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(SALMA) Physiology > MSK > Flashcards

MSK Flashcards

1
Q

list some purposes of the skeleton

A
  1. raises us up from the ground against gravity
  2. determines basic body shape
  3. transmits body weight
  4. forms jointed lever systems for movement
  5. protects vital structures from damage
  6. houses bone marrow
  7. mineral storage
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2
Q

list the 5 different types of bone

A
  1. long
  2. short
  3. flat
  4. irregular
  5. sesamoid
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3
Q

describe long bones

A
  • tubular hollow shaft
  • expanded ends for articulation
    eg femur and humerus
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4
Q

describe short bones

A
  • cuboidal in shape

eg carpals

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5
Q

describe flat bones

A
  • (often curved) plates of bone
  • protective function
    eg bones of the skull
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6
Q

describe irregular bones

A
  • various shapes

eg vertebrae

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7
Q

describe sesamoid bones

A
  • round, oval bones embedded in a tendon

eg patella

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8
Q

what are the 2 types of macro bone structure?

A

cortical and trabecular

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9
Q

what is cortical bone?

A

(macro) COMPACT
- dense and solid
- only spaces are for cells and blood vessels

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10
Q

what is trabecular bone?

A

(macro) CANCELLOUS/spongy
- network of bony struts filled with bone marrow
- cells reside in trabecular, blood vessels reside in holes

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11
Q

what are the 2 types of micro bone structure?

A

woven and lamellar

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12
Q

what is woven bone?

A

(micro)

  • made quickly
  • disorganised
  • no clear structure
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13
Q

what is lamellar bone?

A

(micro)

  • made slowly
  • organised
  • layered structure
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14
Q

what is bone composed of?

A 
50-70% = minerals (hydroxyapatite, a crystalline form of calcium phosphate)
20-40% = organic matrix (90% T1 collagen, 10% non-collagenous)
5-10% = water
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15
Q

what % of bone is minerals?

A

50-70%

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16
Q

what is the main mineral in bone?

A

hydroxyapatite

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17
Q

what is hydroxyapatite?

A

a crystalline form of calcium phosphate (reservoir for calcium and phosphate)

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18
Q

what % of bone is organic matrix?

A

20-40%

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19
Q

what is organic matrix composed of?

A

90% of protein = t1 collagen

10% = non-collagenous proteins

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20
Q

what % of bone is water?

A

5-10%

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21
Q

how is collagen assembled in the bone?

A

in fibrils with crystals situated in the ‘gap’ regions between them

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22
Q

what does collagen provide bones with?

A

stiffness

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23
Q

what do minerals provide bones with?

A

elasticity

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24
Q

what are the 4 main bone cells?

A
  • osteoclasts (multinucleated)
  • osteoblasts (plump, cuboidal)
  • osteocytes
  • bone lining cell
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25
Q

what’s the difference between osteoblasts and osteoclasts?

A 
osteoBlasts BUILD bone
osteoClasts CHEW (break down)
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26
Q

what do osteoblasts do?

A
  • derived from haematopoietic stem cells
  • form bone - in form of osteoid
  • produce t1 collagen
  • act by secreting collagen into matrix (mineralise the extracellular matrix by depositing hydroxyapatite crystal within collagen)
  • high alkaline phosphate activity
  • make non-collagenous proteins
  • secrete factors that regulate osteoclasts eg RANK ligand
  • once collagen becomes calcified (mineralisation), osteoblasts become osteoCYTES
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27
Q

what is osteoid?

A

unmineralised, organic portion of bone matrix that forms prior to bone maturation

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28
Q

what do osteoclasts do?

A
  • resorb bone
  • dissolve the mineralised matrix
  • break down collagen bone
  • secrete collagenases and proteinases
  • high expression of TRAP and cathepsin K
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29
Q

what do osteocytes do?

A
  • form tight junctions with neighbouring osteocytes
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30
Q

what are the 2 ways in which bone shape can be renewed?

