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Musculoskeletal MBCHB > Bone and Joint Diseases > Flashcards

Bone and Joint Diseases Flashcards

1
Q

What is osteoarthritis?

A

Chronic disease involving the imbalance between wear and repair of articular cartilage leading to progressive cartilage loss and accompanying periarticular change.

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2
Q

What is the aetiology of primary OA?

A

Defined as a common complex disorder with multiple risk factors.

Genetic Factors - 40-60%

Constitutional factors - aging, female sex, obesity

Biomechanical factors - joint injury, occupational/recreational usage, reduced muscle strength, joint laxity, joint malalignment

Affects weightbearing or active joints

Presents >50 years

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3
Q

What is the aetiology of secondary OA?

A

Occurs when OA affects an unexpected site due to overuse, previous injury or previous arthritis

Examples of conditions which can lead to secondary OA include rheumatoid arthritis and gout

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4
Q

What are the key pathological changes in osteoarthritis?

A

localised loss of hyaline cartilage and remodeling of adjacent bone with new bone formation (osteophyte) at joint margins

Leads to increased pressure on the bony surfaces and inflammation leads to pain, swelling (inflammatory effusion), thickening of the capsule and stiffness

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5
Q

Describe the development of OA.

A
  1. Chondrocyte injury - genetic and biochemical factors
  2. Chondrocytes proliferate - release inflammatory mediators, proteases, collagen and proteoglycans
  3. Remodelling and degradation of cartilage
  4. Stimulates inflammatory changes in synovium and subchondral bone
  5. Repetitive injury and chronic inflammation
  6. Long term consequences:
    1. Cartilage completely worn away - bone on bone
    2. Subchondral cysts (synovial fluid accumulation)
    3. Surface becomes ‘polished’ - eburnation (subchondral sclerosis)
    4. Formation of osteophytes (disorganised bone remodelling) - can irritate nerves
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6
Q

What is localised OA?

A

can affect hips, knees, finger interphalangeal joints, facet joints of lower cervical and lower lumbar spines

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7
Q

What is generalised OA?

A
  • defined as OA at either the spinal or hand joints and in at least 2 other joint regions (e.g., DIP joints, thumb bases, first MTP joints, knees, hips)
    • Clinical marker of generalised OA is the presence of multiple Heberden’s nodes
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8
Q

What is the typical presentation of osteoarthritis?

A
  • Pain - worse with joint use
  • Pain at night
  • Morning stiffness lasting less than 30 mins
  • Inactivity gelling
  • Instability
  • Poor grip in thumb OA
  • Joint line tenderness
  • Crepitus
  • Deformity
  • Stiff on testing ROM
  • Bony swelling - osteophytes
    • Caused by bony spurs due to chronic trauma
    • Heberden’s node (DIP joints) - only seen in OA (not in RA)
    • Bouchard’s node (PIP joints) - less common, also seen in RA
  • 1st CMC OA - squaring of the thumb
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9
Q

Describe the typical presentation of knee OA?

A
  • Osteophytes
  • Effusions
  • Crepitus and restriction of movement
  • Genu varus and valgus deformities
  • Baker’s cysts
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10
Q

Describe the typical presentation of hip OA?

A
  • Pain may be felt in groin, radiating to knee or anterior thigh
  • Pain felt in hip may be radiating from the lower back
  • Hip movements restricted
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11
Q

Describe the presentation of spine OA?

A
  • Cervical - pain and restriction of movement, occipital headaches may occur
    • Osteophytes may impinge on nerve roots
  • Lumbar - osteophytes can cause spinal stenosis if they encroach on the spinal canal
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12
Q

What are the investigations used to diagnose osteoarthritis?

A
  • Clinical based on S+S
  • Imaging - plain x-rays, MRI scans, USS
    • Don’t tend to perform imaging unless there is doubt over diagnosis
  • X-rays:
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13
Q

What features are seen on an x-ray for osteoarthritis?

A
  • Loss of joint space
  • Marginal osteophytes
  • Sclerosis (subchondral)
  • Subchondral cysts
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14
Q

What are the pitfalls of x-rays in osteoarthritis?

A

insensitive particularly with early disease, correlate poorly with disease activity, common incidental asymptomatic finding in older people

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15
Q

What are the non-pharmacological management for osteoarthritis?

A
  • Education - ensure patient continues to exercise
  • Lifestyle management e.g. weight loss, exercise, walking aids
  • Physiotherapy
  • Activity modification e.g. occupational therapy, hobbies
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16
Q

What are the pharmacological treatments for osteoarthritis?

