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Semester 2 > bone A&P > Flashcards

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
Q

osteoprogenitor

A

stem cells derived from mesenchyme

only bone cells that undergo MITOSIS

develop into OSTEOBLASTS

Part of deep (cellular) layer of periosteum AND ENDOSTEUM

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26
Q

osteoblast

A

bone building

on bone surface

secrete COLLAGEN

form osteoid

TURN OSTEOID into BONE

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27
Q

osteoid

A

“Osteoid is an unmineralized organic tissue that eventually undergoes calcification and is deposited as lamellae or layers in the bone matrix.”

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28
Q

TURN OSTEOID into BONE

A

“assist in depositing the mineral salts (initiate calcification) to turn osteoid into bone”

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29
Q

osteocytes

A

mature bone cells

inside bone tissue

DENDRITIC processes

nutrient/waste exchange
(METABOLIC ACTIVITY OF BONE)

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30
Q

which bone cell type maintains metabolic activity?

A

osteocyte (mature bone cells)

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31
Q

where are osteocytes contained

A

in LACUNAE

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32
Q

where are lacunae?

A

between concentric layers of LAMELLAE

Interconnected via CANALICULI

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33
Q

Osteoclasts

A

break down (resorb) bonew

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34
Q

what is resorption

A

taking Ca2+ from bone

put it back in blood
(OPPOSITE TO OSTEOBLASTS)

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35
Q

what are osteoclasts derived from (common origin)

A

Macrophage (WBC that performs phagocytosis)

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36
Q

which cells are multinucleated?

A

Osteoclasts

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37
Q

where are osteoclasts?

A

also found on surface of bone

grooves called HOWSHIP’S LACUNAE

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38
Q

two types of bone tissue

A

compact

spongy (cancellous/trabecular)

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39
Q

why compact

A

“structure comprising mostly of calcium, phosphate, collagen, and other minerals “

No SPACE between cells

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40
Q

where compact?

A

diaphysis

external layer of all bones

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41
Q

3 types of LAMELLAE in bone matrix

A

concentric lamellae

interstitial lamellae

circumferential lamellae

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42
Q

Osteon

A

individual structural units of bone

made via concentric lamellae

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43
Q

haversian/central canal

A

at centre of concentric lamellae

note lacunae and canaliculi

note osteocytes via lacunocanalicular network

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44
Q

interstitial lamellae

A

between osteons

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45
Q

circumferential lamellae

A

next to medullary cavity

next to periosteum

not part of osteon

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46
Q

haversian canals

A

longitudinally along shaft of bone

blood vessels
lymph vessels
nerves

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47
Q

Volkmann’s canal (PERFORATING canals)

A

perforating canals

perpendicular

interconnect haversian/central canals
(bv/lymph/nerve

superficial to deep

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48
Q

note about canaliculi

A

filipodia of osteocytes

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49
Q

FILIPODIA

A
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50
Q

Spongy bone (trabecular/cancellous)

A

no osteon units – no haversian system

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51
Q

which bone GREATER BLOOD SUPPLY

A

spongy

Red bone marrow
= RBC, WBC, platelets

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52
Q

trabeculae

A

contain lamellae of spongy bone

less organized
weaker

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53
Q

where spongy? …

A

epiphyses of long bones

flat bones – periosteum and thin layer of compact bone – but primarily spongy at centre/core

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54
Q

ossification/osteogenesis

A

“bone formation”

begins during 6th week of embryo development

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55
Q

2 types of bone formation

A

endochondral ossification (replacement of cartilage w/ bone)

intramembranous ossification
(replacement of connective tissue membranes with bone tissue)

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56
Q

ENDOCHONDRAL ossification

A

initial skeleton of embryo = hyaline cartilage

cartilage replaced via endochondral ossification

cartilage is “small model”

occurs in LONG BONES

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57
Q

where endochondral ossification?

A

long bones

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58
Q

6 Steps in endochondral ossification

1 – development of cartilage model

A

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
Q

Steps in endochondral ossification

2 – growth of cartilage model

A

chondroblasts –> chondrocytes

then…
INTERSTITIAL GROWTH
(replication of chondrocytes = LENGTHENING OF CARTILAGE MODEL)

and…
APPOSITIONAL GROWTH
(ECM on cartilage surface & periphery = THICKENING OF MODEL)

60
Q

Steps in endochondral ossification

3 – development of primary ossification centre

A

nutrient artery penetrate to centre

then OSTEOPROGENITOR cells @ perichondrium —-> OSTEOBLASTS

PERICHONDRIUM becomes PERIOSTEUM

cartilage calcifies into bone (spreads towards ends)

61
Q

Steps in endochondral ossification

4 – development of marrow cavity

A

osteoclasts create marrow cavity (diaphysis shaft)

wall of diaphysis replaced with compact bone

62
Q

Steps in endochondral ossification

5 – development of secondary ossification centres

A

epiphyseal plate via epiphyseal arteries

growth outward from epiphysis

cartilage continuously converted to bone

63
Q

6 Steps in endochondral ossification

6 – formation of articular cartilage and epiphyseal plate

A

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
Q

primary / secondary ossification centres – when?

