W10 - Metabolic Bone Disease, Crystal Arthopathy, Sero-neg Arthritis Flashcards
Discuss the definition of osteoporosis
- low bone mass
- microarchitectural deterioration bone tissue
= bone fragility = fracture risk
*DXA bone scan =
Describe the investigations to confirm the diagnosis of osteoporosis as well as significant scoring methods used
DEXA scan = lifestyle interventions
- FRAX = risk assessment tool
- QFracture = prediction algorithm estimates the 10 year absolute risk of osteoporotic fractures and hip fractures in men and women
Discuss the types of drugs used to prevent and treat osteoporosis
(1)
* >BISPHOSPHONATES *
advise good dental health
*drug holiday for 1-2yrs after 10yr use
!oesophagitis; uveitis; CI in CKD, femoral #
> DENOSUMAB MAb against RANKL = ⇩osteoclastic resorption *6mos subcut injection * preferred for renal impairment Pts !hypocalcaemia risk, allergic rash
>Teriparatide (PTH) !rare hypercalcaemia; allergy; COST ----- >Hormone replacement Rx !blood clots ! breast ca risk ! cvd risk
> RALOXIFENE (oestrogen R modulator)
- nil effect on nonvertebral #
- hot flushes, clotting risk, lack of protection at hip site
Associations with Osteoporosis
Endocrine Causes:
Thyroid+++;
Parathyroid(-) and (+)
Cushings
Rheumatic:
RA
Ankylosing Spondylitis
Polymyalgia Rheumatica
GI:
UC & CD
Liver disease
Malabs
Medications:
Steroids, PPI, antiepileptics, warfarin
VitaminD & Calcium Metabolism
The liver converts vitamin D to 25OHD.
The kidney converts 25OHD to 1,25(OH)2D and 24,25(OH)2D.
The liver is the main source for 25-hydroxylation, and the kidney is the main source for 1α-hydroxylation.
*Vit D stimulates calcium and phosphate abs from gut thus allowing their availability for bone mineralisation
Discuss the pathogenesis of osteomalacia
Vit D, Calcium Deficiency = Rickets (Child) / Osteomalacia (Adult)
Discuss the investigations to confirm the diagnosis of osteomalacia
Bloods for vitamin D metabolites, and calcium metabolism
Bone scan
Bone biopsy
Describe the clinical features of osteomalacia and rickets
- wide bones, odd legs, curved out legs
- odd curve to back
bone pain and muscle weakness. The dull, aching pain commonly affects the lower back, pelvis, hips, legs and ribs.
-worse at night or when you put pressure on the bones. –rarely relieved completely by rest.
Describe the biochemical and radiological abnormalities found in osteomalacia
*BMD: bone scan
- high alkaline phosphatase; parathyroid hormone
- low 25-hydroxyvitamin D and calcium and/or low phosphate
- Looser’s Zone Fractures
- Bone biopsy
Discuss the differential diagnoses of osteomalacia with other metabolic disease, including Paget’s disease
Osteomalacia must be differentiated from other diseases that cause lowering bone mineral density (BMD), such as osteoporosis, scurvy, osteogenesis imperfecta, multiple myeloma, and homocysteinuria.
Discuss the principles of prevention and treatment of osteomalacia
> Lifestyle: dietary suppl.
>
Describe the epidemiology and etiology of Paget’s Disease
- Genetic familial component; anglo-saxon origin
- environmental trigger = infective trigger within osteoclast
- > 40yo
Discuss the clinical features of Paget’s disease
Abn bone turnover and remodelling = disorganised bone = risk of deform and #
Presents with bone pain, deform., excessive heat or neurological complications (hearing loss); rarely osteosarcoma
Discuss the investigations to confirm the diagnosis of Paget’s disease and how the results may differ from other metabolic bone disease
Isolated elevation of serum alkaline phosphatase
Discuss the principles of management of Paget’s disease
Skull = Sx intervention
> Intravenous Bisphosphonate therapy
One off zoledronic acid infusion
Crystal Arthropathy Presentation and associated deposits
GOUT = Monosodium urate = Tophi (swolleen bulbous growths)
PSEUDOGOUT = CPPD
= chrondrocalcinosis
= pyrophosphate crystals
CALCIFIC PERIARTHRITIS = BCP
*deposition within joints and peri-articular tissue
Polymyalgia Rheumatica Presentation
Inflamm. condition of the elderly
Polymyalgia Rheumatica > GCA > High ESR, Anaemia
* cycle
- SUDDEN shoulder/pelvic girdle stiffness
- > 70y, F>M, ESR ~100
- Anemia
- Malaise, Wt. loss, fever, depression
Why hyper/hypo uricaemia may occur
(+) malignancy: lymphoproliferative, tumour lysis syndrome severe exfoliative psoriasis drugs: ethanol, cytotox. HGPRT deficiency
(-) Renal impairment HT Thyroid(-) Drugs: alcohol, low dose aspirin, diuretics, cyclosporin Exercise, starvation, dehydration
*endogenous uric acid via purine degradation contributes to 2/3 of body urate pool with rest dietary. Normally then excreted via kidney.
Management of Gout
Dx:
Joint fluid microscopy and culture
Serum uric acid (SUA) (4-6w after acute attack)
Joint X-ray
Acute Mgmt:
> NSAIDs
+PPI?
> COLCHICINE
> STEROIDS
Management of Hyperuricaemia
prophylaxis - lowering uric acid: ensure acute attack settled before reduction attempts
> ALLOPURINOL = consider eGFR
CANAKINUMAB = sfx
+ COLCHICINE
In particular it is important to advise the use of urate-lowering therapy to people with:
Two or more attacks of acute gout in 12 months.
Tophi.
Chronic gouty arthritis.
Joint damage.
Renal impairment (eGFR less than 60 ml/min).
A history of urinary stones.
Diuretic use.
Young age of onset of primary gout.
Polymyalgia Rheumatica Associations
Giant Cell Arteritis; immune complex deposits
Management of Pollymyalgia Rheumatica
Dx:
Hx as well as STEROID RESPONSE
> Pred./day; 18-24mos course
Bone prophylaxis
Lesch Nyan Syndrome
HGPRT deficiency, X-linked recessive
*HGPRT plays aa role in recycling of purine bases into purine
= purine synthesis accelerated
Mgmt of Pseudogout
> NSAIDs
Steroids
nil prophylaxis d/t idiopathic nature
