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Y2 MSK > Bone and joint disorders > Flashcards

Bone and joint disorders Flashcards

1
Q

What is osteoarthritis

A

Chronic disease due to imbalance between wear and repaid of articular cartilage leading to progressive cartilage loss

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2
Q

Risk factors of OA

A

Genetics
Female
Obesity
>50
Repetitive trauma from occupation / sports
Joint malalignment

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3
Q

What is secondary OA

A

OA at an unexpected site due to over use / previous injury / previous arthritis

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4
Q

What conditions can cause secondary OA

A

Gout
RA

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5
Q

Is OA inflammatory arthritis

A

No

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6
Q

How does OA change the structures of the joint (LOSS)

A

Loss of joint space due to cartilage worn away
Osteophytes formation
Subchondral cysts
Subchondral sclerosis

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7
Q

What causes subchondral cysts

A

Synovial fluid seeping into bone due to bone erosion and accumulates there

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8
Q

Why do osteophytes form

A

Due to the bone trying to repair and remodel itself from the damage from OA

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9
Q

Which joints are commonly affected by OA

A

Knee
Hip
Lumbar spine
First MTP joint of big toe
thumb bases
DIP PIP

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10
Q

Presentation of OA

A

Pain at night
Pain worse with activity
Morning stiffness < 30 minutes
Instability
Poor grip in thumb

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11
Q

Differences between OA and inflammatory arthritis

A

OA pain worse with movement
OA pain at night
OA morning stiffness <30 minutes
OA does not affect any other structures apart from joints

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12
Q

How do you differentiate between ankylosing spondylitis and OA which also affects lower lumbar spine

A

AS has inflammatory type of pain hence if it is AS, pain will be worse at rest and morning stiffness >30 minutes

OA does not affect anything else apart from joints whereas AS can affect other structures

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13
Q

Onset of OA

A

Insidious, progresses over months or years

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14
Q

Clinical findings of OA

A

Reduced range of motion
Swelling (but not hot or red)
Crepitus
Deformity
Heberden’s nodes
Bouchard’s nodes

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15
Q

What are Herbeden’s and Bouchard’s nodes

A

Small, hard bony swellings on finger joints

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16
Q

Herbeden’s vs Bouchard’s nodes

A

Herbeden - on DIP
Bouchard - on PIP

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17
Q

Bouchard’s nodes are also seen in

A

RA

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18
Q

Which bony node - heberden or Bouchard, is more specific to OA

A

Heberden’s

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19
Q

OA in the knee can cause

A

Baker’s cysts - swelling behind the knee

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20
Q

OA in the hip can cause

A

Pain in groin radiating to knee or anterior thigh
Pain in hip radiating from lower back

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21
Q

OA in cervical spine can cause

A

Impinge nerve roots
Occipital headaches

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22
Q

OA in lumbar spine can cause

A

Spinal stenosis - narrowing of spinal canal putting on spinal cord and nerve roots

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23
Q

Symptoms of spinal stenosis

A

Pain in legs on activity
Weakness in legs

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24
Q

Investigations for OA

A

Clinical
Imaging Xray/MRI if in doubt

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25
Q

What can be seen on xray for OA (LOSS)

A

Loss of joint space
Osteophyte formation
Subchondral sclerosis
Subchondral cyst

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26
Q

Management for OA

A

Lifestyle management
Drug therapy
Surgery

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27
Q

What are the lifestyle modifications for oA

A

Weight loss
Moderate exercise (avoid weight bearing exercise)
Physiotherapy

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28
Q

Drug therapy for oA

A

Analgesia - paracetamol / NSAID
Intra-articular steroid injections for flare up

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29
Q

Which type of NSAID is avoided in OA management

A

opioids

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30
Q

Which analgesia is particularly effective for knee OA

A

NSAID

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31
Q

Can intra-articular steroid injections be used frequently in OA

A

No, there is a limit to how many injections a patient can have a year due to the side effects and acceleration of OA

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32
Q

When is surgery indicated for OA

A

Severe and providing that the patient is fit enough

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33
Q

When is total knee replacement indicated

A

60+, medically fit patient with end stage arthritis and severe pain

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34
Q

What is considered as severe pain and end stage arthritis to be qualified for TKR

A

Constant severe pain
Sleep disturbance
Pain limiting mobility
Frequent flares

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35
Q

How long does a TKR or Total hip replacement last in a old, low demand patient

A

15-20 years

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36
Q

Complications of TKR and THR

A

Infection
Instability
DVT
Chest infection
Nerve injury
Loosening / breakage

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37
Q

Why is arthroplasty rare in patients under 50 years old (young patients)