A
  • MODELLING = gross shape is altered, bone is added/taken away
  • REMODELLING = all of bone is altered, new bone replaces old
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31
Q

list some reasons for bone remodelling

A
  1. forms bone shape
  2. to replace woven bone with lamellar
  3. to reorientate fibrils and trabecular in favourable direction for mechanical strength
  4. in response to loading (exercise)
  5. to repair damage
  6. to obtain calcium (eg in times of stress such as pregnancy)
  7. dysregulated remodelling = disease
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32
Q

what is the skeleton divided into?

A

axial and appendicular

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33
Q

what is the difference between the axial and appendicular skeleton?

A 
axial = bones of head/trunk
appendicular = upper and lower limbs and girdles (shoulder/pelvis)
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34
Q

discuss primary bones

A

primary bones are the 1st bones that appear in embryonic development and fracture repair

it undergoes bone building in 1st trimester

  • poorly organised structure
  • synthesised from mesenchyme/cartilage
  • bone is often heavy and weak

primary bone is REMODELLED

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35
Q

discuss secondary bones

A

the result of remodelling by osteoblasts/clasts

  • occurs around age 17-18 (after growth stops)
  • well organised structure
  • bone is lighter
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36
Q

what are the 2 main types of ossification (and the difference between them)?

A
  • endochondral ossification (produces LONG bones, cartilage is present)
  • intramembranous ossification (produces FLAT bones, cartilage not present)
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37
Q

how are collagen fibrils formed?

A

3 collagen molecules –> tropocollagen –> collagen fibril

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38
Q

what joins collagen together?

A

covalent cross-links within the tropocollagen molecule and hydrogen bonds between hydroxyproline molecules (within tropocollagen) [requires vit c]

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39
Q

how is collagen broken down?

A

by proteinases - especially collagenases and cathepskin K (in bone)

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40
Q

why is vitamin C important in bone and what condition is associated with this?

A

vitamin c is involved in collagen formation

scurvy = severe vitamin c deficiency

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41
Q

what disease is as a result of not enough collagen?

A

osteogenesis imperfecta aka brittle bone disease

not enough collagen to support minerals in bone thus making bone weak

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42
Q

list 6 diff types of collagen and where they’re found

A

type I = bone marrow, tendon, ligaments, skin
type II = articular cartilage
type III = alongside type I, wound healing
type IV = basal lamina
type V = cell surfaces
type X = growth plate

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43
Q

describe the stages in endochondral ossification

A

remember, it produces long bones

mnemonic: Boys Can’t Pee During Erections

  1. Bone collar formation
  2. Cavitation
  3. Periosteal bud invasion
  4. Diaphysis elongation (diaphysis is the middle portion)
  5. Epiphyseal ossification (epiphyseal = 2 round bits at ends)
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44
Q

describe stage 1 of endochondral ossification

A

BONE COLLAR FORMATION

  • osteoprogenitor cells –> osteoblasts
  • osteoblasts secrete osteoid
  • bony collar formed around shaft (diaphysis)
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45
Q

describe stage 2 of endochondral ossification

A

CAVITATION (cavity formation)

  • cartilage in bone centre begins to ossify [primary ossification centre]
  • inner cartilage can’t get nutrients –> degrades and forms cavity
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46
Q

describe stage 3 of endochondral ossification

A

PERIOSTEAL BUD INVASION

  • vessels in periosteum invade cavity through nutrient foramen
  • vessels bring blood, nutrients and osteoblasts/clasts
  • osteoclasts break down cartilage and osteoblasts secrete spongy bone
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47
Q

describe stage 4 of endochondral ossification

A

DIAPHYSIS ELONGATION

  • increased cell numbers + osteoid –> elongation of diaphysis
  • vessels bud into cartilage at ends of bone [secondary ossification centre]
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48
Q

describe stage 5 of endochondral ossificaiton

A

EPIPHYSEAL OSSIFCATION

  • when completed, hyaline cartilage remains only in epiphyseal plates and articular cartilages
  • ends of bone form spongy bone
  • articular cartilage on end of bone - growth/epiphyseal plate on other side
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49
Q

describe intramembranous ossification

A

(produces flat bones)

  1. ossification centre forms
    - mesenchyme cells –> osteoprogenitor cells –> osteoblasts –> primary ossification centre
  2. calcification
    - osteoblasts secrete collagen/proteins –> forms osteoid (bony matrix)
    - osteoid is calcified –> engulfs osteoblasts to form osteocytes
  3. trabecular formation
    - osteoid is randomly laid down around blood vessels –> trabeculated (osteoblasts are on periphery)
  4. periosteum development
    - peripheral osteoid becomes compact bone –> spongy bone contains bone marrow
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50
Q

what are the 4 hormonal influences on growth?

