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
2
Q
Risk factors of OA
A
Genetics
Female
Obesity
>50
Repetitive trauma from occupation / sports
Joint malalignment
3
Q
What is secondary OA
A
OA at an unexpected site due to over use / previous injury / previous arthritis
4
Q
What conditions can cause secondary OA
A
Gout
RA
5
Q
Is OA inflammatory arthritis
A
No
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
7
Q
What causes subchondral cysts
A
Synovial fluid seeping into bone due to bone erosion and accumulates there
8
Q
Why do osteophytes form
A
Due to the bone trying to repair and remodel itself from the damage from OA
9
Q
Which joints are commonly affected by OA
A
Knee
Hip
Lumbar spine
First MTP joint of big toe
thumb bases
DIP PIP
10
Q
Presentation of OA
A
Pain at night
Pain worse with activity
Morning stiffness < 30 minutes
Instability
Poor grip in thumb
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
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
13
Q
Onset of OA
A
Insidious, progresses over months or years
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
15
Q
What are Herbeden’s and Bouchard’s nodes
A
Small, hard bony swellings on finger joints
16
Q
Herbeden’s vs Bouchard’s nodes
A
Herbeden - on DIP
Bouchard - on PIP
17
Q
Bouchard’s nodes are also seen in
A
RA
18
Q
Which bony node - heberden or Bouchard, is more specific to OA
A
Heberden’s
19
Q
OA in the knee can cause
A
Baker’s cysts - swelling behind the knee
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
21
Q
OA in cervical spine can cause
A
Impinge nerve roots
Occipital headaches
22
Q
OA in lumbar spine can cause
A
Spinal stenosis - narrowing of spinal canal putting on spinal cord and nerve roots
23
Q
Symptoms of spinal stenosis
A
Pain in legs on activity
Weakness in legs
24
Q
Investigations for OA
A
Clinical
Imaging Xray/MRI if in doubt
25
What can be seen on xray for OA (LOSS)
Loss of joint space
Osteophyte formation
Subchondral sclerosis
Subchondral cyst
26
Management for OA
Lifestyle management
Drug therapy
Surgery
27
What are the lifestyle modifications for oA
Weight loss
Moderate exercise (avoid weight bearing exercise)
Physiotherapy
28
Drug therapy for oA
Analgesia - paracetamol / NSAID
Intra-articular steroid injections for flare up
29
Which type of NSAID is avoided in OA management
opioids
30
Which analgesia is particularly effective for knee OA
NSAID
31
Can intra-articular steroid injections be used frequently in OA
No, there is a limit to how many injections a patient can have a year due to the side effects and acceleration of OA
32
When is surgery indicated for OA
Severe and providing that the patient is fit enough
33
When is total knee replacement indicated
60+, medically fit patient with end stage arthritis and severe pain
34
What is considered as severe pain and end stage arthritis to be qualified for TKR
Constant severe pain
Sleep disturbance
Pain limiting mobility
Frequent flares
35
How long does a TKR or Total hip replacement last in a old, low demand patient
15-20 years
36
Complications of TKR and THR
Infection
Instability
DVT
Chest infection
Nerve injury
Loosening / breakage
37
Why is arthroplasty rare in patients under 50 years old (young patients)
Due to high chance of revision surgery
High demand causing the replacement to not last that long
Unexplained moderate - severe pain
38
Risks associated with revision surgery
Substantial blood loss
Increase complications risks
Poorer outcome
Does not last as long
39
Alternatives to a TKR
Unicompartmental knee replacement
Osteotomy
Cartilage regeneration surgery
40
What is unicompartmental knee replacement
Only the worn out area of the knee is replaced
41
Concerns of a unicompartmental knee replacement
Not suitable in many cases
Reoperation rater higher than TKR
Progression of OA in unreplaced one
42
What is osteotomy
Realignment of a bone to correct deformity or redistribute load across an arthritic joint
43
When is osteotomy indicated
Early arthritis in knee and hip
Very active patients who would damage a joint replacement
44
Concerns for cartilage regeneration surgery
Unpredictable results
Does not work for widespread changes of OA
45
What is the hyper mobility syndrome
Ability to move joints beyond the normal range of movement
46
Hypermobility syndrome can cause
Chronic joint and ligament injuries, pain
47
Risk factors for hyper mobility syndrome
Female
Marfan's
Ehlers Danloes
48
Presentation of hyper mobility syndrome
Joint pain
Joint stiffness
Frequent sprains
Dislocations of joints
Thin stretchy skin
49
When does hyper mobility syndrome usually present
Childhood
3rd decade
50
Investigations for hyper mobility syndrome
Beighton score
51
Beighton score that indicates hyper mobility
>4 points
52
What are the 5 manoeuvres used to assess Beighton score
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
53
