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204- MSK > Introduction to diseases the MSK > Flashcards

Introduction to diseases the MSK Flashcards

1
Q

Define the following terms

  • Enthesitis
  • Osteomalacia
  • Osteomyelitis
A

• 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.

  • Osteomalacia – Poor bone mineralisation
  • Osteomyelitis – Bone infection
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2
Q

What can give an onset of myalgia

A
  • Viral infections

- Statins

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3
Q

How do you classify arthritic conditions?

A

Monoarthritis affects 1 joint; oligoarthritis affects 2-4 joints, polyarthritis affects more than 5 joints

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4
Q

Why are MSK injuries important?

A
  • Lower back pain is the leading cause of disability worldwide
  • Cost the NHS 10 billion a year
  • Major barrier to workplace participation, they are less likely to be employed and more likely to retire early
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5
Q

Differential diagnosis. for hot swollen knee

How would you proceed?

A
  • Posttraumatic hemarthrosis
  • Gout
  • Septic arthritis
  • RA?
  • Psoriatic arthritis
  • Osteoarthritis
  • Detailed history, serological tests should be used to support a diagnosis not to look for one
  • Joint aspiration
  • Gram stain
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6
Q

Describe common presentation of septic arthritis

How would you proceed?

A
  • Commonest organism for septic arthritis is street or Steph
  • Not necessarily systemically unwell
  • May be able to weight bear

DONT DELAY ANTIBIOTIC THERAPY

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7
Q

Gout is the most common inflammatory arthropathy

  • Positive join aspiration result?
  • Risk factors?
A
  • Monosodium urate crytals (negatively birefringent rods)–> serum urate > physiological concentrations
    (Crystals form and deposit on cartilage, bone and periarticular tissues or joints)
  • Men >40, women >65
  • genetics
  • chronic kidney disease, metabolic syndrome (and its components), OA, dietary factors which increase uric acid (shellfish, spinach)
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8
Q

How woulda joint aspiration be able to differentiate between gout and pseudo gout?

A

GOUT
- caused by monosodium urate which are negatively birefringent rods

PSEUDOGOUT
- caused by positively birefringent rhomboids – calcium pyrophosphate

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9
Q

State the acute and long term management of gout

A

Acute attack
- NSAIDs (Naproxen), Colchine, steroids

Long term
- Urate lowering therapy (e.g. allopurinol or febuxostat)

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10
Q

RHEUMATOID ARTHRITIS

  • Risk factors
A
  • Women 45-65
  • Smoking: caused citrullination of protein in lung which triggers an immune response by production of anti-citrulinated protein antibody (ACPA)
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11
Q

Which joint component is affected first in OA and in RA

A

OA: cartilage
RA: synovial

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12
Q

Describe the pathophysiology of RA

A
  • Early lymphocyte invasion of synovium
  • Acute inflammatory reaction with swelling and increased vascular permeability
  • Synovial proliferation
  • Pannus formation
  • Cartilage destruction and bone erosion
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13
Q

What are the signs and symptoms of RA

A
  • Variable onset, acute or chronic
  • Symmetrical pain and boggy swelling of small joints of hands and feet (not DIP)
  • early morning stiffness (>1hr)
  • systemically well
  • on examination: pain, swelling, restriction of movement
  • extra-articular manifestations: nodules, bursitis, dry eyes, splenomegaly, anaemia of chronic disease, lung fibrosis, pericarditis, carpal tunnel, renal amyloidosis, leg ulcers, vasculitis, increases Rx of CVD
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14
Q

What investigations would you carry out in suspected RA?

A
  • ESP and CRP
  • FBC: anaemia of chronic disease?
  • Rheumatoid factor positive
  • Anti CCP antibodies
  • Xray
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15
Q

For the following investigations of RA, describe the findings

  1. FBC
  2. Rheumatoid factor
  3. Xray
A
  1. Normochromic normocytic anaemia of chronic disease
  2. IgM antibody against the Fc portion of human IgG antibodies (can be falsely raised by illness)
  3. Normal in early disease. Erosions and periarticular osteoporosis and reduced joint space/cyst later
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16
Q

What are the principles of management of RA?

