Bone and joint disorders Flashcards
What is osteoarthritis
Chronic disease due to imbalance between wear and repaid of articular cartilage leading to progressive cartilage loss
Risk factors of OA
Genetics
Female
Obesity
>50
Repetitive trauma from occupation / sports
Joint malalignment
What is secondary OA
OA at an unexpected site due to over use / previous injury / previous arthritis
What conditions can cause secondary OA
Gout
RA
Is OA inflammatory arthritis
No
How does OA change the structures of the joint (LOSS)
Loss of joint space due to cartilage worn away
Osteophytes formation
Subchondral cysts
Subchondral sclerosis
What causes subchondral cysts
Synovial fluid seeping into bone due to bone erosion and accumulates there
Why do osteophytes form
Due to the bone trying to repair and remodel itself from the damage from OA
Which joints are commonly affected by OA
Knee
Hip
Lumbar spine
First MTP joint of big toe
thumb bases
DIP PIP
Presentation of OA
Pain at night
Pain worse with activity
Morning stiffness < 30 minutes
Instability
Poor grip in thumb
Differences between OA and inflammatory arthritis
OA pain worse with movement
OA pain at night
OA morning stiffness <30 minutes
OA does not affect any other structures apart from joints
How do you differentiate between ankylosing spondylitis and OA which also affects lower lumbar spine
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
Onset of OA
Insidious, progresses over months or years
Clinical findings of OA
Reduced range of motion
Swelling (but not hot or red)
Crepitus
Deformity
Heberden’s nodes
Bouchard’s nodes
What are Herbeden’s and Bouchard’s nodes
Small, hard bony swellings on finger joints
Herbeden’s vs Bouchard’s nodes
Herbeden - on DIP
Bouchard - on PIP
Bouchard’s nodes are also seen in
RA
Which bony node - heberden or Bouchard, is more specific to OA
Heberden’s
OA in the knee can cause
Baker’s cysts - swelling behind the knee
OA in the hip can cause
Pain in groin radiating to knee or anterior thigh
Pain in hip radiating from lower back
OA in cervical spine can cause
Impinge nerve roots
Occipital headaches
OA in lumbar spine can cause
Spinal stenosis - narrowing of spinal canal putting on spinal cord and nerve roots
Symptoms of spinal stenosis
Pain in legs on activity
Weakness in legs
Investigations for OA
Clinical
Imaging Xray/MRI if in doubt
What can be seen on xray for OA (LOSS)
Loss of joint space
Osteophyte formation
Subchondral sclerosis
Subchondral cyst
Management for OA
Lifestyle management
Drug therapy
Surgery
What are the lifestyle modifications for oA
Weight loss
Moderate exercise (avoid weight bearing exercise)
Physiotherapy
Drug therapy for oA
Analgesia - paracetamol / NSAID
Intra-articular steroid injections for flare up
Which type of NSAID is avoided in OA management
opioids
Which analgesia is particularly effective for knee OA
NSAID
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
When is surgery indicated for OA
Severe and providing that the patient is fit enough
When is total knee replacement indicated
60+, medically fit patient with end stage arthritis and severe pain
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
How long does a TKR or Total hip replacement last in a old, low demand patient
15-20 years
Complications of TKR and THR
Infection
Instability
DVT
Chest infection
Nerve injury
Loosening / breakage
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
Risks associated with revision surgery
Substantial blood loss
Increase complications risks
Poorer outcome
Does not last as long
Alternatives to a TKR
Unicompartmental knee replacement
Osteotomy
Cartilage regeneration surgery
What is unicompartmental knee replacement
Only the worn out area of the knee is replaced
Concerns of a unicompartmental knee replacement
Not suitable in many cases
Reoperation rater higher than TKR
Progression of OA in unreplaced one
What is osteotomy
Realignment of a bone to correct deformity or redistribute load across an arthritic joint
When is osteotomy indicated
Early arthritis in knee and hip
Very active patients who would damage a joint replacement
Concerns for cartilage regeneration surgery
Unpredictable results
Does not work for widespread changes of OA
What is the hyper mobility syndrome
Ability to move joints beyond the normal range of movement
Hypermobility syndrome can cause
Chronic joint and ligament injuries, pain
Risk factors for hyper mobility syndrome
Female
Marfan’s
Ehlers Danloes
Presentation of hyper mobility syndrome
Joint pain
Joint stiffness
Frequent sprains
