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227 Cards in this Set
- Front
- Back
intraembryonic cavity
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formed by intercellular clefts in the lateral plate mesoderm, created by lateral folding and creates the future pleural, pericardial and peritoneal cavities
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somatic mesoderm and splanchnic mesoderm layer
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appear when intercellular clefts appear in the lateral mesoderm portion, occur when the plates are divided into two layers
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splanchnic mesoderm layer
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continuous with mesoderm of the wall of the yolk sac
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intraembryonic cavity (body cavity)
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the space bordered by the splanchnic and somatic mesoderm layer, loses connection with the extraembryonic cavity when the body of the embryo folds, forms the cavity extending from the thoracic to the pelvic region
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somatic mesoderm
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lines the intraembryonic cavity, become mesothelial and form the parietal layer of the serous membranes lining the ouside of the peritoneal, pleural and pericardial cavities
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splanchnic mesoderm
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form the visceral layer of the serous membranes covering the abdominal organs, lungs and heart
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dorsal mesentery
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point where the visceral and parietal layers are continuous with each other, it suspends the gut tube in the peritoneal cavity, initially it is a thick band of mesoderm running from the caudal limit of the foregut o the end of the hindgut
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ventral mesentery
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exists only from the caudal foregut to the upper portion of the duodenum and results from thinning of mesoderm of the septum transversum
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mesentery
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a double layer that provides a pathway for blood vessels, nerves and lymphatics of the organ
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septum transversum
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a thick plate of somatic lateral plate mesodermal tissue occupying the space between the thoracic cavity and the stalk of the yolk sac, does not separate the thoracic and abdominal cavities completely, communication through the pericardioperitoneal canals
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pericardioperitoneal canals
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the large openings found where the septum transversum does not separate the thoracic and abdominal cavity, act as a space where the lung buds grow into
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lung buds
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when they begin to grow they expand caudolaterally within the pericardioperitoneal canals, this causes the canals to shrink and the lungs expand into the mesenchyme of the body wall dorsally, laterally and ventrally
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pleuropericardial folds
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develop with lung buds, become part of the thoracic wall, appear as small ridges projecting into the primitive undivided thoracic cavity at first, form the pleuropericardial membranes
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pleuropericardial membrane
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contains common cardial veins and phrenic nerves, divide thoracic cavity into pericardial and two pleural cavities, forms the fibrous pericardium
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components of the mesoderm after lung expansion
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1. definitive wall of the thorax
2. pleuropericardial membranes-extensions of the pleuropericardial folds that contain the common cardinal veins and phrenic nerves |
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pleural cavities
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are derived from the transformation of the pericardioperitoneal canals
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divisions of the thoracic cavity
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1. pericardial cavity
2. two pleural cavities |
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fibrous pericardium
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formed from the pleuropericardial membranes
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pleuroperitoneal folds/membrane
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cresent-shaped folds that closes the opening between the pleural and peritoneal cavities, project into the caudal end of the pericardioperitoneal canals, by the 7th week they fuse with the mesentery of the esophagus and with the septum transversum, thus causing the separation of the thoracic and abdominal cavity
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diaphragm formation
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forms once the rim is established, myoblasts originating in the body wall penetrate the membranes to form the muscular part of the diaphragm
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what structures derive the diaphragm
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1. the septum transversum-forms the central tendon of the diaphragm
2. the two pleuroperitoneal membranes 3. muscular components from the lateral and dorsal body walls 4. the mesentery of the esophagus (where the crura develops) |
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3rd, 4th, and 5th cervical segments
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grow into the septum
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phrenic nerves
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pass into the septum through the pleuropericardial folds, explains why expansion of the lungs and descent of the septum shift the phrenic nerves into the firbrous pericardium, supply the diaphragm with its motor and sensory innervation
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diaphragm at the 6th week
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at the level of the thoracic somites
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repositioning of the diaphragm
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caused by rapid growth of the dorsal part of the embryo compared with that of the ventral part, by the 3rd month some of the diaphragm is at the level of L1
