Biochemical Disorders of Bone Flashcards
Biochemical Disorders
Osteoporosis
osteomalacia
hyperparathyroidism
Paget’s disease of bone
Osteoporosis
Qualitative defect in bone
Bone mineral density less than 2.5 SD below the mean
Osteoporosis Characteristics
Increase bone porosity
Decreased bone mineral density
- normal bone quality just less of it
Osteoporosis Types
Post-menopausal Osteoporosis
Osteoporosis of old age
Post- menopausal Osteoporosis Aetiology
Increased osteoclastic response after the menopause
Decreased oestrogen
Post-menopausal osteoporosis risk factors
Early menopause Genetics Alcohol White caucasian Smoking Lack of exercise Poor diet
Post Menopausal Osteoporosis Fractures
Colle’s Fracture
- Fracture involving the distal radius where the fractured bone is bent backwards
- Can be responsible for carpal tunnel syndrome
Vertebral Insufficiency Fracture
Osteoporosis of Old Age Risk Factors
Females Genetics White Caucasian SMoking Alcohol Lack of exercise Poor diet Chronic disease Lack of sunlight
Osteoporosis of Old Age Fractures
Femoral Neck Fracture
Vertebral Fracture
Osteoporosis of Old Age can be secondary to:
Corticosteroids Alcohol Abuse Malnutrition Chronic Disease - Malignancy - CKD - Rheumatoid Arthritis
Endocrine Disorders
- Cushing’s
- Hyperthyroidism
Osteoporosis Complications
Increased fracture risk
Fragility of bone
Osteoporosis Diagnosis
DEXA bone scan
Normal serum calcium and phosphate
Osteoporosis Treatment
9
Calcium Supplements
Vitamin D
Biphosphonates
- Reduced osteoclast activity
- Best treatment option
- Alendronate, Risedronate, Etidronate
Desunomab
- Monoclonal Antibody
- Decreases osteoclast activity
Strontium
- Increased. osteoblast replication
- Decreases osteoclastic activity
Zoledronic Acid
- Once yearly IV biphosphonate
Raloxifene
- Oestrogen receptor modulator
- Risk off DVT
Hormone Replacement
Intranasal Calcitonin
- Increased risk of breast and endometrial cancer and DVT
- Not preferred
Osteomalacia
Qualitative defect in bone
Abnormal softening of bone due to deficient mineralisation of osteoid
Decrease phosphate and calcium
Osteomalacia Aetiology (6)
Insufficient Calcium
- Lack of intestinal uptake
- low dietary intake
- malnutrition
Deficiency or resistance to Vit. D
- Malabsorption
- lack of sunlight
Phosphate Deficiency
- Increased renal loss
- Refeeding syndrome
- Alcohol abuse
Long term anticonvulsant use
Chronic Kidney Disease
Inherited Disease
Osteomalacia Symptoms
Bone Pain
- Pelvis
- Spine
- Femur
Deformities from soft bones
Pathological fractures
Hypocalcaemia
- Paraesthesia
- Muscle cramps
- Irritability/ anxiety
- Fatigue
- Seizures
- Brittle nails
- Heart failure
Pseudofractures
Pseudofractures common sites
Pubic rami
Proximal femur
Ulna
Ribs
Looser Zones
- incomplete stress fractures that transverse across the bone
- Usually at right angle to associated cortex
Milkman Lines
Osteomalacia Biochemistry
Decrease phosphate
Decreased calcium
Increased ALp
Osteomalacia Treatment
Vitamin D therapy
Calcium Supplementation
Phosphate supplementation
hyperparathyroidism
Overactivity of parathyroid glands resulting in increased PTH
Hyperparathyroidism Aetiology
Primary
- Benign adenoma
- Hyperplasia
- Malignant neoplasm
Secondary
- Physiological overproduction of PTh as a result of hypocalcaemia (Hypocalcaemia as result of Vit. D deficiency, CKD)
- Decreased phosphate excretion and inactive activation of Vitamin D (can lead to osteomalacia, sclerosis of bone and calcification of soft tissues0
Tertiary
- Patients with secondary hyperparathyroidism who develop an adenoma
hyperparathyroidism Consequences
Hypercalcaemia
- Fatigue
- Depression
- Bone pain
- myalgia
- nausea
- thirst
- polyuria
- renal stones
- osteoporosis
Fragility fractures
Lytic lesions in bone: brown tumours (potential skeletal stabilisation may be required)
Hyperparathyroidism biochemistry
Increased PTH
Increased calcium
Normal/ low phosphate
Hyperparathyroidism Treatment
Removal of adenomatous gland
Treatment of underlying cause
-Vitamin D supplement
Treatment of hypercalcaemia
- Iv fluids
- biphosphonates
- calcitonin
Paget’s disease of Bone
Chronic disease of bone causing thickened, brittle and misshaped bone
Paget’s disease of Bone Aetiology
Viral infection with paramyxoviruses
Genetic defects
Paget’s disease of Bone epidemiology
Elderly
Paget’s disease of Bone pathophysiology (4)
- Potentially due to exaggerated Vitamin D response, there is increased osteoclast activity
- In response, osteoblasts become more active. to compensate
- New bone is formed yet fails to successfully remodel
- Resulting bone is thicker and more brittle
Paget’s disease of Bone- bones affected
Pelvis Femur Skull Tibia Ear Ossicles - Conductive deafness
Paget’s disease of Bone Consequences
Arthritis Pathological fractures Deformities Pain High output cardiac failure
Paget’s disease of Bone
Often asymptomatic
Paget’s disease of Bone Appearance on X-ray
Enlarged bone
thickened cortices
thickened and coarse trabeculae
Mixed areas of lysis and sclerosis
Paget’s disease of Bone biochemistry
Raised Alp
normal calcium
Normal phosphate
Paget’s disease of Bone treatment
Biphosphonates
Calcitonin
Joint replacement
Stabilisation of femoral fractures with long intramedullary nails
