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JMP Y2S1 > Week 35- Upper Limb and Bone > Flashcards

Week 35- Upper Limb and Bone Flashcards

1
Q

What is circulating calcium critical to?

A 
Neural function
Muscular function
Blood clotting
Cell replication
Secondary messenger signalling
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2
Q

Does the body respond faster to a low or high blood calcium level?

A

Faster response to decreases in blood calcium concentration

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3
Q

What is the bodies homeostatic response to low calcium levels in the blood?

A
  1. Low calcium levels
  2. Parathyroid gland stimulated
  3. Chief cells in parathyroid gland release PTH
  4. PTH promotes
    - release of Ca2+ from bone ECM
    - Slows loss of Ca2+ in urine
    - Promotes kidneys to release calcitriol (active form of Vitamin D –> increases GIT Ca2+ absorption
  5. Blood calcium raised to normal levels
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4
Q

What is the bodies homeostatic response to high calcium levels?

A
  1. High calcium levels
  2. Thyroid gland stimulated
  3. C-cells in the thyroid gland produce Calcitonin (CT)
  4. CT inhibits osteoclasts (reduced bone demineralisation)
  5. Decreases blood calcium
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5
Q

Where is Fibroblast Growth Factor-23 (FGF23) secreted?

A

From bone in response to increased plasma Hydrogen phosphate (HPO)

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6
Q

What does FGF23 do?

A

Reduces phosphate concentrations in the blood:

  • Increases renal excretion –> by decreasing resorption
  • Decreases gut absorption –> decreases calcitriol production (as phosphate follows calcium)
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7
Q

What are the two main bone textures?

A
  1. Compact –> dense outer layer –> smooth and solid –> 75% of bone is like this
  2. Spongy (cancellous or trabecular) –> honeycomb-like –> deeper than compact bone –> much larger SA –> more metabolically active
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8
Q

What kind of strength does collagen contribute to bone?

A

Tensile

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9
Q

What strength does calcium contribute to bone?

A

Compressive strength

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10
Q

What are the 5 major cell types in bone?

A
  1. Osteogenic cells –> mitotically active –> differentiate into osteoblasts or bone lining cells
  2. Osteoblasts –> mitotically active –> Bone forming cells –> secrete unmineralised bone matrix (osteoid) –> initiates bone resorbtion
  3. Osteocytes –> mature cells –> monitor and maintain bone matrix –> comunicate with blasts and clasts to regulate remodelling
  4. Bone lining cells –>on bone surfaces –> thought to maintain matrix
  5. Osteoclasts –> derived from haematopoietic stem cells –> bone resorbing cells
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11
Q

What secretes osteoid?

A

Osteoblasts

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12
Q

What is in osteoid?

A
  1. Ground substance (proteoglycans and glycoproteins)

2. Collagen fibres

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13
Q

What allows for the resilience of bones?

A

Sacrificial bonds between collagen molecules

  • They stretch and break easily on impact –> dissipates energy and prevents fracture
  • If there is no additional trauma these bonds reform
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14
Q

How much of bone mass is Hydroxyapatites?

A

65%

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15
Q

What is the composition of Hydroxyapatites?

A

Mainly tiny calcium phosphate crystals in and around collagen fibres
Responsible for hardness and resistance to compression

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16
Q

What is the effect of Wnt signalling on bones?

A

Cause mesenchymal stem cells to differentiate into osteoblasts

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17
Q

What does IGF-1 do to osteoblasts?

A

Increases activity

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18
Q

What determines IGF-1 secretion?

A

IGF-1 secretion by the liver is stimulated by GH (growth hormone)

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19
Q

What is the effect of increased vs decreased GH on bones?

A

Increased –> giantism –> increased bone length

Decreased –> dwarfism –> smaller bones

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20
Q

Where do long bones grow from in childhood?

A

Epiphyseal plates - endochondral (cartilage is replaced)

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21
Q

What does the level of bone accretion and bone resorption determine?

A

Bone mass

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22
Q

What happens in over secretion or abuse of GH?

