L39 Parturition Flashcards

1
Q

What is the function of the placenta?

A

The placenta is not important for the first trimester except for producing hormones. After which it is vital, it is responsible for:

- Hormone production 
- Preferential acquisition of nutrients and removal or toxins 
- Gas exchange 

As pregnancy progresses, the placenta senesces - dies off. There is a large reserve of function within the placenta.

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2
Q

Why is there increased foetal oxygen content?

A

Increased foetal oxygen content due to:
• Higher Hb concentrations (17g/dl v 12g/dl)
• Higher affinity for O2 (HbF v HbA)
• Further left shift due to
○ Reduced binding of 2,3-DPG due to foetal Hb gamma chains
Increased pCO2 and relative acidosis on maternal side and vice-versa on the foetal (‘double-Bohr’ effect). This pushes the mothers curve to the left and the babies to the right.

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3
Q

What is the role of foetal lung surfactant?

A

Surfactant is a mixture of phospholipids and apoproteins. It decreases the surface tension at air-liquid interface in the alveoli, enabling them to remain open at end-expiration. Synthesis of surfactant is stimulated by foetal glucocorticoids and thyroid hormones. A lack of surfactant leads to infection prematurity and neonatal respiratory distress syndrome. Surfactant is not produced consistently until 36 week gestation of various stress bring it about and so why premature babies used to die before ventilation.

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4
Q

When is foetal lung surfactant produced?

A

Week 24 - From week 24, type II pneumocytes produce surfactant. This is why the threshold for viability is at the end of the canalicular phase within bronchiole development which occurs at 22-24 weeks of gestation. Above this point, the bronchioles are functional, below this the lungs cannot support the baby.

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5
Q

How does the myometrium prepare for partuition?

A

Myometrium activity - is prepared gradually for labour as pregnancy progresses. There are mechanical stretch which causes a gradual readiness for labour, endocrine and paracrine influences. The effects of this is a:
- Rise in resting membrane potential
Increased intracellular coupling (gap junctions) in particularly connexin 43. This facilitates the transmission of calcium depolarisation through the whole of the myometrium to allow the uterus to contract in coordinate manner to drive the baby out through the birth cannel.

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6
Q

What is the diagnosis of labour?

A

Labour
Diagnosis by 3 conditions (must meet all three):
- Regular painful contractions
- Progressive effacement (shortening) and dilatation of the cervix
Descent of the presenting part

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7
Q

What cause labour at term?

A

Labour is seen with the release of proinflammatory cytokines (TNF-alpha, IL1-beta), prostaglandins and oxytocin. Labour is a inflammatory state. The collagenous bonds dissolve in the cervix allowing it to open up and contraction in the myometrium which produces the driving force to deliver the baby. At term it is an endocrine cause, the baby produces foetal adrenaline androgens (DHEAS) and CRH initiates the signal.

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8
Q

What causes preterm labour?

A

In preterm babies, there is the same common pathway of cytokines, prostaglandins, oxytocin and then labour. The trigger however is changes in the uterine capacity (developmental variant in the shape, size or multiple pregnancy), cervical weakness, placental abruption (the placenta detaches from the wall) and infection (local or systemic) that trigger the pathway.

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9
Q

What are the consequences of preterm birth?

A

Morbidity
• Lung: respiratory distress syndrome (O2 dependence)
• Brain: intraventricular haemorrhage (cerebral palsy)
• Gut: necrotising enterocolitis (malabsorption)
Eye: retinopathy (blindness)

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10
Q

What are the different stages of labour?

A

Labourhas threestages:
• The firststageis when the neck of the womb (cervix) opens to 10cm dilated.
• The secondstageis when the baby moves down through the vagina and is born.
The thirdstageis when the placenta (afterbirth) is delivered.

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11
Q

What is birth asphyxia?

A

Birth asphyxia
During labour the compression of the myometrial arteries stops flow of blood to the myometrial arteries and to the placental bed. Every time there is a contraction, the baby must take a deep breath until the contraction is over. This leads to relative foetal hypoxia. The baby can metabolise anaerobically. There therefore is a gradual build up of lactic acid- the lactic acidosis is very neurotoxic and leads to an increase in the base deficit and a reduction in pH.

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12
Q

What are the consequences of birth asphyxia?

A

Consequences:

  • lactic acidemia
  • tissue acidosis
  • hypoxic-ischemic encephalopathy
  • cerebral palsy

Foetal distress is more likely if:
- Less reserve (low birthweight)
- Long labour
Placental function impaired

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13
Q

Why does the risk of mortality increases after 40 weeks of pregnancy?

A

Pregnancy lasts for 9 months (28 days) at the median. Pregnancy can extend for longer. However the placenta is a senescent organ - it is gradually becoming less and less able to accommodate the respiratory and metabolic demand of the growing baby. The likelihood of perinatal mortality increases after you go after you go beyond 40 weeks. The risk is also great if you deliver early.

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