L13 Introduction to diseases of the MSK system Flashcards

(59 cards)

1
Q

Prefix - problems with bones

A

Osteo

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2
Q

Prefix - problems with muscle

A

My/Myo

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3
Q

Prefix - problems with joints

A

Arth

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4
Q

Prefix - describes cartilage

A

Chond

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5
Q

Bursitis

A
  • Inflammation of bursa. Bursae are synovial membrane lined pockets that serve to allow free movement of adjacent structures where otherwise, there could be friction
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6
Q

Enthesitis

A
  • Inflammation of an enthesis. Entheses are the points where tendons, ligaments or joint capsules insert into bone
  • The largest site is the achilles insertion
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7
Q

Osteoporosis

A
  • Reduced bone density
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8
Q

Osteomalacia

A
  • Poor bone mineralisation
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9
Q

Osteomyelitis

A
  • Bone infection
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10
Q

Osteosarcoma

A
  • An example of malignant bone tumour
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11
Q

Myalgia

A
  • Pain in muscles
  • Very common
  • Commonly associated with viral infections
  • Can be drug induced (eg by statins)
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12
Q

Myositis

A
  • Inflammation of the muscles

- Far less common than myalgia and can be autoimmune

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13
Q

What is a joint

A
  • Formed where two or more bones meet each other
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14
Q

Approach to a patient with MSK disorder

A
  • Full history
  • Physical examination
  • Serological tests - help to support the diagnosis
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15
Q

Some ways of classifying rheumatic disease

A
  • Articular vs non articular/periarticular
  • Inflammatory vs non- inflammatory/degenerative/mechanical
  • Duration of onset
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16
Q

What should be suspected in acute monoarthritis

A
  • Infection
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17
Q

Periarticular vs articular joint pain

A

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

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18
Q

Structures affected by periarticular joint pain

A
  • Bursa
  • Tendon
  • Tendon sheath
  • Ligament
  • others
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19
Q

What to look for if articular joint pain

A
  • Any signs of inflammation

- Features of mechanical problem (locking, catching etc)

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20
Q

Joint inflammation nomenclature

A
  • Monoarthritis - arthritis affecting 1 joint
  • Oligoarthritis - arthritis affecting 4 or fewer joints (2-4)
  • Polyarthritis - arthritis affecting 5 or more joints(>=5)
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21
Q

Soft tissue conditions

A
  • Problems with radiolucent moving tissues

- Very common

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22
Q

Examples of soft tissue conditions

A
  • Tennis elbow (lateral epicondylitis)
  • Golfers elbow (medial epicondylitis)
  • Carpal tunnel (median nerve compression as it passes through the carpal tunnel in the wrist)
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23
Q

Importance of rheumatic disease

A
  • Common and getting more common
  • Expensive
  • Leading cause of disability
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24
Q

Septic arthritis - differential diagnosis

A
  • Differential diagnosis of hot swollen joint is wide

- Always consider joint aspiration and gram stain

25
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
26
Most common organisms - septic arthritis
- Staph and strep
27
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
28
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
29
Conditions associated with gout
- Metabolic syndrome and its components (insulin resistance, obesity, hyperlipidaemia, and hypertension)
30
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)
31
Crystals in gout
- Gout is caused by negatively birefringent rods (monosodium urate) - Pseudogout (CPPD) by positively birefringent rhomboids - calcium pyrophosphate
32
Management of gout
Acute attacks: - NSAIDs eg naproxen - Colchicine - Steroids Long term: - Urate-lowering therapy eg, allopurinol or febuxostat
33
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
34
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
35
Classification and disease duration - 'Normal'
Phase A/B - Genetic and environmental risk factors Phase C - Systemic autoimmunity Induction of autoimmunity
36
Classification and disease duration - 'symptoms'
- symptoms - Phase D - Maturation of the antibody response 0-3 months from symptom onset
37
Classification and disease duration - Swelling
- Unclassified arthritis - Swelling - Phase E 3-6 months from time of onset
38
Classification and disease duration - Fulfilment of classification criteria
- Rheumatoid arthritis - Phase F - No additional changes 6-9 months from time of onset
39
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
40
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
41
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
42
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
43
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
44
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)
45
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
46
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
47
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
48
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
49
OA investigations
- Blood tests not helpful - A clinical diagnosis - X-rays do not correlate well with symptoms
50
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
51
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
52
SLE pathophysiology
1. Genes C1q, C2, C4 HLA-D2,3, 8. MBL. FcR 2A, 3A, 2B, IL-10, MCP-1, PTPN22. Environment, UV light, gender and infection. 2. Abnormal immune response 3. Autoantibodies Immune Complexes 4. Inflammation - Rash, nephritis, arthritis, leukopenia, CNS dz, carditis, clotting --chronic inflammation and oxidation--> 5. Damage - Renal failure, atherosclerosis, pulm fibrosis, stroke and damage from Rx
53
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
54
When is biopsy proven nephritis comparable with SLE
- In the presence of ANA antibodies or anti-dsDNA antibodies
55
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
56
Non-pharmacological management of SLE
- Sun protection - Smoking cessation - CVD RISK modification - Osteoporosis prevention
57
Management of mild SLE
Mild(skin manifestations, arthritis) Treatment: HCQ or MTX +- CS(low dose)
58
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)
59
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