Effect of Pregnancy on Maternal Physiology Flashcards
1
Q
Anatomical Changes during Pregnancy
A
- Weight gain averages 12.5kg - 6kg uterus, foetus and breast. 3kg fat reserves and rest is fluid.
- Pressure on IVC will impede venous return from lower limbs, combined with relaxation of vessels and valves (hormonal effects) results in varicose veins.
- Centre of gravity changes so accentuated lumbar lordosis is developed, leads to backache, waddling gait and anterior flexion of neck.
- Relaxin causes softening of ligaments - Sacroiliac and pubic symphysis pain and pregnancy related pelvic girdle pain (PGP).
- Diastasis Recti - abdominal splitting, rectus abdominus muscle increased with high birth weight and number of pregnancies.
- Striae Gravidarum - stretch marks due to stretching of skin.
- Uterus is palpable around 12 weeks. It displaces intestine and has irregular contractions throught pregnancy.
2
Q
Human Chorionic Gonadotropin (hCG)
A
- peptide hormone synthesised by syncytiorophoblast cells of embryo under direction of progesterone and oestrogens, prevents involution of corpus luteum at end of menstrual cycle.
- nausea and vomiting experienced by women during first 12-14 weeks - precise cause unknown but seems to parallel with rising levels of hCG.
3
Q
Human Placental Lactogen (hPL)
A
Human Chorionic Somatomammotropins (hCS1 and hCS2). Polypeptide hormones structurally related to GH and prolactin secreted by placenta. Synthesised by syncytiotrophoblast cells of placenta. Promotes development of maternal mammary glands. Decreases insulin sensitivity and utilisation of glucose by mother. Plays role in release of free fatty acids from mother’s fat stores.
4
Q
Oestrogens
A
- Enlargement of mother’s uterus, breasts (+growth of ductal structure), and external genitalia.
- Relaxation of pelvic ligaments -sacroiliac joints become limber and symphysis pubis becomes elastic.
5
Q
Progesterone
A
- Development of uterine endometrium and role in nutrition of early embryo (decidual cell development).
- Reduces contractibility of pregnant uterus - reducing spontaneous abortion
- Helps oestrogens prepare mother’s breasts for lactation.
6
Q
Maternal-Placental-Foetal Unit
A
- Although placenta is major source of progesterone and oestrogens during pregnancy, placenta cannot synthesise these hormones by itself. Requires both mother and foetus. It is an imperfect endocrine organ; cannot manufacture adequate cholesterol, lacks 2 crucial enzymes for synthesising estrone and estradiol and lacks enzyme for synthesising estriol. Mother supplies most of cholesterol as LDL particles. Foetal adrenal gland and liver supply 3 enzymes that placenta lacks but foetus cannot synthesis oestrogens as it lacks enzymes to catalyse last two steps.
7
Q
Brain changes induced by pregnancy
A
- Medial preoptic area (mPOA) plays central role in regulating maternal behaviour
- Relaxin produced by corpus luteum. In early pregnancy it stimulates oxytocin and vasopressin neurons.
8
Q
Cardiovascular Changes
A
- Cardiac output increases in 1st trimester (30-40%) and then only slowly during 2nd and 3rd trimesters (30-50% at term).
- Mean arterial pressure usually decreases during 2nd trimester and increases during 3rd trimester although it remains at or below normal, due to decrease in TPR.
- Blood volume increases in 1st trimester, expands rapidly in 2nd trimester and rises at a lower rate in 3rd trimester, then plateaus in last few weeks of pregnancy. Increased due to increased plasma volume and number of erythrocytes (supposedly because elevated progesterone and oestrogens cause vasodilation leading to decrease in peripheral resistance and renal perfusion. Also increases AVP/ADH release so thirst often occurs too. Decreases in blood viscosity improves placental perfusion and reserve during haemorrhage. Haemoglobin in normal range. RBC, EPO, and WBC increased.
- High oestrogen levels stimulate Nitric oxide production + relaxin from corpus luteum causes vasodilation by blocking endothelin induced vasoconstriction.
