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YEAR 1 > Bones - healing/calcium/vit d/collagen > Flashcards

Bones - healing/calcium/vit d/collagen Flashcards

1
Q

What are the 2 types of bone structures?

A

Compact/Cortical bone - closer to the surface

Trabecular/Cancellous/Spongy Bone

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2
Q

What are the 2 types of bone made?

A

Woven bone
- Immature, made rapidly, collagen laid down randomly

Lamellar bone
- Mature bone, collagen laid down in parallel sheets for strength

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3
Q

What is the structure in a compact bone?

A

Made up of Osteons/Haversian Systems, which consist of…

Haversian canals - blood, nerve, lymphatic supply
Columns composed of lamellae
Canals linked together by Volkmans Canals
Lacunae home for osteocytes
Osteoblasts line the surface of the Haversian canals
Osteoclasts found on surface of bone matrix

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4
Q

What are functions of bone?

A 
Mechanical support: Keep us upright
Transmission of forces created by muscle contraction
Protection of vital organs
Calcium homeostasis
Haematopoiesis
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5
Q

What is the process for bone remodelling?

A

ACTIVATION
Osteoblasts sense damage and produce RANKL

RANKL can…

  1. Stimulate osteoclasts
  2. Bind to monocytes to induce formation into osteocytes in presence of M-CSF

RESORPTION
Osteoclasts secrete collagenase to digest collagen and HCL to dissolve hydroxyapatite into calcium and phosphate released into the blood stream, resorbed bone area form Howships Lacuna

REVERSAL
Osteoblasts secrete OPG to bind to RANKL and stop the activity of osteoclasts to stop bone resorption (osteoclasts die by apoptosis)

FORMATION
Osteoblasts secrete osteoid seam to lay down new collagen = osteoid

TERMINATION
This osteoid eventually becomes mineralised via deposit of calcium and phosphate to produce hydroxyapatite

QUIESCENCE
Osteoblasts become incorporated into the bone matrix as osteocytes or become quiescent surface bone lining cells

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6
Q

What is the effect of oestrogen on bone remodelling?

A

Increase expression of OPG to block RANKL
Blocks RANKL with competitive inhibitors(similar to OPG)

… to reduce osteoclast activity

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7
Q

What cells secrete OPG and RANKL?

A

Osteoblasts

Stromal cells

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8
Q

What is the net result of each bone remodelling cycle?

A

Osteon - package of bone where collagen fibres are aligned

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9
Q

What is the first stage in fracture healing?

A

Haematoma - Within 24 hours

Rupture of blood vessels causes the formation of a haematoma.
Haematoma acts as a fibrin mesh which seals the fracture site and provides a scaffold for the influx of inflammatory cells, fibroblasts and support for new capillary growth.

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10
Q

What is the second stage of fracture healing?

A

Soft Callus - After a week

Growth factors…
- Platelet derived growth factor - PDGF
- Fibroblast growth factor - FGF
- Transforming growth factor beta - TGF-beta
Activate osteoprogenitor cells in the periosteum, medullary cavity to stimulate osteoclast and osteoblast activity.

Mass of predominantly uncalcified tissue formed between fracture

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11
Q

What is the third stage of fracture healing?

A

Bony Callus - 3 weeks+

Activated osteoprogenitor cells deposit woven bone
Activated mesenchymal cells surrounding fracture differentiate into chondrocytes that make fibrocartilage and hyaline cartilage

Newly formed cartilage undergoes endochondral ossification forming contiguous network of bone - bridging fracture ends - converting callus to woven bone

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12
Q

What is the 4th and final stage of fracture healing?

A

Remodelling - 12 weeks+

Callus matures as it becomes weight-bearing and portions that are not stressed, are resorbed - this reduces the size of callus + outline of fractures are re-established as lamellar bone
Woven bone replaced by lamellar bone and excess callus resorbed
Healing process complete with restoration of medullary cavity

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13
Q

What can impede fracture healing?

