Physiology in Complications of Pregnancy Flashcards

1
Q

What happens to cardiovascular system in pregnancy?

A
  • Plasma volume increases from 2600 ml to approximately 3800 ml by 32 weeks’ gestation.
  • Cardiac output rises by 40%, from about 4.5 l/min to 6 l/min, plateau by 24–30 weeks’ gestation.
  • 10% increase in heart rate (from approximately 80 beats per minute to 90 beats per minute) and a larger increase in stroke volume.
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2
Q

What happens to the Respiratory System Pregnancy?

A
  • Ventilation increases by 40% in pregnancy.
  • Due to progesterone which acts by stimulating respiratory centre and increasing its sensitivity to carbon dioxide
  • Some patients are aware of this increase in ventilation and feel breathless.
  • This increase in ventilation is achieved by increasing the tidal volume rather than the respiratory rate.
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3
Q

What leads to changes in ventilation in pregnancy?

A
  • Vital capacity does not change during pregnancy, but the tidal volume expands into the expiratory and inspiratory reserve volume.
  • Residual volume decreases by about 200ml, as does the total lung capacity (due to compression from the enlarging uterus).
  • There is no change in FEV1, or peak flow rate.
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4
Q

How does pregnancy lead to chronic hyperventilation?

A
  • Alveolar ventilation - ↑ by 70% during the second to third month of gestation.
  • Oxygen consumption and carbon dioxide production - both ↑ progressively to reach 60% above non pregnant levels at term.
  • The bicarbonate level ↓ to maintain a normal pH and there is a concomitant ↓ in sodium
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5
Q

How does the haematological system change during pregnancy?

A
  • There is an increase in red cell mass, from a non-pregnant level of 1400 ml to 1650–1800 ml.
  • Plasma volume increases proportionately more than red cell mass, resulting in a fall in the haematocrit and haemoglobin concentration such that a haemoglobin level of 10.5 g/dl may be within normal limits – physiological anaemia.
  • The haemoglobin reaches its nadir at about 32 weeks’ gestation when haemodilution is maximal.
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6
Q

What influences the rate of Gaseous exchange?

A

Rate proportional to surface area and inversely to the thickness of the villous membrane. Assisted by the double Bohr shift:

  • Uterine artery = ~ 90mmHg
  • Uterine vein = ~ 45mmHg
  • Umbilical art = ~ 20mmHg
  • Umbilical vein = ~ 30mmHg
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7
Q

What are features of the placenta?

A
  • A discoid organ 20-25 cm in diameter, 3 cm thick weighing 400-750g.
  • Internally it consists of a fetal villous tree bathed directly by maternal blood (villous haemo-chorial type) in the second and third trimesters. Able to hide it HLA to prevent rejection
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8
Q

How does the placenta manipulate the mothers biochemistry?

A
  • Human Chorionic Gonadotrophin (hCG)
  • Human Placental Lactogen (hPL)
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9
Q

What are features of the Human chorionic gonadotrophin (hCG)?

A
  • Glycoprotein with two non-covalently linked subunits
  • Alpha subunit as in FSH, LH and TSH
  • Beta subunit very similar to LH
  • Synthesised in the syncytium
  • Control unknown but synthesis of beta subunit is rate-limiting
  • Acts on LH receptors in corpus luteum and fetal testis – maintains progesterone levels
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10
Q

What are features of Human Placental Lactogen (hPL)?

A
  • 96% sequence homolgy with growth hormone but less growth promoting effects
  • Synthesised in the syncytium
  • Raises maternal FFAs
  • Antagonises peripheral effects of insulin so raises blood glucose levels
  • Induces differentiation of mammary glandular tissues
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11
Q

What are definitions of Pre-existing Hypertension, Pregnancy-Induced Hypertension and Pre-eclampsia?

A
  • Pre-existing Hypertension: BP ≥ 140/90 on 2 separate occasions before 20 weeks gestation
  • Pregnancy-Induced Hypertension: New hypertension which is BP ≥ 140/90 on 2 separate occasions. Occurs after 20 weeks’ gestation
  • Pre-eclampsia: Hypertension PLUS proteinuria (>0.3g in 24hrs or ++ on 2 samples in the absence of UTI)
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12
Q

What is the pathophysiology of Multi-system disorder, pre-eclapmsia in pregnancy?

