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(SG) condensed phase 2a > MSK & Rheumatology > Flashcards

MSK & Rheumatology Flashcards

1
Q

Define osteoarthritis

A

Loss of cartilage, with bone remodelling and inflammation.

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2
Q

Define rheumatoid arthritis

A

Autoimmune inflammation of the synovial joints

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3
Q

Define osteoporosis

A

Progressive skeletal disease with reduced bone mass and micro-deteriorataion

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4
Q

Define osteomalacia

A

Inadequate mineralisation of osteoid framework

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5
Q

How does osteoarthritis clinically present?

A

Joint pain exacerbated by exercise.

Joint stiffness after rest (transient in the morning).

Reduced functionality.

Bony swellings (Distal interphalangeal Heberden’s and proximal interphalangeal Bouchard’s) and deformity.

Crepitus

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6
Q

How does rheumatoid arthritis clinically present?

A

Insidious onset of pain in the distal small jonts.

Morning stiffness (for more than 30 minutes).

Deformities: Ulnar deviation, swan neck and boutonniere.

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7
Q

How does osteoporosis clinically present?

A

Develops asymptomatically.

Bone fragility.

Fracture is often first sign (neck of femur).

Fractures in thoracic vertebrae may lead to kyphosis (widow’s stoop).

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8
Q

How does osteomalacia clinically present?

A

Proximal muscle weakness and pain.

Low bone density.

In children; bowed legs and knock knees.

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9
Q

Rheumatoid arthritis - note

A

DR: ‘Digital Rheumatoid’

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10
Q

Osteomalacia - note

A

‘Rickets’ in children

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11
Q

Pathophysiology of osteoarthritis

A

Progressive destruction of the articular cartilage (loss of articular space).

Exposed subchondral bone becomes sclerotic,

increasing vascularity

and subchondral cyst formation -> repair produces cartilaginous growths which become calcified (osteophytes).

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12
Q

Pathophysiology of rheumatoid arthritis

A

Infiltration of the synovium by inflammatory cells

  • > angiogenic cytokines
  • > Formation of new synovial blood vessels
  • > Synovium proliferates and grows out over the surface of the cartilage producing a pannus
  • > Pannus destroys the cartilage and subchondral bone
  • > bony erosions
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13
Q

Pathophysiology of osteoporosis

A

Inadequate peak bone mass,

excessive bone resorption

and inadequate formation of new bone during remodelling.

Lack of oestrogen increases bone resorption and decreases bone deposition.

Deficiency of calcium -> Increased bone resorption through PTH.

RANKL binds to RANK, activating osteoclasts.

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14
Q

Pathophysiology of osteomalacia

A

Normal bone mineralisation depends on adequate calcium and phosphate.

Vitamin D promotes calcium absorption in the intestines, promotes bone resorption (by increasing osteoclast number).

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15
Q

Cause/s of osteoarthritis

A

Usually primary.

Sometimes secondary to particular joints that have been damaged/frequently used.

RF: Females,

FH, obesity, smoking

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16
Q

Cause/s of rheumatoid arthritis

A

HLA DR4 and DRB1 confer susceptability.

Triggering antigen not known.

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17
Q

Cause/s of osteoporosis

A

Menopause.

Nutritional deficiency, contributes.

Bone density naturally lost from 35.

Steroids can activate osteoclasts.

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18
Q

Causes of osteomalacia

A

Profound vitamin D deficiency.

Lack of exposure to sunlight and/or gastiointestinal malabsorption.

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19
Q

Epidemiology of osteoarthritis

A

Prevalence increases with age.

More common in women.

Most common form of arthritis.

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20
Q

Epidemiology of rheumatoid arthritis

A

1% of population will experience.

More common in women.

Peak incidence in 40s

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21
Q

Epidemiology of osteoporosis

A

More common in women, particularly following menopause.

Being thin.

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22
Q

Epidemiology of osteomalacia

A

More common in pigmented skin

and the elderly.

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23
Q

Diagnostic test for osteoarthritis

A

Examination: Diagnose in >45 yrs,

activity related joint pain,

with either no morning related stiffness

or <30 mins of it Xray: LOSS

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24
Q

Diagnostic test for rheumatoid arthritis

A

Anti-CCP: Most specific.

Rheumatoid factor (also AntiNuclear Antibody).

X ray: Loss of joint space

Erosions

Soft tissue swelling

Soft bones (osteopenia)

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25
Q

Diagnostic test for osteoporosis

A

Bone mass density assessment: DEXA.

