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EMBRYOLOGY
Course Description and Rationale
Birth defects are the leading cause of infant mortality and, together with prematurity, account for
approximately 50% of all infant deaths. Furthermore, 3-6% of children will be born with a major
congenital defect, many of which could have been prevented. As a health care professional, you will
encounter women of childbearing age or who are already pregnant. Therefore, it is imperative that the
care giver realize that she or he may be providing care to two people not one and that whatever procedures
or medications are prescribed may have a serious impact on the unborn child. It is also imperative to
understand what types of health care measures can be used to prevent birth defects. This course will
describe the classical embryological events from fertilization to birth that result in a newborn child and
that provide the rationale for improving maternal and infant health. It will also focus on clinical problems
associated with birth defects and their means of prevention.
Textbook
Langman's Medical Embryology by T.W. Sadler, 14th ed. Lippincott, Williams and Wilkins, 2019.
Additional Teaching Aids
Syllabus: The syllabus is designed to focus your studying, especially the sections labeled The Bottom
Line. Knowing the material in The Bottom Line will enable you to pass the course.
Lectures
Lecture 1: From fertilization to gastrulation
Lecture 2: Derivatives of the Germ Layers and Origin of the Body Cavities
Lecture 3: Musculoskeletal
Lecture 4: Heart Development
Lecture 5: Vascular Development: Fetus and Placenta
Lecture 6: Respiratory System and Digestive System
Lecture 7: Kidneys
Lecture 8: Gonads and Genitalia
Lecture 9: Head and Neck
Lecture 10: Central Nervous System
Lecture 11: Ear and Eye
Lecture 12: Fetal Growth, Birth Defects, and Prenatal Diagnosis
Syllabus
Lecture 1: From Fertilization to Gastrulation (pp 34-71)
Objectives:
- Trace the period of development from zygote to blastocyst formation
- Understand the derivation of the cytotrophoblast and syncytiotrophoblast
- Know the origins of the epiblast and hypoblast
- Know the origins of the amniotic and yolk sac cavities
- Understand the importance of extraembryonic mesoderm in forming the chorionic cavity
- Describe primary villus formation in the placenta and the role of the cytotrophoblast and syncytiotrophoblast
- Define the term ectopic pregnancy and know where this phenomenon usually occurs
- Describe the process of gastrulation and distinguish it from the process of neurulation
- Name the 3 germ layers and describe their origins
- What is the organizer and what does it organize
- Define the term notochord and describe its significance
- When is laterality established
Terms to define: morulla, blastomeres, blastocyst, embryoblast, trophoblast, inner cell mass, outer cell
mass, embryonic stem cells, cytotrophoblast, syncytiotrophoblast, hypoblast, epiblast, extrembryonic
mesoderm, chorionic cavity, primary villi, connecting stalk, ectopic pregnancy, hydatidiform mole,
imprinting, gastrulation, primitive streak, primitive node, primitive pit, notochord, prechordal plate,
the Rectouterine (Douglas’) pouch
Week 2 is the week of 2s: 2 layers to trophoblast: synctio- and cytotrophoblast 2 layers to embryoblast: epiblast and hypoblast 2 cavities: amniotic and yolk sac (actually 3 since the chorionic cavity forms later in the week) 2 layers of extraembryonic mesoderm somatic and splanchnic
Third week: Gastrulation = the process of making 3 germ layers: ectoderm (skin, CNS), mesoderm (blood, bones, connective tissue), endoderm (gut, , gut derivatives, parenchyma of glands).
Epiblast = Forms all 3 germ layers = all of the embryo. Hypoblast disappears
Primitive streak forms at the caudal end of embryo at the beginning of the 3rd^ week: Epiblast cells migrate toward and through the streak and node to form mesoderm and endoderm; Node = organizer = cranial end of streak Cells that migrate through the cranial region of the node form the prechordal plate followed by the notochord: these 2 structures induce the CNS; eventually, the notochord forms the nucleus pulposus in intervertebral discs.
