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HUBS > MidTerms 1 > Flashcards

MidTerms 1 Flashcards

1
Q

When does the cartilaginous model begin ossifying

A

8 weeks

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2
Q

How come bone can repair itself

A

Due to high vascularisation

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3
Q

Is bone made of mostly ECM or mostly cells

A

ECM

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4
Q

What are the 2 types of extracellular components of bone

A
  • organic

- inorganic

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5
Q

How much of ECM is organic?

A

⅓

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6
Q

How much of ECM is inorganic?

A

2/3

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7
Q

What is the organic component of ECM made of?

A

Collagen embedded in ground substance (proteoglycans)

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8
Q

How are the collagen fibres aligned in organic ECM

A

aligned in certain ways depending where forces coming from and to resist tension

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9
Q

What’s in the ground substance of the organic component?

A

Proteoglycans

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10
Q

Function of organic component

A

Resist tension

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11
Q

What happens if organic component is removed?

A

Brittle/breaks easily

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12
Q

What is the inorganic component of bone made of

A

hydroxyapatite (mineral salts)

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13
Q

What gives the bone hardness

A

Hydroxyapatite

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14
Q

Function of inorganic component of bone

A

Resist compression

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15
Q

What happens if inorganic component removed

A

Too flexible = not good for support and movement

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16
Q

Role of OB

A

Build ECM

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17
Q

Role of OCytes

A

OB get trapped in ECM and mature into Octets

  • mature bone cells
  • important for COMMUNICATION in the remodelling process
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18
Q

Role of OC

A

break down ECM

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19
Q

Characteristics of OC

A
  • multinucleated

- giant

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20
Q

What does compact bone look like at gross level

A
  • outer surfaces seem impenetrable
  • foramina/holes: nutrient foramen - provide blood (nutrients) to cells trapped in the compact bone at the microscopic level
  • thickest in shaft
    thin round head
    for load bearing
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21
Q

What is compact bone for

A

Load bearing

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22
Q

Microscopic structure of compact bone

A
  • osteon
  • lamellae
  • central canal
  • lacunae
  • canaliculi
  • periosteum
  • subperiosteal surface of bone
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23
Q

Function of Osteon

A

maintain Ocytes by providing nutrients

- need to bring blood from outside the bone in the gross level to Ocytes

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24
Q

Structure of osteon

A

longitudinal cylinder within compact bone
- foramen on outer surface of bone at gross level which gives opening for blood vessels and nerves to get into osteon systems

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25
Q

Function of lamellae

A
  • resist forces
  • resist tensile forces
  • can resist tensile forces no matter which direction the force is coming from
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26
Q

Structure of lamellae

A

Tubes of ECM with collagen fibres aligned to resist forces
- form a series of cylinders running longitudinally down shaft = osteon
- sheaths of lamella = tubes of ECM
⅓ is collagen
- collagen fibres aligned different ways in each concentric tube to resist tensile forces

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27
Q

Central canal

A

Blood vessel and nerves

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28
Q

Lacunae

A

Lakes of OCytes

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29
Q

Function of canaliculi

A

Channels for Octets through ECM

  • nutrient get between lakes
  • allow cellular chemical communication between the octets, for the ocytes to communicate to OB and OC that remodelling of that osteon needs to occur
  • penetrate lamella
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30
Q

Periosteum

A

Outer surface of bone

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31
Q

Structure of periosteum

A

Fibrous connective tissue sheath go around all surfaces of bone

  • does not cover the ends where bones end to form a joint
  • inserted into bone with fibres
  • blood vessel goes through periosteum before it goes through the bone and into the osteon system
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32
Q

How is periosteum inserted into bone

A

with fibres

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33
Q

Subperiosteal surface of bone

A

where blood vessel penetrates

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34
Q

General overview of remodelling of compact bone (maintenance of normal, mature compact bone)

A
  • osteoclastic front (multinucleate)
  • break down ECM
  • come through by blood as OCytes has communicated that remodelling needs to occur so OC come in
  • OC destroy ECM
  • left with void
  • OB come and build ECM
  • sheets of lamella formed by OB
  • OB gets trapped in ECM and between sheets of lamella
    sit within lacuna and aided in maintenance and survival by central canal that brings blood and nutrients diffused between lacuna by canaliculi
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35
Q

Where is cancellous bond found

A

At bone ends

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36
Q

Describe trabeculae

A

Struts of lamella bone

- sheets of ECM formed together and form honey comb network of trabecular

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37
Q

What fills the cavities in cancellous bone

A

Marrow

- red marrow fill gaps and form RBC

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38
Q

How are OCytes fed in trabeculae

A

Through direct communication with blood

- by blood that is formed and blood vessels penetrating the areas at the ends of the bones

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39
Q

Where are OCytes in spongy bone

A

Housed in lacuna on surfaces of trabeculae

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40
Q

How are OCytes arranged in spongy bone

A

Not arranged in concentric circles but the lacunae and OCytes are found in a lattice-like network of matrix spikes called trabecular

  • each trabecular forms along lines of stress to provide strength to the bone
  • the spaces in some spongy bones contain red marrow, protected by the trabecular, where hematopoiesis occurs.
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41
Q

Where are trabeculae found

A

More shock absorption

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42
Q

How are spongy bone and medullary cavity nourished

A

Receive nourishment from arteries that pass through the compact bone
- the arteries enter through the nutrient foramen
the OCytes in spongy bone are nourished by blood vessels of the periosteum that penetrate spongy bone and blood that circulates in the marrow cavities.

There are no blood vessels within the matrix of spongy bone, but blood vessels are nearby in the marrow spaces.

  • exchange of nutrients, gases etc occurs between the capillaries in the marrow and the interstitial fluid of the marrow.
  • the interstitial fluid extends into the canaliculi and thereby supplies the OCytes.
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43
Q

Are there blood vessels within matrix of spongy bone

A

NO

but blood vessels are nearby in the marrow spaces.

  • exchange of nutrients, gases etc occurs between the capillaries in the marrow and the interstitial fluid of the marrow.
  • the interstitial fluid extends into the canaliculi and thereby supplies the OCytes.
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44
Q

Organisation of trabeculae

A
  • resist compression nada shock absorption

- trabeculae aligned in certain ways to diffuse those forces.

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45
Q

What is the zone of weakness

A

On the superior part of neck
- strengthening on inferior of neck to resist forces, but leaves area with less trabeculae

= area where trabecular do not cross at right ankles - less reinforcement by trabeculae = more potential for injury.

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46
Q

Human Tissue Act 2008

A
  • bodies come from bequests, not condemned criminals or unclaimed bodies
  • informed consent
  • voluntary donation
  • deceased person’s wishes can be overridden by objections of surviving spouse or relative
  • no referente to how long can keep body parts
  • avoid unnecessary mutilation of body
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47
Q

What is the ECM made of

A

Water
proteins
proteglycans

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48
Q

Do tendons stretch during flexion

A

no

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49
Q

Does epithelial tissue have lots of or little matrix

A

Very little

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50
Q

Does connective tissue have lots of or very little matrix

A

Lots of ECM, containing fibres

- sparse cells

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51
Q

Role of nervous tissue

A

Conducting and supporting

- communication and coordination between body parts

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52
Q

Why are unicellular organisms limited in the types of environments they can successfully inhabit

A

Because their immediate surroundings must supply the appropriate nutrients and conditions

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53
Q

Conditions for life (unicellular)

A
  • nutrients
  • solute conc
  • temperature
  • pH
  • toxins (including own wastes)
  • lack of predators
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54
Q

What is the internal environment

A

ECF

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55
Q

Difference between ECF and ECM

A

The ECM comprises a complex system of non-living matter that is important to sustaining the life of the organism.