Clinical.

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26
Q

Diagnostic test for osteomalacia

A

X ray: Defective mineralisation.

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27
Q

Treatments for osteoarthritis

A

Pain relief.

Exercise.

Weight loss.

Assistive devices.

Consider surgery as last resort for debilitating.

Interarticular corticosteroid injection.

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28
Q

Treatments for rheumatoid arthritis

A

DMARDs (sulfasalazine and methotrexate).

NSAIDs.

TNF-a inhibitor (infliximab)

Physiotherapy.

Interarticular corticosteroid injection.

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29
Q

Treatments for osteoporosis

A

Prevent fractures.

Calcium and vitamin D intake.

Bisphosphonates in those who have never had a fracture.

Oestrogen supplement.

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30
Q

Treatment for osteomalacia

A

Oral calciferol.

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31
Q

Complication of osteoarthritis

A

Reduced mobility

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32
Q

Complication of rheumatoid arthritis

A

Social impact

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33
Q

Complication of osteoporosis

A

Fractures

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34
Q

Sequelae of rheumatoid arthritis

A

Depression

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35
Q

Define Systemic Lupus Erythematosus

A

Heterogenous, inflammatory, multisystem autoimmune disease with antinuclear antibodies

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36
Q

Define Antiphospholipid syndrome

A

Autoimmune disorder characterised by arterial and venous thrombosis

and raised levels of antiphospholipid antibodies

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37
Q

Define Sjögrens syndrome

A

Lymphocytic infiltration of exocrine glands

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38
Q

Define Polymyositis

A

Inflammation

and necrosis of skeletal muscle fibres

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39
Q

How does Systemic Lupus Erythematosus clinically present?

A

Vast number of symptoms.

General: Fatigue, malaise, fever, splenomegaly, lympadenopathy, pleuritic chest pain, headache, Raynaud’s, mild hair loss myalgia.

Arthralgia: Symmetrical joint and muscle pain.

Mucocutaneous: Discoid lupus, potosensitive rash, butterfly rash

Pulmonary: pleurisy, fibrosing alveolitis, obliterative bronchiolitis

Cardiovascular: pericarditis, hypertension

Renal: nephritis, haematuria, hypertension, glomerulonephritis

Neuro: Anxiety and depression (almost any neuro manifestation).

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40
Q

How does Antiphospholipid syndrome clinically present?

A

Varied clinical features.

Peripheral artery thrombosis,

deep venous thrombosis,

cerebrovascular disease,

pregnancy loss,

MI,

retinal thrombosis,

pulmonary embolism and pulmonary hypertension.

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41
Q

How does Sjögrens syndrome clinically present?

A

Dry eyes,

dry mouth

and enlargement of the parotid glands.

Possibly blepharitis.

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42
Q

How does Polymyositis clinically present?

A

Symmetrical progressive muscle weakness and wasting, affecting the proximal muscles of the shoulder and pelvic girdle.

Difficulty squatting and with stairs, and with raising hands above head.

Can involve dysphagia and dysphonia if pharyngeal and laryngeal muscles are involved.

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43
Q

Systemic Lupus Erythematosus - note

A

It’s never lupus.

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44
Q

Antiphospholipid syndrome - note

A

Coagulation problems

Livedo reticularis

Obstetric problems

Thrombocytopenia

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45
Q

Pathophysiology of Systemic Lupus Erythematosus

A

Apoptotic cells and cell fragments are cleared inefficiently by phagocytes

  • > transfer to lymphoid tissue
  • > taken up by antigen presenting cells
  • > self-antigens including nuclear components are presented to T cells
  • > T cells stimulate B cells to produce autoantibodies against the antigens.

Clinical manifestations are mediated by antibody formation

and the development and deposition of immune complexes,

complement activation and influx of neutrophils and abnormal cytokine production.

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46
Q

Pathophysiology of Antiphospholipid syndrome

A

Proposed mechanisms for hypercoagulable effect of aPLantibodies include complement activation,

the production of antibodies against coagulation factors,

activation of platelets,

activation of vascular endothelium

and a reaction of antibodies to oxidised low density lipoprotein.

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47
Q

Pathophysiology of Sjögrens syndrome

A

Not fully known.

Possibly inflammation of the glands prompts autoimmune response.

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48
Q

Pathophysiology of Polymyositis

A

Mediated by cytotoxic T cells.

