SM01 Mini3 Flashcards
primary cardiogenic field
horse-shoe shaped zone of heart precursor cells of splanchnic mesoderm (subdivision of lateral plate mesoderm) cranially & laterally to neural plate (if it were on the mesoderm, but it’s really on the ectoderm above)
W3
heart tube
two endothelial lined tubes left & right that fuse lateral body folding
W3
definitive heart tube
single heart tube after fusion of earlier endothelial tubes (through apoptosis of medial cells)
they do NOT fuse at the cranial or caudal extremes
created after lateral body folding, begins cranially and continues caudally
W3
cranio-caudal folding effect on heart
repositions heart tube into presumptive thoracic cavity, caudal to brain & oral cavity
primitive heart tube layers
- inner: endocardial layer
- middle: cardiac jelly
- outer: myocardial layer (muscle)
D22-25 (W4), presence of heart beat
epicardium is derived from
mesodermal cell that migrate from near the developing liver
cardiac jelly
extracellular matrix proteins
unknown function, but required, b/c if it doesn’t form, a spontaneous abortion will occur
middle layer of primitive heart tube
vitelline veins
paired right & left veins that carry deoxygenated blood from the yolk sac to caudal end of primitive heart tube
cardinal veins
paired right & left veins that carry deoxygenated blood from body of embryo to caudal end of primitive heart tube
umbilical veins
paired left & right veins that carry oxygenated body from placenta to the caudal end of primitve heart tube
primitive heart outflow tract
truncus arteriosus (which becomes the aorta & pulmonary thrunk) connects to right & left aortic archs (3 branches/side at this stage)
transverse pericardial sinus
forms from the degeneration of dorsal mesocardium
postnatally: located posteriorly to aorta and pulmonary trunk & anterior to superior vena cava
dorsal mesocardium
initial attachment of heart to posterior thoarcic wall during the development of pericardial cavity
5 dilations of primitive heart tube cranial to caudal
- truncus arteriosus
- bulbus cordis
- primitive ventricle
- primitive artrium
- right & left horns of sinus venosus
blood flows caudally to cranially
heart tube folding
D23 too long to be accomodated in available space
caudal primitive atrium shifts back then up & to the left, dorsocranially & left
cranial primitive ventricle moves ventrocaudally & to the right
D25-28 (end of W4)
blubus cordis & truncus arteriosus are medial & anterior in resulting structure
dextrocardia
when heart is on right instead of left due to abnormal looping
w/situs inversus→ normal or asymptomatic life
in isolation→ accompanied by severe cardiac abnormalities, ex. single ventricle or ventricular septal defect
formation of right atrium
trabeculated part: from right side of primitive atrium
sinus venarum (smooth portion): from right horn of sinus venosus
sinus venarum
smooth part of right atrium on posterior wall near opening of superior vena cava
left horn of sinus venosus derivatives
oblique vein of the left atrium & coronary sinus
crista terminalis
internal ridge demarcating the juntion of smooth portion & trabeculated portion of atria
formation of left atrium
trabeculated portion: left side of primitive atrium
smooth portion: from reincorporated pulmonary vein
single pulmonary vein develops out of posterior wall of left atria→ branches into four & connect to lungs→ proximal portions reincorporate into left atria forming smooth portion of left atria
3 fetal shunt systems
open prenatally, close postnatally
- ductus venosus (to liver)
- foramen ovale (between atria)
- ductus arteriosus (to lungs)
circulation through fetal system
placenta→ umbilical vein→ ductus venosus→ inferior vena cava→ right atria (also receives from superior vena cava)→ right ventricle & thru foramen ovale to left atria (also receives from pulmonary veins)→ left ventricle→ aortic arch & pulmonary trunk (to aortic arch via ductus arteriosus)→ descending aorta→ internal iliac arteries→ umbilical arteries→ placenta
septum primum
thin membranous septum starts at superior medial wall of primitive atrium & grows toward the endocardial cushion