A

growth hormone
- increases growth

thyroid hormone

  • increases metabolic rate
  • required for growth

sex hormones
- stimulates growth at puberty by stimulating GH

cortisol
- inhibits growth

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51
Q

how is calcium distributed?

A

mainly in skeleton - 1200g

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52
Q

what is calcium like in neonates?

A

they have only 30g thus need lots of milk during development

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53
Q

what are the levels of calcium intra/extracellularly? (and why is it needed there)

A

extracellularly - 1g
- needed for blood clotting, muscle contraction and nerve function

intracellularly - trace

  • calcium in the ER
  • major in muscle (SR)
  • important for signalling
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54
Q

what is the total serum calcium?

A

2.4 mmol/L

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55
Q

what are the 3 forms of calcium in serum?

A
  1. ionised (free)
  2. complex eg citrate/phosphate
  3. protein-bound
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56
Q

discuss ionised calcium

A
  • just under half of serum
  • metabolically ACTIVE
  • if serum pH increases (alkalosis) = less ionised calcium
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57
Q

why is there less ionised calcium if serum pH increases?

A
  • albumin is neg charged and a buffer
  • H+ taken away from neg albumin
  • Ca2+ has to take place of excreted H+ to balance charge
  • thus, less circulating ionised calcium
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58
Q

discuss complexed calcium

A
  • metabolically INACTIVE

- filtered by the kidney

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59
Q

discuss protein-bound calcium

A
  • metabolically INACTIVE
  • mainly bound to albumin
  • cannot be filtered by the kidney
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60
Q

what condition is low ionised calcium associated with?

A

tetany

associated with contraction of small muscles of hands/feet

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61
Q

discuss calcium kinetics (3 types of absorption)

A

calcium can be:

  • ABSORBED from gut (excreted in faeces)
  • REABSORBED from kidney (secreted into kidneys)
  • RESORBED from bone (lost in bone formation - helping to mineralise)
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62
Q

name some major and minor dietary sources of calcium

A
  • major: dairy prods (2/3) - milk, yoghurt, cheese

- minor sources: veg (broccoli), cereals, oily fish

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63
Q

what % of dietary calcium is absorbed?

A

30% (actively or passively)

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64
Q

where does active calcium absorption occur?

A

in the duodenum and jejunum (majority)

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65
Q

what is active calcium absorption mediated by?

A

calcitriol (activated vitamin d)

  • low calcium diet = increased calcitriol = increased calcium absorption in duodenum/jejunum
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66
Q

where does passive calcium absorption occur?

A

ileum and colon (to a much lesser extent)

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67
Q

what are the 2 processes in which calcium can be released from the bone?

A
  1. can be released RAPIDLY from exchangeable calcium on bone surface
  2. can be released from osteoclasts during bone resorption which is much SLOWER
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68
Q

what does calcium filtration through the glomerulus depend on?

A
  1. GFR

2. ultra filtrable calcium (ie calcium which is either ionised or complexed to phosphate)

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69
Q

if the GFR is high, is there more or less calcium filtration?

A

more

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70
Q

what % of calcium filtered by the kidneys is reabsorbed back into the blood?

A

98%

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71
Q

if PTH levels are high, does reabsorption of calcium increase or decrease?

72
Q

if filtered sodium levels are high, what effect does it have on calcium filtration?

A

calcium filtration decreases (based on share of channels)

73
Q

is calcium movement out of the nephron active or passive?

74
Q

what % do diff parts of the nephron excrete calcium?

A

65% @ PCT
25% @ LOH
10% @ DCT

75
Q

is reabsorption of phosphate mostly active or passive?

76
Q

what is the difference between calcium and phosphate reabsorption at the kidneys?

