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Phase 1 > MSK💪🩻🦴 > Flashcards

MSK💪🩻🦴 Flashcards

1
Q

Why do we have bones?

A
  • Raises us from the ground against gravity
  • Determines basic body shape
  • Transmits body weight
  • Forms jointed lever system for movement
  • Protects vital structures from damage
  • Houses bone marrow
  • Mineral storage (calcium, phosphorous,
    magnesium
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2
Q

Types of bone classification by shape

A

Long bones
Short bones
Flat bones
Irregular bones
Sesamoid bones

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3
Q

Shape of long bones

A

Tubular shape with hollow shaft and ends
expanded for articulation with other bones

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4
Q

Shape of short bones

A

Cuboidal

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5
Q

Shape of flat bones

A

Plates of bone, often curved, protective function

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6
Q

Two areas of bones and how many in each

A

Apendicular skeleton- 126 bones
Axial skeleton- 80 bones

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7
Q

Shape of irregular bones

A

Various shapes

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8
Q

Shape of sesamoid bones

A

round, oval nodules in a tendon

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9
Q

Cortical bone structure

A

= Compact
Dense, solid, only
spaces are for cells
and blood vessels.

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10
Q

Trabecular bone structure

A

= Cancellous
= Spongy
Network of bony struts
(trabeculae), looks like
sponge, many holes
filled with bone marrow.
Cells reside in
trabeculae and blood
vessels in holes

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11
Q

Woven bone microstructure

A

Made quickly
Disorganised
No clear structure

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12
Q

Lamellar bone microstructure

A

Made slowly
Organised
Layered structure

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13
Q

What do hollow long bones do?

A

Keeps mass away from neutral axis,
minimizes deformation

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14
Q

What do trabecular bones do?

A

Gives structural support while
minimizing mass

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15
Q

What do wide ended bones do?

A

Spreads load over weak, low friction
surface

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16
Q

What do flat bones do?

A

Condensed so protective

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17
Q

Composition of adult mammalian bone

A

50-70% mineral
(Hydroxyapatite, a crystalline form of Calcium Phosphate)
20-40% organic matrix
Collagen (type 1) – 90% of all protein
Non-collagenous proteins -10% of all protein
5-10% water
The collagen assembles in fibrils with mineral crystals situated in ‘gap’
regions between them

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18
Q

How does bone microstructure contribute to function?

A

Bone is a composite
Mineral provides stiffness
Collagen provides elasticity

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19
Q

What are the cells of the bone?

A

Osteoclast - multinucleated
Osteoblast- plump, cuboidal
Osteocyte- stellate, entombed in
bone
Bone lining cell- flattened, lining the bone

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20
Q

Origins of osteoblasts

A

Mesenchymal stem cell -> progenitor cells -> osteoblasts, adipocytes, myoblasts, chondrocytes, fibroblasts

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21
Q

Function/characteristics of osteoblasts

A

Form Bone - in form of osteoid
Produce Type I collagen and mineralize
the extracellular matrix by depositing
hydroxyapatite crystal within collagen
Fibrils
High Alkaline Phosphatase activity
Make non-collagenous proteins
Secrete factors that regulate osteoclasts
ie RANKL

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22
Q

Origin of osteoclasts

A

Haematopoetic stem cells -> determination -> proliferation, survival -> differentiation -> attachment, resorption

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23
Q

Function/characteristics of osteoclasts

A

Resorb Bone
Dissolve the mineralised matrix (acid)
Breakdown the collagen in bone
(enzymatic)
High expression of TRAP and
Cathepsin K

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24
Q

Bone remodelling process

A

Resorption -> reversal phase -> formation -> resting phase -> activation -> back to resorption

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25
Q

Bone modelling

A

Gross shape is altered, bone added or
taken away

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26
Q

Bone remodelling

A

All of the bone is altered, new bone
replaces old bon

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27
Q

Reasons for bone remodelling

A
  • Form bone shape
  • Replace woven bone with lamellar bone
  • Reorientate fibrils and trabeculae in favourable direction for mechanical strength
  • Response to loading (exercise)
  • Repair damage
  • Obtain calcium
  • Dysregulated remodelling = disease!
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28
Q

Different stages of changes of bone

A

0-20 -> development -> modelling
20-50 -> maintenance -> remodelling
50+ -> osteoporosis -> acquired pathology

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29
Q

How do pathological fractures heal?