A
  • Analgesia - paracetamol, NSAIDs (avoid opiates) as needed
  • Local intra-articular steroid injections for flare-up
    • Can give up to 3 per year
    • If given too many can damage joint further and accelerate OA
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17
Q

What are the surgical management for osteoarthritis?

A
  • Joint replacements e.g. knee, hip
  • Arthroscopic surgery to remove loose bodies etc.
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18
Q

What is seen on this xray?

A

Osteoarthritis

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19
Q

What is involved in arthroplasty?

A

Involves either replacement of part of the joint (hemiarthroplasty) or the whole joint (total joint replacement)

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20
Q

What materials can be used for arthroplasty?

A

Joint replacements can be made of stainless steel, cobalt chrome, titanium alloy, polyethylene and ceramic

Components may or may not be cemented (bone cement - PMMA) - advantages and disadvantages of both

The surfaces can consist of a metal‐polyethylene, ceramic‐polyethylene, ceramic–ceramic or metal‐metal bearing couple

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21
Q

Why do joint replacements ultimately fail?

A

Ultimately the joint replacement will fail due to loosening (caused by wear particles producing an inflammatory response or high stresses) or breakage of the joint replacement components

Metal particles can cause an inflammatory granuloma (known as a pseudotumour) which can cause muscle and bone necrosis

Polyethylene particles can cause an inflammatory response in bone with subsequent bone resorption (osteolysis) resulting in loosening

Ceramics can shatter with fatigue due to their brittleness

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22
Q

What are the indications for a total knee replacement?

A
  • Only for older, medically fit appropriate patient with end stage arthritis and severe pain refractory to chronic management
  • Constant severe pain, sleep disturbance, pain limiting function/walking distance, frequent bad ‘flare-ups’
  • Those with milder OA and severe pain tend not to do well - increased chance of developing chronic pain
  • Older patient where replacement will last for good - 60+ as a guide
  • Expect TKR to last 15-20 years in older, low demand patients if put in well
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23
Q

What are the indications for a total hip replacement?

A
  • Pain
  • 90% of cases will be pain free after recovery
  • Vast majority of cases will have large functional improvement
  • In a low demand older patient the estimated lifespan of a THA is around 15 years
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24
Q

What are the early local complications of arthroplasty?

A

infection, dislocation, instability, leg length discrepancy, nerve injury, arterial bleeding/ischaemia, bleeding, DVT

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25
Q

What are the early general complications of arthroplasty?

A

hypovolaemia, shock, acute renal failure, MI, ARDS, PE, chest infection, urine infection

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26
Q

What are the late local complications of arthroplasty?

A

infection (haematogenous spread), loosening, fracture, implant breakage, pseudotumor formation

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27
Q

What is a revision joint replacement?

A
  • Revision joint replacements are a bigger procedure than the primary procedure with often substancial blood loss, increased the complication rates and often poorer functional outcome
  • Revision joint replacements tend not to last as long as primary joint replacement
  • Once a revision fails - risk of fusion or amputation
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28
Q

What are some predictors of complications of joint replacement?

A

young, obesity, psychological distress, preexisting chronic pain, less severe OA

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29
Q

What is unicompartmental knee replacement?

A
  • Only the worn area of the knee is replaced
  • Less invasive, no ligaments removed or lengthened
  • Knee may feel more natural
  • Fairly easy to revise
  • Many cases not suitable
  • Reoperation rate significantly higher than TKR
  • Major concern is progression of OA in unreplaced knee - might regret not doing TKR
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30
Q

What is osteotomy?

A
  • Surgical realignment of a bone which can be used for deformity correction or to redistribute load across an arthritic joint and shift load onto an undiseased part
  • Can be used for early arthritis in the knee and hip
  • Doesn’t remove the damaged joint, controversial
  • Only for very active patients who would damage or loosen a joint replacement
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31
Q

What are the alternatives to a total knee replacement?

A

Unicompartmental knee replacement
Osteotomy
Cartilage Regeneration Surgery
Keyhole clean out surgery

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32
Q

What is involved with cartilage regeneration surgery?

A
  • Cartilage regeneration surgery may be beneficial in a case of small localised area of articular cartilage damage with persistent pain
  • Results unpredictable
  • Does not work for more general/widespread changes of OA or multiple defects
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33
Q

What is involved in keyhole clean out surgery?

A
  • Performed historically to try to alleviate symptoms and prevent knee replacement
  • Usually ineffective, any benefit tends to be short lived
  • Should not be offered on NHS
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34
Q

What are the surgical joint options for smaller joints?

A

Excision or resection arthroplasty
Arthrodesis

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35
Q

What is involved in excision or resection arthroplasty?

