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Year 1 Medicine > Muskuloskeletal > Flashcards

Muskuloskeletal 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 parafollicular C-cells release?

A

Parafollicular C cells of the Thyroid release 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.

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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.

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59
Q

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

A

It converts 7-dehydrocholesterol into cholecalciferol.

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60
Q

What converts 7-dehydrocholesterol into cholecalciferol?

A

UVB light.

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61
Q

What is osteomalacia?

A

An inability to mineralise bone.

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62
Q

What is the usual cause of osteomalacia?

A

Vitamin D deficiency.

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63
Q

What is the DEXA T score range for osteopenia?

A

-1.5 -> -2.5.

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64
Q

What is the DEXA T score range for osteoporosis?

A

-2.5 or lower.

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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.
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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.

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67
Q

What compound is a marker of increased bone turnover?

A

Alkaline phosphatase.

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68
Q

What type of muscle fibres are slow twitch?

A

Type 1.

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69
Q

By what process do type 1 muscle fibres get energy?

A

Oxidative processes and so have lots of mitochondria.

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70
Q

What type of muscle fibres very sensitive to fatigue?

A

Type 2b.

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71
Q

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

A

Type 1.

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72
Q

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

A

Oxidative and glycolytic energy processes.

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73
Q

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

A

Glycolytic processes.

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74
Q

What type of muscle fibres are fast twitch?

A

Type 2a and 2b.

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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.

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76
Q

Define fracture.

A

A breach in the continuity of bone.

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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.
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78
Q

What are the 4 stages of fracture healing?

A
  1. Haematoma (hours after fracture occurs).
  2. Inflammation (days after).
  3. Repair - fibrocartilaginous and bony callus formation (weeks after).
  4. Bone Remodelling (months to years after).
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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.
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80
Q

What happens in the inflammation and fibrocartilaginous callus formation stage of fracture healing?

A
  1. Fibrin clot organisation.
  2. Neovascularisation as capillaries grow into the haematoma
  3. cellular invasion as phagocytes clear away dead cells
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81
Q

What happens in the bony callus formation stage of fracture healing?

A
  1. Callus formation - fibroblasts, chondroblasts and osteoblasts produce fibrous tissue, cartilage and osteoid respectively.
  2. Matrix mineralisation with crystals of hydroxyapatite covert this into a bony callus.
  3. There is High vascularity.
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82
Q

What happens in the remodelling stage of fracture healing?

A
  1. Woven bone is replaced with lamellar bone.
  2. Increased bone strength.
  3. the bony callus undergoes endochondral ossification.
  4. Vascularity returns to normal
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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.
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84
Q

What is a ligament?

A

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

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85
Q

What is a tendon?

A

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

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86
Q

What contains more elastin, ligament or tendon?

A

Ligament.

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87
Q

What contains more type 1 collagen, ligament or tendon?

A

Tendon.

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88
Q

How are fibres arranged in ligaments?

A

Random fibre organisation.

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89
Q

How are fibres arranged in tendons?

A

Organised fibres.

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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.

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91
Q

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

A

80%.

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92
Q

What is the hierarchal structure from tropocollagen to tendon?

A

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

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93
Q

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

A

Endotenon.

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94
Q

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

A

Epitenon.

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95
Q

What is the entheses?

A

Where a tendon or ligament inserts into bone.

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96
Q

What are the two types of insertion into entheses?

A
  1. Fibrous. 2. Fibrocartilage.
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97
Q

How is a fibrous insertion formed?

A

Through intramembranous ossification.

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98
Q

How is a fibrocartilage insertion formed?

A

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

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99
Q

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

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

What can increase tendon and ligament tensile strength?

A

Physical training.

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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.
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102
Q

What are 3 structural classifications of joint?

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

Give an example of a fibrous joint.

A

Teeth, sutures in the skull etc.

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104
Q

Give an example of a cartilaginous joint.

A

Intervertebral discs, costal cartilages etc.

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105
Q

Give an example of a synovial joint.

A

Hip joint.

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106
Q

How are joints classified functionally?

A

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

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107
Q

What are 3 functional classifications of joint?

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

Give an example of a synarthroses joint.

