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Medicine Phase 1 mine > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What are the purposes of the skeleton?

A

Protection, mineral storage, aid movement, transmits body weight, houses bone marrow

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2
Q

What are the two parts of the skeleton?

A

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

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3
Q

What are the shapes of bones?

A

Long bones tubula with hollow shaft, short bones cuboidal in shape, Flat bones plages of bone often curved, irregular bones, sesamoid bones oval or round in a tendon

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4
Q

What are the macroscopic types of bone?

A

Cortical bone compact very dense and only got spaces for cells and blood vessels, Trabecular cancellous spongy bones hollow with spaces

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5
Q

What is the tip of a bone called?

A

Epiphysis

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6
Q

What is the middle of a long bone called?

A

Diaphysis

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7
Q

What is the middle of epyphsis and diaphysis?

A

Metaphysis

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8
Q

What are the types of microscopic bone?

A

Woven bone, Lamellar bone

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9
Q

What is woven bone?

A

Made quickly disorganised no clear structure.

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10
Q

What is lamellar bone?

A

Made slowly organised layered structure often replaces woven bone

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11
Q

What is the purpose of long hollow bones?

A

keeps mass away from neutral axis minimises deformation

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12
Q

What is the purpose of trabecular bone?

A

gives structural support while minimising mass

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13
Q

Why are the heads of bones usually wide?

A

Spreads load over larger area

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14
Q

What is the composition of bone?

A

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

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15
Q

What is an osteoclast like?

A

Multinucleated they are on the surface of the bone they are. they are mesenchymal derived cells

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16
Q

What are osteoblasts?

A

They are plump cuboidal cells on the surfaces of the boen

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17
Q

What are osteocytes like?

A

they are cells with projections into the bone they are inside the bones

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18
Q

What do osteoblasts do?

A

Form bone in form of osteoids, produce type 1 collagen then mieralise it by depositing crystals, tey have high alkaline phosphatase activity and make non collagenous proteins they secrete factors that reculate osteoclasts RANK ligand

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19
Q

Where do osteoclasts come from?

A

Haemopoeitic stem cell lineage

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20
Q

What do osteoclasts do?

A

Resorb bone dissolve mineralsed matrix break down collagen and have high expression of TRAP and cathepisn K

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21
Q

What is bone modelling?

A

Gross shape is altered and bone added or taken away

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22
Q

What is bone remodelling?

A

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

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23
Q

Why does bone remodelling take place?

A

Form bone shape, replaces woven bone with lamellar bone, reoritate fibrils and trabeculae in facourable direction for mechanical strenght, responding to loading, repair damage obtain calcium,

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24
Q

What are the stages of bone healing after a break?

A

Periosteum tears haematoma, callus forms cartilage then becomes bony then remodelling

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25
Q

How can you treat osteoporosis?

A

Stop breakdown, and increase formation

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26
Q

How many types of collagen are there?

A

20

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27
Q

What is the most abundant type of collagen?

A

Fibrillar

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28
Q

What is the strucute of collagen?

A

2 types of protein Alpha 1 and, 3 fibres , has a wavy structure dumbell end at N termina, there are binding sites along the thing

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29
Q

What gives collagen its strength?

A

they interlink fibres that are opposing ends

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30
Q

What do many collagen strands make?

A

Fibrils

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31
Q

What do firbrils make?

A

fibres

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32
Q

What is tropocollagen?

A

It is the fibres that are modified to make the collagen fibre itself

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33
Q

What happens with age in collagen?

A

The bone gets a bit stiffer due to more collagen crosslinks

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34
Q

Why is copper important to collagen?

A

The crosslinks copper helps lysyl oxidase to form links OH-lysine

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35
Q

What are characteristics of copper deficiency?

A

Kinky hair, strange hair, washed out bones

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36
Q

What joins tropocollagen together?

A

Pyridinolines which need vitamin C

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37
Q

What are symptoms of scurvy?

A

Bleeding gums, bruising, loose teeth

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38
Q

How is collagen type one joined?