A

calcium = mostly passive WHEREAS phosphate = mostly active

77
Q

what are the 3 hormones involved in regulation of calcium metabolism and what type of feedback is this?

A
  1. PTH
  2. calcitriol
  3. calcitonin

negative feedback

78
Q

what is calcitriol?

A

activated vit d

79
Q

how is PTH secreted?

A
  • decrease of serum Ca2+
  • sensed by 4 parathyroid glands
  • PT glands then secrete PTH
80
Q

how is PTH inactivated?

A
  • PTH made of 84 amino acids
  • structure needs to be intact for it to be active
  • once Ca2+ levels rise again, PTH is broken down thus inactivated
81
Q

what does PTH do?

A
  • acts on its target cell (bone, kidney)

- activates 2nd messengers eg cAMP, intracellular calcium

82
Q

does PTH increase or decrease phosphate reabsorption at PCT?

A

decreases

hence, it increases phosphate reabsorption at DCT

83
Q

what are the 4 main ways of increasing Ca2+?

A
  • increase calcitriol prod @ kidney
  • increase calcium reabsorption at DCT
  • increase calcium leeching out of bone
  • decrease phosphate reabsorption at PCT (allow more calcium reabsorption at DCT)
84
Q

what % of vit d is from diet?

A

20% - this is D2 (ergocalfierol)

85
Q

where does 80% of vit d come from?

A

breakdown of cholesterol in the skin - this is D3 (cholecalciferol)

86
Q

where does vit d get activated?

A

liver then the kidney

87
Q

which form of vitamin d does the liver produce?

A

25(OH)vit d (calcidiol)

88
Q

which form of vitamin d does the kidney produce?

A

1,25(OH)2vitamin D (calcitriol)

89
Q

what determines how much of the 25(OH)vitD is converted into 1,25(OH)vitD?

A

kidney hormones

  • these hormones are stimulated by PTH or if levels of 1,25(OH)vitD are low
  • low levels of FGF23 also stimulates more
90
Q

what is 1,25(OH)vitD also known as?

A

calcitriol

91
Q

what is 25(OH)vitD also known as?

92
Q

which hormone is secreted in response to an increase in serum calcium?

A

calcitonin

93
Q

what is the difference between fast and slow actions in calcium homeostasis?

A

fast: exchangeable calcium is released from bone surface and decreased calcium excretion from kidney
slow: incr bone resorption, incr fractional absorption by intestine via activated vitD

94
Q

how much phosphate is there in the body (and how is this distributed)?

A

500-800g

1% total body weight
90% in bone mineral

95
Q

what is the normal range for serum phosphate?

A

0.8-1.5 mmol/L

96
Q

what does high phosphate result in?

A

excessive formation of hydroxyapatite and deposition in tissues other than bone

97
Q

what does low phosphate result in?

A

poor bone mineralisation ie low hydroxyapatite

rickets/osteomalacia, pain/fractures

98
Q

name some dietary sources of phosphate

A

animal, dairy, soy, seeds/nuts

99
Q

what is the adult daily recommendation of phosphate?

100
Q

where is phosphate absorbed?

A

in the small intestine

passie diffusion @ hich conc
active transport @ low conc (sodium dependent)

101
Q

what % of phosphate is reabsorbed into the blood at PCT & DCT?

A

80% @ PCT

10% @ DCT

102
Q

what is phosphate metabolism regulated by?

A
  • PTH
  • calcitriol
  • FGF-23
103
Q

what is FGF-23?

A

fibroblast growth factor 23

  • a major regulator of phosphate metabolism
  • produced by osteocytes
  • increases renal excretion of phosphate
  • decreases gut absorption of phosphate
104
Q

what is the main and secondary regulator in phosphate metabolism?

A

main: FGF-23
secondary: PTH

105
Q

what % of body is made of collagen?

106
Q

what is a fracture?

A

breech in continuity of bone

107
Q

what are the 4 fracture healing stages?

A
  1. haematoma (hours)
  2. inflammation (days)
  3. repair (months to years)
  4. remodelling (months to years)
108
Q

what happens during fracture healing stage 1?

