bone A&P Flashcards

1
Q

6 main functions

A

support mush

protect (organs etc)

assist movement

mineral homeostasis (Ca2+, P)

blood cell create
(Red bone marrow = RBC, WBC, platelet)

store fat
(yellow bone marrow)

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2
Q

anatomy of long bone

A

Diaphysis (shaft)

Epiphysis (head/end)
(distal/proximal epiphysis)

Metaphysis (neck)

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3
Q

where is yellow bone marrow?

A

in diaphysis

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4
Q

what is diaphysis made of? (what type of bone?)

A

compact bone (cortical bone)

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5
Q

compact vs cancellous bone (spongy bone)

A
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6
Q

Epiphysis primarily

A

cancellous bone (spongy bone)

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7
Q

where is red bone marrow?

A

in epiphysis

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8
Q

structural characteristic of epiphysis

A

projections and fossae

I.e. forming joints

In other words, around joints are red bone marrow (?)

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9
Q

metaphysis

A

between diaphysis and epiphysis (Zone of transition)

WEAKEST

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10
Q

where is epiphyseal plate

A

in metaphysis

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11
Q

what is epiphyseal line

A

epiphyseal plate becomes epiphyseal line at around 20y.o. when growth (height) stops

epiphyseal plate is area of cartilage where bone growth appears

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12
Q

medullary cavity

A

cavity in diaphysis

contains YBM

contains blood vessels

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13
Q

endosteum

A

lines the medullary cavity

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14
Q

what is endosteum made of? (tissue type?)

A

DENSE IRREGULAR CT

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15
Q

periosteum

A

surrounds bone

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16
Q

two layers of periosteum

A

fibrous layer (Dense irr CT)

cellular layer

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17
Q

function of periosteum

A

covers bone

merges with tendons

sensory nerves

blood vessels

cellular layer holds OSTEOPROGENITOR CELLS (precursors to osteoblasts)

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18
Q

articular (hyaline) cartilage

A

covers epiphysis

reduce friction

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19
Q

reminder: CT is made of

A

CT is made of…
a) specialized cells
b) ECM (ground substance + fibres)

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20
Q

histology of bone

A

GS in bone is very hard

4 main types of cells:
osteoprogenitor
osteoblast
osteocyte
osteoclast

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21
Q

ECM of bone (fibres + GS) – Fibres

A

Collagen fibres (30% bone weight)

= flexibility of bones

ORGANIC COMPONENT OF ECM

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22
Q

ECM of bone (fibres + GS) – GS

A

crystalized mineral salts

only enamel is harder

CALCIUM PHOSPHATE
55% bone weight

HYDROXYAPATITE salts
Calcium phosphate
+
Calcium HYDROXIDE
Also incorporates other salts (e.g. calcium carbonate)

and ions (Na+, Mg2+, F-)