- Normal pregnancy referred to as hypercoaguable state preparing for haemostatic challenge of delivery. Pregnancy is a risk for venous thrombosis and VTE (6x higher). Virchow’s Triad - venous stasis (from 2nd trimester onwards; inhibitors of blood coagulation decrease and fibrinolysis increases), vascular damage (delivery) and hypercoaguable state.
- Normal in pregnant women - peripheral oedema, mild tachycardia, jugular venous distension and lateral displacement of the left ventricular apex.
9
Q
Pre-Eclampsia
A
- Placental problem involving an increase in BP (>140/90mmHg), proteinuria (after 20 weeks) and oedema.
- May involve failure of second wave of trophoblast invasion that normally impairs the capacity of material spiral arterioles to constrict (12-16wks)
- Treatment - delivery of baby
- Occurs in ~2-8% of pregnancies and is more common in 1st pregnancy.
- Risk factors - previous pregnancy with pre-eclampsia, >40yo, family history, obesity, primigravida
- Clinical features - headache, visual disturbances, epigastric pain, oedema.
- Poor placental perfusion can cause foetal growth restriction.
- Increased vascular resistance in placenta causes: decreased blood to placenta, hypertension in mother and renal arterioar endothelial damage causes oedema, glomerular damage and proteinuria (acute atherosis).
10
Q
Eclampsia
A
- Potentially fatal, common in low resource countries, preventable by antenatal care.
- Extreme hypertension (e.g. 180/120) - increased intercranial pressure, seizures, coma, significant risk of cerebral haemorrhage.
- Maternal mortality ~8-36%
- Interventions: magnesium sulphate, antihypertensives, rapid delivery, careful fluid balance.
11
Q
Respiratory Changes
A
- Increase in alveolar ventilation - diaphragm rises approx 4cm which leads to decrease in residual volume and functional residual capacity, increases tidal volume which increases alveolar ventilation.
- Earliest physiologic change is 6wks after fertilisation lol. Direct stimulatory effect of progesterone and oestrogen on medullary respiratory centre (increases sensitivity to CO2), leads to a decrease in maternal arterial pCO2 and higher pO2.
- Respiratory Alkalosis (to maintain maternal pH at 7.4-7.45 increase in excretion of bicarbonate. Buffering capacity is reduced. Results in a slightly reduced ability to buffer a metabolic acid load. The lower pCO2 would shift to the left, but the minimal change in pH and the increased 2,3DPG levels during pregnancy mean there is little change.
- On examination - spirometry parameters unchanged, so abnormal spirometry would be due to an underlying respiratory disease not pregnancy.
12
Q
Chadwick’s Sign
A
increased blood flow to vagina causes a violet colouration
13
Q
Endocrine Changes
A
- hPL maintains foetal glucose levels.
- Foetal adrenals and placenta produce cortisol
- High oestrogen level increase thyroid binding globulin.
14
Q
Renal & Urinary Changes
A
- Blood flow to kidneys increase 35-50% due to increase in cardiac output.
- GFR incrases by about 40-50%
- Urine production increases slightly due to increased fluid intake and load (excretory products).
- Renal tubules reabsorptive capacity for Na, Cl, H2O is increased as much as 50%, due to increased production of steroid hormones by placenta (progesterone) and adrenal cortex (aldosterone)
- Decreased plasma urea, creatinine and uric acid - uric acid is most useful rnal marker in pregnancy as it rises before creatinine in response to impairment (e.g. pre-eclampsia).
- Bladder is compressed by foetus and expanding uterus. Bladder loses tone (progesterone), so pregnancy leads to increased urinary frequency, urgency and sometimes incontinence. Ureters dilated so predispose infection.
15
Q
GI Changes
A
- Constipation more common - uterus pressing against colon and rectum, relaxation of smooth muscle by placental progesterone reduce gut motility and reduction in water content from Angiotensin II and Aldosterone action.
- Gastric Acid Reflux - relaxation of lower oesophageal sphincter, relaxation of GI smooth muscle (progesterone effect), pressure of uterus, worse lying down and aspiration risk during endotracheal intubation.