A

Due to high chance of revision surgery
High demand causing the replacement to not last that long
Unexplained moderate - severe pain

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38
Q

Risks associated with revision surgery

A

Substantial blood loss
Increase complications risks
Poorer outcome
Does not last as long

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39
Q

Alternatives to a TKR

A

Unicompartmental knee replacement
Osteotomy
Cartilage regeneration surgery

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40
Q

What is unicompartmental knee replacement

A

Only the worn out area of the knee is replaced

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41
Q

Concerns of a unicompartmental knee replacement

A

Not suitable in many cases
Reoperation rater higher than TKR
Progression of OA in unreplaced one

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42
Q

What is osteotomy

A

Realignment of a bone to correct deformity or redistribute load across an arthritic joint

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43
Q

When is osteotomy indicated

A

Early arthritis in knee and hip
Very active patients who would damage a joint replacement

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44
Q

Concerns for cartilage regeneration surgery

A

Unpredictable results
Does not work for widespread changes of OA

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45
Q

What is the hyper mobility syndrome

A

Ability to move joints beyond the normal range of movement

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46
Q

Hypermobility syndrome can cause

A

Chronic joint and ligament injuries, pain

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47
Q

Risk factors for hyper mobility syndrome

A

Female
Marfan’s
Ehlers Danloes

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48
Q

Presentation of hyper mobility syndrome

A

Joint pain
Joint stiffness
Frequent sprains
Dislocations of joints
Thin stretchy skin

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49
Q

When does hyper mobility syndrome usually present

A

Childhood
3rd decade

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50
Q

Investigations for hyper mobility syndrome

A

Beighton score

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51
Q

Beighton score that indicates hyper mobility

A

> 4 points

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52
Q

What are the 5 manoeuvres used to assess Beighton score

A

Passively touch the forearm with the thumb while flexing the wrist
Passive extension of the fingers
Touching the floor with palms of hands without bending the knees
Passive hyperextension of the elbow

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53
Q

Treatment of Hypermobility syndrome

A

Supportive
- physiotherapy
- analgesia
- strengthen the muscles to protect the joints
- low impact exercise

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54
Q

What is septic arthritis

A

Joint infection due to pathogens spreading into the synovial fluid

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55
Q

Which pathogens can cause septic arthritis

A

S aureus
Streptococci
Gonococcus (gonorrhoea)
H influenza
E. coli

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56
Q

Most common cause of septic arthritis

A

S aureus

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57
Q

Most common cause of septic arthritis in a patient with prosthetic joint

A

Staph epidermidis

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58
Q

Septic arthritis caused by gonococcus is common in

A

Young sexually active individuals

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59
Q

Septic arthritis caused by E.coli is common in

A

Elderly
IV drug users

60
Q

Risk factors for septic arthritis

A

Joint diseases
Immunosuppression
Prosthetic joints
Chronic kidney disease

61
Q

Symptoms of septic arthritis

A

Acute, asymmetrical monoarthropathy
Red
Hot
Swollen
Painful
Reduced ROM
Systemically unwell

62
Q

Septic arthritis most commonly affects which joint

A

Knee

63
Q

Investigations for septic arthritis

A

Joint aspiration and synovial fluid analysis
Bloods - CRP
Xray

64
Q

Management for septic arthritis

A

Flucloxacillin (before culture)
IV antibiotics after culture
Switch to oral antibiotics after 2 weeks till the end
Joint washout may be required

65
Q

What IV antibiotic is used in septic arthritis

A

Flucloxacillin or clindamycin

66
Q

How long is the antibiotic course for septic arthritis

A

4-6 weeks
IV 2 weeks
Oral the rest if good progress

67
Q

Response to treatment for septic arthritis is based on

A

Clinical
CRP level

68
Q

Risk of prosthetic joint infection

A

Diabetes
RA
Cancer
Use of steroids / anti- TNF
Prior arthroplasty
Prolonged duration of surgery

69
Q

Pathogens causing prosthetic joint infection

A

Staph epidermidis
S aureus
Cutibacterium acnes
E. coli
Pseudomonas aeruginosa

70
Q

Cutibacterium acnes mostly affects which prostheses

A

Upper limb prostheses

71
Q

Early PJI (within 2-3 weeks) suggests

A

acquired during surgery or right after

72
Q

Which pathogens most commonly causes early PIJ

A

S aureus
Staph epidermidis

73
Q

3 weeks + onset of PJI suggests which pathogens

A

S epidermidis
Cutibacterium
Corynebacterium
S aureus

74
Q

Presentation of PJI

A

Fever
Joint pain
Minimal swelling

75
Q

Investigations for PJI

A

Multiple samples of perioperative tissue cultures
Bloods - CRP
Imaging

76
Q

Management of early PJI

A

Debridement
12 weeks antibiotics

77
Q

Management of late PJI

A

Removal of joints
Antibiotics
Revision joint replacement after finishing antibiotics therapy

78
Q

What is osteomyelitis

A

Infection of the bone; acute or chronic

79
Q

Acute osteomyelitis is usually caused by a single/multiple organism (s), while the chronic infection is more likely to be single/polymicrobial.