A

Involves the removal of bone and cartilage of one or both sides of the joint

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36
Q

Why is excision or resection arthroplasty only used for smaller joints?

A
  • Quite disabling for larger joints but can be an effective procedure for smaller joints (e.g., 1st CMC joint in foot for hallux valgus)
  • Occasionally utilized after failure of hip or shoulder replacement
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37
Q

What is arthrodesis?

A
  • Surgical stiffening or fusion of a joint in a position of function
  • The remaining hyaline cartilage of the joint and subchondral bone is removed and the joint is stabilized, resulting in bony union and fusion
  • Alleviates pain but function may be limited, particularly in large joints, and may increase pressure in surrounding joints leading to arthritic change
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38
Q

When is arthrodesis used?

A

Used in end stage ankle arthritis, wrist arthritis and hallux rigidus

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39
Q

What are the surgical options for rheumatoid hand problems?

A
  • Synovectomy
  • Tendon realignment
  • Tendon replacement
  • Fusion
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40
Q

What are the surgical options for elbow arthritis?

A
  • Arthritic change at the radio‐capitellar joint which has failed non-operative management can be treated with surgical excision of the radial head - good pain relief with minimal functional limitation
  • An elbow severely affected by RA or OA at the humero‐ulnar joint which isn’t satisfactorily treated with conservative management can be treated surgically with a Total Elbow Replacement - lifting limited to 2.5kg posteriorly following replacement
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41
Q

What is the lifespan of elbow replacements?

A

Elbow replacements have a limited life span and so are not good for young/active patients

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42
Q

What are the surgical options for shoulder arthritis?

A
  • Anatomic replacement
  • Reverse polarity shoulder replacement for OA secondary to rotator cuff tear
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43
Q

What is joint hypermobility syndrome?

A

Patient with hypermobile joint(s) develops chronic pain lasting 3 months or longer

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44
Q

What is the aetiology of joint hypermobility syndrome?

A
  • Higher incidence in females
  • General or local
  • Rare genetic syndromes e.g. Marfan’s, Ehlers Danlos
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45
Q

What is the typical presentation of joint hypermobility syndrome?

A
  • Usually presents in childhood or 3rd decade
  • Joint pains especially after exercise/physical work
  • Joint stiffness
  • Foot and ankle pain
  • Neck and backache
  • Frequent sprains and dislocations
  • Thin stretchy skin
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46
Q

What are the investigations for joint hypermobility syndrome?

A

Modified beighton score

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47
Q

What is the modified Beighton score?

A
  • > 10° hyperextension of the elbows
  • Passively touch the forearm with the thumb, white flexing the wrist
  • Passive extension of the fingers or a 90° or more extension of the fifth finger
  • Touching the floor with the palms of the hands when reaching down without bending the knees
  • Hypermobility if ≳4/9
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48
Q

What is the management of joint hypermobility syndrome?

A
  • Patient education
  • Physiotherapy
  • Analgesia as required
  • Surgery not recommended
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49
Q

What is septic arthritis?

A

Inflammation of the joint space caused by infection

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50
Q

What are the causative organisms of septic arthritis?

A

Staphylococcus Aureus
Streptococci
Haemophilus influenzae
Neisseria Gonorrhoea
Escherichia coli

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51
Q

What is the most common organism in septic arthritis in adults?

A

Staphylococcus Aureus

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52
Q

What is the most common cause in young adults in septic arthrits?

A

Neisseria Gonorrhoea

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53
Q

What is the most common cause in IV drug users and the elderly in septic arthritis?

A

Escherichia coli

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54
Q

What is the pathophysiology of septic arthritis?

A
  • Haematogenous spread (most commonly)
  • Can be an extension of local infection
  • Suppurative
  • Orthopaedic emergency due to rapid irreversible damage to hyaline articular cartilage
55
Q

What is the typical presentation of septic arthritis?

A
  • Typically presents as an acute monoarthropathy - single warm, red, painful joint with pain whenever the joint moves
    • Any joint that is hot, red and tender is a septic joint until proven otherwise - must aspirate
  • Knee most commonly affected joint
  • Reduced ROM +/- swelling
  • Patients may have systemic fever
56
Q

What is the investigations for septic arthritis?

A
  • Aspiration of joint fluid - microscopy, culture, sensitivity
  • Bloods - CRP may be raised, blood culture if pyrexial (positive in 30-60% of cases)
  • Exclude crystals e.g. gout
  • X ray, consider MRI
57
Q

What is the management of septic arthritis?

