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Samenvatting Humane Ontwikkeling Deel 2
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Samenvatting Humane Ontwikkeling Deel 2 in Nederlands/Engels.
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Summary Human Development (AB_1140) partial exam 1+2+3
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TesT Bank for Larsen’s Human Embryology, 5th Edition, Gary Schoenwolf
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Aantekeningen HO Deel 2 (HC 12-18)12. The skeleton and muscle system
Mesoderm formaton week 3 and 4: the intraembryonic mesoderm is formed, and the
mesoderm cell-specifcaaon is controlled by FGF-8; the intraembryonic mesoderm will be
converted into cardiogenic, paraxial, intermediate mesoderm and the lateral plate and
notochord (future prechordal plate); the extraembryonic mesoderm forms the amnion, yolk
sac, and allantois.
- Lateral plate mesoderm will only form trunk/torso, and the paraxial mesoderm forms
mainly in the medial-cranial part.
- Most muscle assue develops from mesoderm, but diferences by kind of muscles:
Skeletal muscle: paraxial mesoderm.
Smooth muscle: gut and derivaaves from visceral layer, lateral plate mesoderm around
gut tube; pupil, mammary and sweat glands from ectoderm.
Cardiac muscle: visceral layer, lateral plate mesoderm around heart tube.
Somite diferentaton: the somites will diferenaate into dermatome (skin), myotome
(muscle), and sclerotome (spinal vertebrae, skull basis); dermatome and myotome are frst
dermamyotome. -> This diferenaaaon process by epithelial-to-mesenchym transformaaon.
- Epithelial-to-mesenchym transformaton: frst the mesoderm is epithelial forming a
lumen with free cells, ventral and medial part become mesenchymal and migrate around
neural tube/ notochord (then sclerotome); then dermatomyotome forms and from that
the dermatome (upper) and myotome (lower) part forms, the dorsomedial (epimere)
and ventrolateral (hypomere) become muscle cells and these migrate medial and
ventral.
Regulaton dermatomyotome: dorsomedial there is medium BMP4 and high Wnt, and
ventrolateral there is high BMP4 and medium Wnt; later the dermatomyotome will
develop into dermatome wherefore PAX genes are important.
- Factors for somite diferentaton: Shh and FGF (from notochord/neural tube)
upregulates chrodin and noggin, which causes ventral part of somite to become
sclerotome; PAX3+NT3 (neural tube) regulates dermatome (later dermis formaaon);
MYF5 in myotome together with Wnt specifes cells into myotome (later muscle
formaaon), MYOD specifes second group of muscle cell precursor.
- Formaton/development sclerotome: cells migrate around neural tube and notochord,
then fuse with those from other side, and this forms the future vertebra; then
resegmentaton (splits and recombines) with in between nucleus pulposus (only young
children) and annulus fbrosus (intervertebral discs, allows bending).
Resegmentaton: vertebral column splits at Von Ebner’s fssure and recombine (caudal
+ cranial form one underneath) which leads to 8 cervical sclerotomes and 7 cervical
vertebrae; each somite induce outgrowth of spinal nerves (total 8, at ventral part and
are motor neurons) which innervate the corresponding myotomes (muscles).
Occipital bone: skull base of most upper sclerotome.
Vertebrae: has three diferent kinds of vertebrae with each a diferent formaaon, this also
forms the curvature of the vertebral column (not visible in foetus).
I. 7 Cervical vertebrae
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,II. 12 Thoracic vertebrae: mid-secaon of vertebral column, here ribs will develop
(regulated by Hox genes); at 5 weeks the ribs lengthen but separate from vertebrae
at 6-7 weeks; primary ossifcaton centres appear in body of ribs and mostly become
caralaginous during weeks 13-14 of development, secondary ossifcaton centres
appear for head and tubercle of rib at puberty; the true ribs (1-7th) atach through
own caralages to sternum, false ribs (8-10th) atach to sternum through caralage of
another rib, floatng ribs (11th/12th) do not atach to sternum (NL borstbeen).