INORGANIC COMPONENT OF ECM

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23
Q

ground substance in bone

A

made of HYDROXYAPATITE

extremely hard

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24
Q

4 bone cell types

A

osteoprogenitor

osteoblast

osteocyte

osteoclast

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25
osteoprogenitor
stem cells derived from mesenchyme only bone cells that undergo MITOSIS develop into OSTEOBLASTS Part of deep (cellular) layer of periosteum AND ENDOSTEUM
26
osteoblast
bone building on bone surface secrete COLLAGEN form osteoid TURN OSTEOID into BONE
27
osteoid
"Osteoid is an unmineralized organic tissue that eventually undergoes calcification and is deposited as lamellae or layers in the bone matrix."
28
TURN OSTEOID into BONE
"assist in depositing the mineral salts (initiate calcification) to turn osteoid into bone"
29
osteocytes
mature bone cells inside bone tissue DENDRITIC processes nutrient/waste exchange (METABOLIC ACTIVITY OF BONE)
30
which bone cell type maintains metabolic activity?
osteocyte (mature bone cells)
31
where are osteocytes contained
in LACUNAE
32
where are lacunae?
between concentric layers of LAMELLAE Interconnected via CANALICULI
33
Osteoclasts
break down (resorb) bonew
34
what is resorption
taking Ca2+ from bone put it back in blood (OPPOSITE TO OSTEOBLASTS)
35
what are osteoclasts derived from (common origin)
Macrophage (WBC that performs phagocytosis)
36
which cells are multinucleated?
Osteoclasts
37
where are osteoclasts?
also found on surface of bone grooves called HOWSHIP'S LACUNAE
38
two types of bone tissue
compact spongy (cancellous/trabecular)
39
why compact
"structure comprising mostly of calcium, phosphate, collagen, and other minerals " No SPACE between cells
40
where compact?
diaphysis external layer of all bones
41
3 types of LAMELLAE in bone matrix
concentric lamellae interstitial lamellae circumferential lamellae
42
Osteon
individual structural units of bone made via concentric lamellae
43
haversian/central canal
at centre of concentric lamellae note lacunae and canaliculi note osteocytes via lacunocanalicular network
44
interstitial lamellae
between osteons
45
circumferential lamellae
next to medullary cavity next to periosteum not part of osteon
46
haversian canals
longitudinally along shaft of bone blood vessels lymph vessels nerves
47
Volkmann's canal (PERFORATING canals)
perforating canals perpendicular interconnect haversian/central canals (bv/lymph/nerve superficial to deep
48
note about canaliculi
filipodia of osteocytes
49
FILIPODIA
50
Spongy bone (trabecular/cancellous)
no osteon units -- no haversian system
51
which bone GREATER BLOOD SUPPLY
spongy Red bone marrow = RBC, WBC, platelets
52
trabeculae
contain lamellae of spongy bone less organized weaker
53
where spongy? ...
epiphyses of long bones flat bones -- periosteum and thin layer of compact bone -- but primarily spongy at centre/core
54
ossification/osteogenesis
"bone formation" begins during 6th week of embryo development
55
2 types of bone formation
endochondral ossification (replacement of cartilage w/ bone) intramembranous ossification (replacement of connective tissue membranes with bone tissue)
56
ENDOCHONDRAL ossification
initial skeleton of embryo = hyaline cartilage cartilage replaced via endochondral ossification cartilage is "small model" occurs in LONG BONES
57
where endochondral ossification?
long bones
58
6 Steps in endochondral ossification 1 -- development of cartilage model
chemical messages cause MESENCHYME cells to gather in shape of future bone ---> develop into chondroblasts chondroblasts secrete ECM of cartilage --> create hyaline cartilage perichondrium wraps cartilage model
59
Steps in endochondral ossification 2 -- growth of cartilage model
chondroblasts --> chondrocytes then... INTERSTITIAL GROWTH (replication of chondrocytes = LENGTHENING OF CARTILAGE MODEL) and... APPOSITIONAL GROWTH (ECM on cartilage surface & periphery = THICKENING OF MODEL)
60
Steps in endochondral ossification 3 -- development of primary ossification centre
nutrient artery penetrate to centre then OSTEOPROGENITOR cells @ perichondrium ----> OSTEOBLASTS PERICHONDRIUM becomes PERIOSTEUM cartilage calcifies into bone (spreads towards ends)
61
Steps in endochondral ossification 4 -- development of marrow cavity