A

Acute osteomyelitis is usually caused by a single organism whereas chronic is more likely to be polymicrobial

80
Q

Most common causative pathogens of osteomyelitis

A

S aureus
Coagulase-negative staph

81
Q

Risk factors of osteomyelitis

A

Immunocompromised
DIabetes
Peripheral vascular disease
Malignancy
Extremes of age

82
Q

Causative pathogens of osteomyelitis in newborns <4months

A

S aureus
Group A and B strep
Enterobacter sp

83
Q

Causative pathogens of osteomyelitis in children 4m-4yrs

A

S aureus
Group A strep
H influenza
Enterobacter sp.

84
Q

Causative pathogens of osteomyelitis in adults

A

S aureus

85
Q

How does infection spread to bones to cause osteomyelitis

A

Haematogenous infection
Direct inoculation into bone from trauma /surgery

86
Q

Acute osteomyelitis usually occurs in which age group

A

Children

87
Q

Chronic osteomyelitis is usually presented in which bones

A

Spine
Pelvis

88
Q

Chronic osteomyelitis is caused by which infections

A

Haemotogenous spread from pulmonary or urinary infections or infection from intervertebral discs

89
Q

Which pulmonary infection can cause chronic osteomyelitis

A

TB, affects spine the most

90
Q

Symptoms of acute osteomyelitis

A

Gradual onset pain at site of infection
Tenderness
Swelling
red
Hot
Systemic upset

91
Q

Symptoms of chronic osteomyelitis

A

Recurrent pain
Swelling
Redness

92
Q

Acute osteomyelitis in children usually affects

A

Metaphyses of long bones

93
Q

Why is metaphyses of long bones most commonly affected by acute osteomyelitis

A

Because it contains a lot of tortuous blood vessels with sluggish flow -> accumulate bacteria

94
Q

How can osteomyelitis cause septic arthritis in neonates and infants

A

Because certain metaphyses are intra-articular, allowing the infection to spread into the joint

95
Q

Investigations for osteomyelitis

A

Bone biopsy
Bloods
Imaging - Xray, MRI, CT

96
Q

When is Xray indicated in osteomyelitis

A

in chronic osteomyelitis
because x ray may be normal during early stage

97
Q

Which imaging technique should be used for acute osteomyelitis

A

MRI

98
Q

Management of acute osteomyelitis

A

IV Flucloxacillin or clindamycin
+ fusidic acid / rifampicin
switch to oral antibiotics
Surgical debridement if needed

99
Q

Management of chronic osteomyelitis

A

No cure
Surgical debridement
Internal or external fixation if bone is unstable after surgical debridement
IV antibiotics

100
Q

What is osteomalacia

A

abnormal softening of the bone due to deficient mineralization

101
Q

Causes of osteomalacia

A

Deficiencies
Long term anti-convulsant use
Chronic kidney disease

102
Q

Deficiency in what causes osteomalacia

A

Calcium
Phosphate
Vitamin D

103
Q

What causes vitamin D deficiency

A

malnutrition/malabsorption
Lack of sunlight exposure

104
Q

What causes phosphate deficiency

A

Malabsorption
Renal tubular acidosis
Alcohol abuse
Refeeding syndrome

105
Q

What is refeeding syndrome

A

shifts in fluids and electrolytes that may occur in malnourished patients receiving rapid artificial refeeding

106
Q

How does chronic kidney disease lead to osteomalacia

A

Reduced phosphate reabsorption
Failure to activate vitamin D
Secondary hyperparathyroidism -> low calcium

107
Q

Symptoms of osteomalacia

A

Bone pain
hypocalcaemia symptoms (muscle cramps/fatigue/brittle nails..etc)
pathological fractures