III. 5 Lumbar vertebrae
- Defects of spinal vertebrae:
Scoliosis: a mis formaaon in spinal vertebrae can cause the weight to be unequally
divided which results in malformaaon in spine; congenital is when process of splitng
and fusion went wrong, so asymmetric fusion and half a vertebra missing, ofen co-
occurring with other malformaaons; idiopathic has an unknown origin; neuromuscular
is as a result of another primary disease (eg. muscular dystrophy, spina bifda), mostly
progressive.
Flatback syndrome: no curve in botom vertebrae (decreased lumbar lordosis) and
then weight not above hips, this results in a tendency to lean forward when walking or
standing for beter alignment but could faague/aching muscles.
- Openings in vertebrae: spinal cord runs through vertebrae (CNS, neural tube), the
peripheral nerves in dorsal root ganglia (sensory neurons) and ventral root neurons
innervate with muscles.
Skull: two components, the neurocranium (from eyebrow up) and the viscerocranium;
- Neurocranium: has also diferent components; the membranous neurocranium is from
neural crest cells (frontal bone) and paraxial mesoderm, mesenchym from both
undergo ossifcaton without making caralage, typifed by bone spicules that radiate
outwards; the cartlaginous neurocranium (endochrondral bones) is the skull basis.
Skull basis (chondrocranium): iniaally forms caralage intermediate prechordal
chondrocranium (PCC) and hypophyseal chondrocranium form neural crest cells, and
(para)chordal chondrocranium from paraxial mesoderm; PCC/CCC part of pituitary
gland at rostral end of notochord.
- Viscerocranium: is all form neural crest cells form two pharyngeal arches, bones of the
face, facial muscles are from paraxial mesoderm.
Pharyngeal arches: branchial arches, migratory paths of neural crest cells to face,
contribute to formaaon head and neck; head consists of mandibular prominence/
maxillary prominence/nasal prominence; panryngeal pouch gene expression
regulates paterning of pharyngeal arches.
- Around birth: skull bones grow as much as much as brain needs, so microcephaly by
growth retardaaon of brain not skull; the fat bones lie separate with seams of
connecave assue, this is necessary for growth of brain and enabling birth , when >2
bones connect their called fontanelles.
Craniosynosts = premature closure of sutures, closure of one increases growth of
other sutures which results in deformed skull, mutaaons in FGF ligands and receptors
distorts balance between proliferaaon and diferenaaaon in suture.
2
, Spina bifda: neural tube and vertebrae related birth defect,
- SB occulta: efect hidden, failure of vertebral arches to form (neural tube not afected),
not visible as it is covered with skin, characterized by hair tuf overlaying afected region
(not always), could go unnoaced when only one vertebral arch, caudal and cranial end .
- SB aperta: open form of SB, failure of vertebral arches and neural tube closure, neural
tube most cases afected but could funcaon ok.
Meningocele: fuid-flled meninges protrude (sac, is neural crest), but neural tube itself
intact.
Myelomeningocele: neural assue protrudes (neural crest+neural tube), neural tube
could easily be damaged, co-occcurence with hydrocephaly, not simle incomplete
neurulaaon but chemical damage by leakage of amnioac fuid into neural tube
meninges (NL hersenvlies)
Rachischisis: not developed neural tube, caudal and cranial (= anencephaly), not viable.
Prenatal diagnosis: hydrocephaly (90% of myelo-mengingocele cases) detected by ultra
sound and amnioscentesis (high levels of a-feto-protein), prevenaon possible by folic
acid intake.
Treatment: postnatal operaaon with SB aperta, meningocele in frst year afer
birth/myelomeningocele in frst days/rachischisis is it not possible; prenatal operaaon
with SB myelomeningocele has beter treatment outcome and reduces hydrocephaly
and other related SB disorders.
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