A
  • Increased capillary permeability
  • Reduced plasma volume
  • Reduced organ perfusion
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13
Q

What are examples of Maternal Complications?

A
  • Disseminated Intravascular Coagulation
  • CVA
  • Eclamptic Fit
  • Renal Failure
  • Liver Failure
  • Heart Failure – Pulmonary Oedema
  • PE / DVT
  • HELLP (Haemolysis, elevated liver enzymes, low platelets)
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14
Q

What is HELLP syndrome?

A
  • Haemolysis, Elevated Liver Function, Low Platelets.
  • Associated with cell lysis esp. RBCs.
  • Lactate dehydrogenase gives useful measure of severity/recovery in very high 000s.
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15
Q

What are examples of Fetal Complications?

A
  • Fetal Growth Restriction
  • Placental Abruption
  • Prematurity (Preterm delivery, Iatrogenic)
  • Intrauterine Death
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16
Q

How is diagnosis of a foetus made for Pre-Eclampsia?

A

Placental Growth Factor – Pre-eclampsia

  • 287 <35 weeks, PlGF <5th centile had high sensitivity (0.96) and negative predictive value (0.98) for PE in 14 days. Specificity (0.55).
  • AUROC for low PlGF (0.87) predicting PE within 14 days was greater than all other commonly used tests.
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17
Q

How are foetal complications prevented?

A
  • Aspirin may reduce risk of pre-eclampsia
  • Calcium for women who are Calcium deplete
  • Vitamins C and E supplementation do not reduce incidence of PET
  • Tight control of blood pressure in women with pre-existing / PIH may prevent development of severe PIH or pre-eclampsia
18
Q

What is the treatment for foetal complications in pregnancy?

A
  • Ultimate treatment is delivery BUT treatment is gestation dependent & severity dependent
  • Antihypertensives
  • Seizure prophylaxis
  • Fluid Balance
  • Thromboprophylaxis
19
Q

What are the long term outcomes for foetal comlications?

A

Long term FU at GP if remains on antihypertensives

Discuss with mother

  • Regarding eclampsia
  • Recurrence risks
    • Eclampsia ~10%
    • ↑ risk of coronary heart disease
    • ↑ risk of chronic hypertension
    • PET ~10%
20
Q

What is Fetal Growth Restriction?

A
  • Fetal Growth Restriction are fetuses that are failing to grow. Affects 8% of pregnancies
  • Smaller the baby the more likely it is to have FGR.
  • 20-30% of babies <10th centile have FGR
  • 70% of babies <3rd centile have FGR
21
Q

What is Small for Gestational Age?

A

SGA fetuses that are below a specific biometric measurement (e.g. Estimated fetal weight)

  • Different thresholds <10th centile
  • < 2 standard deviations below average

Constitutionally small

Chromosomal abnormalities

Fetal growth restriction

22
Q

What are risk factors of Fetal Growth Restrictions?

A

Fetal

  • Previous FGR
  • Previous Stillbirth

Maternal

  • Age
  • BMI
  • Smoking / Alcohol / Drugs
  • Hypertension
  • Renal disease
  • Cardiac disease
  • Diabetes
  • ?Thrombophilia
  • Multiple Pregnancies
23
Q

How is Fetal Growth Restriction predicted?

A
  • PAPP-A in the lowest 5% at 10-14 weeks gestation is associated with a 50x increase in stillbirth from placental causes
  • AFP (measured in 2nd trimester) in the top 5% have a 2.8x risk of stillbirth
  • PAPP-A cleaves IGF-BP4 – key role in controlling fetal and placental growth
  • AFP made by the fetus, enters maternal circulation through dysfunctional placenta
24
Q

What are consequences of small for gestational age?

A

Immediate Increased risk

  • Stillbirth
  • Fetal hypoxia
  • Intrapartum compromise
  • Neurodevelopmental delay
  • Hypothermia

Delayed Risk

  • Type 2 diabetes
  • Hypertension
  • Cardiovascular risk
25
Q

How is monitoring of SGA/FGR conducted?

A

If SGA severe and early onset

  • Check for structural anomalies
  • Offer karyotyping

Umbilical artery Doppler is primary surveillance tool

  • Reduces perinatal morbidity and mortality and predicts poor perinatal outcomes in SGA foetuses
  • Measures placental resistance
  • SGA / FGR alters placental vascular function, placental infarction and fibrin deposition. It increases placental resistance to fetal blood flow
26
Q

What are biochemical tests of placental fucntion?