as it nears the endocardial cushion, apoptosis occurs in some superior central cells opening the ostium secudum to keep the shunt system in place
ostium primum
opening between growing septum primum & endocardial cushion
allow shunting of blood from right to left atria
ostium secundum
opening of septum primum in superior central portion
allow shunting of blood from right to left atria
endocardial cushions
form in atrioventricular region
dorsal & ventral fuse to partition AV region into left & right canals
septum secundum
thick muscular septum
grows cranial to caudally like septum secundum and just to its right
past ostium secundum, it grows outward a little bit to leave an opening creating the foramen ovales
foramen ovale
opening in caudal portion of septum secundum
prenatally: allows oxygenated blood to bypass lungs to left atrium
postnatally: higher pressure in left atrium prevents backflow of blood into right atrium & septum primum adheres to septum secundum
valve of foramen ovale
higher pressure in right atrium v. left atrium pushes septum primum into left atrium, acting as a primitive valve to foramen ovale shunt system
types of atrial septal defects
10% of congenital heart defects
females more frequent than males
- probe patent foramen ovale
- ostium secunudum defect
- endocardial cushion defect w/ostium primum defect
- sinus venosus defect
- common atria
probe patent foramen ovale
failure of septum primum to adhere to septum secundum after birth
usually small & insignificant
increased risk of migraine
25% of all people
ostium secundum defects
- reabsorption of septum primum in abnormal location
- excessive reabsorption of septum primum
- defect development of septum secundum
- combination of excessive reabsorption of septum primum & large foramen ovale
endocardial cushion defect w/ostium primum defect
septum primum doesn’t fuse w/endocardial cushions→ patent ostium primum
septum secundum never reaches EC either
associated w/mitral valve cleft
mitral valve cleft
slit-like or elongated hole usually involving anterior leaflet
sinus venosus defect
occurs in septum near superior vena cava
causes: incomplete absorption of sinus venosus into right atrium or abnormal development of septum secundum
consequences: pulmonary veins may be attached to right atrium instead of left
requires surgical repair
common atrium
aka cor tricolare biventriculare
three chambered heart= one atrium, two ventricles
very rare
failure to develop septum primum or septum secundum
associated w/heterotaxy (abnormal distribution of organs in the thorax & abdomen)
results of premature closure of foramen ovale
hypertrophy of right heart
under-development of left heart
death shortly after birth
derivatives of truncus arteriosus
proximal aorta & pulmonary trunk
derivatives of bulbus cordis
caudally: smooth right ventricle & smooth left ventricle
cranially: (aka conus cordis) proximal aorta & pulmonary trunk w/truncus arteriosus
derivatives of primitive ventricle
trabeculated portions of left & right ventricles
derivatives of primitive atria
trabeculated portions of left & right atria
derivatives of sinus venosus
right: smooth part of right atrium (sinus venarum)
left: coronary sinus & oblique vein of left atrium
interventricular spectum formation
not as complex as atrial→ don’t need shunting→ complete before birth
muscular & membranous components that fuse
formation of muscular interventricular septum
grows from expanding myocardium of ventricles (end of W4) toward endothelial cushions
stops at W7 before fusion with endothelial cushions, creating interventricular foramen
interventricular foramen
opening of the ventricular septum formed W7 when the muscular interventricular septum does not fuse with the endothelial cushions
Membranous interventricular septum
forms from right endothelial cushions extension toward muscular interventricular septum & tissue from teh airticopulmonary septum growing down from the outflow tract
ventricular spectal defects
most close spontaneously during the first year of life
more frequent in females than males
membranous: most prevalent & often associated with aorticopulmonary septal defects
muscular: single or swiss chesse defects & can fill spontaneously
