Maternal Physiology

Question 1

Why is the fetus not attacked by the maternal immune system? How could this negatively impact and benefit the mum?

Answer 1

Trophoblast cells + placental progesterone stimulate production of HLA (regulates the immune system) -> IL10 cytokines -> T helper cells become type-2 regulatory cells -> inhibits cytotoxic TH1 cells

Negatives: higher attack rate and severity of certain viral pathogens e.g. varicella - immunosuppressed state

Positive: may improve certain autoimmune conditions e.g. psoriasis (post-partum likely relapse)

Question 2

Explain respiratory changes that occur to a pregnant woman, how they occur and why these are necessary

Answer 2

• Tidal volume increases 30-40% (1st trimester subcostal angle changes from 68d up to 103d so chest diameter increases _>2cm)
• Expiratory reserve volume decreases 20%

Later diaphragm elevated by expanding uterus ->
- Total lung capacity decreases 5% (small change)

mum needs 20% more O2

Question 3

What is a normal pH for a pregnant lady, why?

Answer 3

About 7.4-7.47

Increased PaO2 and decreased PCO2

Partially compensated respiratory alkalosis (decreased HCO3-)

Question 4

What are the consequences of increased ventilation in pregnant women? What are some red flag symptoms that could show its more than physiological?

Answer 4

Usually around 2nd trimester 60-70% ‘dyspnea of pregnancy’ (progesterone induced hyperventilation and decreased PaCO2)

Red flags:
Acute onset, cough, pain, auscultations lungs abnormal.
Consider: cardiac problem, anaemia, DVT/ PE, asthma, pneumonia/ ARDS, pulmonary oedema
Do CXR

Question 5

What happens to increase cardiac output in pregnancy?

Answer 5

Early pregnancy: Oestrogen and progesterone act on the kidneys -> renin release (oestrogen also causes liver produce more angiotensinogen) -> renin converts angiotensinogen to angiotensin 1 -> ACE converts this to angiotensin 2 -> adrenal gland produced more aldosterone -> stimulates reabsorption of NaCl and H20 at the kidneys -> increases volume of blood by 30-50%

Late pregnancy: increased HR

(Normally angiotensin 2 also causes vasoconstriction but progesterone overpowers this)

Question 6

What happens to blood pressure during pregnancy?

Answer 6

Initially decreases ->

slight hypertension around end second trimester.
Counteracted by progesterone which relaxes smooth muscles -> decreases SVR and causes a drop in BP

Normal Bp in pregnancy <140/90

Question 7

Why does pregnancy put you in a hypercoagulable state? What are the benefits and negatives of this?

Answer 7

Increased procoagulants (fibrinogen, factor 8, vWF), decreased anticoagulants (protein S), reduced fibrinolysis

Benefits: prevents post- partrum haemorrhage

Negatives: increased risk DVT/ pulmonary embolism

Question 8

What are the problems with increased volume of blood in pregnancy?

Answer 8

Increased RAAS -> peripheral oedema (exacerbated by big uterus compressing vena cava-> venous stasis) swollen ankles/ hands -> CT syndrome

Change in plasma volume&raquo_space; change in RBCs -> dilutional anaemia (consider other causes) treat only if <100 Hb bc treatment gives higher risk of intra-uterine growth restriction and haemorrhage

Question 9

How do you normally diagnose DVT, how is it done in pregnancy?

Answer 9

Normally through D-dimmer blood test but theses are naturally high in pregnancy so instead use a Doppler ultrasound scan

Question 10

How is increased clearance of waste achieved in pregnancy?

Answer 10

Systemic vasodilation increases renal blood flow -> increases GFR by 50% -> decreased serum urea + creatine by 25% (rise in Cr shows marked reduction in kidney function)

Question 11

What are some negative consequences of the renal changes that occur as a result of pregnancy?

Answer 11

Increased blood flow gives less time for absorption in PCT -> glucosuria

Basement membrane increases in pore size -> proteinuria

Smooth muscle relaxation + obstruction -> increased size of kidneys & ureters R>L and decreases speed of urine passage -> backflow of urine up -> hydronephritis/ hydroureter (increased risk ascending UTIs)

Question 12

What are some maternal changes to the kidneys?

Answer 12

Hypothalamus decreased threshold vasopressin release

Afferent and efferent vasodilation

Increases RBF 50-85%

Pelvicalyceal dilation

Increased erythropoietin
Increased RAAS activity

Increased calcium excretion

Decreased reabsorption Uric acid

Question 13

How does progesterone cause gastrointestinal changes? What are some negative changes that may occur as a result?

Answer 13

slows transit time to increase time for absorption of nutrients, minerals and vitamins …

Decreases lower oesophageal sphincter tone (GORD, aspiration)

Decreases small bowel motility for nutrients & Decreases large bowel motility for H20
(Constipation - also retroverted uterus can compress rectum)

Decreases gallbladder contractility (gallstones)

Question 14

What would appendicitis present in a pregnant woman?