A

Periosteum tears
Haematoma
Adjacent bone cell death
Soft tissue damage
Callus
Osteoblasts -> new woven bone
Osteoclasts -> mop up dead bone, remodel strong bone
Osteoblasts lay down lamella bone

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30
Q

Two types of bone treatments

A

Anti-catabolic- stop osteoclasts (more)

Anabolic- stimulate osteoclasts

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31
Q

What is Gly-X-Y?

A

modular building block
(3 residues per turn) up to about 1000 amino acids
X and Y are often proline, hydroxyproline or hydroxylysine
Allows the formation of a helix (alpha-chain)

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32
Q

Outline tropocollagen

A

3 collagen chains – 2 x α1 + 1 x α2
Form the 3-stranded
tropocollagen molecule

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33
Q

How is tropocollagen arranged and what holds it together?

A

The tropocollagen modules are
then assembled into a collagen
fibril
The tropocollagen molecule and
the fibril are held together by
covalent crosslinks (both intraand intermolecular) derived from
lysine/hydroxylysine side-chains

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34
Q

Processing of type I collagen

A

N terminals and c-terminals are cut off the ends

N creates P1NP
C creates P1CP

Can be measured

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35
Q

What joins collagen together?

A

Covalent crosslinks
Hydrogen bonds
Intermolecular crosslinks

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36
Q

Outline covalent crosslinks in collagen

A

– Within and between the triple helix/tropocollagen molecule
= “intra/intermolecular crosslinks” – OH-lysine x2
lysyl oxidase needs copper

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37
Q

Outline hydrogen bonding in collagen

A

– Between hydroxyproline molecules, within tropocollagen
* OH-proline from proline requires Fe2+
* Fe3+ to Fe 2+ requires vitamin C

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38
Q

How are tropocollagen molecules bound together?

A

– = “intermolecular crosslinks” -
– OH-lysine x 3 = pyridinolines

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39
Q

Collagen breakdown

A

Via proteinases esp. collagenases and
cathepsin K (in bone)
Can be a normal process of repair and replacement
(breakdown is balanced by synthesis),
or pathological process
- examples: arthritis, osteoporosis, tumour invasion,
hypertrophic scarring, kidney fibrosis

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40
Q

Breakdown products of type I collagen

A

NTX and CTX
Can be measured to see breakdown

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41
Q

Outline the types of collagen

A

– Type I – bone, tendon, ligaments, skin
– Type II – articular cartilage, vitreous
– Type III – alongside Type I – wound healing
– Type IV - basal lamina
– Type V – cell surfaces
– Type X – growth plate

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42
Q

Outline bone matrix

A
  • Synthesised by osteoblasts
  • 90% collagen
  • Other proteins
  • osteocalcin, osteonectin, osteopontin, fibronectin, bone sialoprotein,
    bone morphogenetic proteins (BMPs)…
  • Contribute to structure
  • Regulate bone cell activity
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43
Q

Outline bone mineralisation

A
  • Alkaline phosphatase hydrolyses pyrophosphate
  • Inorganic phosphate complexes with calcium to form
    hydroxyapatite
  • Hydroxyapatite crystals propagate along collagen
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44
Q

Where does intramembranous ossification occur?

A

*Skull
*Clavicles

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45
Q

Outline endochond

A

Chondrocytes become hypertrophic which attracts blood vessels and so osteoblasts which form the bones

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46
Q

Secondary ossification centres

A
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47
Q

Growth plate fusion

A

Driven by oestrogen

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48
Q

Appositional growth of bone

A

Outward growth of bone
Osteoblasts on osteocortical surface add on bone going outwards
Osteoclasts add on bone growing inwards

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49
Q

Age of peak bone mass

A

About age 25

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50
Q

Enzyme for bone mineralisation

A

Alkaline phosphatase

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51
Q

Outline distribution of calcium in the body

A

*Skeleton is main reservoir
o 1200 g
*Extracellular space has much smaller amount of
calcium (only 1 g), but it is key for
o Muscle contractility
o Nerve function
o Normal blood clotting
Total serum calcium usually about 2.4 mmol/L
Ionised serum calcium about 1.1 mmol/L

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52
Q

Outline the different types of calcium in circulation

A

*Ionised, metabolically active
*Protein-bound, not metabolically active
*Complexed, such as citrate, phosphate

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53
Q

Modulation of ionised calcium by pH

A

At higher pH, albumin binds strongly to calcium

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54
Q

Effect of low ionised/serum calcium

A
  • Low ionised calcium is associated
    with contraction of the small muscles
    of the hands and feet
    o TETANY
    There is depolarization of the long nerves of the upper limb
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55
Q