cor triloculare biatriatum/common ventricle
partitioning of outflow tract
neural crest cells migrate & invade truncal (on truncus arteriosus) & bulbar (on conus cordis-cranial remenant of bulbus cordis) ridges→ grow & twist in sprial fashion→ fuse to form aorticopulmonary septum
aorticopulmonary septum
derived from neural crest cells
partitions the outflow tract to form aorta (ventral &sac) & pulmonary trunk
aortic sac
derived from truncus arteriosus
formed by aorticopulmonary septum
gives rise to right & left horns→ brachiocephalic artery, ascending aorta & proximal segment of aortic arch
persistent truncus arteriosus
always seen w/ventricular septal defect
failure of truncus arteriosus to partition→ common outflow from both ventricles→ oartially deoxygenated blood circulates (cyanosis)→ death in first 2 years
transposition of great vessels
caused by aorticopulmonary partition not spiraling when formed→ pulmonary arteries connect to left ventricle & aorta connects to right ventricle→ oxygenated blood goes back to lungs & blood from body goes around again w/o getting oxygenated
3:1 males to females
risk factors: intrauterine rubella & other viral illnesses
cyanosis in 2/3 day postnatal
incompatible w/life unless shunt system still available
treatment: prostagladin to keep ductus arteriosus open
tetralogy of Fallot
displacement of septum due to four defects:
- pulmonary stenosis (narrosing of blood vessel)
- membranous interventricular septal defect
- overriding aorta (displacement to the right)
- right ventricular hypertrophy (from working harder to get blood through stenosed pulmonary artery)
less blood reaches lungs, poor oxygenation of body, cyanosis
can be corrected surgically
lung bud formation
aka repsiratory diverticulum
W4- appears D22 & grows ventrocaudally
outcropping of endoderm from foregut
surrounding splanchnic mesoderm will form the connective tissue & musculature of the lungs
separates from esophagus by tracheo-esophageal ridges
tracheo-esophageal ridge
separates esophagus dorsally & trachea and lung buds ventrally
tracheo-esophageal fistulas
TEF
more common in males
most associated with esophageal atresia
cause: incomplete division of foregut into esophageal & respiratory portions
can cause polyhydraminos
NOT usually isolated congenital abnormality
tracheo-esophageal fistula w/esophageal atresia
upper portion of esophagus ends & lower portion branches off of posterior trachea (fistula- abnormal or surgical passage)
rapid abdomen distention- air in stomach
aspiration of food (milk) into lungs or ejected
tracheo-esophageal fistula between trachea & esophagus
aka H-type
connecting tube from esophagus to posterior traches
4% of cases
food (milk) may be driven into lungs
VACTERL syndrome
Vertebrate defects
Anal atresia
Cardiac defects
Tracheo-esophageal fistulas
Esophageal atresia
Renal abnormalities
Limb defects
VATER syndrome
Vertebrate defects
Anal atresia
Tracheo-esophageal fistulas
Esophageal atresia
Renal abnormalities
W5 lung formation features
formation of left & right lung buds during partitioning by tracheo-esophageal ridge
main & secondary bronchi (3 on tight & 2 on left)
right is straighter (more vertical) & has larger lumen than left→ more foreign objects get lodged in it
formation of vasculature
W3
sets of paired vessels
arteries: aortic arches, dorsal aorta, vitelline & umbilical arteries
veins: cardinal, vitelline, & umbilical veins
when vascular connection is made between placenta & embryo
W4
where blood vessels begin
embryo & yolk sac
Aortic arches
five paired arteries (L+R): 1, 2, 3, 4, 6 (cranial to caudal)
5’s only purpose is to kickstart the growth of 6 & degenerate
dorsally connect to dorsal aortae
descending aorta formation
fusion of right & left dorsal aorta at T4-L4
adult derivative of first aortic arch
mostly degenerates
remenants: maxillary arteries
adult derivatives of second aortic arch
most degenerates
dorsal end forms hyoid artery which later forms the stapedial arteries, which is a transient connect between external & internal carotid arteries
persistent stapedial artery
manifests as pulsatile mass in middle ear cavity
sometimes causes pulsatile tinnitus
adult derivatives of third aortic arch