A

After long bones fuse –> causes appositional growth (widening)
–> known as acromegaly

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23
Q

What factors is bone accretion dependant on?

A
  1. Sufficient Ca2+
  2. Vitamin D
  3. Sufficient weight bearing activity (most effective if varied and short intense bursts)
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24
Q

What is the bodies main driver of bone resorption?

A

PTH

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25
Q

What factors explain calcium loss with aging?

A
  1. Less osteoblast activity with increased age:
    - Due to decreased IGF-1 and vitamin D production
  2. Decline in sex steroid production in aging:
    - Oestrogen in particular –> important to supress osteoclastic activity
  3. Peak bone density normally attained in early adulthood:
    - Bone density is determined by remodelling processes influenced by:
    - Diet, Age, Hormonal regulation
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26
Q

How does oestrogen supress osteoclast activity?

A

Supresses RANKL –> a ligand that increases osteoclast activity

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27
Q

What non-pharmacological strategies is there to prevent calcium loss?

A
  1. Diet –>
    - calcium intake
    - protein (for collagen synthesis)
    - increased body weight (increases Ca2+ storage potential)
  2. Vitamin D –> increases calcium absorption from diet
  3. Exercise –> weight bearing –> minor damage –> stimulates bone remodelling
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28
Q

What is the three major functions of bone?

A

Structural –> support and insertion sites for muscles and ligaments

Protective –>skull and thoracic cage provide protection

Metabolic –> reservoir of essential minerals (calcium, phosphorus and magnesium)

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29
Q

What is the two divisions of the skeleton?

A

Axial –> the rest –> roles in structure, protection and metabolic function

Appendicular –> limbs –> primarily structural role

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30
Q

What does bones hard matrix consist of?

A
  1. Matrix proteins –> Type 1 collagen (framework), growth factors (bone morphogenetic proteins and transforming growth factor beta (TGF-beta), proteglycans
  2. Minerals –> calcium phosphate most common in complex called hydroxyapatite (provides structural resilience)
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31
Q

What two cell types are present in bone?

A
  1. Osteoblasts –> consisting of osteoblasts (bone forming cells), osteocytes (interconnecting network through bone matrix), lining cells (cover metabolically inactive bone surfaces)
  2. Osteoclasts –> bone reabsorbing cells
    - Mono or multi nucleated cells
    - Monocyte-macrophage lineage
    - Short lived cells
    - Recruited to bone surface of sites of remodelling
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32
Q

How frequently is the adult skeleton completely renewed?

A

7 years

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33
Q

What are the functions of bone remodelling?

A
  1. Release of minerals to maintain levels in circulation
  2. Allow changes in bone structure in response to growth or load bearing
  3. Bone homeostasis –> bone formation = bone resorption
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34
Q

What are the two types of bone?

A
  1. Cortical –> predominately structural or load bearing function
    - Dense bone –> diaphysis (shaft or central part of long bone) of long bones.
  2. Trabecular –> structural and metabolic functions (more prone to disease)
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35
Q

What type of bone disorder is osteoporosis?

A

Metabolic bone disorder:

  • Characterised by significant loss of bone mineral density and loss of microstructure
  • Bone brittle and fragile –> prone to fractures
  • Imbalance between bone formation and resorption
  • Abnormality in the bone remodelling process
  • Mineralisation as well as collagen issue
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36
Q

What is the cycle of bone remodelling?

A
  1. Osteoblasts and osteoclasts transform resting bone into active remodelling sites – bone remodelling units (BMU)
  2. Osteoclasts in the BMU –resorb bone tissue and undergo apoptosis
  3. Osteoblasts migrate to the resorption zone to form new bone matrix which later becomes mineralised
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37
Q

What factors can stimulate osteoclasts?

A
  1. PTH
  2. Glucocorticoids
  3. High dose Vitamin D
  4. Interleukins
  5. Prostaglandins
  6. Tumour necrosis factor
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38
Q

What factors are osteoclasts inhibited by?

A
  1. Calcitonin
  2. Oestrogens
  3. Androgens
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39
Q

What are some types of PRIMARY osteoporosis?

