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25 Cards in this Set
- Front
- Back
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when does lung development start
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lung dev starts at week 4
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pulmonary vasculature begins from
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starts from 6th branchial arch ->
pulmonary vasculature |
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embryonic phase (week 1-6) abnormalitiies
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laryngeal/esophageal/tracheal/bronchial atresia
lung aplasia/hypoplasia bronchogenic cyst extralobar sequestration - lung tissue has no pulmonary airway connection or pulmonary vasculature |
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fetal phase psudoglandular stage - (wk 7-17) abnormalities
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pumonary hypoplasia due to oligohydramnios
intralobar sequesteration congenital cystic adenomatoid malformation pulm lymphagiectasis - problem with lymph vessel development diaphragmatic hernia |
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congenital cystic adenomatoid malformation
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most common
congenital hamartoma, overgrowth of terminal bronchioles, cysts --> pulm hyperplasia |
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canalicular stage (wk 16-25)
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respiratory bronchials appear
acinus development more vascular at completion get surfactant, terminal sacs ready for gas exchange |
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psudoglandular stage (wk 7-17)
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growth of conducting airways
pulmonary vasculature growth cartilage rings |
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surfactant metabolism
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eatin by macrophages or recycled by Type II pneumocytes
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canalicular stage anaomlies
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pulmonary hypoplasia
alverolar capillary dysplasia pulmonary surfactant deficiency |
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terminal sac stage (wk 25-35)
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expansion of gas exchange sites
thinning of interstitilum, epithelium thins, septation |
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T/F type II pneunocytes cells give rise to type I cells
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true: type II cells give rise to both type I and type II
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terminal sac stage abnormalities
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pulmonary hypoplasia
surfactant deficiency pulm hypertension transient tachpnea - due to inability to clear fluid out |
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alveolar stage (36wks - 3 years)
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even more alveoli form
factors that delay interfere: mechanical vent glucocorticoids proinflam cytokines hyperoxia/hypoxia poor nutrition |
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fetal lung fluid
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always filled with fluid after 15 weeks - needed for normal dev
replaced with air later late gestation - get decreased secretion (Cl dependent) labor - increased absorption (Na dependent) enhanced by glucocorticoids c-section disrupt process of removal of fetal lung fluid |
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pulmonary hypoplasia
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disruption of branching process, less area for airway and vasculature and gas exchange\
thoracic compression due to oligohydramnios: 1.premature rupture of membrane 2. renal agenesis (potter syndrome) 3. urinary tract outflow obstruction decreased intrathoracic space: 1. congenital diaphragmatic hernia 2. pleural effusions 3. abdominal distension other: decreased breathing due to CNS damage, Fetal Werdnig- Hoffman |
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tracheoesophageal fistula
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most common lower respiratory tract malformation
most common type is esoph atresia with lower trecha esophageal fistula faulty partition of esoph and trachea during 4-5th week VACTERAL assocation see polyhydramnios |
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polyhydramnios is seen with treachoesophageal fistula because
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fetus can't drink the amnioitic fluid
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surfactant is produced
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34 weeks gestation
use glucocorticoids in mother to stimulate production if need preterm birth test lecithin-to-sphingomyelin ratio after 30 weeks - ratio > 2 is enough surfactant |
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la place law
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P = 2T/R
either reduce the tension or increase the radius to reduce pressure more pressure -> collapse |
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infant respiratory distress syndrome
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not enough surfactant production
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transient tachypnea of the new born
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retain fetal lung fluid
usually self limiting but can -> pulm htn |
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infant pneumonia etiology
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ascending infection from genital tract
colonization during vagtinal delivery transplacental premature rupture of membrane group B strep, ecoli, enterobacter, CMV, listeria |
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pneumothorax auscultation
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no breath sounds on side of pneumothroax
heart sonuds on side opposite of pneumothorax |
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meconium aspiration syndrome
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can pass meconium into utero - infant can aspirate
increased risk during fetal distress, post maturity can occlude airway, cause inflammation |
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persistent pulmonary hypertension of the newborn
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high pulm resistance in utero should go away, but sometimes doesnt
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