Growth Flashcards
(54 cards)
how many lobes around nippe
20
9/10 are functional - all other are vestigial
what inhibit and promote lactogenesis
inhibit
- oestrogen
- progesterone
- dopamine inhibits release of prolactin –> inhibits milk release
- if milk isn’t released
promote
- oxytocin (milk ejection)
- placental lactogen
- prolactin (milk synthesis)
- suckling
- thinking of baby (due to higher areas involved)
what cells contract for milk ejection
myoepithelial
what type of cells do prolactin act on in alveoli to increase milk synthesis
cuboidal
what hormone is mainly responsible for milk production vs milk ejection
production = prolactin from ant. pituitary
release = oxytocin from post. pituitary
name agonists and antagonists for dopamine and their use with breast feeding
antagonists to increase lactation (pre-term birth)
- metacloperamide
- domperidone
agonists to inhibit (rarely done)
- bromocriptine
- cabergoline
5 secretory pathways of milk components
1) exocytosis (proteins/ca/phosphate) from ROUGH ER
2) milk fat globules (lipids) from SMOOTH ER
3) immunoglobulin secretion (IgA)
4) osmosis (ions eg. na / k)
5) paracellular route which opens during pregnancy (leads to higher NaCl and lower lactose/K+ in milk)
so v.preterm women will have different breast milk (higher lactose and higher Na+/K+/Cl-)
why is human milk good
whey is soluble in acid - soluble in stomach and promotes gastric emptying
(human milk has high whey content)
-whey: lactoferrin/lysozymes/iga
contains lipase =activated with bile salts and helps digestion
LCPUFA = brain and retinal development
immunity
-if delivered at term –> igG via placenta if preterm, igG from breast milk too
lactoferrin
inhibits bacterial growth by binding iron - bugs love iron
mother benefits of breast feeding
lose weight
relationship with baby
high oxytocin–> uterus contraction—> dec. risk of postpartum haemorrhage
inhibits oestrogen release—> dec. breast cancer/ovarian cancer due to lowered exposure to oestrogen
lung development (5 stages) + GF involved
- embryonic stage (lung buds from foregut)
- hepatocyte nuclear factor 3b - pseudoglandular (Branching)
- Gli protein - canalicular (development of branching)
- saccular
- VEGF for angiogenesis around - alveolar (even as a child developing)
FGF 10, SSH, BMP4 for outgrowth for new end buds
structural pathology of lung
before 16 weeks = limits branching (irreversible) –> permanent low alveoli number
after 16 weeks = branching already occurred so only alveoli number and function affected
extrinsic restrictions
- congenital diaphragmatic hernia
- effusions
- thoracic dystrophy/ vertebral abnormalities
lung liquid secretion
lung liquid from amniotic fluid
- active pumping of CL- into lung (passive movement of Na in)
- water follows
- positive pressure in lung keeps lung open
lung liquid required for GROWTH not branching therefore important for lung FUNCTION
before birth it is absorbed
- active pumping of Na out to membrane cell
- out of cell via 3Na/2K
- water follows out
during labour, adrenaline stimulates na/k pump
also upon delivery the high O2 will increase Na transport
liquid lung pathologies
- oligohydroamnios (low amniotic fluid–> little/no lung fluid–> lung underdeveloped)
- neuromuscular tone loss
- delivery without labour (no adrenaline to increase absorption of liquid)
concentration of ions of lung liquid
Na and K is similar to plasma
cl> hco3- > protein
surfactant production control
INCREASE
- activation of their B-adrenergic recptors on type 2 pneumocytes
- (dexamethasone-glucocorticoids–> stimulate)
- T4 thyroid hormones
DECREASE
- insulin decreases maturation of type 2
- stretch receptors—> -ve feedback
what is key for ensuring spreading of surfactant
SPA,B,C –> PG
SPD
immune function rather than structural function of surfactant
function = protecting surfactant from external pathogens
what makes up surfactant
protein (SP_) + phospholipids + neutral lipids (main bit that dec. surface tension eg. diplamitoyl-phosphatidycholine)
describe surfactant problems with premature birth
- low number of type 2 pneumocytes + alveoli poorly formed
- later on gestation, pg replaces pi (pg required for spreading of surfactant)
- SP_ protein decifencies –> further structural problems eg. spreading)
when is a baby considered premature
<37 weeks
how is foetal Hb different
2 alpha + 2 GAMMA chains
due to change of one AA
means 2,3DPG doesn’t bind as well to deoxy-Hb = high affinity for O2
2,3DPG difference between normal and pregnant women
normal - binds to deoxy Hb to allow O2 to be released even at high O2 pressures
pregnant - 30% increase so they can release to foetus
at birth what happens to the respiratory structures
cold temp causes umbilical vessels to constrict
decreases BF to umbilical veins/ ductus venosus(connecting umbilical vein and IVC) –> closure
ductus arteriosus closes due to blow from both sides (increased blood flow in pulmonary artery)
there is a decrease of placental PG to the baby therefore this promotes closure of structures including the ductus arteriosus (pulmonary artery and aoorta)
foramen ovale closes due to the pressure of RA and LA equalising
(o2 causes pulmonary artery to dilate–> dec. resistance–> increased flow –> increased blood returning to L.A–> pressure on both sides of foramen ovale causes it to close)