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BIOS1155 > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

What’re the components of bone?

A

Bone matrix

  • collagen
  • ground substance

Minerals

Cells

  • osteoblasts
  • osteoclasts
  • osteocytes
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2
Q

What’s the percentage of the composition of an average bone?

A

30% matrix

70% mineral

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3
Q

Explain what’s a collagen?

A

Collagen fibrils form a triple helix of polypeptide chains

Strength of bone affected by collagen fibre direction

Collagen fibrils overlap and form crosslinkages. Mineral deposited in spaces between collagen fibrils.

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4
Q

What’s the ground substance of the bone matrix?

A

Made up of proteoglycans deposited on a framework of hyaluronic acid

Proteogylcans are proteins which strengthen bone by forming compression resistant networks between collagen fibrils

Proteogylcns control ion movement.

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5
Q

Explain what are bone minerals?

A

Mineral = hydroxyapatite HAP (made from fluid Ca-P compounds in matrix)

Provides compressional strength

Increases strength of bone far beyond what is provided by collagen and mineral components.

Strength = cast iron, half as strong as steel

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6
Q

Explain how mineralisation actually occurs in the bone

A

Mineralisation occurs when local conc of Ca and P is increased by the action of ALP, and after a certain concentration, crystals begin to form (initially amphorous CA-P that transform into HAP)

Ca:P in HAP = 1.3:1, and 2:1

OtheR molecules like Mg, Na, K and CO3- also present but not organised into specific crystals. HAP can incorporate other minerals like, strontium, heavy metals, and radioactive metals

20-30% of HAP remains amorphous, so that the minerals in the HAP are readily available when Ca deficient in blood

P

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7
Q

Are isotopes tolerated by any bone?

A

No, new bones have greater affinity for isotopes than old bone.

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8
Q

What does pathological calcification refer to?

A

Inhibitors inhibit Ca-P salt deposition in soft tissue, but they can sometimes fail and lead to HAP deposited in soft tissue

This can be

  • dystrophic calcification (in dying tissue)
  • metastatic calcification (associated with hypercalcemia)
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9
Q

What’re osteoblasts?

A

Bone making cells

Active on surface of bone

Produce bone matrix (osteoid) - non mineralised matrix with only collagen and ground substance

Once production of matrix is complete, they become osteocytes

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10
Q

What’re osteocytes?

A

Cells located in lacunae of bone matrix, in which they are osteoblasts which have been trapped in the bone.

They maintain bone structure

Linked with other osteocytes and osteoblasts through channels (minerals move through channels)

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11
Q

What are osteoclasts?

A

Bone resorbing cells

They remove bone during repair and remodel

Derived from macrophages (immune cell to combat infection) and do a similar scavenging job

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12
Q

What’re the structure classifications of bone?

A

Cortical

  • makes up hard outer chill and gives shape
  • concentric ting structure
  • in long bones, cortical bone surrounds the medullary cavity

Spongy (Cancellous)
- internal layer at the end of long bones between cortical bone and medullary cavity

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13
Q

How do you classify bones by microscopic appearance ?

A

Woven bone

  • collagen fibres randomly arranged
  • contains many osteocytes
  • found on new bone sites, and some bone disorders and tumours
  • in an adult = pathological process

Lamellar bone

  • collagen fibres arranged orderly
  • laid down on pre existing framework (usually a woven framework)
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14
Q

How would you classify bones by origin?

A

Endochondral ossification

Intramembranous ossification

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15
Q

What is endochondral ossification?

A
  • long bones grow using this method
  • it’s the ossification of a cartilage model (ie. ossification centres)
  • eg. long bones develop from 3 primary ossification centres (diaphysis and 2 epiphysis)
  • bone growth occurs at the ends of diaphysis where layer of cartailage is actively growing, metaphysis/epiphysis is the location. And so cartilage is produced at the ends and pushed down towards diaphysis.
  • when cartilage stops growing, it ossifies and plate closes with no more growth
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16
Q

What is intramenbranous ossification?

A

Forms bones of skull and face (flat bones;)

Occurs in fibrous tissue but has a centre ossification, which extends from the centre to the periphery of bone

Increase in circumference occurs by the ossification of adjacent fibrous tissue

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17
Q

What is referred by the term bone metabolism ?