A

Sutures in the skull, teeth etc.

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109
Q

Give an example of an amphiarthroses joint.

A

Costal cartilages, intervertebral discs etc.

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110
Q

Give an example of a diarthrosis joint.

A

Hip joint.

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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 encases a muscle fasciculi?

A

Perimysium.

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.

143
Q

What are the two parts of the skeleton?

A

The axial skeleton(scull spinal cord 80 bones), appendicular skeleton 126 bones)

144
Q

What is the tip of a bone called?

A

Epiphysis

145
Q

What is the middle of a long bone called?

A

Diaphysis

146
Q

What is the middle of epyphsis and diaphysis?

A

Metaphysis

147
Q

What are the types of microscopic bone?

A

Woven bone, Lamellar bone

148
Q

What is woven bone?

A

Made quickly disorganised no clear structure.

149
Q

What is lamellar bone?

A

Made slowly organised layered structure often replaces woven bone

150
Q

What is the purpose of long hollow bones?

A

keeps mass away from neutral axis minimises deformation

151
Q

What is the purpose of trabecular bone?

A

gives structural support while minimising mass

152
Q

Why are the heads of bones usually wide?

A

Spreads load over larger area

153
Q

What is the composition of bone?

A

Mineral 50-70% hydroxyapetite, 20-40% organic matrix lots of collagen and noncollagenous proteins, 5-10% waterIt is fibres of protein then mineral deposited between them.

154
Q

How many types of collagen are there?

A

20

155
Q

What is the most abundant type of collagen?

A

Fibrillar

156
Q

What is the strucure of tropocollagen and collagen fibrils?

A

Tropocollagen:
3 strands made up of 2x alpha 1 chains and 1x alpha 2 chain.
These are coiled together in a tripple helix.

Collagen fibrils:
Collagen fibrils are formed from multiple tropocollagen fibers bound together via oh-lysine pyridinolone crosslinks

157
Q

What gives collagen its strength?

A

Every 3rd amino acid is a glycine.
Prolines are converted to hydroxyprolines which can bind across the inside of the triple helix with H-bonds to other glycine molecules to hold it together.

Crosslinks are also found at the ends to other tropocollagen molecules side by side.

158
Q

What do tropocollagen strands make?

A

collagen Fibrils

159
Q

What do many collagen firbrils make?

A

collagen fibres fibres

160
Q

What happens with age in collagen?

A

The bone gets a bit stiffer due to more collagen crosslinks

161
Q

Why is copper important to collagen?

A

Helps for crosslinks between the triple helix tropocollagen molecules by aiding lysyl oxidase to oxidise 2x lysine residues.

162
Q

What joins tropocollagen together?

A

hydroxyproline H-bonds to glycine molecules within the triple helix.

163
Q

How is collagen type one joined?

A

Crosslinks between OH-lysine residues (requires copper) between the molecules. These are pryidinolines.

H-bonds between hydroxyproline molecules and glycine within tropocollagen triple helix. (requires vit C)

N terminal and C terminal peptides (P1NP and P1CP are cleaved)

164
Q

How is collagen processed?

A

the collagen molecule is excreted from the cell intact.

The end N terminal and C terminal peptides (P1NP and P1CP) are then cleaved extracellularly

165
Q

What does vitamin C do for the body in collagen synthesis?

A

converts Fe3+ to Fe2+ which is the iron required for the hydroxylation of proline to hydroxyproline.

166
Q

What is osteogenis imperfecta?

A

Common in children bone fragility, bad problems in collagen formation, blue sclera, odd teeth, scholiosis, easily fractures in the back

167
Q

What affects the severity of osteogenesis imperfecta?

A

Number of fractures per year, and how much bone is dammaged

168
Q

What can be the problems with osteogenesis imperfecta?

A

Too much mineral, odd arrangement of collagen fibers

169
Q

How do osteoclasts do to break down bone?

A

make a sealed area around bone and release enzymes

170
Q

What type of growth is bone growth?

A

Appositional where new tissue is grown from the surface.

171
Q

What is the type of bone formed in fast situations?

A

Woven bone

172
Q

What happens in primary bone growth?

