Embryo: Body Cavities & Resp. Development Flashcards

1
Q

As a result of lateral folding, what does the intraembryonic coelom become?

A

The peritoneal cavity.

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2
Q

As a result of the cranial caudal C shaped folding, where do the heart, septum transversum, oral and cloacal membranes, allantois, and connecting stalk move to/from?

A

They move from cranial/dorsal position to ventral position.

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3
Q

what does closure of the ventral body wall cause to happen?

A

Formation of foregut (cranial) and hindgut (caudal) from pouches formed by folding.

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4
Q

What is the gut suspended by in the coelom?

What part of the gut communicated with the yolk sac??

A

Dorsal mesentery (was connected by ventral mesentery as well, but it disintegrates). The midgut is the ONLY gut to connect w/yolk sac.

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5
Q

Septum transversum is the primordial what? What does it grow from, and what cavity does it help form?

A

Main tendon of diaphragm.

Grows from the ventral body wall. This growth causes the formation of the pericardial cavity.

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6
Q

Although separated, how are the pericardial and peritoneal cavities still connected?

A

By 2 pericardioperitoneal canals, which run cranio-caudally on either side of the foregut.

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7
Q

What do the pleuropericardial folds grow from?
What do they contain?
What cavity do they help make?

A

Grow from two lateral buds.
Contain the phrenic nerve
Help the septum transversum in making the pericardial cavity.

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8
Q

What does the pleuropericardial membrane refer to?

What do they eventually become?

A

Refers to the pleuropericardial folds during their growth.

They eventually attach to and become the pericardium.

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9
Q

What makes up the pleuroperitoneal membranes?

A

septum transversum, pleuroperitoneal folds, muscular ingrowth from body wall.

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10
Q

How do the pericardioperitoneal canals close?

A

Pleuroperitoneal membranes grow and fill the canals.

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11
Q
  1. Why does the phrenic nerve end up lengthening?
  2. What does it pass through, and what does it attach to?
  3. What does this cause to happen to the location of the diaphragm?
  4. How long is the phrenic nerve in adults?
A
  1. Due to more dorsal growth compared to ventral, which causes the septum transversum to move posteriorly.
  2. The phrenic nerve passes through pleuropericardial membranes, and becomes attached to the pericardium.
  3. Diaphragm moves to L1 position.
  4. Diaphragm is 30 cm in adults.
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12
Q
  1. What is the first phase of the formation of the lungs/trachea called?
  2. What 5 things form during this phase?
A
  1. Embryonic phase
  2. The laryngotracheal groove, the primordial larynx, primordial trachea, branched bronchi, and the respiratory diverticulum.
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13
Q

What is the laryngotracheal groove?
Forms caudal to which pharyngeal arches?
What primordial structure grows on either side of it?

A
  1. Precursor to the lungs and respiratory structures.
  2. Forms caudal to the 4th pair of pharyngeal arches.
  3. The larynx forms on either side of it (but not epiglottis)
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14
Q

What does the epiglottis form from?

A

The hypopharyngeal eminence.

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15
Q

The respiratory diverticulum separates from esophageal structures via what partition?

A

via a partition called the tracheoesophageal septum

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16
Q

Explain the development of bronchi, starting at laryngotracheal groove/diverticulum.

A
  1. Laryngotracheal diverticulum becomes respiratory diverticulum
  2. Resp divertiulum becomes lung bud.
  3. Lung bud becomes bronchial buds
  4. Bronchial buds become branched bronchi.
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17
Q

smooth muscle, cartilage, and connective tissue of respiratory structures are derived from what? What does it surround?
what else forms at this point?

A

From the splanchnic mesoderm, which surrounds the laryngotracheal epithelium
Primary, secondary, tertiary, and subsegmental bronchi all develop at this point

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18
Q

Explain the roles of TGF-Beta, FGF-10, BMP-4, and Shh in the branching of respiratory epithelium

A

FGF-10 stimulates growth of epithelium, and induces BMP-4
BMP-4 stops growth.
The epithelium secretes Shh, which stimulates mesenchymal proliferation and inhibits FGF-10.
Mesenchyme secretes TGF-Beta, stimulating ECM production to stabilize the growing tip of epithelium.
FGF-10 STILL stimulates growth lateral to the old apex.

This is all possible because Shh and TGF-Beta are below levels to actually stop FGF-10 from doing its job.

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19
Q

What is the 2nd phase in the formation of the trachea/lungs called, and what happens in it?

A

Called the pseudoglandular phase, since it resembles exocrine gland growth.
Lungs continue to branch, and all major elements are formed except those directly involved with gas exchange.

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20
Q

What is the 3rd phase called, and what happens in it?

A

Called the canalicular phase, which is where distal branches associate with capillaries making gas exchange possible. Alveolar cells also form, which make surfactant.

21
Q

What cells make surfactant, and what does it do?

A

Type II alveolar cells. reduces surface tension to keep lungs from collapsing, stabilize alveolar surface, and decrease fluid transfer.

22
Q

What two things are necessary for breathing and mark the point of extrauterine survival being possible?

A

Pulmonary circulation and surfactant production.

23
Q

Earliest survival of fetus extrautero is usually at what point? What is lacking here that limits it?

A

22-24 weeks, with medical care to compensate for lack of surfactant.

24
Q

4th and 5th phases called? Time frame for them? What happens in them?

A

4th phase- Terminal sac phase (week 26 until birth). Terminal sacs form, which become alveoli eventually.
5th phase- Alveolar phase (Week 32 to 8 years). Acceleration of maturation of alveoli. Septal walls of alveoli become thinner. Alveoli are not fully mature until AFTER birth.

25
Q

What percent of mature alveoli form after birth?
Newborn lung has how many alveoli per lung, and what is the surface area?
Adult?

