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MSK - Mid Term 1 > Everything > Flashcards

Everything Flashcards

1
Q

Longitudinal Growth Compact Bone

A

occurs @ epihyseal plate,

as chondrocytes lay the new cartilage at the plate, the cells begin to go through 4 stages to further expand the bone lenght wise.

stage 1 chondrocytes lay the new cartilage
- zone of resting cartilage

stage 2 - chondrocytes begin to divide and proliferate
- proliferating zone

stage 3 - hypertrophic zone
- chondrocytes get bigger

stage 4 - calcification
- osteoclasts eat chondrocytes and signal osteoblasts to lay bone (collagen 1 & 5 )

As this occurs the epihpseal plate gets further away from the chondrocytes and bone

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2
Q

endochondral ossification

A

when type 1 and 5 collagen creplace cartilage and push away the growth plate (last stage- calcification)

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3
Q

cartilage is made from what collagen fibres

A

heterofibrils - Collagen Type 2 & 9 to 11

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4
Q

diameter growth of bone

A

osteons contain osteocytes and lamella. outside of osteons we have osteoblasts adn a couple osteoclasts.

for diameter growth. the osteoblasts begin to fold around the perosteum of the bone, circling the blood vessels, creating more concentrics of the osteons

osteocytes get stuck in here and we get a new osteon for diameter growth.

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5
Q

male vs female diameter growth

A

pre puberty - both same growth

puberty - chicks get thicker
- males grow bigger circumference wise

aging - chicks get a little circumference bigger, but the thickness goes down

guys continue to grow circumference big and a bit thicker

circumferecnce never regressses

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6
Q

hormones bone growth

A

PTH, IGF-1 , Estrogen, TEST , Insulin, TH, progesterone

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7
Q

bone growth is…

A

depositing more than you degrade

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8
Q

remodeling does not equal

A

growth

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9
Q

what cells remodel bone

A

osteoblasts, osteoclasts, osteocytes

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10
Q

tension in bone…..

A

both osteoblasts and osteo cytes can sense tension in bone.

when tension arrives, cytes signal blasts VIA GAP JUNCTIONS and tell them to begin secreting collagen and bone apatite

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11
Q

how does resoprtion of bone work

A

osteoclasts secrete H+ions (acid to break down bone)

osteoclasts secrete MMP to break down bone

osteoclasts eat away the bone and resorb it

REGULATED by - hormones and signals to the cytes and blasts

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12
Q

what do steriods do to tendons

A

fibroblasts are senstiive to steroids.

wehn fibroblasts get steroids they secrete lots of collagen . unfortunately this is unnorganizied collagen annd calcium spots in between fibrils and cannot transmit force very well.

the tendon growns thicker but it doesnt produce the most efficent force.

wehn we take steroids we increase force produciton by the muscle. adn evene though our tendon is getting thicker to withstand more force, the muscles are also getting bigger adn produceing too much force.

this is why there is more risk of rupture.

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13
Q

exercise on tendon

A

exercises increases tension

tension increases fibroblast activity adn number.

more activity adn fibroblasts = more collagen,

tension + collagen = organization

organized fibres equal better at transmitting force.

more collagen = thicler tendon = more force transmission

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14
Q

bone marrow

A

yellow marrow in medullary cavity post puberty

red marrow in epihysis all the time and in cavity pre puberty

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15
Q

osteons made of

A

Extracellular matrix

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16
Q

osteons have blank and blank and trap blank inside

A

nerves and blood vessels
adn trap osteocytes inside inbetwen lamella

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17
Q

chondrocytes

A

initial cartliage layers at growth plate

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18
Q

osteocytes

A
  • inbetween lamella in osteons - signal osteoblasts to lay bone
  • maintain bone via - waste, nutrients, metabolism
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19
Q

osteoblasts

A

outside of osteons - secrete collagen and apatite

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20
Q

osteoclasts

A

HSC Monocytes fused together

  • found in bone compact and spongy
  • secrete H+ and MMP to eat away bone mineral, for resorption

most in endosteum

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21
Q

bone apatite

A

bone mineral - secreted by chondrocytes and osteoblasts within vesicles that layer into type 1 collagen fibrils to give rigidty

