Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
|
What tissue gives rise to the epithelial lining of the trachea and lungs?
|
The respiratory diverticulum, an outgrowth of the embryonic foregut.(endoderm)
|
|
|
What tissue gives rise to the walls (not the linging) of the air passageways and coverings and stroma of the lungs.
|
These tissues are formed from splanchnic mesoderm mesenchyme cells that come to surrond the respiratory diverticulum (endoderm).
|
|
|
What are the 5 phases of lung development?
|
1. Embyronic
2. Pseudoglandular 3. Canalicular 4. Terminal Sac 5. Alveolar "Every Pulmonary Creation Terminates in Alveoli" |
|
|
What major events occur during the embryonic phase of lung development
|
-Formation of the respiratory diverticulum and creation of tracehoesophageal folds
-Fusion of tracheoesophageal folds to form the tracehoesophageal septum separating the trachea from the dorsal esophagus -three rounds of branching (bud, lobar, segmental) |
|
|
In which stage of development would a tracehoesophageal fistula most likely form? What causes this?
|
This would occur in the embryonic phase due to problems with the formation of the tracehoesophageal folds and formation of the tracehoesophageal septum. This defect is often associated with esophageal atresia
|
|
|
During what weeks of lungdevelopment does the embryonic phase take palce
|
4-7
"Every Pumonary Creation Terminates in Alveoli" embryonic= 4-7 pseudoglandular=5-17 canalicular= 16-26 Terminal sac= 26-38 Alveolar=38+ |
|
|
What are the major events of the pseudoglandular phase of lung development
|
-continued branching
-angiogenesis leads to pulomary vascular bed following the branching of the RD -lungs move to more inferior position in thorax |
|
|
Which interactions and signaling molecules are important for proper lung branching during the pseudo glandular phase?
|
-epithelial-mesenchymal signaling
-FGF10 mediates proliferation and outgrowth of endoderm derived RD epithelium -SHH promotes mesenchyme proliferation and differentiation -SHH and BMP-4 direct new bud formation |
|
|
Explain how a new bud is formed during the branching of the RD. What signaling molecules are involved?
|
At the tip of a bud, SHH and BMP4 production lateralize FGF10 expression resultingin two new buds
|
|
|
Disturbances in lung branching may lead to pulmonary hypoplasia and insufficient vascularization. During which stage of lung development does this occur?
|
pseudoglandular
(note that the vascularization that leads to the possiblility for extrauterine survival does not occur until the canalicular stage) |
|
|
When is the pseudoglandular stage
|
wks 5-17
"Every Pumonary Creation Terminates in Alveoli" embryonic= 4-7 pseudoglandular=5-17 canalicular= 16-26 Terminal sac= 26-38 Alveolar=38+ |
|
|
What are the major features of the canalicular phase of lung development
|
-increase in vascular development
-pulomnary acini become associated with capilaries -Type 1 and II pneumocytes differntiate from endoderm derived epithelial cells -ciliated and goblet cells differentiate while surroinding mesenchymal cells make cartilage, smooth muscle, and airway wall components -fluid secretion begins |
|
|
When is the canalicular phase
|
16-26 weeks
"Every Pumonary Creation Terminates in Alveoli" embryonic= 4-7 pseudoglandular=5-17 canalicular= 16-26 Terminal sac= 26-38 Alveolar=38+ |
|
|
The earliest possible extrauterine survival occurs at the interface between which two phases? What features are necessary for survival
|
Occurs at interface of canalicular and terminal sac phase ~26 weeks
Need 1.vasculature 2. surfactant 3. enough terminal sacs |
|
|
When is the terminal sac phase
|
weeks 26-38
"Every Pumonary Creation Terminates in Alveoli" embryonic= 4-7 pseudoglandular=5-17 canalicular= 16-26 Terminal sac= 26-38 Alveolar=38+ |
|
|
What are the major features of the terminal sac phase
|
-distal branches of RD become primitive alveoli with septum that has double layer of capiliaries
-surfactant secreted -ECM compoents are secreted |
|
|
what type of cells secrete surfactant
|
type II pneumocytes
"type II make the goo" |
|
|
Describe Congenital Pulmonary Airway Malformation. What are the features? In which stage does it occur?
|
-defect in terminal bronchiole development
-results in cysts that resemble bronchioles but are not functional -causes respiratory distress, can put pressure on the eosphagus or heart causing polyhydramios or fluid accumulation respectivley -may begin to form in canalicular or terminal sac phase |
|
|
When is the alveolar stage
|
36wks-8 years
"Every Pumonary Creation Terminates in Alveoli" embryonic= 4-7 pseudoglandular=5-17 canalicular= 16-26 Terminal sac= 26-38 Alveolar=38+ |
|
|
What are the major features of the alveolar stage
|
-terminal sacs subdivide into mature alveoli via formation of secondary alveolar septa
-mature alveoli have single layer of capiliaries -reducing in thickness of septal wall -note 95% of alveoli are fomred postnatally |
|
|
Compare the direction of airway formation to that of alveolization
|
Airway formation occurs proximal to distal, alveolization occurs distal to proximal
|
|
|
Insufficient fluid in the fetal lungs can result in...
