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Medicine 3 > 13 maternal adaptation to pregnancy > Flashcards

13 maternal adaptation to pregnancy Flashcards

1
Q

which hormones have a higher plasma level in pregnancy than luteal phase?

does this affect the fetus?

A

progesterone- corpus luteum and then placenta; 200mg/ day by late pregnancy

oestrogen- co-operation of placenta and fetus

no:

  1. placental polarity: prevent too much progesterone and oestrogen
  2. fetus can conjugate steroids to sulfates making biologically inactive
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2
Q

pregnancy hormones

A
  1. placental prolactin (breast changes, behavioural changes)
  2. placental lactogens (maternal insulin and glucose metabolism, lipolysis, erythropoiesis)
  3. CRH from placenta-> increased secretion of cortisol in mother Too high levels affect nutrient transfer and placental clock (risks: pre-term labour, early parturition signals) Male fetus respond more acutely to cortisol levels from mum
  4. aldosterone (plasma volume)
  5. erythropoietin (RBC)
  • Cytokines- pro inflammatory, interleukins, TGF- beta
  • Vasodilatory mediators: VEGF, NO (vasodilation, angiogenesis)
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3
Q

muscular anatomical changes

A
  1. uterine enlargement (expands and increases in weight x20)
  2. hypertrophy of uterine musculature: expulsion of fetus at partruition
    - quiesence of myeometrial contractions during gestation
    - prostaglandin and oxytocin stimulate
  3. diaphragm displaced cranially by gravid uterus (4cm elevation)
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4
Q

cardiovascular anatomical changes

A
  • apex of heart moves anterior and to left (pushed upwards and rotates forwards)
  • LV hypertrophy - cope with increased CO (not permanent
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5
Q

other anatomical changes in pregnancy

A
  • changes in calcium conc in maternal bones ( increased intestinal calcium absorption maternal bone loss may occur in trimester and lactation- reversible)
  • Decidual changes in endometrium to accommodate growing baby
  • Development of mammary glands to form lactating breast
  • Weight gain due to increase maternal blood volume and weight of placenta and baby
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6
Q

cv system: Blood volume and haematological indices

changes in:

blood volume

RC mass

haematocrit and hb

hb values at term

A
  • Increase in blood volume throughout pregnancy: 40% increase by full term (over a litre)
  • Red cell mass increases linearly (30%)
  • Plasma volume increases > cell mass so there is a fall in hematocrit and haemoglobin

Advantage: decreased viscosity -> reduced resistance in flow; better placental perfusion

  • At term: hb values 50%> non pregnant
  • Useful protection blood loss at delivery, 500ml placental maternal blood goes back to mum during delivery
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7
Q

mechanisms of blood volume and haematological indices changes

what is important during pregnancy?

A

Hormonal stimulation:

  1. stimulation RAAS: aldosterone leading to sodium ion and water retention-> increased plasma volume
  2. increased renal erythropoetin: increases red cell mass

supplement iron and folic acid levels to help restore hb levels

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8
Q

CV system: Total peripheral resistance in pregnancy

factors

changes in vascular tone

A
  • Angiogenic, permeability and vasoactive factors: VEGF (permeability), PLGF, NO and progesterone (relaxes arterial smooth muscles)
  • Vascular dilatation and relaxation of peripheral vascular tone
  • New vascular beds (angiogenesis in mum too), including utero-placental circulation -> drop in peripheral resistance
  • Lowers blood pressure (contributes to increased blood volume)

->reduction in peripheral vascular resistance

Reduces about 40% in mid-pregnancy, rising slowly to term

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9
Q

CV system: cardiac output

A
  1. increase in blood volume= more blood enters heart -> increased preload
  2. decrease in peripheral resistance due to vasodilatation-> reduced afterload
  3. increase in stroke volume
  4. increase in maternal heart rate
  5. increase in CO (SV x HR)
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10
Q

why is an increase in CO needed in pregnancy?

A

extra 30-50ml oxygen consumed per minute

  • blood flow to uterus and placenta: 25% maternal CO
  • CO does not fall towards term
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11
Q

how much can CO increase during labour

A

2L/min

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12
Q

what is the blood pressure like during pregnancy?

