Lecture 15: Maternal physiology Flashcards

1
Q

Why does the body need to adapt in pregnancy?

A

Increased waste clearance: increased GFR and hepatocellular stimulation
Nutrition: increased respiration, increased absorption, insulin resistance
Childbirth: changes in clotting factors and MSK structures

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2
Q

What drives the adaptations during pregnancy?

A

Hormones

  • hCG
  • oestrogen
  • progesterone
  • relaxin
  • hPL (human placental lactogen)
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3
Q

What is the role of relaxin?

A
  • softening ligaments

- widens the cervix

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4
Q

Why does immunity change during pregnancy?

A

Because we want the baby to thrive and the mother to be a good host
-usually mother would reject the baby due to immune reaction
(achieved by immune regulation)

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5
Q

What are the adaptations within the immune system in pregnancy?

A

Fetus
-recognised by maternal immune system
-incited allo-response is not cytotoxic
Mother
-in pregnancy undergoes an immunosuppressed state (placental progesterone, upregulation of HLA and therefore IL10 which drives tolerance through Th2 (not cytotoxic) cells, which downregulates Th1 cytotoxic cells)
-may improve certain autoimmune conditions
-higher attack rate and severity of certain viral pathogens (e.g. varicella-chicken pox)
=overall no cytotoxic response but baby is recognised

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6
Q

How is respiration changed during pregnancy?

A

Increased ventilation
-baby needs oxygen delivery and carbon dioxide removal
-mum needs continued oxygen delivery to her organs and periphery
=increased oxygen supply to meet metabolic demand and increased carbon dioxide clearance

  • TV increased by 30-40% (chest diameter can increase in pregnant women)
  • ERV decreased by 20%
  • increased minute ventilation by 40-50% (increased oxygen levels, decrease in carbon dioxide- could lead to pH change)
  • TLC decreased by 5%: at term, the child pushes against the diaphragm

Progesterone relaxes smooth muscle in the airways reducing airway resistance

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7
Q

Why do you commonly see dyspnoea in pregnancy?

A

Occurs in 60-70% of patients

  • multifactorial
  • most likely due to hyperventilation
  • need to consider pathological causes/exacerbating factors
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8
Q

What are the changes to the cardiovascular system and haematology during pregnancy?

A

-baby needs delivery of nutrients
-mum needs to fill utero-placental-fetal circualtion, oxygenate growing uterus (very vascular-high demand), prepare for potential blood loss during delivery, protect from any impairment of venous return
Achieved by
=volume expansion
=clotting mechanisms

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9
Q

How is volume expansion of blood achieved during pregnancy?

A

Increased CO
-early: increased stroke volume
-late: increased HR (no more than 95 bpm)
Progesterone: smooth muscle relaxation, decreasing systemic vascular resistance and a drop in BP
-oestrogen and progesterone act on kidney to active RAAS, and oestogren acts on liver to produce angiotensinogen, this usually causes vasoconstriction but in pregnancy it doesn’t (probably due to smooth muscle relaxation), it still causes release of aldosterone from adrenal gland which acts on the kidneys to stimulate reabsorption of salt and water therfore increasing the SV

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10
Q

What are the clotting mechanisms in pregnancy?

A
  • increased procoagulants (fibrinogen. factor 8, vWF)
  • decreased anticoagulants (protein S)
  • reduced fibrinolysis
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11
Q

What consequences do we see due to changes to the CVS in pregnancy?

A

Increased RAAS: peripheral oedema
Change in plasma volume> change in RBC volume: dilutional anaemia
Hypercoagulable state: increased number of thromboembolitic events

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12
Q

What are the changes to the renal system during pregnancy?

A

-baby needs to remove waste
-mum needs to increase the clearance of waste
Acheived by
=increased GFR by 50% (therefore you see decreased serum urea and creatinine by 25%)
Systemic vasodilation- increased renal blood flow causing increased GFR
Decreased PCT reabsorption
Smooth muscle relaxation (progesterone): increased size of kidneys and ureters, decreased speed of urine passage

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13
Q

Why may you see glucosuria in pregnant women?

A

Due to decreased PCT reabsorption, because of increased filtrate rate and blood flow

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14
Q

Why do you get more UTI’s in pregnancy?

A

Due to decreased speed of urine passage

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15
Q

What is the overall change to the GI system in pregnancy?

A

Slower transit time

  • baby needs nutrients
  • mother needs to feed herself and the baby
  • increased absorption of minerals and vitamins
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16
Q

What are the adaptations to the GI tract in pregnancy?

A

Progesterone causes:

  • decreased small and large bowel motility to increase mineral and water absorption: constipation
  • decreased lower oesophageal sphincter tone: GORD
  • decreased gallbladder contractility: gallstones

(uterus is retroflexed so this displaces the bowel which can cause mechanical obstruction)

17
Q

Are LFT’s affected by pregnancy?