A

Bone is rigid static structure, with constant turnover of minerals of the bone

Bone is flexible, bending forces applied and bone can remodel in response to forces applied

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18
Q

Explain the process of bone remodelling

A

Existing bone is resorber and new bone laid down, this happened continually in the body.
Repairs microscopic bone injuries, and is normally matched by the type of stress experiment by bone ie. areas of greatest stress = greatest thickness

Bone precursor cells located on surface of bone and in vascular channels
Phase 1- stimulus like hormones, drugs, physical stress activates precursor cells to osteoclasts
Phase 2- osteoclasts resorb bone leaving behind a resorption cavity. (2 weeks process)
Phase 3 - osteoblasts lining the resorption cavity lay new bone (4 month process)

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19
Q

Explain the bloody supply necessary for bones

A

Main blood supply = nutrient artery (enters bone during iniatal cartilage phase) supplies inner bone

Outer blood supply = periosteal arteries

Growth plate = own blood supply in which the blood vessels penetrate through the cartilage and allow ossification process

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20
Q

Why does a frvature cause significant bleeding?

A

Cause bones have an abundant blood supply

21
Q

Discuss the complications of blood supply to the bone

A

Blood flow through these vessels is sluggish and the blood can deliver bacteria to the bone and lead to infection (osteomyelitis)

Bones such as the proximal femur and schaphoid are entriely covered by articular cartilage, and so blood vessels can’t penetrate through them for repair if there is a frvature at these regions

And so this can lead to AVN, osteochondritis, osteomyelitis, aseptic necrosis

22
Q

Explain the hormonal control of calcium levels in the bone and blood

A

Vitamin D

  • increases Ca retention
  • potent effect in increasing Ca absorption from GIT and kidneys
  • effects bone deposition and resabsorption
  • activated in liver and kidneys. Synthetic VitD administered if liver and kidneys fail

Parathyroid hormone

  • increases Ca removal (increases Ca in blood)
  • increases Ca and P absorption from bone and into blood (stimulates osteoclasts)
  • decreases Ca excretion in kidneys and increases P excretion
  • PTH acts with VitD to increase Ca resorption from gut

Calcitonin

  • increases Ca retention in bone (opposite of PTH)
  • decreases activity of osteoclasts
  • osteobalstic activty increased
23
Q

What’s hyperparathyroidism?

A

Chronic hypoclcaemia and hypophosphataemia decrease bone mineralisation

PTH levels elevated = increase Ca resorption from bone and phosphate lost in urine

24
Q

Explain the affect of three main hormones related to the growth of bone

A

Thyroid hormone
- major hormone up to 3 years of age then decreases in significance

GH
- stimulates cartilage production at growth plate (importance; 3-15 yo)

Androgens
- most important in age range 12-19. Causes the closure of growth plates

25
Q

What other hormones play a part but minor in terms of bone growth?

A

Glucocorticoids decrease bone formation and increase bone resorption by inhibiting protein synthesis. There is significant bone loss in untreated diabetes msllitus

Hypercalcaemia is a common effect of cancer (Ca withdrawn from bone). Bone metastases cause local erosion. And some tumours produce substances with PTH type activity

26
Q

Name the different types of fractures

A 
Compound 
Torus
Avulsion 
Compression 
Comminuted 
Pathological 
Stress (buttressing effect)
Intra-articular (extends into joints, risk of developing 2 deg OA)
Occult fractures (easily missed. Use CT if overlying strictures present. If non-displaced and no cortical disruption like stress, use MRI)
27
Q

Name the different positioning of fracture lines

A 
Transverse 
Oblique 
Spiral (multiple views needed)
Greenstick 
Segmental
28
Q

Explain how major injuries can be repaired

A

Haematoma formation

  • occurs with vessel damage
  • fibrin (protein substance involved in clotting of blood) forms initial framework for healing. Tissue damage = fibrinogen converted into fibrin at wound

Procallus
- fibroblasts, osteoblasts and capillaries move into the wound to produce granulation tissue

Callus
- osteoblasts deposit disorganised clumps of primitive bone matrix (woven bone). This is the callus

Formation of normal bone with replacement of woven bone

Remodelling of periosteal and endosteal surfaces

29
Q

What’re the factors that can affect the remodelling of bone after a frvature?

A

Local blood supply

Type of fracture
- ie. spiral/oblique faster healing than transverse. Comminuted fracture can have avascular fragment that become sequestrated.

Fixation

  • quality determines healing time.
  • movemntment May lead to non union
  • IM pins may disrupt blood supply

Age

Concurrent infection, disease, nutritional status

30
Q

How do you evaluate if a fracture has completely healed?

A

Continuity of cortex

Calcified complete bridge of callus

No visible line

(Process of 6weeks with adequate fixation)

31
Q

What are the complications of fracture repair?

