MSK COPY Flashcards

1
Q

Give 5 functions of bone.

A
  1. Houses bone marrow.
  2. Protection.
  3. Transmit body weight.
  4. Allows movement.
  5. Mineral storage.
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2
Q

Name 5 types of bone.

A
  1. Long bone.
  2. Flat bone.
  3. Short bone.
  4. Irregular bone.
  5. Sesamoid bone.
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3
Q

Give an example of a long bone.

A

Humerus.

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4
Q

Give an example of a flat bone.

A

The skull.

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5
Q

Give an example of an irregular bone.

A

Vertebrae.

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6
Q

What is the axial skeleton?

A

The part of the skeleton consisting of the head and trunk.

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7
Q

What is the appendicular skeleton?

A

The part of the skeleton consisting of the limbs and the supporting pectoral and pelvic girdles.

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8
Q

What are osteoblasts derived from?

A

Mesenchymal stem cells.

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9
Q

What is the function of osteoblasts?

A

They synthesise a type 1 collagen rich matrix, osteoid. (They contain large amounts of RNA for this function).

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10
Q

What are osteocytes?

A

When osteoid is mineralised with crystals of hydroxyapetite, the osteoblasts are trapped within the bone and become less synthetically active osteocytes.
They respond to changes in tension and pressure in and around your bones

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11
Q

What are osteoclasts?

A

Large and multinucleated bone resorbing cells. They contain large amounts of lysosomes.

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12
Q

What are osteoclasts derived from?

A

Hematopoietic stem cells.

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13
Q

Give 5 reasons for bone remodelling?

A
  1. Replace woven bone for lamellar.
  2. Response to exercise.
  3. Repair damage.
  4. Obtain calcium.
  5. Form bone shape.
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14
Q

Name 3 types of enzymes that are important in bone remodelling.

A
  1. MMPs (Matrix Metalloproteinases) = collagenase
  2. Alkaline Phosphatase (ALP) (mineralistion)
  3. Cathepsins (resorb)

2. MMP’s.

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15
Q

What type of bone does endochondral ossification produce?

A

Long bone.

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16
Q

What type of bone does intramembranous ossification produce?

A

Flat bone.

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17
Q

What type of bone formation uses a cartilaginous pro-former?

A

Endochondral ossification.

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18
Q

Briefly describe process of endochondral ossification.

A
  1. Begins with the creation of hyaline cartilage proformers.
  2. A bony collar is then established around the diaphysis.
  3. Blood vessels penetrate the bony collar and bring in osteoprogenitor cells.
  4. A primary centre of ossification is established. Osteoblasts lay down primary bone.
  5. A secondary centre of ossification is established in the epiphyses.
  6. The amount of cartilage present decreases and is restricted to just to the growth plates.
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19
Q

Briefly describe the process of intramembranous ossification.

A
  1. Bone is directly deposited into mesenchymal tissue.
  2. Osteoblasts deposit isolated islands of bone until a plate of primary bone has been created.
  3. This primary bone is then replaced with denser, lamellar, secondary bone.
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20
Q

Describe primary bone.

A

Newly formed, poorly organised. Calcium is in an amorphous form. This bone is heavy and weak.

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21
Q

Describe secondary bone.

A

Organised collagen. Calcium is in a crystalline form (hydroxyapatite). This bone is lighter and stronger and replaces primary bone.

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22
Q

In the blood approximately how much calcium is bound to plasma proteins?

A

About 50% is bound to plasma proteins, notably albumin.

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23
Q

In the blood approximately how much calcium is ionised?

A

Just less than half.

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24
Q

In the blood approximately how much calcium is complexed?

A

A very small amount is complexed, bound to citrate/phosphate etc.

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25
Q

What are the 3 ways in which the calcium in the blood is distributed?

A
  1. Ionised - metabolically active and is the most important for cellular function.
  2. Bound to plasma proteins - non metabolically active.
  3. Complexed e.g. citrate, phosphate.
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26
Q

What is the affect of alkalosis on ionised calcium?

A

Alkalosis increases the pH, this increases the negative charge on albumin and so affects ionisation as more calcium binds to albumin and less is ionised.

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27
Q

Give 4 dietary sources of calcium.

A
  1. Dairy products.
  2. Oily fish.
  3. Cereal.
  4. Broccoli.
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28
Q

Where in the intestine is calcium actively absorbed?

A

Duodenum and jejunum.

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29
Q

Where in the intestine is calcium passively absorbed?

A

Ileum and colon.

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30
Q

Where does the majority of Ca2+ reabsorption happen in the kidney?

A

At the PCT.

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31
Q

Where does active Ca2+ reabsorption happen in the kidney?

A

DCT - this is where PTH will act.

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32
Q

Where in the body can Calcium come from to enter the blood?