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superior vena cava
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comes from the right common cardinal vein
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ventral body wall defects
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due to incomplete or improper folding or incomplete development of the body wall, bone, muscle and/or skin, failure of the ventral body wall to close
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ectopia cordis
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when the heart protudes through a sternal defect (cleft sternum or absence of the lower third of the sternum) and heart lies outside the body
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omphalocele
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herniation of abdominal viscera through an enlarged umbilical ring, failure of bowel to return after physicological hernia (which is normal during the 6th to 10th week), covered amnion, 59% cardiac, 40% neural tube, INC in alpha fetoprotein
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gastroschisis
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herniation of abdominal viscera through the body wall into the amniotic cavity, lateral to umbilicus usually right side, not covered by amnion which leads to damage, not associated with other defects or chromosomal abnormalities like omphaloceles, INC in alpha fetoprotein, volvulus otherwise prognosis excellent
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cleft sternum
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ventral body wall defect that results from lack of fusion of the bilateral bars of mesoderm responsible for formation of this structure
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Cantrell pentalogy
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a defect that involves both the thorax and the abdomen
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bladder and cloacal exstrophy
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defects in the pelvic region resulting from a lack of closure of the body wall
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diaphragmatic hernia
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failure of one or both pleuroperitoneal membranes to close the pericardioperitoneal canals, abdominal viscera herniates here, 90% left side, a large defect associated with a high rate of mortality from pulmonary hypoplasia and dysfunction (hidden mortality), 1/2000 births
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parasternal hernia
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occurs when a small part of the muscular fibers of the diaphragm fails to develop, found in anterior portion of the abdominal wall, enter chest between the sternal and costal portions of the diaphragm
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esophageal hernia
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thought to be due to congential shortness of the esophagus, upper portions of the stomach are found in the thorax, stomach is constricted at the level of the diaphragm
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respiratory diverticulum (lung bud)
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forms at 4 weeks old, it appears as an outgrowth from the ventral wall of the foregut, along the gut tube
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TBX4
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determines the location of the bud along the gut tube, expressed in the endoderm of the gut tube at the site of the respiratory diverticulum, induces formation of the bud and the continued growth and differentiation of the lungs
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endoderm and lung
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origin of the epithelium of the internal lining of the larynx, trachea, and bronchi as well as that of the lungs
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splanchnic mesoderm and the lung
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is the origin for the cartilaginous, muscular, and connective tissue components of the trachea and lungs
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tracheoesophageal ridges
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two of them, separates the foregut from the lung bud after the diverticulum expands caudally, these fuse form the tracheoesophageal septum
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teacheoesophageal septum
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divides the forgut dorsally into the esophagus and ventrally into the trachea and lung buds
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laryngeal orifice
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maintains communication of the respiratory primordium with the pharynx, changes in shape from a sagittal slit to a T-shaped opening due to rapid proliferation of mesenchyme
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mesenchyme of the 4th and 6th pharyngeal arches
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is the origination point for the cartilage and muscle of the larynx
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thyroid, cricoid and arytenoid cartilages
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fromed from the mesenchyme of the two pharyngeal arches, gives the shape of the laryngeal orifice
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laryngeal ventricles
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a pair of lateral recesses caused from the vacuolization and recanalization of the lumen (caused by proliferation of the laryngeal epithelium), these recesses are bounded by folds of tissue that differentiate into the false and true vocal cords
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larynx in a 12 week embryo
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epiglottis/supraglottis formed from the 4th pharyngeal arch, vocal cords and arytenoid swelling from 6th pharyngeal arch
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purpose of laryngeal development
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to separate the airway and esophagus, larynx separates the trachea and pharynx (esophagus)
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vagus nerve
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CN X, innervate all the laryngeal muscles
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superior laryngeal nerve
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innervates derivatives of the 4th pharyngeal arch
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recurrent laryngeal nerve
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innervates derivatives of the 6th pharyngeal arch
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lung bud gives rise to what?
