MSK/ Rheumatology/ Orthopaedic Surgery Flashcards
(36 cards)
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
What are the functions of vitamin D?
GIT –> increase calcium and phosphate absorption.
KIDNEY –> increase calcium reabsorption + increase phosphate excretion in urine
BONE –> complex actions, stimulates osteoclasts (by stimulating production of RANKL by osteoblasts) + provides calcium for mineralisation.
Explain the cause and risk factors of gout.
HYPERURICAEMIA
Uric acid is an end product of purine metabolism
Can occur due to: 1. INCREASED URIC ACID PRODUCTION - High cell turnover: Tumour lysis syndrome Haemolytic anaemia Psoriasis - Diet rich in purines Red meat Seafood Beer
- DECREASED URIC ACID EXCRETION
Loop and thiazide diuretics
CKD - INBORN ERROR OF METABOLISM
When ECF becomes supersaturated with uric acid –> intra-articular uric crystal precipitation –> phagocytosis by neutrophils –> release of inflammatory mediators –> acute joint inflammation.
An acute attack can be triggered by:
Sudden increase in uric acid - e.g. large meal
Physiological stress - e.g. trauma, surgery
Dehydration
Repeat attacks can lead to tophi - commonly deposited in bone (elbows, knees) and soft tissues (pinna of ear, Achilles tendon sheath)
How would you diagnose gout?
Presumptive diagnosis is made clinically.
Serum uric acid often elevated, but not diagnostic (can be normal in acute gout, and can be elevated w/o gout).
Raised WBC and ESR are typically elevated
Definitive diagnosis is by aspiration of joint fluid.
Shows NEGATIVELY birefringent,
NEEDLE-SHAPED, MONOSODIUM URATE crystals. + Inflammation present (WBCs > 2000/uL and >50% neutrophils) w/ NEGATIVE gram stain and culture
Imaging:
- Not used for dx of acute attacks - does not exclude septic arthritis, but can be supportive if synovial fluid analysis CI
- Shows: BONE EROSION with SCLEROTIC RIM and OVERHANDING EDGE - i.e. PUNCHED OUT.
Joint space is preserved.
DDX of acute monoarticular joint inflammation.
Septic arthritis Gout Pseudogout Trauma Bursitis Psoriatic arthritis
How would you treat gout?
- DRSABCD, VITALS, LOC, STABLE/UNSTABLE?
- Exclude septic arthritis/ trauma
- Treat acute attack:
LIFESTYLE: Rest and ice
PHARMACOLOGIC: NSAIDs, colchicine, corticosteroid (either systemic or intra-articular)
Most effective when started within first 24 hours.
–> these meds do not address hyperuricaemia - Treat recurrent gout to prevent further acute attacks and tophi (indicated when >2 attacks/year, presence of tophi, XR changes showing destructive joint disease, patient preference due to disabling attacks)
LIFESTYLE: limit purine intake, . limit alcohol intake, weight loss/ maintain healthy weight, increase fluid intake
PHARMACOLOGIC: need to lower urate –>
1ST line: Xanthine oxidase inhibitors –> prevent metabolism of xanthine to uric acid
- Allopurinol –> Allopurinol worsens an acute attack of gout!!! DO NOT USE WITHIN 2 WEEKS OF ACUTE FLAIR
- Febuxostat
2ND line: uricosurics –> inhibit uric acid reabsorption in proximal convoluted tubule –> enhance renal clearance of uric acid
- Probenecid
UE: uric acid kidney stones
COLCHICINE
MOA:
Bines to tubulin –> stabilises tubulin –> inhibits microtubule polymerization –> inhibits neutrophil function –> less phagocytosis of urate crystals –> reduced inflammation
USE: to treat acute attack of gout
UE:
GIT most common - diarrhoea, N&V, abdo pain
Narrow therapeutic window –> dose to treat gout is similar to dose that causes GI upset
What findings do you see on analysis of joint fluid in pseudogout?
Weakly POSTIIVELY birefringent RHOMBOID-shaped CALCIUM PYROPHOSPHATE DIHYDRATE crystals \+ inflammation (raised WBCs with >50% neutrophils) NEGATIVE gram stain and culture
How would you treat pseudogout?
- DRSABCD, VITALS, LOC, STABLE/UNSTABLE?
- Exclude septic arthritis/ trauma
- Treat acute attack (as for gout)
If monoarticular –> intraarticular steroid injection
If polyarticular –> NSAIDs, colchicine or systemic steroids
For recurrent acute attacks –>
- Prophylactic colchicine
- Treat any underling metabolic disease
For chronic ongoing symptoms –>
- Anti-inflammatory: NSAIDs, colchicine, low dose prednisone
- Analgesia: paracetamol
Explain the cause and risk factors of pseudogout.
AGE > 60 is the strongest factor.
Previous joint injury (unclear mechanism)
Underlying metabolic disease:
- Hyperparathyroidism
- Haemochromatosis
- Hypo-magnesium
–> if recurrent or chronic attacks of pseudogout, investigate for an underlying cause (CMP, iron studies)
These factors –> CPP crystals deposit into articular cartilage (chondrocalcinosis) –> crystals can enter joint space –> inflammation.