Sources of dietary calcium

A
  • Major sources
    o Dairy products make up 2/3
    − Milk, yoghurt, cheese
  • Minor sources
    o Vegetables, e.g. broccoli
    o Cereals, e.g. white bread
    o Oily fish, e.g. sardines
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56
Q

Recommended intake of calcium

A

700 mg/day

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57
Q

Outline calcium absorption

A

*We absorb about 30% of dietary calcium
o Active absorption in duodenum and jejunum
o Passive absorption in ileum and colon
*Higher fractional excretion when low availability
o More active transport
o Mediated by calcitriol, the active form of vitamin D

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58
Q

Outline release of calcium from bone

A
  • Calcium can be released rapidly from exchangeable
    calcium on the bone surface
    o We don’t know much about this mechanism
  • Calcium can be released more slowly by osteoclasts
    during bone resorption
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59
Q

Outline calcium handling by the kidney

A

*The amount of calcium filtered by the glomerulus depends on
o Glomerular filtration rate
o Ultrafiltrable calcium
− Ionised
− Complexed
* 98% of this filtered calcium is usually reabsorbed
o Reabsorption increased by PTH
o Reabsorption decreased if the filtered sodium is high

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60
Q

Calcium and phosphate reabsorption and excretion

A

Fractional excretion of calcium- 2%
Fractional excretion of phosphate- 10%

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61
Q

Parathyroid hormone effect on serum calcium

A

4 parathyroid glands express
calcium sensing receptor
Decrease in serum calcium means increase in parathyroid hormone

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62
Q

Relationship between serum calcium and PTH

A

Small changes in serum ionised calcium
Big changes in PTH

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63
Q

Parathyroid hormone actions

A

Increase Ca2+ Reabsorption
Increase Phosphate reabsorption
Increase 1 α - hydroxylation of 25-OH vit D
Bone Remodelling
Bone resorption > bone formation
No direct effect
increase of ca2+ absorption because of increased 1,25 (OH) 2 vit D

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64
Q

Response to low calcium diet

A
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65
Q

Vitamin D overdose

A

Increased gut ab

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66
Q

Calcitonin

A
  • Hormone produced by thyroid C cells (parafollicular cells)
    *Secretion stimulated by increased serum calcium
  • Its effect is to lower bone resorption
    *Significance in humans uncertain
    o It is much more important in animals living in a high calcium environment,
    e.g. fish
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67
Q

Outline creation of vitamin D

A

Forms from 7-dehydrocholesterol
Synthesised in the skin
To maintain vitamin D must expose arms for 20mins/day in good sunlight

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68
Q

Outline formation of vitamin D

A

7- dehydroxy cholesterol in skin ->
25 hydroxy D in liver->
1,25 hydroxy D in kidney

Calcitriol is the active form of vitamin D and it is
hydroxylated at positions 1 and 25

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69
Q

Outline the action of calcitriol (vitamin d)

A
  • VDR, vitamin D receptor
  • TRPV6, transient receptor
    potential V6
  • PMCA, plasma membrane
    calcium pump ATPase
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70
Q

Role of phosphate in physiology

A

ATP
DNA
cAMP
Phospholipid bilayer
Bone mineral – calcium hydroxyapatite

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71
Q

Normal phosphate status

A
  • Whole body phosphate 500 - 800g
  • 1% total body weight
  • 90% in bone mineral
  • Serum phosphate 0.8 – 1.5 mmol/l
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72
Q

Presentation of low phosphate

A
  • Poor bone mineralisation
  • Rickets or osteomalacia
  • Pain, fractures
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73
Q

Presentation of high phosphate

A
  • Excessive formation of hydroxyapatite
  • Deposition in tissues other than bone e.g artery calcification and tumoral calcinosis
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74
Q

Dietary sources of phosphate

A
  • Protein
    • Animal
    • Dairy
    • Soy
    • Seeds and nuts
  • Adult recommended daily intake = 700mg
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75
Q

Outline renal phosphate handling

A

In glomerulus unbound phosphate (about 90%) is filtered
80% reabsorbed in PCT- Na cotransporter
10% reabsorbed in the distal tubule
Maximum rate of reabsorption is limited, so excess is excreted

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76
Q

Regulation of phosphate metabolism

A
  • Parathyroid hormone
  • 1,25 dihydroxyvitamin D
  • FGF-23
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77
Q

Impact of parathyroid hormone on phosphate

A

Main function is regulation of calcium
Also affects phosphate
Increases 1,25 vitamin D
Increases active gut absorption
Decreases tubular
reabsorption of phosphate
Increases renal excretion

