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26 Cards in this Set
- Front
- Back
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Describe the structure of pharyngeal arches |
-Boarded by ectoderm (externally) and endoderm (internally) -Core composed of mesenchyme (neural crest cells, paraxial and lateral plate mesoderm) -Each arch has it's own cranial nerve, artery, cartilage |
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Describe how neural crest cells, paraxial/lateral mesoderm contribute to structures of the face |
-Neural crest cells form in the neuroectorderm, migrate ventrally from rhombomeres to the craniofacial region - forming the ectodermal placode. They make up the bones, dermis, connective tissue of the face, sensory ganglia for CN V, VII, IX, X, pia/arachnoid mater, and dentin -Paraxial mesoderm forms the muscles of the head/neck + part of the neurocranium. -Lateral plate mesoderm forms the laryngeal cartilages. |
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What is the significance of the pharyngeal clefts |
-Only the first goes on to form something significant -> external auditory meatus + tympanic membrane -All others obliterated -Sometimes obliteration is incomplete and leaves behind a cervical cyst or fistula |
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Highlight the differentiation of pharyngeal pouches |
-Pharyngeal pouches lined by endoderm, unlike clefts, which are lined by ectoderm -1st pouch -> tympanic cavity + eustachian tube -2nd pouch -> palatine tonsils (adults = tonsillar fossa) -3rd pouch -> dorsal wing into the inferior parathyroid gland, ventral wing into the thymus gland -4th -> dorsal wing into the superior parathyroid gland, ventral wing into the ultimobranchial body (eventually parafollicular cells of the thyroid) |
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Describe tongue development |
-Lingual swellings form from the floor of the pharynx. Swelling are due to the proliferation of the endoderm and underlying mesenchyme -Initially the swelling grow from the first four arches, but the 3rd overcomes the second to form the body (ant. 2/3) and root (pos. 1/3) |
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Describe the formation of the thyroid gland |
-Proliferation of endoderm in the midline floor of the pharynx forms a tube (thyroglossal duct) -This tube opens into the pharynx at the foramen cecum (of the tongue) -Glandular tissue forms at the tip of the thyroglossal duct, and will eventually become the thyroid gland |
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How is neural cell migration regulated |
-HOX genes regulate the migration of neural crest cells -OTX2 drives migration of neural crest cells from midbrain and rhombomeres 1 & 2 to the craniofaical region of the first arch |
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Describe the formation and growth of facial prominences |
-migration of neural crest cells form the frontonasal prominence, two maxillary prominences, and the mandibular arch -Ectoderm thickens on lateral surface of frontonasal prominence to form the nasal placodes -Ectoderm invaginates to form the primitive nares, surrounding mesenchyme forms the nasals processes -Maxillary prominences and nasal processes fuse to form the intermaxillary segment |
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What three segments comprise the intermaxillary segment |
-philtrum, upper jaw and primary palate (boarders 4 incisor teeth) |
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Describe the formaiton of the secondary palate |
-Maxillary prominences fused by the intermaxillary segment -Segments extend dorsally into the oral cavity, forming shelves -Originally the shelves assume a vertical position in the oral cavity -In order to facilitate fusion on the maxillary processes in the oral cavity, the mandible grows forward, allowing the tongue to drop out of the way - the shelves then flip to a horizontal position |
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Describe the role of SHH in the embryology of the face |
-SHH expression establishes midline, this includes separation of the eye fields -Midline establishe at approx. 3 weeks *Midline clefts (failure of med. nasal prominence fusion) are more problematic than lateral clefts since they are assoc. with brain defects + cognitive impairments |
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How do neural crest deficits lead to congenital impairments |
-Neural crest cell migration makes up dermis, connective tissue, bone and more of face. Deficits due to retinoids, alcohol, maternal diabetes or tetratogens may lead to: Treacher-Collins - deficiency in the maxilla and zygomatic arches Robin Sequence - mandible deficiency -> cleft palate, micrognathia, posterior tongue DiGeorge anomaly - velocardiofacialand conotruncal anomalies due to 22q deletion. Most severe due to no thymus development Goldenharsyndrome - unilateral defects in maxillary,temporal, and zygomatic bones, ears and eyes |
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Highlight the three areas of the gut tube |
-Foregut: orpharyngeal membrane to the bile duct -Midgut: bile duct to first 2/3rds of transverse colon -Hindgut: last 1/3rd of transverse colon to cloaca (endoderm derivative) |
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Describe how HOX genes and SHH interact to regulate gut tube development |
-SHH expressed all throughout the gut tube endoderm and stabilizes nested expression of HOX genes in the mesoderm -HOX gene expression is specific to certain areas and instructs the endoderm on what to become -Gut tube differentiation dependent on epithelial-mesenchymal cell interaction |
