musculoskeletal system Flashcards

1
Q

how is micro damage dealt with by bone cells? ex = run

A

if you go for a run and you your shins are a bit sore and you feel you’ve got shin splints,
our bones are designed that actually these BONE BUILDING cells called osteoblasts will sort of rush in to
the site of micro damage and they’ll lay down some new bone and then periodically some BONE CHEWING cells,
osteoclasts will sort of come in behind and and tidy up any mess and make things a bit more organised.

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2
Q

fibro dysplasia

A

where tissue soft tissue should be generated,
bone tissue is mistakenly generated.
And so these bony protrusions result.
=> additional bones, bone fusion,…

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3
Q

functions of bone

A

structural support => allows us to stand

Enables movement – attachment of muscles

Protection of vital organs

Storage of minerals
(Ca2+ = 99% storage of it => can capture and sequester it into circulation, PO43- , Mg)

Haematopoiesis
red Blood cell formation (in bone marrow, some long bones, adolescence mostly adulthood)

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4
Q

what is bone?

A

Collagen fibre framework in a mucopolysaccharide-rich semisolid gel “ground substance”
gives bone its tensile strength
without collagen/ lack of / bones that fracture easily = brittle

Hardened by precipitation of calcium phosphate (hydroxyapatite) crystals within matrix
gives bone its compressional strength
(cartilage is similar to bone but
not calcified)
=> without/ lack of minerals = bendy bones

Made of osteoblasts, osteoclasts
osteocytes = ‘mature blood cells’
Supplied by blood vessels & nerves

Contains bone marrow

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5
Q

long bone structure

A

head = epiphysis => covered by hyaline cartilage => contains spongy bone

Metaphysis (between epiphysis and diaphysis (region of growth in childhood)

shaft = hallow cylinder = medullar cavity with compact bone around is called the diaphysis -> contains bone marrow

periostem = protective tissue covering the bone => contains lots of these active precursor cells that can be triggered to migrate to other parts of the bone to repair damage => fibroblasts synthesize collagen/
mesenchymal cells that can differentiate into osteoblasts and chondroblasts/
osteoclasts

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6
Q

trabecular/ cancellous

A

=> spongy
trabecular, which are these sorts of lines of bone lay down along the lines of stress, and they’re there in order to direct the stress from the head of the bone, down through the shaft of the bone.
if these trabecular were not there, you would quickly result in a situation where if you’ve got a vertical stress bone = going to shatter, it’s going to splinter or break of

gives supporting strength to the ends of the weight-bearing bone

really important site of metabolic activity for ion exchange

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7
Q

cortical

A

solid
will transmit the stresses,
applied to the bone through to other regions of the bone.
bone on the outside forms the shaft of the long bone
provides stiffness and strength

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8
Q

blood supply to bone

A

volkman’s canals carry blood horizontally through bone

haversian’s canals run vertically through bone

macro level => bring blood into and out of bone, the bone cells within compact bone.

Compact bone units = osteons => inside these osteocytes dont have a direct blood supply => oxygen can be transmitted through the bone matrix to cells that are not in direct contact with a blood supply for metabolism to occur,
and equally, waste products can be shipped out of bone.

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9
Q

osteon

A

compact bone arranged in osteons

central blood vessel and then around it osteocytes are arranged in sort of increasing circles.

Haversian canals carry blood along bone
Cells arranged in concentric circles (like onions)
Inside each layer are collagen fibres
Fibres in each layer can be oriented differently - very flexible

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10
Q

trabecular bone arrangement

A

not arranged in concentric circles.

=> easier for
Various agents to be able to access the surface of the trabecular bone.
Fewer lamellular layers in the “spongy” trabecular region
Less coordinated (weaker and more flexible) than compact bone
More open, less dense, site of haemopoiesis in bone marrow

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11
Q

rickets

A

Vitamin D deficiency  failure of Ca2+ absorption

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12
Q

scurvy

A

Vitamin C deficiency  lack of collagen

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13
Q

osteoblast

A

bone forming cell, cover the surface of bone ….forming an osseous matrix in which it becomes enclosed as an osteocyte

When stimulated to form bone will deposit organic matrix (collagen) then hydroxyapatite

Some become entombed during this process  mature in to osteocytes

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14
Q

osteoclast

A

osteophage; a large, multinucleated cell derived from haematopoietic cells…In response to mechanical stresses and physiological demands they resorb bone matrix by demineralization

Release H+ and hydrolytic enzymes to dissolve the mineral, liberate calcium and break down the extracellular matrix

Regulated by hormones (e.g., oestrogens) and osteoblasts

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15
Q

osteocyte

A

bone cell – trapped, “retired” osteoblasts. Mature bone cells - embedded in lacunae, relatively inactive. Maintain bone matrix through cell-to-cell communication (via projections in canaliculi) and influence bone remodelling. Mechanosensing

Embedded within lacunae

Communicate via finger-like projections in canaliculi

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16
Q

Osteoprogenitor cells

A

Stem cell population, gives rise to osteoblasts + other cells

17
Q

bone = dynamic

A

Equilibrium between osteoblast and osteoclast activity is controlled by signalling between the different cells in bone and via the actions of hormones:

Calcitonin ↓ activity of osteoclasts, i.e. ↓ blood Ca2+ levels
Parathyroid hormone (PTH) ↑ activity of osteoclasts, releases Ca2+

18
Q

trabecular bone remodling cycle

A

quiescence
resorption by osteoclasts
surface exposed to osteoprogenitors
osteoblasts differenciate
osteoblasts lay down new bone

19
Q

how often skeleteon remodelled

A

12 yrs

20
Q

cortical bone remodelling

A

Osteoclasts reabsorb bone
Osteoblasts lay down new matrix, eventually get surrounded and become
Osteocytes

21
Q

bone is dynamic and remodelled throughout life - wolff’s law

A

Bone mass and density can increase
- Excessive mechanical stimulation

Bone mass and density can decrease
- Non-weight bearing (immobilisation)
- Sex-hormone deficiency (e.g. menopause)
- Endocrine/nutritional disorders

Wolff’s law
- Bone adapts to the load under which it is placed
Weight-bearing exercise, orthodontic braces, (Amerindian) head binding

22
Q

age related changes

A

bone mass increase till 30
consolidation at 30-40
bone loss at 40 onwards => women lose more bone mass <=> menopause -> reach fracture threshold earlier

23
Q

osteoporotic bone

A

usually dense interconnected strands of bone and interconnected trabecular, whereas osteoporotic bone = there’s a number of fracture sites, missing bone and so on.

24
Q

bone growth

A

starts as a collagen model, completely replaced by bone

Ossification begins in the diaphysis

Primary ossification centre = active before birth = in foetus then after birth

25
Q

2nd ossification

A

Epiphysis
Secondary centre of ossification
Bone is laid down in the shaft and in the head

The bony parts are separated by a plate of cartilage

As long as the plate of cartilage is present and active the bone will increase in length

long bone grows so epiphysial growth plate closes
=> end of growth in height = end of puberty

26
Q

bone fracture reparation

A
  1. Takes 2-4 weeks for healing
    dependent on the severity and position of the fracture and age of patient

Inflammation and additional blood flow lead to
Callus formation
osteoblasts quickly form woven bone, to bridge the gap
woven bone is weak as the collagen fibres are irregular

Lamellar bone laid down
collagen organised in regular sheets to gives strength and resilience

bcs of walff’s law => bone can grow back into its original shape => why cast => Remodelling by osteoclasts to restore original bone shape