pregnancy Flashcards
what is the decidua
uterine lining (endometrium) during pregnancy which forms maternal part of placenta
balance of pro and anti-inflammation in decidualisation
- Pro-inflammatory: HESCs release IL-33 upon decidualisation
- Anti-inflammatory: HESCs → downregulation of ST2L, upregulation of sST2
Poor regulation of this in RPL → imbalance between pro & anti-inflammation → pro-inflammatory time in window of receptivity increased → late decidualisation
Endometrial causes of recurrent pregnancy loss (3)
- Impaired decidualisation of stromal cells → failure of placenta formation
- Dysregulation of pro and anti-inflammation → prolonged endometrial receptivity → delayed implantation (in unsupportive uterine environment)
- Failure of decidualisation → loss of inhibition of implantation factor secretion → loss of embryo recognition and selection
when does decidualisation occur
mid-luteal phase of every menstrual cycle
endocrinology of pregnancy
hCG peak during 1st trimester at ~8 weeks GA
All other hormones (placental lactogen, progesterone, oestrogens) hit peak at end of pregnancy, and fall after delivery
Progesterone levels are highest
Steep fall due to delivery of placenta
All require placental activity though have different regulation
where is hCG produced
Primarily secreted from syncytiotrophoblasts
Cytotrophoblasts can produce some
hCG functions (2)
- Major role: maintenance of oestradiol and progesterone in early pregnancy
hCG → LH receptor on corpus luteum (similar structure to LH) → cAMP → progesterone & oestrogen production from ovary; prevents degeneration of corpus luteum until luteo-placental shift - Stimulation of steroidogenesis in feto-placental unit
High levels of hCG cross from maternal circulation to fetal → androgen production by developing testis
where is prolactin produced (2)
- lactotrophs of pituitary
2. decidualising endometrial cells
hormonal control of breast development
Oestrogen influences duct development
Progesterone and prolactin influence alveolar development
placental production of oestrogen
Placenta lacks key enzyme CYP17 which converts pregnenolone to DHEA
1. Pregnenolone converted to DHEA-S (sulfated form) in fetal adrenals (develop early)
OR DHEA-S produced by maternal adrenals which goes to placenta
DHEA-S inactive as DHEA could affect development in females
2. DHEA-S travels to fetal liver: can either be:
i. Converted to oestrodiol in placenta or
ii. Hydroxylated to 16αOH-DHEA-S, then converted to estriol in placenta
what hormones do the different cells of the placenta produce
Cytotrophoblast layer can produce GnRH and CRH
Syncytium can produce hCG, hPL and progesterone
cardiovascular changes in pregnancy
- ↑cardiac output
- ↓peripheral vascular resistance
- ↑heart rate
Can lead to decreased exercise tolerance, dizziness, palpitations
Parameters begins to return to normal during third trimester
diagnostic criteria for pre-eclampsia
- New onset hypertension (>140/90mmHg)
2. Proteinuria (>0.5g/day) on 2 separate occasions
symptoms of pre-eclampsia (4)
- Headache
- Visual disturbances (due to oedema in the eye)
- Abdo pain (due to stretching of liver capsule)
- Swelling (capillaries leaking)
Can be asymptomatic ∴ screening important
complications of pre-eclampsia (5)
- Eclampsia (fitting)
- Cerebral haemorrhage: due to uncontrolled high BP
- Pulmonary oedema
- Acute kidney injury
- HELLP: haemolysis, elevated liver enzymes, low platelets
cardiovascular changes in preeclampsia
effect of exercise
Pre-eclampsia → concentric remodelling → fibrosis, stiffness, ↓diastolic function
Exercise → eccentric remodelling; better able to cope w increased load
∴ exercise may decrease risk
pathophysiology of preeclampsia
2 causes
- Diminished remodelling of spiral arteries → narrow lumen, smooth muscle hypertrophy → poor blood flow & ↑clotting → release of syncytiotrophoblast microparticles (STBMs) into maternal circulation
- Variable blood flow through spiral arteries → oxygen tension in placenta alters → reoxygenation → ↑release of free radicals and STBMs
STBMs and free radicals:
a. Damage endothelial cells→ cannot release prostacyclin → ↑vasoconstriction and coagulation → hypertension, proteinuria, procoagulant state
b. Activate leukocytes → damage of maternal vasculature
Leads to cycle: high blood flow → coagulation & vasoconstriction → clot breakdown → restoration of blood flow → high blood flow
- phases of cervical dilatation
2. ideal rate of contractions + intervention
- Latent phase: < 3cm dilated, active phase: > 3cm
Can detect whether labour is failing to progress and if intervention needed - Contractions: aim for 3-4 / 10min
Undercontracting → oxytocin
normal values on CTG (4)
- Baseline rate 110-160 (average fetal HR in 10min)
- Variability >5 (how much peaks and troughs of HR deviate from baseline)
Reflection of baby’s autonomic nervous system - Accelerations (abrupt fetal HR increase > 15pbm above baseline for >15s)
- No decelerations (opposite of accelerations)
causes of abnormal CTG
Maternal: 1. Sepsis 2. Placental abruption 3. Uterine scar rupture 4. Spinal/ epidural hypotensive episode 5. Hyperstimulation>5:10 Fetal: 6. Intrauterine growth restriction 7. Cord around neck 8. Cord prolapse 9. Rapid descent 10. Prolonged cord compression
effects of pregnancy on pre-existing diabetes (5)
- More insulin needed
- Nephropathy worsens
- Retinopathy occurs/worsens
- Hypoglycaemia common; ↓awareness of hypos
- Neuropathy/gastroparesis (delayed gastric emptying) may worsen