Extracellular fluid (ECF) bathes cells, and comprises the fluid component of the ECM

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56
Q

What does the external environment provide?

A
  • source of nutrients
  • site for waste disposal
  • changeable
  • pathogens
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57
Q

Proportion of ICF of total body water

A

2/3

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58
Q

Proportion of ECF of total body water

A

1/3

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59
Q

How much of ECF is ISF?

A

4/5

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60
Q

How much of ECF is plasma

A

1/5

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61
Q

What does ECF supply

A

Correct temp, pH, route for nutrient delivery and waste disposal etc

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62
Q

What does ECF also contain

A

Transcellular fluids contained within an epithelial lined spaces

eg synovial fluid in joints, ocular fluid in eye, CSF

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63
Q

Eg of transmembrane fluid

A

Synovial fluid in joints

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64
Q

Define homeostasis

A

The maintenance of relatively constant conditions in the internal environment (ECF) in the face of external (or internal) change

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65
Q

4 statements about homeostasis

A
  1. In our bodies there are mechanisms that act to maintain constancy
  2. any tendency toward change automatically meets with factors that resist change
  3. there are co-operating mechanisms which act simultaneously or successively to maintain homeostasis
  4. homeostasis does not occur by chance, but is the result of organised self-government
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66
Q

Main extracellular cation

A

Na+

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67
Q

Main intracellular cation

A

K+

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68
Q

Function of Na+

A
  • determines ECF vol
  • influences BP
  • people with high BP shouldn’t eat too much salt as ECM will inc. Part of ECM is plasma.
  • important in AP generation in nerve and muscle tissue
  • Na+ must come through specific channels
  • ECF vol and therefore BP
  • AP generation in nerve and muscle tissue
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69
Q

Normal conc of Na+ in ECF

A

135-145 mmol/L

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70
Q

Function of Ca2+

A
  • impt structural component of bone and teeth
  • involved in neurotransmission and muscle contraction
  • essential for blood clotting
  • regulates enzyme function (Ca2+ as a cofactor)
  • muscle contraction
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71
Q

Which ion for AP generation in nerve and muscle tissue

A

Na+

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72
Q

Which ion for neurotransmission and muscle contraction

A

Ca2+

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73
Q

Which ion for blood clotting

A

Ca2+

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74
Q

Which ion as cofactor

A

Ca2+

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75
Q

Total plasma conc of Ca2+

A

2.2-2.6mmol/L

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76
Q

Function of glucose

A
  • used by cells (Esp neutrons) to produce ATP. Neurons are particularly affected by low glucose levels
  • high blood glucose causes other problems (both acute and chronic)
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77
Q

Fasting glucose conc

A

3.5-6mmol/L

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78
Q

Non-fasting glucose conc

A

3.5-8mmol/L

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79
Q

Function of K+

A

main determinant of RMP

- particularly important in excitable tissue i.e. nerve and muscle

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80
Q

Normal conc in ECF of K+

A

3.5-5mmol/L

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81
Q

Osmolarity of ECF and ICF

A

275-300 mosmol/L

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82
Q

normal pH range

A

7.35-7.45

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83
Q

What pH results in coma

A

below 6

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84
Q

Acidosis effect

A
  • depresses nervous system
  • neuronal function dec
  • consciousness dec
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85
Q

Alkalosis effect

A
  • “overexcitability” of nerve and muscle
  • pins and needles
  • muscle spasms
  • convulsions
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86
Q

Core body temp

A

36 - 37.5°C

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87
Q

What is core body temp

A

Chest and head

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88
Q

How does oral and axillary temp differ from rectal (core) temp

A

0.5°C less than rectal

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89
Q

What happens at higher body temps

A

proteins denature

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90
Q

What happens at lower body temps

A

Chemical reactions slow down, preventing normal cell function

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91
Q

Body temp vicious cycel

A

As cells of nervous system become compromised, the ability to thermoregulate is lost -> viscious cycle. Detrimental positive feedback loop
- eg cold = neutrons can’t properly control temp = colder etc

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92
Q

What does diffusion result from

A

the random movement of individual molecules as a consequence of their thermal energy

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93
Q

Relationship between distance travelled and time for diffusion

A

Distance travelled is proportional to square root of time
- four times as long to diffuse twice as far

  • therefore diffusion is very rapid over short distances within cells and between cells and capillaries
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94
Q

Is diffusion effective within cells

A

Very rapid over short distances within cells and between cells and capillaries

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95
Q

Substances that can diffuse directly through the lipid bilayer of our cells

A

O2
CO2
Steroid hormones
Anaesthetic agents

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96
Q

3 types of channels

A

Leak
Ligand gated
Voltage gated

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97
Q

Example of carrier-mediated passive transport

A

Glucose entry into cells when insulin present

- glucose too large to get across cell membrane

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98
Q

What type of entry is glucose into cells when insulin is present

A

Carrier-mediated passive transport

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99
Q

What does the Na+-K+ pump maintain

A
  • ionic gradients

- helps regulate cell volume

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100
Q

Eg of exocytosis

A

Secretion of insulin by beta cells of pancreas

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101
Q

Eg of endocytosis

A

Phagocytosis of microbes by neutrophils

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102
Q

When does osmosis stop

A

when water conc on both sides are equal. No net movement of water

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103
Q

Osmotic pressure

A

the pressure required to stop osmosis

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104
Q

How does water move in regards to osmotic pressure

A

Move from low osmotic pressure to a region of high osmotic pressure

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105
Q

What can differences in solute concentration across cell membrane cause

A
  • fluid shifts

- and create pressure that can damage cells

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106
Q

Differences in solute concentrations across cell membranes can cause fluid shifts and create pressure that can damage cells

A

.

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107
Q

Osmolarity

A

Measure of the total number of solutes per litre of solution

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108
Q

Units of osmolarity

A

osmol/L

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109
Q

Osmolarity of ECF and ICF

A

275-300mosmol/L

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110
Q

Tonicity

A

the effect that solution has on cell volume

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111
Q

C and C tonicity and osmolarity

A

Osmolarity is a property of a particular solution (independent of any membrane)
- tonicity is a property of a solution with reference to a specific membrane

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112
Q

Spacial orientation of ICF, ISF and Plasma

A

ICF
ISF
Plasma

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113
Q

Osmolarity of ICF, ISF and Plasma

A

275-300mosmol/L

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114
Q

What happens if intravenous = water

A

Dilute plasma

  • set up osmotic grad
  • allow water to move into ISF = dilute ISF
  • allow water into cells, through aquaporins, until equilibrium reached (osmolarity in all 3 compartments is the same)
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115
Q

Conc of normal saline

A

0.9%

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116
Q

Assumptions for calculating osmolarity

A
  • NaCl completely dissociates

- particules move in the way we predict

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117
Q

What conc of normal saline is isosmotic and isotonic

A

0.9%

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118
Q

Is 300mosmol/L urea isosmotic and isotonic

A

Urea has conc equal to the solute conc inside cell = ISOSMOTIC

  • but urea can diffuse across the plasma membrane (via transporters) because there is not much of the substances inside the cell (diffuse down its own conc grad)
  • water will follow and enter the cell
  • solution = hypotonic because its effect on cells is to cause them to swell
  • but ISOTONIC
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119
Q

RMP

A
  • 70mV

- inside of a ell neg charged cf external surface

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120
Q

What does the RMP result from

A

the sep of a small number of oppositely charged ions across the lipid bilayer
- overall concentrations of ions in ICF and ECF are not significantly affected

  • due to different concentrations of ions on each side of the membrane and their respective permeabilities to it.
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121
Q

What ion is the major determinant of RMP

A

K+

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122
Q

Why is K the major determinant of RMP

A

as the cell membrane is normally much more permeable to K+ than other ions

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123
Q

When is the RMP established

A

When the amount of K+ leaving the cell down its conc grad is balanced by that moving back in due to the electrical gradient.