A

Chopping p1NP and chop amino and carboxy ends before its joined.

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39
Q

What is the disease with lack of collagenase?

A

More prone to fracture of bone

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40
Q

What does vitamin C do for the body?

A

Helps hydroxylise the collagen

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41
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

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42
Q

What affects the severity of osteogenesis imperfecta?

A

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

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43
Q

What can be the problems with osteogenesis imperfecta?

A

Too much mineral, odd arrangement of collagen fibers

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44
Q

How do osteoclasts do to break down bone?

A

make a sealed area around bone and release enzymes

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45
Q

What type of growth is bone growth?

A

Appositional where new tissue is grown from the surface.

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46
Q

What is the type of bone formed in fast situations?

A

Woven bone

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47
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

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48
Q

How are long bones formed?

A

They grow by endochondral ossification replacement of cartilage with bone

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49
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

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50
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

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51
Q

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

A

Epiphyseal plate

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52
Q

When does bone modelling happen?

A

During growth, formation and resorption to sculpt adult shape

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53
Q

When does remodeling happen?

A

In adult 2 million sites, replace and remove old or dammaged bone, to mobilese minerals

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54
Q

What are osteons?

A

They a feature of growth

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55
Q

What is a primary osteon?

A

A circular part of the bone that doesnt cross lamellae as it is formed during modelling

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56
Q

When is a secondary osteon formed?

A

When bone is tunnelled through to make space for vessels

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57
Q

What is a secondary osteon?

A

It cuts through previous lamellae, formation

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58
Q

What is a Herversian tunnel?

A

Another name for a secodary osteon

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59
Q

What type of joint is the hip?

A

Synovial ball and socket

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60
Q

What are the bumps on the femur?

A

The greater trochanter and lesser trochanter

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61
Q

What is the asitabulum?

A

The articular surface on the pelvis

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62
Q

What does the iliacus muscle do?

A

flexion of the hip joint

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63
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

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64
Q

What is the main artery to the leg?

A

The femoral artery, superficial and profundus

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65
Q

Where does the femoral nerve supply?

A

Front of the leg

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66
Q

What forms the siatic nerve?

A

The lumbar plexus

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67
Q

What is important about the siatic nerve in clinic?

A

You need to avoid it in surgery and intramuscular injection

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68
Q

What are the identifiers of osteoarthiritis on xray?

A

Less space between the point, osteophytes, subarticular cysts and sclerosis

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69
Q

When is osteoarthritis most painful and where?

A

Groin pain, night pain

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70
Q

What increases your risk of hip fracture?

A

Osteoporosis

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71
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

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72
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

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73
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

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74
Q

How much phosphate is there?

A

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

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75
Q

How is phosphate in the blood?

A

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

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76
Q

What happens with high phosphate?

A

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

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77
Q

What happens with low phosphate?

A

Low bone mineralisation

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78
Q

What is difference between rickets and osteomalacia?

A

Kids get rickets

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79
Q

How is phosphate taken in?

A

In chicken milk soy and nuts mainly in animal dairy and soy

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80
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

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81
Q

How does phosphate enter the body?

A

It is absorbed through the GI tract by passive diffusion also sodium dependant active transport that is mediated by vitamin D

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82
Q

How is phosphate processed in the kidney?

A

most goes to filtrate 80% is reabsorbed with sodium cotransporter in PCT, 10% in distal tubule which is passive

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83
Q

How is phosphate levels managed?

A

Parathyroid hormone, IGF-1, FGF-23

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84
Q

How does parathyroid hormone regulate phosphate?

A

it increases 1,25 Vit D and this decreases tubular reabsorption of phosphate so increases increases renal exctretion

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85
Q

What does Fibroblast growth factor 23 do?

A

It increases phosphate excretion through the kidney

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86
Q

What is Autosomal dominant hypophosphataemic rickets?

A

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

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87
Q

What produces FGF-23?

A

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

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88
Q

Where does FGF-23 active?