A
  1. Idiopathic (unknown cause) –> in children and young adults
  2. Type 1 –> Post menopausal –> due to oestrogen deficiency
  3. Type 2 –> Associated with “normal” aging process
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40
Q

What are some types of SECONDARY osteoporosis?

A

Results from other clinical disorders eg:

  1. Hyperthyroidism
  2. Hyperparathyroidism
  3. GIT or renal issues
  4. Long term glucocorticoids
  5. ETC
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41
Q

What does the inside of an osteoporotic bone look like?

A

Healthy bone has small pores –> osteoporotic has large pores

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42
Q

What are the clinical manifestations and complications of osteoporosis?

A
  1. Initially asymptomatic
  2. Progressive loss of height (vertebrae compression) –> kyphosis or scoliosis
  3. Skeletal deformity
  4. Bone pain (due to compression fractures)
  5. Fractures
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43
Q

What is kyphosis?

A

Anterior curvature of the thoracic spine (forwards movement)

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44
Q

What is scoliosis?

A

Coronal movement of the thoracic spine

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45
Q

What is Osteomalacia?

A

Abnormal or deficient mineralisation of the organic matrix

Leads to softening of bones due to a deficiency of the Vitamin D metabolism

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46
Q

What is some causes of osteomalacia?

A
  1. Dietary Vitamin D deficiency
  2. Intestinal malabsorption
  3. Failure to metabolise Vitamin D (renal disease or congenital enzyme deficiencies)
  4. Anticonvulsant treatment –> phenytoin
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47
Q

What is Rickets?

A

Osteomalacia in children –> affects the growing skeleton
Associated with poor mineralisation of the cartilage within the epiphyseal growth plate
(mineral issue)

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48
Q

What are some clinical manifestations of Osteomalacia?

A
  1. Bone pain
  2. Altered mobility
  3. Muscle weakness
  4. Pathological fractures
  5. Dorsal kyphosis
  6. Rickets (children) –> bone growth retardation and deformation in lower extremities
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49
Q

What is Paget’s disease?

A

Disorderly bone remodelling –> forms disorganised osseous (bone) tissue which is weaker than normal bone

  • Doesn’t affect whole skeleton –> tends to be localised to specific areas
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50
Q

What is the affect on osteoclasts in Paget’s disease?

A
  • Affected osteoclasts are dysfunctional and morphologically abnormal (increased size, shape and possess multiple nuclei)
  • Affected osteoclasts show excessive and accelerated bone resorption
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51
Q

What is the cause of Paget’s disease?

A

Aetiology linked to genetic factors –> autosomal dominant inheritance pattern

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52
Q

What are some symptoms of Paget’s disease?

A 
Bone pain
Bone deformation
Fractures
Kyphosis, spinal cord compression, paralysis (pagetic lesions on spine)
Hearing a visual disturbances (impinged cranial nerves)
Vertigo (damage CNVIII)
Nerve root compression
Headaches (pressure on cranial vault)
Hydrocephalus 
Dental problems
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53
Q

What is the primary defect in osteoporosis?

A

Bone loss

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54
Q

What is the primary defect in osteomalacia/rickets?

A

Reduced vitamin D

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55
Q

What is the primary defect in Paget’s disease?

A

Remodelling

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56
Q

What are the 7 classifications of fractures?

A
  1. Complete or incomplete
  2. Closed (simple fractures) –> clean break with intact soft tissue
  3. Comminuted –> splintered with intact soft tissue
  4. Compound fracture –> fracture site communicates with skin surface
  5. Complicated fracture –> involves adjacent structures –> blood vessels, nerves etc
  6. Stress fracture –> small linear fractures
  7. Pathological fractures –> fracture of bones weakened by disease
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57
Q

What is the difference between a simple and compound fracture?

A

Simple –> fractures bone without skin break

Compound –> fractures bone and bone pierces the skin

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58
Q

What are the four stages of bone healing?

A
  1. Haematoma formation
  2. Fibrocartilaginous callous formation
  3. Ossification
  4. Remodelling
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59
Q

What happens in the haematoma stage of bone healing?