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trachea and two lateral bronchial buds
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bronchial buds
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enlarge at the 5th week and form right and left main bronchi, right then forms three secondary bronchi and the left two secondary
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6th week embryo and lungs
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segments of the primitive lobes form, 10 segments on the right and 8 on the left
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8 week embryo and lungs
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segments divide further, pleuroperitoneal folds separate the lobes to form major and minor fissures
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pericardioperitoneal canals
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spaces for the lungs, become more narrow as the lung buds expand into the cavity, lie on each side of the foregut
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primitive pleural cavities
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formed from the pleuroperitoneal and pleuropericardial folds separating the pericardioperitoneal canals from the peritoneal and pericardial cavities
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visceral pleura
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derives from the mesoderm covering the outside of the lung
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parietal pleura
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derives from the somatic mesoderm layer covering the body wall from the inside
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pleuropericardial folds
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separate the pericardial and pleural cavities
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pleural cavity
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space between the parietal and visceral pleura
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tertiary (segmental) bronchi
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form from the further development of the secondary bronchi, ten in the right and 8 in the lef, these form the bronchopulmonary segments of the adult lung, by the end of the 6th month, 17 generations of subdivisions have formed, six more formed during postnatal life
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what regulates branching
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epithelial-mesenchymal interactions between the endoderm of the lung buds and splanchnic mesoderm that surrounds them, involve FGF family
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pulmonary artery development
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grow caudally from the aortic sac positioning themselves next to the bronchial branches, arterial branches completed by 16 weeks, arterioles and capillaries continue to proliferate/grow for several years after birth
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pseudoglanular period
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5-16 weeks, branching has continued to form terminal bronchioles, no respiratory bronchioles or alveoli are present, bronchial branching completes
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canalicular period
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16-26 weeks, each terminal bronchiole divides into 2 or more respiratory bronchioles, which in turn divide into 3-6 alveolar ducts, alveolar ducts open to 10-16 alveoli, respiratory bronchioli/alveolar ducts form
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recognition of respiratory bronchioli
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by thinning of cuboidal epithelial cells into thin, flat cells capable of gas exchange
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terminal sac period
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26 weeks to birth, terminal sacs (primitive alveoli) form and capillaries establish close contact
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alveolar period
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8 months to childhood, mature alveoli have well-developed epithelial endothelial (capillary) contacts
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respiratory bronchioles
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cuboidal in shape, allow for respiration to occur when change to thin, flat cells, intimately associated with numerous blood and lymph capillaries
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terminal sacs (primitive alveoli)
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surrounding spaces of the bronchioles and capillaries, i.e. surround thin, flat cells
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type I alveolar epithelial cells
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line terminal sacs, become thinner, allows surrounding capillaries to protrude into the alveolar sacs, forms blood-air barrier
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mature alveoli
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not present before birth
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type II alveolar epithelial cells
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produce surfactant
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surfactant
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a phospholipid-rich fluid capable of lowering the surface tension at the air-alveolar interace, phospholipids + surfactant proteins (SP-A, SP-B, SP-C, SP-D), measure lecithing/sphingomyelin ratio in amniotic fluid, ratio > 1.9, then phosphatidylglycerol (which comes from phosphotidylinositol) is present = low risk for respiratory distress syndrome
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purposes of surfactant
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decreases surface tension, reduces collapse of alveoli, DEC pressures required to expand lung, controls fluid balance in alveoli, keeps them dry
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fetal breathing movements
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begin before birth and cause aspiration of amniotic fluid, important for stimulating lung development and conditioning respiratory muscles, when respiration begins at birth, most of the lung fluid is resorbed
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postpartum breathing
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bring air into the lungs, growth of lung primarily to an increase in the number of bronchioles and alveoli (formed during the first 10 years of postnatal life)
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esophageal atresia
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abnormaliites in partitioning of the esophagus and trachea by the tracheoesophageal septum, may allow gastric contents or amniotic fluid to enter the trachea and cause penumonitis and pneumonia
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tracheo-esophageal fistulas TEF
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occurs when the esophagus and trachea are attached, associated with other birth defects (cardiac abnormalities), component of the VACTERL association, complication is polyhydramnios (bec. amniotic fluid does not pass to the stomach and intestines)
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Syptoms of TE fistula
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may present with excess salivation/drooling, choking, inability to pass feeding catheter into stomach, X-ray shows dilated upper esophageal pouch, INC air in abdomen and stomach, diagnosis by bronchoscopy
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Type III TEF
