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Medicine phase 2 limbs and back > week 5 > Flashcards

week 5 Flashcards

1
Q

cellular differentiation

A

process of one cell type changing to another cell type

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2
Q

how does differentiation affect a cell

A 
size
shape
membrane potential
metabolic activity
responsiveness to signals
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3
Q

when do limbs start to form

A

week 4

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4
Q

mesenchyme

A

connective tissue found in embryo development
arises from mesoderm
contains loosely packed cells which are non specialised
mesenchymal cells are highly migratory

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5
Q

limb development stages

A

at the end of week 4 - limb buds first become visible
upper limb buds appear first as ridges from ventrolateral body wall
lower limb as small bulges
limb morphogenesis takes place between weeks 4 and 8
lower limbs lag slightly behind
no nerves in early limb bud

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6
Q

where is mesenchyme derived from

A

dorsolateral mesoderm cells of the somites

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7
Q

components of mesenchymal connective tissue

A

matrix of collagen fibres
hyaluronic acid
glycoproteins

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8
Q

structure of a limb bud

A

mesenchymal core - from somatic layer of lateral plate mesoderm
covered by a layer of cuboidal ectoderm
apical ectodermal ridge at distal border

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9
Q

what is the AER

A

apical ectodermal ridge
it is thickened ectoderm at the distal border of a limb bud
has an inductive relationship with mesoderm
remains undifferentiated
key signalling centre in limb development - limbs fail to develop without AER

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10
Q

limb development after AER has formed

A

as limb grows, cells furthest from the AER begin to differentiate into cartilage and muscle
limb outgrowth initiated by secretion of FGF10
position of AER corresponds to border between dorsal and ventral ectoderm

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11
Q

role of FGF10 in limb development

A

signalling molecule first seen in the limb bud
paracrine signalling molecule
FGF family known for mitogenic activity - induce a cell to begin division via triggering a signal transduction pathway

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12
Q

where is radical fringe expressed

A

expressed by dorsal ectoderm

its a signalling molecule

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13
Q

what does the ventral ectoderm express

A

transcription factor called engrailed1

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14
Q

function of FGF 4 and 8 in limb development

A

at distal end keep cells undifferentiated

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15
Q

function of engrailed1 and radical fringe in limb development

A

RF - in dorsal limb it restricts AER to the distal tip

engrailed does the same on the ventral side

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16
Q

function of retinoic acid in limb development

A

at the proximal end starts differentiation into prox components - signals from AER to not reach to prox

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17
Q

what are the factors designating UL and LL

A

t-box family TFs
TBX-5 expressed in the UL
TBX-4 expressed in the LL

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18
Q

mesoderm and ectoderm relationship in AER

A

AER is ectoderm and is acting on mesoderm but its own existence is controlled by mesoderm

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19
Q

week 6 of limb development

A

terminal portion of buds becomes flattened - handplates and footplates
seperated from the proxmal segements by constriction (wrist)
second constriction further divides proximal portion into 2 segments (elbow)

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20
Q

3 components of limb in development

A

stylopod - humerus and femur
zeugopod - radius/ulna and tibia/fibia
autopod - carpels, metacarpals, digits, tarsals/metatarsals

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21
Q

function of HOX genes in limb development

A

regulates positioning of limbs along craniocaudal axis
expressed in overlapping patterns
mis expression will alter limb position

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22
Q

polydactylyl

A

extra digits due to a defect in mesoderm - mutation in HOX genes, Shh or Wnt

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23
Q

what happens after cells start to die in AER

A

cell death in AER separates ridges into 5 parts - 5 digits grow out under influence of 5 ridge parts
mesenchyme condense to form cartilaginous digits
by d56, digit separation is complete

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24
Q

describe limb rotation after development

A

LL develops 1-2 days later
limb development over week 7
UL and LL rotate in opposite directions
rotation occurs from from coronal to the parasaggital plane, then along the long axis

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25
Q

which way does UL rotate in development

A

UL rotates 90 degrees laterally

extensor muscles lie lateral ad posterior side

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26
Q

which way does LL rotate in development

A

rotates 90degrees medially

extensors on anterior surface

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27
Q

appositional growth

A

increase in girth/width

chondroblasts deposit collagen matrix on cartilage beneath the periosteum which initiates growth

