Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BGDA Lectures > Physiology of labour - at or before term > Flashcards

Physiology of labour - at or before term Flashcards

1
Q

What does expulsion of the fetus require?

A

Co-ordinated contractions of the myometrium to increase intrauterine pressure.
Cervical softening (ripening)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the myometrium consist of?

A

Bundles of non-striated muscle fibres, plus connective tissue, nerves, blood and lymph vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why does the myometrial bulk increase during pregnancy?

A

Primarily due to estrogens
Also due to:
* Muscle cell hypertrophy (from 50 to 500 um)
* Hyperplasia
* Increasing glycogen deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are the muscle cells arranged in the myometrium?

A

Circularly in the inner wall and longitudinally on the outer wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why is such a structure important?

A

Contractions from both directions will exert force circumferentially and along the axis of the uterus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do the muscle cells of the myometrium behave as a syncytium?

A

Depolarisation in one cell rapidly moves to the next cell because of special gap junctions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do contractions occur in the myometrium?

A

Spontaneous depolarizing pacemaker potentials occur. If threshold is exceeded, an action potential occurs –> rise in intracellular (Ca2+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are three ways to alter myometrial contractility?

A

1) Change the pacemaker potentials
2) Alter the threshold
3) Alter calcium release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which factors promote and demote mymometrial contraction?

A

Refer to black and white diagram in Chang’s notes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the cervix composed of?

A

High content of connective tissue (collagen fibre bundles in proteoglycan matrix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the key role of the cervix in pregnancy?

A

Resists stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does cervical softening involve?

A

1) Decrease in collagen fibres
2) Increase in glycosaminoglycans
In humans:
* Increase in keratan sulphate (doesn’t bind collagen tightly)
* Decrease in dermatan sulphate (binds collagen tightly)
* Loosening of collagen bundles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which factors cause cervical softening?

A

1) Increased metalloproteases in the cervix
2) Influx of inflammatory cells
3) Increased proinflammatory cytokines (IL2, IL8)
4) Increase in inducible nitric oxide synthase (iNOS) - (an enzyme that makes nitric oxide) –
causing an increase in NO – note that NO relaxes the myometrium. This allows the cervix to soften before contractions begin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical use of prostaglandins?

A

Often used to induce labour or for late abortion.
* PGE2 and PGF2alpha intravaginally or intracervically
* Used for induction of labour and late abortion
* Prostaglandin inhibitors arrest premature cervical ripening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the neuroendocrine reflex?

A

The actual process of labour that commences once the myometrium and cervix are ready.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the steps of the neuroendocrine reflex?

A

Sensory nerves in vagina and cervix –> somatosensory pathway in spinal cord –> brainstem, medial forebrain bundle –> supraoptic and paraventricular nuclei –> oxytocin release from posterior pituitary –> uterine contraction and cervical softening (in interaction with E, P, PGs, NO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is oxytocin synthesised as part of?

A

Preprooxyphysin in the supraoptic and paraventricular nuclei in the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does preprooxyphysin become oxytocin?

A

The leader sequence of this big molecule is removed and the remainder is transported in a secretory granule down the axons in the posterior pituitary. While being transported, the remainder is cleaved into oxytocin and neurophysin 1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does oxytocin increase uterine contractions?

A

1) Acting directly on uterine smooth muscle cells causing contraction
2) Stimulating formation of prostaglandins in the decidua. These PGs enhance the oxytocin-induced contractions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does oxytocin help with milk ejection?

A

Contracts the myoepithelial cells of the breast.

21
Q

How do levels of oxytocin change?

A

Basal maternal plasma levels increase gradually by 3-4 fold during pregnancy.
Pulses increase in frequency, duration and amplitude in late pregnancy and during labour.

22
Q

What is myometrial transformation?

A

The ‘awakening’ of the myometrium to a state of responsiveness to endogenous stimulants (oxytocin, prostaglandins) to produce labour contractions.

23
Q

What does the myometrial transformation involve?

A

Increase in the expression of a group of genes encoding ‘contraction associated proteins’ (CAP)
* Ion channels (Na+, Ca2+)
* Agonist receptors (for oxytocin, PG)
* Gap junctions

24
Q

What does a rise in the estrogen/progesterone ratio cause?

A

Increased synthesis of PGs:
* via release of phospholipase A2 from lysosomes
* estrogen labilizes lysosomes
* progesterone stabilises lysosomes

Increased number of oxytocin receptors
* estrogen increases oxytocin receptors
* progesterone decreases oxytocin receptors

Increased release of PGs
* via increased number of oxytocin receptors
* oxytocin stimulates PG release

Induction of iNOS activity –> produces nitrix oxide to soften the cervix

Facilitation of the neuroendocrine reflex underlying oxytocin synthesis and secretion

Increase in CAP genes associated with uterine transformation

25
Q

What does a mechanical pathway involve?

A

After a rise in the O/P ration, stretching of the uterus contributes to myometrial activation.

26
Q

Why is a mechanical pathway also important to transformation?

A

Endocrine changes are not sufficient

27
Q

What did the study in unilateral pregnant rats show?

A
  • No increase in CAP expression in non-preg horn
  • Mechanical stretch using a polyvinyl tube induced CAP in non-preg horn
  • Mechanical stretch not effective prior to the increased E/P ratio
28
Q

What determines the timing of parturition?

A

In many species the fetus itself determines the timing of parturition via maturational changes in the fetal hypothalamic-pituitary-adrenal axis.

29
Q

Why does ablation of the adrenal gland cause prolonged pregnancy in sheep?

