Embryology Flashcards
What are the 3 germ layers and their derivatives?
Ectoderm, Mesoderm, Endoderm.
Ectoderm: Nervous System, Skin
Mesoderm: Muscle, connective tissue (blood), most organs
Endoderm: Linings of respiratory, GI, urinary tracts
What’s the relative timing of the cranial and caudal ends of the embryo?
Cranial cells develop first, before caudal. Epiblast ingresses through primitive streak during gastrulation in 3rd week of development.
What is a teratoma? Sacroccygeal teratoma?
A tumor composed of tissues from multiple germ layers. If the primitive streak persists due to gastrulation error, can result in a sacrococcygeal teratoma, the most common tumor in newborns.
What tissues become buccopharyngeal and cloacal membranes? What is their location in the trilaminar embryo?
Buccopharyngeal and cloacal membranes are the only two places where ectoderm and endoderm are directly apposed.
What is the prechordal plate and how is it different than the notochord?
Prechordal plate: derived from primitive node, caudal to buccopharyngeal membrane.
Notochord: solid rod from primitive node cells. Signals to neural crest cells in neurulation.
What are the three mesoderm populations and what do they become?
Paraxial: Somites–Dermis, skeletal muscle, skeleton
Intermediate: Genitourinary
Lateral: Somatic (contacts ectoderm) and splanchnic (contacts endoderm)
What occurs during neurulation?
Neural tissue differentiates due to notochord signaling. Ectoderm cells form neural plate, which folds and becomes neural tube.
What is the neural crest and what does it become?
Neural crest cells form as neural tube folds fuse–They dissociate and migrate away becoming PNS, glia, melanocytes, adrenam medulla, connective tissue of face, pharyngeal arches
What is Hirschsprung disease?
Aganglionic megacolon–neural crest cell failure leaves no innervation of distal colon, leading to clogging.
What is amniotic fluid? What is poly/oligohydraminios.
Mom’s water and baby’s urine. 1 L at term. cushions fetus, provides some nutrients/salts/hormones too. Too much (poly) or too little (oligo) can cause birth defects: Potter facies (face flattening) or esophagus/kidney problems
What mesodermal cell population gives rise to the heart? Where is it? How does the heart get to its final location?
Precardiac Mesoderm cranial to buccopharyngeal membrane. Head-fold causes cranial region to fold ventrally.
What cells make the pharyngeal arches? What two syndromes result from a defect in this process?
Neural crest cells that migrate to surround foregut. 6 arches form, but 5th degenerates. Impaired migration leads to Treacher Collins/DiGeorge syndromes.
What 3 veins bring blood to the peripheral heart tube?
Umbilical vein (oxygenated) from placenta Vitelline vein (deoxy) from yolk sac Cardinal vein (deoxy) from embryo body
How does embryonic blood flow travel?
Blood exits heart at cranial end, passes dorsally through pharyngeal arches (aortic arch arteries), then paired dorsal aortae, umbilical arteries, placenta.
What tissues/organs produce RBCs during embryo/fetal stage? What’s the timing?
1) Blood Islands in extra-embryonic mesoderm of yolk sack
2) 4 wk mesoderm of dorsal aortae
3) 6-8 wk Liver (till ~birth)
4) 12 wk Spleen
5) Month 4 Bone Marrow (primary after 6 mo)
What are two major functions encoded by developmental genes?
Transcription factors (eg Hox) Cell-cell signaling (surface proteins or ligand/receptor)
What is a selector gene?
A gene that when expressed activates a particular pathway that leads to the formation of a specific tissue or organ.
What is the function of Hox genes and what patterns of expression are there?
Selector genes of 4 series, with lower numbers more cranial and higher more caudal. Each area receives a mixture which determines its fate.
What is a signaling center? What is induction? What is competence?
SIGNALING CENTERS produce signals that INDUCE COMPETENT cells to differentiate. eg notochord induces ectoderm to become neural tube.
Name 5 signaling ligands and 5 signalling centers
sonic HH, TGFb, EGF, WNT, Retinoic Acid
Primitive node, prechordal plate, notochord, apical ectodermal ridge, zone of polarizing activity
Define and ID defective developmental gene for the following: Achondroplasia, craniosynostosis, polysyndactyly, holoprosencephaly
Achondroplasia: dwarfism, FGF receptor mutation
Craniosynostosis: Malformed cranium, FGFR
Polysyndactyly: several fused digits, HoxD13
Holoprosencephaly: Cyclops-ish, low SHH
What are teratogens? How are teratogen-induced malformations different than inborn errors of development?
Compounds that influence development (eg RA). Inborn errors are genetic mutations, not environmental.
What is the embryonic period in development? What is meant by critical period in organ development? What is a structural vs functional abnormality?
Wk 3-8 is embryonic period ~=Critical period for teratogen exposure. Teratogen during this is structural abnormality, afterward = functional abnormality.
What is retinoic acid embryopathy’s teratogen, developmental genes, structures affected?
Retinoic acid releases HOX from regulatory proteins, hox genes have RA response elements in promoters. It affects the rhombencephalon (hindbrain) and also face/neck/trachea/heart.
Sonic HH
Paracrine, head/face, right/left, Ant/Pos
Wnt
Paracrine
Somites to muscle, limb polarity, kidney, female sex organs
Non-canonical: epithelial planar cell polarity
TGFb
paracrine
right/left, sex, enteric neuron
FGF/RTK
Paracrine
Angiogenesis, mesorderm, axon extension
Integrin/ECM
juxtacrine
movement, gene expression and survival
Notch
juxtacrine
kidney pancreas heart, nervous system receptors
Gap junctions
juxtacrine
blastomeres connected by these
