Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disorders of Gait, Neuro & Eye > Bone path 1 > Flashcards

Bone path 1 Flashcards

1
Q

What are the functions of bone?

A
  • Rigidity
  • protection
  • haematopoiesis
  • resovoir for minerals (calcium and phosphorus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the cellular components of bone?

A

Make bone or cartilage
- osteoblasts -> osteocytes
- line bone trabeculae
- produce osteoid
- once they are mineralised bone matrix = osteocytes

Remove bone (remodelling)
- Osteoclasts - multinucleate phagocytic cells that sit in Howships lacunae and secrete acid and proteinase. Increase PTH -> increase in osteoclast numbers and activity . Osteoclasts have calcitonin receptors, calcitonin inhibits osteoclasts and causes them to detatch from bone surgaces

Bone marrow
- stromal cells
- adipocytes
- erythroid and myeloid precursors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the matrix components of bone?

A

Cone extracellular fluid (bone tissue fluid)
- Functional membrane (osteoblasts and osteocytes) separates bone ECF from general ECF
- Allows regulation of Ca2+ and PO4- ion flow into and out of bone ECF

Lining tissues
- Periosteum
- endosteum

Vascular supply
- Provides nutrients, growth factors/hormones, mineral ions
- Removes waste, mineral ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Key components of calcium homeostasis

A
  • ## tightly regulated - particularly extracellular calcium (kept in a very narrow range). This is critical to cell signalling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is calcium regulated?

A

o Parathyroid hormone
 Bone
* ↑Ca2+ transfer across cellular barrier
* ↑Ca2+ resorption
 Kidney
* ↑Ca2+ absorption in DCT
* ↓ Pi absorption in PCT
* Activation of Vit D
o Calcitonin
 ↓ Bone resorption
 ↓Ca2+ transfer across cellular barrier
o 1,25(OH)2 Vitamin D
 GIT: ↑Ca2+ absorption
 Bone: ↑Ca2+ resorption
 Kidney: Activation of Vitamin D
 Skin: Formation of Vitamin D (UV dependent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causes of hyperparathyroidism?

A
  • Reaction to persistently high serum PO4 (renal failure, vit D toxicity)
  • Persistent secretion of PTH or related proteins (lymphoma, anal sac adenocarcinomas)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What could lead to pathological fractures?

A

Osteodystrophy - sacrifice of skeletal calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does parathyroid hormone influence calcium homeostasis?

A

Parathyroid hormone
- BONE: ↑Ca2+ transfer across cellular barrier and ↑Ca2+ resorption
- KIDNEY: * ↑Ca2+ absorption in DCT, ↓ Pi absorption in PCT and activation of Vit D

Calcitonin: ↓ Bone resorption and ↓Ca2+ transfer across cellular barrier

1,25(OH)2 Vitamin D
- GIT: ↑Ca2+ absorption
- Bone: ↑Ca2+ resorption
- Kidney: Activation of Vitamin D
- Skin: Formation of Vitamin D (UV dependent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does calcium flow between bone and extracellular fluid TO ADD

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What might happen if damage occurs to the growth plate?

A
  • Stunted bone growth
  • Malformation
  • If you get damage to only one section of the growth plate, you might see malformations/deviations in the growth of the bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What might happen if damage occurs to the growth plate?

A
  • Stunted bone growth
  • Malformation
  • If you get damage to only one section of the growth plate, you might see malformations/deviations in the growth of the bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What could lead to imparied osteoclastic activity?

Think viral or toxic causes

A
  • Canine distemper virus
  • Bovine viral diarrhoea
  • Lead poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain Wolffs law

A
  • Bone is deposited at sites where its needed and reabsorbed where it isnt. The abnormal use of a bone can result in a change in shape. Removal of mechanical forces can cause localised osteopenia.
  • Net bone formation at sites of compression, net bone resorption at sites of tension. Trabecular bon aligns along the lines of stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is osteochondrosis?

A

disorder resulting from abnormal growth, injury, or overuse of the developing growth plate and surrounding ossification centers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is osteonecrosis?

A

The death of bone cells due to decreased blood flow. Generally as a reslt of trauma/fractures, pressure from tumours or inflammatory lesions or mechanical pressure, and lastly vasoconstriction from cold or ergotism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What response do we see in periosteal injury?