A

Delayed union - due to motion, infection, age, pathological fracture

Non union - due to motion, avascularity, infection

Signs of non union

  • smooth sclerotic edges with no callus
  • sealed medullary cavity
  • pseudoarthrosis (failure of fusion)

Malunion

  • deformity of bone
  • due to improper reduction or rotation or collapse during healing
32
Q

Define the meaning of different types of abnormalities that can occur

A 
Apalsia = failure to form 
Hypopalsia = fail to grow to normal size 
Dysplasia = abnormal growth 
Hyperplasia = overgrowth
33
Q

What’s Spina bifida? Congenital or developmental abnormality

A

Incomplete closure of neural arches (mostly in lumbosacral)

May cause minor sensory loss (paraplegia)

Often only detected on X-ray

34
Q

Explain what’s scoliosis and kyphosis? Congenital or developmental abnormality

A

Scoliosis = lateral spine curvature

Kyphosis = more posterioly curved

35
Q

What’s a metabolic bone disease and give examples of some ?

A

Abnormal bone structure caused by altered or inadequate biochemical reactions due to genetics, diet, hormones

Ie. osteoporosis, osteomalacia,

36
Q

Explain what is osteoporosis

A

Density or mass of bone reduced, but bone remains normal

  • bone loss is generalised or regional
  • spongy bone is worse affected
  • women more suspectible than men: postmenopausal osteoporosis due to lack of Oestrogen. Oestrogen desensitises osteoclasts to PTH

Causes:
Hypertparahyroidism can cause it

Low Ca diet (excessive Ca can depress VitD and PTH)

High cortisol levels (ie. corticosteroid supplements or Cushings disease can decrease bone mass)

37
Q

What’s regional osteoporosis

A

Associated with disuse or immobilisation

After 8 weeks, significant osteoporosis is present although it will develop faster in <20 yo and >50 yo

38
Q

Exaplain the analysis of osteoporosis

A

Spinal radiographs = vertebral deformity and decreased density

Bone density analysis = post menopausal women in upper 3rd of population not at risk. Bone density should be > 100 mg/cm3 for compression fractures not to occur

39
Q

Explain what is osteomalacia

A

Associated with a lack of VitD

Osteoid production occurs, but conversion of osteoid to bone is inadequate. Thus differntiating from osteoporosis

Due to:

  • poor mineral intake
  • lack of sunlight
  • renal or hepatic disease including biliary obstruction

Known as rickets in children

40
Q

Explain bone tumours and the form of bone tumour

A

Benign or malignant

They can be primary or secondary

Primary: 
vast majority are benign, 
young patients = most are benign 
Older patients = most are malignant 
Slight male predominance

secondary tumours:
metastatic (more common than primary)
spread of adjacent neoplasms,
malignant transformation of pre-existing benign lesions
Metastatic cancers are usually multifocal, adults (over 40 yo) (prostate, breast, kidney, lung), children (in 1st decade)

41
Q

How is radiology involved in cancer diagnosis?

A

Bones involved

Specific site involved (cortex or medulla, epiphysis, diaphysis, or metaphysis)

Tumour margin and contour

42
Q

Compare the differences between metastatic and being tumours?

A

Least amount of pathological damage occurs within benign tumours as they are localised and well defined geographic borders
They oress on surrounding structures causing compression and displacement, and even stress fractures

Invasive, illdegined tumours = malignant

43
Q

Explain what is osteosarcoma

A

Malignant

90% in metaphysis of long bone, especially distal femur

Common = < 20 and >60

On radiographs: moth eaten sunburst appearance

44
Q

Explain what is chondrosarcoma

A

Occurs in metaphysis and diaphysis Of long bones (esp. medullary cavity of femur, humerus and pelvis)

Causes a lucent defect in bone

Occurs in middle age and older

45
Q

Explain what is fibrosarcoma

A

Occurs in middle age, rare

Metaphysis of femur and tibia

Lucent lesions with cortical destruction

46
Q

Explain what is myeloma

A

Affects older than 50

Vertebrae involved

47
Q

Where do metastatic bone tumours originate from?

A

Tumours of the breast, prostate and thyroid commonly metastasise to the bone

48
Q

Explain what is osteomyelitis

A

Bacterial infection with staph aureus (common pathogen), affects children (growth plates of limbs usually) and elderly (metaphysis)

Exogenous infection: direct penetration of open wound
Haematogemous infection: spread from distant sites of body

Intense inflammation caused by periosteal elevation and draining sinuses in skin. AVN of bone fragments common leading to sequestrum formation.

Children; layer of new bone around site (involucrum)

BIOS1155 (19 decks)

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