A
  1. Trauma
  2. Blood collects in the area (from lacerated blood vessels)
  3. Osteocytes in the area die
  4. Clot formation (5 days post) (clot contains fibrin, fibroblasts, macrophages, monocytes and lymphocytes)
  5. New blood vessels form around and into fracture site
  6. Osteoblasts and osteoclasts begin to proliferate
  7. Within 48 hours osteoclasts remove necrotic bone tissue
60
Q

What happens in the second stage of bone healing (fibrocartilaginous callous formation)?

A
  1. Granulation tissue is deposited as fibroblasts
  2. Osteoclasts lay collagen fibres (bridge both sides of fracture and bone fragments)
  3. Chondroblasts fabricate patches of cartilage
  4. Osteoblasts lay organic bone matrix called osteoid
  5. Soft callous is formed in about 1 week
61
Q

What happens in the third stage of bone healing (Ossification)?

A
  1. Soft callous undergoes mineralisation with calcium and mineral salts
  2. Secondary callous is formed (after about 3 months)
62
Q

What happens in the last stage in bone healing (Remodelling)?

A
  1. Osteoblasts continue to lay down bone
  2. Osteoclasts begin to remove excess bone and reshape structure until it resembles its former shape and a medullary cavity is shaped
  3. (can take several years)
63
Q

What are some causes for delayed fracture healing?

A
  1. Excessive movement
  2. Extensive damage
  3. Poor intrinsic blood supply
  4. Severe local tissue injury or tissue blood supply issues
  5. Infection
  6. Interposition of soft tissue in fracture gap or wide separation of fracture ends
64
Q

What are the 5 classifications of soft tissue injuries?

A
  1. Sprains –> ligament injury due to twist or stretch
  2. Strain –> stretch or tear of a muscle or tendon
  3. Dislocation –> displacement of one or more ends of articulating bones due to extreme force and can cause damage to ligaments, nerves and blood vessels
  4. Subluxation –> partial dislocation with lesser damage to ligaments compared to dislocation
  5. Avulsion –> forcible detachment of a tendon, ligament or bone from its point of attachment
65
Q

What are the four stages in soft tissue wound healing?

A
  1. Coagulation/vascular stage
  2. Inflammation stage
  3. Migration/proliferation stage
    Remodelling/maturation stage
66
Q

What happens in the coagulation stage/vascular stage of soft tissue healing?

A
  1. First few hours after trauma (resulting in bleeding)
  2. Platelet aggregation and release of fibrinogen fragments
  3. Formation of fibrin plug (closes wound and dries to become a scab)
  4. Release of pro-inflammatory mediators, growth factors and cytokines
67
Q

What happens in stage 2 soft tissue healing? (inflammation stage)

A
  1. Hours to days
  2. Tissue damage and activation of clotting factors during stage one release inflammatory mediators such as prostaglandins and histamine from mast cells causing blood vessels adjacent to the injured area to become more permeable and vasodilate
  3. This response causes heat, swelling, erythema and discomfort to the site.
  4. Wound exudate is produced –> contains proteins, growth factors and enzymes –> antimicrobial properties and facilitates wound healing by supplying nutrients and cleanses the wound
  5. Exudate also acts as a growth medium for phagocytes
  6. Neutrophils, monocytes and macrophages are attracted to the wound –> prevents infection
  7. New tissue in the wound bed forms
  8. Macrophages control transition between inflammatory response and proliferation stage
68
Q

What happens in stage 3 soft tissue healing? (migration/proliferation)

A
  1. Days after injury
  2. Wound is filled with new connective tissue
  3. Decrease in wound size due to –> granulation, contraction and epithelialisation
    - Granulation –> new wound matrix made of collagen and ground substance in which capillaries grow to form connective tissue
    - Wound contraction –> fibroblasts congregate around the wound margin contracting pulling wound together
    - Re-epithelialisation –> regrowth of epithelial cells across wound margin
69
Q

What stimulates angiogenesis in the proliferation stage of soft tissue healing?

