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Specialities > Clinical Management of osteoporosis and other metabolic bone diseases > Flashcards

Clinical Management of osteoporosis and other metabolic bone diseases Flashcards

1
Q

3 main functions of bone

A

Reservoir of calcium + phosphate

Haemopoiesis
- cancellous bone marrow supplies body with erythrocytes, leucocytes + platelets

Protective + mechanical
- Supports body’s tissues, protects soft internal viscera, provide sites of attachment for muscles that effect body movement and locomotion

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2
Q

2 types of bone structure

A

woven (immature)

lamellar (mature)

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3
Q

describe woven bone structure

A

Rapidly formed – collagen fibres aligned randomly and have no lamellae
Bone weaker but more flexible than lamellar bone
Found in embryonic and neonatal skeleton
Found in metaphyseal regions growing bones (up to age 4) and in fracture callus

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4
Q

describe lamellar bone structure

A

Forms the structural component of cortical and cancellous bone
Osteoblasts lay down collagen matrix in thin layered sheets (lamellae)

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5
Q

2 types of lamellar bone

A

cortical and cancellous

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6
Q

describe cortical lamellar bone

A

Mechanical and protective functions
80% adult skeleton
Found in diaphysis
Haversian system (osteon)

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7
Q

describe cancellous lamellar bone

A

Metabolic regulation of calcium
Found in metaphysis and epiphysis
No Haversian system - less strong than cortical bone

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8
Q

role of osteoblasts

A

baby bone cells
building blocks
Bone forming cells derived from undifferentiated mesenchymal stem cells in marrow
Produce osteoid (bone matrix) containing type 1 collagen

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9
Q

osteoclasts role

A

clean up cells
Found in marrow + circulating blood
Resorb bone

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10
Q

osteocyte role

A

cycle of bone
Osteoblasts that become entrapped by calcified bone matrix
90% bone cell population
Important in controlling calcium + phosphate

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11
Q

3 fates of osteoblasts

A

Become inactive bone lining cells
Surround themselves with matrix and become osteocytes
Disappear (apoptosis)

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12
Q

factors involved in bone remodelling

A 
Vitamin D
Nutrition
Physical activity
Age, hormones
PTH
IL1, TNF,TGF-β
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13
Q

why does bone remodelling occur

A

Allows bone to respond to loads (stresses)
Maintain materials properties
Allows repair of microdamage
Participates in serum Ca2+ regulation

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14
Q

what does bone remodelling involve

A

Cellular activation
Osteoblasts and osteoclasts are continuously recruited
Recruitment occurs at the “cutting” edge
Resorption
Osteoclasts active for ~12 days and then die
Causes release of IGF, FGF, etc., which recruits osteoblasts
Formation and Mineralization
Osteoid is formed by osteoblasts
Mineralization begins ~13 days later (1um/day)
Rate is same as osteoid formation
Mineralization continues after eroded volume filled in

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15
Q

what is ca important for

A

nerve, muscle, hormone function, clotting

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16
Q

absorption of calcium

A

Calcium absorbed from duodenum via active transport (regulated by 1,25-dihydroxycholecalciferol) and via passive diffusion from jejunum

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17
Q

2 roles of vit D in bone metabolism

A

Enhance calcium + phosphate absorption across small intestine
- Enhance osteoclastic resorption from bone

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18
Q

describe the activation process of vitamin D

A

UV light on skin transforms 7-dehydrocholesterol to cholecalciferol (vit D3)
Vit D3 subsequently hydroxylated in liver to inactive 25-hydroxycholecalciferol [25(OH)-Vitamin D3]
Further hydroxylation of 25-hydroxycholecalciferol in the kidney (PCT) to active 1,25-dihydroxycholecalciferol [1,25 (OH)2 vitamin D3]

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19
Q

what activates vitamin D

A

Activation in response to raised levels of PTH or decreased levels of serum calcium or phosphate

Decreased PTH levels or raised calcium or phosphate causes conversion of active form Vit D3 to inactive Vit D3