right & left common carotid arteries
proximal portion of internal carotid branches
adult derivatives of fourth aortic arch
left: arch of aorta
right: proximal right subclavian artery
formation of right subclavian artery
proximally: fourth aortic arch
distally: 7th intersegmental artery
adult derivatives of sixth aortic arch
right: right pulmonary artery & grows toward lungs
left: forms ductus arteriosus (part of shunt system)→ closes after birth & becomes ligamentum arteriosum
recurrent laryngeal nerves
branch off of vagus nerves (runs anterior to arches & just medial to R subclavian & descendin aorta on L)
R: loops under & posterior to 4th aortic arch
L: loops under & posterior to 6th aortic arch (ductus arteriosus)
innervates larynx
coarctation of aorta
constriction or narrowing of aorta
subdivided by location: pre or postductal
postductal coarctations of aorta
restriction occurs below ductus arteriosus
w/ & w/o ductus arteriosus closure, most are closed
most common type of coarctation
collateral circulation thru: subclavian arteries→ internal thoracic→ anterior intercostal arteries→ posterior intercostal arteries (3rd-9th)→ thoracic aorta
dilated tortuous arteries: increased blood flow & palpable pulses (in posterior intercostal spaces)→ rib notching
blood pressure is lower in lower body & lower limbs & higher in upper limbs
preductal coarctation of aorta
restriction of aorta before the ductus arteriosus
w/ & w/o patent ductus arteriosus
patent ductus arteriosus allows blood flow to inferior body, but is deoxygenated
collateral circulation through subclavian arteries does NOT work, reason unknown
double aortic arch
persistent portion of right dorsal aorta cranial to T4
results in vascular ring that can constrict the esophagus & trachea or be asymptomatic
vitelline arteries
paired (R+L) vessels of yolk sac where they anastamose in a vascular plexus→ migrate into embryo as yolk sac regresses→ separate from descending aorta→ reattaches to descending aorta as 3 trunks
celiac, superior & inferior mesenteric arteries
celiac trunk
found at T12
supplies forgut structures (liver & spleen)
superior mesenteric trunk
found at L1
supplies mudgut structures
inferior mesenteric trunk
found at L3
supplies inferior mesenteric structures
umbilical arteries
carry deoxygenated blood & waste from fetus to placenta
initially connectes to dorsal aortae in sacrum→ loose connection (W5)→ connect to proximal segment of internal iliac arteries
thus proximal portion of umbilical arteries form distal segment of internal iliac arteries & superior vesicle arteries; distal degenerates
close a few minutes after birth do to smooth muscle contraction in vessel walls
perment fibrous closure in 2-3 months
vitelline veins
drain blood from yolk sac to heart
initially a pair that drain into sinus horns
cranial L: left hepatocardiac channel→ regresses w/left sinus horn, leaving the left hepatic vein caudally
cranial R: right hepatocardiac channel→ hepatic portion of inferior vena cava & right hepatic vein
central R+L: hepatic sinusoids & ductus venosus (venous plexus in liver)
caudal portions of both: form plexus around duodenum→ portal vein (connects hepatic sinusoids in liver & passes thru septum transversum) & splenic, superior mesenteric, and inferior mesenteric veins
umibilical veins
returns oxygenated blood from placenta to embryo
R: completely obliterated in 2nd month
L: known as definitive umbilical vein, drains into ductus venosus then inferior vena cava
after birth: intraabdominal portion becomes ligamentum teres hepatic or round ligament of the liver
common cardinal veins
drains blood from body to heart of embryo
receives drainage from anterior & posterior cardinal veins
ductus venosus
fetal shunt to bypass liver sinusoids prenatally
shunt connects hepatocardiac channel w/left umbilical vein
adult derivative: ligamentum venosum
left brachiocephalic vein formation
W8
develops form anastomoses of L+R anterior cardinal veins, when caudal left anterior cardinal vein degenerates
functions to shunt systemic blood from L to R
posterior cardinal veins
important for drainage of mesonephroi
majority degenerate
remaining portion forms Root of azygos vein (Right posterior cardinal vein) & common iliac veins