|
hypoplastic lung development
|
|
|
Compare the respiratory movments of a fetus to a newborn imediatelly after birth
|
In the fetus, the respiratory movements are shallow and episodic. At birth, neural changes result in continous and rhythmic respirations
|
|
|
Compare the resistence of the pulmonary vasculature of a fetus to a newborn imediatelly after birth
|
In the fetus the pulmonary resistence is high because there is fluid in the lungs, there is little blood flow into the pulmonary vascular system. At birth, the fluid is replaced by air and the resistence decreases dramatically
|
|
|
Describe the changes to the pulmonary circulation that occur at birth
|
Both the interatrial septum (foramen ovale) and the ductus arteriosus close allowing blood to fill the pulmonary vasculature
|
|
|
As the fetus is being born, the pulmonary fluid is expelled through the mouth and absorebed by the pulomary vasculature. What happens if this does not occur
|
transient tachypnea or wet lung
|
|
|
At what time point is surfactant production sufficient to support extrauterine life?
|
about 35 weeks
|
|
|
What is the function of pulmonary surfactant
|
decreases the surface tension on the alveolar wall (prevents atelectasis) and stabilizes the alveolar surface
also decreases fluid transfer from pulmonary vasculature to surface of alveoli |
|
|
What are the components of surfactant
|
1. phsopholipid
2. protein 3. antioxidant |
|
|
Signs of respiratory distress include
|
rapid breathing, chest retraction, cyanosis, anxious facial expression, flaring nostris, expiratory grunt, rapid heart rate
|
|
|
Name three factors that predispose infants to respiratory distress
|
1. premature (before 37 wks or less than 1.5 kg)
2. male (androgen inhibits alveolar maturity) 3. Maternal diabetes mellitus |
|
|
What is the difference between respiratory distress syndrome and hyaline membrane disease
|
although used interchangeably, respiratory distress syndrome is a clinical picture whereas hyaline membrane disease is a pathological finding
|
|
|
What is a hyaline membrane
|
cell debris in a protein matrix covering the inner surface of alveoli
|
|
|
What is the typical sequence of events that leads to hyaline membrane formation and disease
|
1. injury to type I cells
2. break down of air capilary barrier 3. leakage of serum into alveolar lumen 4. formation of hyaline membrane 5. disruption of surfactant formation 6. problems with lung fxn "I'll bet lungs form dually" |
|
|
What is the underlying cause of death for infants experiencing RDS
|
lung immaturity due to insufficient surfactant production
|
|
|
What is the primary cause of RDS
|
pulmonary surfactant insufficiency
|
|
|
Describe bronchopulmonary dysplasia/ chronic lung disease of infancy
What is dysfunctional? What happens to the lung tissue? What might cause this? |
-often occurs in infants with RDS, disease of immature lungs
-dysfunction VEGF interferes with vascularization of pulmonary circulation that subsequently interfers with normal alveolarization of terminal airways. Normal lung tissue is repalced by fibrotic changes. Factors affecting VEGF signaling= infections and inflammation due to high O2. |
|
|
What are two ways in which pulmonary surfactant insufficiency can be detected
|
1. L/S ratio
2. analysis of Phosphatidylgylcerol Note Phosphatidylgylcerol is more accurate |
|
|
What is the L/S ratio? How is it used to detect surfactant insufficiency
|
the L/S ratio is the ratio of lecithin to sphingomyelin. Lecithin is a PL found in surfactant and sphingomyelin is a baseline PL. If the ratio is more than 2 it is unlikely that surfactant will be insufficient. If it is less than 1.5 it is likley that the infant will be in RDS
hint:Greater than two, you won't be blue, less than one five, you won't be alive |
|
|
How is analysis of phosphatidylglycerol used to predict pulmonary surfactant levels
|
Sampled from the amniotic fluid, phosphatidylglycerol is a drying agent which keeps lecithin dry so that it can function properly
|
|
|
What can be done to improve the outcome of a fetus with insufficeint surfactant production
|
1. administer glucocorticoids to mother 24-48hrs before delivery to enhance fetal lung maturation
2. Give newborn artificial surfactant |
|
|
What 3 things do the lungs need in order to avoid hypoplasia
|
1. adequate fluid
2. adequate space 3. respiratory movements |
|
|
Based on lung development, what is the limit of extrauterine survival
|
22-26 weeks
|
