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Physiology > Bone Objectives > Flashcards

Bone Objectives Flashcards

1
Q

Ectoderm

A

On the external surface of the embryo

- skin, adnexa, neural tissue

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2
Q

Mesoderm

A

Middle layer

- bone, muscle, and all connective tissues

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3
Q

Endoderm

A

Inner layer, is an outpocket of the pharynx

  • epithelial lining of GIT, associated ducts/glands, viscera
  • also lines pharynx, respiratory tract, urethra, bladder
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4
Q

Mesenchyme originates from which tissue layer?

A

Mesoderm

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5
Q

How does undifferentiated mesenchyme become organized and develop into a limb?

A

Mesoderm of left and right lateral body wall forms Wolff’s crest (cylindrical thickening) –> focal ectodermal thickenings occur over Wolff’s crest at sites of future limb placements = apical ectodermal ridge
- AER initiates and organizes limb bud formation and remains throughout limb development

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6
Q

_______ induces mesenchymal cells to condense to form a cartilage model for each bone of the developing limb

A

Apical ectodermal ridge

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7
Q

What is the difference in how bone and cartilage grow?

A

Bones only undergo appositional growth (new chondrocytes applied to existing structure), cartilage tissue grows by appositional growth and by interstitial growth (cartilage tissue expands within)

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8
Q

Long bone development

A

Condensation of mesenchyme to form cartilage model –> formation of perichondrium and invasion of nutrient artery –> degeneration of chondrocytes to form medullary cavity –> perichondrium becomes periosteum –> periosteum forms concentric layers of cortical bone in diaphysis –> vessels at joint capsule insertion invade epiphyseal area –> epiphyseal and metaphyseal physes form

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9
Q

Epiphyseal physis

A

3D growth of epiphysis by proliferation of chondrocytes followed by enchondral ossification to form epiphyseal cancellous and subchondral bone

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10
Q

Epiphyses

A

Ends of long bone

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11
Q

Diaphysis

A

Long compact shaft of the bone

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12
Q

Epiphyseal plate

A

Separates the epiphysis and diaphysis

- growth plate

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13
Q

Metaphysis

A

Transitional spongy bone that joins the diaphysis to the epiphyseal plate

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14
Q

Medullary space

A

Area of spongy bone in the middle of the diaphysis

- is not hollow, consists of bony spicules to provide space for bone marrow (cancellous bone)

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15
Q

Periosteum

A

Outside of bone covered by cells

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16
Q

Endosteum

A

Internal surfaces of bone trabeculae within the marrow cavity
- also lined with osteoprogenitor cells

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17
Q

Osteoblasts

A
  • line periosteal and endosteal surface
  • produce collagen-rich osteoid matrix that later mineralizes
  • main cells involved in ossification process
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18
Q

Osteoclasts

A
  • derived from mononuclear phagocyte cell line
  • fusion of cells to form multinucleated cell, responsible for dissolving bone matrix and collagen to allow reshaping of bone to accommodate stress
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19
Q

How does growth in length occur?

A

Osteoblasts differentiate –> layer of loosely organized collagen matrix is deposited –> new bone matrix calcifies –> osteoclasts move into the metaphysis to resorb the woven bone and calcified cartilage –> new osteoblasts form organized sheets of type 1 collagen
*cells of the zone of proliferation are advancing the growth plate away from the diaphysis, while the ostoblasts/clasts are converting primary woven bone to lamellar bone at the diaphyseal side of the growth plate

20
Q

How does growth in diameter occur?

A

Deposition of new bone on the outside by cells within the periosteum

  • bone resorption is key
  • deposition of new bone is accompanied by resorption of older bone at the interior edge of the shaft of the diaphysis
  • allows marrow cavity within the bone to expand
21
Q

Anatomy of a growth plate

A
  • zone of proliferation: chondrocytes furthest from the diaphysis
  • zone of maturation: chondrocytes are not dividing and are enlarged
  • zone of hypertrophy: hypertrophy and vacuolation of the chondrocytes
  • zone of calcified cartilage: cartilaginous matrix surrounding cells begins to calcify
22
Q

Process of endochondral ossification

A

Proliferating chondrocytes from inner mitotic layer mature to produce collagen and proteoglycan matrix –> mature chondrocytes hypertrophy –> hypertrophic chondrocytes form matrix vessicles and die –> hydroxyappetite crystals form at matrix vesicle sites calcifying the cartilage –> capillary loops with osteogenic mesenchyme invade tunnels formed by dying hypertrophic chondrocytes after cartilage calcifies –> osteoblasts layer woven bone on spicules of calcified cartilage = bony trabeculae –> osteoclasts remodel calcified cartilage spicules and bone trabeculae to produce cancellous bone

23
Q

What allows bone to bend and absorb concussion?

A

Trabecular plates (cancellous bone)

24
Q

What portion of bone is dense and strong?