eg start with cell with K+ inside only

  • conc grad cause K+ to leave the cell
  • electrical grad attracts K+ back in
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124
Q

What must the membrane potential do for excitable tissues (nerve and muscle)

A

The membrane potential must change in order for them to function
- occurs via opening or closing of specific channels

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125
Q

How does membrane potential change

A

via opening or closing of specific channels

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126
Q

Two diseases where excitable tissues can’t function normally

A
  • cardiac arrhythmias

- muscle weakness

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127
Q

What is the reference range

A

values of the regulated variable within acceptable limits

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128
Q

Why a reference range exists

A

For most physiological variables, body cells are
healthy over a range of values

• Within that range, predominantly gene.c factors determine different set points in different individuals (inter!individual varia%on)
• Varia%on may also occur within an individual (intra! individual varia%on)
“ variables fluctuate around the set point in response to normal ac%vity (within the acceptable range)
- e.g. core body temperature, blood glucose, BP, etc

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129
Q

How is the reference range established

A
  • healthy group of people
  • values within 2SD of the mean are considered “normal”
  • 95%
  • 5% of healthy people may fall outside reference range
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130
Q

Interindividual variation

A

Genetic factors eg males vs females

age

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131
Q

Intraindividual variation (2)

A
  • in response to normal activity (within the acceptable range)
  • eg core body temp, blood glucose, BP
- in response to biological rhythms 
eg hormones (but blood glucose isn't a biological rhythm)
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132
Q

Components of negative feedback

A
  1. Sensor
  2. Integrator
  3. Effector
  4. Communication pathways
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133
Q

Sensor

A

monitors actual value of the regulated variable

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134
Q

Integrator

A
  • compares actual and set point values
  • generates an “error signal” if any discrepancy between these
  • determines and controls the response
  • sensor and integrator can be the same cell
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135
Q

Effector

A

produce the responses that restores the regulated variable to its “set point”

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136
Q

Communication pathways

A

carries signals between components

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137
Q

Two physiological communications pathways

A
  1. Neuronal

2. Hormonal

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138
Q

Neuronal Pathway

A
  • involves AP in axons and neurotransmitter release at synapses
  • electrical impulse travel down axon and release neurotransmitter at axon terminal. Bind to receptors on target tissues and bring response
  • FAST
  • SPECIFIC: bring response to a specific group of cells
  • good for when conditions are changing rapidly and where an immediate response is required to prevent tissue damage or loss or homeostatic control
  • good for brief responses
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139
Q

Hormonal pathway

A
  • endocrine cell = any cell that produces hormones
  • hormones released into blood (or ECF)
  • targets ANY cells that have receptors specific (bind to receptors) for the particular hormone, so one hormone can potentially affect several tissues or organs
  • good for widespread, sustained responses eg fluid volume regulation
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140
Q

Which pathway is good for widespread, sustained responses

A

Hormonal

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141
Q

What pathway is good for fast and specific responses

A

Neuronal

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142
Q

Where is the thermoreceptor/integrator

A

Hypothalamus

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143
Q

Responses for cold

A

Cold receptors in the skin detect decreased external temperature and then hypothalamus compares predicted value with set point = feed forward
- decreased core temp detached by the hypothalamus in the brain

  • nerve impulses to muscles = shivering = generate heat = inc body temp
  • nerve impulses to blood vessels in skin = vasoconstriction
  • muscle = piloerection = hair follicles stand.
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144
Q

Responses for hot

A
  • vasodilation - bring warm blood to surface = lose heat
  • sweat (evaporate)
  • conduction
  • convection
  • radiation
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145
Q

Effective heat loss mechanisms when environmental temp > body temp

A

Radiation, conduction, convection are NOT effective heat loss mechanisms when environmental temp > body temp
- only method of heat loss is sweating.

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146
Q

Feedforward

A

Involves detection or anticipation of external (or internal) conditions or situations that COULD alter a regulated variable (or disrupt homeostasis) if some sort of PRE-EMPTIVE ACTION was not taken
- integration center establishes a future “predicted value” for the regulated variable, compares this with the “set-point” and makes anticipatory corrections

eg cold receptors in skin detect decreased external temp and then hypothalamus compares predicted value with set point = feed forward

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147
Q

Two types of feedforward

A
  • behavioural eg putting on a jacket

- physiological eg goosebumps

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148
Q

Positive feedback

A
  • moves controlled variable further away from the “set point”
  • vicious cycle
  • useful when there is a specific end point or purpose
  • must be carefully controlled to prevent inappropriate activation and to limit outcome
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149
Q

Examples of positive feedback

A
  • childbirth: end point when baby born
  • blood clotting: platelets sticking = release stuff that attract more platelets. Needs to be very well controlled to not clot bloodstream
  • must be carefully controlled to prevent inappropriate activation and to limit outcome
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150
Q

Why does the body lose heat faster to water than air

A

Water has a much greater specific heat than air, so can absorb far greater quantities of heat.
- heat conductivity in water is very great in comparison with air.

  • consequently the body loses heat to water faster than to air AND it is virtually impossible for the body to heat a thin layer of water next to the skin to form an “insulating zone” as occurs in air.
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151
Q

How long can skeletal muscle cells be

A

up to 40mm

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152
Q

How are muscle cells arranged

A
  • parallel
  • cylindrical
  • striated - protein arrangement (form a repeated alignment of contractile proteins)
  • sheath formed by TYPE 1 COLLAGEN: useful to create huge forces
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153
Q

Properties of muscle cells

A

Multinuclear

  • cells merged
  • nuclei pushed aside from the cells otherwise would be in the way of contractile mechanisms.
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154
Q

Structures of muscle

A
  • myofilaments in sarcomere = thick and thin proteins
  • myofibril
  • myofibre/myocyte
  • sarcomere (= protein arrangement)
  • sarcolemma
  • sarcoplasmic reticulum
  • sarcomere
  • muscle fibre bundle
  • muscle belly
  • fascia: summative term for all connectives between muscles. Can be extended to tendons.
    - tendons consist of the same type of substructure as fascia
    - bone also consist of type I collagen (protein)
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155
Q

Muscle sheaths

A
  • single muscle fibre wrapped by endomysium
  • fibre bundle wrapped by perimysium
  • epimysium wrap the entire muscle (belly) all the way around
156
Q

Importance of perimysium

A

Blood vessels and nerves

157
Q

Sarcomere

A
  • contractile unit
  • 2 µm
  • actin and myosin fibres: actin frame each of the sarcomeres, cannot be changed in overall length
  • end-on-end along myofibril length
  • Z - line
  • boundaries of sarcomere
  • link actin filaments
158
Q

2 key proteins of muscle

A

actin and myosin

- jointly function to enable contraction

159
Q

2 key metabolites for contraction

A

ATP and Ca2+

  • active sites carry ATP and have small arms
  • under the use of ATP, help muscle fibres to contract
160
Q

Is myosin the thick or thin filament

A

Thick

161
Q

Z line I line and A line

A

Z - connection between one sarcomere and the next
I - in polarised light looks same irrespective of how you look at it. Have actin only
A line - in middle from one end of myosin to another. Consist of end of actin and myosin

162
Q

Function of muscle

A
  • movement
  • heat production: shiver = skeletal muscles 20-30Hz. Create a huge amount of heat for heating up body
  • posture
  • communication
163
Q

frequency of muscle shivering

A

20-30Hz

164
Q

What happens in muscle shortening

A

Thin drawn towards each other over thick

- Z lines move closer together (1µm apart)

165
Q

Important factors for muscle contraction

A
  • actin and myosin interdigitate
  • actin and myosin retain their length: shortening come from actin moving relative to myosin
  • process consumes energy
  • Ca2+ essential
166
Q