supracardinal veins
formed during late embryonic period to take over the role of posterior cardinal artery
disrupted in the region of the kidneys
subcardinal veins
formed during late embryonic period to take over the role of posterior cardinal artery
anastamose with supracardinal veins to for azygos & hemiazygos veins
pseudoglandular period
W5-17
formation of lung division thru terminal bronchioles, but not including respiratory bronchioles
repiration not yet possible
canalicular period
W16-25 (28)
terminal bronchioles give rise to repiratory bronchioles
alveolar ducts form
mesodermal tissue becomes highly vascularized
low chance of survival, but respiration is possible toward the end
terminal sac period
W24-birth
terminal sacs develop & surfactant produced
epithelium thins & capillaries come into contact forming blood-air barrier
alveolar period
birth to 8yrs-old
increasing number of alveoli & respiratory bronchioles
95% formed during this period
type I pneumocytes
differentiates from epithelium
cells across which gaseous exchange takes place
type II pnuemocytes
differentiates from epithelium
secretes surfactant, forms filmover internal wall of terminal sacs to decrease surface tension to facilitate inflation
atelectasis
partial or complete collapse of lung
Respiratory distress syndrome
prime cause: premature birth (W23-30)
signs: labored breathing, increased RR, mechanical ventilation needed, damage to alveolar lining (fluid & serum proteins leak into alveolus), & continued injury may lead to detachment of alveolar lining (causing hyaline membrane dz)
treat w/glucocorticoid to accelerate fetal lung development and surfactant production & artifical surfactant therapy
surfactant B deficiency
causes respiratory distress syndrome
autosomal recessive inheritance pattern
fatal dz
NO treatment
unilateral pulmonary agenesis
failure of one lung to develop
presentation: repiratory distress in 1st year, usually w/lower respiratory tract infection
60% have concurrent congenital abnormalities: cardiac lesions, diaphragmatic hernias, & skeletal anomalies (vetebral or costal)
higher frequency of anomallies seen with R lung agenesis
bilateral pulmonary agenesis
absence of lungs
extremely rare & always lethal
pulmonary hypoplasia
failure to obtain adequate size, but has all components
severity determines amt of compromise
may be associated w/congenital diaphragmatic hernia (abdominal organs in thorax via whole in diaphragm)
congenital cysts of lung
formed by dilation of terminal or larger bronchi
usually drain poorly causing frequent infections
diaphragm formation
divides thoracic & abdominal cavities
from: septum transversum, pleuroperitoneal membranes, dorsal mesentary of esophagus, & muscular ingrowth of somites at cervical levels C3-C5
septum transverseum
derived from mesoderm
begins to divide intraembryonic cavity into thoracic & abdominal cavities
pericardial canals: open channels left on either side from incomplete formation of septum trnasversum (the lungs grow in these)
congenital diaphragmatic hernia
1/2,000 births
when pleuroperitoneal folds fail to form properly, more often on L (called foramen of Bochdalek
results: small bowel enters thorax→ hinders pulmonary formation causing pulmonary hypoplasia
degree determines severity
can be surgically repaired
formation of IVC
Inferior vena cava
- hepatic: derived from hepatocardiac channel (from right vitelline vein)
- prerenal (suprarenal): derived from right subcardinal vein
- renal: derived from supracardinal anastomoses of right subcardinal vein
- postrenal (infrarenal): derived form right supracardinal vein
absence of inferior vena cava
failure of hepatic segment formation, et al form attachesd to azygos
blood will drain via azygos & hemizygos veins
usually associated w/heart malformations
double IVC
inferior portion of left supracardinal vein persists
left IVC typically ends at left renal vein, cross aorta, & joins R IVC
no complications
SVC formation
from an anastomoses of right common cardinal vein & right anterior cardinal vein
double SVC
cause: persistence of left anteriof cardinal vein & failure of left brachiocephalic to form