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78
Q

Outline FGF-23 (fibroblast growth factor 23)

A

Now known to be the major regulator of phosphate metabolism
* Produced by osteocytes
* In response to:
* Rise in phosphate levels
* Dietary phosphate loading
* PTH
* 1,25 vitamin D

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79
Q

Outline inherited rickets

A
  • Presents in childhood or adulthood
  • Bone pain, deformity, fracture
  • Low bone density
  • Low serum phosphate
  • High urine phosphate
  • X-linked hypophosphataemic rickets (XLH)
  • Autosomal dominant rickets (ADR)
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80
Q

Genetic investigation to identify gene for a disease

A
  • Linkage analysis
  • Fixed genetic markers
  • Identify on which chromosome
    and region the abnormal gene is
    likely to be
  • Sequencing
  • Identify where DNA differs
    between affected and unaffected
    people
    White Nature Genetics 2000
    Named FGF-23 because sequence similar to other FGFs
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81
Q

Outline tumour induced osteomalacia

A
  • Rare form of osteomalacia with low phosphate
  • Seen in patients with small benign mesodermal tumours
  • Osteomalacia heals when tumour removed
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82
Q

FGF-23 actions

A
  • Decreases expression of Na transporter in the renal
    tubule
  • Increases renal excretion of phosphate
  • Decreases 1α-hydroxylation of vitamin D
  • Decreases gut absorption of phosphate
  • Decreases whole body phosphate
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83
Q

Comparing calcium and phosphate pathways

A
  • Calcium mostly regulated by hormones that increase
    serum calcium
  • PTH, vitamin D
  • Phosphate mostly regulated by hormones that decrease
    serum phosphate
  • FGF-23, PTH
84
Q

Regulation of bone turnover (remodelling)

A
  • Osteoblasts and osteoclasts must be able to communicate with each other.
  • Coupling
    o Bone formation occurs at sites of previous bone resorption
  • Balance
    o Amount of bone removed by osteoclasts should be replaced by osteoblastic activity
85
Q

Derivation of osteoclasts

A

Macrophages (“big eaters”, makros
= large, phagein = eat)
Involved in chronic inflammation
Phagocytose (ingest) pathogens
Osteoclasts are specialised
macrophages

86
Q

Outline cytokines as inflammatory mediators

A

o A group of proteins and peptides that are used to allow one cell to
communicate with another.
o Released by many types of cells (both haemopoietic and non-haemopoietic)
o Particularly important in immune responses (immunological, inflammatory
and infectious diseases).
o Sometimes these effects are strongly dependent on the presence of other
chemicals and cytokines
* The cytokine system demonstrates great redundancy and great
pleiotropism.

87
Q

What is redundancy in relation to cytokines?

A

Redundancy means that most functions of cytokines can be performed
by many different cytokines.
o Blocking or genetically ablating (“knockout” transgenic technology) a particular
cytokine rarely has widespread or dramatic effects

88
Q

What is pleiotropism in relation to cytokines?

A
  • Pleiotropism means that a single cytokine has many different functional
    effects, on many different cell types or even on the same cell.
    o Overexpression or exogenous administration of a single cytokine frequently has
    several diverse effects.
89
Q

Endocrine and paracrine mediators of osteoclast differentiation and activity

A
  • Hormones (endocrine) including
    o 1,25 dihydroxyvitamin D
    o PTH/PTHrP
    o Oestrogen
    o Leptin
  • Paracrine/autocrine including
    o Prostaglandins
    o Interleukin-1 (IL-1)
    o Interleukin-6 (IL-6)
    o Tumour necrosis factor (TNF)
90
Q

Impact of mediators of osteoclast differentiation activity

A
  • None of them appeared to have significant effects through receptors on
    osteoclasts!
  • They didn’t work in pure osteoclast cultures
  • They only worked in the presence of osteoblasts or other bone marrow
    stromal cells (mesenchymal lineage)
91
Q

Outline osteoprotegerin (OPG)

A
  • Also known as osteoclastogenesis inhibitory factor (OCIF)
  • A member of the tumour necrosis factor (TNF) receptor superfamily.
  • Inhibits the differentiation of myeloid precursors into osteoclasts
  • Decreases resorption by osteoclasts in vitro and in vivo.
  • Works by binding to RANK-ligand, thus blocking the RANK-RANK
    ligand interaction between Osteoblast/Stromal cells and Osteoclast
    precursors
92
Q

Derivation of osteoblasts

A

Mesenchymal stem cells
* Can give rise to
o Osteoblasts
o Adipocytes
o Chondrocytes
o Myocytes
* As we age, more mesenchymal
progenitors are directed down
the adipocyte pathway

