Physiological changes at birth 2 Flashcards
Newborn baby: physiological changes
Neonatal period (1st stage of the postnatal period): extends from birth to 1 month following birth.
Within minutes of the delivery, the umbilical and placental vessels constrict ->increased resistance -> blood flow to placenta stops:
-> Wave of uterine contraction eventually delivers the placenta.
- Umbilical cord is then (usually) clamped.
After birth: the first breath
- Lung aeration (particularly the initial inflation of the lungs) causes important changes to the cardiovascular system of the newborn (adapting it to pulmonary gas exchange).
- There are some triggers for the onset of breathing…
triggers of onset breathing
Pgases are sensed by peripheral and central chemoreceptors: strongest stimulation of respiration is an ↑ in PCO2.
First breath is probably triggered by hypercapnia and cooling (ambient temp.).
fetal lung physiology before and after
Fetal lungs are virtually non-functional: Alveoli are almost collapsed and fluid-filled.
-> The fetus depends on the placenta for gas exchange..!
Fetal lungs are poorly perfused: High resistance to blood flow in the pulmonary capillaries.
Interestingly, breathing movements are seen before birth:
- Begin at ~10th week of gestation: are shallow and irregular until week 34; then display some rhythmicity with periods of activity.
Why?
-> Important in the preparation of the respiratory system for its postnatal function (of gas exchange).
Chemoreceptors are functional during the latter part of gestation: Fetus ‘gasps’ if it experiences hypercapnia.
fetal lung physiology before and after: lung inflation facilitated by surfactant
Surfactant reduces surface tension forces- allows alveoli to expand:
- Week 20: type II epithelial cells appear in developing alveoli.
- Week 28-30: these cells begin secreting phospholipid surfactants (under control of fetal cortisol).
It requires a considerable mechanical effort to expand the lungs for the first time (but it gets easier with each breath)
Lack of surfactant in premature infants (those born before week 28) newborn respiratory distress syndrome (NRDS).
newborn circulation overview
To adapt to pulmonary gas exchange, the 3 fetal shunts must close (/occlude):
- Initiated by the ↑ in pulmonary blood flow (decreased pulmonary vascular resistance; PVR).
newborn circulation steps
- When air enters lungs, blood is forced through the pulmonary arteries (to lungs). Ductus arteriosus closes; becomes ligamentum arteriosum/ductus ligamentosum
- Foramen ovale closes; becomes the fossa ovalis. Blood can no longer flow from right to the left atrium.
- Ductus venosus degenerates; becomes the ligamentum venosum/(teres
- Umbilical vessels are cut: umbilical vein becomes the round ligament of liver.
- Umbilical arteries also degenerate; become the cords of the umbilical arteries/medial umbilical ligaments.
newborn circulation step 2 continuous
After birth & lung expansion (reduced resistance in lungs and increased blood flow via pulmonary arteries to lungs) more blood returns to LA from pulmonary veins: now pressure in LA > RA forces foramen ovale to close.
The 2 unfused septa of the foramen ovale permanently fuse shut within a few days (now fossa ovalis).
fetal vs newborn circulation
Fetus: 2 sides of the heart work in parallel- largely bypass organs with little/no function (via 3 shunts)
Newborn: serial arrangement (like in adult)
Ductus arteriosus remains open for ~10 days after birth; the pressure changes mean blood now flows into the right ventricle (RV):
- Probably closed off by vasoconstriction; eventual fibrosis occurs.
Ductus venosus (not shown below) also closes after birth (likely due to constriction of umbilical vessels); now have adult circulatory form.
-draw both
Congenital heart defects
Can arise by failure of fetal shunts to close:
Patent (i.e. open) ductus arteriosus: “persistent” if duct remains open beyond 3 months in full-term infant:
- Mixing of oxygenated and deoxygenated blood: blood shunted from higher-pressure left (aorta) to lower-pressure right side (pulmonary artery); can be treated/closed surgically:
If not treated pulmonary hypertension; heart failure.
- Patent foramen ovale (an atrial septal defect): also leads to mixing of blood; more frequent in girls than boys (2:1):
If not treated poses long-term risk of pulmonary vascular disease and atrial arrhythmias.
fetal adrenal gland
Adult adrenal glands: Medulla: catecholamines. Cortex: steroids (3 zones).
- Development of the fetal adrenal glands continues beyond birth.
- Fetal zone (of fetal adrenal cortex) produces precursors (e.g. DHEA) needed for the placental synthesis of oestrogens.
- Definitive cortex (of fetal adrenal gland) converts progesterone to cortisol during the last 3 months of pregnancy.
Zona fasciculata: Glucocorticoids
Zona reticularis: Sex hormonenes
Zona glomerulosa: Mineralocorticoids
role of corticotropin-releasing hormone
DHEA: dehydroepiandrosterone (an androgen) is an important steroid produced by the fetal adrenal gland; is used for placental oestrogen prod
- Also, some DHEA from maternal adrenal cortex
-draw flow chart
fetal kidneys
Fetus passes little, if any faeces whilst in utero; contents accumulate as meconium (green-black substance!).
- Play a role in fluid and acid-base balance, and in the control of fetal arterial blood pressure (BP).