A
  • Avoid empirical antibiotics if patient is not septic
    • If septic - flucloxacillin, if under 5 add ceftriaxone (for H. influenzae cover)
    • Adjust when organisms confirmed
  • Once culture comes back: 1-2 weeks IV antibiotics to cultured organism, may require joint washout, if good progress PO antibiotics till 6 weeks antibiotics completed
  • Response to treatment is based on clinical findings and serial CRP
58
Q

What are the risk factors for prosthetic joint infection?

A
  • Presence of comorbidities e.g. rheumatoid arthritis, diabetes, malignancy
  • Use of corticosteroids, TNF inhibitors
  • Prior arthroplasty or prior infection at surgical site
  • Prolonged duration of surgery
  • Postoperative complications
  • Staph. aureus bacteraemia (from another cause)
59
Q

What are the causative organisms for prosthetic joint infection?

A
  • Most commonly staph. aureus and staph. epiderdimis
  • Cutibacterium acnes - upper limb prostheses
  • Rarely strep. sp and enterococcus sp.
  • Gram negatives e.g. E. coli, pseudomonas aeruginosa
  • Very rarely - fungi, mycobacteria sp.
60
Q

What are the mechanisms of infection for a prosthetic joint infection?

A
  • Direct inoculation at time of surgery
  • Manipulation of joint at time of surgery
  • Seeding of joint at a later time (from bacteraemia)
61
Q

What are the classifications of prosthetic joint infections?

A
  • Early (within 2-3 weeks) - acquired during surgery or right after
    • Staph. aureus, coagulase-negative staph (particularly S. epidermis)
  • Chronic (3 weeks +) - most common, symptoms can be subtle
    • CoNS (particularly S. epidermis), cutibacterium, corynebacterium, S. aureus
  • Haematogenous (chronic-late) - abrupt onset, patient can be systemically unwell
    • S. aureus, GNB
62
Q

What are planktonic bacteria?

A

responsible for most symptoms, bacteraemia

63
Q

What are sessile bacteria?

A

phenotypic transformation of planktonic bacteria to form a biofilm encased in an extracellular matrix (Quorum sensing)

64
Q

What is the typical presentation of a prosthetic joint infection?

A
  • Fever
  • Joint pain of affected joint
  • Minimal swelling
65
Q

What are the common investigations of prosthetic joint infection?

A
  • Culture - perioperative tissue (multiple samples)
    • If same organism grows from multiple samples this increases significance
  • Bloods - CRP, blood culture
  • Radiology
66
Q

What is the management of early or haematogenous infection in prosthetic joint infection?

A

Debridement, antibiotics (12 weeks), implant retention

67
Q

What is the management for frail patients with chronic infection in prosthetic joint infection?

A

Removal of joint and antibiotics

68
Q

What is the management for chronic infection in prosthetic joint infection?

A
  • Removal of joint and 6 weeks of aggressive antibiotic therapy
  • Patient left without a joint for the 6 weeks
  • Once the infection is under control (wound healed, clean and dry, CRP reduced) a revision joint replacement is performed with more complex joint replacement components
69
Q

When should rifampicin be used in prosthetic joint infections?

A

Rifampicin PO should be added to antibiotics if culture is positive for rifampicin-sensitive staphylococci

70
Q

What prophylaxis should be used during joint replacement?

A
  • Clean air theatres
  • 24 hours antibiotics starting with induction
  • Antibiotics in cement
  • Laminar flow
71
Q

What is osteomyelitis?

A

Infection of the bone and/or bone marrow

72
Q

What are the risk factors for osteomyelitis?

A
  • Immunocompromised patients
  • Patients with chronic disease
  • Elderly
  • Young
73
Q

What are the causative organisms in newborns in osteomyelitis?

A

S. aureus, Enterobacter sp., and group A and B Strep

74
Q

What are the causative organisms in children aged 4months-4years in osteomyelitis?

A

S. aureus, group A Strep, H. influenzae, Enterobacter sp.

75
Q

What are the causative organisms in children aged 4 years and above and adults in osteomyelitis?

A

S. aureus (80%), group A Strep, H. influenzae, and Enterobacter sp.

76
Q

What are the causative organisms in adults in osteomyelitis?

A

S. aureus, occasionally Enterobacter or Streptococcus sp

77
Q

What are the causative organisms in sickle cell anaemia patients in osteomyelitis?

A

S. aureus the most common, Salmonella species common and fairly unique to sickle cell patients

78
Q

What are the routes of infection for osteomyelitis?

A

Haematogenous and exogenous

79
Q

Describe the haematogenous route of infection in osteomyelitis.

A
  • infection travelled in the blood from another infected site e.g. cellulitis, PWIDs, central lines/dialysis
    • Most commonly due to a single pathogen
    • Common localisation:
      • Children - long bone metaphysis
      • Adults - vertebral involvement is the most common
80
Q

Describe the exogenous route of infection in osteomyelitis.