93
Q

Impact of prostate cancer on bone

A

Increases rank ligand and OPG
Increased osteoblast activity in prostate cancer

94
Q

Outline the Wnt pathway

A
  • Sclerostin (Scl), like Wnt, is a
    secreted glycoprotein.
  • Sclerostin deficiency associated
    with increased Wnt signalling
  • Increased bone formation
  • Decreased bone resorption
  • Anti-sclerostins should have
    anabolic effects on bone
95
Q

Functions of skeletal muscle

A

Produce movement
Support soft tissues
Maintains posture and body position
Communication
Control openings and passageways
Control of body temperature
Breathing via diaphragm

96
Q

Universal characteristics of muscles

A

Responsiveness (excitability)- capable of responding to stimuli
Conductivity- local electrical change triggers a wave of excitation’
Contractability
Extensibility
Elasticity- returns to resting position

97
Q

What are T tubules?

A

Sarcolemma invaginations that help propagating an action potential

98
Q

Myofibre size

A

Length 5cm
Diameter 100um

99
Q

Outline the light band and the dark band

A

Light band- I-band, actin, divided by Z-disc
Dark band- A-band, overlapping of actin and myosin, divided by M-line

100
Q

Thin filament

A

Contains F-actin capped by alpha actinin and CapZ and tropomodulin. Nebulin consists of 35aA acting binding motifs and acts as a molecular ruler

101
Q

Thick filament

A

Contains myosin filaments maintained by Titin which acts as a molecular spring. Titin is the largest protein in our genome with >34000aA

102
Q

Heads of the myosin

A

Each thick filament contains approx 300 myosin heads
Each head cycles 5 times/second

103
Q
A
  1. ATP binds to the myosin head cauring the dissociation o f the actin myosin complex
  2. ATP
104
Q

How is contraction initiated?

A

Motor neurones send an impulse to muscle which communicates via a neuromuscular junction

105
Q

Motor unit

A

A motorneuron and all fibres innervated by it
A motor unit always contains fibres of the same type (slow/fast)

106
Q
A

ACH stimulates acteylcholine gated cation channels w

107
Q

Troponin structure and function

A

Troponin C binds to Ca2+
Troponin I is an inhibitory subunit
Troponin T binds to tropomyosin

108
Q

Tropomyosin

A

Rods cover 7 myosin binding sites on the actin and prevents binding
Binding of Ca2+ to the troponin binding sites which pulls it away from the binding sites

109
Q

Slow oxidative

A

Fatigue resistant
Red- myoglobin
Low glycogen content
Oxidative
Aerobic atp synthesis
High mitochondria
SOleus

110
Q

Fast glycolytic

A

Fatiguable
White
Glycolytic metabolism
High glycogen content
Anaerobic stp

111
Q
A
112
Q

Slow vs fast fibres

A

Slow- half the diameter of fast fibres take longer to contract and

113
Q
A

Creatine is ingested from the diat and transported to tge muscles biva the bloodstream
95% of creatune present in mysdls as P-creatine (60%) or creatine (40%)

114
Q

CAtalyst for conversion of creatine to phosphocreatine

A

Creatube c=kinase- cytoplasmic and mitochondrial isoforms

115
Q

Fatigue

A

progeressive weakeness of the muscle#
ATP shortage due to shortage of glycogen
Lactic axid leveks rise and lover the PH which prevebnts normal workingin the sarcoplasm
Failure of the neuromuscular junction

116
Q

Do skeletal muscles have stem cells?

A

yes

117
Q

Do skeletal muscles have pain receptors?

A

No

118
Q

Classification of joints

A

Structural classification
Functional classification

119
Q

Types of joint- structural

A

fibrous
Cartilaginous
Synoial

120
Q
A

Synarthroses- immovabkle and mostly fibrius
Amphiarothese- slightly moveabke mostly carti
Diarthroses- synovial k

121
Q

Fibrous joints-suture

A

Only sutures of skull
Adjacent bines interdigitate
Junction with very short tissue fibres

122
Q

Fibrous - Syndesmosis

A

Bones connescted by a cord(ligament or interosseous membrane ofn ifbrous tissue
Amount of mvmt permited is proportional to length of fibre
E.g between radius and ulns

123
Q

Fibrous- Gomphoses

A

Peg in socket joint only found in tooth articulation

124
Q

Syncondroses- cartilagenous

A

Bones connected bu hyaline cartilage
Usually amphiarthroses e.g

125
Q

sympheses- cartilagenous joint

A

Here the connecting cartilage is a pad or plate of fibrocartilage e.g pubic symphysis and intervertebral disk

