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Endocrinology - Renee > Metabolic Bone disorders > Flashcards

Metabolic Bone disorders Flashcards

1
Q

Role of Osteoclasts

A

Reabsorb bone
Do so by secreting H, CATK and TRAP
Secrete FGF 23

Develop from mononuclear cells

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2
Q

Role of Osteoblasts

A

Create new bone from osteoid –> mineralised bone

Develop from mesenchymal stem cells

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3
Q

Bone microstructure

A

Matrix of type 1 collagen 35%

Hydroxyapatite crystals 65%

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4
Q

Types of bone

A

Cortical bone:

  • Provides bone strength
  • Dense outer shell of bone
  • 80% of skeletal mass
  • slow turnover rate

Trabecular bone:

  • Provide Calcium and phosphate during times of stress
  • A sponge like network of delicate plates of bone
  • 20% of skeletal mass
  • High turnover rate
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5
Q

What is bone modelling?

A

Uncoupled osteoclast and osteoblast activity which results in bone growth

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6
Q

What is bone remodelling?

A

Mechanism of bone repair and allows for mineral homestasis

Bone goes from resting state –> resorption by osteoclasts –> osteoclasts apoptose and osteoblasts develop –> osteoid formation by osteoblasts –> mineralisation

Coupled osteoclast and osteoblast activity

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7
Q

What happens during osteoporosis?

A

Increased osteoclast numbers –> increased reabsorption of bone with incomplete new bone formation by osteoblasts

Results in thinning of bone and loss of connectivity in trabecular bone and porosity in cortical bone

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8
Q

Mediator of osteoclast formation, function and survivial?

A

RANK- Ligand

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9
Q

Decoy molecule which prevents RANK to RANK-L binding?

A

OPG - binds RANK-L –> cannot bind to RANK –> osteoclast apoptosis

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10
Q

What is Osteoporosis?

A

T score < - 2.5 OR minimal trauma fracture

A metabolic bone disease characterized by low bone mass and deterioration of bone architecture resulting in bone fragility and fracture

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11
Q

What is Z score used for?

A

Z score < - 2 = look for secondary causes of bone loss

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12
Q

Secondary causes of bone loss?

A 
Hypogonadism/menopause
Vitamin D deficiency
Hyperthyroidism
Hyperparathyroidism
Coeliac disease
Multiple myeloma
Corticosteroids
Chronic disease
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13
Q

Rates of osteoporosis?

A

60% of women and 30% of men aged 60yrs or older

People with fragility fractures 3-5% more likely to to have another fracture in the next year

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14
Q

PBS for treatment of OP?

A

T score < - 2.5 aged 70yrs or more OR

Previous low trauma fracture/vertebral fracture >50yrs

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15
Q

Special cases for PBS?

A

Corticosteroids - treat if T score < - 2

Aromatase inhibitors or androgen deprivation treatments = treat if BMD < - 2.5

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16
Q

Glucocorticoid-induced osteoporosis?

A

Bone loss in cancellous bone - rapid in the first year then slows

Fracture in 30-50% on long term Steroids

High risk:

  • > 7.5mg for more than 3 months
  • Age 60-80yrs
  • Underlying inflammatory disease
  • Previous fracture
17
Q

Non-pharm prevention of OP?

A

Falls prevention - vision, proprioception, quads strength, balance

18
Q

Calcium supplementation?

A

1300mg daily for OP patients recommended intake

Supplementation =500-600mg/day

Supplement when:

  • Dietary intake low
  • Taking OP meds
  • Steroids >7.5mg/day for >3/12
  • Elderly and housebound/in NH
19
Q

Vitamin D Supplementation?

A

1000-2000IU/day supplementation

Supplement when:

  • Housebound/NH
  • Work indoors/sun avoiders
  • Dark skin
  • Malabsorption
  • Biliary cirrhosis
  • Antiepileptics
20
Q

SERMs?

A

Selective esterogen receptor modulators

Tamoxifen and raloxifene

Non-hormonal but bind to oestrogen receptors –> anti-osteoclast action in bone

Helps prevent VERTEBRAL fractures only
Reduces rates of ER+ breast cancer

21
Q

Bisphosphonates?

A

Alendronate, Risedronate and Zoledronate

Bind to hydroxyapitate –> inhibits osteoclast activity and causes accelerated apoptosis

Reduce both vertebral and hip fractures

Zoledronate –> AF

22
Q

Denosumab?