A
  1. Absorbed from the intestine.
  2. Resorbed from bone.
  3. Reabsorbed at the kidney.
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33
Q

What stimulates the release of PTH?

A

Low serum Ca2+ detected by receptors in the parathyroid.

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34
Q

Briefly describe the action of PTH

A
  1. It causes bone resorption: increased Ca2+ and phosphate.
  2. It acts on the kidneys causing increased Ca2+ reabsorption and decreased phosphate reabsorption.
  3. It stimulates 1-hydroxylase which increases formation of 1,25 dihydroxyvitamin D (calcitriol) and so increases the absorption of Ca2+ and phosphate from the intestine.
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35
Q

Where in the kidney does PTH act?

A

On the DCT where active reabsorption of Ca2+ takes place.

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36
Q

What do C-cells release?

A

Calcitonin.

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37
Q

What triggers the release of calcitonin?

A

High Ca2+.

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38
Q

What is the action of calcitonin?

A

It reduces bone resorption and so lowers Ca2. It is the antagonist to PTH.

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39
Q

What is the affect of low phosphate levels in the body?

A

Poor mineralisation of bone which can result in rickets, osteomalacia, pain and fractures etc.

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40
Q

Give 3 dietary sources of phosphate.

A
  1. Protein.
  2. Dairy.
  3. Seeds and nuts.
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41
Q

Give 3 regulators of phosphate.

A
  1. PTH.
  2. 1,25 dihydroxyvitamin D / caclitriol
  3. FGF-23 = major regulator!
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42
Q

What is the action of PTH with regards to phosphate homeostasis?

A

It increases phosphate absorption at the intestine and decreases phosphate reabsorption at the kidney.

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43
Q

What triggers the release of FGF-23?

A
  1. High phosphate levels.
  2. PTH.
  3. 1,25-(OH)2-vitD.
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44
Q

What is the action of FGF-23?

A

It acts to decrease phosphate levels!

  1. It increases phosphate excretion at the kidneys.
  2. It decreases 1-hydroxylase meaning less 1,25-(OH)2-vitD is produced and so less phosphate will be absorbed from the intestine.
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45
Q

What is the function of PHEX?

A

It breaks down FGF-23 when phosphate levels have decreased.

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46
Q

What could happen if there was a dysfunction of PHEX?

A

FGF-23 wouldn’t be broken down and so serum phosphate would be very low and urinary phosphate would be high. You would be unable to mineralise bone - osteomalacia.

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47
Q

What is klotho and what is its function?

A

Klotho is a transmembrane protein that modifies FGF receptors making them specific for FGF-23.

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48
Q

What would be the affect on FGF-23 if you were vitamin D deficient?

A

You would have low phosphate levels as less will be absorbed from the intestine and so FGF-23 would be low as its trigger is high phosphate levels.

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49
Q

Define coupling.

A

Bone formation occurs at sites of previous resorption.

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50
Q

Define balance in osteoblast/osteoclast communication.

A

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

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51
Q

What cell releases RANK ligand?

A

Osteoblasts.

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52
Q

What is the function of RANK ligand?

A

It is essential for osteoclast formation, activation and survival.

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53
Q

What is OPG?

A

Osteoprotegerin
OPG inhibits osteoclast formation, function and survival.

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54
Q

How does OPG work?

A

It has a similar binding site as the RANK receptor and so binds RANK ligands which prevents them from stimulating osteoclasts.

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55
Q

Name 2 things that regulate the balance between OPG and RANK?

A

Cytokines and hormones.

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56
Q

What would be the affect on bone if you had unopposed RANK ligands?

A

There would be increased bone loss as more osteoclasts would be stimulated due to the lack of OPG.

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57
Q

What is the affect of increased activity on bone?

A

Increased activity means there are higher than customary strains on the bone and so you get bone formation.

58
Q

What is the affect of decreased activity on bone?

A

Decreased activity means there are lower than customary strains on the bone and so you get bone loss.

59
Q

What is the role of UV light in vitamin D metabolism?

A

It converts 7-dehydrocholesterol into cholecalciferol.

60
Q

What converts 7-dehydrocholesterol into cholecalciferol?

A

UV light.

61
Q

What is osteomalacia?

A

An inability to mineralise bone.

62
Q

What is the usual cause of osteomalacia?

A

Vitamin D deficiency.

63
Q

What is the DEXA T score range for osteopenia?

A

-1.5 -> -2.5.

64
Q

What is the DEXA T score range for osteoporosis?

A

-2.5 or lower.

65
Q

Name 4 risk factors FRAX uses in determining the 10-year probability of osteoporotic fracture.

A
  1. Family history of parental hip fracture.
  2. Smoking status.
  3. Use of glucocorticosteroids.
  4. Diagnosis of rheumatoid arthritis.
66
Q

In osteoporosis what would the blood tests of bone profile look like?

