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TOB > Session 7 > Flashcards

Session 7 Flashcards

0
Q

Describe the development of long bones by endochrondral ossification

A
  • Embryo 5-6 weeks: Cartilage models develops
  • Embryo 6-8 weeks: Collar of periosteal bone forms around the diaphysis (shaft) (intramembranous ossification)
  • Fetus 8-12 weeks: Central cartilage calcifies; nutrient artery penetrates which supplies bone-depositing osteogenic cells; primary ossification centre forms
  • Postnatal: Medulla becomes cancellous bone; cartilage forms the epiphyseal growth plates; secondary centres of ossification develop in the epiphyses
  • Prepubertal: Epiphyses ossify and growth plates continue to move apart which lengthens the bone
  • Mature adult: Epiphyseal growth plates replaced by bone; hyaline cartilage persists at edge of epiphyses
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1
Q

What is endochondral ossification?

A
  • Replacement of a pre-existing hyaline cartilage template by bone
  • Most bones of the body develop in the this way
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2
Q

What are the zones of the epiphyseal growth plate?

A
  • Zone of reserve cartilage
  • Zone of proliferation
  • Zone of hypertrophy
  • Zone of calcified cartilage
  • Zone of resorption
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3
Q

What is the zone of reserve cartilage?

A
  • No cellular proliferation or active matrix production
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4
Q

What is the zone of proliferation?

A
  • Cartilage cells divide and organise into distinct columns

- Cells enlarge and secrete matrix (collagen-mainly type II and XI, and other cartilage matrix proteins)

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5
Q

What is the zone of hypertrophy?

A
  • Cells enlarge greatly

- Matrix is compressed into linear bands between cell columns

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6
Q

What is the zone of calcified cartilage?

A
  • Enlarged cells begins to degenerate

- Matrix calcifies (initial scaffold for new bone)

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7
Q

What is the zone of resorption?

A
  • Calcified cartilage is in direct contact with the connective tissue of the
    marrow cavity
  • Small blood vessels and connective tissue invade the region previously occupied by dying chondrocytes
  • This leaves the calcified cartilage as spicules, onto which bone is laid down
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8
Q

What is intramembranous ossification?

A
  • Condensations of mesenchymal tissue, not the replacement of a pre-existing hyaline cartilage template
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9
Q

What bones develop by intramembranous ossification?

A
  • Flat bones:
    ~ Skull bones (eg parietal, occipital, temporal, frontal)
    ~ Maxilla
    ~ Mandible
    ~ Pelvis
    ~ Clavicle
  • Also contributes to thickening if long bones
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10
Q

How does intramembranous ossification occur?

A
  • Mineral deposits within trabeculae radiate from a central point (primary ossification centre)
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11
Q

What is osteogenesis imperfecta?

A
  • Autosomal dominant group of heritable disorders of connective tissue
  • Caused by mutations in the gene for type I collagen - abnormal collagen synthesis by osteoblasts and fibroblasts
  • Affects the skeleton, joints, ears, ligaments, teeth, sclerae and skin
  • Leads to ‘brittle bones’ - bone fragility which causes predisposition to fractures and deformity
  • Multiple fractures are usually present at/before birth and are often fatal
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12
Q

Where is growth hormone synthesised and stored?

A
  • Anterior pituitary gland
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13
Q

What are the effects of growth hormone on bones before puberty?

A
  • Excessive: Gigantism (promotion of epiphyseal growth plate)
  • Insufficient: Pituitary dwarfism (affects epiphyseal cartilage)
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14
Q

What are the effects of growth hormone on bone as an adult?

A
  • Excessive: cannot cause gigantism as there are no longer epiphyseal growth plates
  • Insufficient: Acromegaly (promotion of periosteal growth by increase in bone width)
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15
Q

What is the effect of sex hormones on bone?

A
  • Influence the development of ossification centres
  • Induce secondary sexual characteristics and pubertal growth spurt
  • Bone growth is retarded because of premature closure (fusion) of epiphyses as a result of precocious sexual maturity (can be caused by tumours producing sex hormone)
  • Prolonged bone growth and tall stature can result if epiphyseal growth plates persist later into life that normal because of sex hormone deficiency
16
Q

What is the effect of thyroid hormone on bone?

A
  • Thyroid hormone deficiency can lead to an infant with cretinism (permanent neurological/intellectual damage) and other abnormalities eg short stature
  • Effects of neonatal hypothyroidism can be reversed with prompt administration of thyroxine
17
Q

What is osteoporosis?

A
  • Metabolic bone disease where bone mass decreases so that it cannot provide adequate mechanical support
  • Incomplete filling of osteoclasts resorption bays
  • Osteoclasts activity is more than osteoblast activity
18
Q

What is the most common type of osteoporosis?

A
  • Primary osteoporosis
    ~ Type 1: occurs in postmenopausal women; caused by an increase in osteoclasts number (result of oestrogen withdrawal)
    ~ Type 2: occurs in the elderly of both sexes (senile osteoporosis) generally occurs after age 70; reflects attenuated osteoblasts function
19
Q

What are some osteoporosis risk factors?

A
  • Genetic: peak bone mass is higher in blacks that whites or Asians
  • Insufficient calcium intake: 800 mg/day is recommended for postmenopausal women
  • Insufficient calcium absorption and vitamin D: decreased renal activation of vitamin D with age (occurs in populations without vitamin D supplementation or elderly confined indoors)
  • Exercise: immobilisation of bone (eg prolonged bed rest/cast) leads to accelerated bone loss as physical activity is needed to maintain bone mass
  • Cigarette smoking: has been correlated with increased incidence of osteoporosis in women
20
Q

What is achondroplasia caused by?

A
  • Autosomal dominant point mutation in the fibroblast growth receptor-3 gene
21
Q

What does the mutation in the gene that causes achondroplasia do?

A
  • Decreased endochondral ossification
  • Inhibited proliferation of chondrocytes in growth plate cartilage
  • Decreased cellular hypertrophy
  • Decreased cartilage matrix production
22
Q

What is achondroplasia?

A
  • Short limb dwarfism
  • Have a normal intelligence and an average lifespan
  • Is heritable
23
Q

Where do we get Vitamin D from?

A
  • Dietary eg fish

- Synthesised by skin using UV ligh

24
Q

What happens to Vitamin D in the body and where?

A
  • Is hydroxylated in the liver

- Undergoes more hydroxylation in the kidney to form active 1,25-dihydroxyvitamion D3

25
Q

What does the hydroxylated, active form of vitamin D do?

A
  • Increase calcium absorption by the small bowel

- Promotes mineralisation of bone

26
Q

What is rickets?

A
  • A childhood disease where bones do not harden due to a deficiency of vitamin D
27
Q

What causes rickets?

A
  • Insufficient calcium deposition for adequate bone rigidity
  • Bones (especially long bones) become soft and malformed
  • Distortion of skull bone (leading to ‘bossing’)
  • Enlargement of costochondral junctions of ribs (rickety rosary)
28
Q

What osteomalacia?

A
  • Adult counterpart of rickets
  • Caused by significant calcium deficiency or a lack of vitamin D (eg because of poor diet, lack of sunshine, intestinal malabsorption, liver/kidney disease
29
Q

What are common symptoms of osteomalacia?

A
  • Bone pain
  • Back ache
  • Muscle weakness
30
Q

What happens to the bone in osteomalacia?

A
  • Trabeculae of cancellous bone have an abnormally large amount of non-mineralised bone (osteoid-uncalcified matrix secreted by osteoblasts) covering the trabecular surface
  • The trabeculae are weakened by insufficient mineralisation

TOB (12 decks)

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