A
  • post-traumatic or contiguous spread
    • Post-traumatic - following deep injury e.g. open fractures
    • Contiguous spread - spread of infection from adjacent tissue e.g. injuries, secondary to infected foot ulcer in diabetic patients, secondary to pressure sore in elderly patients
    • Usually due to multiple pathogens
81
Q

How is an involucrum formed?

A
  • Once infected, enzymes from leucocytes cause local osteolysis and pus forms which impairs local blood flow making the infection very difficult to eradicate
  • A dead fragment of bone known as a sequestrum can form which usually breaks off and once a sequestrum is present, antibiotics alone will not cure the infection
  • New bone will form around the area of necrosis known as an involucrum
82
Q

When does acute osteomyelitis occur?

A

in the absence of recent surgery usually occurs in children
- The metaphysis of children’s long bones contain abundant tortuous vessels with sluggish flow which can result in accumulation of bacteria and infection spreads towards the epiphysis
- In neonates and infants, certain metaphyses are intra‐articular e.g. proximal femur, proximal humerus, radial head and ankle, and infection can spread into the joint causing co‐ existent septic arthritis
- Infants have loosely applied periosteum and an abscess can extend widely along the subperiosteal space

83
Q

How is Brodie’s abscess formed?

A

Children can also develop a subacute osteomyelitis with a more insidious onset and where the bone reacts by walling off the abscess with a thin rim of sclerotic bone - Brodie’s abscess

84
Q

How does chronic osteomyelitis occur?

A
  • Develops from an untreated acute osteomyelitis and may be associated with a sequestrum and/or involucrum
  • In adults the infection tends to be in the axial skeleton (spine or pelvis) with haematogenous spread from pulmonary or urinary infections, or from infection of the intervertebral disc (discitis)
  • Tuberculosis can also cause chronic OM, particularly in the spine through haematogenous spread from the primary lung infection
85
Q

What is the typical presentation of acute osteomyelitis?

A
  • Gradual onset pain at site of infection
  • Point tenderness
  • Swelling, redness, warmth
  • Systemic findings: malaise, fever, chills
86
Q

What is the typical presentation of chronic osteomyelitis?

A
  • Recurrent pain usually following a prior episode of osteomyelitis
  • Swelling, redness
  • In spinal OM, patients present with insidious onset of back pain which is constant and unremitting
87
Q

What are the investigations of choice for osteomyelitis?

A
  • Probe - bone/visible bone, non-healing ulcer, sinus
  • Bloods - CRP useful to monitor response, blood culture
  • Imaging - X ray, MRI, CT, PET scan, bone scan
  • Biopsy - bone biopsy to confirm (gold standard)
    • Wound swap/blood cultures not always diagnostic
    • If first biopsy negative considers another
88
Q

What is the management of acute osteomyelitis?

A
  • ‘Best guess’ antibiotics IV unless there is an abscess which requires drainage
  • If infection fails to resolve - second line antibiotics, surgery to take a sample for culture and remove infected bone/tissue
89
Q

What is the management of chronic osteomyelitis?

A
  • Cannot be cured or eradicated by antibiotics alone
  • Active infection can be suppressed with antibiotics but this may prove unsuccessful
  • Surgery is usually recommended to gain deep bone tissue cultures, to remove any sequestrum and to excise any infected or non‐viable bone (debridement)
  • If debridement of bone results in instability, the bone must be stabilized by internal or external fixation
  • Other strategies may include local antibiotic delivery systems and bone grafting
  • Plastic surgery may be required if skin and soft tissue coverage of bone is not possible
  • IV antibiotics are continued for several weeks after surgery
90
Q

What is osteoporosis?

A

Quantitative defect of bone characterised by reduced bone mineral density and increased porosity

91
Q

What is the general aetiology of osteoporosis?

A
  • Loss of bone mineral density is physiological - starts at ~30 years
  • Females tend to lose more bone mineral density after the menopause due to an increase in osteoclastic bone resorption with the loss of protective effects of oestrogen
92
Q

What is Type I osteoporosis?

A
  • Exacerbated loss of bone in the post‐menopausal period
  • Early menopause may have an influence
  • Familial and environmental factors (white Caucasians at particular risk)
  • Further risk factors include smoking, alcohol abuse, lack of exercise and poor diet
  • Colles fractures and vertebral insufficiency fractures tend to occur in this group
93
Q

What is Type II osteoporosis?

A
  • Osteoporosis of old age with a greater decline in bone mineral density than expected
  • Risk factors are similar with the added risks of chronic disease, inactivity and reduced sunlight exposure (Vitamin D)
  • Femoral neck fractures and vertebral fractures predominate in this group
94
Q

What is secondary osteoporosis?

