Respiratory Development Flashcards
endodermal part of lung
endoderm of respiratory diverticulum gives rise to the mucosal lining of bronchi and epithelial cells of alveoli (so, the wet stuff)
mesodermal part of the lung
picked up as the lungs travel through mediastinum into pleural space…. everything else… mesoderm-muscle, cartilage supporting bronchi, visceral pluera covering lung)
failure of tracheoesohageal folds to fuse
tracheosophageal septum isnt formed, tracheoesopogeal fistula (TEF), communication between foregut and esophagus. VACTERL assocation
VACTERL
vertebral anomalies, anal atresia, cardiac defects, tef, ea, renal anomalies, limb anomalies
dorsal and ventral portions of the foregut
ventral=trachea and lung buds, dorsal= esophagus
respiratory primordium maintains communication with pharynx through
laryngeal orifice
type c tef
polyhydroaminos, blind esophagus, respiratory distress, choking, secretions, tube doesn’t make it to the stomach, air in stomach. septum doesn’t form. foregut and trachea not completely separated. radiographic, endoscopic. air to stomach. sonogram
type h tef
least symptomatic, no esophageal atresia, ng tube makes it to the stomach, chronic lung infections. aspiration pnuemonia
precursor to the epithelial lining of larynx and the cartliages
epithelial–endoderm of respiratory diverticulum
cartliages–4th and 6th pharyngeal arches
development of the canal in larynx
mesenchyme proliferates to make arytenoid swellings which make lumen into slit. laryngeal epithelial cells (endoderm) proliferate rapidly to close slit. recanalization occurs at week 10.
what occurs during the recanalization process of the larynx
production of the laryngeal ventricles, and their folds create vocal folds and vestibular folds.
clincal correlation of failure of recanalization of larynx
laryngeal atresia. CHAOS. distal to atresia or stenosis, airways are dilated, lungs enlarges and filled with fluid, diaphram is flattened or inverted, and fetal ascites/hydrops…edema.
incomplete atresia, incomplete recanalizaton. membranous web forms at vocal cords, partially blocking air.
epiglottis formed by
hypopharyngeal eminence, proliferation of mesenchyme
innervation of larynx
vagus, recurrent laryngeal branch. (myoblasts from 4th and 6th arches)
endodermal lining of laryngotracheal tube
epithelium and glands of the trachea and pulmonary epithelium
splanchnic mesenchyme surrrounding laryngotracheal tube
mesoderm. cartilage, connective tissue, and muscles
what is the difference between the right and left main stem bronchus
embryonic right main bronchus is larger, more vertical
development of bronchial tree
trachea–>r/l bronchial buds (two lungs and r/l primary bronchi)–>3 r secondary branches, 2 l secondary branches (lobes)–>10 tertiary bronchi, both sides (bronchiopulmonary segments of mature lung)–>terminal bronchioles–>respiratory bronchioles (highly vascularlized mesodermal tissue)–>craniocaudal branching of “stubby branches–>terminal sacs (primitive alveoli) surround terminal stubby branches–>mature alveoli
differentiation of primitive alveoli to mature alveoli
continued thinning of sqaumous epithelial lining of the terminal sacs
5 stages of lung development
EPCSA
Embryonic, psuedoglandular, canalicular, saccular (terminal sac), alveolar
embyronic stage
respiratory diverticulum
three rounds of branching (two lungs, lobes, and bronchiopulmonary segments
trachea and larynx
26-6 weeks
psuedoglandular
terminal bronchioles (14 branches) at 16 weeks, all major elements of lung except gas exchange think:pseudo is false... you think you can breath because you have all the structures, but you cant
canalicular
terminal bronchiole to respiratory bronchioles (now respiration is possible)
respiratory vasculature (canal of blood)
epithelium differentiates
at end, respiration possible, terminal sacs have developed (primordial alveoli)
blood-air barrier
26 weeks
limit of viability of premature infants
22-23 weeks. respiration only possible after blood air barrier. end of this period (canalicular) could survie, but ICU
saccular
terminal sacs are formed completely
division of respiratory bronchioles to produce terminal sacs
capillaries bulge (alveoli)
establishment of blood-air barrier
type II pnuemoncytes secrete pulmonary surfacant (phospholipids and proteins)
saccules-primordial alveoli
purpose of surfactant during saccular stage
counteracts the surface tension at air-alveolar interface, facilitating the expansion of saccules, and preventing atelectasis
alveolar
maturation of gas exchange structures and alveoli
respiratory distress syndrome
inadequate production of surfactant
AKA hyaline membrane disease, glassy or hyaline membrane
provide steroids if afraid premature
only premature babies.
ground glass, peripherally extending air bronchograms.
total surface area for gas exchanged depends on
number of alveoli and density of alveolar capillaries, need thin walls.
which type of alveolar cells secrete surfactant
type II
pulmonary surfactant composition
90% phospholipid
10% protein
AD–hydrophilic, host defence
BC–hydrophobic, surface-active properties of surfactant
hereditary surfactant protein b deficiency
respiratory failure. autosomal recessive. complete absence or mutation of the genes. respiratory distress syndrom.
pulmonary hypoplasia causes
oligiohydrominos (insufficient amniotic fluid) (bilateral renal agenesis)
CDH
bilateral renal agensis results in
potter’s sequence. and oligiohydrominos. deformed limbs, wrinkly, dry dink. abnormal facial appearnce.
CDH
failure of pleuroperitoneal canal to close during 6th week of development.
eft side 4-8 times more, left pericardioperitoneal canal larger, closes later. posterolateral bochdalek hernia. lung hypoplasia.
failure of diaphragm to completely form. push lungs and heart anteriorly. prolonged is lung underdevelopment.
medial do not really result in lung hypoplasia
presentation of newborn with CDH
respiratory distress, cyanosis, decreased bronchial breath, scaphoid abdomen. smaller lung on hernia side
bowel gas in ches and shift of mediastinal structures
proximal diverticulum
larynx and trachea