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most common, occurs 86% of the time, occurs when the upper portion of the esophagus ends in a blind pouch and the lower segment forms a TEF, affects amniotic fluid volume
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H-type (V-type) fistula
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forms an H shaped fistula in which there is communication of esophagus with the trachea at one point, does not present with esophageal atresia
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isolated esophageal atresia
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no TEF forms, just two esophageal atresias
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tracheal stenosis/agenesis
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vascular compromise to the developing trachea, shrinking of the trachea
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congenital laryngeal cleft
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very rare, deficiency in the separation of the larynx from the hypopharynx, symptoms include aspiration, choking, weak voice
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shape of larynx in infants
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CROUP, funnel shape in infants, cylindrical in adults
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respiratory distress syndrome (RDS)
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cause: surfactant deficiency (causing INC surface tension, collapse (atelectasis) of lungs, INC alveolar fluid), ventilator induced trauma, hypoxia, acidosis (damage to capillary endothelial cells, leakage of proteinaceous fluid “hyaline membranes”)
occurs: after 23 weeks gestation, potentially viable 20% of deaths in newborns |
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hyaline membrane disease (HMD)
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AKA of RDS, hyaline membrane consists of protein, dead epithelial cells, fibrin clot formation
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treatment of RDS or HMD
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surfactant treatment (DECes surface tension within mins/hrs.), at 72 hours pulmonary macrophages will appear, other complications include infection, ventilator damage, oxygen toxicity, INC lung fluid from other causes such as PDA
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Dochdalek type congenital diaphragmatic hernia
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most common and sever, 80-85% left sided, abdominal organs migrate into the left chest wall, heart pushed over to the right, moderate-severe lung hypoplasia of left lung, mild hypoplasia of right lung
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morgagni type congenital diaphragmatic hernia
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parasternal defect, incomplete muscularization of the diaphragm, so significant pulmonary hypoplasia, mild or no respiratory distress
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hypoplastic lung
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leads to smaller airways, alveoli and pulmonary vascular bed, DEC gas exchange surface area
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hypoxemia
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INC constriction of pulmonary blood vessels, pulmonary vascular resistance and pulmonary artery pressures, a right to left shunting of blood
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ectopic lung lobes
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arise from the trachea or esophagus, formed from additional respiratory buds of the foregut
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congential cysts of the lung
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formed by dilation of terminal or larger bronchi, gives honeycomb appearance to lung, these structures normally drain poorly and lead to chronic infections
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when is the vascular system established
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during the middle of the third week when the embryo is no longer able to satisfy its nutritional requirements by diffusion alone
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where are cardiac progenitor cells
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lie in the epiblast lateral to the primitive streak, they then migrate through the streak in a sequential cranial -> caudal order, proceed toward the cranium and position themselves rostal to the buccopharyngeal membrane and neural folds residing in the splanchnic mesoderm, then induced by the pharyngeal endoderm to form cardiac myoblasts, blood islands also appear to form blood cells and vessels
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cardiogenic field
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horseshoe-shaped endothelial tube composed of cardiac myoblasts
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pericardial cavity
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the intraembryonic cavity over the cardiogenic field
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dorsal aortae
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blood islands that appear bilaterally, parallel and close to the midline of the embryonic shield
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growth of the brain and the position of the heart tube
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causes the buccopharyngeal membrane to be pulled forward while the heart and pericardial cavity move first to the cervical region and finally to the thorax
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heart tube
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angiogenic cell clusters coalesce to form right and left endocardial tubes, embryo folds cephalocaudally and laterally, endocardial tubes fuse via programmed cell death (PCD) forming a continuous tube with an inner endothelial lining and an outer myocardial layer
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where does venous drainage occur in the heart tube
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at the caudal pole
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where does blood get pumped out of
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the first aortic arch into the dorsal aorta at its cranial pole
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dorsal mesocardium
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a fold of mesodermal tissue that attaches the tube to the dorsal side of the pericardial cavity
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transverse pericardial sinus
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created by the disappearance of the dorsal mesocardium, connects both sides of the pericardial cavity, suspends the heart in the cavity by blood vessels at its cranial and caudal pole
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proepicardium
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formed from the mesothelial cells on the surface of the septum transversum, is near the sinus venosus and migrate to the heart to form epicardium, rest of epicardium comes from mesothelial cells from the outflow tract (cephalic end)
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three layers of the heart tube
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1. endocardium-forms the internal endothelial lining of the heart, surrounded by cardiac jelly which separates it from the myocardium
2. myocardium-forms the muscular wall 3. epicardium or visceral pericardium-covering the outside of the tube, responsible for formation of the coronary arteries, including their endothelial lining and smooth muscle |
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creation of the cardiac loop