A

Angiogenesis is stimulated by macrophages and hypoxia due to blood vessel damage (transforming growth factor (TGF) –promotes formation of new tissue and blood vessels and Tumour necrosis factor (TNF) –breaking down necrotic tissue) stimulates proliferation.

70
Q

What happens in the remodelling/maturation stage of soft tissue healing?

A
  1. Weeks to months post trauma
  2. Scar tissue formation –> avascular, no hair/sebaceous or sweat glands
  3. Remodelling of scar tissue is stimulated by macrophages
  4. Extra cellular matrix degradation with reorganisation of collagen fibres
  5. Change from fibroblasts to myofibroblasts
71
Q

Does chronic inflammation inhibit tissue healing?

A

Yes

72
Q

What is the difference between the cause of acute vs chronic inflammation?

A
  1. Acute –> single injury

2. Chronic –> permanent presence of the causing agent eg bacteria, foreign object

73
Q

What does a chronic inflammatory response drive infiltration of into a wound?

A

Macrophages
Lymphocytes
Fibroblasts

74
Q

What does chronic inflammation driven cell infiltration lead to?

A

Persistent inflammation
Fibroblast proliferation
Scar formation

75
Q

What are some factors that can affect wound healing?

A
  1. Infection
  2. Movement
  3. Poor nutrient supply
  4. Poor oxygen delivery (developing tissue has increased metabolic demands)
  5. Drug therapy
  6. Poor blood flow (nutrient delivery and waste removal)
76
Q

How does wound healing in avascular tissue differ?

A
  1. Wound healing normally determined by vasculature of damaged tissue
  2. But in eyes for example the transparent structures of the eye are avascular –> yet are still subject to repair and fibrosis
  3. Resulting scars often remains avascular in the eyes and can lead to blindness
  4. Normally in vascular healing early wound healing components are delivered by blood (eg by platelets –> the glycoprotein thrombospondin 1 (TSP1)
  5. However in ocular cells involved in avascular repair are capable of synthesising the protein themselves.
77
Q

What is osteoporosis?

A

Reduction in bone mass (resorption greater than formation) –> issues with mineralisation and collagen structure

78
Q

What is osteomalacia?

A

Reduced bone mineralisation –> vitamin D deficiency

79
Q

What is Paget’s disease?

A

Distortion of bone resorption and remodelling –> areas of increased osteoclastic activity and other areas of increased osteoblastic activity
Odd bone formation –> mainly an issue of osteoclastic activity with large overachieving osteoclasts

80
Q

Compare the roles of RANKL and OPG?

A

RankL –> osteoclast receptor activator –> increases osteoclast function

OPG –> osteoprotegerin –> decoy ligand –> stops RANKL binding –> decreases osteoclast function

81
Q

What is the role of antiresorptive drugs?

A

Decrease bone loss

82
Q

What is the role of anabolic agents?

A

Increase bone formation

83
Q

What kind of bone metabolism drug is bisphosphonates?

A

Antiresorptive drug

84
Q

What are bisphosphonates?

A

They are enzyme-resistant analogues of pyrophosphate (normal constituent of bone)

85
Q

What is the general mechanism of bisphosphonates?

A
  1. Bind to calcium in bone matrix
  2. Released by osteoclasts during resorption
  3. Deposits elsewhere or internalised by osteoclast
  4. In osteoclast drives apoptosis
  5. Reduces bone resorption
86
Q

What are the two classes of bisphosphonates and their mechanisms?

A
  1. Simple bisphosphonates (etidronate)
    - Very similar to pyrophosphate (normal in bone)
    - Incorporates into ATP analogues in osteoclasts
    - Incorporation in ATP leads to apoptosis
    - Bone resorption decreased
  2. Amino-bisphosphonates (pamidronate, alendronate)
    - Potent inhibition of bone resorption
    - Interferes with anchoring of cell surface proteins to osteoclast membrane
    - Reduces osteoclast attachment
    - Leads to apoptosis of osteoclast
    - Reduces bone resorption
87
Q

What kind of bone metabolism drug is denosumab?