A

Everything would be normal! Normal calcium, phosphate, PTH, alkaline phosphate etc. Osteoporosis is a problem with bone density not mineralisation.

67
Q

What compound is a marker of increased bone turnover?

A

Alkaline phosphatase.

68
Q

What type of muscle fibres are slow twitch?

A

Type 1.

69
Q

By what process do type 1 muscle fibres get energy?

A

Oxidative processes and so have lots of mitochondria.

70
Q

What type of muscle fibres very sensitive to fatigue?

A

Type 2b.

71
Q

What type of muscle fibres would be found in postural muscles?

A

Type 1.

72
Q

By what process do type 2a muscle fibres get energy?

A

Oxidative and glycolytic energy processes.

73
Q

By what process do type 2b muscle fibres get energy?

A

Glycolytic processes.

74
Q

What type of muscle fibres are fast twitch?

A

Type 2a and 2b.

75
Q

When muscle fibres are stained to demonstrate the presence of fibrillar ATPase, which muscle fibres appear darker stained?

A

Type 1 muscle fibres, they have lots of fibrillar ATPase for oxidative energy processes and lots of mitochondria.

76
Q

Define fracture.

A

A breach in the continuity of bone.

77
Q

What 5 things need to be considered in describing a fracture?

A
  1. Site - which bone? Proximal/distal?
  2. Pattern - oblique, transverse, spiral etc.
  3. Displacement - % displaced, angulation.
  4. Joint involvement (intra-articular).
  5. Skin involvement - breach in skin is an orthopaedic emergency.
78
Q

What are the 4 stages of fracture healing?

A
  1. Haematoma (hours after fracture occurs).
  2. Inflammation (days after).
  3. Repair (weeks after).
  4. Remodelling (months to years after).
79
Q

What happens in the hameatoma stage?

A
  1. Bleeding of endosteal and periosteal vessels.
  2. Decreased blood flow.
  3. Periosteal stripping.
  4. Osteocyte death.
80
Q

What happens in the inflammation stage?

A
  1. Fibrin clot organisation.
  2. Neovascularisation.
  3. Cellular invasion - osteoclasts, mesenchymal stem cells etc.
81
Q

What happens in the repair stage?

A
  1. Callus formation - fibroblasts, chondroblasts and osteoblasts produce fibrous tissue, cartilage and osteoid respectively.
  2. Matrix mineralisation.
  3. High vascularity.
82
Q

What happens in the remodelling stage?

A
  1. Woven bone is replaced with lamellar bone.
  2. Increased bone strength.
  3. Vascularity returns to normal.
83
Q

What are the 3 principles of fracture management?

A
  1. Reduce the fracture, alignment.
  2. Immobilize the fracture - stability!
  3. Rehabilitate the patient.
84
Q

What is a ligament?

A

Attaches bone to bone. Ligaments aidsmechanical joint stability and guide joint motion. Ligaments also prevent excessive motion.

85
Q

What is a tendon?

A

Attaches bone to muscle. Tendons transmit tensile loads and aid joint stability.

86
Q

What contains more elastin, ligament or tendon?

A

Ligament.

87
Q

What contains more type 1 collagen, ligament or tendon?

A

Tendon.

88
Q

How are fibres arranged in ligaments?

A

Random fibre organisation.

89
Q

How are fibres arranged in tendons?

A

Organised fibres.

90
Q

Briefly describe the composition of ligaments and tendons?

A

Dense connective tissue consisting of parallel fibres. There are fibroblasts that synthesise and remodel the ECM. The tissue is sparsely vascularised.

91
Q

What percentage of ligaments and tendons is the extra cellular matrix (ECM)?

A

80%.

92
Q

What is the hierarchal structure from tropocollagen to tendon?

A

Tropocollagen -> collagen -> microfibril -> subfibril -> fibril -> fascicle -> tendon.

93
Q

What is the name of the connective tissue that surrounds fascicles?

A

Endotenon.

94
Q

What is the name of the connective tissue that surrounds tendons?

A

Epitenon.

95
Q

What is the entheses?

A

Where a tendon or ligament inserts into bone.

96
Q

What are the two types of insertion into entheses?

A
  1. Fibrous.

2. Fibrocartilage.

97
Q

How is a fibrous insertion formed?

A

Through intramembranous ossification.

98
Q

How is a fibrocartilage insertion formed?

A

Through endochondral ossification. There is a gradual change: ligament -> fibrocartilage -> mineralised cartilage -> bone.

99
Q

Name 3 things that can decrease the tensile strength of tendons.

A
  1. Ageing.
  2. Pregnancy and postpartum.
  3. Immobilisation.
100
Q

What can increase tendon and ligament tensile strength?

A

Physical training.

101
Q

Give 3 functions of joints.

A
  1. Allows movement in 3 dimensions.
  2. Bears weight.
  3. Transfers load evenly onto the musculoskeletal system.
102
Q

What are 3 structural classifications of joint?

