Musculoskeletal Flashcards
What is Osteomyelitis
Inflammatory condition of the bone caused by an infective organism, most commonlyStaphylococcus aureus (except in SCA patients → salmonella species more common
Usually involves a single bone, may occur in the peripheral or axial skeleton
What is Haematogenous Osteomyelitis
Results from bactaraemia and is usually monomicrobial
- Most common form in children
- Vertebral osteomyelitis → most common form of haematogenous osteomyelitis in adults
- Risk Factors: sickle cell anaemia, IV drug use, immunosuppression, infective endocarditis
What is Non-Haematogenous Osteomyelitis
Results from contagious spread of infection from adjacent soft tissues to the bone or from direct injury/trauma to bone
- Poly microbial, most common form in adults - Risk Factors → diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease
What are the Risk Factors of Osteomyelitis
previous osteomyelitis, penetrating injury, IV drug misuse, diabetes, HIV infection, recent surgery, distant or local infections, sickle cell anaemia
What are clinical features of Osteomyelitis
Limp or Reluctance to weight-bear→ common presentation fo acute osteomyelitis in children
- Non-specific Pain at site of infection
- Malaise, Fatigue, Fever, Chills
- Local inflammation, tenderness, erythema, or swelling
- Local Back Pain with systemic symptoms → native vertebral osteomyelitis
What Investigations are needed for Osteomyelitis
Bone MRI→ most definitive imaging modality
Bone Biopsy→ Gold Standard before administering antibiotics. Identification of infection and the causative microorganism, so appropriate treatment
Blood Culture → may be positive, indicating the infective organism
WCC, ESR & CRP → raised
What treatments are needed for Osteomyelitis (name antibiotic)
Antibiotic Therapy →flucloxacillin (IV)
- Abx treatment for 2-4 wks
- If Penicillin Allergic → clindamycin
Example causes of Primary Osteoporosis
postmenopausal osteoporosis (decreased oestrogen leads to increased bone resorption due to increased osteoclast activity)
senile osteoporosis (gradual loss of bone mass as patients age)
rheumatoid arthritis
Example causes of Secondary Osteoporosis
drug induced (long term corticosteroid therapy, or anticonvulsants, anticoagulants, PPIs), hypogonadism, hyperthyroidism, Cushings syndrome, immobilisation, hyperparathyroidism
Osteoporosis vs Osteomalacia
Loss of bone density vs Loss of Bone mineral
DEXA scan vs Blood Vit D and serum calcium
DEXA scan value for Osteoporosis?
DEXA → T-score ≤-2.5 indicates osteoporosis. (Osteopenia = -1 to -2.5)
What is the management plan for Osteoporosis?
Bisphosphonates (Alendronate) → inhibit osteoclasts leading to reduced bone resorption. If patients can’t tolerate alendronate (due to upper GI side effects), give risedronate.
Denosumab→ 2nd line treatment for postmenopausal women with osteoporosis
Calcium and Vitamin D supplementation (Ergocalciferol)
Teriparatide→ PTH analogue
Avoid or minimise use of glucocorticoids
What are the main side effects of Bisphosphonates and what else can they be used for?
Have side effect of dyspepsia and reflux due to oesophageal reactions (oesophagitis).
Can also cause osteonecrosis of the jaw
Can also be used for hypercalcaemia, Pagets disease and pain from bone metastases
What are the main clinical features of temporal arteritis?
unilateral vision loss, headache, jaw claudication (pain when chewing), scalp tenderness
Tender, palpable temporal artery
What is the main aetiology for Polymyalgia Rheumatica?
Aetiology → genetic predisposition + association with giant cell arteritis
What is the main differentiating factor regarding Polymyalgia Rheumatica (steroid related)?
Rapid response to Steroids
What is the management plan for Polymyalgia Rheumatica?
- 1st Line →Corticosteroids (Prednisolone)
If patients don’t respond to steroids, alterative diagnosis should be considered. Increase dose if treatment-resistance or relapse.