osteoclasts create marrow cavity (diaphysis shaft) wall of diaphysis replaced with compact bone
62
Steps in endochondral ossification 5 -- development of secondary ossification centres
epiphyseal plate via epiphyseal arteries growth outward from epiphysis cartilage continuously converted to bone
63
6 Steps in endochondral ossification 6 -- formation of articular cartilage and epiphyseal plate
final stage hyaline cartilage --> articular cartilage hyaline cartilage also remains @ epiphyseal (growth) plate until adulthood (around 20) -- when plate closes and becomes epiphyseal line
64
primary / secondary ossification centres -- when?
primary = prenatal secondary = after birth
65
intramembranous ossification
bone formation without cartilage model mesenchyme (Stem) cells differentiate into osteoblasts occurs in deep layers of dermis bones called DERMAL BONES / membrane bones E.g. some bones of skull lower jaw (mandible) clavicle sesamoid bones (patella)
66
steps of intramembranous ossification 1 -- development of ossification centres
chemical messages cause mesenchymal cells to cluster --> become osteoprogenitors osteoprogenitors --> osteoblasts osteoblasts secrete bone ECM
67
Steps in intramembranous ossification 2 -- calcification
ECM secretion stops osteoblasts become osteocytes within lacunae extend processes into canaliculi calcium and other minerals are deposited and ECM hardens (calcifies)
68
Steps in intramembranous ossification 3 -- formation of trabeculae
matrix continues to harden forms trabeculae RBM forms within spongy bone trabeculae
69
Steps in intramembranous ossification 4 -- development of periosteum
outer layer of mesenchyme becomes PERIOSTEUM compact bone replaces spongy bone @ OUTER layer spongy @ inner remodeling continues until adult size/shape
70
bone growth types
length (interstitial) thickness (appositional)
71
interstitial (length)
via epiphyseal plate = hyaline layer of cartilage in metaphysis plate becomes line after skeletal maturity (around 20)
72
4 zones of epiphyseal plate
1) resting cartilage zone 2) proliferating cartilage zone 3) hypertrophic cartilage zone 4) calcified cartilage zone
73
1) resting cartilage zone
nearest to epiphysis small chondrocytes connect epiphyseal plate to epiphysis "RESTING" b/c not involved in bone growth
74
2) proliferating cartilage zone
large chondroblasts replicate and divide replace old chondrocytes "Stack of coins" apperance
75
3) hypertrophic cartilage zone
large mature chondrocytes columns
76
4) calcified cartilage zone
dead chondrocytes area is calcified osteoblasts take over create ECM convert from calcified cartilage to NEW DIAPHYSIS
77
about interstitial bone growth and puberty
@ puberty, hormones stimulate increased bone growth epiphyseal cartilage is replaced osteoblast activity OUTPACES chondroblast/chondrocyte activity Thus, Epiphyseal plate/cartilage closes = "Epiphyseal closure" leaves epiphyseal line
78
note about anatomical neck of the humerus and the residual epiphyseal plate/line
79
APPOSITIONAL GROWTH (growth in thickness of bone)
bone diameter increase osteogenic cells differentiate osteoblasts --> add bone matrix (ECM) under periosteum adds layers of CIRCUMFERENTIAL lamellae Trapped osteoblasts become osteocytes osteoclasts adjust size of MEDULLARY cavity
80
bone blood supply
rich supply why? constant remodeling Blood cell production
81
major arteries/veins supporting bone tissue
Periosteal arteries/veins Nutrient artery/vein metaphyseal arteries/veins epiphyseal artery/vein (?)
82
periosteal blood vessels
via Volkmann's Canals (PERFORATING CANALS) transport blood @ PERIOSTEUM @ outer portion of compact bone
83
nutrient artery/vein
enter via NUTRIENT FORAMEN of Diaphysis = nutrient foramen location depends on bone supply blood @ @ inner portion of compact bone @ proximal portion of spongy bone (?)
84
metaphyseal arteries/veins
enter @ metaphysis blood supply to... = metaphysis = to RED BONE MARROW
85
Epiphyseal artery/vein
enter @ epiphysis blood supply to... = epiphysis = to RED BONE MARROW
86
bone remodeling
mature bone tissue removed replaced by new bone tissue
87
why Remodeling?
structural integrity strengthen bone areas specifically (where stress) fracture repair micro-stress blood calcium homeostasis
88
2 processes of remodeling
1) resorption 2) deposition
89
1) resorption
