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Year 2 - T3 Theme 2 > L13 Introduction to diseases of the MSK system > Flashcards

L13 Introduction to diseases of the MSK system Flashcards

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
Q

What can increase the possibility of a diagnosis being septic arthritis

A
  • 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
Q

Most common organisms - septic arthritis

A
  • Staph and strep
27
Q

Gout

A
  • 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
Q

Who gets gout

A
  • 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
Q

Conditions associated with gout

A
  • Metabolic syndrome and its components (insulin resistance, obesity, hyperlipidaemia, and hypertension)
30
Q

Risk factors for gout

A
  • 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
Q

Crystals in gout

A
  • Gout is caused by negatively birefringent rods (monosodium urate)
  • Pseudogout (CPPD) by positively birefringent rhomboids - calcium pyrophosphate
32
Q

Management of gout

A

Acute attacks:

  • NSAIDs eg naproxen
  • Colchicine
  • Steroids

Long term:
- Urate-lowering therapy eg, allopurinol or febuxostat

33
Q

Rheumatoid arthritis

A
  • 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
Q

Main problem in inflammatory arthritis vs osteoarthritis

A
  • The main problem in inflammatory arthritis is with the synovium whereas in osteoarthritis, the main problem is with the cartilage
35
Q

Classification and disease duration - ‘Normal’

A

Phase A/B - Genetic and environmental risk factors

Phase C - Systemic autoimmunity

Induction of autoimmunity

36
Q

Classification and disease duration - ‘symptoms’

A
  • symptoms
  • Phase D
  • Maturation of the antibody response
    0-3 months from symptom onset
37
Q

Classification and disease duration - Swelling

A
  • Unclassified arthritis
  • Swelling
  • Phase E
    3-6 months from time of onset
38
Q

Classification and disease duration - Fulfilment of classification criteria

A
  • Rheumatoid arthritis
  • Phase F
  • No additional changes
    6-9 months from time of onset
39
Q

Rheumatoid arthritis pathophysiology

A
  • Early lymphocyte invasion of the synovium
  • Acute inflammatory reaction - swelling and increased vascular permeability
  • Synovial proliferation
  • Pannus formation
  • Cartilage destruction and bone erosion
40
Q

Symptoms and signs of rheumatoid arthritis

A
  • 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
Q

Extra-articular manifestations of RA

A
  • 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
Q

RA investigations

A
  • 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
Q

RA principles of management 1

A
  • 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
Q

RA principles of management 2

A
  • 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
Q

RA principles of management 3

A

Multidisciplinary team input:

  • Nurse specialist(education and disease monitoring)
  • Physiotherapy (improve strength and stamina)
  • Occupational therapy (work, home environments)
  • Podiatry
46
Q

Osteoarthritis

A
  • 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
Q

Osteoarthritis pathophysiology

A
  • 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
Q

Clinical features of osteoarthritis

A
  • Age > 50 years
  • Morning stiffness < 30 mins
  • Persistent joint pain aggravated on use
  • Crepitus
  • No inflammation
  • Bony enlargement and/or tenderness
49
Q

OA investigations

A
  • Blood tests not helpful
  • A clinical diagnosis
  • X-rays do not correlate well with symptoms
50
Q

RA vs OA

A

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
Q

Systemic lupus erythematosus (SLE)

A
  • 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
Q

SLE pathophysiology

A
  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–>

  1. Damage - Renal failure, atherosclerosis, pulm fibrosis, stroke and damage from Rx
53
Q

SLE - 2012 SLICC classification criteria

A

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
Q

When is biopsy proven nephritis comparable with SLE

A
  • In the presence of ANA antibodies or anti-dsDNA antibodies
55
Q

SLE investigations

A

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
Q

Non-pharmacological management of SLE

A
  • Sun protection
  • Smoking cessation
  • CVD RISK modification
  • Osteoporosis prevention
57
Q

Management of mild SLE

A

Mild(skin manifestations, arthritis)

Treatment: HCQ or MTX +- CS(low dose)

58
Q

Management of moderate SLE

A
  • 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
Q

Management of severe SLE

A
  • 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

Year 2 - T3 Theme 2 (17 decks)

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