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22
Q

mechanical stims simple

A

any mechanical stim to bone or CT causes adaptiations that make them become more resistant and stronger

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23
Q

(3) possibel causes for CT adaptation

A
  • increase fibro activity/ number of fibroblasts
  • increased collagen density
  • type of collagen
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24
Q

how do me measure collagen turnover

A

terminal pro-peptides (snippets off of tropocollagen)

  • taken from ECM
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25
Q

72 hours post exercise

A

collagen synthesis increases heavy

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26
Q

4 weeks (1 months)

A

msot collagen synthesis

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27
Q

11 weeks (3 months)

A

still lots of synthesis but not as much as 1 month. ( comes back down a bit)

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28
Q

acute exercise causes collagen sytheiss

A

acute exercise causes collagen synthesis to stop during the workout and then turn on afterwards (72hours)

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29
Q

why is a biggger tendon good?

A

bigger tendon is good because -

increase the amount of load/ stress via increasing CSA

decrease the amount of deformation per load.

stress = force/area

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30
Q

can we increase performance with a bigger tendon?

A

yes V02 seems to decrease as the tendon increases due to expenditure of energy becomes more economical.

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31
Q

trained mice

A
  • more fibroblasts
  • bigger tendons
  • stress fibres of costameres had more contractile phenotype
  • this means that he myosin and actin were mroe dense - genereating more contractile force intracellularly
  • more type 1 collagen
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32
Q

run training did what

A

increased torque and force

decreased deformation

increased tendon stifness

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33
Q

Research Article (RA) - how many people

A

15

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34
Q

RA explain control and experimental

A

control group adn experimental group were both volunteers with tendonosis 2-6cm above achilles insertion.

control group - did surgery adn regualar

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35
Q

protiens

A

amino acid + amino acid + amino acid…. bonds between AA are covalenet

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36
Q

how are proteins folded

A

folds occur between R groups on the amino acids that are attracted to eachother based on how electronegative a molecule is. they attract and fold

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37
Q

DNA down the line

A

DNA - mRNA - ribosomes - proteins -

dna makes instructions

mRNA copies instructions

Ribosomes read instructions
and make proteins to then be added to the AA chain

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38
Q

functions of proteins

A

structure
motors - produce force
enzymes
hormones/recpetors/signals

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39
Q

pH and Temp

A

proteins work at optimal ranges - pH and Temp denature proteins

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40
Q

post transcriptional modification

A

after proteins are in their chain and DNA has formed a protein with an original function, a modification occurs to the protein changing its finction ( phosphorylation) - turning it on or off

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41
Q

sk. muscle layers

A

epimysium - protector and force transducer
perimysium - fascicle man
endomysium -between myofibres
BM -
(reticular lamina)
(basal lamina)
plasmolemma (sarcolemma + BM)
myofibre
myofibril
sarcomere
myofilament

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42
Q

what makes up CT

A

collagen 1-6 and elastin

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43
Q

how are endomysium and BM bound together

A

dense collagen fibres of endomysium and loose collagen fibres of BM (reticular lamina), velcro together.

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44
Q

BM proteins

A

collagen
acetylecholine esterase - cancels contraction
laminan and fibrrenectin- connect fibre to BM

45
Q

BM membrane is lined with what types of proteins

A

Glycoproteins

46
Q

Basement membrane functions

A

connect endo to fibre
cancel contractions
attract motor neurons - muscle repair

47
Q

Plasmalemma Proteins

A

Integrins / Dystroglycan Complex - transmit force and anchor between fibre and contractile proteins

Kinases - for integrin and target protein phosphorylation

Signals
Channels
Receptors

48
Q

stress equation

A

stress=force/area

  • more area = less stresss
  • less force = less stress
49
Q

highest point of tension

A

highest point of tension on a muscle is where the area is the lowest - therfore the myotendinous junction (tendon) - high force created in middle of tendon, passed down to little area of MTJ

50
Q

tendon composition

A

60% water
39% protein (80% of that is collagen)
1% groundsubstance - glycans

51
Q

tendon layers like muscle layers are..