osteoclasts break down bone ECM remove COLLAGEN & minerals I.e. Calcium released to blood
90
2) Deposition
Osteoblasts create new bone ECM osteoblasts create OSTEOID (osteoid becomes lamellae (ECM)) OSTEOID receives minerals via osteoblasts (CALCIUM via blood)
91
resorption and deposition
continuously & simultaneously
92
Wolff's law
bone tissue deposition along LINES OF STRESS bone markings via muscle attachments Wolff's law = bone added where demand, lost where no demand (stress)
93
exercise and bone
strengthens bone stresses bone = more bone deposition Wolff's law = bone added where demand, lost where no demand (stress)
94
bone growth important factors
minerals vitamins hormones
95
bone growth important factors (Minerals)
Calcium phosphorus fluoride magnesium manganese
96
bone growth important factors (vitamins)
Vitamin A (osteoblasts) Vitamin C (Collagen) Vitamin D (Calcitriol) = helps Calcium absorbtion in GI tract Vitamin K (bone proteins) Vitamin B12 (" proteins)
97
bone growth important factors (hormones)
T3 & T4 (thyroid hormones) GH (growth hormone) = stimulate IGFs = from liver = bone growth Sex hormones = testosterone = bone growth Calcitonin & PTH (parathyroid hormone) = Calcium homeostasis
98
calcium important functions
nerve/muscle cell function (Ca2+ ion muscle contract) blood clotting (acts as enzyme --> clotting factors) other chemical reactions (as "COFACTOR")
99
blood calcium homeostasis
8.5 - 10.5 mg/dL
100
hypercalcemia hypocalcemia
hypercalcemia (>10.5mg/dL) = cardiac arrest hypocalcemia (<8.5mg/dL) = respiratory arrest
101
blood homeostasis where? (3 locations
3 locations: 1) Bone = bone resorption increase blood Ca2+ = bone reposition decrease blood Ca2+ 2) Kidney = increased calcium reabsorption increase blood Ca2+ = decreased calcium reabsorption decrease blood Ca2+ 3) GI tract = increased vs decreased absorption
102
3 hormones that regulate calcium homeostasis
1) Calcitonin = decrease blood Ca2+ = puts calcium in bone 2) Parathyroid hormone (PTH) = increase blood Ca2+ = puts calcium in blood 3) Calcitriol = activated form of Vitamin D = INCREASE blood Ca2+
103
1) Calcitonin
via Parafollicular cells (C CELLS) of THYROID GLAND decrease blood Ca2+ effect antagonistic to PTH and Calcitriol
104
How does Calcitonin decrease blood Ca2+ (TWO ways)
1) Decreases bone resorption = inhibit OSTEOCLASTS = Osteoblasts outpace Osteoclasts = more deposited than resorbed 2) Decreases Kidney reabsorption of Calcium = more Calcium stays in Urine = leaves body
105
2) PTH (parathyroid hormone)
via Parathyroid glands = increase blood Ca2+ antagonist to Calcitonin synergist to Calcitriol
106
How does PTH increase blood Ca2+? (THREE ways)
1) Increase bone resorption = osteoclasts activity outpaces Osteoblasts = more resorbed than deposited 2) Increase kidney reabsorption of Calcium = less Ca2+ lost in urine 3) Activates Calcitriol/Vitamin D = in kidney (?)
107
PTH/Calcitonin and negative feedback system
regulated by negative feedback loop
108
3) Calcitriol
made in EPIDERMIS = via Cholesterol precursor = precursor activated by UV radiation Increase blood Ca2+ levels antagonistic to Calcitonin synergistic to Calcitriol
109
how does Calcitriol increase blood Ca2+ (one way)
increase GI tract absorption of Ca2+ increase amount of Ca2+ in blood
110
menopause and osteoporosis
osteoblasts activate osteoclasts ESTROGEN protection = blocks activation of osteoclasts sudden drop in estrogen = active Osteoclasts Active osteoclasts = more resorption = increased chance of Osteoporosis
111
Bone pathologies
fractures osteoporosis rickets/osteomalacia
112
fracture
any break in bone types, severities, locations, causes
113
open fracture
aka compound fracture broken ends of bones protrude through skin complications: = infection = non-union (not healing after 3 months -- fracture persists for 9 months) treatment: = surgery = antibiotics via plate/screws
114
closed fracture
aka simple fracture broken ends don't protrude through skin may or may not require surgery
115
comminuted fracture
2 or more spots forms fragments requires surgery internal fixation (e.g. plate/screws) external fixation = metal frame/scaffolding outside leg = not quite same as cast (?)
116
greenstick fracture
incomplete/partial fracture one side broken, other side bent common in children b/c bones not fully ossified (more organic material)
117
impacted fracture