A

Osteoporosis can also occur secondary to other conditions including:

  • Drugs especially corticosteroid use and aromatase inhibitors (breast cancer)
  • Alcohol abuse
  • Malnutrition
  • GI disorders - hepatic insufficiency, malabsorption, malnutrition, deficiency of vitamin C and D
  • Chronic disease - CKD, malignancy, rheumatoid arthritis
  • Endocrine disorders - Cushing’s, hyperthyroidism, hyperparathyroidism
  • Immobilisation
95
Q

What is localised osteoporosis?

A

Localised osteoporosis can develop through disuse of particular bones

96
Q

What is the pathophysiology of osteoporosis?

A
  • Peak bone mass occurs in young adulthood
    • Determined by hereditary factors (polymorphisms in genes regulating bone metabolism) and environmental factors (physical activity, muscle strength, diet and hormonal stasis
  • After peak bone mass has been reached, there will be average bone loss of 0.7% per year (normal part of aging)
  • In older age, the proliferative and biosynthetic capacity of osteoblasts is reduced and response to growth factors is attenuated
    • Also as we age there tends to be reduced physical activity
  • The reduced density and increased porosity increases the fragility of bone → increases fracture risk
    • Fractures after little or no trauma, vertebral compression fracture
97
Q

What is the direct effect of corticosteroids on bone?

A
  • Reduction of osteoblast activity and lifespan
  • Suppression of replication of osteoblast precursors
  • Reduction in calcium absorption
98
Q

What is the indirect effect of corticosteroids on bone?

A

Inhibition of gonadal and adrenal steroid production

99
Q

Where are the common osteoporotic fracture sites?

A
  • Neck of femur
  • Vertebral body - often not identified at the time of injury as stress can be minimal e.g. coughing
    • Result in thoracic kyphosis and loss of height
    • Once patient has had one vertebral body fracture they are at increased risk of additional fractures
  • Distal radius
  • Humeral neck
100
Q

What are the investigations of choice for osteoporosis?

A

Fracture risk calculator
DEXA Scanning
- To ensure treatment is safe, and check there is no additional underlying condition contributing to the decreased bone density
- U+Es, LFTs, FBC, PV, TSH
- Consider:
- Protein electrophoresis/Bence Jones proteins - to rule out multiple myeloma
- Coeliac antibodies
- Testosterone
- 25OH vitamin D
- PTH

101
Q

When is a risk assessment tool used for osteoporosis?

A
  • Use an 10 year osteoporotic fracture risk calculator to assess:
    • Anyone over 50 years with risk factors
    • Anyone under 50 years with very strong clinical risk factors - early menopause, glucocorticoids
102
Q

Describe DEXA scanning in osteoporosis?

A
  • Measure of bone mineral density - predicts fracture risk independently of other risk factors
    • For every decrease in 1 SD below the mean, fracture risk doubles
  • Anyone with a 10 year risk assessment for any OP fracture of at least 10% should be referred for a DEXA scan, as well as any patient over 50 years with a low trauma fracture
  • Osteoporosis is diagnosed when bone density is 2.5 standard deviations below the mean peak value of young adults of the same race and sex
103
Q

When is severe osteoporosis diagnosed?

A

defined as bone density is 2.5 standard deviations below the mean peak value of young adults of the same race and sex WITH a fragility fracture

104
Q

When is osteopenia diagnosed?

A

Osteopenia is an intermediate stage where bone mineral density is between 1 to 2.5 standard deviations below mean peak value

105
Q

What are the non-pharmacological treatments for osteoporosis?

A
  • Increase calcium intake - postmenopausal women aim 1000 mg calcium per day (700 mg recommended for general population)
  • High intensity strength training
  • Low-impact weight-bearing exercise
  • Avoidance of excess alcohol
  • Avoidance of smoking
  • Fall prevention
106
Q

What are the pharmacological treatments for osteoporosis?

A
  • Calcium and/or vitamin D supplements if dietary intake is poor/limited sunlight exposure
    • Calcium supplements should not be taken within 2 hours of oral bisphosphonates
  • Oral bisphosphonates (alendronic acid, risedronate, etidronate) - reduce osteoclastic resorption, first line for the majority of patients
    • Consider treatment with when T score </= -2.5
    • If ongoing steroid requirement >/= 7.5mg prednisolone for 3 months or more or if there is a prevalent vertebral fracture, consider treatment with T score < -1.5
  • Zoledronic acid - once yearly intravenous bisphosphonate, second line for majority of patients e.g. patients with side effects with oral bisphosphonates
  • Desunomab - monoclonal antibody which reduces osteoclast activity, another second line alternative to oral bisphosphonates
107
Q

What are the alternative options for treatment for osteoporosis?