A

It decreases vitamin d activation so reduces absorption in the GI tract and increases excretion in kidney so less in more out

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89
Q

What is Klotho?

A

Trans membrane protein that is associated with FGF-23 it allows it to act

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90
Q

What is Paget’s disease?

A

Focal bone disease like osteoporosis

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91
Q

What is coupling in bone?

A

When bone formation occurs at sites that have previously undergone bone resorption

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92
Q

Where do osteoclasts come from?

A

Haemopoetic progenitor and myeloid porgenerator

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93
Q

What is arthritis?

A

Focal erosion periarticular osteoporosis and generalised osteoporosis

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94
Q

What is pleiotropism?

A

Having many functions in the same and different tissues in conjunction with others

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95
Q

What is redundancy in cytokines?

A

Many cytokines can do the same role so won’t make a difference if you remove it

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96
Q

What affects osteoclast activity?

A

PTH 1,25 dihydroxyvitamin D, osetrogen, leptin, IL-1 IL-6 prostaglandins TNF

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97
Q

What controls remodeling?

A

Osteoblasts

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98
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

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99
Q

What produces rank ligand?

A

Osteoblasts

100
Q

What is rank?

A

A receptor on osteoclasts

101
Q

What is probably responsible for coupling?

A

Release of growth factors

102
Q

Where do osteoblasts come from?

A

Mesenchymal progenetors

103
Q

Where is calcium in the body?

A

Mainly in bone, in extracellular space but needed

104
Q

Where is calcium in the blood?

A

Most is ionised or protein bound small aount complexed

105
Q

Which part of calcium is metabolically active?

A

Ionised

106
Q

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

A

Adjusted calcium from albumin levels

107
Q

What happens in alkalosis to calcium binding?

A

More bind to protein less ionised

108
Q

What is tetany?

A

When low calcium levels cause muscle problems

109
Q

Where is calcium transported?

A

Bone formation resorption, calcium is rebsorbed and excreted in kidney, dietary intake

110
Q

Where does calcium come from in diet?

A

Milk and dairy products, other sorces are minor like cerial and vegetables

111
Q

How is calcium absorbed?

A

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

112
Q

How can calcium be released?

A

In osteoclastic bone destruction and fast transfer

113
Q

What happens to calcium in the kidney?

A

Most is reabsorbed. lots filterd apart from protein bound, PTH causes more reabsorption and less is reabsobed if sodium is high, active resoprtion in DCT most is passsive reabsorption.

114
Q

How is calcium level controlled?

A

Drop in calcium causes PTH release this means more reabsorption in DCT and in GI tract

115
Q

How is PTH released?

A

Detects calcium changes and leasdd with seccond messengers to secrete PTH

116
Q

What is the biosynthesis of Vitamin D?

A

7 dehydroxycholesterol and light turns it to Vit D, then can be hydroxylated 25OH Vit D, Then very active 1,25 OH vit D

117
Q

How is 1,25 Vit D production affected?

A

PTH stimulates it inhibits itelf and byt FGF-23

118
Q

What does calcitriol do for calcium?

A

It inuces expression of calcium transfer proteins in the intestine,

119
Q

What does calcitonin do?

A

C cells in thryroid responds to high calcium and lowers bine resorption

120
Q

What does PTH do?

A

It acts in bone kidney. uses second messnegers in kidney it increases resorption decrease phosphate, increases Vit D, increases bone resporption, no direct effect in GI tract but Vit D has effect

121
Q

What do ligaments connect?

A

Attach bone to bone usually, tooth to bone

122
Q

What is the function of ligaments?

A

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

123
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

124
Q

What is the composition of tendons and ligaments?

A

Dense connective tissues, fibroblasts, low cell number and low cell turnover. most is ectracellular matrix most is water other parts are collagen and proteins low vascularisation

125
Q

Are tendons flexible?

A

They are slightly extensible but not very

126
Q

What units build a tendon?

