leucopenia
11) Lymphopenia
12) Thrombocytopenia
When is biopsy proven nephritis comparable with SLE
- In the presence of ANA antibodies or anti-dsDNA antibodies
SLE investigations
Urinalysis - urinary protein:creatinine ratio
FBC
Urea and electrolytes
ESR
CRP
Liver function test
Antibodies: ANA; ENA; Anti-dsDNA; Lupus anticoagulant; Anti C1q; C3, C4
Non-pharmacological management of SLE
- Sun protection
- Smoking cessation
- CVD RISK modification
- Osteoporosis prevention
Management of mild SLE
Mild(skin manifestations, arthritis)
Treatment: HCQ or MTX +- CS(low dose)
Management of moderate SLE
- Mild-to-moderate nephritis
- Thrombocytopenia
- Major serositis
Treatment -
Induction therapy
- iv. MP(1 g/day for 3 days) followed by:
AZA(2 mg/kg/day) or MMF(2-3g/day)
GC(0.5-0.6 mg/kg/day for 4-6 weeks, then taper)
Maintenance therapy -
AZA(1-2 mg/kg/day) or MMF(1-2g/day), GC(0.25 mg/kg every other day)
Management of severe SLE
- Severe nephritis (class IV, III + V, IV + V or III-V with renal impairment)
- Severe refractory thrombocytopenia
- Severe refractory hemolytic anaemia
- Lung involvement (hemorrhage)
- CNS(cerebritis, myelitis)
- Abdominal vasculitis
Induction therapy:
iv. MP (1 g/day for 3 days)
iv. CYC (1 g/m/month x 7 doses)
Maintenance therapy:
iv. CYC (1 g/m^2 every 3 months for 1 year)
Add rituximab calcineurin inhibitors iv. IG