A

Antiresorptive drug

88
Q

What is denosumab?

A

Recombinant human monoclonal antibody

89
Q

What does denosumab do?

A

Binds and inhibits RANKL –> reduces osteoclast activation –> reduces bone resorption

90
Q

What kind of bone metabolism drug is Raloxifene (SERMs)?

A

Antiresorptive drug

91
Q

What is the mechanism of Raloxifene?

A

Selective oestrogen receptor modulators

  1. Binds to oestrogen receptor –> causing tissue selective effects on target tissue
  2. Different to HRT because AGONIST activity in bone and ANTAGONIST activity in endometrium and breast
  3. Activates oestrogen receptors in osteoblasts
  4. Reduces osteoblast RANKL transcription
  5. Reduces Osteoclast activation
  6. Stimulates Osteoblast activity
92
Q

What kind of bone metabolism drug is HRT?

A

Antiresorptive drug

93
Q

What is the mechanism of HRT (oestrogen) on bone resorption?

A
  1. Lowers transcription of RANKL in osteoblasts/T cells
  2. Reduced cytokines eg IL6
  3. Reduced osteoclast proliferation, differentiation, activation
  4. Reduction in bone resorption
94
Q

What is the downsides of using HRT for bone resorption issues alone?

A
  1. Normally given in an oestrogen + progestogen combination
  2. Both have actions at many sites in the body
  3. Can lead to unwanted effects
95
Q

What does PTH do at the bone level?

A
  1. Activates PTH receptors on osteoBLASTS
  2. Activates RANKL release in these osteoblasts
  3. RANKL stimulates osteoclast differentiation and activity
  4. Bone resorption in increased –> to increase Ca2+ in circulation
96
Q

What kind of bone metabolism drug is recombinant PTH Teriparatide?

A

Anabolic agent

97
Q

What is recombinant PTH?

A

Synthesised version only containing the functional part of PTH, amino acids 1-34
PTH normally 84 amino acids long

98
Q

How is recombinant PTH eg Teriparatide administered to give a net increase in bone formation?

A
  1. Delivered by subcutaneous injection as has 0% oral bioavailability
  2. Must be done as an INTERMITTENT treatment to have a net increase in bone formation
99
Q

What is the mechanism behind recombinant PTH for bone development?

A
  1. Intermittent teriparatide –> binds and activates PTH receptor on osteoblasts
  2. Stimulates Gas (G.alpha.S) –> increases cAMP
  3. Has an antiapoptotic effect on osteoblasts
  4. Promotes osteoblast release of insulin like growth factor (IGF-1) –> induces osteoblast maturation
  5. Result –> increased bone mass, structural integrity, bone strength by an increased number of osteoblasts and activating osteoblasts already in the bone.
100
Q

What kind of bone metabolism drug is cathepsin-k inhibitors?

A

Antiresorptive drug

101
Q

What is the mechanism of cathepsin-k inhibitors as an antiresorptive drug?

A
  1. Inhibits cathepsin K protease expressed by osteoblasts and released from their lysosomes
  2. Cathepsin K protease degrades type 1 collagen –> degrades bone
  3. Hence inhibiting Cathepsin K protease –> reduces bone resorption
102
Q

What kind of bone metabolism drug is sclerostin inhibitors?

A

Anabolic agent

103
Q

What is the mechanism behind sclerostin inhibitors?

A
  1. Sclerostin is produced by osteoblasts
  2. Transported to bone surface
  3. Acts on osteoblasts to reduce bone formation
  4. Stimulates production of RANKL by osteocytes
  5. Stimulates osteoclast bone resorption
  6. HENCE inhibiting this sclerostin:
    - Increases bone formation by osteoblasts
104
Q

How does the drug calcimimetic work?

A
  1. Enhances the sensitivity of PTH calcium-sensing receptors to serum calcium levels
    - So the PTH thinks that serum calcium serum levels are higher than reality
  2. Leads to the decreased secretion of PTH and a reduction in serum Ca2+ levels
105
Q

What are calcium salts and what are they used for?