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caused by the bending of the cephalic portion (ventrally, caudally and to the left) and the caudal portion (dorsocranially and to the right), start at day 23 with a series of expansions, constrictions and folds, completed by day 28, normal is folding to the left
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five dilations of the heart tube (cephalic -> caudal, ventral -> dorsal)
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1. aortic roots-remains outside the pericardial cavity after looping
2. bulbus cordis-divided into truncus arteriosus, conus cordis and trabeculated part of the right ventricle 3. primitive ventricle 4. primitive atrium-goes inside the pericardial cavity after looping 5. sinus venosus-remains outside the pericardial cavity after looping |
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what does the formation of the cardiac loop create
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1. normal position of heart chanber
2. changes a single circuit system into an assymetrical system -> pulmonary and systemic circulations |
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atrial portion
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initially a paried structure outside the pericardial cavity, forms a common atrium and is incorporated into the pericardial cavity
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atrioventricular junction
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forms the atriventricular canal, connects the common atrium and the early embryonic ventricle
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bulbous cordis
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narrow, proximal end of bulbus forms the trabeculated part of the right ventricle
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conus cordis
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will form the outflow tracts of both ventricles, midportion of bulbus
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truncus arteriosus
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distal part of the bulbus, will form the roots and proximal portion of the aorta and pulmonary artery
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primary interventricular foramen
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junction between the ventricle (left) and the bulbus cordis (which eventually makes the right), externally indicated by the bulboventricular sulcus
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primitive left ventricle
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formed from the primitive ventricle when it is trabeculated
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primitive right ventricle
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formed from the proximal third of the bulbus cordis when it is trabeculated
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sinus venosus
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initially on the dorsal end in association with the septrum transversum, in the middle of the 4th week (24 day) it receives venous blood from the right and left sinus horns and gives it to the atria, entrance shifts to the right venous return caused by left to right shunts of blood (35 days), IVC, SVC and coronary sinus all open into here, contains crista terminalis (conducting fiber tract SA node to AV node)
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right vitelline vein
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becomes the IVC
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right anterior cardinal vein
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becomes the SVC
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left sinus horn
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coronary sinus and oblique vein of the left atrium
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right sinus horn
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blends into the right posterior wall of the right atrium becoming the smooth area sinus venarum
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pulmonary veins
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come from the smooth portion of the left atrium
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where do sinus horns receive blood from
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1. vitelline or omphalomesenteric vein
2. umbilical vein 3. the common cardinal vein |
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when is the right umbilical vein and left vitelline vein obliterated?
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fifth week,
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when is the left common cardinal vein obliterated
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10 weeks, mostly due to the fact that venous drainage occurs entirely on the right side now
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what remains of the left sinus horn after the 10th week
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oblique vein of the left atrium and the coronary sinus, empty into the sinus venosus
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sinuatrial orifice
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entrance of the right horn into the right atrium, flanked on each side by right and left venous valves
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septum spurium
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caused by the fusion of the right and left venous valves dorsocranially
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right venous valve and its formation of great vessel valves
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superior portion is obliterated, inferior portion forms the valves of the IVC and coronary sinus
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crista terminalis
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forms the dividing line between the original trabculated part of the right atrium and the smooth walled sinus venarum which originates from the right sinus horn
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when are the septa formed
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27th to 37 days
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theories of cardiac septa formation
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1. two actively growing masses (endocardial cushions) approach each other until they fuse, dividing the lumen into two separate canals
2. one actively growing mass that makes its way to the other end 3. does not envolve cushions, occurs when the atria and ventricle grow while a narrow ridge does not forming a septa, such a septa never completely divides the original lumen, closed secondarily by neighboring proliferating tissues |
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endocardial cushions and formation of cardiac septa
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splanchnic mesoderm, addition of neural crest cells in the conotruncal area or AV region, play a role in formation of septa and valves and cardiac defects
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AV and conotruncal area
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help in formation of the atrial and ventricular (membranous) septa, the atrioventricular canals and valves and the aortic and pulmonary channels
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septum primum
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thin membranous septa, first portion is a small sickle shaped crest that grows in the roof of the common atrium into the lumen, extend toward the endocardial cushions in the AV canal, perforations made in the upper portion through cell death
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ostium (foramen) primum