A

95%.
Newborn= 75 alveoli/lung, surface area of 3 m squared.
Adult= more than 150 alveoli/lung, surface area of 70 m squared.

26
Q

Formation of airway occurs in what direction?

What about terminal differentiation?

A

Proximal to distal. However, terminal differentiation happens distal to proximal.

27
Q

Without amniotic fluid in pre-natal lungs, what would happen to them?

A

They would become hypoplastic (underdeveloped)

28
Q

What pulmonary changes occur after birth to allow for atmospheric breathing?

A

1/3 of fluid expelled by mouth, and the rest is absorbed by pulmonary vasculature. 10% absorbed into lymph.

29
Q

What circulatory changes happen to allow for atmospheric breathing?
Neural?

A

Interatrial shunt and ductus arteriosus close, and pulmonary vessels fill with blood.
As respiratory movements begin at birth, sympathetic NS is stimulated which leads to less fluid secretion by lungs.

30
Q

Explain the air/liquid interface in the lungs, and surfactant’s role in it.

A

Fluid coats the lungs, making the interface. This fluid exerts a surface tension on the alveoli, which makes it so they can’t expand fully. Surfactant breaks up this surface tension, allowing the alveoli to expand properly.

31
Q

At what week is there a massive increase in surfactant production?

A

Week 35

32
Q

Alveoli without surfactant require how much more pressure to inflate?

A

10X more.

33
Q

Without medical intervention, at what point could a fetus survive out of the uterus?

A

At week 35, when the surfactant is dramatically increased.

34
Q

Phospholipids make up most of surfactant. How many lipids are there, and what is the main one?
What other molecules are present?

A

2, main one is lecithin. About 10% is protein, and there are also antioxidants.

35
Q

How can lung maturity be measured?
What number indicates higher survival possibility?
At what number would respiratory distress be indicated if born?
When is there a sharp increase in lecithin, as compared to surfactant in general?

A

Using the Lecithin-sphingomyelin ratio (L-S) in the amniotic fluid.
A ratio of 2 or more (lecithin to sphingomyelin) indicates higher survival.
A ratio of 1.5 or less would indicate distress.
Week 32 marks a large increase in lecithin, followed by the large surfactant increase at week 35.

36
Q

What drug can be given to the mother to enhance fetal lung maturation 1-2 days before birth?
What can be given to the newborn?

A

glucocorticoids

Artificial surfactant can be used for the newborn.

37
Q

What is a congenital diaphragmatic hernia (CDH), and what causes it?
Detection rates?
Treatment?

A

Failure of pericardial membrane to fuse with parts of diaphragm. Results in opening usually on the left side, with intestines herniating into thorax and causing hypoplasia of lungs. Mortality rate is high.
Detected prenatally 50% of the time.
If the newborn survives, surgery can fix it.

38
Q

What causes eventration of the diaphragm, and what is it?

Treatment?

A

Defective development of diaphragm. There is no opening in it, but the weakened muscle allows the intestines to push up into thorax on one side, without actually pushing through.
Treatment is surgery to put a prosthetic patch in, or to graft a part of the latissimus dorsi to it.

39
Q

What causes a tracheoesophageal fistula?
What type is most common? What happens in this type?
Symptoms?
Often results in what?

A
  1. Results from incomplete fusion of tracheoesophageal folds in 4th week, leading to defective tracheoesophageal septum.
  2. Type A is most common (85%). Esophagus ends blindly, called esophageal atresia, with the lower part connecting to the trachea where it bifurcates.
  3. Symptoms: Drooling at rest, regurgitation of fluid, gastro/intestinal reflux into trachea/lungs causing pneumonitis and respiratory compromise.
  4. Often results in polyhydramnios, meaning there is too much amniotic fluid around fetus because it cannot be swallowed successfully.
40
Q

Respiratory distress characterized by: (7 ish)

A
  1. Rapid breathing (>60 breaths/min)
  2. Flaring nostrils
  3. chest retractions
  4. expiratory grunt
  5. often cyanotic (blue)
  6. rapid HR
  7. anxious expressions
41
Q

What are some possible causes of respiratory distress? (One is especially important to know)

A

INSUFFICIENT PULMONARY SURFACTANT
meconium aspiration, wet lung, bilateral choanal atresia, pneumonia, congenital diaphragmatic hernia, congenital heart disease, pulmonary hemorrhage, pneumothorax

42
Q

what are risk factors for pulmonary distress? 3

A
  1. Premature infants: Less than 37 weeks, less than 1-1.5 Kg
  2. Male infants (androgens inhibit alveolar development)
  3. Mothers with poorly controlled diabetes
43
Q

Hyaline membrane disease/Respiratory distress syndrome (same thing) characterized by? What does it do?
Outlook?

A

Respiratory distress; usually premature. Often develop a hyaline membrane in lungs that covers surface of alveoli. Disrupts/interferes with function of surfactant. Usually lethal.

44
Q

What causes a hyaline membrane to form on alveoli? How does the membrane form?

A

Damage to Type I alveolar cells. serum leaks into alveolar lumen, which catalyzes formation of the membrane.

45
Q

What is atelectasis?

A

loss of lung volume due to decrease/absence of air from collapsed alveoli

46
Q

developmental pathway of the epithelium of the larynx, trachea, bronchi, and lungs?

A

Endoderm—– pharynx (cranial foregut—– respiratory diverticulum—- epithelial lining of larynx, trachea, bronchi, lungs

47
Q
Developmental pathway of cartilage, smooth m, elastic tissue and fibrous CT of: 
Larynx??
Trachea
Bronchi
Lungs
A

Mesoderm— lateral plate mesoderm— splanchnic mesoderm— all those things.

48
Q

Do fetal lungs have high or low pulmonary vascular resistance?

A

High