A

Dietary calcium supplement –> to increase Ca2+ levels in circulation

106
Q

What are some adverse effects of calcium salts?

A
  1. Belching
  2. Flatulence
  3. Abdominal distension
  4. Constipation
  5. Hypercalcaemia (infrequently) –> can lead to nausea, vomiting, constipation, anorexia, apathy, muscle weakness, headache, thirst, polyuria
107
Q

What are Vitamin D analogues used for?

A

Help regulate calcium homeostasis and bone metabolism

108
Q

What are the two main types of used vitamin D analogues and what are their differences?

A

Calcitriol –> active form of Vitamin D3

Cholecalciferol –> Vitamin D3

109
Q

What are some adverse effects of using Vitamin D analogues?

A

Hypercalcaemia

- If hypercalcaemia persists –> renal failure, kidney stones, calcification, cardiovascular damage

110
Q

What are some of the risk factors for falls?

A
  1. Fear of falling
  2. Limitations in mobility and undertaking ADLs
  3. Impaired walking pattern (gait)
  4. Impaired balance
  5. Visual impairment
  6. Reduced muscle strength
  7. Poor reaction times
  8. Some medications –> benzodiazepines, antidepressants, antipsychotics, other psychoactive medications
111
Q

What are risk factors for fractures?

A
  1. Advancing age
  2. Personal history of fragility fracture
  3. Low BMI
  4. Long-term glucocorticoid therapy
  5. Smoking
  6. Excess alcohol
112
Q

What are clinical signs of fracture?

A
  1. Swelling or bruising over a bone
  2. Deformity of an arm or leg
  3. Pain on movement or pressure on the affected area
  4. Inability to bear weight
  5. Loss of function in area
  6. Protruding bone
113
Q

What are the 7 classifications of fractures?

A
  1. Complete or incomplete
  2. Closed (simple fractures) –> clean break with intact soft tissue
  3. Comminuted –> splintered with intact soft tissue
  4. Compound fracture –> fracture site communicates with skin surface
  5. Complicated fracture –> involves adjacent structures –> blood vessels, nerves etc
  6. Stress fracture –> small linear fractures
  7. Pathological fractures –> fracture of bones weakened by disease
114
Q

What are some acute complications of fractures?

A
  1. Neurovascular damage
  2. Soft tissue damage
  3. Blood loss
  4. Localised contamination/infection
115
Q

What are some long term complications of fractures?

A
  1. Malunion
  2. Embolic complications
  3. Osteomyelitis (bone infection)
  4. Loss of function
116
Q

What is the importance of immobilisation of a fracture?

A
  1. Allows the fracture to be immobilised after being positioned correctly
  2. Protects the damaged area
  3. Restricting movement will accelerate the healing process (less disturbance)
117
Q

What is the difference between casting, internal fixation and external fixation for fractures?

A
  1. Casting –> a way to encase the area of fracture to immobilise (normally made of plaster)
  2. External fixation –> surgical treatment where rods are screwed into the bone and exit the body to be attached to a stabilising structure on the outside of the body
  3. Internal fixation –> Surgical implementation of implants to repair a bone (screws, plates etc)
118
Q

What are the risk factors for osteoporosis?

A
  1. Female
  2. Smoking
  3. Poor nutrition
  4. Malabsorption
  5. Low estrogen levels:
    - Menopause
    - Surgical removal of ovaries
    - Chemotherapy
    - Amenorrhea (loss of menstrual period in young women)
  6. Chronic disease–> RA, chronic hep C, liver infection
  7. Immobility
  8. Hyperthyroidism
  9. Hyperparathyroidism (accelerates calcium removal from bones)
  10. Vitamin D deficiency
  11. Medications –>heparin, anti seizure medication, long term corticosteroids
119
Q

How is osteoporosis assessed?

A
  1. Patient history/presentation
  2. Bone density scan (DEXA)
  3. Bone density scan are reported as T-scores and Z-scores
120
Q

What is the T-score in an osteoporosis assessment?