Dislocations of joints
Thin stretchy skin
When does hyper mobility syndrome usually present
Childhood
3rd decade
Investigations for hyper mobility syndrome
Beighton score
Beighton score that indicates hyper mobility
> 4 points
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
Treatment of Hypermobility syndrome
Supportive
- physiotherapy
- analgesia
- strengthen the muscles to protect the joints
- low impact exercise
What is septic arthritis
Joint infection due to pathogens spreading into the synovial fluid
Which pathogens can cause septic arthritis
S aureus
Streptococci
Gonococcus (gonorrhoea)
H influenza
E. coli
Most common cause of septic arthritis
S aureus
Most common cause of septic arthritis in a patient with prosthetic joint
Staph epidermidis
Septic arthritis caused by gonococcus is common in
Young sexually active individuals
Septic arthritis caused by E.coli is common in
Elderly
IV drug users
Risk factors for septic arthritis
Joint diseases
Immunosuppression
Prosthetic joints
Chronic kidney disease
Symptoms of septic arthritis
Acute, asymmetrical monoarthropathy
Red
Hot
Swollen
Painful
Reduced ROM
Systemically unwell
Septic arthritis most commonly affects which joint
Knee
Investigations for septic arthritis
Joint aspiration and synovial fluid analysis
Bloods - CRP
Xray
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
What IV antibiotic is used in septic arthritis
Flucloxacillin or clindamycin
How long is the antibiotic course for septic arthritis
4-6 weeks
IV 2 weeks
Oral the rest if good progress
Response to treatment for septic arthritis is based on
Clinical
CRP level
Risk of prosthetic joint infection
Diabetes
RA
Cancer
Use of steroids / anti- TNF
Prior arthroplasty
Prolonged duration of surgery
Pathogens causing prosthetic joint infection
Staph epidermidis
S aureus
Cutibacterium acnes
E. coli
Pseudomonas aeruginosa
Cutibacterium acnes mostly affects which prostheses
Upper limb prostheses
Early PJI (within 2-3 weeks) suggests
acquired during surgery or right after
Which pathogens most commonly causes early PIJ
S aureus
Staph epidermidis
3 weeks + onset of PJI suggests which pathogens
S epidermidis
Cutibacterium
Corynebacterium
S aureus
Presentation of PJI
Fever
Joint pain
Minimal swelling
Investigations for PJI
Multiple samples of perioperative tissue cultures
Bloods - CRP
Imaging
Management of early PJI
Debridement
12 weeks antibiotics
Management of late PJI
Removal of joints
Antibiotics
Revision joint replacement after finishing antibiotics therapy
What is osteomyelitis
Infection of the bone; acute or chronic
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
Most common causative pathogens of osteomyelitis
S aureus
Coagulase-negative staph
Risk factors of osteomyelitis
Immunocompromised
DIabetes
Peripheral vascular disease
Malignancy
Extremes of age
Causative pathogens of osteomyelitis in newborns <4months
S aureus
Group A and B strep
Enterobacter sp
Causative pathogens of osteomyelitis in children 4m-4yrs
S aureus
Group A strep
H influenza
Enterobacter sp.
Causative pathogens of osteomyelitis in adults
S aureus
How does infection spread to bones to cause osteomyelitis
Haematogenous infection
Direct inoculation into bone from trauma /surgery
Acute osteomyelitis usually occurs in which age group
Children
Chronic osteomyelitis is usually presented in which bones
Spine
Pelvis
Chronic osteomyelitis is caused by which infections
Haemotogenous spread from pulmonary or urinary infections or infection from intervertebral discs
Which pulmonary infection can cause chronic osteomyelitis
TB, affects spine the most
Symptoms of acute osteomyelitis
Gradual onset pain at site of infection
Tenderness
Swelling
red
Hot
Systemic upset
Symptoms of chronic osteomyelitis
Recurrent pain
Swelling
Redness
Acute osteomyelitis in children usually affects
Metaphyses of long bones
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
How can osteomyelitis cause septic arthritis in neonates and infants
Because certain metaphyses are intra-articular, allowing the infection to spread into the joint
Investigations for osteomyelitis
Bone biopsy
Bloods
Imaging - Xray, MRI, CT
When is Xray indicated in osteomyelitis
in chronic osteomyelitis
because x ray may be normal during early stage
Which imaging technique should be used for acute osteomyelitis
MRI
Management of acute osteomyelitis
IV Flucloxacillin or clindamycin
+ fusidic acid / rifampicin
switch to oral antibiotics
Surgical debridement if needed
Management of chronic osteomyelitis
No cure