A

5 tropocollagen forms microfibril and then fibrils fascicles and form the tendon, there is epitenon and paratenon aroung the fasicles

127
Q

How is the hierachical structure of tendons formed?

A

Mainly type 1 also 3 5 6 9, they control the fibril diameter, proteglycans which act as lubricant to help glide over eachother

128
Q

How is collagen synthesis?

A

3 left coled chains join to make a right handed triple one that is released into ECM and self assembles outside the cell N and C ternminals cleaved Lysyloxidase

129
Q

Are tendons elastic/

A

No but do contain some elastin especially in the spine

130
Q

What are the main differences between tendons and ligaments?

A 
Ligament vs Tendon
bone to bone vs muscle to bone
Lower ype one vs higher type one
Hight elastin vs very little elastin
more random arrangement of fibres
blood from insertion, can get from the perimysium from the muscle or the bone
131
Q

What is an alternative name for insertion site?

A

Entheses

132
Q

What are the two types of insertion?

A

Fibrous insertion or fibrocartilage insertion

133
Q

What is a fibrous insertion like?

A

Calcified anchorage from collagen fibres sharpeys fibres into bone

134
Q

What is fibrocartilage insertion like?

A

Gradual change from collagenous ligament into fibrocartialge into mineralised cartilage into bone

135
Q

What hapens with stress and strain in tendons and ligaments?

A

Intitally extends lowering strain from crimps extending after a while it breaks slow extension initially and then lots of extension the breaks 15% extension

136
Q

What is inside tendons?

A

Golgi tendon organ

137
Q

What does the golgi tendon organ do?

A

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

138
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

139
Q

How do tendons change over life?

A

Up to 20 years increase in diabeter and quantity, as you ages the collagen content decreases and so the strength decreases, pregnancy relaxes

140
Q

How do tendons respond to strain?

A

physical strain can lead to tensile stregth and ligament- bone interface strength. ligaments become stronger and stiffer in immobilisation there wll be decreae of tensile strenght and more elongation and decrease in crosslength 8 weeks mmpbile 12 months to recover strength

141
Q

What is the cause of most sports injuries?

A

Over use 30-50% obesity is a risk factor

142
Q

What can cause tendon failure?

A

direct trauma actute tensile fiaure indirect tensile overload

143
Q

When are ligaments usually broken?

A

Traumatic injuries, ligament avulsion from from bone at slow rates

144
Q

What happens after a dislocation?

A

Destabilise joint and leads to abnormal load bearing

145
Q

What affects healing of things?

A

location for resting and vascularisation

146
Q

What are the stages of healing in tendons?

A

Short inflamtory phase days, proliferative phase in weeks, remodelling and maturation over months

147
Q

What are the functons of joints?

A

3D movements bear weight transfer load evenly to MSK

148
Q

What are the tissues associated with a joint?

A

Bone, Muscles, cartilage, synovium, synovial fluid, dense fibrous tissue(capsule) tendons and ligaments

149
Q

What are the classification methods of joints?

A

Structural, which components hold it together

Functional classification about degree of movement

150
Q

What are the types of structural joints?

A

Fibrous, cartilaginous, synovial

151
Q

What are the functional classifications of joints?

A

Synarthroses immovable mostly fibrous, Amphiarthroses slight movement cartilagenous and intervertebral disks, diarthroses freely moveable, hip

152
Q

Give an exampe of a fibrous joint?

A

Sutures in the skull short tissue fibres, syndesmoses, bones conneced by a ligament amount of movement proportional to the length of the fibre, gomphoses teeth

153
Q

What are cartilagenous joints?

A

Synchondroses hyaline cartilage of ribs, sympheses fibrocartilage plate,

154
Q

What makes up a synovial joint?

A

Articular cartilage, Joint capsule with synovial membrane on inner side, joint synovial cavity, synovial fluid, reinforcing ligaments

155
Q

What other component are associated with synovial joints?

A

Bursae fluid filled sacs, menisci discs of fibrocartilage

156
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

157
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

158
Q

Which joint is a first class lever?