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28
Q

interstitial growth

A

increase in length

achieved by growth plate up until puberty - cartilage can do this not bone

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29
Q

endochondral ossification

A

cartilage model laid down as a precursor to bone

mainly in long bones

30
Q

intramembranous ossification

A

cartilage not involved
condensation of mesenchyme which is converted straight to bone
see this in flat bones

31
Q

stages of limb bone development

part 1

A

as external shape is being established, mesenchyme in the buds becomes condensed
cells differentiate to chondrocytes - driven by expression of BMPs
at week 6 - hyaline cartilage models can be seen
areas where chondrogenesis is arrested makes joints - cell proliferation, increased density, differentiation then cell dealth - induced by WNT 14
bones formed by week 8
centres of ossification form in diaphyses and epiphyses
primary centres of ossification present in all long bones by week 12
growth plates of cartilage remain

32
Q

stages in limb bone development

part 2

A

cells in centre of cartilage model proliferate, enlarge, make new kind of matrix - can be calcified
calcified cartilage matrix does not allow diffusion of nutrients so cartilage cells die
left with spicules of calcified cartilage matrix - acts as a scaffolding on which bone can be deposited
periosteum is vascular connective tissue around model where blood vessels grown in - BVs bring in progenitor cells
osteoprogenitor cells become osteoblasts - line up on spicules and start producing bone matrix
core of calcified cartilage matrix removed by osteoclasts
trapped osteoblasts become osteocytes

33
Q

during growth period, what remodels bone to maintain overall shape and proportion

A

osteoclasts

34
Q

achondroplasia

A

disorder of bone growth that affects endochondral ossification via cartilage

35
Q

achondroplasia mutation

A

mutation in FGFR3 - normally down regulates cartilage and bone growth and it inhibits cell proliferation and differentiation
mutation in receptor results in permanent expression so protein is overactive - results in reduced chondrocyte activity

36
Q

examples of where hyaline cartilage is located in the body

A

skeletal - articular, costal, growth plate
trachea
larynx
nose

37
Q

examples of where elastic cartilage is located in the body

A

ear

epiglottis

38
Q

examples of where fibrocartilage is located in the body

A

meniscus

IVDs

39
Q

describe articular cartilage

A

smooth lubricated surface for articulation
facilitate load transmission and create low friction environment
cells - chondrocytes
ECM - collagen, water, proteoglycans/proteins - hyaluronan and aggrecan
it is avascular, aneural, non-immunogenic

40
Q

function of chondrocytes and ECM in articular cartilage

A

c - synthesise and maintain ECM

ECM - protects chondrocytes from loading forces

41
Q

what is involved in the degradation part of cartilage turnover

A

MMPs - degrade collagen/proteoglycans

TIMPs prevent degradation of MMPs

42
Q

what is involved in the synthesis part of cartilage turnover

A

collagen, proteoglycans and proteins
increase in GFs, IGF-1 and TGF-beta
decrease in cytokines

43
Q

issue with cartilage healing

A

injury must penetrate subchondral bone to allow bleeding - inflammatory cells, platelets, mesenchymal cells to synthesise collagen type I (not as good as II)

44
Q

stages of cartilage healing

A

inflammation
repair
remodelling

45
Q

issue with meniscal tears

A

cant heal as no blood supply

46
Q

composition of fibrocartilage

A

cells - fibrocartilage

ECM - collagen type I, water, proteoglycans, glycoproteins, elastin

47
Q

acute and chronic cartilage injuries

A

a - trauma, sports, infection

c - osteoarthritis, previous injury

48
Q

diagnosis of cartilage injury

A

xray
mri
arthroscopy

49
Q

treatment of cartilage injury

A 
physiotherapy
medical - paracetamol, NSAIDs
arthroscopy
cartilage transplantation 
joint replacement
50
Q

two types of bone

A 
mature/lamellar:
all cortical and cancellous bone
osteoblasts lay bone matrix in sheets - lamellae
parallel, organised collagen fibres
immature/woven:
randomly aligned collagen fibres
51
Q

cortical bone

A

mature bone laid down in concentric rings
80% of the skeleton
slow turnover rate/metabolic activity

