Endocrinology: Physiological Adaptations to Pregnancy Flashcards

1
Q

Hypothalamic-pituitary-gondal axis

A
  • Complex hormonal system
  • Involved in regulation of reproductive function in mammals
  • Consists of hypothalamus, pituitary gland and gonads (testes and ovaries)
  • GnRH (gonadotropin releasing hormone) is released by the hypothalamus into the portal system; stimulates release of gonadotropins from pituitary gland
  • LH (luteinising hormone) and FSH (follicle-stimulating hormone) released by pituitary: LH stimulates testes to produce testosterone, ovaries to produce estrogen/ progesterone, trigger ovulation; FSH supports spermatogenesis and follicle development in ovaries/ production of estrogen
  • Gonads respond to gonadotropins (LH and FSH) to produce sex hormones (testosterone, estrogen, progesterone) and release eggs during ovulation
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2
Q

Hormonal changes during the menstrual cycle if fertilisation doesn’t occur

A

Luteal phase of menstrual cycle: days 14-28
- Corpus luteum is a progesterone factory with a limited life span
- Progesterone induces endometrial secretory phase
- Endometrium (thick and secreting) required for implantation
- If no fertilisation, no need for implantation and no need for endometrium: progesterone decreases, endometrium becomes ischaemic and lost

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3
Q

Hormonal changes during the menstrual cycle if fertilisation occurs

A
  • Zygote formed, begins dividing
  • Implants into uterus around 6-7 days after fertilisation (up to 10 days post-ovulation)
  • Need secretory endometrium
  • Therefore, need progesterone
  • Levels stay high until end of gestation
  • Uterus: maintains endomentrium, decreases contraction of myometrial cells (important for quiescence vs. labour)
  • Lung: increases tidal volume
  • Breast: preparation for lactation
  • GIT: smooth muscle relaxation
  • Bone marrow: increase erythropoiesis
  • Kidney: natriuretic properties (offset by aldosterone
  • Corpus luteum is ‘rescued’ by human chorionic gonadotrophin (hCG)
  • Glycoprotein synthesised by zygote – even before implantation
  • Placental (trophoblast) cells produce and release hCG into maternal circulation
  • ‘Tells’ corpus luteum to continue making progesterone and oestrogens (which it does until ~ wk8), then placenta take over production of progesterone and oestrogens
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4
Q

Hormonal changes during the menstrual cycle (regardless of whether fertilisation occurs or not)

A
  • Oestrogens
  • Regulates secretion of progesterone by placenta
  • Vital for development of foetus
  • Stimulates hypertrophy of myometrial and placental cells
  • Stimulates breast development
  • Human placental lactogen (hPL)
  • Also called human chorionic somatotropin (hCS)
  • Lactogenic and diabetogenic: decreases maternal glucose utilisation
  • Relaxin
  • Produced by corpus luteum and placenta
  • Mediates hemodynamic changes (increase cardiac output, arterial compliance and renal blood flow)
  • Relaxes pelvic ligaments and softens cervix
  • Insulin
  • Decrease in sensitivity (insulin resistance) in 2nd half due to increased cortisol, prolactin and human placental lactogen
  • High plasma insulin levels, normal to high plasma glucose
  • Thyroid axis
  • Increase total T3 and T4: hCG exerts some ‘TSH like’ activity
  • Increase free (active) T3 and T4 due to oestrogen, increasing TBG
  • Aldosterone and corticosteroids
  • Adrenal cortical hormones elevated during pregnancy
  • Stimulate sodium (and water) retention; expansion of ECF
  • Prolactin
  • Secreted by the anterior pituitary
  • Preparation of breast for lactation (hypertrophy of alveoli)
  • Stimulation of milk production postpartum
  • Calcitriol (activated vitamin D)
  • Calcium demand increased
  • Calcitriol increases calcium absorption from intestines
  • PTHrp (parathyroid hormone-related peptide)
  • Placental hormone
  • Mobilises calcium from maternal bones to ensure calcification of the foetal bones
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5
Q

Plasma and extracellular fluid changes during pregnancy

A
  • ~50% increase in plasma and ECF
  • Includes sequestering of sodium in placenta and amnion
  • Mediated by increased aldosterone and cortisol (opposed by progesterone and atrial natriuretic peptide)
  • Oedema clinically identifiable in 50% of pregnancies
  • Hypothalamic osmostat is ‘reset’: thirst increased at lower than usual osmolarity, helps protect lower osmolarity
  • Increased water reabsorption: decrease plasma oncotic pressure (due to dilution of plasma protein conc), increased hydrostatic (venous) pressure, contributes to oedema
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6
Q

Haematological changes during pregnancy

A
  • Erythropoiesis (RBC production) increases: not as much as plasma volume decreased haematocrit, Hb conc normal
  • Increased fibrinogen and clotting factors
  • Decreased endogenous anticoagulants
  • Helps to stop bleeding after delivery but increases risk of thrombosis and thromboembolism (further increased by venous stasis due to vasodilation and compromised venous return)
  • Mild haemodilution is normal in pregnancy
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7
Q