A
  • Teriparatide - recombinant parathyroid hormone; stimulates bone growth rather than reduces bone loss (anabolic)
    • Recommended to reduce risk of vertebral and non-vertebral fractures in postmenopausal women with severe osteoporosis
    • Recommended over oral bisphosphate in postmenopausal women with at least 2 moderate or 1 severe low trauma vertebral fracture to prevent vertebral fracture
  • Romosozumab - monoclonal antibody that binds to and inhibits sclerostin to increase bone formation and reduce bone resorption
    • Recommended for postmenopausal women with severe osteoporosis who have had a fragility fracture and are at imminent risk of further fracture (24 months)
108
Q

What are the prevention measures for osteoporosis?

A

Building up peak bone mineral density by way of exercise, good diet and healthy levels of sunlight exposure before bone density starts to decline may reduce the risk of osteoporosis

109
Q

What is osteomalacia?

A

qualitative defect of bone with abnormal softening of the bone due to deficient mineralization of osteoid (immature bone) secondary to inadequate amounts of calcium and phosphorus

110
Q

What is Ricketts?

A

Osteomalacia in children which has subsequent effects on the growing skeleton

111
Q

What are the causes of osteomalacia and Rickets?

A
  • The principal causes of osteomalacia and rickets involve either insufficient calcium absorption, or phosphate deficiency caused by increased renal losses
  • Vitamin D deficiency - malnutrition/malabsorption, lack of sunlight exposure
  • Hypophosphatemia
    • Re‐feeding syndrome
    • Alcohol abuse - impairs phosphate absorption
    • Malabsorption
    • Renal tubular acidosis
  • Long term anticonvulsant use
  • Chronic kidney disease - reduced phosphate resorption and failure of activation vitamin D, resulting in secondary hyperparathyroidism
    • Some renal diseases are inherited disorders (X‐linked hypophosphatemia or vitamin D resistant rickets)
112
Q

Wha is the pathophysiology related to Vitamin D deficiency and osteoporosis?

A
  • Vitamin D stimulates absorption of calcium from GI tract, kidney and bone, also induces osteoblasts to release osteocalcin
  • Vitamin D deficiency leads to hypocalcaemia and elevated PTH
  • This increases calcium absorption, osteoclastic activity, and release of Ca2+ from bone
  • Results in impaired mineralisation of newly formed osteoid (thick osteoid seams)
  • Bone is weakened - prone to fracture (micro-fractures or gross fractures)
113
Q

What is the typical presentation of osteomalacia and Ricketts?

A
  • Bone pain - pelvis, spine and femora
  • Symptoms of hypocalcaemia - paraesthesia, muscle cramps, irritability, fatigue, seizures, brittle nails
  • Sustain pathological fractures easily
  • Deformities from soft bones (particularly in rickets)
  • Proximal myopathy
  • Dental defects (caries, enamel)
114
Q

What are the investigations related to osteomalacia and ricketts?

A
  • X-ray - pseudofractures (aka Looser’s zones), particularly of the pubic rami, proximal femora, ulna and ribs, poor cortico-medullary differentiation
  • Bloods - ↓ calcium and serum phosphate, ↑ serum ALP
115
Q

What is the management of osteomalacia and Ricketts?

A
  • Involves vit D therapy with calcium and phosphate supplementation
    • D3 tablets (400-800IU per day after loading with 3200IU per day for 12 weeks) - calcitriol (1-25 dehydroxycholecalciferol), alfacalcidol (1⍺ hydroxycholecalciferol)
    • Combined vitamin D and calcium tablets e.g. adcal D3
116
Q

What considerations should be taken for patients with chronic renal disease and osteomalacia/rickett’s?

A
  • Patients may have a very high 25-OH vitamin D so make sure to check 1-25 OH vitamin D
  • Titrate treatment to PTH levels
  • Phosphate binders
117
Q

What is Paget’s disease of the bone?

A

Chronic condition involving cellular remodeling and deformity of one or more bones

118
Q

What is the aetiology of Paget’s disease?

A
  • Cause uncertain
    • Genetic elements that increase activity of Nf ⲕβ
    • Viral infection may play a role
  • Rare in people < 50 years
  • Predominantly affects long bones, pelvis, lumbar spine and skull
119
Q

What are the three stages of Paget’s disease?

A
  1. Osteolytic - restoration pits with large osteoclasts
  2. Mixed - osteoclasis and osteoblastic activity
  3. Osteosclerotic
120
Q

What are the effects on the bone for Paget’s disease?