108
Q

What are the hypocalcaemia symptoms

A

Muscle cramps
fatigue
brittle nails
irritability
seizures

109
Q

Where is bone pain usually presented in osteomalacia in adults

A

Lower back
Pelvis
Femur

110
Q

Investigations for osteomalacia

A

Bloods
Xray

111
Q

Blood test results for osteomalacia

A

Low calcium
Low phosphate
High PTH
High ALP

112
Q

Management of osteomalacia

A

Lifestyle advice
Vitamin D therapy
Calcium / phosphate supplements

113
Q

Describe the vitamin D therapy for osteomalacia

A

If vitamin D deficient -> high dose vitamin D3 -> maintenance
If not deficient -> maintenance

114
Q

What vitamin D is used for osteomalacia

A

D3 tablets
- calcitriol
- alfacalcidol

115
Q

If patient was vitamin D deficient and was treated with high dose Vitamin D what needs to be checked within 1 month

A

Calcium level

116
Q

Presentation of rickets in children

A

Knock knees
Wrist swelling
Skull softening
Delayed tooth eruption
Bone pain
Bowing of the legs

117
Q

What is knock knees

A

Where a child stands straight and the knees touch but ankles are apart (valgus knees)

118
Q

What is seen on xray for rickets

A

Joint space widening - due to insufficient mineralisation of the bones

119
Q

What is Paget’s disease

A

Chronic condition involving cellular remodelling and deformities of one or more bones

120
Q

Cause of Paget’s

A

Abnormal osteoclast activity followed by increased osteoblast activity
= disorganised bone breakdown and formation
= reduced strength of bone

121
Q

Risk factors of Paget’s

A

> 50
Family history
Anglo-Saxon descent

122
Q

Paget’s disease commonly affects which bones

A

Pelvis
Skull
Lumbar spine
Femur

123
Q

Which bones are less commonly affected by Paget’s

A

Small bones

124
Q

Symptoms of Paget’s

A

Often asymptomatic
Pain over affected bones
Pathological fractures

125
Q

Signs of Paget’s

A

Affected bone may feel warmer on palpation
Bowing of femur
Deformities
Hearing loss
Spinal stenosis
Nerve compression

126
Q

Paget’s increases the risk of

A

osteosarcoma
fibrosarcoma
High output heart failure

127
Q

How may Paget’s cause hearing loss

A

Vestibulocochlear nerve compression
Ossicle ossification

128
Q

How does Paget’s cause high output heart failure

A

Because the new bone that forms contains more blood vessels than normal bone which means that the heart needs to work harder to pump blood to everywhere

129
Q

Why does the bone affected by Paget feel warmer on palpation

A

Due to increase in blood vessels hence blood flow

130
Q

Investigations for Paget’s

A

Bloods - ALP, Ca, phosphate
Xray

131
Q

Blood test results that suggest Paget’s

A

Increase in ALP
Normal Ca2+
Normal phosphate

132
Q

What can be seen on xray in Paget’s

A

Osteolysis
Increased bone size
Osteosclerosis
Coarse trabecular pattern

133
Q

cause of course trabecular pattern in Paget’s

A

Thickening of the white lines of trabecular tissue

134
Q

Management of Paget’s

A

Analgesia
Bisphosphonates

135
Q

What finding is used to monitor Paget’s disease activity

A

ALP level

136
Q

Risk factors for avascular necrosis

A

Males
35-50 years old

137
Q

Which bones are commonly affected by avascular necrosis

A

Femoral head
Wrist
Humeral head

138
Q

Causes of avascular necrosis

A

Steroids
Trauma
Radiation
Sickle cell disease
Pregnancy
SLE
NSAID
Idiopathic

139
Q

Pregnancy, SLE, sickle cell disease can cause avascular necrosis due to

A

Increased coagulability of the intraosseous microcirculation

140
Q

How does steroid use and alcoholism lead to avascular necrosis

A

Alters fat metabolism resulting in mobilisation into circulation
Sludges up the capillary system and promotes coagulation

Increased fat content in bone can compress venous outflow

141
Q

Symptoms of avascular necrosis

A

Can be asymptomatic
Pain
Stiffness
Femoral head ACN causes insidious onset of groin pain exacerbated by stairs
Reduced ROM (if late stage)

142
Q

Investigations for avascular necrosis

A

MRI for early stages
Xray

143
Q

What is a late sign of AVN on xray

A

Hanging rope sign - thin sclerotic line that crosses femoral neck

144
Q

2 types of managements of AVN

A

If AVN is reversible
If AVN is irreversible

145
Q

What is considered as irreversible AVN

A

If the articular surface has collapsed -> secondary OA

146
Q

Management of irreversible AVN

A

Joint replacement
Osteotomy

147
Q

Management of reversible AVN

A

Bisphosphonates
Core decompression
Curettage
Bone grafts

Y2 MSK (19 decks)

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