A

(bone density scan)

Comparison of a persons bone density with the bone density of a healthy 30-year old of the same gender

121
Q

What is the Z score in an osteoporosis assessment?

A

(Bone density scan)

Comparison of a persons bone density with the bone density of an average person of the same age and gender

122
Q

What is the function of the T score vs the Z score?

A

T score –> used to diagnose osteoporosis
Z score –> used to identify if there is need to investigate the existing osteoporosis (as it may show a greater bone density loss than someone of your age.

123
Q

What are some non-pharmacologic ways to mitigate osteoporosis?

A
  1. calcium and vitamin D supplementation
  2. weight-bearing exercise
  3. muscle strengthening
  4. fall prevention.
124
Q

What is the role of Vitamin D in Osteoporosis?

A
  1. Assists in the GIT absorption of Calcium from the diet to provide substrate for the mineralisation of bon –> helps prevent osteoporosis
  2. High circulating calcium reduces PTH release (PTH activates osteoclasts)
125
Q

What is the role of calcium the development of osteoporosis?

A
  1. Calcium give substrate for mineralisation

2. High blood calcium reduces osteoclast activation by PTH

126
Q

What can be done to boost bone health to prevent osteoporosis?

A

Weight bearing exercise can increase bone formation

127
Q

What is the role of physiotherapy in recovery from an injury?

A
  1. Strategies to transition back to function without further damage
  2. Can facilitate clinically significant effects on pain, range of motion (ROM), muscle performance, functional ability and patient quality-of-life
128
Q

What is the role of Physiotherapists in the hospital system?

A

Physiotherapistsassess and diagnose the problem, then plan and provide treatment programs that aim to restorefunctionor minimise dysfunction after disease or injury.

129
Q

What is meant by a greenstick injury?

A

Fracture where the bone bends and cracks instead of breaking into separate pieces
Mostly occur in children under 10

130
Q

What is a salter-harris fracture?

A

Growth plate fracture –> long bones

131
Q

How many types of salter-harris fractures are there?

A

9

132
Q

What is a colles fracture?

A

A Colles Fracture is a complete fracture of theradius of the forearm close to thewrist resulting in an upward (posterior) displacement of the radius and obvious deformity. It is commonly called a “broken wrist” in spite of the fact that the distal radius is the location of the fracture, not the carpal bones of the wrist

133
Q

Where does the ulna connect to the wrist?

A

Scaphoid

134
Q

Tendons vs ligaments?

A

Tendons –> bone to muscle

Ligaments –> bone to bone

135
Q

What is the enthesis?

A

The connection point of tendons or ligaments onto bones

136
Q

What is the entire upper limb and scapula hanging on to the skeleton by?

A 
One bony joint --> sternoclavicular joint
Sits centrally (sternum)
137
Q

Where do you start an upper limb examination?

A

Sternoclavicular joint

138
Q

What is the acromion?

A

Tip of the scapula near the shoulder

139
Q

Main bony structures of upper limb?

A

Sternoclavicular joint –> clavicle border –> acromion (first bit of scapula) –> drop down to the greater tuberosity of the humerus –> feel capsule NB dont forget scapula spine

140
Q

What is the difference between active vs passive movement of a joint?

A

Active –> patient is moving of their own

Passive –> you are moving the joint for the patient

141
Q

What classes of rotation are there for the shoulder joint?

A

Externa rotation –> arm away from body
Interna rotation –> arm into body
Abduction – arm movement away from body
Adduction –arm movement into body

142
Q

Bones in elbow joint?

A

Humerus
Ulna
Radius

143
Q

What part of the ulna takes part in the elbow joint?

A

Olecranon process

144
Q

What type of joint is the elbow?

A

Hinge joint

145
Q

Is the glenohumeral joint weak or strong?

A

Relatively weak –> needs lots of support

146
Q

Is dislocation or fracture of the shoulder joint more common?

A

Dislocation

147
Q

What is the palpable bits of the elbow?

A

Medial epicondyle
Lateral epicondyle
Olecranon process

JMP Y2S1 (24 decks)

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