Treatment of Hypermobility syndrome
Supportive
- physiotherapy
- analgesia
- strengthen the muscles to protect the joints
- low impact exercise
54
What is septic arthritis
Joint infection due to pathogens spreading into the synovial fluid
55
Which pathogens can cause septic arthritis
S aureus
Streptococci
Gonococcus (gonorrhoea)
H influenza
E. coli
56
Most common cause of septic arthritis
S aureus
57
Most common cause of septic arthritis in a patient with prosthetic joint
Staph epidermidis
58
Septic arthritis caused by gonococcus is common in
Young sexually active individuals
59
Septic arthritis caused by E.coli is common in
Elderly
IV drug users
60
Risk factors for septic arthritis
Joint diseases
Immunosuppression
Prosthetic joints
Chronic kidney disease
61
Symptoms of septic arthritis
Acute, asymmetrical monoarthropathy
Red
Hot
Swollen
Painful
Reduced ROM
Systemically unwell
62
Septic arthritis most commonly affects which joint
Knee
63
Investigations for septic arthritis
Joint aspiration and synovial fluid analysis
Bloods - CRP
Xray
64
Management for septic arthritis
Flucloxacillin (before culture)
IV antibiotics after culture
Switch to oral antibiotics after 2 weeks till the end
Joint washout may be required
65
What IV antibiotic is used in septic arthritis
Flucloxacillin or clindamycin
66
How long is the antibiotic course for septic arthritis
4-6 weeks
IV 2 weeks
Oral the rest if good progress
67
Response to treatment for septic arthritis is based on
Clinical
CRP level
68
Risk of prosthetic joint infection
Diabetes
RA
Cancer
Use of steroids / anti- TNF
Prior arthroplasty
Prolonged duration of surgery
69
Pathogens causing prosthetic joint infection
Staph epidermidis
S aureus
Cutibacterium acnes
E. coli
Pseudomonas aeruginosa
70
Cutibacterium acnes mostly affects which prostheses
Upper limb prostheses
71
Early PJI (within 2-3 weeks) suggests
acquired during surgery or right after
72
Which pathogens most commonly causes early PIJ
S aureus
Staph epidermidis
73
3 weeks + onset of PJI suggests which pathogens
S epidermidis
Cutibacterium
Corynebacterium
S aureus
74
Presentation of PJI
Fever
Joint pain
Minimal swelling
75
Investigations for PJI
Multiple samples of perioperative tissue cultures
Bloods - CRP
Imaging
76
Management of early PJI
Debridement
12 weeks antibiotics
77
Management of late PJI
Removal of joints
Antibiotics
Revision joint replacement after finishing antibiotics therapy
78
What is osteomyelitis
Infection of the bone; acute or chronic
79
Acute osteomyelitis is usually caused by a single/multiple organism (s), while the chronic infection is more likely to be single/polymicrobial.
Acute osteomyelitis is usually caused by a single organism whereas chronic is more likely to be polymicrobial
80
Most common causative pathogens of osteomyelitis
S aureus
Coagulase-negative staph
81
Risk factors of osteomyelitis
Immunocompromised
DIabetes
Peripheral vascular disease
Malignancy
Extremes of age
82
Causative pathogens of osteomyelitis in newborns <4months
S aureus
Group A and B strep
Enterobacter sp
83
Causative pathogens of osteomyelitis in children 4m-4yrs
S aureus
Group A strep
H influenza
Enterobacter sp.
84
Causative pathogens of osteomyelitis in adults
S aureus
85
How does infection spread to bones to cause osteomyelitis
Haematogenous infection
Direct inoculation into bone from trauma /surgery
86
Acute osteomyelitis usually occurs in which age group
Children
87
Chronic osteomyelitis is usually presented in which bones
Spine
Pelvis
88
Chronic osteomyelitis is caused by which infections
Haemotogenous spread from pulmonary or urinary infections or infection from intervertebral discs
89
Which pulmonary infection can cause chronic osteomyelitis
TB, affects spine the most
90
Symptoms of acute osteomyelitis
Gradual onset pain at site of infection
Tenderness
Swelling
red
Hot
Systemic upset
91
Symptoms of chronic osteomyelitis
Recurrent pain
Swelling
Redness
92
Acute osteomyelitis in children usually affects
Metaphyses of long bones
93
Why is metaphyses of long bones most commonly affected by acute osteomyelitis
Because it contains a lot of tortuous blood vessels with sluggish flow -> accumulate bacteria
94
How can osteomyelitis cause septic arthritis in neonates and infants
Because certain metaphyses are intra-articular, allowing the infection to spread into the joint
95
Investigations for osteomyelitis
Bone biopsy
Bloods
Imaging - Xray, MRI, CT
96
When is Xray indicated in osteomyelitis
in chronic osteomyelitis
because x ray may be normal during early stage
97
Which imaging technique should be used for acute osteomyelitis
MRI
98
Management of acute osteomyelitis
IV Flucloxacillin or clindamycin
+ fusidic acid / rifampicin
switch to oral antibiotics
Surgical debridement if needed
99
Management of chronic osteomyelitis
No cure
Surgical debridement
Internal or external fixation if bone is unstable after surgical debridement