A
  • Net result is thick excess bone with abnormal reversal lines - mosaic pattern
  • Bone matures but is soft and porous
  • Can affect all bones - usually axial, small bones less commonly affected
121
Q

Describe the pathophysiology of Paget’s disease?

A
  • Abnormal osteoclastic activity followed by increased osteoblastic activity results in abnormal bone structure with reduced strength and increased fracture risk
  • May be single site (monostotic) or multiple sites (polyostotic)
122
Q

What is the typical presentation for Paget’s disease?

A
  • Often asymptomatic
  • Pain - micro-fracture or nerve compression
  • Enlargement and abnormal shape of bone → leontiasis ossea, platybasia, sabre tibia
  • Increased metabolism → heat (warm skin), AV shunt, effectively high output heart failure
123
Q

What are the investigations of choice for Paget’s Disease?

A
  • X-ray
    • Initial lytic phase results in well defined lucency
    • Later sclerotic phase with enlarged bone, increased density and coarse trabecular pattern
  • Isotope bone scan - shows distribution of disease
  • Biochemistry - ↑ alkaline phosphatase with otherwise normal LFTs
124
Q

What is the management of Paget’s disease?

A

Treat with bisphosphonates if pain not responding to analgesia

125
Q

What are the complications of Paget’s disease?

A

Risk of secondary malignancy within the affected bone - osteosarcoma, fibrosarcoma

126
Q

What is avascular necrosis?

A

Failure of the blood supply to the end of a bone, resulting in ischaemic necrosis of bone and marrow

127
Q

What is the aetiology of avascular necrosis?

A
  • Greater incidence in males
  • Typical age 35-50 years
  • Most commonly affects the head of the femur, but can affect other bones too e.g. wrist, head of humerus
128
Q

What is the pathophysiology of idiopathic avascular necrosis?

A
  1. Coagulation of the intraosseous microcirculation
  2. Venous thrombosis causes retrograde arterial occlusion
  3. Intraosseous hypertension
  4. Decreased blood flow results in necrosis of a segment of bone
  5. There will be patchy sclerosis before subchondral collapse and irregularity of the articular surface occurs
  6. Resultant bone and joint damage can lead to significant structural collapse of the bone → secondary OA
    1. Can also secondarily affect osteoarthritic joints causing collapse of the articular surface and rapid deterioration
129
Q

What are the risk factors for idiopathic avascular necrosis?

A
  • Irradiation
  • Trauma
  • Increased coagulability - thrombophilia, sickle cell disease, antiphospholipid deficiency in SLE, pregnancy
  • Dysbaric disorders (decompression sickness - Caisson disease)
    • Rare cause which causes AVN from nitrogen gas bubbles forming in the circulation after too rapid a depressurization after deep sea diving
  • Alcoholism and steroid (ab)use
    • Alter fat metabolism which can result in mobilisation of fat into the circulation
    • Sludges up the capillary system and promotes coagulation within prone areas of bone
    • Increased fat content of the marrow can compress venous outflow from the bone causing stasis and ischaemia
  • Hyperlipidaemia - increased fat in circulation
130
Q

What is the pathophysiology of AVN associated with trauma?

A
  • Secondary to fractures (femoral neck, proximal humerus, waist of scaphoid and talar neck) - the fracture disrupts the blood supply to an entire portion of bone
  • Decreased blood flow → necrosis → collapse
131
Q

What sites are commonly affected by avascular necrosis?

A
  • Femoral head
  • Femoral condyles
  • Head of the humerus
  • The capitellum
  • The proximal pole of the scaphoid
  • The proximal part of the talus
132
Q

What is the presentation of AVN?

A
  • Can be asymptomatic
  • Examination is usually normal unless disease has advanced to collapse/OA

Femoral head AVN

  • Insidious onset of groin pain exacerbated by stairs or impact
  • Bilateral disease in 80% of cases
133
Q

What is the management of reversible AVN?

A
  • If the articular surface has not collapsed in an amenable site, AVN can be reversed
  • Bisphosphates
  • Core decompression - drilling performed under fluoroscopy to ‘decompress’ the bone to prevent further necrosis and help healing
  • Curettage and bone grafting
  • Vascularised fibular bone graft
134
Q

What is the management of irreversible AVN?

A
  • If the articular surface has collapsed, generally joint replacement is usually required in the hip, knee or shoulder to control symptoms
  • Rotational osteotomy can be considered if less than 15% of femoral head damaged (rare)
  • Fusion can be considered in the wrist or foot/ankle

Musculoskeletal MBCHB (21 decks)

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