results: left SVC drains venous blood from left & drains into coronary sinus, which dilates to accommodate increased blood flow
no ill effects
left SVC in isolation
cause: failure of degeneration of left anterior cardinal vein→ anastomoses of left common cardinal vein & left anterior cardinal vein→ L SCV formation AND degeneration of right common cardinal & caudal portion of right anterior cardinal veins
no left brachiocephalic vein formed
results: blood drains to L SVC→ coronary sinus→ right atrium
left brachiocephalic formation
from anastomoses of left & right anterior cardinal veins
when caudal part of left anterior cardinal vein degenerates
changes in circulation after birth
- alveoli expand
- pulmonary vessels open & resistance reduces
- placental blood flow ceases
- above events initiate closure of shunts
- high oxygen saturated blood enters ductus arteriosus→ increase in localized O2 tension→ constriction of ductus arteriosus
- immediately after birth
- complete obliteration intima in 1-3 months
- foramen ovale closure due to pressure changes in atria
- fusion (permenant closure) takes about 1yr
patent ductus arteriosus
most common among preterm babies
can close spontaneously
treatment: in preterm, use of NSIDS or indomethacin to help close by blocking prostagladin E1 (which is keeping it open)→ will NOT work in full term babies or adults
formation of primitive gut tube
creeated by lateral folding in W3+4
all 3 layers in concentric tubes around lume
foregut
cranial portion of primitve gut tube
blood supply: celiac trunk @ T12
midgut
portion of primitive ut tube attached to the yolk sac
blood supply: superior mesenteric @ L1
hindgut
caudal portion of primitive gut tube
blood supply: inferior mesenteric @ L3
vitelline duct
opening/passageway from midgut to yolk sac
formation of vitelline duct
end of W4
constriction of midgut connection to yolk sac as craniocaudal folding takes place
incorporated into proximal umbilical cord
*formed at the same time as allantois*
ileal diverticulum
aka Meckel’s diverticulum
persistence of vitelline duct postnatally
may become inflammed & mimic appendicitis
2% pop
2” length
w/in 2’ of ileocecal valve
found under age of 2
males 2x over females
(other persistence of vitelline duct: enterocyst or vitelline fistula)
derivatives of foregut
pharynx, esophagus, stomach, superior 1/2 of duodenum
derivatives of midgut
inferior 1/2 of duodenum, jejunum, ileum, cecum, ascending colon, R 2/3 transverse colon
derivatives of hindgut
L 1/3 transverse colon, descending colon, sigmoid colon, rectum, & upper portion of anal canal
stomodeum
mouth opening created by the rupture of the buccopharyngeal (oropharyngeal) membrane
W4
cloacal membrane rupture
W7
creats opening for anus & urethra
layers of gut tube
lumen outward
- mucosa (epithelium [endodermic origin], lamina propria, & muscularis mucosae)
- submucosa
- muscularis
- serosa/adventitia
derived from splanchnic mesoderm
formation of esophagus
W3 w/formation of esphagotracheal septum
cranially: pharynx
caudally: esophagus
W4-7: elongation
histological changes: simple columnar→ stratified columnar→ multilayered ciliated→ straified squamous non-kartinated epithelium
short esophagus
cause: failure to elongate in proportion to neck & thorax development
result: congenital hiatal hernia (part of stomach displaced into thorax)
esophageal stenosis
caused: incomplete recanalization of lumen
Barret’s Esophagus
CELLO (columnar epithelium lined lower oesophagus)
- congenital: cells did not complete histological evolution→ tendency toward GERD
- acquired: abnormal change in cells, possibly caused by chronic acid exposure or reflux esophagitis
- premalignant condition
- 1-5% develop cancer
formation of stomach
end of W4/beginning W5, fusiform dilation of foregut
attached to anterior & posterior walls via ventral & dorsal mesentery respectively
dorsal grows more to create greater curvature
L+R vagus nerve run on either side
makes 90º turn counter-clockwise: greater curvature is L, lesser curvature is R, R vagus n. becomes posterior vagus n., L vagus n. becomes anterior vagus n., & dorsal mesentery is L as greater omentum
anteropsterior axis rotation: pyloris up & cephalic portion down