A
  • Inadequate immobilisation - prevents normal callus maturation = delayed or non-union
  • Displace/comminuted fractures can lead to deformity
  • Open fractures - risk of nutrition
  • Malnutrition
  • Skeletal dysplasia - congenital abnormalities
  • Excessive trauma - systemic complications
  • Avascular necrosis
  • Intra-articular fracture
  • Weakened bone - by radiation/disease/tumour
  • Older age
  • Diabetes
  • Smoking
  • Drugs - steroids
  • Dependant on bone fractured
    • Tibia heals more slowly
    • Fractures of the diaphysis heal slower than of the metaphysis
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14
Q

Why can fractures involving joints have impaired healing?

A

Synovial fluid contains fibrinolytic agents - preventing haemotoma formation

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15
Q

What are the 2 types of ossification?

A

Intramembraneous ossification

- Bone develops directly within a sheet of mesenchymal or immature connective tissue
- Ossification of flat bones of the face, skull bones, clavicles

Endochondral ossification

- Bone develops by replacing hyaline cartilage which acts as a template
- Ossification of bones at the base of skull and long bones, fractures
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16
Q

What is the role of osteocytes?

A

Regulate calcium in and out of cells

Canaliculi junctions for communication with other cells on the bone surface

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17
Q

What type of cells are osteoblasts?

A

Plump, cuboidal cells, single nuclei

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18
Q

What type of cells are osteoclasts

A

Large mutlinucleated cells

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19
Q

How can you estimate bone turnover?

A

Bone marrow biopsy from iliac crest

Stain with tetracycline at 2 different times to see rate of bone formation

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20
Q

What are clinical markers for bone formation?

A

P1NP - pro-collagen peptides

Alkaline phosphatase - released by osteoblast during mineralization of osteoid

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21
Q

What are clinical markers for bone resorption?

A

CTX - released from collagen breakdown

NTX

Acid phosphatase - if osteoclast very active

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22
Q

Difference between periosteal apposition and endosteal resorption?

A

Periosteal apposition - thickening of periosteum

  • Common in men - have stronger bones
  • Estrogen suppresses this
  • Androgens stimulate this

Endosteal resorption - resorption of inner layer
- More in females as they age

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23
Q

What is the recommended minimum vitamin D intake for female, male, adolescent, osteoporotic patient?

A

Average adult - 700mg

Female - 350mg
Male - 450mg
12-19 - 750mg
Osteoporosis - 1500mg

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24
Q

What are the 3 forms that calcium exist as in the blood?

A
  1. Free, ionic in the blood
  2. Bound to albumin
  3. Bound to anions - phosphate, citrate
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25
Q

What is free calcium essential for?

A

Muscle contraction
Release of neurotransmitters and hormones
Enzyme activity
Blood coagulation

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26
Q

What is adjusted calcium?

A

Total free calcium adjusted for albumin concentration.

Gives a better reflection of ionised calcium in the blood as this is the calcium that is physiologically active

Diseases can cause low albumin which can adjust calcium levels and mask total free calcium

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27
Q

How does calcium affect PTH and what is the role of PTH in calcium homeostasis?

A

LOW calcium INCREASES PTH production

PTH…

  • Increase calcium reabsorption in the kidneys
  • Stimulate osteoblasts to secrete RANKL to stimulate osteoclasts for bone resorption
  • Calcitriol increases calcium absorption in the gut (PTH converts calcidiol to calcitriol in the kidneys)
  • Increase phosphate excretion in the kidneys
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28
Q

What must be present for the release of PTH?

A

Magnesium

29
Q

What is the affect of calcium on calcitonin and what is its role in calcium homeostasis?

A

HIGH calcium stimulates calcitonin

  • Decreases bone resorption, stops osteoclasts
  • Decreases calcium resorption in the kidneys
  • Decreases phosphate resorption in the kidneys
30
Q

What effect does alkalosis have on calcium-protein binding in the blood?

A

Increased calcium binding with proteins

Decreased free calcium in the blood

31
Q

What effect does acidosis have on calcium-protein binding in the blood?

A

Decreases binding of calcium with proteins

Increased free calcium in the blood

32
Q

What are symptoms of hypocalcaemia?

