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Yr 2 - Reproductive System > Parturition > Flashcards

Parturition Flashcards

1
Q

What is haemochorial placentation?

A

Maternal blood comes in direct contact with the fetal chorion,

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2
Q

What is the placenta responsible for?

A
  • hormone production
  • preferential acquisition - nutrients and removal of toxins
  • gas exchange (CO2, O2)
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3
Q

What does the placenta consist of?

A

A few layers of cells that separate maternal from fetal blood

Large surface are created by folding villi

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4
Q

Describe the foetal Oxygen-Hemoglobin Dissociation Curve

A

Shifted to the lift

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5
Q

How does this foetal Oxygen-Hemoglobin Dissociation Curve affect placental O2 exchange?

A

Increased foetal O2 content due to:

  • Higher Hb conc
  • Higher affinity for O2
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6
Q

What is a further left shift of the foetal Oxygen-Hemoglobin Dissociation Curve caused by?

A
  1. Reduced binding of 2,3-DPG to fetal Hb gamma chains

2. Increased pCO2 and relative acidosis on maternal side and vice-versa on the fetal (‘double-Bohr’ effect)

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7
Q

Describe HbF

A

2x alpha and 2x gamma chains

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8
Q

Why is there reduced binding of 2,3-DPG to fetal Hb gamma chains?

A

2,3 DPG binds preferentially to beta chains in HbA shifting curve to right

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9
Q

When does surfactant begin to be produced? What is it produced by?

A

From 24 weeks of pregnancy

Produced by type II pneumocytes

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10
Q

When can lungs begin to start supporting ventilation?

A

From beginning of production of surfactant

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11
Q

What is surfactant made of?

A

Mixture of phospholipids (PC and PG) and apoproteins (SP-A, B, C, D)

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12
Q

What is purpose of surfactant?

A

Decreases surface tension at air-liquid interface in the alveoli, enabling them to remain open at end-expiration

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13
Q

What is foetal lung surfactant triggered by?

A

Synthesis stimulated by foetal glucocorticoids and thyroid hormones (less so)

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14
Q

What can a lack of surfactant be caused by?

A

Prematurity, infection

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15
Q

What can a lack of surfactant cause?

A

Neonatal respiratory distress

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16
Q

What therapies are available for treating lack of foetal surfactant?

A

Promote production antenatally (maternal glucocorticoid administration)
- Given if believed baby will be delivered early

Replace in neonatal period (artificial surfactant: Curosurf)

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17
Q

What are the 3 layers of the uterus?

A
  1. Endometrium
  2. Myometrium
  3. Perimetrium
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18
Q

What is the perimetrium?

A

Outer layer

An outer tunica serosa, the perimetrium, a thick tunica muscularis

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19
Q

What is the myometrium?

A

Middle layer

20
Q

What is the endometrium?

A

Inner layer where implantation takes place

21
Q

What is the main function of the myometrium?

A

Induce uterine contractions

22
Q

How are contractions enabled in the myometrium?

A

Through generation of electrical potential (any cell can act as a pacemaker, generating an action potential)

23
Q

How is an action potential generated in myometrium?

A

Depolarisation mediated by calcium ions

  • intercellular (gap junctions)
  • intracellular (Ca channels and intracellular stores)
24
Q

How are electrical potentials propagated in the myometrium?

A
  • Rapid action potential wave (global)
  • Slower intercellular calcium wave (local)

Enabling coordinate and sustained contractions

25
Q

How does myometrial activity change as pregnancy progresses?

A

Rise in resting membrane potential

Increased intercellular coupling (gap junctions)

26
Q

How is labour diagnosed?

A
  1. Regular painful contractions

AND

  1. Progressive effacement and dilatation of the cervix

AND

  1. Descent of the presenting part
27
Q

Define parturition

A

Childbirth

28
Q

What is typically released during labour?

A
  • Oxytocin
  • Prostaglandins
  • Cytokines
29
Q

Where is oxytocin secreted from?

A

Posterior lobe of pituitary gland

30
Q

What is the function of oxytocin during labour?

A

Oxytocin stimulates the uterine muscles to contract and also increases production of prostaglandins, which increase the contractions further

31
Q

How do cytokines play a role in labour?

A

Pro inflammatory cytokines (TNF-a, IL-1b) set the cascade off (stimulate local production of prostaglandins and collagenases)

32
Q

What are the key inflammatory cytokines to look out for during labour?

A

TNF-a, IL-1b

33
Q

How do collagenases play role during labour?

A

Collagenous bonds in cervix dissolve, allowing it to open up

34
Q

What is linked to preterm labour?

A
  • Uterine capacity (e.g. twins are 50% likely to be delivered preterm)
  • Cervical weakness
  • Placental abruption
  • Infeciton
35
Q

What is placental abruption?

A

When placenta comes away from wall of womb

Presence of thrombin and antithrombin in uterine cavity is a potent inflammatory mediator and will trigger labour

36
Q

What is perinatal asphyxia?

A

Medical condition resulting from deprivation of oxygen to a newborn infant that lasts long enough during the birth process to cause physical harm, usually to the brain.

37
Q

What is birth asphyxia?

A

During labour contractions, compression of myometrial arteries causes cessation of flow to placental bed

This leads to lack of gas exchange and relative foetal hypoxia

Baby begins anaerobic metabolism and there is gradual lactic acidosis

38
Q

What is dangers of lactic acidosis?

A

Neurotoxic –> reduced pH and increase in base deficit

39
Q

When is foetal distress more likely?

A
  • Less reserve (low birthweight)
  • Long labour
  • Placental function impaired
40
Q

Describe the first stage of labour

A
  1. Contractions of uterine muscles force baby toward cervix

2. Cervical opening thins and widens as contractions of lengthwise uterine muscles pull it open

41
Q

Describe the second stage of labour

A
  1. Uterine contractions are aided by mother’s involuntary pushes with abdominal muscles
  2. Head moves through dilated cervix and birth canal
  3. Shoulders and rest of body move through cervix and birth canal
42
Q

Describe third stage of labour

A

Placental separates from uterine wall and is delivered through the vagina

43
Q

What are the consequences of preterm birth?

A
  • lung: respiratory distress syndrome (O2 dependence)
  • brain: intraventricular haemorrhage (cerebral palsy)
  • gut: necrotising enterocolitis (malabsorption)
  • eye: retinopathy (blindness)
44
Q

How can the risks during preterm birth be reduced?

A

Using corticosteroids, ventilation, artificial surfactant

45
Q

What are the potential consequences of birth asphyxia?

A
  • lactic acidemia
  • tissue acidosis
  • hypoxic-ischemic encephalopathy
  • cerebral palsy
46
Q

How can birth asphyxia be managed?

A
  • fetal heart rate monitoring
  • measurement of fetal scalp pH
  • monitor ST segment changes in fECG
  • expedite delivery by cesarean section (first stage) or forceps (second stage)

prognosis good if cord arterial pH >7.00 and BE better than -12 mmol/l

Yr 2 - Reproductive System (30 decks)

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