Muscle form determines function (3)

A
  1. length of muscle fibres
  2. number of muscle fibres
  3. arrangement of muscle fibres
167
Q

length of muscle fibres

A
  • fibre can shorten up to 50% of resting length
  • large ROM required means long muscle fibres needed
  • length -> ROM
168
Q

Number of muscle fibres

A
  • tension (= force) is directly proportional to CSA
  • greater number of fibres = greater CSA = grater tension
  • origin at proximal
  • insertion at distal
169
Q

Arrangement of muscle fibres

A

Fibres oblique to muscle tendon
= pennate

  • more fibres into same space
  • reduced shortening but increased CSA
    = FIBRE PACKING
170
Q

Anatomical vs physiological CSA

A
  • anatomical: cut muscle in standard anatomical plane = not representative of the max force the muscles can exert
  • physiological CSA: muscles aligned to oblique = more force due to CSA = contract obliquely
  • Anatomical CSA of straight and pennate are the same but physiological is different.
  • higher for pennate
171
Q

Do pennate fibres have more or less shortening and CSA

A

LESS shortening

MORE CSA

172
Q

Pennate arrangement

A
  • oblique to line of pull (uni-, bi-, multi-). Multi eg scapula eg rectus abdomens
  • PSA for uni and bi and multipennate allows more fore than arranged longitudinally
173
Q

Muscle tone

A

Even relaxed muscles are slightly active

  • nerve impulses activating muscle fibres
  • does NOT produce movement
  • without nerves innervating muscles, can become hypertrophic or even atrophic
  • synapses release ACh, which helps to depolarise the muscle cell to liberate Ca2+, thereby helping contraction
174
Q

Function of muscle tone

A

Keeps muscles firm and healthy

  • help stay metabolically active
  • eg taking off cast = loss of proteins in muscle.
  • become hypertrophic
  • helps stabilise joints and maintain posture
175
Q

Process of Synaptic transmission

A
  1. Action potential reaches the end of the motor neuron
  2. ACh released into the NMJ/synapse, which depolarises the muscle cell
  3. ACh diffuses across synaptic cleft and binds to ACh receptors on the motor endplate of the muscle fibre
  4. ACh receptors regenerate action potential (by allowing entry of Na+)
  5. AP propagates into the T-tubules
  6. Depolarisation of the T-tubule triggers Ca2+ release from the sarcoplasmic reticulum
176
Q

2 fibre types

A

Fibre type I

Fibre type II

177
Q

Fibre type I

A
  • high enzyme activity
  • aerobic, slow twitching: require O2 to stay active at all times
  • eg for posture
  • marathon runners
178
Q

Fibre type II

A
  • low enzyme activity
  • anaerobic, fast twitching
  • many contractions in a short time frame
  • sprinters.
179
Q

When does cartilage being to turn into bone

A

8 weeks

180
Q

What is the process of transforming cartilage to bone called

A

Ossification

181
Q

What does the cranial vault bones ossify from

A

Membranes, not cartilage

182
Q

Where is the primary centre of ossification

A

Diaphysis

183
Q

Where is the secondary centre of ossification

A

Epiphysis

184
Q

Which centre ossifies first?

A

Epiphysis

185
Q

Can there be more than one secondary center

A

yes

186
Q

Function of secondary center

A

Bones meet at the ends at the joints

  • those parts undergo different forces as we grow and move
  • therefore need to develop separately to the primary centre
187
Q

Epiphyseal plates

A
  • made of cartilage
  • as the bone grows in length, growth plate is continually turned into bone tissue
  • at the top of growth plate = purely cartilage
  • in the middle towards bottom, cartilage cells being transformed and destroyed by OB as OB’s job is to reproduce bone tissue, so OB form more bone tissue below themselves (At the the bottom of growth plate)
  • therefore, at bottom = bone
  • as you go up its transforming into bone
  • at top = cartilage
  • in tibia, growth = upwards
  • at distal end = downwards
  • in xray, more bone can be seen (As cartilage doesn’t show up)
188
Q

Process of ossification (known..)

A
  • known rate
  • known sequence
  • for estimating age
  • for seeing if growth is normal
  • eg which epiphyses should have been ossified at a certain age
  • but difficult for different pop’s due to different growth standards in different countries etc
189
Q

How does bone grow in length

A
  • occurs through childhood
  • through epiphyseal plates
  • during adolescence, hormonal surge = growth spurt
  • drop in hormonal surge at the end of adolescent support = growth plates transform completely into bone

If bones just grow longer, then bone would be thin so the shafts of the long bones must also grow thicker at the same time they are getting longer -> moulding.

190
Q

Growth in width/moulding

A

OB in periosteum inc width

  • OB lay down new bone to the outside of the shaft at the sub-periosteal surface (surface under the periosteum)
  • on inner layer of periosteum, there are OB -> lay down new bone tissue on outside of shaft

OB from endosteum mood the bone shape and form the medullary cavity

  • remove bone where it needs to be removed
  • inside of diaphysis
  • in endosteum

Dead bone = empty cavity.

  • shaft = tube of thick compact bone
  • in adults, filled with yellow marrow
  • in children = filled with red marrow (entire bone is filled with red marrow) due to rapid and continual growth in length and width and moulding. Need high vascularisation to allow the bone to continue to grow
191
Q

Epiphyseal fusion

A

fusion of the epiphyses to diaphyses (After growth is complete)

  • occurs at a known rate and sequence
  • can use for estimating age in skeletal populations and forensics
  • measuring whether growth is normal
192
Q

Late fusing epiphyses

A
  • medial clavicle
  • pelvis (Esp impt for females, into early twenties)
  • all growth complete mid-twenties
193
Q

bone pathology

A

an imbalance of OB or OC activity

194
Q

How is bone homeostasis maintained

A
  • diet high in Ca2+
  • moderate exercise
  • Ca2+ homeostasis maintained by OC and OB etc
195
Q

Osteoporosis

A

OC take over OB

- OC take away more bone than OB can produce

196
Q

Process of osteoporosis

A
  1. Compact bone become thinner and porous
    - more vulnerable to fracture
  2. Cancellous bone has a loss of volume
    - COMPRESSION FRACTURES of vertebrae
    - spine hunched as it is anterior
  • trabeculae thinner as OC remove bone tissue
  • fewer trabeculae
197
Q

What happens to trabeculae in osteoporosis

A
  • thinner as OC remove bone tissue

- fewer trabeculae

198
Q

Causes of osteoporosis

A
  • ageing- loss of estrogen, esp post-menopausal women
  • lack of exercise: exercise stimulates bone cells to keep remodelling. Lack of exercise = don’t get signals to continue remodelling. Astronauts -> atrophy
  • nutritional factors: diet high in Ca2+
  • peak bone mass - bone as a bank
199
Q

Stage 1 fracture healing

A

Vascular damage initiates the highly regulated process

Lots of bleeding due to high vascularisation
Soft tissue damage
- haematoma (immediately)
hepatoma quickly becomes “organised”, develops a firkin mesh, and transforms into a soft mass of granulation tissue containing inflammatory cells, fibroblasts, bone and cartilage forming cells and new capillaries.
- capillaries invade site and bring phagocytes
- phagocytes clean up debris

200
Q

Stage 2 fracture healing

A

Been ends must be spliced so soft callus doesn’t break. Correct alignment

  • FB (can differentiate into other cells)
  • chondroblasts (differentiated from fibroblasts)
  • fibrocartilaginous callus ( pro callus). Helps to anchor the ends of the fractured bone more firmly, but offer no structural rigidity for weight bearing.
  • approx 3 weeks
201
Q

Stage 3 fracture healing

A
  • bony callus. 6 weeks for OB top turn cartilage into bone
  • OB invade cartilaginous callus
  • bony callus lasts for 3-4 months
202
Q

How long does it take for OB to turn cartilage into bone

A

6 weeks

203
Q

How long does the bony callus last for

A

3-4 months

204
Q

How long does the soft callus last for

A

3-4 weeks

205
Q

Stage 4 of fracture healing

A
  • remodelling
  • back into osteon network of mature bone
  • take a few weeks
  • 6 months for complete remodelling
206
Q

Can see bony callus?