A

It produces wavy surfaces and this can cause areas to be missed that get filled in later

173
Q

How are long bones formed?

A

They grow by endochondral ossification replacement of cartilage with bone

174
Q

What is the seconday ossification centre in a long bone?

A

It is an area that is at the end of the long bone that is separate to the shaft where tissue grows

175
Q

What are the layers of the tissue at the growth plate?

A

Resting zone, germinal zone, hypertrophic zone, degenerative zone, cartilage resorption and bone formation

176
Q

What is the technical name for the growth plate in a bone?

A

Epiphyseal plate

177
Q

When does bone modelling happen?

A

During growth, formation and resorption to sculpt adult shape

178
Q

What are osteons?

A

Osteons are formations characteristic of mature bone and take shape during the process of bone remodeling, or renewal.

179
Q

What is a primary osteon?

A

A circular part of the bone that is the functional unit. it contians blood vessles within the haversian canal

180
Q

When is a secondary osteon formed?

A

When bone is tunnelled through to make space for vessels

181
Q

What is a secondary osteon?

A

secondary osteons are formed by the replacement of primary woven bone with secondary lamella bone

182
Q

What is a Herversian canal?

A

Haversian canals are a series of tubes (arteries, veins, nerves, lympatics) around narrow channels formed by lamellae.

183
Q

What type of joint is the hip?

A

Synovial ball and socket

184
Q

What are the bumps on the femur?

A

The greater trochanter and lesser trochanter

185
Q

What is the acetabulum?

A

The articular surface on the pelvis where the head of the femur articulates.
Also the point where the 3 pelvic bones fuse

186
Q

What does the iliacus muscle do?

A

flexion of the hip joint

187
Q

What is the clinical significance of the abductor muscles of the hip?

A

It elevates the pelvis on the non weight bearing side of the body

188
Q

What is the main artery to the leg?

A

The femoral artery, superficial and profundus

189
Q

Where does the femoral nerve supply?

A

Front of the leg

190
Q

What forms the sciatic nerve?

A

The lumbar plexus

L4-S3

191
Q

What is important about the siatic nerve in clinic?

A

You need to avoid it in surgery and intramuscular injection

192
Q

What is an intracapsular fractrue of the hip?

A

Happens on the neck of the femur and is serious as breaks blood supply to the head

193
Q

What is developmental dysplasis of the hip?

A

found often in first 5 years of life, is developed out of the joint and doesnt grow and doesnt have an ossification centre

194
Q

What is the use of phosphate in the body?

A

Phospholipids for bilayer, seccond messengers cAMP, involve in post-translational protein modification, in DNA, in bone minerals

195
Q

How much phosphate is there?

A

1% 500-800g it is mainly intracellular and a lot in the bone

196
Q

How is phosphate in the blood?

A

50% free ions
35% complexed with Na Ca Mg and
10% bound to protein

197
Q

What happens with high phosphate?

A

Hydroxyapitite is formed excessively and deposited in other places such as vessels and soft tissue

198
Q

What happens with low phosphate?

A

Low bone mineralisation

199
Q

What is difference between rickets and osteomalacia?

A

Kids get rickets

200
Q

Where is phosphate processed?

A

In GI absorbed in and out of bone kidney filtres and brings it back some lost in stool and some secreted

201
Q

What is Autosomal dominant hypophosphataemic rickets?

A

It is a genetic lack of ability to retain phosphate through the kidneys

202
Q

What produces FGF-23?

A

Osteocytes and osteoblasts in response to a rise in phosphate and high 1,25 Vit D and PTH

203
Q

What is Paget’s disease?

A

Focal bone disease like osteoporosis

204
Q

What is arthritis?

A

inflammation of the articular joints

205
Q

What is pleiotropism?

A

Where a single cytokine has many different functional effects on many different cell types or even on the same cell

206
Q

What is redundancy in cytokines?

A

means most functions of cytokines can be performed by many different cytokines

207
Q

What affects osteoclast activity?

A

PTH 1,25 dihydroxyvitamin D, oestrogen, Osteoprotegerin

208
Q

What controls remodeling?

A

Osteoblasts

209
Q

What is osteoprotegrin?

