Sinnot Flashcards
List 4 risk factors for hyaline membrane disease i.e. infant respiratory distress syndrome
(1) Premature birth
- 20% if 32-36 weeks
-60% if < 28 weeks
(2) Maternal diabetes
- hyperinsulinemia impairs surfactant synthesis.
(3) Amniotic fluid aspiration
(4) C-section
- Results in less glucocorticoid release compared to vaginal delivery: generally released in response to contractions and are needed to mature fetal lungs
-vaginal delivery helps squeeze out amniotic fluid.
List 4 complications of IRDS
(1) Alveolar rupture
(2) Intracranial hemorrhage/Periventricular leukomalacia -> cerebral palsy
(3) Infection
(4) Patent ductus arteriosus
Where is surfactant synthesised? What is its composition
Synthesised in ER of type II pneumocytes.
Composed of hydrophobic and hydrophilic components. Mainly:
(i) Phospholipids (dipalmitoyl phosphatidylcholine)
(ii) Surfactant apoproteins
(iii) Calcium ions.
What is the timeline of surfactant production to mature levels?
22-24 weeks type II’s start to synthesise it
28-32 weeks begins distribution
35 weeks mature levels.
What group of drugs can be given to delay a premature labour to allow for steroid therapy? List 3 types and how long they can delay labour for
Tocolytics
(1) Oxytocin Antagonist
-Atosiban
-inhibits binding of oxytocin to myometrium
-2-7 days delay
(2) Beta 2 Agonist
-Salbutamol
-Hyperpolarised myometrial cells thereby preventing AP propogation + smooth muscle contraction.
1-2 days
(3) Calcium channel blocker
-Nifedipine
-Inhibits calcium influx
-2-7 days
What drug can be given in early pregnancy to protect the fetal brain?
Magnesium sulphate
What is considered the threshold of viability ?
23+0 weeks
From what week of gestation is steroid therapy started if expected to delivery in 7 days?
What 2 drugs can be given?
23-33 weeks
IM Betamethasone (2 dose 24 hrs apart)
IM Dexamethasone (4 doses, 12 hours apart)
Why are fetal alveoli more susceptible to collapse? Consider Laplace Law
Laplace law states that the pressure within the alveolus is directly proportional to the surface tension and indirectly proportional to the radius.
P = 2 x T / R
This means that the smaller the alveolus, the greater the pressure required to remain open and not collapse under increased surface tension. Considering this in terms of IRDS - the increased surface tension (lack surfactant) coupled with the small alveoli means the alveolus will collapse on expiration.
Account for the fluid filled lungs of a fetus in utero.
Fetal lungs are filled with fluid as a result of ion exchange across the type II pneumocytes.
-NKCC channels on basolateral end allow for influx of Cl- and Na+
- Cl- exits into the alveoli lumen at the apical end having travelled down its electrochemical gradient
- Na+ follows by electrochemical gradient
- This movement of ions creates an osmotic gradient thereby drawing water into the alveolus lumen.
Account for the aeration of fetal lungs at birth
- At birth, oxygen, catecholamines and glucocorticoid increase expression of ENAC on the apical surface of type II pneumocytes. These channels allow for influx of sodium from the alveoli into the type II pnuemocytes. The sodium is then pumped out the basolateral side via Na+/k+ ATPase pumps.
- At birth, type II pneumocytes stop secretion of chloride ions into alveolar space. This reduces the fluid secretion into the alveoli. Additionally, the electrochemical gradient created by efflux of sodium draws chloride out of the alveoli.
- The movement of sodium and chloride causes an osmotic gradient which draws fluid from alveoli which can then be drained into lympathics/venous system.
What 3 factors allow for efficient gas exchange at the plateta?
(1) Double bohr effect
- Gaseous exchange is facilitated by the acidity/alkalinity of the blood.
-As Co2 diffuses from fetal blood into maternal blood, down its concentration gradient, the increased acidity of Co2 (due to formation of H+ ions) decreases the maternal hemoglobin’s affinity for O2/ rightward shift -> O2 released.
- As more Co2 is released from fetal blood, the fetal blood becomes more alkaline. This causes a left shift in fetal hemoglobin dissociation curve/ increased affinity for oxygen.
(2) Haldane effect
- Relates to O2 effect on Co2
- As more oxygen binds to fetal hemoglobin, the affinity for CO2 decreases, resulting in more CO2 being released from fetal blood.
-As oxygenation of maternal hemoglobin decreases, the affinity for CO2 increases, facilitating the uptake of CO2 by maternal hemoglobin.
(3) Fetal hemoglobin’s higher affinity for O2
- The presence of the gamma chains (has a serine instead of histidine) in fetal hemoglobin give HbF a net negative charge. Because 2,3 BPG is also negatively charged, it means that HbF has a lower affinity for 2,3 BPG and so therefore has a higher affinity for O2.
What are the components of the interface between maternal and fetal blood
Maternal spiral arteries pierce the decidual plate and flood the intervillous spaces with blood, which are lined with syncytium.
Chorionic capillaries of the fetus are bathed in the maternal blood, allowing for gas exchange to occur.
Gas exchange occurs across the thin barrier composed of:
Syncytiotrophoblast
Cytotrophoblast (if present)
Basement membrane
Endothelial cells of the fetal capillaries within the chorionic villi
What components separate the maternal and fetal blood at the placenta
Syncytiotrophoblast
Cytotrophoblast (if present)
Basement membrane
Endothelial cells of the fetal capillaries within the chorionic villi
Define still birth
In Ireland, a stillbirth is defined as a baby born with no signs of life at 24 weeks gestation or later, or with a birthweight of 500g or more