A

HAEMATOMA (hours)

  • bleeding from endosteal and periosteal vessels/muscles
  • decreased blood flow to fracture site = leads to perinatal stripping and osteocyte death
109
Q

what happens during fracture healing stage 2?

A

INFLAMMATION (days)

  • fibrin clot organisation bc of platelets
  • neurovascularisation
  • cellular invasion (osteoclasts resorb dead bone, mesenchymal stem cells stimulate new bone etc)
110
Q

what happens during fracture healing stage 3?

A

REPAIR (months to years)

  • callus formation (fibroblasts prod fibrous tissue, chondroblasts prod cartilage, osteoblasts prod osteoid)
  • progressive matrix mineralisation
  • high vascularity provides nutrition and blood supply
111
Q

what happens during fracture healing stage 4?

A

REMODELLING (months to years)

  • woven bone structure from repair stage is replaced by lamellar bone
  • increased bone strength
  • vascularity returns to normal
  • healing w/o scar tissue
112
Q

list 3 functions of joints

A
  1. allow movement in 3D
  2. to be weight-bearing
  3. to transfer load evenly to MSK system
113
Q

what are the 2 classifications of joints?

A

structural (by degree of movement) and functional (by the components which hold the joint together)

114
Q

what are the 3 types of joints according to structural classification?

A
  • fibrous eg teeth sockets
  • cartilaginous eg IVD
  • synovial eg metacarpophalangeal
115
Q

what are the 3 types of joints according to functional classification?

A
  • synarthroses eg skull sutures
  • amphiarthroses eg IVD
  • diarthroses eg hip
116
Q

what are synarthroses?

A

immovable joints, mostly fibrous

eg skull sutures

117
Q

what are amphiarthroses?

A

slightly moveable joints, mostly cartilaginous

eg IVD

118
Q

what are diarthroses?

A

freely moveable joints, mostly synovial

eg hip joint

119
Q

what are fibrous joints connected by?

A

a cord (ligament) or sheet (interosseous membrane) of fibrous tissue

120
Q

what are cartilaginous joints connected by?

A

hyaline cartilage

usually amphiarthroses ie slightly moveable eg costal cartilage

121
Q

list the 5 characteristic features of synovial joints

A
  1. articular cartilage
  2. joint capsule (inner layer = synovial membrane)
  3. joint (synovial) cavity
  4. synovial fluid
  5. reinforcing ligaments
122
Q

what are bursae?

A

fluid filled sacs lined by synovial membrane

123
Q

what are menisci?

A

discs of fibrocartilage

124
Q

what is cartilage composed of?

A

water, proteoglycans, collagen

125
Q

what is the diff between tendons and ligaments?

A
  • tendons connect bone to muscle

- ligaments connect bone to bone

126
Q

which group of muscles help in stabilisation of the shoulder joint?

A

rotator cuff muscles

  1. subscapularis
  2. supraspinatus
  3. infraspinatus
  4. teres minor
127
Q

what type of joint is the shoulder joint?

A

ball and socket (synovial)

128
Q

what does synovial fluid do?

A

increases lubrication of the joint

129
Q

are tendons/ligaments well vascularised?

A

no, so generally have poor capacity for healing

130
Q

what are tendons and ligaments mainly composed of?

A

collagen (mainly type I)

131
Q

what is the precursor of collagen?

A

procollagen

132
Q

how do ligaments and tendons differ in their elastin content?

A

ligaments have a higher elastin content

133
Q

what is the place of insertn of a tendon or ligament into bone called?

134
Q

what effect does physical training have on ligaments?

A

they become stronger/stiffer

collagen fibres incr in diameter

135
Q

what does ACL of the knee do?

A

provides rotational stability and resists anterior translation of the tibia

136
Q

what does PCL of the knee do?

A

resits post translation of femur

137
Q

what does MCL do?

A

resists valgus (inwards) force on the knee

138
Q

what does LCL do?

A

resists varus (outwards) force

139
Q

what causes gout?

A

high uric acid levels cause uric acid crystals to deposit in joints. these cause inflammation which causes swelling, pain n redness

140
Q

how does pH affect uric acid solubility?