Cranial-caudal axis established by Anterior Visceral Endoderm (AVE): Secretes genes essential for head formation Head mesoderm (dorsal mesoderm = paraxial mesoderm) is organized by Goosecoid and other genes that antagonize BMP-4. BMP-4 secreted throughout the embryonic disc = ventralizes mesoderm = forms intermediate and lateral plate mesoderm: Antagonized by Goosecoid and other genes expressed by the node; hence the node is the organizer Brachyury (T gene) controls formation of dorsal mesoderm in regions caudal to the head: Expressed by the node and notochord: If decreased T gene, then results in caudal dysgenesis. PITX2 = master gene for laterality = establishes left sidedness: Upregulated by serotonin (5HT), nodal and FGFs Caudal dysgenesis (Sirenomelia; Mermaid syndrome) = insufficient mesoderm formed by gastrulation = missing kidneys, fused lower limbs.
Situs inversus = transposition of the viscera = usually no other defects Laterality sequences = incomplete situs inversus such that organ reversal only involves a few organs = often have other defects. Antidepressants causing laterality problems Trophoblast = forms villi for placenta: Primary villi = core of cytotrophoblast covered by syncytiotrophoblast; Secondary villi = core of extraembryonic mesoderm, covered by cyto, covered by with each other and to umbilical vessels to form the fetal circulation.
Week 3 = week of 3s: 3 germ layers: ectoderm, mesoderm, endoderm 3 cavities: amniotic, yolk sac, chorionic
Ectoderm: skin, CNS, PNS, eyes, internal ear, neural crest cells(bones & connective tissue of the face and part of the skull) Mesoderm: bones, connective tissue, urogenital system, cardiovascular system Endoderm: gut and gut derivatives(liver, pancreas, lungs, etc.)
Lecture 2: Derivatives of the Germ Layers and Origin of the Body Cavities (pp 72-105)
Objectives:
- Name the major derivatives of the three germ layers
- Explain why the embryonic period is considered the most critical time in human development for the induction of birth defects
- Describe the process of neurulation and understand that it overlaps with the period of gastrulation
- What is a homeobox gene? What role do they play in specifying the craniocaudal axis?
- What is the embryological basis for caudal dysgenesis (sirenomelia) and sacrococcygeal teratomas
- Determine the origin of the intraembryonic cavity
- Describe the processes of cephalocaudal and lateral folding of the embryonic disc and their significance with respect to establishment of body form
- What is the embryological basis for gastroschisis versus omphalocoele and ectopia cordis?
- Describe the subdivisions of the intra-embryonic mesoderm and the role this tissue plays in development of the intra-embryonic coelomic cavity
- Describe the role of the pleuropericardial folds in establishing the pericardial and pleural cavities
- Describe the formation of the diaphragm and explain the origins of diaphragmatic hernias Terms to define: neural plate, neural tube, neuropores, neural crest, placode, mesenchyme, paraxial
mesoderm, intermediate mesoderm, lateral plate mesoderm, somite, dermamyotome, sclerotome,
vasculogenesis, angiogenesis, head fold, tail fold, cloaca, vitelline duct, crown rump length,
intraembryonic coelom (cavity), visceral and parietal mesoderm, Homeobox genes, serous membrane,
septum transversum
(buccopharyngeal membrane) and caudal (cloacal membrane) ends: Cloaca = expanded portion of hind gut = later forms urogenital sinus and part of anal canal
Body cavity = same as intraembryonic cavity (coelom) = eventually becomes the cardiac, pleural, and peritoneal cavities = all 3 cavities derived from space between the 2 layers of the lateral plate mesoderm:
- splanchnic (visceral) layer = surrounds gut tube, heart, and lungs; 2) somatic (parietal) layer = lines body wall
2 sides of cavity are brought together by embryonic folding = caudal and cranial folds and 2 lateral folds = draws everything around the umbilical region: Failure of the folds to close = ventral body wall defects = ectopia cordis, gastroschisis, and bladder and cloacal extrophy Omphalocele = ventral body wall defect, but is not due to a closure problem; it is due to a failure of bowel loops to return to the abdominal cavity following umbilical herniation
2 layers of lateral plate mesoderm form serous membranes that secrete fluid for lubrication. 2 layers continuous at the root of each organ Gut is suspended by dorsal mesentery = double layer of peritoneum = where 2 layers are continuous
Division of cavities: Septum transversum = block of mesentery derived from splanchnic mesoderm around the heart: moves to the region between the thoracic and peritoneal cavities due to cranial folding that curved the heart into the thoracic region. Pericardioperitoneal canals = posterior to septum transversum = connect primitive pleuropericardial and peritoneal cavities Pleuroperitoneal membranes close pericardioperitoneal canals Pleuropericardial folds (membranes) grow around the heart and separate the pleural and pericardial cavities = form the fibrous pericardium
Diaphragm formed by Pleuroperitoneal membranes: form the central tendon & provide scaffold for migrating muscle cells Muscular components = from cervical myotomes C3, 4, 5 = carry phrenic nerve with them Mesentery of the esophagus = crura
Diaphragmatic hernia = usually on left = failure of muscle cells to reinforce pleuroperitoneal membrane to close pericardioperitoneal canal; can also be caused by short esophagus = abdominal organs may compress lungs and heart
Homeobox genes = contain conserved DNA binding motif from the homeotic gene complex of Drosophila; grouped into 4 clusters; regulate anterior-posterior (craniocaudal) patterning of the embryo
Period of organogenesis = 3rd to 8th weeks = very sensitive to teratogenic insult because organ primordia are forming. Embryo also sensitive in 1st and 2nd weeks when craniocaudal and left right axes are forming. Lecture 3: Musculoskeletal (pp 147-178) A. Muscular System
Objectives:
- Describe the regions of a somite that give rise to muscle cells
- Describe the muscular derivatives of the epimeres and hypomeres
- Describe the origins of the innervation of the segmental musculature
- Know the origins of head, body, limb, smooth, and cardiac musculature
Terms to define: dermomyotome, epimere, hypomere, dorsal primary ramus, ventral primary ramus,
Poland anomaly
The Bottom Line :
Muscles: Skeletal muscle: from paraxial mesoderm = myotomes form from somites and somitomeres Myotome: formed by cells at the ventrolateral lip (VLL) of the prospective myotome region and by cells from the dorsomedial lip (DML) DML contributes cells to the primaxial domain of mesoderm (also includes sclerotome and dermatome cells). VLL contributes cells to both the primaxial and abaxial domains of mesoderm. Abaxial and primaxial domains are separated by the Lateral Somitic Frontier = border between each somite and lateral plate mesoderm. Primaxial domain contains only cells from paraxial mesoderm: forms muscles of the back, shoulder girdle (rhomboids, levator scapulae, and Latissimus dorsi), and intercostals. Abaxial domain forms limb and abdominal wall (obliques and tranversus abdominus) muscles. Regardless of their final position, migrating muscle cells receive innervation from their spinal segments of origin and carry these spinal nerves with them as they migrate. Paraxial cells also form dermis on the back (from dermatomes), vertebrae, and bony parts of the ribs (from sclerotome) Abaxial cells form dermis in the body wall (from lateral plate mesoderm) and rib cartilages (from sclerotome cells that migrate across the lateral somitic frontier).
Head musculature formed by somitomeres = tongue, eye (except those of the iris = pupillary muscles = derived from the optic cup) and pharyngeal arches. Muscles in the head are patterned by connective tissue that is formed by neural crest
Limb muscles formed by VLL cells: patterned by connective tissue formed by lateral plate mesoderm regulated by Myo D genes = transcription factors
Cardiac muscle formed from splanchnic mesoderm around heart tube
Larger spaces between bones = fontanelles = “soft spots” Craniosynostosis = early fusion of the sutures = abnormal skull = many of these defects result from mutations in fibroblast growth factor receptors (FGFRs).
Viscerocranium = face = mostly from the frontonasal prominence and the 1st and 2nd pharyngeal arches = neural crest cells 1st arch = maxilla, mandible, malleus, incus; 2nd^ arch = stapes, part of hyoid bone
Limbs = buds form during 4th and 5th weeks at positions specified by HOX genes Forelimb structures specified by TBX5; hindlimb by TBX AER = apical ectodermal ridge = proximodistal growth = FGFs maintain a rapidly proliferating population of cells adjacent to the ridge = the progress zone Cell death in ridge = digits; cell death between digits separates each finger ZPA = zone of polarizing activity = cranial to caudal(anterior-posterior) patterning, thumb to little finger = sonic hedgehog (SHH) and retinoic acid = morphogens Bone patterning = HOX genes Amelia = no limbs; meromelia = short limbs; Thalidomide = limb defects, now an anticancer, anti AIDS drug so seeing thalidomide type limb defects again Polydactyly = too many digits, syndactyly = fused digits; brachydactyly = short digits
Vertebral Column: derived from somites(scleretome) and from notochord(nucleus pulposus of intervertebral disc). Caudal part of one sclerotome fuses with cranial part of another = intersegmental so that muscles bridge the vertebra to act on them = resegmentation
Lecture 4: Heart Development (pp 179-206)
Objectives:
- Determine the identity of the tinman
- Explain the role of cephalocaudal and lateral embryonic folding in positioning of the heart tube
- Define the term cardiac looping and describe its formation
- Identify the bulbus cordis, conus cordis, and truncus arteriosus and name their derivatives
- Describe the contributions of the sinus venosus to atrial development
- Describe the processes involved in septation of the atria, ventricles, and truncus arteriosus, including the role of the endocardial cushions
- Explain the embryological origins of ventricular septal defects (VSD), atrial septal defects (ASD), and transposition defects of the great vessels
- Understand that heart defects may arise very early during the establishment of laterality or later during cardiac looping and septation
- Explain the roles of the primary (PHF) and secondary (SHF) heart fields in normal and abnormal cardiac development
Terms to define: epicardium, endocardium, myocardium, cardiac loop, bulbus cordis, dextrocardia, sinus venosus, endocardial cushions, septum primum, septum secundum, ostium primum, ostium secundum, foramen ovale, heart-hand syndromes, tetralogy of Fallot, transposition of the great vessels
The Bottom Line :
Heart development starts during gastrulation when cells migrating through the lateral edges of the primitive node move in a cranial direction to establish the primary heart field(PHF). The PHF is a horseshoe shaped collection of splanchnic mesoderm cells that unite to form a tube cranial to the cranial neural folds: Later, the tube is moved to the thoracic cavity by cranial folding; lateral folding causes fusion of the 2 sides of the horseshoe shaped tube so that a single heart tube forms. BMP-2 (TGF- family) induces NKX 2-5(tinman gene) that establishes the cardiogenic field. TBX5 (T Box transcription factor) regulates septation.
The horseshoe shaped region of cardiac mesoderm represents the primary heart field and contains cardiac progenitor cells responsible for forming the left ventricle and part of the atria. These cells are patterned during the establishment of left-right symmetry as the form the PHF. The rest of the heart, including the right ventricle and the outflow tract, and part of the atria are formed by the secondary heart field (SHF), a region of splanchnic mesoderm ventral to the pharynx. These cells are responsible for lengthening the outflow tract and are regulated by FGFs secreted by neural crest cells.
Endocardium = lines heart cavity = same as the endothelial wall of blood vessels Myocardium = muscle cells = from surrounding splanchnic mesoderm Epicardium = same as visceral pericardium: parietal pericardium lines inside of fibrous pericardium. Fibrous pericardium comes from pleuropericardial folds
Cardiac looping = cranial end of the heart tube grows ventrally and to the right; caudal end grows dorsally and to the left; as this process occurs regions of the tube begin to differentiate into atria, ventricles, and outflow tract: Looping helps delineate these regions and sets the stage for septation Dextrocardia: Looping occurs in opposite direction. Can be induced during patterning of the PHF (Days 16-18) or during cardiac looping (4 th^ week)
Atrioventricular junction = canal = will be separated into 2 channels = right and left AV canals
Outflow tract = conus cordis into truncus arteriosus = will become pulmonary and aortic channels
Sinus venosus = primitive venous receiving end of the heart that has right and left sinus horns: Each horn receives umbilical, vitelline, and common cardinal veins. Veins shift to right = left sinus horn diminishes, right increases in size and is incorporated into the wall
Ventricular septal defects (VSDs) = most common: Most (80-90%) occur in muscular portion of the septum, but disappear postnatally. More serious ones usually in the membranous portion. Due to effects on PHF or with endocardial cushion growth.
Outflow tract defects due to effects on: 1) PHF (Double outlet right ventricle [DORV], transposition of the great vessels [TGA]; 2) SHF (DORV, Tetralogy of Fallot [pulmonary stenosis, over-riding aorta, VSD, and right ventricular hypertrophy]; 3) Neural crest cells [common truncus arteriosus]
Dextrocardia: heart loops the opposite way, usually associated with transposition of other organs = situs inversus = loss of left/right symmetry. May be caused during establishment of laterality or during looping. Almost any type of heart defect can be produced by abnormal laterality signaling.
Lecture 5: Vascular Development: Fetus and Placenta (pp 110-120; 206-222)
Objectives:
- Know the derivatives of the 3rd, 4th, and 6th aortic arches
- Understand that arteries shift to the left and veins to the right during development
- Describe the origin of the umbilical vein, the portal system, and the inferior vena cava
- Trace the patterns of pre- and postnatal blood flow and describe the changes that occur at birth
- Understand the importance of extraembryonic mesoderm in forming the chorionic cavity
- Describe primary villus formation in the placenta and the role of the cytotrophoblast and syncytiotrophoblast
- Understand the structure and function of the term placenta
- Know the relationship between the amnion, chorion, and uterine cavity
Terms to define: aortic arches, ductus arteriosus, double aortic arch, coarctation of the aorta, ductus
venosus, cytotrophoblast, syncytiotrophoblast, primary villi, chorion, chorion frondosum, decidua,
deciduas basalis, amniochorionic membrane, cotyledons, hemolytic disease of the newborn,
erythroblastosis fetalis
The Bottom Line :
Vascular development: Fetus Arterial System Aortic arches (5 prs.) associated with pharyngeal arches = arise from aortic sac off the heart outflow tract, course through pharyngeal arches, undergo modification: due to cell death (apoptosis) and blood flow patterns.
aortic sac splits into brachiocephalic and 1st^ part of the aortic arch
1st arch = mostly disappears, leaves maxillary artery
2nd arch = mostly disappears, leaves hyoid and stapedial arteries
3rd arch = carotid system
4th arch = persists on both sides = subclavian on the right and part of the aortic arch on the left
6th arch = forms pulmonary arteries = on left, the distal part persists and connects to the aorta as the ductus arteriousus = allows for circulation to bypass the lungs
Vitelline arteries supply the gut: celiac = foregut; superior mesenteric = midgut; inferior mesenteric = hindgut
Umbilical arteries: Form in mesoderm in the connecting stalk and make connections with the common iliac arteries: ultimately become internal iliac and superior vesicular arteries and medial umbilical ligaments
Arterial Defects: 1). Patent ductus 2). Coarctation of aorta: preductal and postductal (80%) = blood finds ways around the block. 3). Double aortic arch = difficulty swallowing = both parts of dorsal aorta remain 4).Interrupted aortic arch = abnormal regression of the 4th arch on the left 5). Abnormal right subclavian artery Venous system Vitelline v = gut and liver, left disappears; right forms hepatic sinusoids, hepato cardiac portion of inf vena cava, portal v., sup mesenteric v.
Umbilical v: right disappears; left connects placenta to inf vena cava= ductus venuosus = bypasses Liver: right umbilical v ultimately becomes the ligamentum teres; ductus venosus becomes ligamentum venosum
Cardinal v: drain body wall bilaterally: As organs form, new veins develop to drain these organs and primary vessels form on the right so that left to right connections are made to the right side Anterior and post cardinal v drain to common cardinals to primitive atrium A left to right anastomosis occurs between ant card v = left brachiocephalic v: Ant card v on both sides form jugular system Post card v disappear and are replaced by: 1) supracardinals = body wall via intercostals; right forms the azygous v, left forms hemiazygous v: left to right connection forms between them; 2)subcardinals = kidneys; left to right connection = left renal v; 3) sacrocardinals = lower limbs = left to right connection = left connom iliac v
Chorion fuses with outer wall of uterus obliterating uterine cavity Cotyledons = septa from deciduas basalis that separate villi into clusters: total = 15-
Placental circulation: fetal separate from maternal, but still get some fetal cells into maternal circ = can lead to an antibody response by mother against fetal red blood cells = erythroblastosis fetalis (hemolytic disease of the newborn Placental functions: Exchange gases, nutrients etc., transmission of antibodies, hormone production = progesterone
Lecture 6: Respiratory System & Digestive System (pp 223-255)
A. Respiratory System
Objectives:
- Know how the lung bud forms and is separated from the gut tube
- Understand the origin of tracheoesophageal fistulas
- Understand the origin and relationships of the visceral and parietal pleura and the pleural cavity
- Describe the factors involved in lung maturation, including the role of alveolar type I and II cells
- Define the terms respiratory distress syndrome and hyaline membrane disease
Terms to define: respiratory diverticulum, tracheoesophageal septum, pleural cavity, visceral and
parietal pleura, alveoli, type I and II alveolar cells, respiratory distress syndrome, hyaline membrane
disease, surfactant
The Bottom Line :
Lung bud (respiratory diverticulum) grows off foregut: endoderm forms lung cells, splanchnic mesoderm surrounding gut tube forms connective tissue and bronchial cartilages Tracheoesophageal septum = separates esophagus and trachea Tracheoesophageal atresia with or without fistulas results from abnormal septation
Lung bud divides = bronchial buds = divides and branches into lungs to create bronchopulmonary segments and ultimately alveoli. Lungs keep making divisions (6) postnatally
Cells in lungs = alveolar cells = derived from endoderm: Type I alveolar cells form the blood air barrier = very thin Type II alveolar cells make surfactant, a phospholipid, that decreases surface tension = essential to keep alveoli open = not made until 28 weeks = premature
babies have trouble breathing because they have not made enough surfactant = respiratory distress syndrome (hyaline membrane disease): Treat with steroids and artificial surfactants Pleura: visceral (around lung, derived from splanchnic mesoderm); parietal = around body wall. Two are continuous at hilus area: space between layers = pleural cavity
B. Digestive System
Objectives:
- Understand the relationship of the visceral and parietal peritoneum, mesenteries, and the peritoneal cavity
- Know the location and ultimate fate of the ventral mesentery
- List the derivatives of the fore-, mid-, and hindgut regions and briefly describe their morphogenesis
- Describe the formation of the liver and its function during fetal life
- Describe the process of gut rotation and its role positioning the derivatives of the gut table
- Understand that the mesentery to the midgut and hindgut remains as a continuous structure even though parts of the gut fuse to the posterior body wall. This continuity is important for surgical procedures involving the abdominal cavity.
- Describe the origin of the lesser sac and epiploic foramen (of Winslow)
- Describe the vascular supply of the primitive gut tube. How does this arrangement compare to that in the adult?
- Define the term physiological umbilical herniation and the time and reasons for its occurrence
- Describe the embryological origin of the following defects: congenital umbilical hernia, left sided colon, Meckel's diverticulum, gut atresia and stenosis, gastroschisis, and omphalocele
Terms to define: parenchyma, mesentery, intraperitoneal, retroperitoneal, omental bursa, lesser omentum, epiploic foramen (of Winslow), falciform ligament, portal triad, primary intestinal loop, vitelline duct, physiological umbilical herniation, annular pancreas, mobile cecum, volovulus, omphalocele, gastroschisis, Meckel’s diverticulum, gut atresia and stenosis, urorectal septum, urorectal fistula, rectovaginal fistula
The Bottom Line : Mesentery = double layer of peritoneum that maintains gut tube and its derivatives in their normal anatomical positions. Visceral peritoneum = around the organ , derived from splanchnic (visceral) mesoderm surrounding the gut tube; parietal peritoneum = on body wall, derived from somatic (parietal) mesoderm Both visceral and parietal layers are continuous where parietal layer leaves body wall = forms a mesentery in this region
Mesenteries = suspend organs from body wall = allow for passage of blood and lymph vessels and nerves Dorsal mesentary, = a continuous sheet of tissue extending from the caudal region of the esophagus to the end of the hind gut. Regions of dorsal mesentery named according to their attachment to gut tube.
Omphalocoele = gut fails to return = usually associated with other defects, also with increased AFP Gastroschisis = gut herniates directly through the body wall due to failure of the body wall to close = usually few other defects Vitelline duct = connects yolk sac to midgut = if remains = Meckel's diverticulum Atresias and stenosis of midgut = vascular accidents
Hindgut extends from left third of the transverse colon to upper two thirds of anal canal ends in cloaca Urorectal septum separates cloaca from hindgut: Hindgut portion forms rectum and upper part of the anal canal (lower portion of the anal canal is derived from proliferation of ectoderm to formthe anal pit); Remainder of cloaca becomes the urogenital sinus Anal canal supplied by superior and middle rectal arteries (upper two thirds) and inferior rectal artery (lower third, because the lower part is derived from ectoderm) Failure of the urorectal septum to separate hindgut form cloaca results in urorectal fistulas (males) and rectovaginal fistulas (females) Imperforate anus = ectoderm from anal pit fails to contact caudal end of the hindgut Congenital megacolon(Hirschsprung’s disease = no ganglia in smooth muscle of gut = no neural crest = no mobility Lecture 7: Kidneys (pp 256-266) Objectives:
- Describe the role of the intermediate mesoderm in development of the urinary system
- Define the terms pronephros, mesonephros, and metanephros
- List the derivatives of the ureteric bud and the metanephric mesoderm
- Understand the importance of epithelial mesenchymal interactions in kidney development
- Describe the embryological origin of congenital cystic kidney, renal agenesis, double ureter, and horseshoe and pelvic kidneys
- Describe the formation of the urinary bladder and the urogenital sinus
Terms to define: pronephros, mesonephros, metanephros, urogenital ridge, ureteric bud, calyces,
nephron, glomerulus, renal corpuscle, Bowman’s capsule, pelvic kidney, horseshoe kidney, urachus,
urorectal septum, bladder extrophy
The Bottom Line :
Urogenital system = mostly from intermediate mesoderm
3 kidneys in succession: pronephros = cervical = non-functional mesonephros = thoracolumbar; may function for a short time: duct = mesonephric duct
metanephros = definitive kidney; begins to function in the 12th^ week
Collecting system = ureteric bud off mesonephric duct grows into and induces metanephric blastema = (intermediate) mesoderm. Bud continues to divide = forms ureter, renal pelvis, major and minor calyces, collecting tubules
Metanephric mesoderm induced by ureteric bud forms filtration system = glomerulus, Bowman's capsule, proximal convoluted tubule, loop of Henle, and distal convoluted tubule. WT 1 gene is the master gene for kidney development and it allows mesoderm to be induced by the ureteric buds: Development continues to be dependent upon an interaction between branches of the ureteric bud and the metanephric blastema: Mutations in WT cause Wilm’s tumor Renal agenesis occurs when induction between the epithelium of the ureteric bud and mesoderm from the metanephric blastema fails (another example of an epithelial- mesenchymal interaction)
Congenital polycystic kidney = cysts = form from collecting ducts (= autosomal recessive form of the disease, which is progressive and usually causes renal failure in infancy or early childhood); or from all parts of the nephron = autosomal dominant form = less progressive and more common
Kidneys form in pelvis: Differential growth moves them into lumbar region. If kidneys fuse = horseshoe kidney = gets stuck on inferior mesenteric artery
Urorectal septum, a wedge of mesoderm, grows caudally and divides the cloaca into the anorectal canal (hindgut), posteriorly and urogenital sinus, anteriorly: Bladder forms from upper part of urogenital sinus: Expansion of this region causes an incorporation of the mesonephric ducts into the posterior wall of the bladder (the trigone) and causes the ureters to enter the posterior wall: Expansion of the posterior wall causes the mesonephric ducts to move lower to enter urethra where prostate forms. In the female the portion of the mesonephric ducts that is not incorporated into the bladder degenerates
Urachus (old allantois) extends from the urogenital sinus to the umbilicus: Normally it degenerates to become the median umbilical ligament; if it stays open = urachal fistula
Lecture 8: Genital System (pp 267-283)
Objectives:
- Define the terms genital ridge and indifferent gonad and describe the changes that occur when the primordial germ cells arrive carrying either an XX or XY chromosome complement
- Contrast the development of the mesonephric and paramesonephric duct systems and their derivatives in the male and female
- Describe the formation of the vagina