one end forcefully driven into other (of 2 fractured ends)
118
transverse fracture
perpendicular to length
119
oblique fracture
@ an angle
120
spiral fracture
warps around shaft like corkscrew shape via fracture during twisting motion
121
Pott's fracture
distal fibula via ankle sprain
122
Colle's fracture
distal radius fracture distal end moves posteriorly = dinner fork deformity
123
avulsion fracture
bone attached to ligament or tendon pulled away young athletes common @ @hip @foot/ankle @elbow Note also... MALLET finger = small bone fragment pulled away with extensor digitorum tendon
124
stress fracture
micro-fracture repetitive stress E.g. running, jumping, dancing can be missed by X-ray
125
Growth plate fracture
break in growth plate of child/teen if goes through growth plate, can result in shortened/crooked limbs
126
vertebral compression fracture (VCF)
vertebral body fracture can become compressed via injury/trauma more common in those w/ osteoporosis
127
osteoporosis
"porous bone" loss of bone mass resorption frequently outpaces deposition
128
osteoporosis some causes
decreased estrogen in women (post-menopause) decreased testosterone in males poor diet/low calcium intake lack of exercise drug use e.g. also steroids smoking genetics
129
osteoporosis more common in
women and elderly
130
bone pathologies numbers
2.3 million Canadians with osteoporosis 1.3 million fractures per year 1/3 females experience fracture due to osteoporosis 1/5 males experience fracture due to osteoporosis best prevention = regular exercise = healthy diet
131
osteomalacia and rickets
failure of bones to calcify in children, called "Rickets" in adults, called osteomalacia osteomalacia = "soft bones" organic matrix present calcium salts not deposited lack of vitamin D lack of sunlight poor diet extreme/prolonged calcium or vitamin D deficiency soft bones = bow legs pain, tenderness, fractures
132
osteoporosis vs osteomalacia
in osteoporosis bone mass decreases bone mineral to matrix is same in osteomalacia bone volume not necessarily different bone mineral to matrix ratio is lower note Vitamin D deficiency
133
4 steps in fracture repair
1) formation of fracture hematoma (reactive phase) 2) fibrocartilage callus formation 3) bony callus formation 4) bone remodeling
134
1) formation of fracture hematoma (reactive phase) -- (SEVERAL WEEKS)
damaged blood vessels form clot (hematoma) circulation stops bone cells in area DIE inflammation via DEAD cells Phagocytes/osteoclasts remove DEBRIS (dead cells) = SEVERAL WEEKS
135
2) Fibrocartilage callus formation (THREE WEEKS)
fibroblasts create COLLAGEN fibres CHONDROCYTES (from periosteum) = CREATE fibrocartilage FC callus is formed THREE WEEKS
136
3) Bony Callus formation (FOUR MONTHS)
osteogenic cells (OSTEOPROGENITOR CELLS) = become osteoblasts = convert FC callus into SPONGY BONE trabeculae = join bone fragments with bone bony/hard callus = 3-4 (FOUR) MONTHS
137
4) Bone remodeling
osteoclasts resorb remaining dead portions COMPACT BONE replaces SPONGY bone (around periphery)
138
X-ray (radiography) discovered by...
in 1895 by William Conrad Roentgen in Germany "He was experimenting with an electron accelerator, called a cathode, and discovered that a nearby barium plate became fluorescent due to the massive exposure of electrons. Roentgen called these fluorescent beams 'X' for their unknown quantity. X-rayed his wife’s hand soon after and received Nobel prize for physics same year."
139
how X-ray (radiography) works
via electron beams soft tissue & air does not reflect " hard/dense objects do E.g. metal, bone, teeth, etc.
140
note radiopaque vs radiolucent
"Radiolucent Refers to structures that are less dense and permit the x-ray beam to pass through them. Radiolucent structures appear dark in the radiographic image." "Radiopaque Refers to structures that are dense and resist the passage of x-rays."
141
DEXA scan
dual energy X-ray absorptiometry scan measures bone density tracks bone loss as you age diagnose osteoporosis
142
radioactive tracer
chemical substance injected "taken up" by bone scanning device detects area of activity (via tracer) hot spot = higher metabolism (= potential pathologies) cold spot = lower metabolism E.g. healed fracture degeneration arthritis etc.
143
most useful bone scan method?
via radioactive tracer efficiency, accuracy
144