A

the lower the pH, the less soluble it becomes

141
Q

what does uric acid come from?

A

purines (adenine/guanine)

142
Q

list some sources of purines

A

diet (meat, offal, seafood, fish), breakdown of nucleotides from tissues, synthesis in the body

143
Q

how does uric acid leave body?

A

70% excreted in urine

30% broken down in gut

144
Q

what impact does oestrogen have on uric acid excretion in urine?

A

promotes it

145
Q

list 4 purines

A

adenine, guanine, hypoxanthine, xanthine

146
Q

what is the metabolic end prod of purine metabolism?

147
Q

what is hyperuricaemia as a result of?

A
  • over production or under excretion of uric acid
148
Q

list 3 functions of bone

A
  • protect vital soft organs eg brain
  • allow muscles to work to move us around
  • store mineral and house marrow cells
149
Q

what are the 3 types of muscle?

A

skeletal
smooth
cardiac

150
Q

describe skeletal muscle

A
  • multinuclated
  • long, unbranched fibres
  • voluntary contraction
  • transverse tubules
  • sarcoplasmic reticulum
151
Q

describe smooth muscle

A
  • uninucleate
  • unbranched fibres
  • involuntary contraction
  • unstriated
152
Q

describe cardiac muscle

A
  • branched fibres
  • intercalated discs
  • purkinje fibres
  • fairly striated
  • inherent rhythm
153
Q

list some types of synovial joints

A
  • plane joint eg wrist/ankle
  • hinge joint eg elbow/knee
  • ball and socket joint eg shoulder
154
Q

what enhances the strength of collagen molecules?

A

cross-linking between alpha chains (remember, 3 alpha chins are coiled in the left hand helix and same with right)

155
Q

where are collagen molecules synthesised and then assembled into fibrils?

A
  • collagen molecules are synthesised inside the cell
  • they are then secreted into extracellular space
  • outside the sell, collgaen fibrils self assemble
156
Q

how are ligaments and tendons formed?

A

tropocollagen –> microfibrils –> sub fibrils –> fibrils –> fibres –> fascicles –> tendon

157
Q

what is an enthesis?

A

place of insertion of tendon or ligament into bone

158
Q

what are the 2 types of insertion (entheses)?

A

fibrous and fibrocartilagenous

159
Q

what does enthusis insertion depend on?

A

cellular processes involved during their formation

160
Q

what are entheses innervated by?

A

proprioceptive and pain receptors

161
Q

what is the main difference between fibrous and fibrocartilage insertion at entheses?

A

fibrous: formed through intramembranous ossification
fibrocartilage: formed through endochondral ossification

162
Q

describe fibrous insertion (entheses)

A

calcified anchorage is by calcified collagen fibres (Sharpey’s fibres) into bone

163
Q

describe fibrocartilage insertion (entheses)

A

gradual change from collagenous ligament –> fibrocartilage –> mineralised cartilage –> bone

164
Q

how can you describe fractures?

A
  • site
  • pattern
  • displacement/angulation
  • joint involvement
  • skin involvement
165
Q

what is coupling?

A

bone formation occurs at sites of previous bone resorption

166
Q

what is balance?

A

amount of bone removed by osteoclasts should be replaced by osteoblastic activity

167
Q

what are osteoclasts derived from?

168
Q

what activates osteoclasts?

A

RANK ligand

169
Q

what is RANK ligand secreted by?

A

osteoblasts

170
Q

what is bone remineralisation also known as?

A

calcification

171
Q

what is calcitonin produced by?

A

c cells of thyroid gland

172
Q

what does calcitonin do?

A

lowers calcium levels

  • suppresses calcium release from bones, dampens calcium absorption in intestine and discourages kidney reabsorption of calcium
173
Q

what is osteopenia?

A

decreases bone density but not to extent of osteoporosis

174
Q

what is osteoporosis?

A

osteopenia to a greater degree

decreased bone density

175
Q

what is osteomalacia?

A

decreased mineralisation of newly formed bone (caused by severe vit D deficiency or cold that cause low blood phosphate levels)

(SALMA) Physiology (12 decks)

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