A

Calcium level <2.2mmol/L

Muscle spasm, cramps, tetany

Paraesthesia

Cardiac abnormalities

Seizures

Coma

Chvosteks sign - facial nerve twitch

33
Q

What causes hypocalcaemia?

A
  • Renal failure
  • Hypoparathyroidism
  • Vitamin D deficiency/malabsorption
  • Pancreatitis/Rhabdomyolysis
  • Adrenal insufficiency
  • Genetics
34
Q

What are signs and symptoms for hypercalcaemia?

A

Ca > 2.6mmol/L

Nausea

Constipation

Peptic ulcers

Mental disturbance/depression

Renal failure, renal stones, polyuria

Soft tissue calcification

Thinning of bones - PTH driving resorption of bone

35
Q

What are causes of hypercalcaemia?

A
  • Hyperparathyroidism - primary
  • Hypercalcaemia of malignancy - lung, breast, blood - tumours produce a factor that acts similar to PTH = PTHrP
  • Vitamin D intoxication
  • Sarcoid, GH excess, Vitamin A excess, Addisons
  • Drugs - lithium, thiazides
  • Idiopathic infantile hypercalcaemia
  • Familial benign hypercalcaemic hypocalciuria

Always check PTH when have high calcium

36
Q

What form of vitamin D to we test in the blood and why?

A

Calcifidiol - 25-hydroxycholecalciferol

Reflects the production

Testing the active form uses PTH so would be skewed

37
Q

What are causes of vitamin D deficiency?

A
  • low sunshine exposure
  • low dietary supply
  • low absorption
  • obesity
  • high loss/utlisation
38
Q

Who are at increased risk of vitamin D deficiency?

A
  • Dark skinned individuals
  • Concealing dress style
  • Little UVB exposure
  • Obesity
  • Adolescents
  • Frail elderly
  • Exclusively breast-fed babies
  • Winter
  • Co-morbidities - renal disease, coeliac disease, liver disease, GI disorders, CF, TB, HIV
39
Q

What diseases can occur as a result of vitamin D deficiency?

A
  • Osteomalacia in adults

- Rickets in children

40
Q

What are clinical symptoms of vitamin D deficiency?

A
  • Non-specific
  • Fatigue
  • Generalised muscle, joint and bone pain
  • Hyperalgesia
  • Fragility fractures
  • Waddling gait
41
Q

What is the process of Vitamin D metabolism?

A

7-dehyrdocholesterol in the skin - inactive

(activated by UV)

Cholecalciferol in the blood - inactive

(activated by 25-hydroxylase)

25-OHD - Calcidiol in the liver - inactive

(activated by 1alpha hydroxylase)

1-25OH2D - Calcitriol in the kidney - ACTIVE

42
Q

What is the active form of vitamin D and what is its role in calcium metabolism?

A

Calcitriol - activated in the kidney

Increases absorption of calcium and phosphate in the GI tract
Increases reabsorption of calcium and phosphate in the kidneys
Increases osteoclast activity of bone

Increases calcium and phosphate in the blood

43
Q

What is the role of calcium on vitamin D metabolism?

A

Low calcium stimulates release of PTH

PTH activates 1-alpha hydroxylase

1-alpha hydroxylase converts calcidiol to active calcitriol

44
Q

What is the role of FGF23?

A

Suppresses kidney reabsorption of phosphate to increase urinary excretion

Blocks activation of calcidiol into calcitriol

Blocks PTH

(secreted by osteocytes)

45
Q

What is the effect of calcitriol on bone?

A

Stimulates bone resorption

  • Stimulates FGF23
    • Inhibits activation of calcidiol
    • Inhibits release of PTH
46
Q

What are the 3 main amino acids in collagen?

A

Glycine
Proline
Hydroxyproline

47
Q

What is the structure of collagen?

A

Procollagen: 3 alpha chains of repeating amino acid triplet

(Stablised by collagen proteases and hydrogen bonds)

Tropocollagen: Triple helix of collagen

48
Q

Why is vitamin C crucial for collagen?