A

Cortical bone of the diaphysis

- compact bone

25
Q

What strengthens the bone?

A

Osteons

26
Q

What 3 things generally result from decreased calcium?

A
  • limb deformity during growth
  • osteomalacia
  • Bran’s disease: big head, hyperparathyroidism (weak bones, lameness)
27
Q

What occurs as a result of inadequate Ca during growth?

A

Faulty endochondral ossification

  • poor calcification of cartilage in physis
  • delayed bone formation
  • wide unstable cartilage zone in physis
  • limb deviation
28
Q

What occurs as a result of inadequate Ca in diet of mature horses?

A

Bran disease
- osteoclasts reabsorb bone to maintain serum Ca level –> osteoblasts produce too much osteoid to compensate for lost bone –> osteoid fails to mineralize in low Ca conditions –> bone is fibrous and thickened

29
Q

Ca effect on the nervous system

A

Essential for nerve conduction by stabilizing voltage gated channels

  • decreased Ca leads to nerve cell hyperexcitablity with tetany (eclampsia), or paralysis in cows
  • too much calcium allows channels to become resistant to opening = nerve transmission stops
30
Q

Ca effect on the blood

A

Essential for blood clotting

  • decreased Ca leads to inadequate clot formation
  • ex: EDTA chelates Ca to stop its effect on coagulation
31
Q

Hypercalcemia

A

Depresses nervous system and muscle activity

  • apparent at Ca levels > 12 mg/dl
  • decreased appetite
  • constipation
32
Q

How are Ca levels in plasma tightly regulated?

A
  • increase/decrease GI absorption
  • increase/decrease renal losses
  • move Ca into or out of bone
33
Q

What systems are involved in controlling Ca levels?

A
  • vitamin D
  • parathyroid hormone via chief cells of parathyroid gland
  • calcitonin via C cells of the thyroid
34
Q

Vitamin D

A

D3 must be activated to have an effect on Ca levels

  • active vit D increases intestinal absorption of Ca
  • is necessary for parathyroid hormone to work on bone
35
Q

PTH

A
  • Most powerful mechanism of controlling Ca and phosphate
  • increases Ca by increasing GI absorption, and increasing reabsorption of Ca and P from bone
  • decreases renal losses of Ca, increases excretion of P
36
Q

Calcitonin

A

Stimulated by increased plasma Ca

  • decreases Ca (opposite of PTH)
  • decreases absorptive action of osteoclasts
  • decreases formation of new osteoclasts
  • minor effect on kidneys and GIT
  • limited effect compared to PTH (no lasting effect after thyroids are removed)
37
Q

Milk fever

A

Need for adequate Ca at motor end plate is more pronounced in cows than other species

  • decreased Ca causes decreased Ach release = nerve excitability in cows
  • paralysis and death
38
Q

Where is Ca stored/located in the body?

A
  • bone
  • kidneys
  • GIT
39
Q

What are the 3 forms of Ca found in plasma?

A
  • ionized: diffusible thru membranes (50%)
  • protein bound: nondiffusible (41%)
  • complexed to negative ions and nonionized (9%)
40
Q

How much total Ca is in plasma?

A

9.4 mg/dl = 2.4 mmol

41
Q

Hypoparathyroidism

A

Inadequate PTH secretion

  • decreases osteocyte/clast bone resorption
  • Ca level in ECF drops
  • bone stays strong
42
Q

Hyperparathyroidism - primary

A

Excess PTH secretion (due to tumor)

  • extreme osteoclastic reabsorption of bone
  • weak bone with fractures
  • high Ca levels and low P levels in ECF
  • crystals deposit in tissues
  • mild elevations lead to kidney stones
  • high Ca = nerve depression, constipation, death
43
Q

Hyperparathyroidism - secondary

A

Poor nutrition and decreased Ca intake

  • causes low serum Ca
  • seen also when kidney damage causes inadequate activation of vitamin D = inadequate intestinal absorption of Ca, low serum Ca
  • stimulates PTH to maintain blood levels –> increased PTH leads to Ca reabsorption from bone
  • nutritional form common in horses, renal form common in dogs/cats with chronic renal failure
44
Q

Rickets

A

Inadequate vitamin D

  • usually seen in spring after staying indoors during winter
  • Ca absorption from bone prevents clinical signs for a few months, liver stores of D3 are depleted by spring
  • mildly low Ca in ECF, pronounced decrease in P
  • weak bones due to increased PTH
  • late stage: tetany as bone stores are depleted and ECF Ca drops
45
Q

Excessively rapid administration of Ca containing solutions

A

Used to treat milk fever in cows

  • monitor heart rate
  • too rapid administration slows heart = death
  • stop administration if arrhythmia noted
46
Q

Excessively rapid administration of Ca depleting solutions

A

Rapid IV tetracycline antibiotic administration

  • chelates Ca and takes it out of solution
  • acute death due to hypocalcemia and cardiac arrhythmia

Physiology (33 decks)

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