A

primary = prenatal

secondary = after birth

65
Q

intramembranous ossification

A

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
Q

steps of intramembranous ossification

1 – development of ossification centres

A

chemical messages cause mesenchymal cells to cluster –> become osteoprogenitors

osteoprogenitors –> osteoblasts

osteoblasts secrete bone ECM

67
Q

Steps in intramembranous ossification

2 – calcification

A

ECM secretion stops

osteoblasts become osteocytes

within lacunae

extend processes into canaliculi

calcium and other minerals are deposited and ECM hardens (calcifies)

68
Q

Steps in intramembranous ossification

3 – formation of trabeculae

A

matrix continues to harden

forms trabeculae

RBM forms within spongy bone trabeculae

69
Q

Steps in intramembranous ossification

4 – development of periosteum

A

outer layer of mesenchyme becomes PERIOSTEUM

compact bone replaces spongy bone @ OUTER layer

spongy @ inner

remodeling continues until adult size/shape

70
Q

bone growth types

A

length (interstitial)

thickness (appositional)

71
Q

interstitial (length)

A

via epiphyseal plate

= hyaline layer of cartilage in metaphysis

plate becomes line after skeletal maturity (around 20)

72
Q

4 zones of epiphyseal plate

A

1) resting cartilage zone
2) proliferating cartilage zone
3) hypertrophic cartilage zone
4) calcified cartilage zone

73
Q

1) resting cartilage zone

A

nearest to epiphysis

small chondrocytes

connect epiphyseal plate to epiphysis

“RESTING” b/c not involved in bone growth

74
Q

2) proliferating cartilage zone

A

large chondroblasts

replicate and divide

replace old chondrocytes

“Stack of coins” apperance

75
Q

3) hypertrophic cartilage zone

A

large mature chondrocytes

columns

76
Q

4) calcified cartilage zone

A

dead chondrocytes

area is calcified

osteoblasts take over

create ECM

convert from calcified cartilage to NEW DIAPHYSIS

77
Q

about interstitial bone growth and puberty

A

@ 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
Q

note about anatomical neck of the humerus and the residual epiphyseal plate/line

A
79
Q

APPOSITIONAL GROWTH (growth in thickness of bone)

A

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
Q

bone blood supply

A

rich supply

why?
constant remodeling
Blood cell production

81
Q

major arteries/veins supporting bone tissue

A

Periosteal arteries/veins

Nutrient artery/vein

metaphyseal arteries/veins

epiphyseal artery/vein

(?)

82
Q

periosteal blood vessels

A

via Volkmann’s Canals (PERFORATING CANALS)

transport blood
@ PERIOSTEUM
@ outer portion of compact bone

83
Q

nutrient artery/vein

A

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
Q

metaphyseal arteries/veins

A

enter @ metaphysis

blood supply to…
= metaphysis
= to RED BONE MARROW

85
Q

Epiphyseal artery/vein

A

enter @ epiphysis

blood supply to…
= epiphysis
= to RED BONE MARROW

86
Q

bone remodeling

A

mature bone tissue removed

replaced by new bone tissue

87
Q

why Remodeling?

A

structural integrity

strengthen bone areas specifically (where stress)

fracture

repair micro-stress

blood calcium homeostasis

88
Q

2 processes of remodeling

A

1) resorption

2) deposition

89
Q

1) resorption

A

osteoclasts break down bone ECM

remove COLLAGEN & minerals
I.e.
Calcium released to blood

90
Q

2) Deposition

A

Osteoblasts create new bone ECM

osteoblasts create OSTEOID (osteoid becomes lamellae (ECM))

OSTEOID receives minerals via osteoblasts
(CALCIUM via blood)

91
Q

resorption and deposition

A

continuously & simultaneously

92
Q

Wolff’s law

A

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
Q

exercise and bone

A

strengthens bone

stresses bone = more bone deposition

Wolff’s law = bone added where demand, lost where no demand (stress)

94
Q

bone growth important factors

A

minerals

vitamins

hormones

95
Q

bone growth important factors (Minerals)

A

Calcium

phosphorus

fluoride

magnesium

manganese

96
Q

bone growth important factors (vitamins)

A

Vitamin A (osteoblasts)

Vitamin C (Collagen)

Vitamin D (Calcitriol)
= helps Calcium absorbtion in GI tract

Vitamin K (bone proteins)

Vitamin B12 (“ proteins)

97
Q

bone growth important factors (hormones)

