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30 Cards in this Set
- Front
- Back
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factors for closure of ductus arteriosus |
Bradykinin release O2 concentration (must be above 50mmHg) TGF-Beta |
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Patent Ductus arteriosus |
Causes high BP aortic blood into pulmonary circulation = raises pulmonary circulation pressure Left to right shunt = non-cyanotic heart Right to left shunt = cyanotic heart (Eisenmeger's syndrome) Trtmnt = NSAIDS = inhibit prostaglandin synthesis (prostaglandins administered in fetuses to keep PDA) |
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Placenta fxn in 3rd trimester |
Lungs and kidneys |
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Fetal components of placenta |
Synctiotrophoblasts Some cytotrophoblasts Chorionic villus (from extraembyronic mesoderm) Umbilical artery and vein
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Maternal components of placenta |
Decidua basalis Decidua parietalis Spiral arteries and veins that supply intervillous space |
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Battledoor insertion of umbilical cord |
Insertion of umbilical cord at margin of the placenta |
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Velamentous insertion of umbilical cord |
Attachment to fetal membranes (amnion and chorion) and NOT to placenta Umbilical vessels leave cord and travel between amnion and chorion = easily torn; baby exsanguinates |
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Maternal vs Fetal layer of placenta |
Maternal = rough (cause of cotyledons = projections of chorionic villi) Fetal = smooth (cause of the amnion) |
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Tetralogy of Fallot (4 factors and primary clinical sign) |
Conus Septum develops too far anteriorly = Large aorta and stenotic pulmonary trunk Due to neural crest cell migration problems 1) Pulmonary stenosis 2) Ventricular septal defect = septum if too far anterior to contribute to septum 3) overriding aorta = straddles the VSD 4) hypertrophy of right ventricle (shunting of blood from left to right = increase in RV pressure = RV walls expand) Primary clinical sign = presents w/ cyanosis but not necessarily at birth |
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Transposition of the great vessels |
Aorta = from right ventricle; pulmonary trunk = left ventricle Deoxygenated RA blood goes to aorta in RV = deoxygenated blood goes to rest of body Oxygenated blood in LA goes to LV = goes to pulmonary trunk back to lungs Cause = defective migration of neural crest cells to move into conus arteriosus region = truncoconal swellings don't grow in normal spiral direction ALSO 1) ventricular septal defect and 2) patent ductus arteriosus = make life possible for a short time Primary clinical sign = intense cyanosis that doesn't improve w/ O2 administration |
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Respiratory distress syndrome |
Hyaline Membrane disease Major cause = surfactant deficiency (normally secreted by type 2 alveolar cells weeks 20-22) Lungs underinflated and contain fluid w/ high protein content that resemble glassy/hyaline membrane Surfactant deficiency could be due to intrauterine asphyxiation which permanently messes up type 2 alveolar cells Trtmnt = maternal glucocorticoids (corticosteroids and thyroxine) or betamethasone in preterm labor |
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Congenital oomphalacele |
Failure of intestines to return after mid-gut herniation Results from impaired growth of mesodermal and endodermal components of abdominal wall Critical failure of growth at this time (gastrulation) = other defects involving cardiovascular and urogenital systems Produces a swelling in umbilical cord present at birth = intestinal loops; covered by epithelium derived from amnion |
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Umbilical hernia |
Intestines return to abdominal cavity in 10th week but return due to imperfectly closed umbilicus (defect in linea alba) Diff. from oomphalacele = covered by subcutaneous tissue and skin Easily reduced, no surgery necessary until ages 3-5 |
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Initiation of phenotypic sexual differentation |
No difference until week 7 Primary factor = presence or absence of TDF on the SRY-gene of the Y-chromosome |
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Male sexual differentiation |
Primitive sex cords react to TDF and become testis cords (become the Wolffian ducts = mesonephric ducts = vas deferens) Gonadal cords become seminiferous cords = primordia of seminiferous tubules Part of seminiferous cords that enter medulla of testes = rete testis |