A

BP= CO X resistance

Systolic bp stable in pregnancy.

In early pregnancy, diastolic pressure does not fall reaching a nadir at around 20 weeks, rises to normal by term

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13
Q

ECG changes during pregnancy

A

leftward deviation of 15 degrees. Flattening/inversion of T wave in lead III; ST segment depression.

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14
Q

what does enlarging uterus cause when mother lies supine

A

IVC and aorta compression

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15
Q

what happens if IVC is compressed?

A
  • reduces venous return to heart (fall in pre- load and CO)
    • Resultant fall in bp- can be severe for loss of consciousness
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16
Q

what happens if the aorta is compressed

A
  • reduces uteroplacental and renal blood flow
    • Last trimester: maternal kidney function lower in supine than lateral position
  • Fetal transplacental gas exchange may be compromised
17
Q

respiratory system: structural changes

A

increased chest expansion, displaced diaphragm, increases vascularisation of upper respiratory tract

18
Q

respiratory system: ventilatory adaptations

A
  1. Progesterone- mediated hypersensitivity to CO2 increases RR by 15%
  2. Tidal volume by 40%
  3. Alveolar ventilation- 70% higher at end of gestation

fall in arterial and alveolar CO2 tensions: 4.1 kPa by end of first trimester (25% decrease). PaO2 increases to 13-14 kPa

19
Q

respiratory system changes: consequences to baby

A
  • Higher PaO2 on maternal side of placenta facilitates oxygen transfer to fetus
  • Lower PaCO2 facilitates transfer of CO2 in reverse direction
20
Q

maternal renal function: anatomical changes

A
  • Kidneys enlarge (1cm increase in size) due to increased vasculature, vascular dilatation and interstitial space increases
  • Renal parenchymal volumes increase in pregnancy, glomerular (Bowman’s capsule) diameters are greater
  • Dilatation of calyces, renal pelvis and ureter (progesterone and local pressure effect)- increases chance UTI
  • Bladder loses tone: increased urinary freq and urgency
21
Q

maternal renal function: physiological changes

A
  • Increase RPF, decrease renal vascular resistance
  • Changes in GFR and GFF (filtration fraction)
  • Changes in tubular re-absorption
22
Q

renal haemodynamics alterations in pregnancy

A

FF= GFR/ RPF

  1. RPF increases 50-80% between conception and mid pregnancy (and then decreases in third trimester)
  2. GFR increases but less than RPF

-> FF declines in early pregnancy

Non pregnant state FF= 20%. Similar to late pregnancy

23
Q

changes in glucose handling

A

FF declines, increased renal flow-> more glucose in filtrate.

  • Filtered load of glucose rises in pregnancy and exceeds maximal rate of reabsorption
  • Urine is not glucose free
  • Excretion can be 10x higher than non pregnant
  • Glycosuria
  • Increased chances of UTI
24
Q

what determines fetal glucose levels

A

maternal glucose levels

net flux of glucose from mother to fetus (fick’s principle)

25
Q

Increase glucose excretion in mother- is there a glucose deficit in the mother?

A

evidence for:

  1. Fasting blood glucose 10mg/dl lower than non- pregnant
  2. Ketones found in maternal blood

‘accelerated starvation’

evidence against

  • Fasting hypoglycaemia in first trimester, decrease in glucose levels reach nadir around 12 weeks gestation
  • Then reverts to normal in second and third trimester
26
Q

how do glucose levels revert to normal in early pregnancy?

A
  • Progesterone increases maternal appetite (and stimulates deposition of glucose in fat stores)
  • Increased insulin secretion- favours lipogenesis and storage of fat
27
Q

how do maternal levels revert to normal in mid pregnancy? (5)

A
  • Increased absorption of glucose from gut
  • Increased maternal gluconeogenesis and total glucose production (glycogenolysis)
  • Mobilisation of FFA and lipolysis (influenced by placental lactogen)
  • Enhanced lipolysis- increases FFA and oxidation and ketones. Alternative fuel used by mother, thus reducing own need for glucose- spared for fetus
  • Maternal tissue becomes progressively insulin insensitive (50-80% decline in insulin sensitivity in skm).
    • Development mild insulin resistance
    • Decrease uptake of glucose by maternal tissue
  • After 20 weeks, plasma glucose levels are normal