A

Not in children. In adults, process slowed down = can see lump.

207
Q

Pseudoarthroses

A

False joint

- ends of bones continue to move on each other if not fixed

208
Q

Closed, simple

A
  • minimal soft tissue damage

- not a lot of movement of bones on each other

209
Q

Open, compound

A
  • displacement of bone ends
  • bone can penetrate skin = lots of soft tissue damage (muscles, nerves)
  • if bone goes outside of skin = prone to infection
210
Q

Greenstick

A
  • not a complete discontinuation of the bone
  • more common in children as their bones not as mineralised
  • can get fractures though epiphyseal plate.
211
Q

Intramembranous ossification

A

A few flat bones are formed within fibrous membrane, rather than cartilage, in the process of intramembranous ossification

212
Q

Endochondreal Ossification

A
  • The cartilage model of a typical long bone, such as the tibia, can be identified early in embryonic life
  • the cartilage model then develops a periosteum that soon enlarges and produces a ring, or collar, of bone.
  • bone is deposited by OB, which differentiate from cells on the inner surface of the covering periosteum.
  • soon after appearance of the ring of bone, the cartilage begins to calcify, and a primary ossification centre forms when a blood vessel enters the rapidly changing cartilage model at the midpoint of the diaphysis
  • endochondral ossification progresses from the diaphysis toward each epiphysis, and the bone grows in length
  • the process is called INTERSTITIAL GROWTH
  • eventually, secondary ossification enters appear in the epiphyses, and bone growth proceeds toward the diaphysis from each end.

until bone growth in length is complete, a layer of the cartilage, known as the epiphyseal plate, remains between each epiphysis and the diaphysis.

  • during periods of growth, proliferation of epiphyseal cartilage cells brings about a thickening of this layer.
  • ossification of the additional cartilage nearest the diaphysis follows, that is, osteoblasts synthesise organic bone matrix, and the matrix undergoes calcification
  • as a result, the bone becomes longer.
  • it is the epiphyseal plate that allows the diaphysis of a long bone to inc in length.
213
Q

Epiphyseal plate structure

A

4 layers:

  • cells closest to epiphysis is composed of “resting” cartilage cells. These cells are not proliferating or undergoing change. This layer serves as a point of attachment firmly joining the epiphyses to the shaft
  • proliferating zone: composed of cartilage cells that are undergoing active mitosis. As a result to mitotic division and increased cellular activity, the layer thickens and the plate as a whole increases in length.
  • zone of hypertrophy: composed of older, enlarged cells that are undergoing degenerative changes associated with calcium deposition
  • ossification zone: thin layer composed of dead or dying cartilage cells undergoing rapid calcification. As the process of calcification progresses, this layer becomes fragile and disintegrates. The restyling space is soon filled with new bone tissue, and the bone as a whole grows in length.
214
Q

Direction of length inc of epiphyseal plate activity

A

Grows upwards at the proximal end

- grows downwards at distal end.

215
Q

Process of bone remodelling

A
  • the first osteons formed in lamellar bone are called primary osteons.
  • to form a primary osteon, OC in the endosperm that surrounds a blood vessel first demineralise a cone or tube around a blood vessel.
  • this leaves a cavelike hollow filled with collagenous fibres and lined with endosperm
  • OB in the endosperm then form layer upon layer (lamellae) along the inside wall of the tube, trapping OCytes between the lamellae.
  • eventually, the concentric lamella run out of space to mineralise - leaving only the central canal with its tightly packed blood vessels, nerves and lymphatic vessels
  • as bone develops, primary osteons are later replaced through the same process with secondary osteons.

Bones grow at their outer margins by the ossification of fibrous tissue by OB

  • long bones grow in diameter by the combined action of OB and OC
  • OC enlarge the diameter of the medullary cavity by eating away the bone of its walls
  • at the same time OB from the periosteum build new bone around the outside of the bone.
  • by this dual process, a bone with a larger diameter and larger medullary cavity is produced from a smaller bone with a smaller medullary cavity.
216
Q

What is important in homeostasis of blood Ca2+ levels

A
  • remodelling activity of OC and OB
217
Q

What two processes balance each other out

A

Ossification and reabsorption proceed concurrently.

  • these opposing processes balance each other during the early to middle years of adulthood.
  • the rate of bone formation equals the rate of bone destruction.

During childhood and adolescence, ossification occurs at a faster rate than bone reabsorption. therefore bone grow larger

Older:

  • bone gain occurs slowly at the outer, or periosteal surfaces of bones
  • bone loss at endosteal surfaces and takes place at a somewhat faster pace.
218
Q

Remodelling of trabecula

A

under mechanical stress, cancellous bone remodels its trabecular in different directions and thicker diameters to better withstand the stress.

219
Q

Remodelling in compact bone

A

formation of new (secondary osteons) when bones are stressed.
- the higher the mechanical load on a bone, the narrower the tube hollowed out by OC as they prepare for new osteon.
- thus the bones that bear the greatest weight have the narrowest osteons.
- these narrower osteons also have denser mineralisation
the dense mineralisation along with more numerous, narrower osteons gives the bone great strength to resist the stress.

220
Q

What is a joint

A
  • hold bones together
  • where bones meet = articulation
  • involves bone shapes and soft tissues
  • allow free movement/or control movement
221
Q

Soft tissues associated with joints

A
  • have no inorganic component
  • cartilage:
    1. fibrocartilage
    2. hyaline/articular cartilage
  • find hyaline cartilage between ends ribs and sternum, and cartilage model that the skeleton begins growing from
  • growth plate is also hyaline cartilage
222
Q

What type of cartilage is the cartilaginous model

A

Hyaline

223
Q

What type of cartilage is growth plate

A

Hyaline cartilage

224
Q

General cartilage composition

A
  • collagen fibres in a ground substance. Collagen = protein. In FIBRES
  • chondrocytes (produce ECM) live in lacuna
  • nutrients diffused through by matrix by JOINT LOADING- i.e. not vascular
  • osteon unit distribute nutrients to bone. Done by vascularisation
  • for cartilage, only way nutrients can get diffused to the chondrocytes is by loading into the cartilage -> i.e. by normal movement of the body
  • not vascular -> need to push tough tissue to stay alive. Can’t regenerate like bone can.
225
Q

Which cartilage has amorphous structure

A

Hyaline

226
Q

Compare collagen fibre arrangement in hyaline vs fibro

A

In hyaline - collagen fibres barely visible

In fibrocartilage - collagen fibres form bundles throughout matrix

227
Q

Which cartilage have more collagen

A

Hyaline has less collagen than fibrocartilage

228
Q

How is collagen fibres aligned in fibrocartilage

A
  • orientation of fibres aligns with stresses
229
Q

Which type of cartilage has high water content in matrix

A

Hyaline

230
Q

Function of hyaline cartilage

A
  • resist compression only DUE TO HIGH WATER CONTENT
  • resist compression ONLY, not tension (whereas fibrocartilage does resist compression)
  • provide frictionless surface for movement of bones in synovial joints
231
Q

Function of fibrocartilage

A
  • resist compression (due to ground substance)