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List the mesenteries of the gut tube and their derivatives |
Ventral mesentery -> forms FROM the thinning of mesoderm in the septum transversum into the falciform ligament and the lesser omentum. Coronary ligaments are also derived from the ventral mesentery Dorsal mesentery -> forms the greater omentum |
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Describe the rotation of the stomach and how this drives rearrangement of the mesenteries |
-First the stomach rotates around the longitudinal axis 90 degreees, so now anterior part is right, posterior past is left -Next the stomach rotates around the anterior-posterior axis -As a result the ventral mesentery is pulled to the right and the dorsal mesentery is pulled to the left (pancreas now secondarily retroperitoneal) |
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Describe how the omental bursa is formed |
-rearrangement of the mesenteries causes formation of a space in between the liver and pancreas. -This space, the omental bursa, is posterior to the lesser omentum bordered by the layered greater omentum. These layer fuse obliterating this part of the greater sac and then fuse with the mesentery of the transverse colon to form the lesser sac *Epiploic foramen |
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Define the cloaca and the viteline duct |
Cloaca = sewer, connects receives connections form the hindgut and urogenital structures Viteline duct = connects the midgut through the umbilical region, eventually obliterated and forms meckel's diverticulum |
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How does Retinoic acid play a role in differentiation of the gut tube |
-Specification is initiated by an RA concentration gradient -Little/no RA in the pharynx as opposed to the colon with see high RA -Gradient causes specific transcription factors to be expressed in different regions of the gut tube -SOX2 to stomach, PDX1 to pancreas and duodenums -Expression if special transcription factors is stabilized by SHH express in the endoderm |
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Describe the formation of the liver and gall bladder |
-Liver growth begins as bud off the foregut - proliferation of foregut endoderm -Liver grows into the mesoderm of the septum transversum, which thins to form the central tendon of the diaphragm and lesser omentum -The endoderm will become the hepatocytes while the mesoderm becomes the blood vesells, connective tissue -Connection between liver outgrowth and foregut narrows forming bile duct. A small outgrowth off of the duct will form the cystic duct and gall bladder |
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Describe the molecular regulation of liver growth |
-Initially ALL of the gut tube has the capacity to form the liver -However inhibitive factors secreted by the noncardiac mesoderm, ectoderm, and notochord prevent liver outgrowth -FGF secreted by the cardiac mesoderm INHIBIT liver growth inhibitors, and thus inhibit bud growth -BMP upregulates FGF to enhance their activity |
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Describe the formation of the pancreas |
-Begins as the development of two buds - one ventral (off the liver bud outgrowth) and one dorsal -gradually the ventral bud moves around to lie underneath the dorsal bud (caused by gut rotation and differential growth) -Eventually they two buds fuse with ventral bud contributing uncinate process and dorsal bud contributing the head, body, tail |
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Describe formation of the primary loop |
-Midgut rotates 90 degrees counterclockwise, using the SMA (supplies midgut) as the axis of rotation -Rotation creates a physiological herniation -Cephalic limb of the primary intestinal loop becomes the forms the small intestine to 1/2 point of ileum. Caudal limb forms 1/2 ileum to large intestine -By week 10 loops begin to return, upon return they rotate 180 degrees (total rotation: 270) -Ascending + descending colon fuse to the posterior wall, not retro peritoneal |
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List some of the anomalies that occur during rotation |
-Sometimes initial 90 degree rotation is made (primary loop), but 180 rotation is not made, in this case most of the colon ends up on the left side -Other times the primary loop rotates clockwise, in this case the colon lies posterior to the duodenum -Problems that arise from rotation anomalies -> volvulus bowel compromises blood supply |
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Describe the difference between omphalocele and gastroschisis |
Omphalocele = gut tube fails to return to the bodycavity after umbilical herniation (high mortality rate). Tube is covered by amnion, unlike in gastrochisis, as the intestines herniate through the umbilical cord Gastrochisis = closure of theventral body wall fails and gut loopsherniate through the opening in the abdomen wall into the amniotic cavity |
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Describe the formation of the hindgut |
-Cloacal membrane (endoderm) and ectoderm constitute the cloacal plate, which sits at the bottom of an indentation called the prodectum -Urorectal septum (mesoderm) grows to separate anterior portion (eventual urinary bladder) from posterior as develops into the perineal body -The cloaca is now split into two canals: one is the anal canal formed cranially from the endoderm of the hindgut and caudally by an invagination of ectoderm (the anal pit). The junctions b/w these two regions is the pectinate line -Separation is reflected in blood flow and innervation: superior rectal from IMA, and inferior rectal from internal pudendal. And inferior hypogastric plexus vs inferior rectal of pudendal |