Involves autoimmune factors.

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49
Q

Cause/s of Systemic Lupus Erythematosus

A

Unknown.

Likely multifactorial.

Strong genetic association.

Ultraviolet light causes onset of rash.

Higher incidence premenopausal -> oestrogen has an effect.

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50
Q

Cause/s of Antiphospholipid syndrome

A

Unknown.

Some genetic association.

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51
Q

Cause/s of Sjögrens syndrome

A

Can be idiopathic (primary)

or associated with another autoimmune condition (secondary),

often rheumatoid arthritis.

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52
Q

Causes of Polymyositis

A

Unknown.

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53
Q

Epidemiology of Systemic Lupus Erythematosus

A

More common in premenopausal females.

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54
Q

Epidemiology of Antiphospholipid syndrome

A

Higher prevalence in black people.

Occurs most commonly in women of fertile age.

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55
Q

Epidemiology of Sjögrens syndrome

A

Classicallly disease of middle aged women.

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56
Q

Epidemiology of Polymyositis

A

Presents between 30 and 60 (small peak at 15).

Twice as common in females.

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57
Q

Diagnostic test for Systemic Lupus Erythematosus

A

FBC, ESR and antinuclear factor.

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58
Q

Diagnostic test for Antiphospholipid syndrome

A

Screen for aPL antibodies.

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59
Q

Diagnostic test for Sjögrens syndrome

A

Serum antibodies.

Schirmer’s test: Whether the eye can self hydrate.

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60
Q

Diagnostic test for Polymyositis

A

Muscle biopsy.

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61
Q

Treatments for Systemic Lupus Erythematosus

A

Avoid sunlight and smoking.

NSAIDs and coritcosteroid for arthralgia.

Immunosuppressives for severe symptoms.

Rituximab.

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62
Q

Treatments for Antiphospholipid syndrome

A

Healthy lifestyle.

Acute management of thrombosis: Heparin

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63
Q

Treatment for Sjögrens syndrome

A

Artificial tear and saliva replacement.

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64
Q

Treatment for Polymyositis

A

Oral prednisalone.

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65
Q

Complications of Systemic Lupus Erythematosus

A

Depends on organ involvement

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66
Q

Complications of Antiphospholipid syndrome

A

Stroke. MI

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67
Q

Complications of Sjögrens syndrome

A

Infection of eyes or mouth.

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68
Q

Complications of Polymyositis

A

Interstitial lung disease,

dysphagia,

infection.

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69
Q

Sequelae of Systemic Lupus Erythematosus

A

Characterised by relapse and remission.

70
Q

Define Raynaud’s phenomenon

A

Paroxysmal vasospastic

–> vasodilatory events in peripheral arteries.

71
Q

How does Raynaud’s phenomenon clinically present?

A

Usually following cold: Pallor of distal portion of one or more digits

  • > Numbness/pain and cyanosis of the digit
  • > Hyperaemic; red and warm
72
Q

Pathophysiology of Raynaud’s phenomenon

A

Abnormalities in the blood vessel wall,

neural control mechanisms

and intravascular circulating factors are thought to combine.

73
Q

Cause of Raynaud’s phenomenon

A

Primary (Raynaud’s disease): Genetic cause, usually.

Secondary: Depends on underlying disease.

74
Q

Epidemiology of Raynaud’s phenomenon

A

Primary: Usually young women.

Smoking and hand vibration (tools) associated.

75
Q

Diagnostic test for Raynaud’s phenomenon

A

Examination of affected region.

76
Q

Treatments for Raynaud’s phenomenon

A

Primary: smoking cessation,

calcium channel blockers if symptomatic .

Secondary: Treatment of the underlying cause.

77
Q

Sequelae of Raynaud’s phenomenon

A

About 13% of patients -> Scleroderma.

78
Q

Define Ankylosing spondylitis

A

Inflammatory disorder of the spine

79
Q

Define psoriatic arthritis

A

Inflammatory arthritis associated with psoriasis

80
Q

Define reactive arthritis

A

Inflammatory arthritis that usually follows a GI or GU infection

81
Q

Types of reactive arthritis

A

Post-enteric

Post-venereal

82
Q

How does Ankylosing spondylitis clinically present?

A

Increasing pain and prolonged morning stiffness in the lower back and buttocks.

Improves with exercise.

Progressive loss of spinal movement.