- resist tension AS WELL

232
Q

Example of fibrocartilage

A

Meniscus of knee joint = concave discs of fibrocartilage

  • deepens articulation at knee
  • can adapt its shape to stresses on joint in movement
233
Q

how does hyaline cartilage attach

A

Moulds to surface of the bones where they articulate

234
Q

How does hyaline cartilage degrade

A
  • degrades with age (lose water content, becomes friable and brittle) -> osteoarthritis
  • degrades with trauma
235
Q

Bony congruence

A

sum of the bone surfaces that form an articulation
- less BC = more soft tissue support
eg femoral head’s entire head is covered by hip socket = less soft tissue support needed
- eg in shoulder, very shallow bony articulation = less bony congruence cf hip = more vulnerable to injury. Most of the support is from muscles

236
Q

Meniscus of the knee location

A

Sit on top of the hyaline cartilage that’s sitting on top of the bone

237
Q

What is the meniscus

A
  • concave discs of fibrocartilage
  • deepen the articulation at the knee joint
  • where femur articulates with knee is flat, therefore deepening of the articulation help stabilise knee joint
  • can adapt shape to stresses on joint in movement
  • anchored to bone on outer surface
  • more loose on inside, able to move
238
Q

Can the meniscus adapt shape to stresses on joint in movement

A

Yes

239
Q

Inside of meniscus vs outside

A
  • anchored to bone on outer surface

- more loose on inside, able to move

240
Q

Force distribution over meniscus

A
  • forces from above, through knee down tibia and into foot
  • presence of meniscus = diffuse forces from above over a wider area over the tibia -> resist compression
  • if removed = no cushioning, forces come into a smaller area of tibia = articular cartilage more likely to be damaged -> osteoarthritis
241
Q

Cartilage in intervertebral disc

A
  • cartilaginous joint
  • anchored onto bone by a small ligament
  • rings show how collagen is aligned = can resist tensile forces from all directions
  • nucleus pulposus = fell-like, squishy ball bearing.
  • can be compressed and can move with the movement of torso.
242
Q

What is a slipped disc

A

Nucleus purposes gets squished out

  • if tear is posterior, then impact on spinal cord
  • if lateral, can impact on spinal nerves
243
Q

What are ligaments and tendons made of

A

DFCT

244
Q

DFCT

A

fibres as main matrix element.

  • type 1 collagen
  • crowded between collagen fibres are rows of fibroblasts that generate fibres.
  • form strong, rope-like structures eg tendons and ligaments
245
Q

How is collagen aligned in DFCT

A

in one direction

246
Q

What are the cells that make up DFCT

A

Fibroblasts(cites) that mature into firbocytes.

- embedded in matrix

247
Q

Function of ligaments and tendons

A

resist tension

248
Q

Is there vascularity in ligaments and tendons

A

Some vascularity but minimal compared to bone

- therefore very slow healing compared to bone which is highly vascularised

249
Q

Ligaments

A

Bone to bone

250
Q

Function of ligaments

A 
Restrict movement (inside and around joints)
- movement is restricted away from itself
- eg lateral restricts adduction
- eg medial restricts abduction
eg ankle: weight through ankle. Don't want ankle to move medially or laterally.
251
Q

Do ligaments stretch

A

No.

- placed in such a way that restricts movement

252
Q

How long for ankle repairmen (of ligament)

A

3 months to repair 50% of normal strength of ligament

- up to a year for 90%

253
Q

Tendons

A

Muscle to bone

254
Q

Function of tendons

A

On outside of muscle belly has fibrous sheath. Sheet merges into DCFT of tendon.

  • tendon inserts into bone
  • contraction of bone -> shortens -> pulls on tendon -> tendon pulls on bone. Occur because made of DFCT which will not lengthen if pulled on as it is to resist tension

Function = facilitates and controls movement
- contraction

255
Q

Do tendons stretch

A

No

- it resists tension

256
Q

How does over adduction affect ligament

A

Ligament pull away from bone = damage to bone as well

- evulsion fracture.

257
Q

Another name for fibrous joints

A

Synarthroses

258
Q

Another name for cartilaginous joints

A

Amphiarthroses

259
Q

Another name for synovial joints

A

Diarthroses

260
Q

What tissue makes up fibrous joints

A

DFCT

- function of DFCT is to resist tension

261
Q

What tissue makes up cartilaginous joints

A

Fibrocartilage

- resists compression and tension

262
Q

What tissue makes up synovial joints

A

All of the tissues

  • hyaline cartilage
  • fibrocartilage
  • DFCT
263
Q

What is the structure of fibrous joints

A

Ligament

- goes directly between 2 bones and articulates them and joins them together

264
Q

What is the structure of synovial joints

A
  • articular cartilage

- subchondral bone is smooth

265
Q

Function of fibrous joints

A

limited movt/stability

266
Q

Function of cartilaginous joints

A

Some movement

  • special functions and various structures
  • find where compressive forces and some movt between the bones
267
Q

Function of synovial joints

A

Free-moving

- most limb joints

268
Q

example of fibrous joints

A
  • cranial suture (principal function is to protect the brain)
  • distal tibiofibula joint (weight of body going through ankle -> don’t want tibia and fibula to move apart = more vulnerable to injury
  • between roots of teeth and jaw bone
269
Q

Example of cartilaginous joints

A
  • intervertebral disc = structure
  • pubic symphysis = joint. Anterior of pelvic girdle
  • need some movement because all forces go through posterior part of pelvic girdle, but still go to the anterior part. If had fibrous joint that does not allow any movement = more vulnerable to injury
270
Q

Example of synovial joints

A

hip

knee

271
Q

Structure of Synovial joints

A
  • complex association of tissues and structures
  • facilitation of free movement AND control of movement
  • bone ends determine the range of motion at a knee joint

hip vs knee

  • hip: lots of bony congruence due to hip socket = stable Less soft tissue support needed
  • knee: fibrocartilage meniscus deepen the articulation and make up for lack of bony congruence. Lots of soft tissue support
  • articular cartilage covers bone ends where they articulate AND move over each other
  • subchondral bone is smooth (cf roughed areas where ligaments and muscles attach)
272
Q

Capsular ligament/joint capsule function

A

Hold bones together

- go around and insert into the other bone

273
Q

Structure of joint capsule

A
  • tight and thick where more support is required
  • thickening of capsule where more support is required
  • losse and thin on sides where movement is allowed
  • collateral ligaments of knee
  • eg knee: thick tight ligaments on medial and lateral. Don’t want tibia to move side to side on femur, but thin and loose on posterior and anterior aspects to allow flexion and extension.
  • very thin and loose on shoulder joint, therefore support must come from other structures -> muscles
  • potential space
  • not a real space. If there is a space: due to trauma or synovial fluid being produced in response to trauma.
  • synovial membrane lines the inner surface of the capsule and secretes synovial fluid = lubrication of joint
274
Q

Collateral ligaments of knee

A

Medial restricts abduction
Lateral restricts adduction

eg phalanges also have collateral ligaments (part of joint capsule)

275
Q

Function of intracapsular ligaments

A
  • restricts movement between bones
  • stop femur from moving anteriorly or posteriorly on the tibia
  • eg going up stairs, femur slide off posteriorly tibia
    going down, femur slide off anterior off tibia
276
Q

Eg of intracapsular ligaments

A
  • cruciate ligaments
  • arise form tibia and insert into femur
  • ACL restricts posterior displacement of femur
  • PCL restricts anterior displacement of femur
  • can be damaged from external forces: fixation of tibia but rest of body still moves eg skiing
277
Q

What is meniscus made of

A

Fibrocartilage

  • deepening articulation between femur and tibia
  • diffuse compressive forces
278
Q

Structural difference between fibrous joint and synovial joint

A

Fibrous joint and cartilaginous joints: tissues glue bones together to either stop movement entirely or allow some movement
Synovial - capsule goes from one bone to another. Leaves bone ends free to move over each other.