52
Q

cancellous bone

A

spongy or trabecular bone

high turnover rate and undergoes greater remodelling

53
Q

inorganic part of bone matrix

A

calcium and phosphorus

54
Q

organic part of bone matrix

A

collagen, mucopolysaccharides, non-collagenous proteins

55
Q

3 blood supplies of bone

A

periosteum blood supply is most important supply in children
nutrient artery enters centre of diaphysis - high pressure
vessels enter at metaphysis and epiphysis - communicate with nutrient artery but enter separately

56
Q

two types of fracture healing

A

indirect and direct

57
Q

indirect fracture healing process

A 
haematoma:
haemopoetic cells secrete GFs
fibroblasts, osteoprogenitor cells, mesenchymal cells, immune cells
granulation tissue forms
soft callus:
1 week - 1 month
10% strain at failure
hard callus:
soft callus becomes mineralised 
disorganised woven bone
remodelling:
stable bridge with low strain environment 
osteoclasts go across and dissolve mineralised bone, osteoblasts form new bone
58
Q

direct fracture healing

A

unique ‘artificial’ surgical situation - forms low strain environment
direct formation of bone without formation of callus - via osteoclastic absorption and osteoblastic formation
fracture stable - no movement under physiological load
relies upon compression of the bone ends - osteoblasts and osteoclasts can cut across gap that has been compressed

59
Q

which fractures are prone to problems with union or necrosis bc of blood supply problems

A

proximal pole of scaphoid fractures
talar neck
intracapsular hip
surgical neck of humerus

60
Q

inhibition of fracture healing factors

A 
increasing age
diabetes
anaemia
malnutrition
peripheral vascular disease
hypothyroidism 
smoking
alcohol
61
Q

why are there increasing numbers of people with a disability

A

population growth
increase in chronic disease
medical advances which extend and prolong life

62
Q

a disabled person

A

someone with a physical or mental impairment that has a long term effect on his/her ability to carry out normal daily activities
even if condition is controlled by medication etc it still counts as a disability - except eyesight controlled by glasses

63
Q

impairment

A

is due to an injury, illness or congenital condition that causes or is likely to cause a loss or difference of physiological or psychological function

64
Q

causes of disability in young people

A 
prenatal
premature
birth injury - cerebral palsy
congenital - downs syndrome
accident
infection - meningitis
violence
disease
65
Q

barriers children with disabilities experience

A 
physical disability
locomotor disability - movement
cosmetic disability 
sensory eg blind, deaf
cognitive impairment
66
Q

promoting factors for young disabled people in the work participation

A 
male
education level
parental education level
higher level of psychosocial functioning
lower scores on depression scales
67
Q

hindering factors for young disabled people in the work participation

A 
lower educational factors 
female
inpatient treatment - can affect education
motor impairment
wheelchair use
functional limitations
multiple health problems
low mental health perception, dependent coping strategy
68
Q

adjustments to work with a disability

A

adjustments to equipment, work station - voice activated software
support - supervision
change in duties
modification of hours and place
absence due to treatment or rehabilitation
may involve moving to lower grade job if that is what they are competent of now

69
Q

embryonic folding

A

occurs in 2 directions:
lateral folding - driven by somites - creates embryo body - creates tube with endoderm in the middle
cephalocaudal/head to tail folding - driven by CNS - creates c shape as tube bends
the folds happen simultaneously and somatic LPM fuses to close the body wall to create tube like structure

70
Q

what does the dermomyotome form

A

becomes dermis and skeletal muscle

71
Q

what does the sclerotome form

A

vertebrae and ribs

72
Q

process of intramembranous ossification

A

begins with condensation of the mesenchymal stem cells - they undergo proliferation and undergo morphological changes and differentiate into osteoprogenitor cells which will develop into osteoblasts
osteogenic cells start to deposit bone matrix which are arranged in bony spicules
differentiating osteoblasts arrange themselves along the spicules and begin to secrete more bone matrix
as more matrix gets laid down, the spicules increase in size and will fuse together
as these grow, they will fuse with more and more spicules and this results in the formation of trabeculae

Medicine phase 2 limbs and back (6 decks)

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