126
Q

Synovial joints

A

Atriculating bines are separated by a fluid filled cavity
most body

127
Q
A
  1. articular (hyaline cartilage
  2. Joint capsule- inner layer is synovial membrane
    Joint synovial cavvity
    synovial fluid
    reinforcing ligamnets
128
Q

Additional components associated with some synovial joints

A

Bursae- fluid filled sacs lined by synovial membrane
Menisci- discs of fibrocartilage allow for friction free memt

129
Q

Articular (hyslaune cartiklaeg

A

Almost fricitionless
resistes compressibve loads
high water contednt
low dcell contrent
no blood supply

130
Q

Synovial fluid

A

civers articykaitg surfaces with a thin fillm
Modifird from pkasma by synovual membrana( synoviocytes)
Fluid, proteins, charges sugars that bind water e,g hyaluronic acid
Result: slimy fluid (loke eggwhite)
Reduces friction during articulation

131
Q
A

Sits on inside f joint capsule and encloses synivual cavity’inky a dw cels thich
may have villi to increase SA

132
Q

Types of synovial joints

A

Ball and socket joint- knee
Condyloid joints- metacarpal and phalanges
Glifing joint- between carpals
Hinge joint- elbow
Pivot joint- between c1 and 2
Saddle joint-base of the thumb

133
Q
A

Attatch bone to bone
prevent excessive motion
goide joint motion
augemnt mechanical stbilty

134
Q
A

Connect muscle to bone
Transmit tenske loads form muscle to bone
Prosuce joint torqu
Stabilisis joint during oisometric contration
ensbles joint motion siring isptonic
stabilises

135
Q

Dense connective tissue

A

Clls fibroblasts 20% od tussye synthesis anr enremodle the ecm

80% ectracelllular matrix- 70% wet 30% solid
spparselu vascularised

136
Q
A

Collagen type 1 90-95% dry weight
proteoglycan and ither types od collagen

137
Q

how does ligament have slight mvmt

A

fibres slighlt crimoed together allowing fir sime movement

138
Q
A

influences elsasitn in tendons and ligaments
little in tendons
mroe in liagamebtum flavum

139
Q
A

lower colagen content 90% of dry weight
more elastin
bllodd supply from isertion point
fibres less organisd

140
Q

Entheses

A

Places of insertion of thendon or ligament into bone
pain and proprioceptive receptors
Important for disease
e.g epicondyles of elbow
achillies tehn

141
Q

load bearing

A

transmit forces
tendos aee viscoelsasic- voth viscous and elastic can treform hsape
themilw loads cause elongathom

142
Q

Typical elongation load

A

1- toe regiom small loas and crimped fibres straighten
2. linear curve as fibres straigten and stifness increases rapide
3. pmax - maximal deformation ant tensile tstrength
4. yeild point- after which is complete failure to support structures

143
Q

Golgi tendon organ

A

encapsuleated sensory recepotis proprioceptirs activated by stretch or active mucle contraction
Associated intendons near insertion (mostly but also a nit in orougun’consists if thin capsule
enclosing cillahem gibres

144
Q

Inverse myotatic reflex protective reflex

A
145
Q

factors affec

A
  • maturation and ageing- up to 20 years
    aging preganancy and postpartuk
    physical training- increase tendon tensile strenght
    immobilisation decrease thensile strength
146
Q

Size of the problem of inactivity

A

Only 59% of adults in England meet DoH
recommended levels of PA
▫ 28% meet all aspects of guidelines
* Drops to <10% in over 85s
* 23% do <30 min exercise TOTAL per week
* 5.3million 25-64 yo would find 3mph walk
“vigorous” activity
* Total cost of inactivity in UK >£20 billion/year

147
Q

What is cardiorespiratory fitness?

A

The ability of the circulatory and respiratory systems
to supply oxygen to skeletal muscles and the muscles’
ability to absorb and utilise the oxygen, during
sustained physical activity”

148
Q

What is fitness?

A

The condition of being physically fit and healthy

149
Q
A
150
Q

What is gout?

A

High uric acid levels in the blood cause urate/uric acid crystals to deposit in the joints.
The crystals cause inflammation, which then causes the swelling, pain & redness.
Toe is the most commonly affected joint

151
Q

Key features of uric acid

A

Poorly soluble in plasma
The lower the pH the less soluble it becomes

152
Q

Where does uric acid come from?