What is the investigation and management plan for Temporal Arteritis?
- Ix ⇒ raised ESR (first investigation). Temporal artery biopsy should be done (may show skip lesions).
- Tx ⇒ high dose steroids (prednisolone - given before biopsy done) and urgent Opthalmology review (same day)
No visual loss = high dose oral prednisolone. Vision loss = IV methylprednisolone.
What 2 types of infection tend to cause Reactive Arthritis
gastrointestinal or urinary tract infection
What are the main clinical features of Reactive Arthritis?
Arthritis → clinical symptoms develop 1-4 weeks after onset of infection. Usually larger joints in lower extremity.
Inflammation leads to painful, swollen, warm, red and stiff joints (normal ROM unlike septic), especially in morning.
Swelling of digits. May also get lower back pain.
Conjunctivitis or Uveitis
Symptoms from preceding infection → diarrhoea, dysuria, urethritis
What constitutes as a Seronegative Spondyloarthropathy?
negative for rheumatoid factor and has a strong genetic association with HLA-B27
What is the management plan for Reactive Arthritis?
- First Line → NSAIDs (Naproxen, Ibruprofen, Diclofenac)
- If NSAIDs don’t work → Corticosteroids (Prednisolone)
- Chronic Cases (refractory to both NSAIDs and corticosteroids) → DMARDs (Sulfasalazine)
Key differences Septic Vs Reactive Arthritis
Reactive is Sterile
Reactive the ROM is preserved
What is the management plan for Septic Arthritis?
Joint Drainage→ therapeutic arthrocentesis
IV Antibiotics which cover gram-positive cocci → flucloxacillin (or clindamycin if penicillin allergic)
- Course should be taken for at least 4-6 weeks
What is SLE?
Multisystem autoimmune disease that predominantly affects women of childbearing age
- Type 3 hypersensitivity reaction
- F>M (9:1), onset usually at 20-40 yrs old, more common in Afro-Caribbeans
- Aetiology → genetic predisposition (HLA-DR2 and HLA-DR3), hormonal factors (hyperoestrogenic states), environmental factors (cigarette smoking)
What syndrome is SLE associated with?
Associated with Anti-Phospholipid Syndrome →
increased risk of thrombus formation (recurrent PEs and DVTs) and recurrent miscarriages.
Prolonged APTT (paradoxical) and low platelets (thrombocytopenia).
Associated with anti-cardiolipin antibodies.
How is Anti-Phospholipid Syndrome managed?
1st Line Managed with warfarin (after inital thromboembolic event - avoid warfarin in pregnant women).
if contraindicated- LMWH or aspirin
What are the main clinical features of SLE?
- Malar (Butterfly) Rash
- Photosensitive Rash → rash occurs after sun exposure. Can be painful and pruritic and usually lasts a few days, healing without scarring
- Joints → arthritis and arthralgia. Distal symmetrical polyarthritis.
- Oral Ulcers
- Constitutional Symptoms → fatigue, fever, weight loss
- Raynaud’s Phenomenon → colour changes of the digits induced by cold (white → blue → red)
- CVS → pericarditis (and pleural effusion) or myocarditis
What are the investigations for SLE?
-
Antinuclear Antibody (ANA) → very sensitive, however may be positive in many other conditions so low specificity (hence useful as a ruleout test)
- ANA is very unspecific antibody
- Anti-dsDNA → highly specific for SLE, less sensitive
- ESR → elevated (CRP often normal, may be high if patient has infection)
- Decreased Complement Levels (C3/C4)
- Urinalysis (urine dipstick) → check for proteinuria and renal involvement
What is the management plan for SLE?
- 1st Line → Hydroxychloroquine
- Requires visual acuity testing as can lead to severe and permanent visual loss. Baseline ophthalmological examinationand annual screening is generally recommened. Safe for use in pregnancy.
- General → NSAIDs, avoid smoking and UV light
- Topical Steroids for skin manifestations