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opening between the lower rim of the septum primum and the endocardial cushions, closed with further development of the endocardial cushions on the end of the septum primum
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ostium (foramen) secundum
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coalescence of the perforations found in the septum primum, maintains right and left shunt bypassing the pulmonary circulation
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septum secundum
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second crest fold formed, a thick muscular septum forms to the right of the septum primum, never forms a complete partition, only overlapping the ostium secundum
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oval foramen
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forms by incomplete closure of the septum secundum maintaining a right to left shunt, foramen ovale closes right after birth
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closure of the foramen ovale
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DEC in right atrial pressure from occlusion of placental circulation and INC left atrial pressure due to INC pulmonary venous return, a functional closure at birth, anatomical closure at 3 months when the septum primum and septum secundum fuse
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pulmonary vein
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develops as an outgrowth of the posterior left atrial wall, to the left of the septum primum, gains connections with veins of the developing lung buds, eventually formes the smooth walled part of the adult atrium, eventually 4 enter the left atria
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AV endocardial cushions
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appears at the superior and inferior borders of the Av canal, project into the lumen and fuse, results in a complete dicision of the canal into right and left AV orifices by end of 5th week
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bulbo(cono) ventricular flange
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` separate the bulubus from the left ventricle, terminates at the end of the 5th week
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lateral AV endocardial cushions
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appear on the right and left borders of the canal,
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formation of AV valves
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after fusion of cushions, orifice is surrounded by proliferations of mesenchymal tissue, bloodstream hollows out tissue on the ventricular side of the proliferations forming valves connected to the wall by muscular cords, muscular cords replaced with dense connective tissue, connected to papillary muscles by chordae tendinae
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truncus swellings (ridges)
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forms aorticopulmonary septa dividing truncus into aortic and pulmonary channels, lie on the right and left superior wall, right swelling grows distally and to the left while the left grows distally and to the right (growth toward the aortic sac), left and right twist around each other (to make sure that the correct outflow tract is lined up with the correct ventricle)
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conus swellings (ridges)
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forms the outflow tracts of the right (anterolateral) and left (postereomedial) ventricles, develop along the right dorsal and left ventral walls, unite with the truncus septum
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neural crest cells and partitioning of the truncus arteriosus and conus cordis
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contributions to both swellings to form CT and smooth muscle of the aorticopulmonary septum
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partitioning of the primitive ventricle
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end of the 4th week, muscular intervetricular (IV) septum develops midline on the floor of primitive ventricle from merging medial walls of the two ventricles, IV foramen between free edge of muscular IV septum and fused AV cushions allows for communication between the two ventricles, eventually closes through outgrowth of inferior AV cushions
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interventricular forman
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above the muscular portion of the interventricular septum shrinks once the conus septum is made
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expansion of the primitive ventricles
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due to growth of the myocardium on the outside and continuous diverticulation and trabecula formation on the inside
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membranous IV septum
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formed from complete closure of the IV foramen
1. right and left bulbar ridges 2. inferior AV cushions |
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semilunar valves
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two pairs, visible as small tubercles found on the main trunucs swelling, tubercules hollow out at their upper surface and form the valves, neural crest cells contribute to the formation of the valves
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pacemaker of the heart
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initially in the caudal part of the left cardiac tube, later sinus venosus assumes this function, incorporated into the right atrium, replaced with pacemaker tissue and forms SA node at base of interatrial septum
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bundle of His
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derived from cells in the left wall of the sinus venosus, and cells from the AV canal
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vasculogenesis
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one form of blood vessel development, vessels arise by coalescence of angioblasts, makes major vessels like the dorsal aorta and cardinal veins
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angiogenesis
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another form of blood vessel development, vessels sprout from existing vessels, forms remainder of vessels
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vascular endothelial growth factors (VEGF)
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pattern the system of vessel formation
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aortic arch arteries
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arise from the aortic sac (expansion of cranial end of the truncus arteriosus), ventrally and connect to the left and right dorsal aortae dorsally
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aortic arches
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six pairs originate in aortic sac (the 5th though sometimes never forms or forms incompletely the regresses) and terminate in right and left dorsal aortae, give arterial supply to each of the pharyngeal arches
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adult arterial system
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develops from aortic arches 3, 4 and 6 (these develop asymmetrically and make major contributions) and the right and left dorsal aortae, aortic arches 1 (disappear by day 27, before arch 6 is made), 2 and 5 disappear
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brachiocephalic artery
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the right horn of the aortic sac
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aortic arch