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20
Q

what cells secrete PTH

A

chief cells

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21
Q

what causes secretion of PTH

A

Secreted by chief cells of 4 parathyroid glands in response to extracellular calcium via calcium-sensing receptor
Secreted in response to decreased serum calcium + phosphate

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22
Q

what inhibits PTH release

A

Production inhibited by elevated serum calcium or (active) Vit D3

23
Q

effects of PTH

A

Kidney
Stimulation of hydroxylation of 25(OH)-vitamin D3
Increasing reabsorption of filtered calcium in kidney
Promotes urinary excretion of phosphate from kidney

Bone
Stimulation osteoclasts and precursors–> bone resorption

OVERALL
Serum calcium levels increased
Phosphate levels decreased

24
Q

what secretes calcitonin?

A

parafollicular C-cells of thyroid gland

25
Q

what stimulates calcitonin release

A

elevated serum calcium

26
Q

what inhibits calcitonin release

A

Inhibited by decreased serum calcium

27
Q

effect of calcitonin

A

Directly inhibits osteoclasts (have calcitonin receptors) causing transient decrease in serum calcium

28
Q

role of oestrogen in bone metabolism

A

Inhibits bone resorption (so prevents bone loss)

Also inhibits bone formation (so does not increase bone density)

29
Q

what is osteoporosis

A

Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture

30
Q

signs and symptoms of osteoporosis

A

Asymptomatic

Fragility fractures
Chronic pain
Deformity (kyphosis)
Impaired mobility

31
Q

risk factors for osteoporosis

A 
Non-modifiable
Sex (female)
Age
Ethnicity
Genetics
Early menopause
Small stature
(Potentially )Modifiable
Alcohol
Vit D deficiency
Smoking
Malnutrition
Inactivity
Heavy metals
PPIs
Medical conditions
Hypogonadal states
Menopause, amenorrhoea, Turner syndrome…
Endocrine disorders
Cushing’s, ↑PTH, ↑T4, ↓T4
Malabsorption
Coeliac, Crohn’s, UC, CF, short gut…
Rheumatological conditions
RA, Ank Spond, SLE…
Renal insufficiency
Haematological diseases
MM, lymphoma, leukaemia…
Inherited disorders
Medications - Steroids, Phenytoin, Anticoagulants (warfarin, heparin) PPIs
32
Q

pathophysiology of osteoporosis

A 
Low peak bone mass
Genetics (>20 genes)
Oestrogen
Environment factors
Excessive bone resorption
Inadequate bone formation

Bone formation < Bone resorption

33
Q

diagnosis of osteoporosis

A

Bone Mineral Density (BMD)
The difference between your measurement and that of a young healthy adult is known as a T score

Thedifference between your measurement and that of someone of the same age is known as a Z score

N: T >-1.0
osteopenia -2.5

34
Q

3 types of osteoporosis

A

1: postmenopausal- loss of trabecular bone
2: senile- loss of corticol and trabecular bone
3: secondary- loss of corticol and trabecular bone

35
Q

mechanisms for falls

A 
Intrinsic factors
CVS
Neuromuscular
Visual acuity
Locomotor
Alcohol

Extrinsic factors
Lighting
Flooring

36
Q

common fracture sites in osteoporosis

A

vertebra
hip
distal radius

37
Q

clinical signs and symptoms of vertebral fractures

A

Signs

  • Kyphosis
  • Loss of height
  • Tummy bulges due to loss of space under the ribs

Symptoms

  • neck becomes weak and head falls forward
  • pain in whole or part of back
  • breathing difficulties
  • indigestion and GORD
  • stress incontinence
  • difficulty with mobility
38
Q

classification of osteoporosis

A

Primary
Post menopausal
Idiopathic osteoporosis in men
Osteoporosis in older people

Secondary
Disease e.g. rheumatoid arthritis, organ Tx
Iatrogenic e.g. steroids

39
Q

Ix for osteoporosis

A 
Full blood count
Biochemistry
Myeloma screen
Gonadal function
Vitamin D and PTH 
Bone density measurements
40
Q

indications for referral for bone densitometry

A

Low trauma fracture (defined as a fracture which is either spontaneous or following a fall from the upright position)