A

collagen fibril
collagen fibre
1st collagen bundle
endotenon - perimysium and BM (tougnness)
2nd collagen bundle
endotenon - BV and Nerves
3rd collagen bundle
endotenon
epitenon
paratenon - synovial

52
Q

where are fibroblasts in tendons

A
  • fibroblasts in tendons can be found in between the primary collagen bundles
53
Q

where are fibroblasts found in muscle

A

fibroblasts in muscle can be found in between myofibres

54
Q

which tenon (epi, endo, para) transmits force and what do the others do

A

endotenon doesnt transmit force - it just divides collagen bundles

epitenon transmit force as it is the most superficial portion of tendon

paratenon - decrease friction agianst other tissues

55
Q

what is a fibroblast

A
  • a mesenchymal cell
  • large fairly
  • 1 nucleus
  • stress fibres are connected to the connective tissue that surrounds them by FAKs - Focal Adhesion Kinases
  • contains a cytoskelton - called stress fibres ) makes its own tension
  • responds to tension to secrete collagen
56
Q

where do we find stress fibres -

A

cytoskelton of fibroblasts

57
Q

tension organizes what

A

tennsion organizes tropocollagen to fibrils

tension organizes fibrisl to fibres

58
Q

how many myofibres

A

up to 1000

59
Q

do myofibres have nuclei

A

yes and satellite cells

60
Q

myonuclei vs satellite cells

A

satellite cells used for tissue repair
satellite cells are found under the basement membrane but above the plasma lemma - and they have their own membrane

myonuclei under both

61
Q

mitchondria are where in muscle

A

mitochonrdria squish beteween myofibrils

62
Q

two types of mitochondria

A

mitochondria have two differeetn pools

subsarcolemma poools -
intramyofibrular- (IMF) - IMF are the highly aerobic pools

IMF and Subsarcolemma Pools of Mitochondria

63
Q

mitochondria pools

A

IMF and subsarcolemma decrease with age

mitochondria are highly branched

64
Q

branching fibres? fibrils?

A

myofibres arent branched, fibrils are

in the heart myocardial fibres are branched

65
Q

myofibril (contractile)

A

sarcomere - myosin actin all that jazz

66
Q

myosin

A

2 heavy chains 4 light chains

67
Q

actin

A

actin with tropomyosin and troponin

68
Q

how many thin surround thick filaments

A

6 thin around 1 thick

69
Q

what is titin?

A

titin is a structural/accesory protein that spans the entire lenght of a sarcomere - from z-line to m-line

largest protein in our body

gives resting tension to our muscles

allows myosin and actin to contact eachother

can scaffold for other protiens, like dystopphin or inte

coiled up at z disk

when lengthened muscle (relaxed) titin uncoils and reveals tension sensors and signalling proteins.
thesse proteins phosphorylate down to another target protein, chanign gits turning it on configuration therfore important for muscle hypertrophy and growth

70
Q

titin uncoiled

A

titin uncoilded shows its kinase domains as wwell as signalling proteins, thesse proteins phjsophorylate and signal target proteins that can lead to adaptation

71
Q

z disk proteins

A

nebulin, desmin and plectin

72
Q

nebulin

A

lets actin build off it

73
Q

intergrins

A

interns connect the basement mebrane to the fibre

they transmit force alongside dystroglycan complexes - pulling on the contractile fibres of actin via accesory proteins (FAK)