A
  • Serum/plasma more reliable than urine
  • Placental growth factor best at differentiating SGA from appropriately grown infants
27
Q

What is Preterm Labour?

A

Labour before 37 weeks gestation.

  • Significantly poorer outcome before 34 weeks gestation
  • 7-12% of all deliveries
  • 85% of neonatal morbidity / mortality
  • 20% is iatrogenic (medically caused)
28
Q

What are causes of Preterm Labour?

A
  • 30% - preterm rupture of membranes
  • 30% - infection
  • 20% - spontaneous preterm birth
29
Q

What are risk factors for Preterm Labour?

A
  • Previous preterm birth
  • Twins
  • Cervical surgery
  • Afro-Caribbean
  • Low socio-economic status
  • Uterine anomaly
30
Q

What is the pathogenesis of Preterm Labour?

A
  • Sub-clinical infection. Labour is an inflammatory process
  • Cervical weakness
31
Q

What are signs and symptoms of Preterm Labour?

A
  • Uterine contractions
  • Bleeding
  • Sensation of pelvic pressure
32
Q

What are features shown on examination of preterm labour patients?

A
  • Shows cervical dilatation

Can also be:

  • Fever
  • Abdominal tenderness
  • Contractions
33
Q

What are treatments of Preterm Labour?

A
  • Exclude reasons to stop labour
  • Bedrest
  • Tocolysis (to break labour)
  • Steroids to mature fetal lungs
  • Magnesium sulphate better neonatal outcome
34
Q

What are drugs used for Tocolysis?

A
  • Nifedipine (Calcium channel blocker)
  • Atosiban (Oxytocin antagonist)
35
Q

What is the definition of Stillbirth?

A
  • WHO definition: A fetus born without signs of life after 22 completed weeks gestation
  • UK definition: A fetus born without signs of life after 24 completed weeks gestation
36
Q

What are risk factors for Stillbirth?

A
  • Extremes of maternal age
  • Non-Caucasian ethnicity
  • Smoking
  • Drug use
  • Previous FGR, Stillbirth
  • Previous induced abortion
  • Twins
  • Maternal medical conditions: Diabetes Mellitus, Anti-cardiolipin antibodies
37
Q

What are causes of Stillbirth?

A

Depends on classification system used. Extended Wigglesworth used by CEMACH

  • Congenital 8.2%
  • Unexplained 76.2%
  • Intrapartum 6.4%
  • Infection 3.5%
  • Other specific causes 4.9%
  • Accident 0.2%
  • Unclassifiable 0.7%
38
Q

What are classification of Stillbirth using ReCoDe?

A
  • Lethal Congenital Anomaly (14.9%)
  • Infection (3.0%)
  • Abruption (6.9%)
  • Fetal Growth Restriction (43.0%)
  • Constricting loop of cord (2.9%)
  • Intrapartum (3.2%)
  • Unclassified (15.2%)
39
Q

What are investigations after Stillbirth?

A
  • Gold standard test is Post-Mortem: Reveals new information in 40% of cases but take up rates are 45%. Low take-up rate in Asian families
  • Alternatives: External examination of fetus, MRI, X-ray survey of fetal skeleton
  • Placental histology (by an experienced histopathologist) decreases unexplained SB – useful information in 30% of cases
  • Fetal karyotype (+ Parental karyotype if abnormal) – useful information in 8% of cases
    • Cord insertion
    • Fetal skin
40
Q

What are maternal blood tests on Stillbirth?

A
  • Full blood count
  • HbA1c
  • Bile acids
  • Liver function tests, Urate
  • Kleihaur
  • Infection screen – including Parvovirus B19, TORCH screen, Syphilis (if not done already)
  • Lupus anticoagulant / Anticardiolipin antibodies
  • Thrombophilia screen (better if delayed until 6 weeks)
41
Q

What is Kleihaur?

A
  • Looks at foetal blood cells in maternal circulation
  • Do it when the patient is rhesus negative to see if there is potential sensitization.
  • Estimate from the amount of foetal red cells how big the haemorrhage. Should be done at the point of birth