Characteristic abnormalities: Loss of lumbar lordosis,

increased kyphosis

and limitation of lumbar spine mobility.

83
Q

How does psoriatic arthritis clinically present?

A

Ranges from mild synovitis to severe progressive erosive arthropathy, usually preceded by the rash.

Skin disease can be as minor as an occult rash.

Nail changes are characteristic.

84
Q

How does reactive arthritis clinically present?

A

2-4 weeks following a GI or GU infection.

Acute onset, with malaise, fatigue and fever.

Low back pain common.

Asymmetrical, oligoarthritis (no more than 6 joints).

Can’t see, can’t pee, can’t climb a tree (Conjunctivitis urethritis, arthritis).

85
Q

Seronegative spondyloarthopathies (this encompasses Ankylosing spondylitis, psoriatic and reactive arthritis) - note

A

Seronegative spondyloarthopathies share five main traits:

Predilection for axial inflammation,

Asymmetrical peripheral arthritis,

Absence of rheumatoid factor,

Inflammation of the enthesis

and a Strong association with HLA-B27

86
Q

Pathophysiology of Ankylosing spondylitis

A

Ankylosis occurs by forming syndesmophytes following inflammation.

This leads to the fusion of the vertebrae.

The cause of the inflammation is not known, but thought to involve CD8 T cells.

87
Q

Pathophysiology of psoriatic arthritis

A

Exact mechanisms unknown.

88
Q

Pathophysiology of reactive arthritis

A

Persistent bacterial antigen in the inflamed synovium of affected joints is thought to drive the inflammation.

89
Q

Cause of Ankylosing spondylitis

A

Unknown.

Strong genetic association.

90
Q

Cause of psoriatic arthritis

A

Autoimmune mediated, with defined HLA associations (HLA-B27, -B17, -CW6, -DR4, -DR7).

91
Q

Cause of post-enteric reactive arthritis

A

Usually infection by Campylobacter, Salmonella and Shigella.

92
Q

Cause of pose-venereal reactive arthritis

A

Usually infection by Chlamydia trachomatisor with HIV.

93
Q

Epidemiology of Ankylosing spondylitis

A

Usually young males.

More common and severe in males.

94
Q

Epidemiology of psoriatic arthritis

A

20% of patients with psoriasis.

95
Q

Epidemiology of reactive arthritis

A

Typically affects young males.

96
Q

Diagnostic test for Ankylosing spondylitis

A

X ray: normal, or show erosion and sclerosis of the margins of the sacroiliac joints -> ankylosis.

Bamboo spine from rehealing of the enthesitis.

97
Q

Diagnostic test for psoriatic arthritis

A

Xray: Pencil in cup deformity.

98
Q

Diagnostic test for reactive arthritis

A

Once arthritis discovered, cultures show negative;

take serum antibodies.

99
Q

Treatments for Ankylosing spondylitis

A

NSAIDs, TNF-alpha inhibitors (infliximab).

Surgery: Can correct spinal deformities to repair damage.

Possibly hip/shoulder replacement.

100
Q

Treatments for psoriatic arthritis

A

Drugs: NSAIDs, DMARDs, TNF-alpha inhibitor (infliximab)

Surgical: Can correct deformed joints

101
Q

Treatments for reactive arthritis

A

Aspirate synovial effusions.

Physiotherapy.

NSAIDs, Corticosteroids.

Antibiotics for causative organism.

102
Q

Complications of Ankylosing spondylitis

A

Small chance of spinal fusion

-> severe kyphosis.

103
Q

Complication of psoriatic arthritis

A

Joint destruction,

psycho social damage.

104
Q

Complication of reactive arthritis

A

Minority may develop destructive enthesitis or spondylitis.

105
Q

Sequelae of reactive arthritis

A

High recurrence by new infection or stress.

106
Q

Define gout

A

Deposition of monosodium urate monohydrate crystals wthin joints.

107
Q

Define pseudogout

A

Deposition of calcium pyrophosphate crystals within joints.

108
Q

How does gout clinically present?

A

A joint becomes swollen, tender and erythmatous.

Florid synovitis,

extreme tenderness,

with overlying erythema.

Usually affects the metatarsalphalangeal joint of the big toe.

109
Q

How does pseudogout clinically present?

A

Often asymptomatic.

Joints become swollen tender and erythmatous (as above).

Usually affects knee or wrist.

In chronic condition, destructive changes as in OA.