- Urine is produced by 8th week; fetal kidneys cannot effectively concentrate it produce hypotonic urine (compared to plasma): Fetal urine contributes to the amniotic fluid volume.
- At birth, newborn’s kidneys take over some placental functions: e.g. become fully responsible for waste disposal (and fluid balance).
- Glomerular filtration rate (GFR), urine output and the ability to concentrate urine increase gradually in newborn (as organ matures): With respect to latter, there is a risk of dehydration.
lactation- structure of breast
Structurally, the breast consists of fat, fibrous connective tissue, and glandular tissue. Ducts branch, and converge at nipple.
Lactation 1. Mamogenesis
The pre-pubertal mammary gland is largely composed of lactiferous ducts.
At puberty, gonadotrophins secreted in large amounts…
Oestrogen stimulates growth and proliferation of the ductile system.
Progesterone release stimulates growth and development of the ductile and alveolar secretory epithelium.
In pregnancy, under the influence of the placental hormones the alveoli mature, and breast acquires the potential for milk secretion.
Alveolar epithelium assumes a secretory state in preparation for lactation
Ducts dilate near the areola (brown-ish pigment surrounding the nipple) form lactiferous sinuses
Lactation 2. Lactogenesis- after birth
Alveoli: primary sites of milk production and secretion.
Lactogenesis: synthesis and secretion of milk from breast alveoli.
- As alveoli mature, balls of granular cells become ‘hollowed out’ so that they surround a central lumen (drain into lactiferous ducts).
During lactation, milk is secreted by alveolar cells:
- Specifically, by epithelial (secretory) cells; possess microvilli (luminal side).
- Myoepithelial cells are contractile move milk into lactiferous ducts prior to ejection from nipple (galactokinesis).
lactogenesis- why after birth
Lactation is initiated by the fall in placental steroid levels at birth
- Lactation is stimulated by prolactin, but its action (i.e. to induce milk production) is prevented until after delivery - >inhibited by high levels of progesterone and oestrogens.
- Regular suckling stimulates pulses of prolactin secretion ->maintains milk production (galactopoiesis).
Lactogenesis: milk pathways
Milk consists of simple sugars (carbs), lipids, proteins, vitamins and minerals dissolved in water: account for >80% of its volume.
- Major milk proteins: casein, α-lactalbumin, lactoglobulin.
- Most abundant milk sugar: lactose (disaccharide).
- Alveolar epithelial cells synthesise, package and export the key milk constituents.
- Mechanism for fat/lipid secretion is unique to the mammary gland:
Most consist of triglycerides synthesised from glucose and fatty acids; prolactin controls lipid secretion into lumen.
5 milk secretion pathways
- secretory pathway
- transcellular endocytosis/ exocytosis
- lipid pathway
- trascellular salt and water transport through channels and transporters
- paracellular pathway for ions and water
- look at picture
milk secretion pathway 3: lipid pathway
3, lipid: manufactured in SER; lipid droplets migrate to lumen; microdroplets fuse within cytosol (get bigger); ‘pushes’ cell membrane; eventually, membrane ‘pinches off’ (enters lumen).
composition of human milk
Breast milk composition changes gradually over the first few weeks after delivery:
- Colostrum (week 1): yellow-ish, low in fats, lactose; rich in proteins, certain vitamins, etc; lots of immunoglobins (IgAs).
- Week 2 onwards: ↓ in IgAs and proteins; milk now much richer in fats and sugars.
Important to follow safe guidelines for drug use (e.g. dosing) when a woman is pregnant or lactating: many drugs cross the placenta and enter breast milk..!
lactation 3. Galactokinesis- ejection of milk
Oxytocin stimulates milk ejection in response to suckling (‘let-down’):
- Causes contraction of mammary gland myoepithelial cells to squeeze milk towards the nipple.
- Many stimuli can cause secretion e.g. baby cry.
Uterine contractions:
- Helps expel fetus and placenta (labour).
-> Positive feedback.
lactation 4. Galactopoiesis- maintenance of lactation
TRH = thyrotropin-releasing hormone.
Besides being the primary lactogenic hormone, high levels of prolactin are also required to sustain lactation:
- Recap: regular suckling stimulates pulses of prolactin secretion -> maintains milk production (galactopoiesis).
- Suckling (/nipple) stimulus is considered the single most important factor in the maintenance of established lactation:
Neuroendocrine reflex: suckling causes release of prolactin from the anterior pituitary.
- Afferent impulses travel to the hypothalamus ->fall in dopamine (aka prolactin inhibitory hormone, PIH) -> ↑in prolactin secretion
-draw mechanism
suckling and associated neuroendocrine
- Interestingly, suckling ‘blocks’ ovulation: probably due to the inhibition of GnRH neurons and thus secretion of gonadotropins.
- look at picture
lactation 5. Involution- after weaning -suckling stopped
In absence of mechanical stimulation (suckling), prolactin secretion declines lactogenesis slows down:
- Takes ~2-3 weeks for milk production to stop.
Complete involution of mammary gland takes ~3 months (i.e. gland is remodelled back to its original adult, non-pregnant state):
- Apoptosis of alveolar cells; ductal systems start to dominate.