A

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

159
Q

What is an example of 2nd class lever?

A

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

160
Q

what the names for joints from movement?

A

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

161
Q

What does the ACL of the knee do?

A

Rotational stability and resists tibia moving forwards

162
Q

What does the PCL of the knee do?

A

It resists posterior translation of the femur

163
Q

What does the MCL of the knee do?

A

It resists valgus force n the knee

164
Q

What does the LCL do?

A

It resists varus force

165
Q

What are some common knee conditions?

A

OA RA, Ligment injuries meniscal pathology patelofemoral disorders knee dislocation

166
Q

How can OA be divided?

A

Primary or secondary after infection or trauma

167
Q

What investigations for knee issues?

A

weight bearing, Xrays, MRI for other things

168
Q

What is osteotomy?

A

Remove bone to realign

169
Q

What is an arthroplasty?

A

Replacement of all or part of the joint?

170
Q

What is an acute knee?

A

Short time frame, time frame, blood thinner, injection, gout, pseudo gout

171
Q

Where are the menisci of the knee?

A

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

172
Q

What causes knee problems of menisci?

A

Twisting in flexion acute pain but often not severe gradual swelling

173
Q

What is locking?

A

The meniscus blocks extension but not flexion

174
Q

Who hurts ACL most?

A

Men probably stupidity, women are more likely to though and women land differently,

175
Q

What do you do with ACL?

A

Operate if very active, or just rehab

176
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

177
Q

What are the characteristics of muscle /

A

Conductivity, excitability, contractility, extensibility and elasticity

178
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

179
Q

What is the function of nebulin?

A

It dictates the maximum lenth of the actin

180
Q

What are the thick filaments of muscle like?

A

Maintained by titin, like a spring, has heads

181
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

182
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

183
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

184
Q

What are the three types of muscle fibres?

A

slow oxidative of slow twitch fatigue resistant fibres, fast oxidative IIa and fast glycolytic IIb

185
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

186
Q

How do muscles get energy aerobicly?

A

Trhough the generation of ATPin mitochondria.

187
Q

How do muscles get energy anaerobicly?

A

they use glycolusis only and use lactic acidto export waste, also use creatine phosphate to generate ATP and creatine

188
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

189
Q

How is gout diagnosed?

A

From clinical syptoms, inflamation in joint and from blood test slightly

190
Q

What is gout?

A

Uric acid crystals in the joint,what causes dammage

191
Q

What are the properties of uric acid?

A

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

192
Q

Where does uric acid come from?

A

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

193
Q

How does uric acid leave the body usually?

A

In the urine or broken down in the gut

194
Q

Where can purines come from?

A

Purine synthesis diatery intake and tissue nucleotides

195
Q

Why do some people get gout?

A

Men have higer levels in blood, less in women and children, dietary factors

196
Q

What food contains a lot of purines?

A

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

197
Q

How can alcohol affect purine metabolyism?

A

Increased tissue breakdown and decreased extretion

198
Q

How can gout be treated?

A

Rest ice elevate joints and anti inflamatories

199
Q

What are some other causes of gout?

A

cancers, Polycythemia rubra vera, trauma starvation

200
Q

What can an ageing population lead to?

A

Strains on the pension service increasing demand of healthcare and staff long term care and ageism becomes worse

201
Q

What are the two types of ageing?

A

Intrinsic, natural universal inevitable

Extrinsic such as exposure to UV smoking and air pollution that can be changed

202
Q

What happens in physical aging?

A

Loss of skin elacticity, hair color and hair, size weight loss of flexability lower immunity less efficient memory and learning ability sensory effectiveness, smaell hearing and vision

203
Q

What is the gender balance in aging/

A

20% biological from protective hormones in women 80% in environmental life choices

204
Q

What diesease affect older people?

A

Arthritis, cancers mainly chronic conditions

205
Q

What are the types of dementia?