A

it allows bone to be dense it inhibits differentiation of myeloid precursors into osteoclasts. it binds to rank ligand so rank rankligand interaction is blocked

210
Q

What produces rank ligand?

A

Osteoblasts

211
Q

What is rank?

A

A receptor on osteoclasts

212
Q

What is probably responsible for coupling?

A

Release of growth factors

213
Q

Which part of calcium is metabolically active?

A

Ionised

214
Q

What should you take into account when you get calcium rating?

A

Adjusted calcium from albumin levels

215
Q

What happens in alkalosis to calcium binding?

A

More bind to protein less ionised

216
Q

What is tetany?

A

When low calcium levels cause muscle problems

217
Q

How is calcium absorbed?

A

In duodenum jejunum active absorption and passibe in ileum vitamin D switches on actie transport

218
Q

What is the biosynthesis of Vitamin D?

A

7 dehydroxycholesterol is converted to cholecalciferol by UVB light. This can then be converted to 25-hydroxyvitamin D by 25 hydroxylase in the liver. 25-OHvitamin D is then activated by 1-hydroxylase in the kidney to form 1,25-Hydroxyvitamin D (the active form of vitamin D)

219
Q

How is 1,25 Vit D production affected?

A

PTH stimulates it

Inhibited production by itself and FGF-23

220
Q

What is the function of ligaments?

A

They augment mechanical stability of joints, guide joint motion and prevent excessive motion

221
Q

What is the function of tendons?

A

Muscle to bone, transmit load from muscle, produce joint torque, stabilise joints enable joint motion, dynamic joint restraint

222
Q

Are tendons flexible?

A

They are slightly extensible but not very

223
Q

How is collagen synthesis?

A

3 left coiled chains join to make a right handed triple helix that is released into ECM
It self assembles outside the cell the N and C terminal peptides (P1NP and P1CP) are cleaved by Lysyloxidase

224
Q

What is an alternative name for insertion site?

A

Entheses

225
Q

What are the two types of insertion?

A

Fibrous insertion or fibrocartilage insertion

226
Q

What is a fibrous insertion like?

A

Calcified anchorage from collagen fibres sharpeys fibres into bone

227
Q

What is inside tendons?

A

Golgi tendon organ

228
Q

What does the golgi tendon organ do?

A

It has nerves around the tendon fibres, tey sense muscle tension

229
Q

Explain the myotatic reflex.

A

Golgi tendon organ is stimulated, nerve impuse travels to spinal chord by 1b, interneurone alpha motor neurone to muscle goes and this prevents the muscle from contracting to stop damage to tendon

230
Q

What other component are associated with synovial joints?

A

Bursae fluid filled sacs, menisci discs of fibrocartilage

231
Q

What are the features of hyaline cartilage articuation?

A

Almost frictionless surface, resists compressive loads, high water cntent, low cell content no blood supply

232
Q

What is in synovial fluid?

A

Covers the articular surfaces with a thin film, modified from plasma by synovial contains charged sugar like hyluronate gives viscosity

233
Q

Which joint is a first class lever?

A

elbow for triceps the resistance has the fulcrum between it and the load

234
Q

What is an example of 2nd class lever?

A

temporomandibular the resistance is between the fulcrum and the force stading on tip toes

235
Q

what the names for joints from movement?

A

Ball and socket, condoloid, gliding joint, hinge joint, pivot joints and saddle joints

236
Q

What does the ACL of the knee do?

A

Rotational stability and resists tibia moving forwards

237
Q

What does the PCL of the knee do?

A

It resists posterior translation of the femur

238
Q

What does the MCL of the knee do?

A

It resists valgus force n the knee

239
Q

What does the LCL do?

A

It resists varus force

240
Q

Where are the menisci of the knee?

A

Lateral and medial meniscis. lateral is often torn as takes more area

241
Q

What is the function of skeletal muscle?

A

To produce movements of body parts, suppport soft tissues comunication cotrol of opennings and passage ways to maintian boy temperature

242
Q

What are the characteristics of muscle /

A

Conductivity, excitability, contractility, extensibility and elasticity

243
Q

What are the thins filaments of muscle like?