A

Vitamin C is a cofactor for the collagen proteases that hydroxylate collagen which is key for stability

49
Q

Where are the 4 types of collagen found in the body?

A

Type I: Bone, Skin, Tendons

Type II: Cartilage

Type III: Reticulin, Blood vessels

Type IV: Basement membranes

50
Q

What is the role of elastin, what is it made of and where is it found?

A

Recoil and stretch

Elastin + Fibrillin-1 + Fibrillin-2 crosslinked

Found in blood vessels, ligaments, skin and lungs

51
Q

What are properties of proteoglycans?

A

Negative charge which traps water in tissues
Keep cells hydrated and cushioned
Resist compression

High content in cartilage
Protein core and chain of sugars
Fill space between cells

Hyaluronic acid, aggregan, fibromodulin, decorin

52
Q

What are symptoms of vitamin C deficiency and what is it called?

A

Scurvy

Swollen, bleeding gums
Bruising
Poor wound healing
Skin lesions
Joint pain/weakness
53
Q

What are signs and symptoms of Marfans Syndrome?

A 
Long, tall human - long fingers/toes
Scoliosis
Flexible joints
Stretch marks on the skin
Aorta dilation, aneurysm, dissection, rupture
Mitral valve prolapse
54
Q

What kind of inheritance is Marfan syndrome and what is the mutation?

A

Autosomal dominant inheritance

Mutations in Fibrillin-1 gene

55
Q

What kind of inheritance is osteogenesis imperfecta and what is the mutation?

A

Autosomal dominant inheritance

Type I collagen mutation of glycine

56
Q

What are signs and symptoms of osteogenesis imperfecta?

A

Brittle bones - deformities, fractures
Eyes - blue sclarae
Teeth - Small, blue teeth
Ears - Hearing loss

57
Q

What are the main 2 types of EDS?

A

Autosomal dominant inheritance

Classic
- Mutation in type 5 collagen

Vascular
- Mutation in type 3 collagen

58
Q

What are signs and symptoms of EDS?

A

Stretchy skin
Easy bruising
Flexible joints

59
Q

What other types of EDS can you have if the mutation is not in collagen?

A

Mutations in the enzymes in collagen synthesis

Kyphoscoliotic EDS - defect in lysyl hydroxylase
Musculocontractual EDS - defect in collagen peptides

60
Q

What is Alport Syndrome - signs and mutation?

A

X linked dominant
Mutations in type 4 collagen

Haematuria
Proteinuria
Renal insufficiency - renal failure
Renal hypertension
Hearing loss
Eye issues

** Differential diagnosis - Goodpasture’s Syndrome - similar presentation of glomerulonephritis - caused by anti-GBM antibodies **

61
Q

What bone disease has normal calcium, phosphate, ALP, PTH values?

A

Osteoporosis

62
Q

What bone disease has…
decreased calcium and phosphate
increased ALP, PTH values?

A

Osteomalacia

63
Q

What bone disease has…
normal calcium, phosphate, PTH
increased ALP values?

A

Paget’s disease

64
Q

What disease has…
decreased phosphate
increased calcium, ALP, PTH values?

A

Primary hyperparathyroidism

65
Q

What would be the lab values of secondary hyperparathyroidism? (CKD)

A

Decreased calcium

Increased phosphate, ALP, PTH

66
Q

What are early complications of fractures?

A

Compartment syndrome
Infection
Fat embolism
Thromboembolism

67
Q

What are immediate complications of fractures?

A

Nerve palsy
Haemorrhage
Skin tear
Ischaemia

68
Q

What are late complications of fractures?

A 
Malunion
Non-union
Delayed union
Osteoarthritis 
Avascular necrosis 
Growth disturbance
Stiffness and pain
Osteomyelitis
69
Q

What are causes of pathological fractures?

A 
Pagets 
Tumours - benign/malignant 
Bone metastases 
Infection
Osteogenesis imperfecta
Osteomalacia/rickets 
Osteoporosis

YEAR 1 (17 decks)

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