IV antibiotics
100
What is osteomalacia
abnormal softening of the bone due to deficient mineralization
101
Causes of osteomalacia
Deficiencies
Long term anti-convulsant use
Chronic kidney disease
102
Deficiency in what causes osteomalacia
Calcium
Phosphate
Vitamin D
103
What causes vitamin D deficiency
malnutrition/malabsorption
Lack of sunlight exposure
104
What causes phosphate deficiency
Malabsorption
Renal tubular acidosis
Alcohol abuse
Refeeding syndrome
105
What is refeeding syndrome
shifts in fluids and electrolytes that may occur in malnourished patients receiving rapid artificial refeeding
106
How does chronic kidney disease lead to osteomalacia
Reduced phosphate reabsorption
Failure to activate vitamin D
Secondary hyperparathyroidism -> low calcium
107
Symptoms of osteomalacia
Bone pain
hypocalcaemia symptoms (muscle cramps/fatigue/brittle nails..etc)
pathological fractures
108
What are the hypocalcaemia symptoms
Muscle cramps
fatigue
brittle nails
irritability
seizures
109
Where is bone pain usually presented in osteomalacia in adults
Lower back
Pelvis
Femur
110
Investigations for osteomalacia
Bloods
Xray
111
Blood test results for osteomalacia
Low calcium
Low phosphate
High PTH
High ALP
112
Management of osteomalacia
Lifestyle advice
Vitamin D therapy
Calcium / phosphate supplements
113
Describe the vitamin D therapy for osteomalacia
If vitamin D deficient -> high dose vitamin D3 -> maintenance
If not deficient -> maintenance
114
What vitamin D is used for osteomalacia
D3 tablets
- calcitriol
- alfacalcidol
115
If patient was vitamin D deficient and was treated with high dose Vitamin D what needs to be checked within 1 month
Calcium level
116
Presentation of rickets in children
Knock knees
Wrist swelling
Skull softening
Delayed tooth eruption
Bone pain
Bowing of the legs
117
What is knock knees
Where a child stands straight and the knees touch but ankles are apart (valgus knees)
118
What is seen on xray for rickets
Joint space widening - due to insufficient mineralisation of the bones
119
What is Paget's disease
Chronic condition involving cellular remodelling and deformities of one or more bones
120
Cause of Paget's
Abnormal osteoclast activity followed by increased osteoblast activity
= disorganised bone breakdown and formation
= reduced strength of bone
121
Risk factors of Paget's
> 50
Family history
Anglo-Saxon descent
122
Paget's disease commonly affects which bones
Pelvis
Skull
Lumbar spine
Femur
123
Which bones are less commonly affected by Paget's
Small bones
124
Symptoms of Paget's
Often asymptomatic
Pain over affected bones
Pathological fractures
125
Signs of Paget's
Affected bone may feel warmer on palpation
Bowing of femur
Deformities
Hearing loss
Spinal stenosis
Nerve compression
126
Paget's increases the risk of
osteosarcoma
fibrosarcoma
High output heart failure
127
How may Paget's cause hearing loss
Vestibulocochlear nerve compression
Ossicle ossification
128
How does Paget's cause high output heart failure
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
Why does the bone affected by Paget feel warmer on palpation
Due to increase in blood vessels hence blood flow
130
Investigations for Paget's
Bloods - ALP, Ca, phosphate
Xray
131
Blood test results that suggest Paget's
Increase in ALP
Normal Ca2+
Normal phosphate
132
What can be seen on xray in Paget's
Osteolysis
Increased bone size
Osteosclerosis
Coarse trabecular pattern
133
cause of course trabecular pattern in Paget's
Thickening of the white lines of trabecular tissue
134
Management of Paget's
Analgesia
Bisphosphonates
135
What finding is used to monitor Paget's disease activity
ALP level
136
Risk factors for avascular necrosis
Males
35-50 years old
137
Which bones are commonly affected by avascular necrosis
Femoral head
Wrist
Humeral head
138
Causes of avascular necrosis
Steroids
Trauma
Radiation
Sickle cell disease
Pregnancy
SLE
NSAID
Idiopathic
139
Pregnancy, SLE, sickle cell disease can cause avascular necrosis due to
Increased coagulability of the intraosseous microcirculation
140
How does steroid use and alcoholism lead to avascular necrosis
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
Symptoms of avascular necrosis
Can be asymptomatic
Pain
Stiffness
Femoral head ACN causes insidious onset of groin pain exacerbated by stairs
Reduced ROM (if late stage)
142
Investigations for avascular necrosis
MRI for early stages
Xray
143
What is a late sign of AVN on xray
Hanging rope sign - thin sclerotic line that crosses femoral neck
144
2 types of managements of AVN
If AVN is reversible
If AVN is irreversible
145
What is considered as irreversible AVN
If the articular surface has collapsed -> secondary OA
146
Management of irreversible AVN
Joint replacement
Osteotomy
147
Management of reversible AVN
Bisphosphonates
Core decompression
Curettage
Bone grafts