110
Q

Gout - note

A

‘One of the most painful acute conditions human beings can experience’.

111
Q

Pseudogout - note

A

Calcium pyrophospate dihydrate crystal deposition disease.

112
Q

Pathophysiology of gout

A

Monosodium urate (derived from purine breakdown) precipitates and forms deposits in joints.

Crystals formed are very painful.

Can form tophi; asymmetrical chalky appearance, firm nodules.

113
Q

Pathophysiology of pseudogout

A

Excess of pyrophosphate and calcium in the blood

-> crystal deposition in synovium.

114
Q

Causes of gout

A

Hyperuricaemia.

Often idiopathic Impaired excretion: CKD, diuretics, hypertension

Increased uric acid production (rarer): PPS overactivity, increased turnover.

115
Q

Causes of pseudogout

A

Unknown.

Precipitated by dehydration, steroids, hyperparathyroidism.

In younger patients, associated with; haemochromatosis and wilson’s disease.

116
Q

Epidemiology of gout

A

Much more common in males.

RF: Meat, seafood, alcohol, diuretics

117
Q

Epidemiology of pseudogout

A

Usually affects elderly women.

118
Q

Diagnostic test for gout

A

Joint fluid microscopy: MSU negatively birifringent needle crystals or

Examination: tophi confirm diagnosis.

119
Q

Diagnostic test for pseudogout

A

Joint fluid microscopy: rhomboid positively birifringent crystals.

120
Q

Treatment for gout

A

Acute: ice pack,

rest,

elevation.

NSAIDs (diclofenac), colchicine (if NSAIDs aren’t tolerated).

Long term: Allopurinol.

121
Q

Treatment for pseudogout

A

Joint aspiration with NSAIDs or colchicine.

Possibly corticosteroids.

122
Q

Complications of gout

A

Nephrolithiasis,

infection.

123
Q

Complications of pseudogout

A

Pain.

124
Q

Sequelae of gout

A

Recurrence, usually within first year.

125
Q

Define Paget’s disease of bone

A

Increased bone turnover

-> enlarged misshapen bones

126
Q

Define Degenerative disc disease

A

Pathological process of degeneration of intervertebral discs.

127
Q

Define Fibromyalgia

A

Chronic widespread pain and sensitivity to pressure.

128
Q

Define Mechanical back pain

A

Back pain as a result of physical wear and tear.

129
Q

How does Paget’s disease of bone clinically present?

A

Commonly asymptomatic.

When presents; often bone pain and/or deformity.

Localised to one or a few bones.

Bone fragility -> Pathological fractures

130
Q

How does Degenerative disc disease clinically present?

A

Chronic low back pain,

sometimes radiating to the hips,

or the buttocks.

131
Q

How does Fibromyalgia clinically present?

A

Chronic, widespread pain associated with unrefreshing sleep and tiredness.

Often occurs with inflammatory and osteo arthritices.

Symptoms generally worse in the cold, and under stress.

132
Q

How does Mechanical back pain clinically present?

A

Back pain in lumbosacral.

History of bowel / bladder dysfunction suggestive of cauda equina.

133
Q

Paget’s disease of bone - note

A

There is also a Paget’s of breast,

and Juvenile Paget’s.

134
Q

Pathophysiology of Paget’s disease of bone

A

Lytic phase: Increased bone resorption with abnormal osteoclast activity

  • > Rapid increase in bone formation by osteoblasts
  • > New bone is mechanically weaker, more vascularised and poorly organised (pathological fractures)
135
Q

Pathophysiology of Degenerative disc disease

A

Degenerative fibrocartilage and clusters of chondrocytes present.

Fibrocartilage replaces the gelatinous mucoid material of the nucleus pulposus as the disc chagnes with age.

Possibly splits in the anulus fibrosus allow nucleus pulposus to herniate out.

There may be shrinkage of the nucleus pulposus that produces prolapse or folding of the anulus fibrosus with secondary osteophyte formation at the margins of the adjacent vertebral body.

Pathology: Protrusion, spondylolysis, and/or spinal stenosis.

136
Q

Pathophysiology of Fibromyalgia

A

Unknown.

Theories include; peripheral and central hypersensitivity,

altered pain perception,

somatisation.

137
Q

Pathophysiology and cause of Mechanical back pain

A

Nerve root: Nerve root impingement due to herniated discs.

Could also be cauda equina syndrome.