A

Alzheimer’s disease, vascular dementia, mixed, dementia with lewy bodies fronto-temporal dementia

206
Q

What is the role of the GP for elderly people

A

joining services preventing loss of function helping deal with symptoms

207
Q

Why do bones respond to exercise?

A

So that they won’t break under load

208
Q

What happens to bones under load?

A

They deform under load

209
Q

How is strain valued?

A

Deformation/ length

210
Q

What are the variables in strain?

A

Magnitude, rate, frequency, dwell number of cycles

211
Q

What is SSCSS?

A

Site specific customary strain stumulus

212
Q

What can affect customary strain?

A

Age sex hormones and drugs can change these levels

213
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

214
Q

Which bones measure strain?

A

Osteocytes

215
Q

How fast does bone respond to strain?

A

Within 5 minutes

216
Q

How is the understanding of bone used clinically?

A

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

217
Q

What is achondroplasia?

A

dwarfism

218
Q

What can affect growth plate differentiation rate?

A

FGF-23

219
Q

what is alkaline phosphate?

A

it inhibits bone formation

220
Q

What does alkaline phosphatase do?

A

It breaks down alkaline phosphate to allow bone formation

221
Q

What is periostial elevation/

A

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

222
Q

What are the radiological features of rickets?

A

Cupping splaying fraying osteopaenia periosteal elevation

223
Q

How can inherited enzyme vitamin d activation?

A

They give supliments at a later step to jump it over

224
Q

Should children have same levels of phosphate?

A

No they should have higher levels

225
Q

What usually causes low phosphate?

A

too much loss rather than low intake

226
Q

What can be used to treat low phosphate?

A

Anti FGF23 antibodies to reduce its effects

227
Q

What causes problems at the end of the bones?

A

Alkaline phosphatase hypophosphatase.

228
Q

What is a fracture?

A

A breach in continuity of the bone

229
Q

When do fractures occur?

A

Non-physiological when loads applied to normal bone

Physiological loads applied to abnormal bone

230
Q

What can make bone more ikely to fracture?

A

Osteoporosis, osteomalacia, tumours also bone disease

231
Q

What ways can a fractures be described?

A

Site pattern displacement or angulation, joint involvement skin involvement

232
Q

How can the site of a fracture be described?

A

proximal middle distal

233
Q

What can pattern of the fracture be described as?

A

Transvers, oblique, spiral, comminuted, segmental, avulsed, impacted, torus greenstick

234
Q

How can joint involvement be described?

A

Intra-articular or extra articular

235
Q

What are inflamation of fracturs?

A

The bone fills with blood breaking dead things with growth factors with clotting and immune cell bodies

236
Q

What is a callus?

A

Fibrous tissue around a bone from fibroblasts and chondrocytes and cartilage

237
Q

How shoudl you deal with a bone fracture?

A

Reduce if required immobilise and rehabilitate

238
Q

Does a plated fracture help healing?

A

Very good position but can take a lot longer to work

239
Q

What can affect fracture healing?

A

Patient- Age nutrition Smoking drugs
Tissue- bone type site vascularity pathology infection
Treatment- type of care with the fracture

240
Q

What are early local effects of the fracture?

A

Vessel damage, Nerve damage, Compartment syndrome, infection

241
Q

What are early general effects of the fracture?

A

Hypovolaemic shock, ALI/ARDS VTE fat embolysms

242
Q

What are late local effects of the fracture?

A

mal/ non-union. Avascuar necrosis Ischaemic contractures joint stiffness, myostis ossifcans artheritis

243
Q

What are late general effects of the fracture?

A

Poor mobility, disability pressure sores disuse osteoporosis

244
Q

What type of collagen is scar collagen?

A

3 rather than 1

245
Q

Which diseases contribute to frailty?

A

Cardiovascular deterioration, Risk of stroke, respiratory capacity reduction, depression anxiety cognitive imparement

246
Q

How are falls linked to frailty?

A

after a fall knocks confidence and makes it harder

Medicine Phase 1 mine (21 decks)

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