Conflict with concept of pregnancy being example of accelerated starvation

28
Q

explain response to glucose load in post pregnant and third trimester (38 weeks)

A

post pregnancy:

  • plasma glucose reaches peak 30mins after ingestion
  • returns to baseline after 60 mins

third trimester:

  • plasma glucose slower to reach peak
  • peak is higher (*)
  • returns to baseline after 2h

Prolonged duration of postprandial hyperglycaemia in pregnancy

29
Q

insulin levels in response to glucose load- last trimester

A
  • Higher glucose peak-> higher insulin secretion
  • Insulin reaches peak after 1h (*)
  • Declines slowly but not back to basal levels in pregnancy (vs post pregnant values)

Postprandial hyperinsulinmea. Evidence of insulin resistance

30
Q

is increased insulin resistance a cause of GDM

A

possible cause

  • Initially silent period begins as insulin gets higher (2nd trimester), silent period when most damage is done

resistance also higher in maternal obesity

31
Q

immunulogical role of placenta

A

(fetus has MHC and macrophages)

  • structural barrier stopping direct contact of maternal blood with the fetus
    • Fetus has major histocompatibility antigens (MHCs), but placenta, specifically syncytiotrophoblast surface does not. Acts as immunological barrier
  • Fetus hides behind placenta
  • Syncytial structure of syncytiotrophoblast (SN)- maternal immune cells cannot cross to the fetus without going through cytoplasm and being downgraded (lyosomal system)
  • If they transcytose to placental stroma, fetal macrophages (Hofbauer cells) phagocytoses maternal immune cells
32
Q

how does fetus avoid rejection?

A
  1. Syncytial knots, exosomes, cell free DNA, fetal stem cells shed into maternal circulation are phagocytosed by maternal immature dendritic cells
  2. Phagocytosed debris contains intracellular fetal HLA (Class I & II)
  3. These fetal peptides presented by maternal dendritic cells to T cells in endometrium
  4. Induces a) t cell apoptosis and b) conversion to T reg suppressor cells (avoid high levels of T cells)

Peripheral tolerance of fetal HLA develops. Tolerance by the maternal immune system is achieved (changing maternal ‘self’ hypothesis)

33
Q

immune function of endometrium

A
  • Endometrial mucosa is an immunologically privileged site
  • Must mount immune response against microorganisms and be able to tolerate sperm and allogenic fetus
  • No trafficking of endometrial lymphocytes to other mucosa
  • Under influences of pregnancy hormones, T helper cells decline relative to suppressor cells or Treg in endometrium
  • Treg act to decrease immune function. Suppresses response from dwindling t cells and help maintain materno-fetal tolerance
34
Q

immune cells in endometrium

A

Dendritic (APC) cells

Th cells

T reg cells

Uterine NK cells

35
Q

Mechanisms of tolerance at fetal-maternal interface

A

Soluble factors may provide local immunoprotection of fetus

  • Secretion of endometrial glycoproteins by decidual stromal cells suppress uterine NK cells. uNK cells produce cytokines kill fetal cells
  • Secretion of placental galectins- immunosuppressive
  • Production of anti-inflammatory factors: TGF-b and IL-10 by the decidua and the placenta aids apoptosis of T cell and their conversion to T reg.

Extra-villous trophoblast cells (EVTs)- invade endometrium and remodel spiral arteries, lack conventional class I and II MHCs

  • Unique HLA class I antigens: HLA-C,-G and -E
  • HLA-G is not expressed in any other maternal or fetal cells
36
Q

what is the role of Invading EVTs

A
  • uNK contain killer cell immunoglobulin-like receptors
  • can recognise HLA-G on invading trophoblast cells
  • binding of HLA-G with KIR on uNK inhibits cytokine production by uNK (negative signal)
  • inhibits uNK cells capacity to secrete cytokines which cause fetal cell lysis, thus controlling maternal immune response
37
Q

acquired immunity: can cell transfer of maternal igG become a problem?

A
38
Q

what is the role of MHC I IgG

A

supress immune reactions

Medicine 3 (31 decks)

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