A
  1. Fibrous.
  2. Cartilaginous.
  3. Synovial.
103
Q

Give an example of a fibrous joint.

A

Teeth, sutures in the skull etc.

104
Q

Give an example of a cartilaginous joint.

A

Intervertebral discs, costal cartilages etc.

105
Q

Give an example of a synovial joint.

A

Hip joint.

106
Q

How are joints classified functionally?

A

Functional classification focuses on the amount of movement at a joint.

107
Q

What are 3 functional classifications of joint?

A
  1. Synarthroses - immovable.
  2. Amphiarthroses - slight movement.
  3. Diarthroses - freely moveable.
108
Q

Give an example of a synarthroses joint.

A

Sutures in the skull, teeth etc.

109
Q

Give an example of an amphiarthroses joint.

A

Costal cartilages, intervertebral discs etc.

110
Q

Give an example of a diarthrosis joint.

A

Hip joint.

111
Q

Give 5 features of a synovial joint.

A
  1. Articular cartilage - hyaline.
  2. Joint capsule.
  3. Joint cavity.
  4. Synovial fluid.
  5. Reinforcing ligament.
112
Q

What are bursae?

A

Fluid filled sacs lined by synovial membrane.

113
Q

What are menisci?

A

Discs of fibrocartilage.

114
Q

What is the function of hyaline cartilage in a synovial joint.

A

It provides a frictionless surface and acts to resist compressive loads.

115
Q

Describe hyaline cartilage.

A

High water content, low cell content and no blood supply.

116
Q

What is the function of synovial fluid?

A

It lubricates the joint by covering the articulating surfaces. It acts to reduce friction.

117
Q

Give 5 classes of synovial joint.

A
  1. Saddle e.g. thumb
  2. Pivot. atals axis
  3. Ball and socket e.g. hip.
  4. Gliding e.g. carpals.
  5. Hinge e.g. elbow.
118
Q

What are the clinical consequences of high uric acid?

A

Hyperuricemia can lead to the formation of uric acid crystals. These crystals are deposited in the joints and can cause inflammation, pain, swelling and redness. Hyperuricemia

119
Q

What clinical condition can be caused by hyperuricemia?

A

Gout.

120
Q

What is the end product of purine metabolism?

A

Uric acid.

121
Q

What is the effect on the solubility of uric acid if the pH decreases?

A

It becomes less soluble.

122
Q

Give 2 examples of purines.

A
  1. Guanine.

2. Adenine.

123
Q

What is the function of purines?

A

They are important building blocks of DNA and RNA.

124
Q

Name 5 dietary sources of purines.

A
  1. Meat.
  2. Offal; liver, heart, kidney.
  3. Seafood.
  4. Soya, yeast extracts.
  5. Fructose.
125
Q

Why are men more commonly affected by gout than women?

A

Oestrogen promotes uric acid excretion.

126
Q

Give 5 risk factors of gout.

A
  1. CHD.
  2. Diabetes.
  3. Obesity.
  4. High blood pressure.
  5. Excessive alcohol consumption.
127
Q

What does a bone profile blood test look at?

A
  1. Minerals.
  2. Proteins.
  3. Enzymes.
128
Q

What would the bone profile for osteomalacia look like?

A
  1. Low serum calcium.
  2. Low serum phosphate.
  3. High parathyroid hormone (release is triggered by low Ca2+).
129
Q

What is the function of T-tubules?

A

Conduct stimulatory impulses.

130
Q

What is the function of sarcoplasmic reticulum?

A

Sequestration of Ca2+.

131
Q

What is the function of titin?

A

Maintains the functional integrity of myofibrils.

132
Q

What connective tissue binds fasciculi to form muscles?

A

Epimysium.

133
Q

What connective tissue binds muscle fibres to form fasciculi?

A

Perimysium.

134
Q

What connective tissue is found in between each muscle fibre?

A

Endomysium.

135
Q

A patient has low calcium but normal phosphate. What two hormones are responsible?

A

PTH and calcitonin.

136
Q

What enzyme, expressed in osteoclasts, resorbs bone?

A

Cathepsin K.

137
Q

Give 3 places where osteoporotic fractures are common.

A
  1. Hip.
  2. Wrist.
  3. Vertebral column.
138
Q

What is the average recommended daily intake of calcium?

A

700mg.

139
Q

Name 3 hormones involved in calcium homeostasis.

A
  1. Calcitonin.
  2. PTH.
  3. 1,25-dihydroxyvitamin-D.
140
Q

What has been injured in the knee that results in hyperextension?

A

Posterior cruciate ligament.

141
Q

How would you describe a fracture with more than 2 bone fragments?

A

Comminuted.

142
Q

What is a compound fracture?

A

An injury in which bone pierces the skin.