A

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
Q

calcium important functions

A

nerve/muscle cell function
(Ca2+ ion muscle contract)

blood clotting (acts as enzyme –> clotting factors)

other chemical reactions (as “COFACTOR”)

99
Q

blood calcium homeostasis

A

8.5 - 10.5 mg/dL

100
Q

hypercalcemia

hypocalcemia

A

hypercalcemia (>10.5mg/dL)

cardiac arrest

respiratory arrest

101
Q

blood homeostasis where? (3 locations

A

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
Q

3 hormones that regulate calcium homeostasis

A

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
Q

1) Calcitonin

A

via Parafollicular cells
(C CELLS)
of THYROID GLAND

decrease blood Ca2+

effect antagonistic to PTH and Calcitriol

104
Q

How does Calcitonin decrease blood Ca2+ (TWO ways)

A

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
Q

2) PTH (parathyroid hormone)

A

via Parathyroid glands

= increase blood Ca2+

antagonist to Calcitonin
synergist to Calcitriol

106
Q

How does PTH increase blood Ca2+? (THREE ways)

A

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
Q

PTH/Calcitonin and negative feedback system

A

regulated by negative feedback loop

108
Q

3) Calcitriol

A

made in EPIDERMIS

= via Cholesterol precursor
= precursor activated by UV radiation

Increase blood Ca2+ levels

antagonistic to Calcitonin
synergistic to Calcitriol

109
Q

how does Calcitriol increase blood Ca2+ (one way)

A

increase GI tract absorption of Ca2+

increase amount of Ca2+ in blood

110
Q

menopause and osteoporosis

A

osteoblasts activate osteoclasts

ESTROGEN protection
= blocks activation of osteoclasts

sudden drop in estrogen = active Osteoclasts

Active osteoclasts = more resorption = increased chance of Osteoporosis

111
Q

Bone pathologies

A

fractures

osteoporosis

rickets/osteomalacia

112
Q

fracture

A

any break in bone

types, severities, locations, causes

113
Q

open fracture

A

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
Q

closed fracture

A

aka simple fracture

broken ends don’t protrude through skin

may or may not require surgery

115
Q

comminuted fracture

A

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
Q

greenstick fracture

A

incomplete/partial fracture

one side broken, other side bent

common in children
b/c bones not fully ossified
(more organic material)

117
Q

impacted fracture

A

one end forcefully driven into other (of 2 fractured ends)

118
Q

transverse fracture

A

perpendicular to length

119
Q

oblique fracture

A

@ an angle

120
Q

spiral fracture

A

warps around shaft

like corkscrew shape

via fracture during twisting motion

121
Q

Pott’s fracture

A

distal fibula

via ankle sprain

122
Q

Colle’s fracture

A

distal radius fracture

distal end moves posteriorly

= dinner fork deformity

123
Q

avulsion fracture

A

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
Q

stress fracture

A

micro-fracture

repetitive stress

E.g. running, jumping, dancing

can be missed by X-ray

125
Q

Growth plate fracture

A

break in growth plate of child/teen

if goes through growth plate, can result in shortened/crooked limbs

126
Q

vertebral compression fracture (VCF)

A

vertebral body fracture

can become compressed

via injury/trauma

more common in those w/ osteoporosis

127
Q

osteoporosis

A

“porous bone”

loss of bone mass

resorption frequently outpaces deposition

128
Q

osteoporosis some causes

A

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
Q

osteoporosis more common in

A

women and elderly

130
Q

bone pathologies numbers

A

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
Q

osteomalacia and rickets

A

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
Q

osteoporosis vs osteomalacia

A

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
Q

4 steps in fracture repair

A

1) formation of fracture hematoma (reactive phase)

2) fibrocartilage callus formation

3) bony callus formation

4) bone remodeling

134
Q

1) formation of fracture hematoma (reactive phase) – (SEVERAL WEEKS)

A

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
Q

2) Fibrocartilage callus formation (THREE WEEKS)

A

fibroblasts create COLLAGEN fibres

CHONDROCYTES (from periosteum)
= CREATE fibrocartilage

FC callus is formed

THREE WEEKS

136
Q

3) Bony Callus formation (FOUR MONTHS)

A

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
Q

4) Bone remodeling

A

osteoclasts resorb remaining dead portions

COMPACT BONE replaces SPONGY bone
(around periphery)

138
Q

X-ray (radiography) discovered by…

A

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
Q

how X-ray (radiography) works

A

via electron beams

soft tissue & air does not reflect “

hard/dense objects do
E.g.
metal, bone, teeth, etc.

140
Q

note radiopaque vs radiolucent

A

“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
Q

DEXA scan

A

dual energy X-ray absorptiometry scan

measures bone density

tracks bone loss as you age
diagnose osteoporosis

142
Q

radioactive tracer

A

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
Q

most useful bone scan method?

A

via radioactive tracer

efficiency, accuracy

144
Q
A

Semester 2 (14 decks)

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