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the left horn of the aortic sac
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arch 1
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gives rise to maxillary artery
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arch 2
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gives rise to hyoid and stapedial arteries
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arch 3
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common, external and part of the internal carotid artery
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arch 4
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left: part of the arch of the aorta
right: most prosimal segment of the right subclavian |
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arch 6
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left: left pulmonary artery and the ductus arteriosus
right: right pulmonary artery |
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recurrent laryngeal nerves
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left: nerve hooks where the ligamentum arteriosum is
right: moves up and hooks around the right subclavian |
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vitelline arteries
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initially a number of paired vessels supplying the yolk sac, form the vessels in the dorsal mesentery of the gut (celiac, SMA, IMA)
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derivation of coronary arteries
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1. angioblasts formed elsewhere and distributed over the heart surface by migration of the proepicardial cells
2. epicardium |
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inflow tract remodeling
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1. above the diaphragm-remodeling begins with a shift to the right of the venous return
2. below the diaphragm- |
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vitelline system below the diaphragm
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gives rise to the liver sinusoids (including the ductus venous), the portal system (portal vein, SMV, IMV and its components) and a portion of the IVC, carries blood from the yolk sac to the sinus venosus
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right umbilical vein below the diaphragm
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disappears and the left umbilical vein anastomoses with the ductus venous, originates in the chorionic villi and carry oxygenated blood to the embryo from the placenta
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cardinal veins
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drain the body of the embryo proper, form the main venous dranage system of the embryo initially
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how does oxygenated blood from the placenta reach the heart
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via the single umbilical vein and the ductus venosus
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ductus venosus
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direct communication between the left umbilical vein and the right hepatocardiac channel, bypasses the sinusoidal plexus of the liver
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ligamentum venosum
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obliterated left umbilical ductus venosus
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anterior cardinal veins
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drain the cephalic part of the embryo
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posterior cardinal veins
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drain the rest of the embryo
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common cardinal veins
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joining of the anterior and posterior cardinal veins before reaching the sinus horn
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subcardinal veins
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drain the kidney
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sacrocardinal veins
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drain the lower extremities
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supracardinal veins
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drain the body wall by way of the intercostal veins, taking over the function of the posterior cardinal veins
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left brachiocephalic vein
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created by the anastomosis between the anterior cardinal vein
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left superior intercostal vein
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receives blood from the second and third intercostal spaces, comes from the left posterior cardinal vein
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superior vena cava
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formed by the right common cardinal vein and the proximal portion of the right anterior cardinal vein
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left renal vein
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formed from the anastomosis between the subcardinal veins
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left gonadal vein
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also forms from the subcardinal veins
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left common iliac vein
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comes from the anastomosis between the sacrocardinal veins
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azygos and hemiazygos veins
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come from the right and left supracardinal vein
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fetal circulation
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well oxygenated blood returns from the placenta via the umbilical vein, half passes through the hepatic sinusoids, other half bypasses the liver and goes through the ductus venosus, into the IVC (right to left shunt), blood goes into the right atrium, then most through the foramen ovale into the left atrium (right to left shunt) into the left ventricle and out the ascending aorta, best oxygenation to head, neck and upper limbs, small amount of blood from the right ventricle enters pulmonary trunk, some goes to the lungs but most passes through the ductus arteriosus into the aorta (right to left shunt), umbilical arteries return blood to the placenta for re-oxygenation
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where does oxygenated blood meet non-oxygenated blood in fetal circulation
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1. liver
2. IVC 3. right atrium 4. left atrium 5. ductus arteriosus |
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saturation levels of blood in the umbilical arteries that goes back to the placenta
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58%
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neonatal circulation
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at birth, the three shunts that permitted most of the blood to bypass the liver and the lungs cease to function, the foramen ovale, ductus arteriosus, ductus venosus and umbilical vessels are no longer needed
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how are the unnecessary fetal circulation shunts obliterated
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1. aeration of the lungs provides a dramatic fall in vascular resistance, causes INC in pulmonary blood flow -> INC of lest atrial pressure above that in the right atrium -> closing of the foramen ovale
2. constriction of the ductus arteriosus 3. constriction of the ductus venosus 4. constriction of the umbilical vessels |