A

Because ACTH (adrenocorticotrophic hormone) from the foetal pituitary stimulates production of cortisol in the adrenal gland which converts progesterone into oestrogen.

30
Q

Why is the human placenta unable to change progesterone into oestrogen?

A

It does not contain enzyme 17alpha-hydroxylase

31
Q

How could the initiating factor be CRH?

A

CRH and CRH-BP are synthesised in the placenta and secreted into both maternal and fetal circulations.
As maternal levels of CRH-BP are high, only modest increases in ACTH and cortisol result.
Maternal plasma levels of CRH increase exponentially with gestation.
During the last month of pregnancy, CRH-BP drops –> rise in free CRH.

32
Q

How does CRH affect the fetus?

A

In the fetus:
* CRH stimulates the pituitary gland (increases ACTH) and exerts a direct action on the fetal zone of the adrenal cortex –> increasing DHEAS.
* This increases placental production of estrogen –> increasing E/P ratio.

33
Q

How does CRH affect the uterus?

A
  • Stimulation of CRH receptors:
  • increased production of locally acting prostaglandins (especially PGE2 & PGF2alpha)
  • potentiates the contractile response of smooth muscle to oxytocin (via a prostaglandin dependent mechanism)
  • NOTE: the CRH receptor isoforms change towards term from those favouring relaxation to those favouring contraction.
34
Q

What are uterine contractures?

A

During the pregnancy the uterus shows recurring contractile events of low amplitude (3-10mmHg) and low frequency (0.5-3/h) with a duration of 3-15 min.

34
Q

What is the flow of cell-free fetal DNA being the trigger?

A

Term gestation –> placental maturation and senescence of palcental trophoblast cells –> increased cell-free fetal DNA in maternal plasma –> TLR9 activation –> innate immune response by the chorion, decidua, myometrium and cervix –> increased proinflammatory cytokines and chemokines –> increased uterine-activation protein expression by the chorion, decidua, myometrium and cervix –> cervical ripening, membrane rupture, phasic uterine contractions –> parturition

34
Q

What are contractions?

A

High frequency, high amplitude and short duration tightening known as contractions.

35
Q

What are the two functionally distinct segments of the uterus?

A

1) Upper uterine segment: muscular
2) Lower uterine segment: relatively thin and amuscular. Unifies with the vagina during labour to provide a relatively passive fibromuscular birth canal.

36
Q

What marks the start and end of the first stage of pregnancy?

A

The onset of regular, painful contraction associated with dilation and shortening of the cervix. Ends with full dilation of the cervix.

37
Q

What are key features of the first stage of pregnancy?

A

Subdivided into:
Latent phase (slow dilation until about 3cm)
Active phase (rapid dilation)

  • Each muscle cell becomes thicker and shorter; each contraction is followed by relaxation in which initial length is not regained
  • Fundal musculature becomes thicker and uterine volume decreases
  • The lower uterine segment does not contract - becomes continuous with the vaginal wall (effacement)
  • The retraction ring gradually moves upwards
38
Q

What starts and ends the second stage of pregnancy?

A

Begins at full dilation of the cervix and ends at complete delivery of fetus.

39
Q

What is the key feature of the second stage of pregnancy?

A

Uterine contractions (aided by abdominal wall contractions) push the fetus down and through the pelvis.

40
Q

What marks the start and end of the third stage of pregnancy?

A

Begins at the end of fetal expulsion and ends at delivery of the placenta.

41
Q

What are key features of the third stage of pregnancy?

A
  • A few min after delivery of the fetus and clamping of the cord, the placenta becomes detached from wall.
  • The placenta is completely expelled by uterine contractions often aided by the midwife or obstetrician.
  • Active management of Stage 3 involves:
  • Oxytocin or syntometrine (oxytocin + ergometrine)
  • steady traction on the umbilical cord
42
Q

How can you calculate the expected date of delivery?

A
  • Most infants deliver 280 +- 14 days after the first day of the last normal menstrual period (266 days post conception)
  • Add 7 days to the date of the LMP, count back 3 months and add 1 year
43
Q

What are the main risk factors for premature labour?

A

1) Premature rupture of the membranes
2) Previous preterm labour or low birth weight
3) Uterine and cervical abnormalities
* Short cervix
* Cervical incompetence
* Repeated 2nd trimester abortions
3) Uterine overdistension
* Multiple pregnancy
* Polyhydramnios
4) Infection - could be responsible for up to 40% of cases of preterm labour
* Bacterial vaginosis in early pregnancy carries high risk
* Urinary tract infection

44
Q

What are some other risk factors for premature labour?

A
  • Bleeding e.g placental abruption, abnormal placentation
  • In vitro fertilization (even after correction for multiple births)
  • Fetal abnormality/birth defect/intrauterine fetal death
  • Medically indicated
  • maternal complications like severe hypertension
  • endangered fetus e.g fetal growth restriction, fetal distress
45
Q

What are the smaller risk factors for premature labour?

A

Extreme stress, work/standing more than 2h a day, age < 17 or >35, short conception cycle, reduced BMI, smoking, drug abuse, low SES, male fetus

46
Q

How is pre-term labour managed?

A
  • Corticosteroids (betamethasone)
  • Antibiotics if membranes ruptured
  • Magnesium sulphate (neuroprotection <30 weeks)
  • Totolytic agents
  • calcium channel blockers (nifedipine)
  • beta-antagonists (salbutamol)
  • prostaglandin synthase inhibitors (indomethacin)
  • oxytocin antagonists (atosiban)
  • Progesterone - high risk pregnancies
  • vaginal
  • injections (17alphaOH progesterone caproate)

BGDA Lectures (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions