Brainscape's Knowledge GenomeTM

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


See full index

YR 3 - Illness and Wellbeing > Bone Disorders > Flashcards

Bone Disorders Flashcards

1
Q

what’s bone made of?

A

non-cellular mineralised matrix
- type 1 collagen = osteoid
- calcium phosphate
- protein and growth factors

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

why is mineralisation important?

A

to make the osteoid hard, makes bone stiff and strong

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

what is the function of bone?

A
  • physical integrity and support
  • protection for organs
  • attachment for muscles and tendons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the 3 main cellular elements of bone and their functions?

A

osteoblasts
- secrete collagen/osteoids
- mineralisation

osteocytes
- inactive osteoblasts
- trapped inside bone

osteoclasts
- stem from macrophages
- resorb bone

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

what is the difference between woven and lamellar bone?

A

woven bone = immature bone
- random osteoid
- rapid turnover
- remodelled to lamellar bone

lamellar bone
- parallel sheets
- normal healthy adult bone
- compact or trabecular/cancellous

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

which is stronger, woven or lamellar bone?

A

lamellar bone
- due to regular arrangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

the 2 types of bone

A

compact/cortical

trabecular/cancellous

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

describe cortical bone

A

hard outer shell
organised and regular
haversion system
surrounds cancellous bone

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

describe cancellous bone

A

spongy
marrow

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

describe the bone remodelling cycle

A
  1. activation
    - hormones or damage activate osteoblast
    - cytokines secreted
    - osteoclasts sticks to surface of bone
  2. resorption
    - osteoclasts secrete substance and resorb bone
    = pits on surface
    - apoptosis or migration of clasts
  3. reversal
    - monocytes clear debris
  4. formation
    - osteoblasts secrete matrix
    - mineralisation
    - some blast incorporate as osteocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is osteoarthritis?

give aetiology.

A

progressive erosion of articular cartilage

aetiology
- primary - just happens
- secondary - pre-existing joint damage, metabolic disease, systemic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the pathogenesis of osteoarthritis?

A
  • erosion of articular cartilage
  • bone exposed
  • abnormal growth = osteophytes
  • cysts in the bone
  • narrow joint space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does osteoarthritis clinically feature?

A

symptoms
- pain
- limited function

signs
- bony enlargements
- crepitus - crunch
- instability

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

how is osteoarthritis investigated and treated?

A

blood test
x-ray

physical
medications
surgery - joint replacement

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

what is rheumatoid arthritis

A

autoimmune condition with persistent inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe the pathogenesis of rheumatoid arthritis.

A
  • citrullination of arginine to citrulline
  • protein modification, becomes foreign
  • autoimmune response
  • T cells and cytokines
  • macrophages
  • fibroblasts
  • synovium proliferation and inflammation
  • synovitis
17
Q

how is rheumatoid arthritis investigated and managed?

A

blood tests
x-rays

no cure
medications - DMARDS
= disease modifying anti-rheumatic drugs

18
Q

what is padgets disease?

A

bone turnover is disordered
- more woven bone

19
Q

describe the pathogenesis of padgets disease.

A
  1. hot phase
    - osteoclast activity
  2. mixed phase
    - osteoblast and osteoclast activity
  3. cold phase
    - no activity
20
Q

how does padgets disease clinically present?

A

bone deformations
high fracture risk
bone pain
hypercementosis - cotton wool appearance
nerve compression - hydrocephalus

21
Q

how is pagets disease treated? also used for osteoporosis

A

bisphosphonates
- inhibit clasts resporption
= slow bone loss

22
Q

what is the biggest worry of using bisphosphonates?

A

the chance of developing BRONJ
- hinders bone healing

23
Q

what is osteomyelitis?

give aetiology.

A

inflammation of bone marrow

aetiology
- from infection
- staphlococcus aureus

24
Q

how does osteomyelitis clinically present?

A

fever
bone pain
tenderness

25
Q

treatment for osteomyelitis?

A

immobilise
antibiotics

26
Q

what is osteonecrosis?
- aetiology.

A

infarction of bone marrow

aetiology = vascular insufficiency
- alcohol
- steroids
- fractures

27
Q

osteonecrosis is asceptic, wym?

A

not due to infection

28
Q

describe the pathogenesis of osteonecrosis.

A
29
Q

how does osteonecrosis clinically present?

give management

A

joint pain
collapse of articular bone

  • grafts
  • joint replacement
30
Q

what is osteomalacia AKA rickets?
give aetiology.

A

defective mineralisation of bone osteoid

rickets = kids
osteomalacia = adults

aetiology - anything that interferes with bone mineralisation
- vitamin D deficiency - blood calcium drops
- renal failure

31
Q

dental complications of rickets

A

hypophosphataemia
- thin enamel
- globular dentine
- dental abscess more common

hypoplasia
missing teeth

32
Q

osteogenesis imperfecta
- definition
- aetiology

A

brittle bone disease

  • type 1 collagen has gene mutation
33
Q

describe the clinical features of osteogenesis imperfecta

A

increased fractures
small discoloured teeth

34
Q

achrondoplasia
- definition
- aetiology

frank from always sunny has achondroplasia

A

woven bone remodelled to lamellar bone
= endochondral ossification
- short limbs

intramembral ossification
- in the maxilla, skill and mandible

aetiology
- FGFR-3 mutation
- impairs cartilage growth

35
Q

define fracture

A

a loss of bone integrity and loss of the mechanical strength

36
Q

how are fractures classified?

A

simple
comminuted - fragments
compound - out of the skin
displaced - ends not aligned

37
Q

describe the phases of fracture healing

A
  1. inflammatory phase
    - haematoma forms - blood
    - lump of haemopoietic cells
    - macrophages, neutrophils, platelets activate cytokines
    - fibroblasts at site
    - granulation tissue
    - neovascularisation
    - fibrosis = callus formation - a scar within the site
  2. reparative phase
    - primary callus
    - endochondral ossification converts soft cartilage to woven bone
  3. remodelling phase
    - woven bone into cortical bone

YR 3 - Illness and Wellbeing (31 decks)

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