Causes a sharp, well-localised pain, can be associated with paresthesia

MSK pain: myofascial pain syndromes and fibromyalgia

Other: Osteomyelitis, sacroiliitis and malignancy.

138
Q

Cause of Paget’s disease of bone

A

Genetic component: autosomal dominance in some cases.

Unclear what causes attacks.

Possibly mechanical stress.

139
Q

Cause of Degenerative disc disease

A

Disease of aging;

increased fragility of the cartilage of the disc can lead to the onset of pathology.

140
Q

Cause of Fibromyalgia

A

Unknown.

Some genetic association.

141
Q

Epidemiology of Paget’s disease of bone

A

1-2% of white adults over 55.

UK has highest incidence in the world. S

lightly more common in males.

142
Q

Epidemiology of Degenerative disc disease

A

More common in the elderly.

143
Q

Epidemiology of Fibromyalgia

A

More common in women.

Middle age.

144
Q

Epidemiology of Mechanical back pain

A

2/3 affected at some point.

145
Q

Diagnostic test for Paget’s disease of bone

A

Xrays: Deformity

Bloods: Bone specific alkaline phosphatase raised

146
Q

Diagnostic test for Degenerative disc disease

A

CT and/or MRI

147
Q

Diagnostic test for Fibromyalgia

A

Clinical, 9 pairs of sites to assess for tenderness

148
Q

Diagnostic test for Mechanical back pain

A

CT and/or MRI

149
Q

Treatment for Paget’s disease of bone

A

Bisphosphates inhibit bone resorption by reducing osteoclast activity.

150
Q

Treatment for Degenerative disc disease

A

Physical therapy,

NSAIDs,

epidural steroids.

If no effect; surgery to relieve pain.

151
Q

Treatment for Fibromyalgia

A

Drugs: Analgesic ladder (strong opioids not advised).

Psychosocial: exercise and strength training.

152
Q

Treatment for Mechanical back pain

A

NSAIDs,

analgesics,

and muscle relaxants.

153
Q

Complications of Degenerative disc disease

A

Sciatica,

ankylosis.

154
Q

Sequelae of mechanical back pain

A

Recurrence.

155
Q

Define septic arthritis

A

Infection producing inflammation in a joint.

156
Q

Define osteomyelitis

A

Infection of the bone marrow.

157
Q

Types of septic arthritis

A

Acute

Chronic

158
Q

How does septic arthritis clinically present?

A

Single swollen joint with pain on movement, usually the knee.

Joint swollen, warm, tender.

159
Q

How does osteomyelitis clinically present?

A

Fever, local pain and erythema.

In chronic: sinus formation.

160
Q

Septic arthritis - note

A

Medical emergency: can destroy a joint in 24hrs.

161
Q

Pathophysiology of septic arthritis

A

Infection of the joint can cause damaging inflammation, and loss of function.

162
Q

Pathophysiology of osteomyelitis

A

Results in inflammatory destruction of bone.

When dead bone detaches from healthy, it forms a sequestrum.

Large sequestrum that remains in situ acts as a focus for infection.

New bone can form around this and often causes deformity.

163
Q

Cause of septic arthritis

A

Direct injury or blood-borne infection.

Prosthetic joints are more susceptible.

Mostly Staphylococcus aureus.

Gram negative are more common in the elderly.

164
Q

Cause of osteomyelitis

A

Local infection (usually following trauma)

or due to metastatic haematogenous spread.

Usually Staphylococcus,

but sometimes Haemophilus influenza and Salmonella.

165
Q

Epidemiology of septic arthritis

A

Increases with age.

Immunocompromised.

166
Q

Epidemiology of osteomyelitis

A

Increasing due to increase of predisposing conditions such as diabetes.

167
Q

Diagnostic test for septic arthritis

A

Bloods: ESR and CRP elevated.

Synovial fluid exam: culture.

168
Q

Diagnostic test for osteomyelitis

A

CT, MRI or bone scan.

169
Q

Treatment for septic arthritis

A

Immediate empirical antibiotics (flucloxacillin usually).

Splinting.

Aspiration to drain the joint.

170
Q

Treatment for osteomyelitis

A

Flucloxacillin and fusidic acid IV.

171
Q

Complications of septic arthritis

A

Delay in treatment can cause joint destruction

and long-term disability.

172
Q

Complications of osteomyelitis

A

Bone abscess,

bacteraemia,

growth arrest,

chronic infection.

(SG) condensed phase 2a (9 decks)

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