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fetal remnants
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1. and 2. umbilical arteries -> internal iliac arteries and medial umbilical ligaments
2. umbilical veins -> ligamentum teres of liver 3. ductus venosus -> ligamentum venosum 4. ductus arteriosus -> ligamentum arteriosum 5. foramen ovale -> obliterated |
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lympathic system
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appears later than the circulatory system, 5th week, may form from mesenchyme in situ, two jugular, two iliac, one retroperitoneal and one cisterna chyli
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dextrocardia
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folding to the right, heart lies on right, resulting in mirror image of the heart
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isolated dextrocardia
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associated with other severe cardiac anomalies
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dextrocardia with situs inversus (inversion of the all viscera)
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not associated with sever cardiac defects, normal physiology, slight risk of heart defects
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heterotaxy
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where sidedness is random in the organs, some reversed some not, classified as laterality sequences
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probe patency of the foramen ovale
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incomplete anatomical fusion of septum primum and septum secundum, present in approx. 25% of the population, of no clinical importance
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ASD (atrial septal defects)
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2:1 femal to male prevalence, can be ostium secundum defects (most clinically significant ASD), cor triloculare biventriculare (common atrium), or ostium primum defects
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ostium secundum ASD
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characterized by a large opening between the left and right atria, caused by either excessive cell death and resorption of the septum primum or by inadequate formation of the septum secundum, may cause intracardiac shunting from left to right
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cor triloculare biventriculare
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complete absence of the atrial septum, is always associated with serious defects elsewhere in the heart
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ostium primum ASD
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partially fusion of AV canal, defect in atrial septum, usually combined with a cleft in the anterior leaflet of the tricuspid valve
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tricuspid atresia
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obliteration of the right AV orifice, characterized by the absence or fusion of the tricuspid valves, symptoms include patency of the oval foramen, ventricular septal defect, underdevelopment of the right ventricle and hypertrophy of the left ventricle
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endochondral cushions and heart defects
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cushions play a role in ASD, VSD, transposition of the great vessels, tetralogy of Fallot , if cushions fail to fuse results in persistent atrioventricular canal
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conotruncal cushions and heart defects
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neural crest cells cause both heart and craniofacial defects in the same individual
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transposition of the great vessels (TGA)
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failure of the aorticopulmonary septa to develop in a spiral fashion (so aorta lines up with the right ventricle and the pulmonary trunk leaves with the left), leads to cyanosis, complete TGA is incompatible with life if there is no associated septal defect or patent ductus arteriosus (allows for connection between the arch of aorta and pulmonary arteries
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persistent truncus arteriosus
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no formation of the AP septum, a single arteriole vessel leaves the heart giving rise to the aorta and pulmonary trunks, usually accompanied by a defect in the IV septa, cyanosis
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teratology of fallot
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failure of outflow tract openings to align with ventricles, cyanosis, most freq. occurring of the conotruncal regions, four classic findings
1. overriding aorta that arises directly over the septal defect 2. pulmonary stenosis 3. rt. ventricular hypertrophy bec. of higher pressure on the right 4. IV septa defect |
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ventricular septum defects
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most common cardiac defect, occurs in about 25% of children with congenital heart disease, occurs through failure of the membranous IV septum to form or muscular VSD which arises from single or multiple perforations in the muscular IV septum
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acyanotic congential cardiac anomalies
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1. anomialies of the aortic arches
a. right arch of aorta b. double arch of aorta c. retro-esophageal right subclavian artery 2. coarctation of aorta |
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usually acyanotic congenital cardiac anomalies (left right shunts)
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1. persistent ductus arteriosus
2. interatrial septal defects 3. interventricular septal defects |
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cyantoci congenital cardiac anomalies (right left shunts)
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1. complete transposition of great vessels
2. truncus arteriosus communis 3. teratology |
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patent ductus arteriosus
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a ductus arteriosus that does not close, can be isolated or accompany other heart defects
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coarctation of the aorta
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occurs when the aortic lumen below the origin of the left subclavian artery is narrowed
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retro-esophageal right subclavian artery
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near where the left subclavian is, must cross the midline and posterior to the esophagus to reach the right arm, does not usually cause problems with swallowing or breathing though
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double aortic arch
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the right dorsal aorta persists, forms a junction with the left arch of the aorta and a vascular ring is present that surrounds the trachea and esophagus and commonly compresses the structures
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right aortic arch
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arch of the aorta is on the right side bec. left is obliterated, can cause swallowing complaints
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interrupted aortic arch
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caused by obliteration of the 4th aortic arch on the left side, combined with an abnormal origin of the right subclavian
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