A

Purines are in the blood (e.g Adenine and guanine + hypoxanthine and xanthine)

153
Q

Sources of purines

A

Diet
Breakdown of nucleotides from tissues
Synthesis in the body

154
Q

Where does uric acid leave the body?

A

Excreted in the urine
Breakdown in the gut

155
Q

Why is gout not common in children and pre-menopausal women but is more common in older men?

A

Oestrogen helps to promote excretion of uric acid

156
Q

Dietary purines

A

Meat
Offal – heart, liver & kidney
Seafood - muscles
Fish – herring and sardines
Also – oatmeal, soya & yeast extracts
Fructose – found in soft drinks

157
Q

Risk factors for gout

A

Metabolic syndrome
Obesity
Raised triglycerides
Raised blood pressure

Coronary heart disease
Diabetes

158
Q

WHat is metabolic syndrome

A

Increases risk for CHD and gout
combination of obesity raised triglycerides, raised blood pressure

159
Q

How does alcohol affect uric acid conc.?

A

Synthesis increased and excretion decreased
Mainly beer, spirits and port wine
Wine in moderation doesn’t increase risk of gout

160
Q

Medications that have an effect on uric acid

A

Thiazide diuretics
Low dose aspirin
Ciclosporin
Levodopa
Ethambutol
Pyrazinamide

161
Q

How does reduced kidney function lead to increased uric acid conc.?

A

Reduced kidney function can lead to reduced excretion of uric acid

162
Q

Key steps in uric acid formation

A

Purines —–xanthine oxidase—> xanthine —- xanthine oxidase —–> Uric acid

163
Q

Complications of gout

A

Damage to the joint (degenerative arthritis)
Secondary infections
Nerve damage

164
Q

Outline kidney stones

A

Consequence of high uric acid
Urate crystals can form in the kidneys
Causes damage to the kidneys & reduces kidney function

165
Q

How does increased turnover of nucleic acids increase uric acid conc.?

A

Increased tissue nucleotides and body purine nucleotides so increased purines and increased uric acid

166
Q

What causes an increased turnover of cells

A
  • Rapidly growing malignant tissue
    • Leukaemia
    • Lymphoma
    • Polycythaemia rubra vera
  • Increased tissue breakdown
    • Tumour lysis syndrome
    • Trauma
    • Starvation
  • Psoriasis
167
Q

Outline salvage of purines

A

Hypoxanthine & guanine are recycled back to precursors by enzyme HPRT.
If enzyme missing leads to increased production of uric acid.

168
Q

Functions of bone

A

Bones protect the vital soft organs
– brain, heart, lungs etc
Bones allow muscles to work to move us around
Bones store mineral and house marrow cells

169
Q

How do bones respond to loading?

A

Loading increases bone mass
Off-loading decreases bone mass

170
Q

Is loading all over or site specific?

A

Loading response is site-specific and localised

171
Q

What happens to bones when they are loaded?

A

Deformation and strain
Force (F) causes deformation ( change in length)
Change in Length / Length
femur: 600mm
Deformation= 0.6 mm
Strain = 0.6/600= 0.1%

172
Q

Strain variables

A

Magnitude
Rate (up and down)
Frequency
Dwell (hold/rest periods)
Number of cycles

173
Q

Non-direct things that affect bone formation

A
  • Sex and age
  • Age
  • Hormones, cytokines
  • Drugs/medicines/nutraceutical
174
Q

What is mechanostat theory?

A
  • There is not a single mechanostat
  • Our skeletons contain vast numbers of small units of
    bone, each of which has its own dynamically regulated
    mechanostat
175
Q

Maximising response to loading

A
  • Bone responds maximally to only a few loading cycles each
    day
  • Exercise in the previous 4 hours increases the response to
    subsequent loading
  • Bone responds to very brief mechanical events
    (milliseconds)
  • Rest periods between single loading events (~10 seconds)
    increase their effect
176
Q

How do osteocytes sense loading?

A

Fluid flow shear stress
Deformation of bone cause movement of fluid which signals the osteocytes
The osteocytes then signal the other bone cells- extends processes to cells

177
Q

Outline changes in trabecular architecture with ageing

A

Trabecular loss more pronounced for
non load-bearing horizontal trabeculae

178
Q

Definition of a fracture and when do they occur

A

breach in continuity of bone
Fractures occur when:
non-physiological loads applied to normal bone
Physiological loads applied to abnormal bone

179
Q

Diseases that can lead to abnormal fractures of bone

A

Tumour
-Benign
-Malignant
-Metastatic
Metabolic bone disease
-Osteoporosis
-Paget’s Disease
-Osteogenesis Imperfecta

180
Q

How to describe fractures to colleagues?