Osteopenia or vertebral fractures on X-ray
Steroid therapy
Early menopause
Secondary causes of osteoporosis
Strong family history of osteoporosis
41
Q

Mx of high risk osteopenia

A 
Offer DEXA (rpt ~2 years)
Bone-sparing drug tx if T-score
42
Q

Mx for low risk osteopenia

A

Lifestyle advice, review <5 years

43
Q

drugs for treatment of osteoporosis

A

Antiresorptive drugs

  • Hormone replacement therapy
  • Selective oestrogen receptor modulators
  • Bisphosphonates

Bone formation drugs
-Teriparatide

Calcium & Vitamin D (All patients with osteoporosis)

44
Q

define osteomalacia

A

‘A metabolic bone disease wheredefective mineralizationresults in alarge amount or unmineralized osteoid’
Qualitativedefect as opposed to a quantative defect like osteoporosis
Rickets and osteomalacia are manifestations of the same pathologic process

45
Q

causes of nutritional osteomalacia

A

Vitamin D deficiency

  • Lack of adequate sunlight
  • Low intake of vitamin D
  • GI diseases

Calcium deficiency
-Dietary

Phosphate deficiency

  • TPN
  • Chronic phosphate binder therapy
46
Q

RFs for osteomalacia

A 
vitamin-D deficient diets
malabsorption e.g. celiac disease
renal osteodystrophy
hypophosphatemia
chronic alcoholism
tumors (tumor-induced osteomalacia)   
drugs
47
Q

clinical features of osteomalacia

A 
Bone pain
Proximal weakness
Symptoms from hypocalcaemia
Deformity 
Fracture
48
Q

Ix for osteomalacia

A 
Low Ca
Low Phosphate
Low vitamin D
Raised PTH
X-ray / bone scan abnormalties
Investigation for underlying abnormalities

Radiograph findings
Looser’s zones (insufficiency fractures)
medial femoral cortex
pubic ramus
scapula
fractures (especially in the proximal femur/femoral neck)

Bone scan: increased activity

49
Q

treatment for osteomalacia

A

Underlying cause Eg coeliacs disease

Vitamin D supplements

  • Oral Vitamin D3
  • Oral 1,25 Vitamin D
  • Intramuscular vitamin D3
50
Q

what is Paget’s disease

A

A condition ofabnormal bone remodelling
excessivebone resorption and abnormal new bone formation
Disease of osteoclasts
Osteoclasts show abnormal morphology and are increased in number
Focal areas of increased and disorganised bone turnover
Focal bone is common

51
Q

clinical features of Paget’s disease

A 
Frequently asymptomatic
Orthopaedic manifestations
Pain  (e.g. stress #, increased vascularity)
Deformity
Osteoarthritis
Fracture
Neurological symptoms
Sarcomatous transformation
less than 1% will develop malignantPaget's sarcoma(secondary sarcoma)
Cardiac failure
52
Q

Ix for Paget’s disease

A

Markers of bone turnover

  • Alkaline phosphatase (serum)
  • Collagen cross-link (urine)
X-rays
-coarsened trabeculaewhich 
give the bone ablastic appearance
-remodeled cortices
-Long bone bowing

Isotope bone scans

Bone biopsy

53
Q

Ddx for Paget’s disease

A 
Raised alkaline phosphatase
Metastatic bone disease
Osteomalacia
Hyperparathyroidism
Liver disease
Similar radiographic appearance
Metastatic disease
Lymphoma
Fibrous dysplasia
Chronic osteomyelitis
54
Q

Tx for Paget’s disease

A

Conservative
physiotherapy, NSAIDS, oral analgesics

Medical
Bisphosphonates
-Drugs which promote osteoclast apoptosis
-Reduce bone turnover
-Reduce woven bone formation
-Increase lamellar bone formation
-Improves bone strength

Surgical
E.g. arthroplasty

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