Lecture 4 - Parturition Flashcards

1
Q

What does the placenta do and how does it form?

A
haemochorial placentation
effective from end of first trimester
senesces as pregnancy progresses
large reserve
-responsible for - hormone production, preferential acquisition nutrients and removal of toxins
-gas exchange (CO2, O2)
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2
Q

placenta function

A

consists of a few layer of cells
large surface area
-folding villi

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3
Q

Explain the saturation of fetal and maternal haemoglobin at different partial pressures

A

At lower partial pressures below 80% - foetal haemoglobin has a greater affinity for oxygen
under optimal conditions - maternal and fetal haemaglobin has the same o2 saturations.

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4
Q

Increased foetal oxygen content is due to

A
higher Hb concentrations
higher affinity for O2
further left shift 
- reduced binding of DPG to fetal hb
- Increased pCO2 and relative acidosis on maternal side (right shift)
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5
Q

Role of surfactant in the fetal lung

A

from 24 weeks of pregnancy - produced by type 2 pneumocytes
produced surfactant
mixture of phospholipids (PC and PG) and apoproteins (SP-A,B,C,D)
decreases surface tension at air-liquid interface in the alveoli - remain open during expiration

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6
Q

What stimulates release of fetal surfactant

A

stimulated by fetal glucocorticoids and thyroid hormones

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7
Q

Lack of surfactant

A

leads to neonatal respiratory distress

replace in neonatal period - curosurf

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8
Q

Myometrial activity

A

rise in membrane potential
increased intercellular coupling
mechanical/endocrine/paracrine influences

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9
Q

Diagnosis of labour

A

regular painful contractions
progressive effacement and dilation of uterus
descent and presenting of the part

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10
Q

Endocrine effects

A

production of cytokines, prostaglandins, oxytocin facilitate labour
progesterone, estrogen,
increased DHEAS, CRH, progesterone and estrogens

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11
Q

causes for preterm labour

A
uterine capacity
placental abruption
cervical weakness
infection - local/systemic
triggers release of cytokines
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12
Q

Birth asphyxia (oxygen compromised)

A
compression of myometrial arteries
cessation of flow to placenta
lack of gas exchange
relative fetal hypoxia
anaerobic metabolism -lactic acidosis
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13
Q

Consequences of birth asphyxia

A
lactic acidaemia
tissue acidosis
hypoxic - ischemic encephalopathy
cerebral palsy
fetal distress more likely 
- low birth weight
long labout
impaired placental function
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14
Q

Management of birth asphyxia

A

fetal heart rate monitoring
measurement of fetal scalp pH
monitor ST segment changes
expedite delivery by cesarean section or forceps
prognosis good if cord arterial pH > 7 and base excess better than - 12 mmol/l

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