A

F actin it binds to make a chain, capped by tropomodulin and cap Z alpha actin to help it be stable

244
Q

What is the function of nebulin?

A

It dictates the maximum lenth of the actin

245
Q

What are the thick filaments of muscle like?

A

Maintained by titin, like a spring, has heads

246
Q

What happens to initiate muscular contraction?

A

The nerve releases acetylcholine onto the neuromuscuar junction the ACh binds to receptors on the muscle cells and this allows sodium to enter the cell causing voltage gated calcium channels to open and this activates the sliding mechanism

247
Q

How can drugs interact with muscle contraction?

A

Thy can have potassim channels blocked on presynaptic also sodium calcium and can block ACh release, also block the ACh receptro chanel on the muscle

248
Q

What does botulinum toxin do?

A

Muscle weakness paralysis leading to death they stop the proteins neeeded for exocytosis of ACh stops the vesicle bnding or inhibitin the binding site on membrane or the protein on the vesicle

249
Q

How does reaction time in muscles work?

A

fast fibres react quickly and contract for short time while slow fibres take longer to react and contract for longer

250
Q

What is muscle fatigue?

A

The weakness of contraction of muscles that happens when ATP synthesis decreases from low glycogen, lactic acid levels rise or failure of motorneurones form lack of Calcium

251
Q

What are the properties of uric acid?

A

Poorly soluble in plasma, lower pH of blood less soluble it becomes

252
Q

Where does uric acid come from?

A

Purines that come from the break down of DNA Adenine and Guanine hypoxanthine and xanthine

253
Q

How does uric acid leave the body usually?

A

In the urine or broken down in the gut

254
Q

Where can purines come from?

A

Purine synthesis diatery intake and tissue nucleotides

255
Q

What food contains a lot of purines?

A

Meat (organs), seafood fish oatmeal soya yeast extract but mainly meat

256
Q

How can alcohol affect purine metabolyism?

A

Increased tissue breakdown and decreased extretion

257
Q

How can gout be treated?

A

Rest ice elevate joints and anti inflamatories

258
Q

Why do bones respond to exercise?

A

So that they won’t break under load

259
Q

What happens to bones under load?

A

They deform under load

260
Q

How is strain valued?

A

Deformation/ length

261
Q

What are the variables in strain?

A

Magnitude, rate, frequency, dwell number of cycles

262
Q

What causes bone to strengthen itself?

A

Maximally to a small number of loading cycles, exercise prior can help can respond to events that happen in miliseconds

263
Q

Which bone cells measure strain?

A

Osteocytes

264
Q

How fast does bone respond to strain?

A

Within 5 minutes

265
Q

How is the understanding of bone used clinically?

A

Increase bone mass in younger ages and help prevent loss in older age

266
Q

What is achondroplasia?

A

dwarfism

267
Q

What can affect growth plate differentiation rate?

A

FGF-23

268
Q

what is alkaline phosphate?

A

it inhibits bone formation

269
Q

What does alkaline phosphatase do?

A

It breaks down alkaline phosphate to allow bone formation

270
Q

What is periostial elevation/

A

When the periosteum is lifted from the bone either from bleeding or from bone growth (in children)

271
Q

How can inherited enzyme vitamin d activation?

A

They give supliments at a later step to jump it over

272
Q

Should children have same levels of phosphate?

A

No they should have higher levels

273
Q

What usually causes low phosphate?

A

too much loss rather than low intake

274
Q

What causes problems at the end of the bones?

A

Alkaline phosphatase hypophosphatase.

275
Q

When do fractures occur?

A

When Non-physiological loads are applied to normal bone

When Physiological loads applied to abnormal bone

276
Q

What type of collagen is scar collagen?

A

3 rather than 1

277
Q

Explain the Process of Bone remodelling

A

Cells lining the bone surface are activated to form or recruit osteoclats in response to injury.

Osteoclasts attach to the bone surface and secrete acids that dissolve the bone mineral to form resorption cavities.

Osteoblasts are recruited to the resorbed bone and secrete osteoid matrix which is mainly comprised of collagen.

Over time the osteoid matrix is mineralised with hydroxyapatite crystals to form bone.

Year 1 Medicine (25 decks)

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