279
Q

What is the reference range

A

The values of a controlled variable that is within an acceptable range

280
Q

Where are hormonal signals transmitted

A

Via the blood stream

281
Q

Type I diabetes mellitus

A

When the patient cannot produce insulin in response to stimuli

282
Q

When does the diaphysis fuse to the epiphyses, hence ceasing vertical growth?

A

Adolescence

283
Q

Does fibrocartilage have a high water content to resist compression

A

NO

hyaline does

284
Q

Cells of DFCT

A

Fibrocytes/fibroblasts

285
Q

Why is there a reference range rather than a single correct value

A
  • within that range, genetic factors can determine different set points in different individuals
  • set point may change in a regular way in response to biological rhythm
  • body cells are healthy over a range of values
  • variables fluctuate around the set point in response to normal activity (within an acceptable range)

NOT because different individuals have different levels of homeostatic strength

286
Q

How does the hormonal communication systems work

A

Targeting by expression of specific receptors on target cells

287
Q

What’s the time frame for soft callus formation

A

3 days to 2 weeks

  • fibroblasts differentiate into chondroblasts to form a fibrocartilaginous callus
288
Q

What happens in remodelling of bone in middle-aged adult?

A

Ossification proceeds concurrently with resorption at equal rates.

289
Q

How do OCytes in cancellous bone receive blood and nutrients

A

normal blood supply because OCytes are not embedded in a hard matrix

290
Q

Purpose of menisci

A

To inc bony congruence in the joint
help with normal movement of the joint
to help stabilise the joint
to distribute weight over a large area

291
Q

Function of T tubules

A

To conduct impulses into the muscle cell

292
Q

In mid swing, the knee starts to extend. It is INITIALLY controlled by

A

Gravity

293
Q

During mid stance what MAIN role does the quadriceps femoris play?

A

Stabilising

294
Q

When human run, what is it called when both feet are on the ground?

A

No time when both feet are on the ground

295
Q

Double stance

A

when both feet are on the ground

296
Q

What mainly helps to keep us stable when standing (i.e. not falling over flat on our face)

A

Soleus

297
Q

Two factors that determine peripheral skin temperature?

A

Room temperature and clothing

298
Q

Muscle structure

A
  • myofilaments in sarcomere (thick and thin)
  • myofibrils
  • myocyte
  • sarcoplasmic reticulum
  • sarcolemma
  • muscle bundle
  • muscle belly
  • fascia
299
Q

Epimysium

A

around entire muscle

300
Q

perimysium

A

around muscle fibre bundles

301
Q

important of perimysium

A

key structure to supply vascular supply and nerve supply to muscles

  • allowing sliding of the muscle fascicles one relative to the other
  • otherwise will have “shear off” phenomena and mechanical muscle destruction whenever contracts.
302
Q

Endomysium

A

connect sheath around muscle fibre

303
Q

Is myosin thicker than actin

A

yes

304
Q

What is the human mscuoloskeletal system and its motion mainly based on

A 
proteins
- muscle
- ligaments
- tendons 
Not all of these proteins are contractile, but allow for locomotion.
305
Q

What is muscle function largely driven by

A

nerves

306
Q

Where do nerves that drive an excitation that causes a contraction sit?

A

at the ventral root of spinal cord

- must travel axon all the way down

307
Q

How far does the axon go? (muscle)

A

only go as far as the proximal insertion of a muscle begins

  • as proximal as possible
  • to inc velocity of signal transduction
  • to save material (to save material of axon)
308
Q

What is the feedback of the NMJ provided by

A
  • feedback provided by the spinal root and root ganglion (which sits slightly outside spinal cord)
  • receives feedback of how the muscle is situated in space
  • signals integrated from tendons and muscles are integrated via the nerves that are situated in the spinal root ganglion.
309
Q

Transformation of signals

A

Electrical -> chemical -> electrical.

310
Q

motor endplates

A

Com from axons of neurons

- for skeletal muscles, those axons are myelinated

311
Q

Chemical signal diffusion

A

Diffusion signal takes a long time

- therefore at the outer surface of axon, have an electrical signal (time-saving mechanism)

312
Q

Transformation of signal

A

Signal from spinal cord to the terminals of axons electrically

  • electrical stimuli transmitted into neurotransmitters -> Ash (also for smooth muscle contractions as well)
  • ACH in synaptic cleft can also become the site of neurological diseases -> myasthenia graves
  • muscle cells, due to ACH, retransfers the chemical signal back to electrical, to twitch up to 30Hz
313
Q

Cellular components involved in contraction

A 
NMJ
Sarcolemma
T tubules (transport Ca2+ and make available in the muscle fibres so they can contract simultaneously)
SR
Ca2+
314
Q

Why is Ca2+ so important for contraction?

A

Ca2+ is responsible for the ends of the myosin to make a movement to allow contraction

  • movement of the ends of the myosin proteins (hundreds)
  • Ca2+ bound in the ER when not contracting, but released upon contraction.
  • tropomyosin between actin strands, which makes available myosin binding sites
  • which cannot be attached unless Ca2+ is liberated
315
Q

What does ATP and Ca2+ do?

A

Under the influence of ATP and Ca2+, the proteins, without changing length, approach each other, allowing muscle shortening.

316
Q

What is the motor unit

A

all the muscle fibres being innervated by a single nerve fibre

  • motor neuron
  • axon
  • branches
  • plus ALL the muscle fibres it innervates
  • size varies
317
Q

Precise vs forceful contractions due to motor unit size

A

Eye muscles

  • capable of making small, tiny movements
  • tiny movements possible by a few fibres being innervated by a single motor neurone
  • max of 30 fibres/motor neuron
  • refined

Quadriceps femoris

  • huge motor units
  • up to 2000 fibres/unit
  • forceful and powerful contraction
  • huge force to ground and to joints
318
Q

Myasthenia gravas

A

Neuromuscular disease

  • auto antibodies act against receptors of ACh
  • cannot open their eyes properly
  • due to the eye of the muscles around the eye (huge number of muscle fibres) are using and wasting ACh within the synaptic cleft
  • diplopia - seeing 2 images at the same time
  • can’t contract diaphragm -> being unable to breathe by themselves.
319
Q

Displayed activation of fibres

A

Motor unit displays ALL or NONE activation of fibres

  • different sizes of motor units = graded range of contraction
  • how is the force of contraction of whole muscle then graded?
320
Q

How is the force of contraction of whole muscle graded

A
  • not only by the number of excitations from the nerve fibres
  • also come from the number of fibres being excited to get a muscle contracted
321
Q

What does the force of contraction of whole muscle depend on (3)

A
  1. characteristics of muscle fibres: length, number, arrangement
  2. characteristics of motor units: size, number, rate of firing that the motor neurone in the spinal cord generates
  3. muscle attachments: size, number, rate of firing
322
Q

Anatomical lever

A

bone = lever

  • bones do not independently move without muscle
  • for arm flexion, the ulna and radius are the bones that act as levers

joint = pivot

load = external or internal eg just your hand

muscle contraction = pull

323
Q

Type I lever

A

pivot in middle between force and resistance

324
Q

Type one lever function

A

Stabilise joint position

  • prevent head drooping
  • force of gravity on opposite side compared to muscle contraction
325
Q

Type 2 lever

A

Axis -> resistance -> force

326
Q

Type 2 lever function

A

effective at overcoming loads

  • axis of motion is distant compared to both resistance and force
  • resistance between axis and force

eg standing on tip toes

  • balls of feet = axis
  • achilles tendon = force
  • ankle = resistance
327
Q

Type 3 lever

A

Axis -> force -> resistance

328
Q

Type 3 lever function

A
  • large range of movement and speed
  • force between resistance and axis
  • huge lever
329
Q

What allows a muscle to be lengthened

A

An opposing muscle or gravity
eg extension at elbow from a flexed position
- in most cases, an eccentric muscle or a neutralisation of a joint position is taking place by gravity
- eg jaw TMD drops during talking due to gravity, but contract actively back up.