A

ALP levels increased due to placental synthesis

18
Q

What are the adaptations of the thyroid during pregnancy?

A

Fetal dependency on maternal thyroxine up to around 12 weeks

  • oestrogen stimulates TBG hepatic production (thyroxine binding globulin)
  • need to increase thyroxine production so we get free thyroxine, as we need free thyroxine to avoid binding of TBG to provide the fetus
  • hCG has a similar alpha-subunit to TSH so stimulates the thyroid
19
Q

What is the adaptation to PTH and calcium?

A

Calcium is required for development of baby’s bones
-Ca2+ reduces due to baby using it
-this stimulates the parathyroid glands to increase PTH, causing increased 25(OH)D (intermediate of vit D), placenta causes increased 1-alpha-hydroxylase which converts 25(OH)D to 1,25(OH)2D (active form of vit D)
=increased Ca2+ and phosphorus absorption in gut (maintain equilibrium of calcium, so we don’t see changes to mums bones to accomodate)

20
Q

How does glucose metabolism change during pregnancy?

A

Insulin resistance: increase glucose levels, allowing glucose for fetus (due to constant hyperglycaemia allowing for glucose flux)
=diabetogenic pregnancy

21
Q

What hormones cause insulin resistance?

A
  • tumour necrosis factor alpha
  • human placental lactogen
  • placental growth hormone
  • oestrogen
  • cortisol
  • progesterone
22
Q

What is gestational diabetes mellitus?

A

Onset of elevated blood sugar levels during pregnancy

Increased insulin resistance so more glucose going to baby (due to obesity/physical inactivity/ethnicity/PCOS)
-increase in glucose flux
-defective insulin secretion, can’t secrete enough
-enhanced size of fetal growth: issues with delivery
Results in increased risk of diabetes later in life

23
Q

What is the increase in weight with a pregnancy?

A

11-15kg

24
Q

What are the adaptations in MSK during pregnancy?

A
Change in centre of gravity
-increased lordosis and kyphosis 
-forward flexion of neck
Stretching of abdominal muscles 
-impede posture
-strain paraspinal muscles
=back pain, shoulder pain, tension headaches

-increased mobility of sacroiliac joints and pubic synphysis
-anterior tilt of pelvis
=pelvic pain

Fluid retention (due to increased volume in circulatory system) can compress structures such as median nerve e.g. carpal tunnel

25
Q

What are the adaptations in skin during pregnancy?

A
  • spider angioma, palmar erythema due to oestrogen increase

- increase in melanocytic stimulating hormone: hyperpigmentation (linea nigra)

26
Q

What is preeclampsia?

A

Hypertension and proteinuria

  • usually presents in the third trimester
  • multisystem disorder
  • impaired invasion of the trophoblast leading to shallow invasion of spiral arteries
  • leads to hypoperfusion and ischaemia
  • this also causes systemic endothelial dysfunction in mum
27
Q

What are some risk factors of preeclampsia?

A
  • diabetes
  • obesity
  • FHx
  • chronic/gestational hypertension
  • renal disease
  • first pregnancy
  • extremes of age
  • IVF
  • preeclampsia in prior pregnancy
28
Q

What are the complications of preeclampsia?

A

Maternal (vasoconstriction due to systemic endothelial dysfunction)

  • seizure (eclampsia): serious
  • cerebral haemorrhage
  • renal failure
  • pulmonary oedema
  • DIC and thrombocytopenia
  • hepatic failure

Fetal

  • growth restriction
  • fetal distress
  • stillbirth
  • placental infarction
  • premature delivery
  • oligohydramnios (reduced amniotic fluid)
29
Q

When is hCG detectable in urine/serum?

A

Urine: 14 days after fertilisation
Serum: 7 days after fertilisation

30
Q

Can tubal pregnancies always be diagnosed by USS?

A

No

31
Q

What is placenta accreta and placenta percreta?

A

Placenta accreta: fertilised ovum invades beyond the endometrium into the myometrium
Placenta percreta: fertilised ovum ivades full width of uterus

32
Q

Why is fat laid down in the first half of pregnancy?

A

Helps mother meet the demands of the fetus later on in the pregnancy when the fetus is most demanding
-progesterone also increases appetite in the first half of pregnancy and diverts glucose into fat synthesis

33
Q

Why may you get flow mumurs and upwards displacement of the apex beat during pregnancy?

A

Due to increased plasma volume

34
Q

What hormones stimulate breast growth?

A
  • oestrogen
  • progesterone
  • prolactin
35
Q

How do you manage eclampsia?

A

Deliver the baby and the placenta