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Medicine Phase 1 > MUSCULOSKELETAL > Flashcards

MUSCULOSKELETAL 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.

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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 2 types of enzymes that are important in bone remodelling.

A
  1. Collagenases.
  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 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-(OH)2-vitD 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-(OH)2-vitD.
  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

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.
  2. Pivot.
  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.

Medicine Phase 1 (16 decks)

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