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Sertoli cells |
Support cells = secrete Anti-mullerian hormone (AMH) which suppresses the paramesonephric ducts Arise from coelemic epithelial cells |
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Leydig cells |
Produce T and DHT Arise from mesenchymal cells in response to AMH Androgens produced maintain the wolffian ducts that become epididymus |
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Female sexual differentiation |
Absence of Y-chromosome (no SRY gene = no TDF = no AMH) primary sex cords degenerate and new sex cords develop (secondary or cortical sex cords) Cortical sex cords break up into clusters = primordial follicles = oogonium surrounded by follicular cells Ovaries develop = mesonephros degenerate; ovaries become suspended by mesovarium |
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Cranial, horizontal, and caudal parts of paramesonephric ducts in females (and general equivalent in males) |
Cranial = fallopian tube and ampulla Horizontal = remainder of uterus and fundus of uterus Caudal = uterovaginal primordium = cervix and fornix of vagina Males = appendix of epididymus |
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Esophageal atresia |
Superior part of esophagus ends blindly Associated w/ esophageal fistula 85% of time Causes polyhydramnios = fetus can't swallow amniotic fluid to pass through umbilicus = amniotic fluid accumulates Signs = can't pass catheter through stomach and regurgitation of oral feeding |
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Duodenal atresia |
Signs = inability to keep food down after 15-30 minutes, epigastric distention, polyhydramnios, double bubble CT signs, bilious emesis Bilious emesis = blockage usually distal to common bile duct Polyhydramnios = prevents normal intestinal absorption Double bubble = distended and gas filled stomach + proximal duodenum = 2 bubbles |
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Ventricular septal defect |
upper part of ventricular septum failed to fuse w/ endocardial cushions, aorticopulmonary septum, and musculature of IV septum VSD = acyanotic (left to right shunt) |
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Formation of ECC's |
ECC's divide AV canal into right and left AV canals Develop on dorsal and ventral walls of heart Start as cardiac jelly, get invaded by post EMT ECC's Express the SLUG gene Hyperglycemia (maternal) can mess up baby by prohibiting EMT via inhibiting VEGF that is normally released from myocardium = increases cardiac defect 3X |
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3 causes of pulmonary stenosis |
Obstruction from flow of right ventricle to pulmonary artery Pulmonary valve stenosis = cusps fuse and leave a small opening (symptom of ToF) Infundibular stenosis = conus arteriosus is underdeveloped (CA = becomes PT) Unequal division of aorticopulmonary trunk = severe enough = same symptoms as ToF |
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Symptoms of pulmonary stenosis |
Resistance in right ventricle = hypertrophy of RV Failure of RV = pressure in RA increases, could open up the foramen ovale = shunting of deoxygenated blood from right to left = cyanosis |
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Stages of respiratory development |
Pseudoglandular state: 6-16 weeks Canalicular state = 16-26 weeks Terminal sac stage = 26 weeks to birth Alveolar stage = 32 weeks to 8 years |
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Pseudoglandular stage |
6-16 weeks All major elements of respiratory system are forming EXCEPT those involved w/ gas exchange |
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Canalicular stage |
16-26 weeks lumina of bronchi and terminal bronchioles enlarge and vascularize Respiration BARELY possible due to thin walled terminal bronchiole sacs (primordial alveoli) Fetuses born towards 26 weeks may survive w/ intensive care but usually die later |
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Terminal sac stage |
26 weeks - birth Epithelium around terminal sacs thins out = blood-air barrier; permits gas exchange if fetus born early Type 1 and Type 2 alveolar sacs (pneumocytes) Type 1 = gas exchange occurs Type 2 = secretes surfactant (film that counteracts surface tension at air-alveolar interface = facilitates expansion of sacs) |
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Alveolar stage |
32 weeks -8 years sacs analagous to alveoli form at week 32 but 95% of alveoli form postnatally |