A
  1. Early and aggressive treatment to reduce inflammatory and joint damage
  2. NSAIDs for short term
  3. Corticosteroid intraarticular joint injections
  4. DMARDS: synthetic e.g. methotrexate or biological agents e.g. anti-TNF, anti-B cell, anti IL6 receptor blocker, anti-T cell selective co stimulator modulator
  5. MDT involvement
17
Q

OSTEOARTHRITIS

  • what is it?
  • whose most affected?
  • whats most affected?
  • characterisation
A
  • common degenerative disease which increases in prevalence with age
  • 70% 65
  • mostly affects knees, hips and small joints of hand (DIP, PIP, 1st CMCJ)
  • characterised by joint pain and very variable degrees of functional limitation
18
Q

Outline the pathophysiology of osteoarthritis

A
  1. Metabolically active, dynamic process involving all joint tissues (cartilage, bone, synovium, capsule, ligaments/muscles)
  2. Focal destruction of articular cartilage
  3. Remodelling of adjacent bone = hypertrophic reaction at joint margins (osteophytes)
  4. Remodelling and repair process (efficient but SLOW)
  5. Secondary synovial inflammation and crystal deposition
19
Q

Outline the clinical features OA

A
  • > 50yo
  • Morning stiffness <30 minutes
  • Persistent joint pain aggravated on use (mechanical)
  • Crepitus (crackling sound)
  • no inflammation
  • bony enlargement/ tenderness
  • no clinical correlation between the radiological changes and symptoms
20
Q

Why might relying on investigations prove difficult to obtain a diagnosis of OA

A
  • Blood tests not helpful, it is not a clinical diagnosis it is based on the experiences symptoms
  • X rays do not correlate well with symptoms
21
Q

What does management of OA look like?

A
  • Education, advice
  • Strengthening aerobic exercise
  • Weight loss if overweight
  • Topical NSAIDs, paracetamol
  • Joint arthroplasty, supports and braces, capsaicin, orals NSAIDs, opioids, intraarticular corticosteroid injections, local heat and cold
22
Q

Compare RA to OA in terms of

  • types of disease
  • anatomical location
  • stiffness
  • relieveing/exacerbating factors
  • inflammation
  • cohort
  • systemic features
  • cause
  • Fhx
A
  • RA: synovial disease, OA: cartilage disease
  • Both bilateral and symmetrical
  • RA affects MCPs and PIPs, OA affects DIPs and 1st CMCJs
  • RA relieved by some activity, OA worse on exertion and at the end of the day
  • RA has raised inflammatory markers
  • RA affects 3x more women, OA affects 2x more women
  • RA has extra-articular features , OA is just a joint disease
  • RA is an AID. OA is “wear and tear”
  • Both have family history
23
Q

SLE

  • Describe its course
  • Prevalence
  • Onset
A
  • Chronic, relapsing, remitting systemic disease
  • 97/100,000, 10-20 women per man
  • Peak onset between 15-40
  • Commonest and most severe in Afro-caribbean, India, hispanic, Chinese
24
Q

Outline the pathophysiology of SLE

A
  • Genetic (C1q, c2,c4, HLA- D2,3,8, MBL) and environment (UV light, infection)
  • Abonrmal immune responses
  • autoantibody immune complexes
  • inflammation: rash, nephritis, arthritis, leukopenia, neurological damage and affective disorder , carditis, clotting
  • image caused by chronic inflammation and oxidation: renal failure, atherosclerosis, pulm fibrosis, stroke
25
Q

State the clinical signs of SLE

A
  • Malar/discoid rash
  • Leukopenia
  • Anti-nuclear antibodies
  • Glomerulonephritis
  • Arthritis
  • Spenomegaly
  • Inflammation of lung
  • Neurological disorder/ affective disorder
26
Q

Which investigations would you carry out in suspected SLE?

A
  • Urinalysis- urinary protein:creatinine ratio
  • FBC
  • U&E
  • ESR
  • CRP
  • LFT
  • Antibodies: ANA, ENA, Anti-dsDNA, Lupus anticoagulant, Anti C1q/C3/C4
27
Q

How do you manage SLE?

A
  • Non pharmalogical management (sun protection, smoking cessation, CVD risk modification, osteoporosis prevention)

204- MSK (16 decks)

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