HUBS3511 · Human Reproduction And Pregnancy
Maternal Adaptations
Pregnancy forces the mother’s body to up-rate every supply system — more blood, more cardiac output, more ventilation, more renal filtration — to feed a fetus and pre-pay for delivery blood loss. The exam’s favourite twist is that several of these changes look like disease but are normal: the classic is dilutional (physiological) anaemia, where plasma volume rises faster than red-cell mass so haemoglobin concentration falls even though total red-cell mass increased. HUBS3511 asks for the cardiovascular numbers (blood volume and cardiac output both up ~30–50%, SVR and BP down), why pregnancy anaemia is dilutional and therefore normal, the respiratory change (↑ tidal volume → mild respiratory alkalosis) and renal change (↑ GFR → ↓ creatinine), and the lactation system — a clean two-hormone split in which prolactin makes milk and oxytocin ejects it, with synthesis starting only once progesterone falls at birth.
What this chapter covers
- 016.1 Cardiovascular adaptation: ↑ blood volume & CO, ↓ SVR & BP
- 02Dilutional (physiological) anaemia — normal, not pathology
- 036.2 Respiratory: ↑ tidal volume → mild respiratory alkalosis
- 04Renal: ↑ GFR ~50% → ↓ creatinine & urea; mild glucosuria
- 05Metabolic: hPL-driven insulin resistance spares glucose for the fetus
- 06Adaptation vs disease: the discriminators
- 076.3 Lactation: prolactin (MAKE) vs oxytocin (EJECT)
- 08The suckling reflex and the progesterone brake on milk synthesis
Worked example: why is pregnancy anaemia normal?
- +1Both rise, unequally: in pregnancy both plasma volume and red-cell mass increase, but plasma rises ~40–50% while red-cell mass rises only ~15–20%.
- +1Concentration falls: because plasma rises faster, haemoglobin concentration falls even though total red-cell mass has increased.
- +1Name it: this is dilutional (physiological) anaemia — a normal adaptation, not iron deficiency. The mantra is “normal adaptation ≠ pathology”.
- +1The red flag: a failure of BP to fall mid-pregnancy (or rising BP) with proteinuria after 20 weeks points to preeclampsia — a genuine pathology, not an adaptation.
Key terms
- Dilutional anaemia
- The fall in haemoglobin concentration in pregnancy caused by plasma volume rising faster (~40–50%) than red-cell mass (~15–20%). Total red-cell mass increases; it is a normal physiological adaptation, not iron deficiency.
- Cardiac output (in pregnancy)
- CO = HR × SV, which rises ~30–50% — early via increased heart rate, later via increased stroke volume — to supply the low-resistance placental circuit and the fetus.
- Respiratory alkalosis (of pregnancy)
- The mild alkalosis from progesterone-driven increased tidal volume, which blows off CO₂ and lowers maternal PaCO₂. This is deliberate: it steepens the gradient for fetal CO₂ to offload across the placenta.
- Prolactin
- The anterior-pituitary hormone that drives milk SYNTHESIS in alveolar cells, making milk for the next feed. It is released when suckling suppresses hypothalamic dopamine (PIH).
- Oxytocin (let-down)
- The posterior-pituitary hormone that contracts the myoepithelial cells around the alveoli to EJECT milk into the ducts (the let-down reflex). It can be conditioned and is inhibited by stress.
Maternal Adaptations FAQ
What happens to blood pressure and creatinine in pregnancy?
BP falls slightly (lowest mid-pregnancy) because progesterone lowers systemic vascular resistance. Blood creatinine and urea also fall, because GFR rises ~50% and clears them faster — so a “normal” non-pregnant creatinine may actually be abnormally high in pregnancy.
Do prolactin and oxytocin make or eject milk?
Prolactin MAKES milk (synthesis, anterior pituitary); oxytocin EJECTS milk (let-down via myoepithelial cells, posterior pituitary). Do not swap them, and note the different pituitary lobes. Both are triggered by infant suckling.
Why does milk only ‘come in’ after birth?
Because high progesterone during pregnancy blocks actual milk synthesis. After delivery the placenta is gone, progesterone falls, and the brake is released so prolactin can drive synthesis. This is why retained placental fragments (still making progesterone) can delay milk coming in.
How do I tell a normal adaptation from a disease?
Each adaptation has a pathological mimic the exam pairs it with: dilutional anaemia vs iron-deficiency anaemia; the normal BP fall vs preeclampsia (BP rises); physiological insulin resistance vs gestational diabetes; mild glucosuria vs frank diabetes. Know which side of the line each sits on.
Why is a mild respiratory alkalosis a good thing in pregnancy?
The increased tidal volume blows off CO₂, lowering maternal PaCO₂. That steepens the gradient for fetal CO₂ to diffuse across the placenta into the mother — a feature, not a bug.
Exam move
Anchor the whole chapter on the mantra “normal adaptation ≠ pathology” and build a two-column table of each adaptation against its pathological mimic (dilutional vs iron-deficiency anaemia; BP fall vs preeclampsia; physiological insulin resistance vs gestational diabetes). Memorise the cardiovascular numbers (blood volume and CO both ↑30–50%; SVR and BP down, lowest mid-pregnancy) and the two tell-tale lab clues (mild respiratory alkalosis from ↑ tidal volume; ↓ creatinine from ↑ GFR). For lactation, the single most-tested fact is the prolactin/oxytocin split — use the mnemonic (proLactin makes the Liquid; oxyTocin = eT ejection) and remember both fire on the suckling reflex while synthesis waits for progesterone to fall.