330
Q

Which muscle action involves the muscle being active and developing tnsion

A

Concentric
Static/isometric
Eccentric

331
Q

Which muscle action involves a change in joint position

A

Concentric and eccentric

isometric does NOT result in a change in joint position

332
Q

How does muscle length change for each of the muscle actions

A

Shortened in concentric
No change for isometric
Lengthened for eccentric.

333
Q

Which type of lever allows for a large range of movement and speed

A

type 3

334
Q

Agonist

A
  • exert a certain movement at a certain joint position
    eg BB shortens
  • act concentrically
335
Q

Antagonist

A
  • opposes agonist
  • supported by muscles on the opposite side on the relative joint
  • TB -> lengthens
  • act eccentrically
336
Q

Stabiliser

A
  • when a muscle is active to hold a joint STILL

eg holding a heavy book
BB = stabiliser
BB = isometric
no change in the length of BB

eg quads when standing

  • do not have to sit on either side of the joint
  • guide movement
  • save energy
337
Q

Neutraliser

A

Muscle eliminates an unwanted movement caused by another muscle

  • can eliminate unwanted movement by another muscle (stabilising)
  • but can also restore initial joint position without acting on the joint with large force
eg BB
- drinking from a glass
- flexion - yes
- supernation - no
"pronator" muscle neutralise supinating effect of BB
338
Q

Functions of the skeleton

A
  1. support
  2. movement
  3. protection
  4. storage
  5. RBC formation
339
Q

Where is compact bone found

A

WHere strength and load bearing needed

340
Q

Where is cancellous bone found

A

Where shock absorption is needed

341
Q

Function of long bones

A

levers for movt

342
Q

Function for short bones

A

weightbearing/shock absorption

343
Q

Function of flat bones

A

protection - cranial bones

muscle attachemnt - scapula

344
Q

Structure of long bone

A

longer than wide
diaphysis and epiphyses
thicker compact bone in shaft

345
Q

Structure of short bones

A

near equal width and length

mostly cancellous bone

346
Q

Structure of flat bones

A

thin plates of compact bone - some cancellous

347
Q

Axial skeleton

A

Skull:

  • cranium: frontal, parietal, occipital, temporal
  • facial bone
  • mandible

Vertebral column

  • cervical (7)
  • thoracic (12)
  • lumbar (5)
  • sacrum (5 fused)
  • coccyx (2-5 fused)

Rib cage

  • ribs
  • sternum
348
Q

Appendicular skeleton

A
  • limbs

- regions: arm, forearm, thigh, leg

349
Q

What is the upper limb designed for

A

Manipulation

350
Q

What is the lower limb designed for

A

Stability and locomotion

351
Q

Structure of limbs

A

single proximal long bone
two distal long bones
hands and feet

352
Q

Attachment

A

pectoral girdle: clavicle and scapula

pelvic girdle: hip bones (2) and sacrum

353
Q

Bones of forearm

A

radius and ulna

354
Q

bones of leg

A

tibia

fibula

355
Q

bones of hand

A

carpals (8)
metacarpals (5)
phalanges (3x 4 + 2)

356
Q

Bones of foot

A

tarsals (7)
metatarsals (5)
phalanges (3)

357
Q

Bursae

A

Synovial membrane and enclosed products.
if fully enclosed and independent of the joint, but still provides cushioning = bursae

  • if it communicates = recess
358
Q

Homeostasis of glucose

A 
Pancreas: (Receptor/Controller)
Receives input (glucose level) and releases appropriate hormone

Liver (also muscle and body cells): (Effector)
Liver and muscle cells store or release glucose as appropriate, other body cells can take up excess glucose for use in respiration but can’t store it

Blood system:
Transports hormones from pancreas, throughout body to liver, muscle and body cells

When we eat food, carbohydrates are digested and broken down into glucose.

This increases our blood glucose level
So the pancreas releases the hormone insulin, which allows the glucose to move from the blood into cells where the glucose is converted into ATP in the mitochondria (respiration), or converted to glycogen in the liver (and muscles) for storage.
Blood glucose drops, insulin production stops, no more glucose leaves the blood.

When we haven’t eaten for a while or exercise, glucose is used up in cellular respiration.

This decreases our blood glucose level
So the pancreas releases the hormone glucagon, which allows to break down of glycogen in the liver and muscle cells into glucose which is released into the blood.
Blood glucose increases, glucagon production stops, no more glucose enters the blood.

359
Q

What do growth plates allow

A

Provide a convenient means of allowing growth of a long bone without distorting the intricate shape at the joint surface.

360
Q

Where does bone thickening and bone removal occur

A

Thickening of bone occurs at subperiosteal surface

Bone removed/resorbed by OC at the endosteal surface

361
Q

How is bone removed

A

OC remove bone by releasing lysosomes and acid

- enzymes break down the organic part of bone tissue, and acid breaks down the inorganic part.

362
Q

Factors predisposing to osteoporosis

A

Lack of biomechanical stress (lack of exercise, reduced gravity, paralysis)

Diet lacking in Ca2+

Cigarette smoking

Use of corticosteroids

Interference with oestrogen production

363
Q

When does stage 1 occur

A

0 -3 days

364
Q

When does stage 2 occur

A

3 days to 2 weeks

365
Q

What is the soft callus made of

A

Fibrocartilage

366
Q

how is the soft callus formed

A

Fibroblasts enter, produce collagen fibres

- some cells differentiate into chondroblasts

367
Q

When does stage 3 occur

A

3-4 weeks

368
Q

What happens in stage 3

A

OB transforms the fibrocartilage callus into a bony callus

369
Q

What bone makes up the bony callus

A

cancellous bone

370
Q

When does stage 4 occur

A

2-3 months

371
Q

How long may remodelling take

A

up to 2 years

372
Q

What influences final shape of bone

A

quality of “setting”

reduction of fracture

373
Q

Does the thickness of epiphyseal plate change when bone lengthens

A

No.

  • bottom layer of calcified cartilage becomes bone.
  • bone added to diaphysis
374
Q

Features of quadrupelda standing

A

Base of support
legs flexed at several joints
energetic expenditure

375
Q

Features of biepdal standing

A

Relatively small area of contact
plantar surface of feet
energy efficient

376
Q

Where is the line of gravity in relationship to hip, ankle and knee

A

Posterior to hip
anterior to ankle
anterior to knee

377
Q

What happens to hip joint when standing

A

Joint pushed into extension

  • extension = ligaments are tight = LOCKED
  • capsular ligaments of the hip joint are spiral -> don’t need contraction of quads or iliopsoas just when standing = prevent from falling back
378
Q

Is the hip joint locked when standing

A

yes

379
Q

What happens to the knee when standing

A

Joint pushed into extension

extension = ligaments are tight = LOCKED

380
Q

IS THE KNEE JOINT LOCKED WHEN STANDING

A

YES

381
Q

What happens to the ankle when standing

A

falls into dorsal extension
NOT LOCKED
plantar flexors stabiliser
energy consumed

382
Q

Is the ankle joint locked when standing

A

NO

383
Q

Is energy consumed at the ankle joint when standing

A

yes

384
Q

bipedal stadngin summary

A

feet form base of support but insufficient size to provide only balance solution

  • standing achieved with very little muscle effort - mot at ankle joint
  • gait is characteristics
  • gait is learnt.
385
Q

when does primary ossification occur

A

when a blood vessel enters the cartilage model at the diaphysis

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