A

Injured periosteum often forms bone. Usually see spicular bone that is orientated perpendicular to the log axis of the cortex (nodular lesions = osteophytes, osteophytes at insertions or tendons or ligaments are referred to as enthesiophytes). This spicular bone may be admixed with cartilage (esp. under low oxygen tension).

16
Q

What is ectopic mineralisation/ossification?

A

Ectopic mineralisation: Mineralisation in areas of the body outside of the skeletal system

Ectopic ossification: Ectopic ossification is a biologic process in which new bone is formed in tissues which normally do not ossify.

17
Q

What are the forms of ectopic mineralisation?

A

Metastatic and dystrophic

18
Q

Give an examle of metastatic forms of ectopic mineralisation

A
  • Hypercalcaemia or hyperphosphataemia
19
Q

Give an examle of dystrophic forms of ectopic mineralisation

A
  • Calcinosis cutis - Mineralisation of collagen fibres in the skin, strongly assoicated with cell injury
  • Tumouralcalcinosis/calcinosis crcumscripta - often near joints, mass lesion due to depostiion of chalky accumulation of calcium salts
20
Q

What can cause bone fractures?

A

Either
- Traumatic fractures - excessive force on NORMAL bone
- Pathological fractures - abnormal bone, minimal trauma as a result of neoplasia, inflammatory disease, osteodystrophies

21
Q

What are the types of fractures?

A
  • Transverse/oblique/spiral
  • comminuted
  • greenstick
  • physeal (salter-harris I-V) - refer to image
22
Q

Why is the distal ulnar physis easy to damage?

A

Because its conically shaped

23
Q

What are the stages of healing following a fracture?

A

→ Haematoma
→ Local ischaemic necrosis of bone ends and local tissues
→ Acute inflammation, fibrinolysis, phagocytosis
→ Proliferation of mesenchymal cells (periosteal, endosteal) -> dominated by periosteal proliferation in the beginning stages
→ Loose connective tissue callus
→ Mesenchymal cells differentiate into chondroblasts
→ Cartilaginous callus, while osteoclasts remove dead bone
→ Osteoblasts proliferate and make woven bone
→ Bony callus (primary callus)
→ Modelling to mature lamellar bone (secondary callus)
→ remodolling continues for the remainder of the animals life

24
Q

How would you promote high vascularity to promote bone formation?

A
  • Minimise dead space
  • Minimise dead tissue present
25
Q

What are the aims of the treatment of fractures?

A

aimed at ensuring stability, maintaining blood supply, removing infectious agents and promoting normal function to optimise the healing process

26
Q

In fracture repair, what does poor oxygen tension promote?

A

Poor oxygen tension promotes increased cartilage in the callus -> ont as strong as woven bone but will eventually form bone via endochondrial ossification

27
Q

What would a lack of stabilisation mean in fracture repair?

A

↑ movement & tension, promoting development of mature fibrous tissue in the callus and may lead to non-union Infection

28
Q

What diseases might impact fracture repair?

A

Neoplasia and or degenerative bone disease

29
Q

List some adverse outcomes of fractures

A

o Delayed union
o Non-union
o Malunion
o Osteomyelitis
o Disuse atrophy of bone and musculature
o Physical disruption of surrounding tissue by the callus
o Angular limb deformity

30
Q

How can inflammation induce a pathological fracture?

A

Exudate may accumulate in the medullary cavity
- Increased intramedullary pressure
- Compression of vessels
- Thrombosis and infarction

Stimulation of bone resorption
- Inflammatory mediators stimulate bone resorption by osteoclasts
- Enzymes from inflammatory cells and activation of matrix metalloproteinases promote matrix resorption

31
Q

In a pathological fracture, what would cause a change to the matrix?

A
  • Cellular infiltration from inflammation or neoplasia
  • Change to the composition/amount of matrix as a result of osteodystrophies or congenital abnormalities of the bone or cartilage
32
Q

Name some specific diseases that can result in a pathological fracture?

A
  • Osteoporosis
  • legg-calve-perthes disease in small dogs -> ishaemic necrosis of the femoral head
  • Slipped capital physis in cats -> usually in overwight males, disorganised cartilage with delayed physeal closure
  • Bucked shins -> dorsal cortex of MCIII in horses, repetative stress may cause periosteal damage, microfractures are in cortical bone

Disorders of Gait, Neuro & Eye (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions