1 Muskuloskeletal Development Towards the end of the fourth week the limbs begin to develop from limb buds made up of mesenchyme somatic mesoderm covered with surface ectoderm ID: 774837
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SYSTEMIC EMBRYOLOGY
Friday, June 14, 2013
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Slide2Muskuloskeletal Development
Towards the end of the fourth week the limbs begin to develop from limb buds made up of mesenchyme (somatic mesoderm) covered with surface ectoderm. The apical ectodermal ridge at the tip of each limb bud induces the mesenchyme beneath it to elongate. At the end of each limb the hand or foot first develops as a single flat outgrowth, then programmed death of selective cells (apoptosis) causes it to divide into distinct digits.
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Slide3Movement of Limbs
Initially the limbs develop high on the trunk where they are supplied by the ventral rami of adjacent spinal nerves. Spinal roots C5 – T1 supply the upper limb bud and L2 – S3 supply the lower limb bud. During weeks six through eight the limbs descend to their adult height taking their nerve supply with them.
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Slide4To attain adult anatomical position, the upper and lower limbs rotate in opposite directions and to different degrees, with the result that the adult elbow points posteriorly and the adult knee points anteriorly.
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Slide5Skeletal Elements
Cartilaginous bones begin to develop from chondrification centers early in the fifth week. Ossification of the long bones (osteogenesis) begins from primary ossification centers, which appear in the middle of the long bones in the seventh week. Ossification of the carpal (wrist) bones does not begin until approximately the first year after birth. The skeletal muscle of the limbs is derived from myotomal cells that migrate into the limbs, followed by the branches of their associated spinal nerves.
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Slide6Limb Malformations
Amelia is complete absence of one or more limbs. Phocomelia is a defect wherein the upper portion of a limb is absent or poorly developed, so that the hand or foot attaches directly to the body by a short, flipperlike stump. These defects are often due to a failure of inductive signaling factors, and may inherit in a Mendelian fashion.
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Slide7Malformations of Hands and Feet
Syndactyly is congenital anomaly characterized by two or more fused fingers or toes. Macrodactyly (megadactyly) is enlargement of one or more digits. Polydactyly is a condition wherein there are extra digits, whereas in ectrodactyly there are fewer than normal.
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Slide8Clubfoot (talipes equinovarus)
Clubfoot is a common foot malformation (1/5,000 infants) characterized by abnormal positions of the foot (e.g., inverted). Some cases result from compression of the infant in the uterus (e.g., with oligohydramnios)
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Slide9Achondroplasia
One form of congenital dwarfism resulting from improper development of cartilage at the ends of the long bones.
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Slide10Cardiovascular System
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Slide11Early Development
The heart and major blood vessels arise from blood islands or hemangioblastic tissue derived from the mesoderm.The heart begins to form in the third embryonic week.One embryonic and two extraembryonic (umbilical and vitelline) vascular circuits are completed by the end of the first month of development.
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Slide12Development of the Heart and Vascular Circuits
The endocardial tubes are formed deep to the epimyocardial (myocardial mantle) thickenning of splanchnic mesoderm by the coalescence of blood islands.These tubes run longitudinally and are deep to the horse-shoe shaped prospective pericardial cavity.
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Slide13With the lateral folding and forward growth of the embryo, the endocardial tubes are shifted ventrocaudally and fuse in the midline.The adjacent epimyocardium fuses in the midline around the fused endocardial cavity by the dorsal mesocardium.The coalescence of other blood islands in the embryo forms blood vessels that in continuity with the heart tube.In the embryonic circulation, paired anterior and posterior cardinal veins drains the embryo cranial and caudal to the heart, respectively, and join to form the paired common cardinal veins (ducts of Cuvier).
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Slide14These veins drain into the caudal extent of the endocardial tube at the sinus venosus.Blood leaves the cranial extent of the endocardial tube and is distributed into five paired aortic arches that pass dorsally around the forgut in the branchial arches to empty into the paired dorsal aortae.Blood then circulates through branches of the aortae to capillaries that are in continuity with tributaries of the cardinal veins.
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Slide15Blood vessels developing in the placenta (chorion) are linked to the embryonic circuit to form an umbilical (i.e. allantoic, placental) circuit.In this circuit, umbilical arteries arise from the aorta, pass through the body stalk, and go to capillaries of the placenta.Oxygenated and nutritive blood returns by the left umbilical vein to the sinus venosus.The right umbilical vein disappears soon after it is developed.The vitelline circuit involves vascular channels in the yolk sac.
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Slide16Vitelline (omphalomesenteric) arteries arise from the abdominal aorta and pass along the yolk stalk to capillaries in the yolk sac.Blood returns to the sinus venosus by vitelline (omphalomesenteric) veins.After birth, the umbilical arteries will remain, in part, as a portion of the internal iliac and superior vesical arteries and the lateral umbilical ligaments.The umbilical veins persists as the round ligaments of the liver.Portions of the vitelline veins become the portal vein.The vitelline arteries fuse with each other and give rise to the superior mesenteric artery.
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Slide17Folding and Partitioning of the Heart
With fusion of the endocardiac tubes, several dilatations becomes apparent.These are, from cephalic to caudal, the bulbus cordis (truncus arterosus plus the cornus arterosus), ventricle, atrium and sinus venosus.
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Slide18Arteries leave the cephalic end of the bulbus cordis from a swelling called the aortic bulb (aortic sac).Veins enter at the sinus venosus.With the lost of dorsal mesocardium, except where the veins and arteries enter and leave, the heart begins to flex into an S-shaped structure.
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Slide19The first flexor occurs at the junction of the bulbus cordis and ventricle.The second flexure causes sinus venosus and atrium to shift dorsally.The adjacent bulboventricular walls disappear, and this part of the bulbus and primitive ventricle become part of a common ventricular chamber.
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Slide20The atrium becomes sandwitched between the pharynx dorsally and the rest of the cornus and truncus ventrally, causing the antrium to bulge laterally into a right and left swelling.The sinus venosus is shifted to the right and eventually is incorporated into the primitive right atrial swelling.
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Slide21The pattern of blood flow is from veins to common atrium, to common ventricle, to conus, to truncus, to aortic bulb, and then to aortic arches,During the second month of the development, the heart is partitioned into four chambers (two atria and two ventricles); atrioventricular (A-V) valves are formed, and conus to truncus and aortic bulb are partitioned into ascending aorta and pulmonary trunk.
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Slide22In partitioning of the antrium, endocardial tissue from the dorsal and ventral walls fuses into an endocardial cushion that separates the A-V communication into right and left A-V canals.While this is taking place, an endocardial septum primum grows towards the endocardial cushion from the dorsal wall of the antrum.Before fusing with the cushion, an ostium primum exists temporarily between the free margin of the septum primum and the cushion.The ostium will not disappear before an ostium secundum arises from the degeneration of the septum primum cephalically.
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Slide23In the seventh week of development, , a septum secundum grows dorsocaudally to the right of the septum primum and leaves a crescentic free area only by septum primum.The communication from the right to the left atrium through the crescentic opening and ostium secundum is the foramen ovale.The valve of the foramen ovale is part of the septum primum. The interatrial septum thus arises from septum primum and septum secundum.
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Slide24The sinus venarum of the right atrium is formed by the incorporation of the sinus the sinus venosus into the right atrium so that the developing great veins enter independently.The smooth-surface portion of the left atrium arises after the absorption of the common trunk of the pulmonary veins, thus leaving four pulmonary veins entering at the boundaries of this area.In septation of the aortic bulb, truncus arteriosus, a ridge of endocardial tissue develops on opposite walls of each these structures.These ridges fuse in the middle of the lumen to form a bulbar(i.e. aortic conal, truncal) septum.The septum spiral about 180 degrees as it descends from the aortic bulb into the conus, thus establising a pulmonary trunk that interwines with ascending aorta.
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Slide25Semilunar valves develop in these vessels and are localized swellings of endocardial tissue.The conal septum eventually descends to help close the interventricular septum.In development of A-V valves, subendocardial and endocardial tissues project into the ventricle just below the A-V canals.These bulges of tissue are excavated from the ventricular side and invaded by muscle.Eventually all of the muscles disappears, except that remaining as papillary muscles, and three right cusps of the right A-V valve and two cusps of the left A-V valve remain as fibrous structures.
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Slide26Fates of Embryonic Dilatations of the Primitive Heart Tube
Embryonic DilatationAdult StructureSinus venosusSmooth part of right atrium (sinus venarum), coronary sinus, oblique vein of left atriumPrimitive atriumTrabeculated parts of right and left atriaPrimitive ventricleTrabeculated parts of right and left ventriclesBulbis cordisSmooth part of right ventricle (conus arteriosus), smooth part of left ventricle (aortic vestibule)Truncus arteriosusAorta, pulmonary trunk
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Slide27Development of Major Arteries
Five pairs of aortic arches develop cephalocaudally in the branchial arches.The bridge from the ventral aortic roots to the dorsal aortae.In comparative studies, the five aortic arches, the 1st , 2nd , 3rd , 4th , and 6th aortic arches.
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Slide28In humans, the first, second and the distal part of the right sixth arches (fifth) disappear.The remaining aortic arches, ventral aortic roots, and dorsal aortae give rise to major arteries.The internal carotid arteries develop from the 3rd aortic arches and the dorsal aortae cephalic to the 3rd arches.
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Slide29The common carotids arise from the ventral aortic roots and the proximal part of the 3rd arches.The external carotids arise in a similar position to the ventral aortic roots lying cephalic to the 3rd arches.The right subclavian artery arises from the right 4th arch, the 7th dorsal intersegmental artery, and the intervening portion of the right dorsal aorta.
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Slide30The left subclavian artery arises from the left 7th dorsal intersegmental artery.The arch of the aorta develops from the left 4th aortic arch and some septation of the aortic bulb.The pulmonary arteries arise from the proximal portions of the 6th arches along with some new vascular buds.The ductus arteriosus, linking the pulmonary trunk with the aorta, is the distal portion of the left 6th arch.
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Slide31The brachiocephalic artery originates from the right ventral aortic root between the 4th and the 6th arches.The right dorsal aorta caudal to the right 7th dorsal intersegmental arteries disappears down to the embryonic low thoracic region where the paired dorsal aortae had fused into one midline vessel.The dorsal aortae between the 3rd and 4th arches degenerate.
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Slide32Development of Major Veins
The superior and inferior vena cavae and the portal veins arise from early embryonic vessels.The superior vena cava forms from the right common cardinal vein and a caudal portion of the right anterior cardinal vein up to the entrance of the left brachiocephalic vein.This vessel arises from a thymicothyroid anastmosis of veins.
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Slide33The right brachiocephalic develops from the right anterior cardinal vein between the anastomotic venous attachment and the right 7th intersegmental vein (right subclavian).The left common cardinal vein and part of the left horn of the sinus venosus become the coronary sinus, which drains the heart wall into the right atrium.
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Slide34The inferior vena cava, from the heart to the common iliacs, arises from the following vessels:A small portion of the right vitelline veinA new vessel in the mesenteric fold of the degenerating mesonephros,The right subclavian vein, and A sacrocardinal vein joining the caudal extent of the posterior cardinal veins.
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Slide35The subcardinals and their anastomosis, which developed to drain the mesonephros, also gives rise to the renal, gonadal, and suprarenal veinsThe azygos venous system arises mostly from the supracardinal veins and their anastomosis.The most cephalic portion of the azygos vein is derived from the right posterior cardinal vein.The portal and hepatic veins arise from the vitelline veins and their anastomosis.
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Slide36Fetal Circulation
The circulation of the blood in the embryo results in the shunting of well-oxygenated blood from the placenta to the brain and the heart, while relatively desaturated blood is supplied to the less essential structures.Blood returns from the placenta by the way of the left unbilical vein and is shunted in the ductus venosus through the liver to the inferior vena cava and then to the right atrium.
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Slide37Relatively little mixing of oxygenated and deoxygenated blood occurs in the right atrium because the valve overlying the orifice of the inferior vena cava directs the flow of oxygenated blood from the vessels through the foramanen ovale into the left atrium, and deoxygenated blood from the superior vena cava is directed through the tricuspid valve into the right ventricle.
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Slide38From the left atrium, the oxygenated blood and a small amount of deoxygenated blood from the lungs pass into the left ventricle and then into the ascending aorta from which it is supplied to the brain and the heart through the vertebral, carotid, and coronary arteries.
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Slide39Because the lungs of the fetus are inactive, most of the deoxygenated blood from the right ventricle is shunted by the way of the ductus arteriosus from the pulmonary trunk into the descending aorta.This blood supplies the abdominal viscera and the inferior extremities and is carried to the placenta for oxygenation through the umbilical arteries arising from the aorta.
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Slide40Production of Blood
Production of blood (hemopoiesis or hematopoiesis) begins first in the yolk sac wall about the third week of development. Erythrocytes produced in the yolk sac have nuclei. Blood formation does not begin inside the embryo until about the fifth week. Erythrocytes produced in the embryo do not have nuclei (unucleated). Hematopoiesis inside in the embryo occurs first in the liver, then later in the spleen, thymus, and bone marrow.
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Slide41Circulatory Changes at Birth
At birth, placental blood flow ceases and lung respiration begins. The sudden drop in right atrial pressure pushes the septum primum against the septum secundum, closing the foramen ovale. The ductus arteriosus begins to close almost immediately, and may be kept open by the administration of prostaglandins. Other embryonic circulatory vessels are slowly obliterated and remain in the adult only as fibrous remnants.
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Slide42Adult Remnants of Fetal Circulatory Structures
Fetal StructureAdult RemnantForamen ovaleFossa ovalis of the heartDuctus arteriosusLigamentum arteriosum Left umbilical vein Extra-hepatic portionLigamentum teres hepatis Intra-hepatic portion (ductus venosus)Ligamentum venosum Left and right umbilical arteries Proximal portionsUmbilical branches of internal iliac arteriesDistal portionsMedial umbilical ligaments
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Slide43Congenital Anomalies of the Heart and Blood Vessels
The complicated sequence of development in the heart and the major vessels accounts for many congenital abnormalities that, alone or in combination, may affect these structures.These include:Septal defectsInterventricular Septal defectsCongenital pulmonary stenosisTetralogy of FallotTransposition of the great vesselsAorta stenosis and Aorta coarctionAbnormal development of the aortic arches
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Slide44Septal Defects
Septal defects include paten foramen ovale and other atrial or ventricular septal defects.Anostium secundum (foramen ovale) defect lies in the interatrial wall and is relatively easy to close surgically.An ostium primum defect lies directly above the A-V boundary and is often associated with a defect in the membranous part of the interventricular septum and in the A-V valves.A high interatrial septal defect may result, which most likely is an improper shifting and incorporation of the sinus venosus into the right atrium.
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Slide45Interventricular Septal Defects
Interventricular Septal Defects usually involve the membranous part of the interventricular septum and are due mostly to improper formation of the conal septum.Rarely, the septal defect is so large that the ventricle forms a single cavity, resulting in a trilocular heart.This defect is caused by improper development of primitive muscular interventricular septum.Failure of closure of the interventricular foramen also may be caused by defective development of the septum membranaceum contribution from the fused endocardial cushions
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Slide46Congenital Pulmonary Stenosis
Congenital Pulmonary Stenosis may involve the trunk of the pulmonary artery and its valve or the infundibulum of the right ventricle.If this is combined with an interventricular septal defect, the conpensatory hypertrophy of the right ventricle develops sufficiently high pressure to shunt blood through the defect into the left side of the heart.This mixing of blood results in the child’s being cyanosed at birth.
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Slide47Tetralogy of Fallot
Tetralogy of Fallot is the most common congenital abnormality causing cyanosis.It is comprised of pulmonary stenosis, right ventricular hypertrophy, an interventricular septal defect with an overriding aorta, the orifice of which lies cranial to the septal defect and receives blood from both ventricles.
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Slide48Transposition of the Great Vessels
Transposition of the Great Vessels is caused by improper spiraling of the bulbar septum in the formation of the great vessels.This results in either complete transposition, in which the aorta is from the right ventricle and the pulmonary trunk is from the left ventricle, or in incomplete transposition in which both vessels are reversed but both exit from the right ventricle.
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Slide49Aortic Stenosis and Aortic Coarction
Aortic Stenosis is caused by either bulbar septum displacement or localized improper growth in supravulvular, vulvular, and subvulvular regions of the aorta.Aortic Coarction is caused by abnormal retention of the fetal isthmus of the aorta or to incorporation of smooth muscle from the ductus into the wall of the aorta.
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Slide50Abnormal Development of the Aortic Arches
Abnormal Development of the Aortic Arches may result in the arch of the aorta lying in the right or actually being double.Double aorta is caused by retention of the right dorsal aorta between the 7th dorsal intersegmental artery and the point of fusion of the aortae.If this portion remains and the right 4th aortic arch disappears, then the right subclavian arises from the aorta.
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Slide51Respiratory System
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Slide52Respiratory System
The primordium of the lower respiratory system develops in about the fourth week. The laryngotracheal diverticulum arises from endoderm on the ventral wall of the foregut. Tracheoesophageal folds develop on either side and join to form a tracheoesophageal septum that separates it from the rest of the foregut.
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Slide53This divides the foregut into the laryngotracheal tube (ventral) and the esophagus (dorsal). The caudal end of the laryngotracheal diverticulum enlarges to form the lung bud, which is surrounded by splanchnic mesenchyme.
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Slide54Larynx
The opening of the laryngotracheal tube becomes the inlet of the larynx. The laryngeal cartilages are derived from the fourth and sixth pharyngeal arches.
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Slide55Trachea
The epithelium and glands of the trachea develop from the endoderm of the laryngotracheal tube. The cartilage, connective tissue, and smooth muscle are derived from the surrounding splanchnic mesenchyme.
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Slide56Bronchi
At the end of the fourth week the lung bud divides into two bronchial buds, which enlarge to form the primary bronchi. The right bronchus is larger and more vertically oriented than the left one, and this relationship persists throughout life. In the fifth week, each bronchial bud divides into secondary bronchi. In the eighth week the secondary bronchi divide to form the segmental bronchi (tertiary bronchi), ten in the right lung and eight in the left.
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Slide57Each segmental bronchus becomes a bronchopulmonary segment (segment in a lung). The smooth muscle, connective tissue, and cartilaginous plates in the bronchi are derived from splanchnic mesenchyme.
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Slide58Stages of Lung Development
Time periodStageNotesWeeks5 – 17PseudoglandularDeveloping lungs resemble an exocrine gland. Respiration is not possible. Fetuses born during this period cannot survive. Weeks16 – 25CanalicularTerminal bronchioles divide and primitive alveolar sacs (terminal sacs) develop. Some respiration may be possible towards the end of this stage. Fetuses born towards the end of this period (weeks 22-25) can survive if given intensive care but often die anyway.Week 24 – birthTerminal sacMany more alveoli develop, and the epithelium lining the terminal sacs become thin enough to allow respiration. Type I and Type II pneumocytes develop. Type II pneumocytes begin producing pulmonary surfactant, which counteracts surface tension and facilitates expansion of the terminal sacs at birth. Fetuses born after 24 weeks may survive, and those born after 32 weeks have a good chance of survival.Birth – year 8AlveolarRespiratory bronchioles, terminals, alveolar ducts continue to increase in number
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Slide59Tracheoesophageal Fistula
An abnormal communication between the trachea and esophagus due to incomplete separation of the trachea and esophagus during the fourth week of development. It is commonly associated with esophageal atresia. Newborn infants with these malformations cough and choke during eating due to the aspiration of food and saliva into the lungs.
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Slide60Respiratory Distress Syndrome
Respiratory Distress Syndrome is common in premature infants and is due to a deficiency of surfactant. It is commonly associated with hyaline membrane disease in which the alveolar surfaces of the lungs are coated with a glassy hyaline membrane. Treatment with thyroxin and cortisol can increase production of surfactant.
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Slide61Pulmonary Hypoplasia
Pulmonary hypoplasia results when lungs are compressed by abnormally positioned abdominal viscera and cannot develop normally or expand at birth. It is commonly caused by congenital posterolateral diaphragmatic hernia.
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Slide62Diaphragmatic Hernias
Diaphragmatic Hernias can arise from improper formation to the septum transversum, the pleuroperitoneal folds, or muscular components from the body wall
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Slide63Digestive System
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Slide64Development of the Gut
The endodermal foregut gives rise to the pharynx, esophagus, stomach, liver, pancreas and a pair of the duodenum.The midgut gives rise to the rest of the small intestine, ascending colon, and proximal two-thirds of the transverse colon.
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Slide65The hindgut develops into the rest of the large intestine as far as the upper part of the anal canal.The lower part of the rectum and much of the anal canal is established by the separation of the cloaca into dorsal anorectal canal and ventral urogenital sinus by urorectal septum.The rest of the anal canal develops from an ectodermally lined anal pit.
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Slide66The stomach appears in the 4th embryonic week as a dilation of the foregut.As it shift caudally from its position above the septum tranversum, it rotates so that its original left surface faces anteriorly and its dorsal greater curvature extends to the left.The intestines develop from the caudal part of the foregut and the cephalic and caudal limbs of the midgut loop that extends into the belly stalk.
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Slide67The cephalic limb extends from the upper duodenum to the yolk stalk.It gives rise to the rest of the small intestines, except the last portion which includes 40 to 50 cm of ileum.The caudal limb extends from the yolk stalk to the hindgut, and it gives rise to the rest of the ileum, the cecum, the ascending colon, and the proximal two-thirds of the transverse colon.
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Slide68As the loop develops, it rotates counterclockwise ( in anteroposterior view) around the omphalomesenteric (vitelline) artery, which becomes the superior mesenteric artery.This rotation places the transverse colon above the jejunum and ileum anterior to the duodenum, and just below the stomach.
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Slide69By the 10th week of development, the abdomen enlarges, and the gut loop reenters the abdomen.The cephalic limb enters first, crowding the descending colon to the left.Partial persistence of the yolk stalk may remain as a Meckel’s diverticulum attached to the ileum 40 to 50 cm from the ileocolic junction.
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Slide70Development of the Liver
The liver arises in the 4th embryonic week as a ventral diverticulum of the foregut.This diverticulum grows through the ventral mesentery and into the caudal face of the septum transversum.The more proximal part of the hepatic diverticulum gives rise to the common bile duct, cystic duct, gallbladder, and hepatic ducts.
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Slide71The more distal portion differentiates into the hepatic plates and the smaller bile ducts.Because the liver grows in the septum transversum and bulges from the caudal face, it is covered by peritoneum lining the septum transversum except at the bare area of the liver where it abuts directly against the diaphagm
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Slide72Development of the Pancreas
The pancreas form from the dorsal and ventral endodermal buds located at the level of the duodenum.The dorsal bud grows into the dorsal mesentery.The proximal portion of the ventral bud joints with the common bile ducts, whereas the distal portion grows into the dorsal mesentery and fuses with the dorsal bud.
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Slide73The anterior portion of the duodenum grows more exclusively than the dorsal part does.The pancreatic duct (of Wirsung) develops from the ventral bud and the distal part of the dorsal primordium.The proximal portion of the dorsal bud may gives rise to the accessory duct (of Santorini).
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Slide74Abdominal, Mesenteries and Spleen
The abdominal mesenteries develop primarily from the embryonic dorsal mesentery.The ventral mesentery may give rise to the lesser omentum and the falciform ligament.Although the falciform ligament is formed from a shearing of peritoneum covering the anterior body wall, the peritoneum covering the liver reflects the bare area of the liver to form the coronary and triangular ligaments of the liver.
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Slide75Much of the dorsal mesogastrum suspending the stomach fuses with the dorsal body wall to form the dorsal lining of the lesser sac.The rest of the dorsal mesogastrium fuses with the embryonic transverse mesocolon to form the definitive mesentery of the transverse colon and then drapes over the small intestine to become the greater omentum.The spleen develops from the mesoderm of the dorsal mesogastrium.
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Slide76Most of the dorsal mesentery of the duodenum fuse with the dorsal body wall, making it and the pancreas, secondarily retroperitoneal.The dorsal mesentery of the jejunum and ileum becomes the mesentery proper.Most of the dorsal mesentery of the ascending and descending colon fuses with the dorsal body wall.The dorsal mesentery of the rest of the hindgut becomes the transverse mesocolon and the sigmoid mesocolon.
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Slide77Summary of the Derivatives of the Three Parts of the Primitive Gut
RegionArteryVentral Mesentery DerivativesDorsal Mesentery DerivativesForegutCeliac arteryFalciform ligament, lesser omentum, capsule of the liverGreater omentumMidgutSuperior mesenteric artery…………………….Mesentery part of transverse mesocolonHindgutInferior mesenteric artery………………………..Part of transverse mesocolon, sigmoid colon
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Slide78Congenital Malformations of the GIT
Clinical Correlations includeEsophageal AtresiaCongenital Hypertrophic Pyloric StenosisAnnular PancreasIleal Diverticulum (Meckel’s Diverticulum)OmphaloceleMalrotations of the MidgutSub-hepatic Cecum and AppendixStenosis and Atresia of the Small IntestineCongenital Aganglionic Megacolon (Hirschsprung’s disease)Anorectal AgenesisAnal Agenesis, and Imperforate Anus
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Slide79Esophageal Atresia
Esophageal atresia usually results from abnormal division of the tracheoesophageal septum. The fetus is unable to swallow and this results in polyhydramnios (excessive amount of amniotic fluid) because amniotic fluid cannot pass into the intestines for return to the maternal circulation.
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Slide80Congenital Hypertrophic Pyloric Stenosis
Overgrowth of the longitudinal muscle fibers of the pylorus creates a marked thickening of the pyloric region of the stomach. The resulting stenosis (Gk. severe narrowing) of the pyloric canal obstructs passage of food into the duodenum, and as a result after feeding the infant expels the contents of the stomach with considerable force (projectile vomiting).
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Slide81Annular Pancreas
The ventral and dorsal pancreatic buds form a ring around the duodenum, thereby obstructing it.Ileal Diverticulum (Meckel’s Diverticulum)A remnant of the proximal part of the yolk stalk that fails to degenerate during the early fetal period results in a finger-like blind pouch that projects from the ileum. While this condition occurs in about 1/50 people, it is usually asymptomic and only occasionally leads to abdominal pain and/or rectal bleeding.
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Slide82Omphalocele
The midgut fails to retract into the abdominal cavity. At birth, coils of intestine covered with only a transparent sac of amnion protrude from the umbilicus.
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Slide83Malrotations of the Midgut
The midgut does not rotate normally as it retracts into the abdominal cavity. This usually presents as symptoms of intestinal obstruction shortly after birth. Malrotation also predisposes the infant to a volvulus of the midgut, wherein the intestines bind and twist around a short mesentery. Volvulus usually interferes with the blood supply to a section of the intestines, and can lead to necrosis and gangrene.
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Slide84Sub-hepatic Cecum and Appendix
The cecum and appendix adhere to the inferior surface of the liver during the fetal period, and are carried upwards with it.This results in an abnormal anatomical position that may create difficulties in diagnosing appendicitis.
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Slide85Stenosis and Atresia of the Small Intestine
Failure of recanalization of ileum during the solid stage of development leads to stenosis (narrowing) or atresia (complete obstruction) of the intestinal lumen. Some stenoses and atresias may be caused by an infarction of the fetal bowel owing to impairment of its blood supply (cf. volvulus).
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Slide86Congenital Aganglionic Megacolon (Hirschsprung’s disease)
This results from the failure of neural crest cells to migrate and form the myenteric plexus in the sigmoid colon and rectum. The resulting lack of innervation results in loss of peristalsis, fecal retention, and abdominal distention.
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Slide87Anorectal Agenesis
Abnormal formation of the urorectal septum causes the rectum to end as a blind sac above the puborectalis muscle.
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Slide88Anal Agenesis
Abnormal formation of the urorectal septum causes the rectum to end as a blind sac below the puborectalis muscle.
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Slide89Imperforate Anus
The anal membrane fails to break down before birth. The anus must be reconstructed surgically, with severity depending on the thickness of the intervening tissue.
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Slide90Development of The Head and Neck
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Slide91Development and Fate of the Branchial Arches
During the 3rd and 4th week of development, the embryo develops head and tail folds that result in the incorporation of the dorsal portions of the primitive yolk sac endoderm as foregut, midgut and hindgut.
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Slide92The rostral portion of the foregut (primitive pharynx) develops five lateral pairs of pharyngeal pouches.These and the flow of the pharynx gives rise to the tongue, pharynx, trachea, lungs. Eustachian tubes, middle ear cavity, thyroid gland, parathyroid glands and the thymus.The more caudal portion of the foregut develops into the esophagus, stomach, part of the duodenum, the liver, and the pancreas.
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Slide93While the pharyngeal pouches are forming internally, five pairs of branchial (pharyngial arches) appear externally.These are numbered 1, 2, 3, 4 and 6.They are separated by branchial (pharyngeal) groove that are aligned with the pharyngeal pouches to form branchial (pharyngeal) membranes consisting of outer ectodermal and inner endodermal layer.
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Slide94Each groove is numbered according to the arch that lies rostral to it.Each branchial arch is comprised of an outer ectodermal layer and inner endodermal lining with a vertical bar of mesoderm and a cranial nerve interposed between two layers.Some of the mesoderm will condense to form a cartilage and some will contribute to the formation of the aortic arches.The remainder of the mesoderm will contribute to the formation of muscles
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Slide95Derivatives of the Branchial Arches
The first arch is divisible into the mandibular and maxillary arches.The surface ectoderm of these arches will become the epidermis of the upper and lower jaws, the epithelium of most of the oral cavity, the parenchyma of most of the salivary glands, and the enamel of the teeth.
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Slide96The mandibular and maxillary divisions of the trigerminal nerve course in these arches and supply the skin of the face and the mucosa of the oral and nasal cavities with sensory nerves and muscles of mastication with motor nerves.The muscles developing from the mandibular arch are the temporalis, masseter, medial and lateralpterygoids, mylohyoid, anterior belly of the digastric, tensor vili palatini, and tenso tympani.
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Slide97Mesenchyma and the neural crest of the mandibular arch develop into a transitory Meckel’s cartilage before forming a mandible, malleus and incus, mesenchyma of the maxillary arch forms the maxilla.The first branchial groove gives rise to external acoustic meatus.
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Slide98The first branchial membrane develops into the tympanic membrane, and the first pharyngeal pouche presage part of the auditory tube (eustachian) , and middle ear cavity.The second arch, also known as the hyoid arch, grows back over arches 3 to 6 and fuse with them, obliterating branchial groove 3 to 6 and resulting in a transitory cervical sinus.
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Slide99The sinus normally obliterates, but if it persists, it can develop into a cervical sinus cysts.Cervical (branchial) fistulas may remain if communications are retained externally or internally through branchial membranes.Because the ectoderm of the second arch gives rise to the epidermis of much of the neck, the opening of the external branchial fistulas occur in the neck along the anterior margin of the sternocleiddomastoid muscle.
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Slide100Internal fistulas most often occur into the second pouch, opening into the tonsilar region because the tonsil develops from the second pharyngeal pouch.Mesenchyma of the second arch gives rise to the muscle of the facial expression (mimetic muscles), stapedus, posterior belly of the digastric, and stylohyoid muscles.Along with neural crest, mesenchyma gives rise to the stapes, styloid process, stylohyoid ligament, and lesser cornua of the hyoid bone.The facial nerves runs in the second arch and supplies innervations to muscles developing from this arch.
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Slide101The 3rd pharyngeal arch gives rise to the stylopharyngeus muscles, supplied by the glossopharyngeal nerve, and to the body and greater horn of the hyoid bone.The endoderm of the dorsal part of the 3rd pharyngeal pouch gives rise to the inferior parathyroid glands.The ventral part of the third pharyngeal pouch becomes the thyroid gland.
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Slide102The the 4th and 6th arches gives rise to the laryngeal cartilage and the pharyngeal, palatal, and laryngeal muscles.All of these muscles, except the tensor veli palatini and the stylipharyngeus, are innervated by the vagus nerve, with the superior laryngeal nerve supplying the 4th arch and the recurrent laryngeal nerve supplying the 6th .The dorsal part of the 4th pharyngeal pouch gives rise to the superior parathyroid gland.The fate of the ventral part is not certain.
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Slide103The fifth (sixth) pharyngeal pouch gives rise to the ultimobranchial body, which with neural crest involvement, gives rise to calcitonin-producing cells of the thyroid gland.Aortic arches arise from the aortic bulb and enters each branchial arch where they run cheifly caudal to the cranial nerve in each arch.The first aortic arch contributes to the development of the maxillary artery, the second aortic arch largely disappears.The 3rd aortic arch becomes part of the carotid artery.The 4th aortic arch become part of the subclavian artery
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Slide104Summary of the Derivatives of the Brachial Arches
Arc 1Arc IIArc IIIArches IV-VICartilageMeckel’sReichert’………..……………….SkeletalMalleus, Incus Stapes, styloidGreater horn and body of hyoid boneIntrinsic and extrinsic laryngeal cartilagesMusclesMasticationFacialStylopharyngeusLaryngealNerveTrigeminalFacialGlossopharyngealVagusVesselMaxillary arteryHyoid and Stapedial arteriesCarotid arterySubclavian and aortic archPouchLining of pharynxTonsillar fossaInferior parathyroids, thymusSuperior parathyroids , parafollicular cellsGrooveExternal auditory meatus
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Slide105Development of the Face, Nasal and Oral Cavities
By the 6th week of embryonic development, a frontal prominence overhangs the cephalic end of the stomodeum.The medial portion of the horseshoe-shaped elevation is the mesomedial process; the lateral portion is the nasolateral process
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Slide106The nasolateral process is delimited from the maxillary process by the nasooptic furrow.The developing oral cavity is bounded inferiorly by the distal fusion of the mandibular processes of the first branchial arch.
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Slide107As the maxillary process becomes more prominent, they fuse with the nasomedial process and push them towards the midline.This displaces the frontal prominence upwards and leads to the fusion of the nasomedial process in the midline.The fused nasomedial process (i.e. intermaxillary segment), primary palate) give rise to the medial part of the upper lip, distal nose, incisor teeth and associated upper jaw, and the primary palate (median palatine process).
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Slide108The maxillary process gives rise to the rest of the upper lip, teeth, and jaw and the palatine shelves, forming the secondary palate.The lower lips, jaw, and teeth are formed from the mandibular processes. The nasolacriminal duct is formed at the point of obliteration of the nasooptic furrow by fusion of the nasolateral and maxillary processes.Inability of these processes to fuse leads to an oblique facial cleft.
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Slide109The nasolateral processes give rise to the alae of the nose.The nasal pits become deeper and break through the bucconasal membrane into the primitive oral cavity.Towards the end of the second embryonic month, the palatine shelves of the maxillary processes grow medially and fuse with the primary palate nostrally, and with each other and with the inferiorly growing nasal septum caudally.
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Slide110The lateral palatine processes thus give rise to a secondary palate, which separates the nasal cavity above from definitive oral cavity below.The caudal free border of the palatine shelves project as the soft palate into the pharynx, dividing it into an upper nasopharynx and a lower oropharynx.
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Slide111Congenital Malformations of the Face, Nasal and Oral Cavities
Incomplete degeneration of the bucconasal membrane can lead to choanal atresia.Failure of the palatine shelves to fuse in the midline or to fuse with the primary palate produces cleft palate.Such clefts can be divided into three groups:Those occuring between the palatine shelves and the primary palateThose occuring posterior to the incisive foramen at the point of fusion of the palatine shelves with each other, &Those involving defects in both the anterior and posterior palate.
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Slide112The anterior and complete types may be associated with cleft lip if the nasomedial and maxillary processes fail to merge and fuse.Median cleft of the upper lip and jaw is caused by the lack of fusion of the nasomedial processes with each other.
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Slide113Urogenital System
The urinary and reproductive systems originate from the urogenital sinus and the intermediate mesoderm
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Slide114Development of the Kidney and Ureter
Three pairs of embryonic kidneys develop in humans:The pronephrosMesonephros, &MetanephrosThe pronephros and mesonephros will degenerate, but their development is essential for the establishment of metanephros, which becomes the definitive kidney.
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Slide115Pronephros
The pronephros arises at the C3 to T1 vertebral levels by the dorsal proliferation of cord of cells from the intermediate mesoderm.The cords become pronephric tubules.They grow caudally and link up with the other pronephric tubules, forming a common pronephric duct that extends caudally towards the cloaca.The pronephric kidney does not function, but the pronephric duct is important for the normal formation of mesonephric kidney
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Slide116Mesonephros
The mesonephros develops by the formation of mesonephric tubule from the intermediate mesoderm of the C6 to L3 vertebral levels.The distal end of the mesonephric tubules tap into the pronephric duct and contribute to the caudal growth.This enlarged pronephric duct taps into the cloaca, and it then becomes the mesonephric (wolffian) duct.The extensive growth of the mesonephros produces a large urogenital ridge projecting from the dorsal body wall.
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Slide117Metanephros
Metanephros arises from two sources: the ureteric bud and metanephrogenic intermediate mesoderm of the L4 to S1 vertebral levels. The ureteric bud arises as a tubular outgrowth from the mesonephric duct near its entrance into the cloaca.It grows towards the intermediate mesoderm, where its blind end becomes capped by metanephrogenic tissue.The ureteric bud elongates as the ureter, and its blind end enlarges as the renal pelvis and undergoes a series of branching.
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Slide118The branchings give rise to the major and minor calyces and the collecting tubules.The metanephrogenic condensations capping the blind ends of the collecting tubules develop into nephrons.One end of the blind nephron froms a Bowman’s capsule around a glomerulus of capillaries.The other end taps into the collecting tubule.
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Slide119Development of the Urinary Bladder and Urethra
The urinary bladder and the urethra develop from the endoderm of the urogenital sinus and allantois.In early development, the allantois is a diverticulum of the cloaca.A urorectal septum of the mesoderm arises between the allantois and hindgut, grows caudally, and divides the cloaca into a dorsal rectum and ventral urogenital sinus.With this division, the mesonephric duct empties into the urogenital sinus.
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Slide120As the urogenital sinus and a small adjacent portion of the allantois enlarges to form the urinary bladder, portions of mesonephric and metanephric (ureter) ducts are incorporated into the walls of the urogenital sinus.This results in the ureter entering the bladder and the mesonephric duct enterying more caudally into the less dilated portion of the urogenital sinus.This distal portion of the urogenital sinus will become the urethra of the male and the urethra vestibule, and part of vagina of the female.
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Slide121Development of the Reproductive System
Even though the sex of the embryo is determined at fertilization, the gonads, ducts, and external genitalia pass through an undifferentiated stage of development in which male and female components have the same appearance.This stage last until about the 6th week of embryonic development.
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Slide122Development of Male and female Genital Ducts
In the different stages, gonads form one of the medial wall of the urogenital ridge.Starting in the 3rd week, primordial germ cells migrate from the endoderm of the yolk sac to the urogenital ridge.By the 6th week, the coelomic epithelium has proliferated, invaginated, and surrounding the primordial germ cells to form the primitive gonadal (primary sex) cords in the underlying mesoderm of the gonad.
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Slide123In the undifferentiated stage of the genital duct formation, both mesonephric and Müllerian (paramesonephric) ducts are present.The Müllerian ducts arise as longitudinal invaginations of the coelomic epithelium on the lateral wall of the urogenital ridge.Cranially, this duct remains open to the coelom.Caudally, it opens through the dorsal wall of the urogenital sinus.
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Slide124In its craniocaudal course, it lies at first lateral to to the mesonephric duct, then passes anterior to it, and finally fuse with the opposite Müllerian duct medial to the mesonephric duct.During this fusion, the urogenital ridges of the two sides are brought together to form a genital cord between the developing bladder anteriorly and the rectum posteriorly
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Slide125Summary of Development of Male and female Genital Ducts
Embryonic StructureMale derivativeFemale DerivativeYolk sac primordial germ cellSpermatogoniaOögoniaMesonephric cortxTunica albugineaCortical sex cords, Follicle cells of the ovary.Mesonephric medullaMedullary sex cords, seminferous tubules of testis……………………..Mesonephric tubulesEfferent ductules and rete testisEpoöphoronMesonephric ductEpididymis, vas defeernsParoöphoronparamesonephric ductAppendix of testis, prostatic utricleOviduct, uterus, upper part of vagina
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Slide126Development of External genitalia
In the undifferentiated stage of development of the external genitalia, mesoderm invades the lateral walls of the external opening of the urogenital sinus producing elevations called urogenital folds.These folds unite anterior to the urogenital opening at the genital tubercle.Labioscrotal swelling develop lateral to the urogenital folds.
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Slide127Male Reproductive System Development
In the development of the male reproductive system, the gonadal cords become testis cords, which differentiate into seminiferous tubules and rete testis.The primordial germ cells become spermatogonia.Efferent ductules develop from adjacent mesonephric tubules.The developing testes produces müllerian-inhibiting hormone and androgens, which leads to the degeneration of the müllerian duct and to the differentiation of the mesonephric duct into the ductus epididymis, vas deferens, and ejaculatory duct.
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Slide128The seminal vesicle arises as an outgrowth of the mesonephric duct.The urogenital tubercle enlarges and carries with it inferiorly, a urethral plate of the endoderm.This plate is transformed into the penile (cavernous) urethra after the lateral urogenital folds fuse ventrally.The urethral plate, urogenital folds, and genital tubercle give rise to the definitive penis.The scrotum is formed by the ventral fusion of the labioscrotal swellings.
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Slide129The testes descend late in gestation from their retroperitoneal abdominal location.They anchored in the scrotum by the gubernaculum testis, which is derived from the mesoderm of the urogenital ridge and caudal to the testis.The path of the descent is indicated by the inguinal canal.This follows the embryonic pathway of the process vaginalis eveginating from the peritoneum.
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Slide130Female Reproductive System development
In the development of the female reproductive system, the initial gonadal cords degenerate and the second series of ovarian cords develop from the primordial germ cells and ovarian epithelium.The germs cells grow to follicles towards the surface of the developing ovary.Each primitive ovarial follicle consists of a developing sex cell, surrounded by a flattened layer of follicular cells.The sex cells complete the prophase of the first meiotic division and are in the arrested dictyotene stage by the time of birth
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Slide131From the 6th month until parturition, there is a tremendous rate of degeneration of the primitive follicles, the number decreasing from about 6 million to about 400, 000 or less.The unfused portion of the müllerian duct develop into the uterine tubes.The fused portion gives rise to the uterus and part of the vagina.The genital cord remains as the broad ligaments of the uterus.The proper ligaments of the ovary and the round ligaments of the uterus arise from the mesoderm of the urogenital ridge caudal to the ovary.
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Slide132The mesonephric duct and the tubules degenerate and the lower part forms part of the vagina.The urogenital sinus caudal to the vaginal opening becomes enlarged as the vestibule.In the female, the genital tubercle remains relatively small as clitoris.The urethral folds become the labia minora and the labioscrotal swellings develop into the labia majora.The hymen forms from the endoderm of the vaginal plate.
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Slide133Summary of the origins of Male and female External genitalia
Embryonic StructureMale derivativeFemale derivativeGenital tubercleGlans and body of penisGlans and body of clitorisUrogenital SinusPenile urethraVestibule of vaginaUrethral foldsCorpus spongiosum surrounding urethraLabia minoraLabioscrotal swellinhScrotumLabia majora
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Slide134Congenital Malformations of the Urogenital System
These include:Horseshoe kidneyBifid UreterDouble pelvisExstrophy of the bladderCongenital hydrocelHypospadiesDouble vaginaHermaphroditism etc
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Slide135Renal Agenesis
Absence of a kidney results when the ureteric bud fails to develop or regresses after development. If both kidneys are absent (bilateral renal agenesis) the fetus cannot urinate and amniotic fluid is deficient (< 400ml) resulting in oligohydramnios and characteristic physical deformations known as Potter facies (flattened nose, low-set ears, thickened, tapering fingers).
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Slide136Congenital Polycystic Disease of the Kidneys
An autosomal recessive condition manifest by the presence of many heterogeneous cysts within the parenchyma of the kidney. The cause and pathogenesis is unknown.
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Slide137Horseshoe Kidney
Horseshoe kidney occurs when the inferior poles of the kidneys fuse together. The combined kidney is not able to ascend to its adult physiological location because it gets “hung up” on the inferior mesenteric artery.
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Slide138Pelvic Kidney
A pelvic kidney is one that has failed to migrate to its adult anatomical location. In crossed ectopia one kidney and its associated ureter migrate to the opposite side of the body.
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Slide139Urachial Fistula
If the lumen of the allantois persists as the urachus forms it may give rise to an abnormal communication between the urinary bladder and the umbilicus known as an urachal fistula. Often with this condition urine will dribble from the umbilicus when the baby cries. A blind-ending communication that will not drain urine is known as an urachal sinus.
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Slide140Malformations of the Uterus and Vagina
If the two paramesonephric ducts fail to fuse correctly it can result in duplication of the uterus and vagina (double uterus and double vagina). If one paramesonephric duct fails to develop it results in formation of a single uterine tube and single horn of the uterus (unicornuate uterus).
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Slide141Hypospadias
Incomplete fusion of the urogenital folds creates abnormal openings of the urethra on the ventral aspect of the penis. This malformation occurs in about 1/300 infants.
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Slide142Cyrptorchidism
Failure of the testes to descend into the scrotum (cryptorchidism) is the most common malformation of the male genital system, resulting in infertility and an increased risk of testicular cancer. The testes may remain anywhere between the abdomen and the scrotum.
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Slide143Intersexuality
Rare true hermaphrodites have both ovarian and testicular tissues, usually possessing a 46,XX karyotype. The internal and external and external genitalia are variable. Female pseudohermaphrodites are more common, possessing a 46, XX karyotype, and typically result from exposure to excess androgens during embryologic development (as in congenital virilizing adrenal hyperplasia). Male pseudohermaphrodites have testes and a 46, XY karyotype. This condition results from an inadequate production of androgens by the testes, or when embryonic genital tissues lack a specific receptor needed to respond to normal levels of the hormone.
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Slide144Congenital Inguinal Hernia
A large patency of the tunica vaginalis can allow a loop of intestine to herniate into the scrotum. This must typically be corrected surgically.
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Slide145Endocrine System
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Slide146Pituitary
The pituitary gland or hypophysis, develops from two primordia.The anterior lobe also known as the adenohypophysis is glandular in appearance and developed as a dorsal outgrowth from the primitive oral cavity.This diverticulum, although initially hollow, becomes solid and forms the anterior lobe, pars intermedia, and pars tubularis of the pituitary gland.
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Slide147The posterior lobe is also known as pars nervosa and develops as a ventral diverticulum of the diencephalon of the brain.It remains connected to the hypothalamus by way of the infundibular stalk.The cells that produce posterior lobe hormones are located in the hypothalamus.From here, they are transported into the posterior lobe of the pituitary, where they are stored and secreted.
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Slide148Thyroid Gland
The thyroid gland begins development as a ventral diverticulum of the primitive pharynx.Initially, it is connected to the floor of the pharynx by the way of thyroglossal duct.This connection is eventually lost as the thyroid gland migrates caudally in the anterior neck to assume its final position over the upper tracheal rings.The origin of the thyroglossal duct is evident in the adult as the forammen caecum, which is found on the dorsal surface of the tongue between the anterior two-thirds and posterior one-third of the tongue.
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Slide149The thyroid becomes bilobed, with the lobes connected across the midline by an isthmus.In addition, to the thyroid follicular cells, which produce thyroxin, the thyroid gland contains parafollicular cells, which produce a calcium-regulating hormone called calcitonin.These cells develop from the neural crest and migrate into the thyroid gland as it is migrating in the neck
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Slide150Parathyroid Glands
The endoderm of the 3rd and 4th pharyngeal pouches is responsible for the development of the inferior and superior parathyroid glands, respectively.The inferior parathyroids arise from the dorsal endoderm of the 3rd pharyngeal pouch in conjunction with the thymus.As the thymus migrates caudally to the mediastinium, the parathyroid glands migrate to an inferior position behind the lobes of the thyroid gland.The superior parathyroids arise from the dorsal endoderm of the 4th pouch, but maintain a more superior position behind the lobes of the thyroid gland.
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Slide151Adrenal Glands
The adrenal or suprarenal glands develop from two sources.The outer cortex is derived from condensation of the posterior body wall mesenchyme.It differentiates into three zones, characteristics of the adrenal cortex.The adrenal medulla, which consists of nor-epinephrine and epinephrine-secreting cells, is derived from the neural crest.
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Slide152Nervous System
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Slide153Neural Tube Formation
The nervous system begins its development as a thickened midline area of ectoderm called the neural plate.A longitudinal neural groove develops in the neural plate.The sides of the groove are flanked by raised neural folds.By the end of third week of development, the neural folds begin to fuse in the midline, beginning in the center of the neural plate and proceeding simultaneously in the rostral and caudal direction.
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Slide154This results in an open area of the neural fold rostrally, known as the rostral neuropore, and a similar area caudally, known as the caudal neuropore.The rostral neuropore closes at about day 26, and the caudal neuropore closes at about day 28, thus completing the formation of the neural tube.
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Slide155Neural Crest
As the ectoderm of the neural folds fuse to form the neural tube, some of the lateral ectoderm buds off and migrates throughout the embryo as the neural crest.Neural crest has been identified as the origin of many structures throughout the body including sensory and autonomic ganglia, neurolemmocyte of the peripheral nerves, skeletal elements of the head, components of some of the endocrine glands, and melanocytes.
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Slide156Differentiation of the Neural Tube
Three concentric zones develop in the walls of the neural tube.The innermost layer, which lines the space within the neural tubes is the ependymal zone.Cells in this layer differentiate into two types of cells:Spongioblasts, which develop into the glial cells, and Neuroblasts, which develop into neurons.Both of these types of cells migrate into the mantle zone where they complete their development.The area of gray matter that is developing adjacent to the ependymal zone is the mantle layer.The outermost zone of developing white matter is the marginal zone.
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Slide157Laterally on each side of the developing neural tube, paired masses of cells developed.These are separated from each by a longitudinal groove called sulcus limitans.The mass dorsal to the sulcus limitans is the alar plate, which will give rise to the sensory component of the central nervous system.The mass ventral to sulcus limitans is the basal plate and will give rise to motor components of the nervous system.The caudal end of the neural tube will develop into the spinal cord, and the rostral end of the neural tube will undergo extensive bending folding to develop into the brain.
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Slide158Development of the Spinal Cord
The spinal cord develops from the caudal end of the neural tube.For the first 12 weeks of development, it is equal in length with the vertebral column.Spinal nerves emerge from intervertebral foramina, which they are associated.During postnatal growth and development, the vertebral column progressively lengthens, causing an upward shift in the caudal end of the spinal cord, the conus medullaris.
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Slide159This results in the lengthening of the caudal nerve roots in order to reach their respective intervertebral foramina.These elongated nerve roots are termed the caudal equina.At birth, the conus medullaris is located opposite the L3 vertebral level. In the adult, it is opposite the intervertebral disc between L1 and L2.
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Slide160Embryonic Development of the Brain
During the first 26 days of development: Ectoderm thickens along dorsal midline to form the neural plateThe neural plate invaginates, forming a groove flanked by neural foldsThe neural groove fuses dorsally and forms the neural tube
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Slide161Embryonic Development
Figure 12.2
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Slide162Primary Brain Vesicles
The anterior end of the neural tube expands and constricts to form the three primary brain vesiclesProsencephalon – the forebrainMesencephalon – the midbrainRhombencephalon – hindbrain
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Slide163Secondary Brain Vesicles
In week 5 of embryonic development, secondary brain vesicles formTelencephalon and diencephalon arise from the forebrainMesencephalon remains undividedMetencephalon and myelencephalon arise from the hindbrain
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Slide164Adult Brain Structures
Fates of the secondary brain vesicles:Telencephalon – cerebrum: cortex, white matter, and basal nucleiDiencephalon – thalamus, hypothalamus, and epithalamusMesencephalon – brain stem: midbrainMetencephalon – brain stem: pons and the Cerebellum.Myelencephalon – brain stem: medulla oblongata
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Slide165Adult Brain Structures
Figure 12.3c, d
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Slide166Adult Neural Canal Regions
Adult structures derived from the neural canalTelencephalon – lateral ventriclesDiencephalon – third ventricleMesencephalon – cerebral aqueductMetencephalon and myelencephalon – fourth ventricle
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Slide167Adult Neural Canal Regions
Figure 12.3c, e
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Slide168Congenital Malformations of the Nervous System Development
Spina BifidaAnencephalyMicrocephalyHydrocephalusArnold-Chiari MalformationFetal Alcohol Syndrome
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Slide169Spina Bifida
Spina bifida occulta is a defect of the vertebral column only, and is a common problem affecting as many as 10% of live births.Spina bifida with meningocele (spina bifida cystica) is a defect of the vertebral column with protrusion of the meninges through the defect.Spina bifida with myelomeningocele is a defect of the vertebral column protrusion of the meninges and herniation of the spinal cord through the defect.
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Slide170Spina bifida with myeloschisis results from the failure of the caudal neuropore to close at the end of the fourth week of development. Newborn infants are paralyzed distal to the lesion.These defects usually occur in the cervical and/or lumbar regions and may cause neurologic deficits in the lower limbs and urinary bladder. Neural tube defects can be detected by the presence of alpha-fetoprotein (AFP) in the fetal circulation after the fourth week of development.
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Slide171Anencephaly
Anencephaly is the failure of the anterior neuropore to close, resulting in a failure of the brain to develop.
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Slide172Microcephaly
Microcephaly (small head) results from microencephaly (small brain), or the failure of the brain to grow normally. This can be the result of exposure to large doses of radiation up to the sixteenth week of development, or from certain infectious agents (cytomegalovirus, herpes simplex virus, and toxoplasma gondii)
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Slide173Hydrocephalus
Hydrocephalus is an accumulation of CSF in the ventricles of the brain, caused most commonly by stenosis of the cerebral aqueduct. In the absence of surgical treatment in extreme cases the head may swell to three times its normal size.
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Slide174Arnold-Chiari Malformation
Arnold-Chiari malformation is herniation parts of the cerebellum (medulla oblongata and cerebellar vermis) through the foramen magnum of the skull.
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Slide175Fetal Alcohol Syndrome
Ingestion of alcohol during pregnancy is the most common cause of infant mental retardation. It also causes microcephaly and congenital heart disease.
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Slide176Development of the Eye and Ear
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Slide177Development of the Eye and Ear
The eyes and ears begin to develop during the fourth week.These special sense organs are very sensitive to teratogenic infectious agents (e.g. cytomegalovirus and rubella virus).The most serious defects result from disturbances of development during the fourth to sixth week.Defects of sight and hearing may result from the infection of tissues and organs by certain microorganisms during the fetal period (e,g, syphilis).
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Slide179The Eye
The visual organs of the eye develop from three sources:Neuroectoderm of the forebrainSurface ectoderm of the head, &Mesoderm between these layersThe ectodermal outgrowth from the brain becomes the retina, iris, and optic nerveThe surface ectoderm forms the lens, and the surrounding mesoderm gives rise to the vascular and fibrous coats of the eye.
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Slide180Eye formation is first evident at the beginning of the fourth week of development.Grooves called optic sulci appear in the neural folds at the cranial end of the embryo.As the neural folds fuse to form the forebrain vesicle, the optic sulci evaginate to form hollow diverticula called optic vesicles.These vesicles project from the sides of the forebrain into the adjacent mesenchyma.The cavities of the optic vesicles, are continuous with the lumen of the forebrain vesicle.
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Slide181The formation of the optic vesicle is induced by the mesenchyma adjacent to the developing brain.As bulb-like optic vesicles grow laterally, their distal ends expand, and their connections with the forebrain constrict to form a hollow optic stalks.The optic vesicles soon come in contact with the surface of the ectoderm, and their lateral surfaces become flattened.
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Slide182Concurrently, the surface ectoderm adjacent to the vesicles thickens to form lens placodes, which are the primordia of the lenses.The formation of lens placodes is induced by a signal produced by the optic vesiclesThe central region of each lens placode soon invaginates and sinks deep to the surface, forming a lens pit.The edges of the pit gradually approach each other, and fuse to form a spherical lens vesicle, which is soon pinched off from the surface ectoderm.The lens vesicle develop into the lens of the eye.
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Slide183As the lens vesicles are developing, the optic vesicles invaginate and become double-walled structures called optic cups.The opening of each optic cup is large at first, but the rim of the optic cup infolds and converges around the lens.By this stage, the lens vesicles have lost their connection with the surface ectoderm and give rise to the cavities of the optic cups.Linear grooves called choroid fissures develop on the ventral surface of the optic cups and along the optic stalks.
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Slide184The choroid fissures contain vascular mesenchyma from which the hyaloid blood vessels will develop.The hyaloid artery, a branch of the opthalmic artery, supplies the inner layer of the optic cup, the lens vesicle, and the mesenchyma in the optic cups.The hyaloid vein returns blood from these structures.
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Slide185As the edges of the optic fissure approach each other and fuse, the hyaloid vessels are enclosed within the optic nerve.The distal portions of the hyaloid vessels eventually degenerate, but their proximal portions presist as the centarl artery and vein of the retina.
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Slide186The Retina
The retina develops from the walls of the optic cups.The outer layer becomes the pigmented epithelium and an inner layer the neural epithelium.During embryonic and early fetal periods, the two retinal layers are separated by an intraretinal space, which eventually disappear and the two layers fuseThe Cells of the neural epithelium finally differentiate to light-sensitive cells containing photoreceptors (rods and cones) and many axons of ganglion cells to form the optic nerve.
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Slide187The Ciliary Body
The pigmented portion is derived from the outer layer of the optic cup and continuous with retinal epithelium.The non-pigmented portion is the anterior prolongation of the neural retina in which no neural elements differentiate.The ciliary muscle develop from fibroblasts located in the edge of the optic cup in the region between the anterior scleral condensation and the ciliary pigment epithelium.
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Slide188The Iris
The iris develop from the anterior part of the optic cup, and grows inward and partially covers the lens.In this area the two layers of the optic cup have remained thin.The epithelium of the iris represents both layers of the optic cup.It is continuous with the ciliary body and with the retinal neural epithelium.The vascular connective tissue of the iris is derived from mesenchyma located anterior to the rim of the optic cup.
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Slide189The Lens
The lens develops from the lens vesicle, a derivative of the surface ectoderm.The rim of the lens is known as the equatoral zone, because it is located midway between the anterior and posterior poles of the lensThe lens is made up of lens fibers and supplied by hyaloid artery, and eventually become avascular during the fetal period.Thereafter, it depends on diffusion for its physiological function.
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Slide190The Choroid and Sclera
The mesenchyma surrounding the optic cup differentiates into an inner vascular layer, the choroid, and an outer fibrous layer, the sclera.The sclera develops from a condensation of the mesenchyma external to the choroid.The blood vessels appear from the 5th week and by the 22th week, arteries and veins can be distinguished.The sclera is continuous with the substantia propia of the cornea.
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Slide191The Eyelids
The eyelids develop from two surface ectodermal folds.The meet and adhere by the tenth to the twenty sixth week.The lids open on the 27th week.The eyelashes and glands are derived from the surface ectoderm.The orbicularis oculi muscle is derived from the second branchial or pharyngeal arch.As a result, it is supplied by the 7th cranial nerve.
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Slide192The Lacrimal Gland
At the superolateral angles of the orbits, the lacrimal glands develop from a number of solid buds from the surface ectoderm.These branch and become canalized to form the ducts and alveoli of the glands.The lacrimal glands are small at birth and do not function fully for about six weeks.Hence, the newborn baby does not produce tears when it cries.
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Slide194Congenital Abnormalities of the Eye
Because of the complexity of the eye development, many abnormalities can occur such as:Coloboma of the Eyelid, iris, & RetinaCongenital glaucomaCongenital CataractCongenital AniridiaCryptophthalmos
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Slide195Coloboma of the Eyelid, iris, & Retina
These are defects of the closure of the optic fissure which should have normally closed during the sixth week.Coloboma of the eyelid appears as a result of a developmental disturbance in the growth of the eyelid.Coloboma of the iris result in a key-hole in the pupil and are hereditary and transmitted as an autosomal dominant characteristics.Coloboma of the retina is a defect characterized by a localized gap in the retina, usually anterior to the optic disc.
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Slide196Congenital Glaucoma
This is an abnormal elevation of the intraocular pressure in newborn babies as a result of abnormal development of the drainage mechanism of the aqueous humor during the fetal period.Intraocular tension rises because of the imbalance between production of aqueous humor and its outflow.Congenital gloucoma is usually caused by recessive mutant genes,, but the infection may result from rubella infection during early pregnancy.
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Slide197Congenital Cataract
In this condition, the lens is opaque resulting in blindness.Many lens opacities are inherited, and some are caused by teratogenic agents particularly rubella virus that affect early development of the lenses.They are vulnerable to rubella virus between the 4th and 7th weeks when primary lens fibers are forming, therefore Rubella immunity to woman at reproductive age prevents this condition.Another cause of cataract is an enzymatic deficiency, congenital galactosemia that appears weeks after birth.
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Slide198Congenital Aniridia
This is a congenital abnormality in which there is almost complete absence of the iris.This condition is the result of an arrest of development at the rim of the optic cup during the 8th week.Congenital Aniridia may be associated with gloucoma and other eye abnormalities.Aniridia may be familial, transmission being dominant or sporadic
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Slide199Cryptophthalmos
This is called the Hidden Eye, and occurs due to the failure of the eyelids to develop; As a result, skin covers the eye.The eyeball is small and defective, and the cornea and conjunctiva usually do not develop.Fundamentally, the defect means absence of the palpebral fissure but usually there is varying absence of eyelashes and eyebrows.Cryptophthalmos is an autosomal recessive condition.
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Slide200The Ear
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Slide201The Ear
In adults, the ear consists of three anatomical parts: External, middle , and inner ear.The external and middle parts are concerned with the transference of sound waves from the exterior to the inner ear.The inner ear contains the Vestibulocochlear organ concerned with equilibrium and hearing
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Slide202Inner Ear
The first indication of the developing ear can be found on the 22nd day as the thickening of the surface ectoderm on each side of the rhombencehpalon.These thickenings, the otic placodes, invaginate rapidly and form the otic or auditory vesicles (otocysts).During later development, each vesicle divides into a ventral component that give rise to the saccule and cochlear duct and a dorsal component that forms the utricle, semicircular canals, and endolymphatic duct.Together, these epithelial structures form the membranous labyrinth.
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Slide203Saccule, Cochlea, and Organ of Corti
In the 6th week of development, the saccule forms a tubular outpocketing at the lower pole.This outgrowth, the cochlear duct, penetrates the surrounding mesenchyma in the spiral fashion until the end of the 8th week, when it has completed 2.5 turns.Its connection with the remaining portion of the saccule is then confined to a narrow pathway, the ductus reuniens.
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Slide204Mesenchyma surrounding the cochlear duct soon differentiates into cartilage.In the 10th week, this cartilaginous shell undergoes vacuolization, and two perilymphatic spaces, the scala vestibuli and scala tympani, are formed.The cochlear duct is then separated from the scala vestibuli by the vestibular membrane and from the scala tympani by the basilar membrane.The lateral wall of the cochlear duct remains attached to the surrounding cartilage by the spiral ligament.
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Slide205The median angle of the cochlear duct is connected to and partly supported by a long cartilaginous process, the modiolus, the future axis of the bony cochlea.Initially, epithelial cells of the cochlear duct are alike.With further development, however, they form two ridges: the inner ridge, the future spiral limbus, and the outer ridge.The outer ridge forms one row of inner and three of four rows of outer hair cells, the sensory cells of the auditory system.
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Slide206They are covered by the tectorial membrane.The sensory cells and tectorial membrane together constitute the organ of Corti.Impulses received by the organ of Corti are transmitted to the spiral ganglion and then to the nervous system by the auditory fibers of the cranial nerve VIII.
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Slide207Utricle and Semicircular Canal
During the 6th week of development, semicircular canals appear as flattened outpocketing of the utricular part of the otic vesicle.Central portions of the walls of these outpocketting eventually appose each other and disapppear, giving rise to semicircular canals.Whereas one end of each canal dilates to form the crus ampullare, the other, the crus nomampulare, does not widen.
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Slide208Because two of the latter type fuse, however, only five crura enter the utricle, three with an ampulla and two without.Cells in the ampullae form a crest, the crista ampullaris, containing sensory cells for maintenance of equilibrium.Similar sensory areas, the macula acusticae, develop in the walls of the utricle and saccule.Impulses generated in the sensory cells of the cristae and maculae as a result of a change in position of the body are carried to the brain by vestibular fibers of cranial nerve VIII
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Slide209During formation of the otic vesicle, a small group of cells breaks away from its wall and forms the statoacoustic ganglion.Other cells of these ganglion are derived from the neural crest.The ganglion subsequently splits into cochlear and vestibular portions , which supply sensory cells of the organ of Corti and those of the saccule, utricle, and semicircular canals respectively.
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Slide210Middle Ear: Tympanic Membrane and Auditory Tube
The tympanic membrane, which originates from the ectoderm, is derived from the 1st pharyngeal pouch.This pouch expands in lateral direction and comes in contact with the floor of the 1st pharyngeal cleft.The distal portion of the pouch, the tubotympanic recess, widens and gives rise to the primitive tympanic cavity, and the proximal part remains narrow and forms the auditory tube (eustachian tube), through which the tympanic cavity communicates with the nasopharynx.
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Slide211Middle Ear: Ossicles
The malleus and incus are derived from cartilage of the 1st pharyngeal arch, and the stapes is derived from that of the second arch.Although the ossicles appear during the first half of the fetal life, they remain embedded in the mesenchyma until the 8th month, when the surrounding tissues dissolve. The endodermal epithelial lining of the primitive tympanic cavity is now at least twice as large as before.When the ossicles are entirely free of the surrounding mesenchyma, the endodermal epithelium connects them in a mesentery-like fashion to the walls of the cavity.
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Slide212The supporting ligaments of the ossicles develop later within these mesenteries.Because the malleus is derived from the 1st pharyngeal arch, its muscle, the tensor tympani, is innervated by the mandibular branch of the trigeminal nerve.The stapedius muscle, which is attached to the stapes, is innervated by the facial nerve, the nerve to the 2nd pharyngeal arch.
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Slide213During late fetal life, the tympanic cavity expands dorsally by vacuolization of surrounding tissue to form the tympanic antrum.After birth, the epithelium of tympanic cavity invades the bone of the developing mastoid process, and epithelium-lined air sacs are formed (pneumatization).Later, most of the mastoid air sacs come in contact with the antrum and tympanic cavity.
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Slide214External Ear: External Auditory Meatus
The External Auditory Meatus develops from the dorsal portion of the 1st pharyngeal cleft.As the beginning of the 3rd month, epithelial cells at the bottom of the meatus proliferate, forming a solid epithelial plate, the meatal plug.In the 7th month, the plug dissolves, and the epithelial linings of the floor of the meatus participates in formation of the definitive eardrum.Occasionally, the meatal plug persists until birth, resulting in congenital deafness.
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Slide215External Ear: Eardrum and Tympanic Membrane
The eardrum is made up of:An ectodermal epithelial lining at the bottom of the auditory meatus.An endodermic epithelial linningof the tympanic cavity, and An intermediate layer of connective tissue that forms the fibrous stratum.The major parts of the eardrum is firmly attached to the handle of the malleus, and the remaining portion forms the separation between the external auditory meatus and the tympanic cavity.
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Slide216External Ear: Auricle
The auricle develops from 6th mesenchymal proliferations at the dorsal ends of the 1st and 2nd pharyngeal arches, surrounding the 1st pharyngeal cleft.These swellings (auricular hillocks), three on each side of external meatus, later fuse and form the definitive auricle.As fusion of the auricular hillocks is complicated, developmental abnormalities of the auricle are commonInitially, the external ears are in the lower neck region, but with development of the mandible, they ascend to the side of the head at the levels of the eyes.
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Slide217Congenital Abnormalities of Ear Development
These include:Congenital deafnessAuricular AbnormalitiesPreauricular sinusesAtresia of the external Acoustic Meatus, &Congenital Cholesteatoma.
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Slide218Congenital Deafness
Because formation of the internal ear is independent of the development of the middle and external ears, congenital impairment of hearing may be the result of maldevelopment of the sound-conducting apparatus of the middle and external ears or of the neurosensory structures of the internal ear.
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Slide219Most types of deafness are caused by genetic factors.In deaf-mutism, the ear abnormality is usually perceptive in type.Congenital deafness may be associated with several head and neck abnormalities as part of the first arch syndrome.Rubella infection during the critical period of embryonic development of the internal ear, particularly during the 7th and 8th weeks, can cause maldevelopment of the spiral organ.Congenital deafness may also be associated with maternal goiter, which may result fetal hypothyroidism.
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Slide220Congenital fixation of the stapes results in conductive deafness in an otherwise normal ear.Failure of differentiation of the anular ligament, which attaches the base of the stapes to the fenestra vestibuli, results in fixation of the stapes to the bony labyrinth.Abnormalities of the malleus and incus are often associated with the first arch syndrome.
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Slide221Auricular Abnormalities
There is a wide normal variation in the shape of the auricle.These could be Auricular appendages which appear anterior to the auricleAbsence of the auricle (anontia) due to the failure of the auricular hillocks to develop.Microtia (small auricle) which results from suppressed development of the auricular hillocks.
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Slide222Preauricular Sinuses
These are pitlike , cutaneous depressions located in a triangular area anterior to the auricle.They are symptomatic and have only minor cosmetic importance.However, they often develop infections of the ear.
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Slide223Atresia of the External Acoustic Meatus
Blockage of this canal is the result of failure of the meatal plug to canalize.Usually, the deep part of the meatus is open, but the superficial part if blocked by bone or fibrous tissue.Most cases are associated with the first arch syndrome.The auricle is also usually affected and abnormalities of the middle and/or inner ear are sometimes present.Atresia of the External Acoustic Meatus usually results from autosomal dominant inheritance.
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Slide224Congenital Cholesteatoma
This is a group of epithelial cells that appears as white, crystlike structure medial to or within the tympanic membrane.These are cells from the meatal plug that were displaced during recanalization.Congenital Cholesteatoma originates from an ectodermal formation which normally involutes by 33 weeks gestation.
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Slide225Integumentary System
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Slide226Integumentary System
This system consists of the skin, sweat glands, nails, hairs, sebaceous glands, and errector pili muscles.It also includes the mammary glands and teeth.The latin word integumentum means a covering.At the external orifices (e.g. of the digestive tract), the mucous membrane and the integument are continuous.
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Slide227Skin
The skin and its appendages develop from ectoderm and mesoderm.The epidermis is derived from ectoderm.The melanocytes are derived from neural crest cells that migrate into the epidermis.The dermis develops from mesenchyma that differentiates from mesoderm.Cast-off cells from the epidermis mix with secretions of the sebaceous glands to form the whittish, greasy coating of the skin known as vernix caseosa.It protects the epidermis, making it more waterproof, and facilitates birth due to its slipperiness.
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Slide228Hair, Sebaceous, & Mammary Glands
Hairs develop from downgrowth of the epidermis into the dermis.By the 20th week, the fetus is completely covered with fine, downy hairs called lanugo.These hairs are shed by birth or shortly thereafter and are replaced by coarse hairs.Most sebaceous glands develop as outgrowth from the side of the hair follicles.Some sebaceous gland develop as downgrowth of epidermis to the dermis.Sweat glands also develop from epidermal downgrowth into the dermis.Mammary glands develop in a similar way.
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Slide229Teeth
Teeth also develop from the ectoderm and mesoderm.The enamel is produced by ameloblasts, which are derived from the oral ectoderm.All other dental tissues develop from mesoderm
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Slide230Congenital Abnormalities of the Integumentary System
These include abnormalities of the:SkinDisorders of keratinizationCongenital Ectodermal DysplasiaAngiomas of the SkinAlbinismAbsence of skinHairsAtrichia congenitaHypertricosisNailsAnonychia
Mammary GlandsAthelia and AmastiaAplasiaSupernumerary breasts and nipplesInverted NipplesTeethNatal TeethEnamel HypoplasiaRicketsAbnormalities of ShapeAbnormal size of TeethFused TeethDiscolored teeth
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Slide231Congenital Abnormalities of the Skin(Disorders of Keratinization )
Disorders of Keratinization is a group of disorders resulting from excessive keratinization.They are characterized by excesive dryness and fishskin-like scaling of the skin, invovling the entire body surface.The skin is thickened, ridged and cracked.Affected babies die within weeks of deliveryThese disorders are inherited as autosomal recessive traits.
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Slide232Congenital Abnormalities of the Skin(Congenital Ectodermal Dysplasia)
This is a hereditary disorder in which there is partial failure of the epidermis and its appendages to develop.In severe cases, there are dental abnormalities and absence of body hair.
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Slide233Congenital Abnormalities of the Skin(Angiomas of the Skin)
These vascular abnormalities are developmental defects in which some transitory and/or surplus primitive blood or lymph vessels persistAngiomass composed of lymphatics are called cystic lymphangiomas.Angiomas are benign tumors of endothelial cells
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Slide234Congenital Abnormalities of the Skin(Albinism)
In generalized albinism, an autosomal recessive trait, the skin, hair, and retina lack pigments, but the iris usually shows some pigmentation.The condition occurs when melanocytes fail to produce melanin due to the lack of enzyme tyrokinase.The localized albinism, or piebaldism, an autosomal dominant trait, there is lack of melanin in patches of the skin and/or hairs
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Slide235Congenital Abnormalities of the Skin(Absence of Skin)
In rare cases, small areas of skin fail to form, giving the appearance of ulcers.The area usually heals by scarring unless a skin graft is performed.Absence of patches of skin is most common in the scalp.
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Slide236Congenital Abnormalities of Hairs(Gray Hairs in Infants)
Gray hairs in infants is associated with albinism, which results from the lack of melanin in the skin.The lack of pigments in the melanocytes of the bulbs of the hairs amounts to the lack of color in the hairs.
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Slide237Congenital Abnormalities of Hairs(Congenital Alopecia)
Congenital Alopecia or Atrichia Congenita is the absence or loss of hairs may occur alone or with other abnormalities of the skin and its derivatives.The hair loss may be caused by failure of hair follicles to develop or it may result from follicles producing poor quality hairs.
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Slide238Congenital Abnormalities of Hairs(Hypertrichosis)
Hypertrichosis is excessive hairiness results from the development of supernumerary hair follicles or from the persistence of hairs that normally disappear during the perinatal period.It may be localized (e.g. on the shoulders and back) or diffuse.Localized hypertrichosis is often associated with spina bifida occulta.
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Slide239Congenital Abnormalities of Hairs(Pilli Torti)
Pilli Torti is a hair disorder in which the hairs are twisted and bent.Other ectodermal defects (e.g. distorted nails) may be associated with this condition.Pilli torti is usally first recognized at two to three years of age.
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Slide240Congenital Abnormalities of Nails(Anonychia)
Anonychia is the absence of nails and occur as a result of failure of the nail fields to form.It can also result from the failure of proximal nail folds to give rise to the nail plates.The abnormality is permanent.It may be associated with congenital absence of extremely poor development of the hair and with abnormalities of the teeth.Anonychia may be restricted to one or more nails of the digits of the hand and/or feet.
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Slide241Congenital Abnormalities of Nails(Deformed Nails)
Deformed Nails is a disorder occurring occasionally and may be a manifestation of a generalized skin disease or systemic disease.There are number of congenital diseases with nail defects.
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Slide242Congenital Abnormalities of the Mammary Glands(Athelia and Amastia)
The absence of Nipples (Athelia) and absence of the Breast (Amastia) are rare congenital abnormalities that may occur bilaterally or unilaterally.They are the result of failure of development or from complete disappearance of ridges.These conditions may also be the result of failure of a mammary bud to form.More common is hypoplasia of the breast, often found in association with gonadal agenesis and Turner syndrome.
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Slide243Congenital Abnormalities of the Mammary Glands(Aplasia of Breast)
The breast of a postpubertal female often differ somewhat in size.Marked differences are regarded as deformities because both glands are exposed to the same hormones at puberty.In these cases, there is often associated rudimentary development of muscles, usually the pectoralis major.
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Slide244Congenital Abnormalities of the Mammary Glands(Supernumerary Breast and Nipples)
An extra breast (polymastia) or nipple (polythelia) occurs in about 1% of the female population and is an inheritable condition.Supernumerary nipples are also relatively common in males.They are often mistaken for moles (nevi).An extra breast or nipple usually develops just inferior to the normal breast.
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Slide245Congenital Abnormalities of the Mammary Glands(Inverted Nipples)
Sometimes the nipples fail to elevate above the skin surface i.e., they remain in their newborn location.Inverted nipples may make breast-feeding of an infant difficult, but special exercise can be used to prepare the nipple for feeding an infant.
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Slide246Congenital Abnormalities of Teeth(Natal Teeth)
These are teeth that are erupted at birth.There are usually two in the position of the mandibular incisors.Natal teeth may produce maternal discomfort due to biting of the nipple during breast-feeding.In addition, the infant’s tongue may be lacerated or the teeth may detach and be aspirated.For these reasons, natal teeth are extracted.
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Slide247Congenital Abnormalities of Teeth(Enamel Hypoplasia)
Defective enamel formation causes pits and/or fissures in the enamel.These defects are a result of temporary disturbance in enamel formation.Various factors may injure the ameloblasts (e.g. nutritional deficiency, tetracycline therapy, and infectious disease such as measles.
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Slide248Congenital Abnormalities of Teeth(Rickets)
Rickets during the critical period of permanent tooth development is the most common known cause of enamel hypoplasia.Rickets is caused by a deficiency of vitamin D, especially during infancy and childhood.It is characterized by a disturbance of ossification.
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Slide249Congenital Abnormalities of Teeth(Abnormalities in Shape)
Abnormally shaped teeth are relatively common.Occasionally, spherical masses of enamel called enamel pearls are attached to the tooth.They are formed by aberrant groups of ameloblasts.The maxillary lateral incisor teeth may assume a slender, tapering shape.Congenital syphillis affects the differentiation of the permanent teeth resulting in screw-driver shaped incisors with central notches in their incisive edges.
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Slide250Congenital Abnormalities of Teeth(Numerical Abnormalities)
One or more supernumerary teeth may develop or the normal number of teeth may fail to form.Supernumerary teeth usually appear at the level of the maxillary incisors, where they disrupt the position and eruption of normal teeth.The extra teeth commonly erupt posterior to the normal ones.
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Slide251Congenital Abnormalities of Teeth(Abnormal Size of Teeth)
Disturbances during differentiation of teeth may result in gross alterations of dental morphology e.g. macrodontia (large teeth) and microdontia (small teeth)
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Slide252Congenital Abnormalities of Teeth(Fused Teeth)
Occasionally a tooth bud divides or two buds partially fuse to form fused teeth.This condition is commonly observed in the mandibular incisors of the primary dentition.Twinning of teeth is the results of division of the tooth bud.In some cases the permanent tooth does not form.This suggests that the deciduous and permanent tooth primordia fused to form the primary tooth.
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Slide253Congenital Abnormalities of Teeth(Dentigerous Cysts)
In rare cases cyst develops in the mandible, maxilla, or maxillary sinus that contains an unerupted tooth.The cyst develops due to cystic degeneration of the enamel reticulum of the enamel organ of an unerupted tooth.Most of these cysts are deeply situated in the jaw and are associated with misplaced or malformed secondary teeth that have failed to erupt.
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Slide254Congenital Abnormalities of Teeth(Amelogenesis Inperfecta)
The enamel is soft and friable because of hyocalcification and the teeth are yellow to brown in color.This autosomal dominant trait affects about one in every 20,000 children
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Slide255Congenital Abnormalities of Teeth(Dentinogenesis Inperfecta)
This condition is relatively common in white children,The teeth are brown to gray-blue with a apalescent sheen.The enamel tends to wear down rapidly, exposing the dentine.This anomaly is inherited in an autosomal dominant trait.
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Slide256Congenital Abnormalities of Teeth(Discolored Teeth)
Foreign substances incorporated into the developing enamel will cause discoloration of the teeth.Hemolysis associated with erythroblastosis fetalis may produce blue-black discoloration of the primary teeth.Tetracyclines are extensively incorporated into the enamel of teeth is given by 18th week (prenatal) to 12 years and may produce brownish-yellow discoloration.Tetracyclines should not be administered to pregnant women or to children if they can be avoided because these drugs adversely affect tooth development
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Slide257THIRD MONTH TO BIRTH
THE FETAL DEVELOPMENT
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Slide258Introduction
The transformation of an embryo to a fetus involves dramatic transformations in eight weeks.Development during the fetal period is primarily concerned with rapid growth of the body and differentiation of tissues and organs.A notable change during fetal period is the rapid slow down in the growth of the head compared to the rest of the body.The rate of body growth is very rapid especially between the 9th and 16th week, and fetal weight gain is phenomenal during the terminal weeks.
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Slide259Fetal Age
The length of the fetus is usually indicated as the crown-rump length (CRL) (sitting height) or as crown heel length (CHL), the measurement from the vertex of the skull to the heel (standing height).The measurement s are correlated with the age of the fetus in weeks or months.Growth in length is particularly striking during the 3rd, 4th, and 5th months, while an increase in weight is most striking during the last 2 months of gestation.
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Slide260In general, the length of pregnancy is considered to be 280 days or 40 weeks after the onset of the last normal menstrual period (LNMP) or, more accurately, 266 days or 36 weeks after fertilization.In our course, age is calculated from the time of fertilization and is expressed in weeks or calendar months
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Slide261Growth in Length and Weight During the Fetal Period.
Age (Weeks)Crown-Rump Length (cm)Weight (g)9-125-810-4513-169-1460-20017-2015-19250-45021-2520-23500-82026-2924-27900-130030-3428-301400-210035-3831-342200-290039-4035-363000-3400
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Slide262Nine to Twelve Weeks
At the beginning of the 9th week, the head constitute one half of the CRL of the fetus.Subsequently growth in body length accelerates so that by the end of the 12th week, the CRL has more than doubled.At 9th week, the face is broad, the eyes, widely separated with fused eyelids.By the end of the 12th week, ossification centers appear in the skeleton, especially in the skull and long bones.
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Slide263Limbs develop, with the upper limb reaching the final relative length but the lower limb still not well develop to their final length.Intestine and the liver develop and the liver starts erythropoiesis which is relayed by the spleen in the 12th week.Urine formation begins and the urine is discharged into the amniotic fluid.Fetal waste products are transferred to the maternal circulation by passing across the placental membranes.
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Slide264Thirteen to Sixteen Weeks
Growth is very rapid during this period.The head is relatively small and the lower limbs relatively lengthens as compared to the 12-week fetus.Limb movements which first occur at the end of embryonic period (8th Week), becomes coordinated by the 14th week but are too slight to be felt by the mother.Ossification of skeleton is active during this period
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Slide265Seventeen to Twenty Weeks
Growth slows down during this period but the fetus still increases in its CRL by about 50 mm.The lower limb reach their final portion and fetal movements known as quickening are commonly felt by the mother.The skin is now covered with a greasy material called vernix caseosa, and fine downy hairs called lanugo.Eye brows and head hair are also visble by the 20th week.
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Slide266By the 18th week, the uterus is formed and canalization of the vagina has begun.By this time, many primordial ovarian follicles containing oogonia have formed.By the 20th week, the testes have begun to descend but still located in the posterior abdominal wall, as are the ovaries in the female fetuses.
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Slide267Twenty-One to Twenty-Five Weeks
There is substantial weight gain during this period.The skin is wrinkled, pink to red, and more translucent.At 21st week, rapid eye movement begins, and blink-startle responses starts from the 22nd week.By the 24th week, pneumatocytes in the lungs starts secreting surfactant and fingernails appear.Although a 25-week fetus born prematurely may survive if given intensive care, it may die during early infancy because its respiratory system is still immature
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Slide268Twenty-Six to Twenty-Nine Weeks
The respiratory system develops sufficiently to provide adequate gas exchange.The CNS matures to a point to control breathing and body temperature.The eyes re-opens at 26th week, and lanugo and head hairs are well developed.Toenails becomes visible and subcutaneous fats is now present under the skin, smoothing out the wrinkles.The fetal spleen is now as the site of erythropoiesis is relayed by bone marrow by 28th week.
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Slide269Thirty to Thirty-Four Weeks
The skin is pink and smooth and the limbs have a normal appearance.Fetuses 32 weeks and older usually survive if born prematurely.If a normal weight fetus is born during this period, it is premature by date as opposed to being premature by weight.
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Slide270Thirty-Five to Thirty-Eight Week
Fetuses at 35 weeks have a firm grasp and exhibit a spontaneous orientation to light.As term approaches, The Nervous system is sufficiently mature to carry out some coordinated functions.There is slowing of growth during this finishing period as the time of birth approaches.Normally fetuses usually reach a CRL of 36 cm and a weight of about 3400 gm.In general male fetuses are longer and weigh more at birth than females.
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Slide271Time of Birth
The expected time of birth is 266 days or 38 weeks after fertilization i.e. 280 days or 40 weeks after LNMP.About 12% of babies , however, are born one to two weeks after the expected date of confinement (EDC).Prolongation of pregnancy for three or more weeks beyong the EDC occurs in 5 to 6% of women.
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Slide272Parturition (Birth)
For the first 34 to 38 weeks of gestation, the uterine myometrium does not respond to signals for Parturition (Birth).During the last 2 to 4 weeks of pregnancy, this tissue undergoes a transitional phase in preparation for the onset of labor.Ultimately, this phase ends with the thickening of the myometrium in the upper region of the uterus and a softening of the lower region and cervix.
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Slide273Labor itself is divided into three stages:Effacement (thickening and shortening) and dilation of the cervix, (this stage ends when the cervix is fully dilated),Delivery of the fetus, andDelivery of the placenta and fetal membranesStage 1 is produced by the uterine contractions that force the amniotic sac against the cervical canal until it ruptures.Stage 2 is also due to uterine contraction that leads to a great contraction of abdominal muscles.Stage 3 combines uterine contraction with the abdominal muscle contractions.
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Slide274As the uterus contracts, the upper part retracts, creating a smaller and smaller lumen, while the lower part expands, thereby producing direction to the force.Contractions usually begin about 10 minutes apart; then during the second stage of labor, they may occur less than 1 minute apart and last from 30 to 90 seconds.Their occurrence in pulses is essential to fetal survival, as they are of sufficient force to compromise uteroplacental blood flow to the fetus
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Slide275Clinical Correlates of the Fetal Development or Gestation Period
These include twin defects and preterm birth.Twin defects may be vanishing twins that result in fetus pyraceus in which only develops and the other is desorbed in the first trimester.Twin transfusion syndrome result in maternal blood supply only to one and the other therefore fail to develop.At later stages of development, partial splitting of the primitive node and streak may result in conjoined twinsDelivery of premature infant before 34 weeks is preterm birth caused by several factors.
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