Lecture 4 - Parturition Flashcards
What does the placenta do and how does it form?
haemochorial placentation effective from end of first trimester senesces as pregnancy progresses large reserve -responsible for - hormone production, preferential acquisition nutrients and removal of toxins -gas exchange (CO2, O2)
placenta function
consists of a few layer of cells
large surface area
-folding villi
Explain the saturation of fetal and maternal haemoglobin at different partial pressures
At lower partial pressures below 80% - foetal haemoglobin has a greater affinity for oxygen
under optimal conditions - maternal and fetal haemaglobin has the same o2 saturations.
Increased foetal oxygen content is due to
higher Hb concentrations higher affinity for O2 further left shift - reduced binding of DPG to fetal hb - Increased pCO2 and relative acidosis on maternal side (right shift)
Role of surfactant in the fetal lung
from 24 weeks of pregnancy - produced by type 2 pneumocytes
produced surfactant
mixture of phospholipids (PC and PG) and apoproteins (SP-A,B,C,D)
decreases surface tension at air-liquid interface in the alveoli - remain open during expiration
What stimulates release of fetal surfactant
stimulated by fetal glucocorticoids and thyroid hormones
Lack of surfactant
leads to neonatal respiratory distress
replace in neonatal period - curosurf
Myometrial activity
rise in membrane potential
increased intercellular coupling
mechanical/endocrine/paracrine influences
Diagnosis of labour
regular painful contractions
progressive effacement and dilation of uterus
descent and presenting of the part
Endocrine effects
production of cytokines, prostaglandins, oxytocin facilitate labour
progesterone, estrogen,
increased DHEAS, CRH, progesterone and estrogens
causes for preterm labour
uterine capacity placental abruption cervical weakness infection - local/systemic triggers release of cytokines
Birth asphyxia (oxygen compromised)
compression of myometrial arteries cessation of flow to placenta lack of gas exchange relative fetal hypoxia anaerobic metabolism -lactic acidosis
Consequences of birth asphyxia
lactic acidaemia tissue acidosis hypoxic - ischemic encephalopathy cerebral palsy fetal distress more likely - low birth weight long labout impaired placental function
Management of birth asphyxia
fetal heart rate monitoring
measurement of fetal scalp pH
monitor ST segment changes
expedite delivery by cesarean section or forceps
prognosis good if cord arterial pH > 7 and base excess better than - 12 mmol/l