Cardiac physiology changes during pregnancy

A
  • Cardiac output increased by 30-50%
  • Heart rate increases by 15 beats/ min
  • Stroke volume increases by 10%
  • Often heart murmurs can be heard due to increased blood flow through heart, altered heart configuration, mammary vessels: difficult to distinguish on auscultation from those due to significant cardiac or vascular disease
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8
Q

BP changes during pregnancy

A
  • Increased CO, decreased vascular resistance
  • Same systolic pressure, decreased diastolic pressure during 1st half by ~15mmHg
  • Due to peripheral vasodilation
  • Mediated by progesterone, prostaglandin E2 and prostacyclin; increased NO production
  • Triggers volume expansion (via RAAS)
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9
Q

Renal physiology changes during pregnancy

A
  • Increased GFR (up 50% by end of first trimester)
  • Increased renal plasma flow: decreased pre- and post-glomerular resistance
  • Decreased plasma urea and creatinine (increased clearance)
  • Microalbuminuria (due to haemodynamic, permeability and tubular reabsorption changes)
  • Glucosuria (glucose in urine): increased filtration rate of glucose, impaired reabsorption, may increase chances of UTI
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10
Q

Respiratory physiology changes during pregnancy

A
  • Progesterone increasing sensitivity of respiratory centre to CO2
  • Increase tidal volume x respiratory rate = increase minute ventilation; helps meet increased O2 demand
  • Keeping maternal pCO2 low encourages CO2 removal from foetus
  • Renal excretion of HCO3- maintains normal pH
  • Breathlessness (dyspnoea) not unusual
  • Lung volume changes
  • Increased tidal volume
  • Expiratory reserve volume and functional residual capacity (FRC) decrease
  • The enlarging uterus can elevate the diaphragm by as much as 4cm the transverse chest diameter can be increased by 2cm
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11
Q

Gastrointestinal system changes during pregnancy

A
  • Taste often altered
  • Reduced gastric secretion
  • Delayed gastric emptying
  • Reduced gut motility; constipation
  • Nausea and vomiting common (~50% of pregnancies)
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12
Q

How do pregnancy hormones affect the brain?

A
  • Oestrogen and progesterone: enlarge cell bodies of neurons of the medial preoptic area of the hypothalamus (maternal behaviour), increase SA of neuronal branches in the hippocampus (memory and learning)
  • Oxytocin: stimulates the hippocampus
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13
Q

How can pregnancy cause insomnia?

A
  • Increased awareness of foetal movements at rest
  • Feeling too hot due to peripheral vasodilation
  • Nocturia
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14
Q

How can pregnancy darken skin?

A
  • Hyperpigmentation occurs due to increased secretion of melanocyte stimulating hormone (MSH) – from pars intermedia of pituitary gland
  • Promotes linea nigra (dark line down abdomen), darkening of areola, facial chloasma/ melasma ‘pregnancy mask’
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15
Q

Impacts on pregnancy on oral health

A
  • Vomiting (morning sickness) can contribute to enamel erosion
  • Changes in feeding habits (grazing, food fads), decreased oral hygiene (tiredness, nausea) and reduced dental visits can be detrimental for dental health
  • Pregnancy gingivitis: usually in 2nd trimester; hormonal excesses causes gums to react differently to bacteria. Periodontitis has been linked to preterm labour (increase prostaglandins)
  • Pyogenic granuloma (pregnancy tumours); rare, inflammatory, benign growths that develop on the gums as part of an exaggerated response to plaque. Pregnancy tumours usually subside shortly after childbirth
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16
Q

Considerations for pregnant patients during appointments

A
  • Counsel on importance of receiving adequate vitamin A, C, D, calcium, and phosphorus
  • Safe to receive dental treatment at any time during pregnancy however best to schedule non-emergency treatment for 2nd semester
  • Delay extensive treatment until after delivery (for comfort and wellbeing of mother/ foetus)
  • To avoid supine hypotensive syndrome, use a semi-supine chair position and elevate right hip; displace gravid uterus away from vena cava
  • Avoid radiographs in 1st sem if possible; lead apron must be used
  • Many drugs not acceptable; NSAIDs, codeine, nitrous oxide, tetracyclines; general anaesthesia should be avoided
  • Refrain from removing or fitting amalgam fillings: avoids any potential risk of mercury crossing the placenta
17
Q

Possible implications for the oral health of infant, related to the mother

A
  • Foetal alcohol syndrome: increased incidence (3.4x) of orofacial clefts. Can also lead to cranio-facial dysmorphism
  • Enamel hypoplasia in young children; linked with prolonged/ difficult deliveries; viral infections; uncontrolled diabetes during pregnancy
  • Low birth rate increased risk of periodontal disease
  • Positive attitude of oral health from parents likely to be carried over to growing infant