MSK/ Rheumatology/ Orthopaedic Surgery Flashcards
Outline DDX for acute back pain.
IV DISC = degeneration, herniation
MUSCLE = strain, sprain
ARTHRITIS = OA, RA, ankylosing spondylitis
OSTEOPOROSIS/ FRACTURE
CANCER = primary, metastatic
INFECTION = septic arthritis, osteomyelitis, abscess (epidural, paraspinal)
VISCERAL =
AAA
Renal
GIT = pancreatitis, gallbladder, perforation
Endometriosis, PID
List red flags for acute back pain.
VITAL SIGNS = abnormal SYSTEMIC FX = fevers, chills, night sweats, unintentional weight loss PATIENT FX = age > 50 years PRESENTING COMPLAINT FX = Worse with rest or lying down Night pain, esp. waking from sleep assoc. with bladder/bowel dysfunction PMH/PSH = Cancer Immunosuppression Osteoporosis Significant major trauma IVDU Current bacterial infection MEDS/ALLERGIES: corticosteroids
Outline treatment of acute low back pain w/o red flag features.
Conservative management.
EDUCATION = will likely resolve within 4 wks with conservative management, investigations are not required.
BE AS ACTIVE AS POSSIBLE
HEAT
SIMPLE ANALGESIA = paracetamol +/- NSAIDs
PHYSIO may be beneficial
What is the aetiology of osteoporosis?
(1) Failure to attain normal peak bone mass.
- genetic causes: e.g. gene polymorphisms - RANKL, oestrogen receptor, IGF1
- environmental: calcium deficiency, immobility, growth hormone deficiency
(2) Uncoupling of bone resorption and bone formation.
- Lack of oestrogen (post-menopausal) –> increased RANKL expression –> increased osteoclasts (increased differentiation, activity and longer lifespan) and decreased osteoblasts.
- Secondary causes:
Endocrine: Cushing, hyperparathyroidism, hyperthyroidism
GIT: coeliac, IBD
Chronic disease
Deficiencies: vitamin D, calcium
Drugs: corticosteroids, aromatase inhibitors, anti-androgen therapy in men (e.g. for tx of prostate ca)
What are the pathologic features of osteoporosis?
Loss of bone mass
Loss of trabeculae
What are the indications for DEXA?
- all women 65+ years
- post-menopausal women <65 with risk factors for fracture
- history of fragility fracture
- starting corticosteroids
Explain your approach to treatment of osteoporosis.
(1) LIFESTYLE:
- weight-bearing exercise
- calcium and vitamin D supplementation if dietary intake not sufficient (daily intake 800 IU vit D and 1g calcium).
- smoking cessation
- healthy body weight
- healthy alcohol intake
- reduce risk of falls: correct vision, balance disorders, medication reconciliation (prevent polypharmacy, sedating drugs etc.), OT to address trip hazards etc.
(2) MEDICATION: bisphosphonates, denosumab, teriparatide
Begin pharmacotherapy if T score of -2.5 or osteopenia with high risk of fracture (using FRAX calculator)
BISPHOSPHONATES
Alendronate, risendronate are oral
Zolendronic acid is IV
MOA: synthetic analogue of pyrophosphate –> incorporated into bone –> inhibition of osteoclasts
USE: Treatment of osteoporosis & fracture prevention; hypercalcemia
Risendronate,
PRECAUTIONS:
Osteonecrosis of jaw - dental assessment and procedures before starting bisphosphonate.
UE:
GIT: N&V, oesophagitis/gastritis, erosions and ulcers
Bone pain
Atypical femoral fracture
Flu-like symptoms for 1-2 days after IV bisphosphonates.
MONITOR: CMP
Ensure adequate calcium and Vit D intake.
TERIPARATIDE
MOA: teriparatide is a PTH analogue –> promotes bone formation by increasing osteoblast activity (only anabolic therapy for osteoporosis)
USES: osteoporosis
CI: hyperparathyroidism, hypercalcaemia
Given SC daily
Lifetime max use of 24 months due to risk of osteosarcoma.
Monitor CMP
Ensure adequate calcium and vit D intake.
DENOSUMAB (PROLIA)
MOA: antibody to RANKL –> binds to RANKL –> prevent activation of RANK –> decreased osteoclast formation and activity.
USE: osteoporosis, hypercalcemia
Given SC every 6 months. Must not miss dose –> increased fracture risk.
Monitor CMP.
Ensure adequate calcium and vit D intake. CI if hypocalcaemic as can decrease serum calcium further.
Explain the pathophysiology of rickets and osteomalacia.
Defect in mineralisation of bone.
If occurring in childhood –> rickets
If occurring after epiphyseal plate closure –> osteomalacia.
Occurs due to:
VITAMIN D DEFICIENCY = the MOST COMMON cause of osteomalacia
(1) Decreased sunlight exposure –>
- sunscreen
- skin covered by clothing/veil etc.
- dark skin pigmentation
- insufficient time outdoors
(2) Insufficient activation of vitamin D –>
- CKD
- anticonvulsants affect production of vitamin D (affect the production of 25-hydroxy-vitamin D in the liver)
(3) Inadequate dietary intake of vit D
INADEQUATE CALCIUM OR PHOSPHATE INTAKE
(1) Inadequate dietary intake of Ca or PO4
(2) Malabsorption - e.g. CF, coeliac disease
(3) Paraneoplastic syndrome - tumour producing FGF-23
Compare and contrast CMP, vit D, ALP and PTH levels in osteoporosis, osteomalacia/rickets and Paget’s disease.
OSTEOPOROSIS: usually normal
OSTEOMALCIA/RICKETS: low Ca and low PO4, low vit D, high ALP, high PTH
PAGET’s DISEASE: high ALP, otherwise normal.
What are the main causes of raised ALP?
Alkaline phosphatase elevation is most commonly caused by LIVER or BONE disease.
LIVER = mainly cholestasis
BONE = increased bone formation - primarily Paget’s disease (can be raised by metabolic bone disease e.g. osteomalacia, osteoporosis, and bone tumours)
Outline the metabolism of vitamin D.
7-dehydro-cholesterol in skin –> converted into pre-vitamin D by UVB light –>
OR dietary vitamin D (mainly dairy, also eggs, fish, fortified cereals)
–>
in the liver are converted by 25-hydroxy-vitamin D –> in the kidney the enzyme 1-alpha-hydroxylase produces 1,25-hydroxy-vitamin D.
What factors affect the activity of 1-alpha-hydroxylase in the kidney?
PTH and low phosphate –> increase enzyme activity
FGF-23, calcium and vitamin D –> decrease enzyme activity
