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cardiac cresent/primary heart field
horseshoe shaped distribution of angiogenic/cardiogenic cells migrating from the lateral mesoderm at the cranial end of the unfolded embryo (third week)
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blood islands
differentiated angiogenic cells which unite to form 2 endothelial lined tubes on either side of the midline
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heart tube
 fusion of the 2 endothelial tubes during embryonic folding to form a single heart tube made up of 5 regions: aortic roots, bulbus cordis, primitive ventricle, primitive atrium and sinus venosus
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aortic roots
rostral most end of the heart tube which remains rostral throughout development and develops into the aorta
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bulbus cordis
part of heart tube that will go on to form most of the right ventricle - moves inferiorly, anteriorly and to the right during heart looping
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primitive ventricle
part of the heart tube between the bulbus cordis and primitive atrium which will go on to form the left ventricle by moving to the left of the bulbus cordis which forms most of the right ventricle
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primitive atrium
part of the heart tube between the primitive ventricle and sinus venosus which goes on to form the right and left atria by moving superiorly and posteriorly to end up posterior to the bulbus cordis and primitive ventricle areas
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sinus venosus
caudal most part of the heart tube which goes on to form the superior vena cava by moving posteriorly and superiorly together with the primitive atria; left sinus horn forms connections with the umbilical vein
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heart looping
folding of the heart tube during the fourth week to form the atrioventricular structure of the heart
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atrioventricular canal
internal opening between primitive ventricle and primitive atrium
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truncus arteriosus
outflow tract from primitive ventricle formed from the rostral part of bulbus cordis, will eventually form the aorta and pulmonary trunk
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endocardial cushions
ventral and dorsal outgrowths from the atrioventricular canal between the primitive ventricle and atrium after heart folding which will fuse to separate the right and left atrioventricular canals forming the "fused" endocardial cushions
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septum primum
downgrowth from the roof of the primitive common atrium towards the fused endocardial cushions at the end of the fourth week (thin, membraneous tissue)
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ostium/foramen primum
closing gap between the septum primum and endocardial cushions connecting the RA and LA allowing shunting of blood away from pulmonary circulation
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ostium/foramen secundum
hole that forms through septum primum by apoptosis as ostium primum closes
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septum secundum
second downgrowth from roof of RA towards the endocardial cushions which forms the borders of the foramen ovale (thick and muscular tissue compared to septum primum); finishes growing at end of 6th week
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valve of the foramen ovale
result of the degeneration of the upper part of septum primum and ostium secundum leaving only the lower part of septum primum which covers the foramen ovale
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fossa ovalis
thinned oval part of the interatrial septum formed by the fusion of the septum primum (valve of foramen ovale) with the septum secundum due to pressure changes
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atrial septal defect
failure of the interatrial septum to fully form due to excessive resorption or absence of one or both septa
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interventricular septum
muscular outgrowth from floor of common ventricle up towards endocardial cushions which almost completely separates the ventricles bar the very upper part which is the interventricular foramen
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interventricular foramen
opening between muscular ventricular septum and fused endocardial cushions
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membranous part of interventricular septum
outgrowth of thin tissue from endocardial cushion which fuses to the muscular interventricular septum to completely separate the ventricles
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ventricular septal defect
failure of either of the components of the interventricular septum to develop properly
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conotruncal ridges/truncoconal swellings
two ridges of tissue that appear on the sides of the truncus arteriosus which grow towards each other and make a spiral shaped septum called the aorticopulmonary septum
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aorticopulmonary septum
outgrowths of the conotruncal ridges to form the barriers between the aorta and pulmonary trunk in the truncus arteriosus
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transposition of the great vessels
when the aorticopulmonary septum connects in such a way that the aorta is continuous with the right ventricle and the pulmonary trunk is continuous with the left ventricle
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AV valve formation
migration of dense mesenchymal tissue of the endocardial cushion and walls of atria downwards to form atrioventricular valves while myocardium migrates up to form papillary muscle
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pulmonary valvular atresia
blockage of outflow tract from right ventricle to pulmonary trunk which is only compatible with life in the presence of ventricular septal defect allowing deoxygenated blood in the right side of the heart to be recycled through the aorta (with some being shunted to the lungs via the ductus arteriosus
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periods of greatest susceptibility to teratogens
3-8 weeks period of greatest sensitivity
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causes of gross malformations
gene defects, chromosomal defects, maternal infections, maternal disease, constraint, drugs/chemical exposure BUT MOSTLY UNKNOWN/MULTIFACTORIAL
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stages of respiratory development
- Embryonic - lung buds form bronchioles
- Pseudoglandular - terminal bronchioles, undifferentiated cuboidal epithelium
- Canalicular - respiratory bronchioles, vasculature, epithelial differentiation
- Saccular - terminal sacs, primitive alveoli, type II pneumocytes
- Alveolar - vascular and epithelial proliferation, septation and maturation of alveoli
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respiratory diverticulum/lung bud
ventral outpouching at week 4 of cranial endoderm (primitive foregut) which branches into LR lung buds and then further to bronchopulmonary segments
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pseudoglandular respiratory development
formation of terminal bronchioles from lung buds which have cuboidal undifferentiated epithelium (weeks 5-16, well into second trimester)
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canalicular respiratory development
Branching and differentiation of each terminal bronchiole into two or more respiratory bronchioles, with formation of vasculature and epithelial differentiation to squamous, during weeks 16-25 (most of second trimester)
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saccular respiratory development
formation of terminal sacs with thin squamous type I epithelium and penetration of capillary endothelial cells to form primitive alveoli; differentiation into type II pneumocytes from week 28-
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alveolar respiratory development
from week 32 and into childhood, there is maturation of alveoli by proliferation of vasculature and type I epithelium causing septation and increased SA as well as increasing numbers of type II pneumocytes
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tracheo-esophageal fistula
opening of esophagus into trachea increasing risk of aspiration to the lung
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esophageal atresia
esophagus is blind ended pouch from the mouth which must be immediately modified to allow for feeding
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IRDS
infant respiratory distress syndrome occurring particularly in premature babies whose lungs have yet to reach maturity required - low volume/surface area and high surface tension due to lack of surfactant
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surfactant
amphipathic lipoprotein produced by type II pneumocytes from week 28 onwards which reduces surface tension between alveolar membranes to increase overall lung compliance; this reduces the pressure difference required to expand the lungs during inspiration (decreases work of breathing)
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pathophysiological features of IRDS
CRAACS: compliance low, residual volume low, alveolar collapse, airway closure, capillary leak, shunting
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embryonic components of diaphragm
all derived from mesoderm (intraembryonic coelem): septum transversum, pleuroperitoneal membranes, mesoderm of body wall, esophageal mesenchyme
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septum transversum
cranial-most end of intraembryonic coelom continuous with amnion (derived from mesoderm)
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pleuroperitoneal membranes
cranial intraembryonic coelom formed from embryonic folding of mesoderm which extends towards the anterior septum transversum to close off the pericardioperitoneal canal
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pericardioperitoneal canal
closing gap between septum transversum and pleuroperitoneal membranes
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congenital diaphragmatic hernia
defect in barrier between thoracic and abdominal viscera causing abdominal GIT to herniate through to thorax preventing normal development of lungs
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