A

RANK Ligand inhibitor

–> inhibits osteoclast formation, function and survival

Reduces vertebral and hip fractures

Can have rebound vertebral fractures on discontinuation –> transfer to another agent like bisphosphonates

23
Q

Rare side effects of Antiresorptives?

A

Osteonecrosis of the jaw:

  • Bisphosphonates and denosumab
  • Usually after 2yrs of treatment
  • Usually in the mandible
  • Treat with daily rinses and antibiotics –> surgery if not healed
  • Requires dental review prior to commencement of treatment

Atypical femoral fractures:

  • Bisphonates
  • Stress fractures in mid thigh
  • Usually have pain prior to fracture
  • Usually after 7yrs of treatment
  • TX –> stop bisphos and nail fixation
24
Q

Skeletal anabolics?

A

PTH

  • Gives as once daily injection –> stimulates new bone formation
  • Only can give 18 months of treatment –> PTH causes late stimulation of osteoclasts
25
Q

? LRP5 activation?

A

Sclerosteosis = high bone density due to LRP5 mutation

–> inactivation of sclerostin –> increased wnt signalling –> increased osteoblast proliferation

26
Q

Osteomalacia?

A

Deficiency of mineralised bone

High osteoid

27
Q

Presentation?

A

Bone pain
Fractures
Waddling gait

Elevated ALP
Check Ca, PO4, 25OHD, PTH
Urinary PO4

28
Q

Causes of Osteomalacia?

A

Vitamin D deficiency

Hypophosphataemia - fanconi or tumour induced

RENAL DISEASE:

  • FGF-23
  • Iron infusions
  • Phosphate leak - fanconis or tenofovir
29
Q

Role of FGF-23?

A

Secreted by osteoclasts

Results in increased urinary phosphate and low Vitamin D

30
Q

Hypophosphatasia?

A

Usually presents in childhood

Results in high phosphate loss in urine and low serum PO4 and Vitamin D
Low ALP on bloods

Rickets
Recurrent fractures and psuedofractures
Soft teeth
Chrondocalcinosis common

Treatment is PTH

31
Q

Paget’s disease?

A

Increased osteoclast activity –> increased and abnormal bone formation

Present with:

  • Bone pain
  • Bone deformity
  • OA
  • Fractures
  • HIGH ALP

Treat with bisphosphonates if pain or if bone growth is causing damage to critical structures

32
Q

Calcium metabolism

A

IN = INTESTINE + VITAMIN D
The active absorption of calcium from the gut is regulated by the calcitriol concentration in the blood.

OUT = KIDNEY + PHOSPHATE + PTH
Increased excretion by increased PO4 and low PTH

STORAGE = BONE
Calcium release from bone is regulated by PTH in conjunction with calcitriol under the influence of PTH.

33
Q

Vitamin D Metabolism

A

Calcitriol is a cholesterol derivative.

Under the influence of ultraviolet light on the skin, cholesterol is converted to previtamin D3 which spontaneously isomerizes to vitamin D3.

Under the influence of parathyroid hormone, the kidneys convert cholecalciferol into the active hormone, 1,25 dihydroxycholecalciferol.

34
Q

Causes of Hypercalcaemia?

A

PTH dependant:

  • Primary or tertiary hyperparathyroidism
  • Abnormal CaSR = familial hypocalcinuric hypercalcaemia

PTH independant:

  • CANCER - myeloma, PTHrP, bone metastasis, vitamin D
  • Excess vitamin D - sarcoidosis and granuloma disease
  • Milk-alkali syndrome
  • Endocrine disorders - Hyperthyroid, pheo, cortisol deficiency, VIPoma
  • IMMOBILISATION

Medications:

  • Li
  • Thiazide diuretics
  • Vitamin D
  • Ant-acids
35
Q

Primary Hyperparathyroidism

A

Mostly asymptomatic
High Ca and high PTH

–> increased bone loss by stimulation of osteoblasts

Results in fractures and kidney stones

–> parathyroidectomy as treatment if surgical candidate or bisphosphonates is not

REPLACE VITAMIN D
Ask about family history - ? MEN1

36
Q

What is romosozumab?

A

A monoclonal antibody against sclerostin

Sclerostin produced by osteocytes to decrease osteoblast proliferation
If blocked –> increased wnt signalling –> increased osteoblast proliferation

Endocrinology - Renee (7 decks)

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