74
Q

costamere

A
  • at the z disk of sarcomeres - act as the anchors and traducers of tension (integrins adn dystroglycan complexs)
75
Q

myotendinous junctin (MTJ)

A

sarcolemma invaginates the tendon at its ECM

high density of costameres, and integrins because lots of tension here

76
Q

FAK

A

focal adhesion kinases - act as the costameres in fibroblasts and in sarcomeres, are connected to integrins which phosphorylate subsequent protiens to their target protein in order to change configuration, important for hypertophy of muscl and growht

77
Q

Muscular Dystophy types

A

Duchene and Beckers - duchene more common - worse

beckers less common and not as bad

78
Q

muscular dytrophy what is

A

something wrong with your dystophin protien whihc connects plasmalemma and contractile proteins - allows us to tranduice force

79
Q

muscular distrophy rates

A

1/20000 have a hereditary myopathy

1/3500 boys have dystrophy = common

80
Q

muscular distrophy cycle

breakdown regeneration cycle

A

fibres chronically breakdown
imfllamatory cells go to the site adn secrete collagen
satellite cells help to repair - but this happens so much those deplete adn then we lose the regeneeration part

81
Q

chromosome linked muscular dystophy

A

x recessive

xx okay xy no good

82
Q

collagen type 1

A

all mysiums /tendon

83
Q

collagen type 2

A

cartliage

84
Q

collagen type 3and 5

A

mysiums and MTJ

85
Q

collagen type 4

A

BM non fibrillar

86
Q

collagen type 6

A

BM to endo

87
Q

collagen fibres are non fibrillar are?

A

collagen 4 and 6 in BM

88
Q

flexibility depends on…

A

addition of sarcomeres
ECM pliability
sensory neuromuscular feeback (ROM)

89
Q

more force = less flixibilty therfore

A

more flexibility = less force

90
Q

more fibres, density, type, crimp, glycation, organization, determine

A

flexibility and stifness

91
Q

free cells

A

blood cells

92
Q

fixed cells

A

everything else

93
Q

whats its pair

irregular and loose

A

dense and regular

94
Q

endomysium tissue is what type

A

dense irregular

95
Q

epi and parimysium CT is waht type

A

dense regular

96
Q

25% of protein mass in our bodies is what protein

A

collagen

97
Q

acute bone remodeling

A

lack of Ca+ in blood, osteoclasts send Ca+ to blood - osteoclasts activsated by PTH

98
Q

what activates osteoclasts to send calcium to blood

A

Para Thyroid Hormone

99
Q

osteoclasts purpose adn make up

A

made up of HSC - monocytes that fuse together with osteoblasts

these resorp bone mineral

100
Q

osteoclasts secrete

A

H+ioons and MMP to breakdown bone for resorption

101
Q

resorption is based on

A

activity of osteoclasts and number of osteoclasts.

102
Q

what nhibits resorption

A

estrogen and testosterone

103
Q

4 roles of estrogen

A

tells mature osteoclasts to kill themselves

slows release of PTH from PT

stims IGF production in osteoblasts

stims epiphyseal plate closure in late puberty by inhibitj g IGF

104
Q

exercise and bone

A

more exercise = more tension = more osteoblasts/cytes = more collagen/apatite = more BMD

105
Q

OsteoTEndinous Junction

A

the oppostie to the MTJ

high degree of osteoblast/cyte acitivty here

more dense none at these insertion points as this is where most force gets exerted too,

106
Q

4 zones of OTJ

A

tendon - fibroblasts T1C
fibrocartilage - chondrocytes T2C some T1
mineralized fibro cartilage - more chondrocytes w/ apatite mainly TYPE 2C
bone - sharpeys fibres connect thriug perisosteum into mineralized fibrocartilage as anchors

107
Q

osteoporosis -

A

low BMD (more than 2.5vStandard Deviations from average)

108
Q
A

MSK - Mid Term 1 (1 decks)

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