Answer 14

Due to bowel displacement will be higher - flanks or RUQ rather than RIF

Question 15

How is pregnancy kept at a euthyroid state and why is this important?

Answer 15

It’s important because the foetus is dependent on maternal thyroxine until 8-12 weeks (important for regulating metabolic/ cardiac/ lung functions, brain development, muscle control, bone maintenance)

Oestrogen stimulates thyroid- binding globulin production from liver which increases thyroxine production

hCG has a similar alpha- submit to TSH so weak stimulating effect on thyroid

Question 16

What happens to [Ca2+] in pregnancy and how?

Answer 16

Ca needed for baby bones development and later for lactation

Small drop in Ca2+ -> increased PtH -> kidneys produce hydroxylase (placenta also produces this) -> this converts inactive VD to the active form (calcitriol)

VD aids absorption of ca in small intestines

If adequate dietary intake of Ca minimal bone resorption should occur

Question 17

How is glucose metabolism regulated in pregnancy? What happens if a woman had impaired glucose metabolism pre-pregnancy?

Answer 17

Pregnancy = diabetigenix bc increased insulin resistance (due to lactogen + other placental hormones) so need the pancreas to increase insulin secretion

Oestrogen increases gluconeogenesis in liver

HPL (human placental lactogen) increases breakdown of lipids into FAs

Due to both insulin resistance and increased substrates -> increased glucose levels (+1 on urine DIP normal)

So if impaired before e.g. from obesity, polycystic ovaries then need even more insulin -> pancreas can’t keep up -> hyperglycaemia (insulin coat cross placenta but glucose can) -> foetus needs to reduce its own insulin (similar growth factors) -> >4.5kg baby macrosomic

Question 18

What is gestational diabetes? What are the consequences?

Answer 18

Onset of elevated blood sugar levels during pregnancy (includes type 1&2), 18% women globally

Screening for high risk women often done in second trimester when HPL highest by oral glucose tolerance tests

Consequences: macrosomia of babies -> increased risk of shoulder dystopia, instrumental delivery -> perineal trauma

Risk of resp problems (high glucose prevents lung maturation & surfactant development) and re-bound hyperglycaemia in babies. Risk DM type2 mothers.

Maternal and neonatal mortality

Question 19

What are some changes that occur to the MSK system and what problems can these cause for the woman?

Answer 19

Change in centre of gravity -> increased lordosis and kyphosis, forward flexion of neck, shoulders down, Stretching of abdo muscles -> impede posture, strain pararspinal muscles
❌back pain, shoulder pain, tension headaches

Increased mobility of sacroiliac joints and pubic symphysis, anterior tilt of of pelvis, widen genital hiatus, posterior vaginal wall relaxes, stance widens
❌pelvic pain

Question 20

What skin changes occur and why?

Answer 20

Increases in oestrogen -> palmar erythema and vascular spiders (large BV in skin which smaller vessels extend from)

Melanocytes stimulating hormone increases -> hyperpigmentation of face (chloasma/ melasma), nipples, umbilicus, abdo line (linea nigra)

Question 21

What are the risk factors for pre-eclampsia and how common is it?

Answer 21

Risks: 
Chronic/ gestational hypertension,
Renal disease, 
Diabetes,
Obesity, 
FH, 
First pregnancy,
Extremes age,
Multiple gestation,
IVF 

5-6% of all live births
Usually presents third trimester resolves after delivery but can occur postpartum

Question 22

It’s unclear but what is the predicted pathogenesis of pre-eclampsia?

Answer 22

Impaired invasion of trophoblast into endometrium leading to shallow invasion of spiral arteries -> hypoperfusion of utero-placental circulation and ischaemia & systemic endothelial dysfunction

Question 23

Signs and symptoms of pre-eclampsia

Answer 23

Main two for mum: hypertension + proteinuria

Mild: elevated BP, elevated proteinuria, weight gain exceeding 2LBS/ week, water retention and swelling

Severe: headaches, changes in vision, nausea/ combing, pain in abdomen and back

(+/- decreased urine output, SOB, hyperreflexia, clonus - tremor uncontrolled muscle contractions and relaxations)

Question 24

maternal Complications of pre-eclampsia

Answer 24

Maternal:
Seizure (eclampsia)

Cerebral haemorrhage - uncontrolled BP

Renal failure - vasoconstriction

Pulmonary oedema - fluid overload

DIC and thrombocytopenia

Hepatic failure or rupture

Question 25

Fetal complications of pre-eclampsia

Answer 25

Growth restriction

Oligohydramnios (lower levels amniotic fluid)

Placental infarct or abruption (detached from endometrium)

Fetal distress

Premature delivery

Stillbirth

Question 26

Treatment of pre-eclampsia

Answer 26

Stabilise Bp

Monitor blood results

Monitor baby

If no fetal distress consider delivery (induced/ caesarean)

MgSO4 for neuroprotection and seizure prevention

Fluid restrict and monitor output