histologenesis of stomach
rugae & gastic pits of epithelium form during late embryonic period
cell differentiation during early fetal period
HCl production just before birth
congenital pyloric stenosis
cause: incomplete recanalization of pyloric lumen during development
symptoms: projectile vomitting during 2nd week, formation of pyloric mass, infrequent stool, dehydration & loss of subcutaneous fat
male 4x more than female
1:200 live births
Tx: surgery
derivatives of embryonic ventral mesentery
lesser omentum (hepatoduodenal & hepatogastric ligaments), falciform ligament of liver, coronary ligament of liver, & triangular ligament of liver
derivatives of embryonic dorsal mesentery
greater omentum (gastrorenal, gastrosplenic, gastrocolic, & splenorenal ligaments), mesentery of small intestine, mesoappendix, transverse mesocolon, & sigmoid mesocolon
Formation of omental bursa
aka lesser peritoneal sac
space behind stomach formed when the dorsal mesogastrium is pulled to the L during longitudinal rotation
Greater Sac
peritoneal cavity opening on left & anterior of stomach & mesentery after longitudinal rotation
epiploic foramen of Winslow
opening if the lesser omentum (between stomach & liver) connection the greater & lesser sacs
formation of greater omentum
dorsal mesogastrium extends to forma double layer sac over small intestine & transverse colon
2 layers fuse to form greater omentum, hanging from greater curvature of the stomach to protect the small intestine & transverse colon
formation of the duodenum
derivative of foregut & midgut
duodenum & head of pancreas are pressed dorsally aginst body wall after stomach rotation (retroperitoneal)
dorsal mesoduodenum fuses w/peritoneum
lesser omentum is formed from
ventral mesogastrium
development of midgut
expands to U-shpaed midgut loop in W5
cranial limb→ distal duodenum, jejunum, & upper ileum
caudal limb→ rest of ileum & rest of midgut
rapid growth of liver→ forces physiological herniation of midgut into umbilical cord in W6 & rotates 90º counterclockwise around superior mesenteric artery→ W10 abd expansion allows return to abd cavity→ +180º counter-clockwise rotation during regression & **viteline duct looses connection to intestines*→ mesenteries of ascending & descending colon fixed to peritoneum of posterior wall (retroperitoneal)
histological development of small intestine
M2, epithelium proliferates to obliterate lumen→ recanalization as multi-layered epithelium→ rearrangement of tissue to yield villi & crypts w/stem cells (simple columnar epitelium)
cell types formed by end of 2nd trimester (M6)
omphalocoele
failure of intestinal loop to return to abd cavity following physiological herniation
seen by fetal US
variation in size
has shiny coverings
frequently associated w/: fetal liver herniation w/small abd size & pulmonary hypoplasia (small lungs)
other risks: other birth defects, intestinal malrotation, & urinary anomalies
tx: bag covering & slowly push intestines inside until abd defect can be sewn shut, takes time
gastrochisis
aka cleft stomach
no shiny covering, but otherwise looks similar to omphalocoele (but rarer)
no known cause
1: 3000 births
tx: bag covering & slowly push intestines inside until abd defect can be sewn shut, takes time
congenital umbilical hernia
more common in premature births
2x male over female
intestines return to abd cavity, but ventral abd wall doesn’t close umbilical ring
protruding bowel still covered by skin
some resolve spontaneously by 2yrs-old
sx by 4yrs-old if symptomatic
non-rotation of midgut
results in small intestine on R & large intestine on L
usually asymptomatic
Mixed rotation of midgut
failure to complete last 90º rotation
results in cecum inferior to pylorus fixed to posterior abd wall by peritoneal bands
volvulus
twisting of intestines
impedes intestinal contents & compromises blood supply
cloaca
endodermal lined pouch at terminal end of hindgut
partitioned by urorectal septum into rectum, upper anal canal, & urogenital sinus
proctoderm
surface ectoderm
joined with cloaca to form cloacal membrane
cloacal membrane
joining of proctoderm & cloaca
partitioned to form anal membrane & urogenital membrane