A

Site
Pattern
Displacement / angulation
Joint involvement
Skin involvement

181
Q

How to describe site of bone fracture

A

WHich bone
Part of bone (prox., mid., or dist.)

182
Q

Patterns of fractures

A

Transverse
Oblique
Spiral
Comminuted
Segmental
Avulsed
Impacted
Torus
Greenstick

183
Q

Describing displacement/angulation

A

Displacement (%)
Angulation – of distal part

184
Q

Outline joint involvement in fracures

A

Extra-articular
Intra-articular

185
Q

Outline skin involvement in fractures

A

Open / closed
Open fracture = breach in skin communicates with #
Orthopaedic emergency
Requires urgent treatment
Soft tissue injury determines outcome

186
Q

Fracture patterns unique to children

A

Epiphyses open and bone more ‘plastic’
∆ fracture types

Heal quickly
 deformity remodelling

187
Q

Fracture healing stages

A

Haematoma (hours)-> inflammation (days) -> repair (weeks)-> remodelling (months to years

188
Q

Haematoma after a fracture

A

Bleeding
endosteal and periosteal vessels, muscle etc
Decreased blood flow
Periosteal stripping
Osteocyte death

189
Q

Inflammation stage of fracture healing

A

Fibrin clot organisation
Platelets rich in chemo-attractants
Neovascularisation
Cellular invasion
Haematopoietic cells
clear debris
express repair cytokines
Osteoclasts
resorb dead bone
Mesenchymal stem cells
building cells for repair

190
Q

Repair stage of fracture healing (callus formation)

A

‘Callus’ formation
Fibroblasts produce fibrous tissue (high strain)
Chondroblasts form cartilage (strain <10%)
Osteoblasts form osteoid (strain <1%)
Progressive matrix mineralisation
High vascularity
Soft callus 2-3 weeks
Hard callus weeks to 5 months

191
Q

Remodelling stage of fracture healing (months to years)

A

Woven bone structure replaced by lamellar bone
osteonal remodelling
Increased bone strength
Vascularity returns to normal
Healing without scar - unique

192
Q

Principles of fracture management

A

Reduce fracture-> Immobilise the part-> rehabilitate the patient

193
Q

Types of fracture fixation

A

Slings
Casts and splints
Extra-medullary devices
plates and screws
Intra-medullary devices
nails
External Fixation

194
Q

Rigidity of primary bone healing

A

Strain <2%
Intramembranous
Haversian remodelling
Occurs with rigid fixation e.g plates and screws

195
Q

Secondary bone healing

A

Strain 2%-10%
Responses in the periosteum and external soft tissues
Endochondral healing
Occurs with non-rigid fixation-casts

196
Q

Combined secondary/primary bone healing

A

Semi-rigid fixation- i.m nail

197
Q

Fibrous response

A

Strain >10%
Results in non-union

198
Q

Factors that influence fracture healing

A

Patient
Age
Nutrition
Smoking
Drugs – NSAIDs, steroids
Tissue
Bone type: cancellous vs. cortical
Bone site: upper limb vs. lower limb
Vascularity / soft tissue damage
Bone pathology - # in metastatic deposit does not heal
infection
Treatment
Apposition of fragments
Stability (ability to resist force without deforming)
Micromotion (<1mm)

199
Q

Early complications of fractures

A

Local-
Vessel damage
Nerve damage
Compartment syndrome
infection
General-
Hypovolaemic shock
ARDS
VTE
Fat embolism

200
Q

Late complications of fractures

A

Local
Malunion
Non-union
Avascular necrosis
Ischaemic contractures
Joint stiffness
Myositis ossificans
Complex regional pain syndrome
Osteoarthritis
General
Poor mobility
Functional disability and social isolation
Pressure sores
Disuse osteoporosis
Loss of income / job

201
Q

Which nerve is affected by shoulder dislocation and fracture of the humeral head?

A

Axillary nerve

202
Q

Which muscles do the axillary nerve supply?

A

Deltoid and teres minor

203
Q

What area of skin does the axillary nerve supply?

A

Area at the top of the shoulder

204
Q

Nerve most likely to be affected by a mid shaft femur fracture?

A

Radial nerve

205
Q

What does radial nerve do?

A

Wrist extension

206
Q

Nerve at risk from elbow dislocation

A

Ulnar nerve

207
Q

How to test ulnar nerve?

A

Altered abduction and adduction of fingers
sensation to little finger and that part of hands

Phase 1 (22 decks)

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