Surgical debridement
Internal or external fixation if bone is unstable after surgical debridement
IV antibiotics
What is osteomalacia
abnormal softening of the bone due to deficient mineralization
Causes of osteomalacia
Deficiencies
Long term anti-convulsant use
Chronic kidney disease
Deficiency in what causes osteomalacia
Calcium
Phosphate
Vitamin D
What causes vitamin D deficiency
malnutrition/malabsorption
Lack of sunlight exposure
What causes phosphate deficiency
Malabsorption
Renal tubular acidosis
Alcohol abuse
Refeeding syndrome
What is refeeding syndrome
shifts in fluids and electrolytes that may occur in malnourished patients receiving rapid artificial refeeding
How does chronic kidney disease lead to osteomalacia
Reduced phosphate reabsorption
Failure to activate vitamin D
Secondary hyperparathyroidism -> low calcium
Symptoms of osteomalacia
Bone pain
hypocalcaemia symptoms (muscle cramps/fatigue/brittle nails..etc)
pathological fractures
What are the hypocalcaemia symptoms
Muscle cramps
fatigue
brittle nails
irritability
seizures
Where is bone pain usually presented in osteomalacia in adults
Lower back
Pelvis
Femur
Investigations for osteomalacia
Bloods
Xray
Blood test results for osteomalacia
Low calcium
Low phosphate
High PTH
High ALP
Management of osteomalacia
Lifestyle advice
Vitamin D therapy
Calcium / phosphate supplements
Describe the vitamin D therapy for osteomalacia
If vitamin D deficient -> high dose vitamin D3 -> maintenance
If not deficient -> maintenance
What vitamin D is used for osteomalacia
D3 tablets
- calcitriol
- alfacalcidol
If patient was vitamin D deficient and was treated with high dose Vitamin D what needs to be checked within 1 month
Calcium level
Presentation of rickets in children
Knock knees
Wrist swelling
Skull softening
Delayed tooth eruption
Bone pain
Bowing of the legs
What is knock knees
Where a child stands straight and the knees touch but ankles are apart (valgus knees)
What is seen on xray for rickets
Joint space widening - due to insufficient mineralisation of the bones
What is Paget’s disease
Chronic condition involving cellular remodelling and deformities of one or more bones
Cause of Paget’s
Abnormal osteoclast activity followed by increased osteoblast activity
= disorganised bone breakdown and formation
= reduced strength of bone
Risk factors of Paget’s
> 50
Family history
Anglo-Saxon descent
Paget’s disease commonly affects which bones
Pelvis
Skull
Lumbar spine
Femur
Which bones are less commonly affected by Paget’s
Small bones
Symptoms of Paget’s
Often asymptomatic
Pain over affected bones
Pathological fractures
Signs of Paget’s
Affected bone may feel warmer on palpation
Bowing of femur
Deformities
Hearing loss
Spinal stenosis
Nerve compression
Paget’s increases the risk of
osteosarcoma
fibrosarcoma
High output heart failure
How may Paget’s cause hearing loss
Vestibulocochlear nerve compression
Ossicle ossification
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
Why does the bone affected by Paget feel warmer on palpation
Due to increase in blood vessels hence blood flow
Investigations for Paget’s
Bloods - ALP, Ca, phosphate
Xray
Blood test results that suggest Paget’s
Increase in ALP
Normal Ca2+
Normal phosphate
What can be seen on xray in Paget’s
Osteolysis
Increased bone size
Osteosclerosis
Coarse trabecular pattern
cause of course trabecular pattern in Paget’s
Thickening of the white lines of trabecular tissue
Management of Paget’s
Analgesia
Bisphosphonates
What finding is used to monitor Paget’s disease activity
ALP level
Risk factors for avascular necrosis
Males
35-50 years old
Which bones are commonly affected by avascular necrosis
Femoral head
Wrist
Humeral head
Causes of avascular necrosis
Steroids
Trauma
Radiation
Sickle cell disease
Pregnancy
SLE
NSAID
Idiopathic
Pregnancy, SLE, sickle cell disease can cause avascular necrosis due to
Increased coagulability of the intraosseous microcirculation
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
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)
Investigations for avascular necrosis
MRI for early stages
Xray
What is a late sign of AVN on xray
Hanging rope sign - thin sclerotic line that crosses femoral neck
2 types of managements of AVN
If AVN is reversible
If AVN is irreversible
What is considered as irreversible AVN
If the articular surface has collapsed -> secondary OA
Management of irreversible AVN
Joint replacement
Osteotomy
Management of reversible AVN
Bisphosphonates
Core decompression
Curettage
Bone grafts
