Uterine Motility Flashcards

1
Q

Briefly identify and describe the main layers of the uterus.

A

1) Perimetrium (serosa)
– Single thin outer layer of epithelium, not evident clinically
2) Myometrium
– Thick middle layer of smooth muscle
3) Endometrium
– Inner layer with glands, blood vessels, lymphatics and epithelial cells

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2
Q

Describe the physiological control of uterine motility.

A

1) Uterine contractions depend on gap junctions for phasic propagation of depolarisation
– Connexin 43

2) Hormonally influenced
– Menstrual cycle
– Pregnancy
– Labour

3) Minimal influence of autonomic innervation on contractions under physiological conditions.

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3
Q

Define connexin 43.

A

“Component of gap junctions, which allow for gap junction intercellular communication (GJIC) between cells.” (important for function of uterus including muscle contraction)

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4
Q

Distinguish between the junctions found in the heart, in vascular/intestinal smooth muscle, and in uterine muscle.

A

Gap junctions:

1) Cardiac muscle
– Constitutively expressed
– Arranged in intercalated discs

2) Vascular/intestinal smooth muscle
– Constitutively expressed
– Not concentrated in specialised areas (exception of myenteric interstitial cell of Cajal)

3) Uterine smooth muscle
– Inducible (especially hormonally).
– Fundal dominance during labour may arise from anatomical arrangement of expressed gap junctions.

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5
Q

Describe the expression of connexin 43 in rates during pregnancy.

A
  • Uterus of pregnant rats.
  • Immunofluorescence is absent day 4, evident day 14 and prominent day 20 (term).
  • Disappears postnatally.
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6
Q

Describe innervation of the uterus.

A

• Sympathetic, parasympathetic and sensory

• Innervation of vascular smooth muscle and
myometrium

• Sympathetic outflow effect depends on receptor type
– a-adrenoceptors - contraction
– b-adrenoceptors - relaxation

• Ratio of sympathetic receptor types influenced by hormonal status.

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7
Q

Identify the main posterior pituitary hormones. Where are they produced ? secreted ?

A

Oxytocin and ADH/vasopressin (both created in the hypothalamus and secreted from the posterior pituitary into the circulation)

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8
Q

Compare the structure of ADH, and Oxytocin.

A

ADH and oxytocin are both 9 amino acid peptides, 2 amino acids different.

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9
Q

What are the main actions of ADH and Oxytocin ?

A

Both stimulate contraction of the uterus
ADH primarily acts on kidneys
Oxytocin also acts on mammary glands

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10
Q

What is the primary factor influencing number of Oxytocin receptors ?

A

Oxytocin receptor numbers and effect on uterine contraction are influenced by sex hormone levels.

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11
Q

Describe the number of oxytocin receptors in pregnancy.

A

At the start, few oxytocin receptors. At term, much increased (need oxytocin to trigger uterine contractions)

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12
Q

Describe the nature of uterine contractions in labour.

A

Increasingly regular, co-ordinated contractions that travel from the fundus to the cervix (fundal dominance) (stimulated by oxytocin)

Uterus relaxes completely between contractions.

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13
Q

Why are uterine relaxations in between contractions important ?

A

Because otherwise fetus would not receive enough blood

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14
Q

Identify groups of drugs which may modulate physiological control of uterine motility.

A

1) Uterine stimulants (oxytocics) (stimulate uterine contractions)
2) Uterine relaxants (tocolytics)

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15
Q

Identify the main clinical uses of oxytocics.

A

– Induce abortion.
– Induce and accelerate labour.
– Contract the uterus after delivery to control postpartum
haemorrhage (PPH).

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16
Q

Identify the main clinical uses of toxolytics.

A

– (Treat menstrual cramps/dysmenorrhoea).
– Prevent or treat preterm labour.
– Facilitate obstetric manoeuvres.
– Counteract (iatrogenic) uterine hyperstimulation.

17
Q

Identify the main groups of oxytocics, and the main clinical uses of each.

A

– Oxytocin (induce or accelerate labour + after delivery to control postpartum haemorrhage)
– Ergometrine (for bleeding related to early pregnancy complications such as miscarriage (oxytocin is not effective)
– Syntometrine (combination of oxytocin and ergometrine for the third stage of labour)
– E and F series prostaglandins

18
Q

How is therapeutic Oxytocin administered ?

A

• IV infusion to induce or accelerate labour
• IV or IM injection after delivery to control postpartum
haemorrhage (PPH)

19
Q

Briefly state the mechanism of action of Ergometrine.

A

Causes sustained powerful uterine contractions.

20
Q

To what extent can Ergometrine be used for prophylaxis PPH ?

A

Largely obsolete for postpartum haemorrhage (PPH) prophylaxis owing to stability, inadvisability in the presence of hypertension (vasoconstriction), adverse effect of nausea/vomiting.

21
Q

Which parts of the uterus produce prostaglandins ?

A
  • Endometrium/deciduaand myometrium have significant prostaglandin synthesising capacity
  • Amniotic fluid also contains prostaglandins (so can break membranes to release these)
22
Q

Identify the main prostaglandins which occur naturally.

A

Prostaglandin F2a (PGF2a) generated in large amounts. Prostaglandin I2 (PGI2)/prostacyclin and prostaglandin E2 (PGE2) also occur naturally.

23
Q

State the main effects of E and F series Prostaglandins.

A

F series more vasoconstrictor, E series vasodilator, both act on cervical ripening and induce oxytocin receptors.

24
Q

Identify the main medicinal Prostaglandins, stating which naturally occurring Prostaglandin each is equivalent to.

A

• Dinoprostone
– Equivalent to prostaglandin E2 (PGE2), naturally occurring

• Carboprost
– Synthetic analogue of prostaglandin F2a (PGF2a)

• Gemeprost
– Synthetic analogue of prostaglandin E1 (PGE1)

• Misoprostol
– Synthetic analogue of prostaglandin E1 (PGE1)

25
Q

Identify the main clinical uses + administration of Misoprostol.

A

USES
– Treatment/prevention of peptic ulcers (initially).
– Medical abortion, myometrium sensitised by mifepristone (progesterone receptor antagonist) then misoprostol.
– Induction of labour.
– Control of postpartum haemorrhage (PPH) secondary to uterine atony (not as effective as IV/IM oxytocin).

ADMIN
– Oral, vaginal, sublingual or rectal routes of administration (room temperature storage)

26
Q

Identify the main groups of tocolytics.

A

1) b2-agonists
2) Calcium channel blockers and Magnesium Sulphate
3) Non-steroidal anti-inflammatory drugs (NSAIDs)
4) Oxytocin receptor antagonist
5) Nitrates

27
Q

b2-agonists

  • Examples
  • Mode of action
  • Side effects
A

• b2-agonists
– Ritodrine, terbutaline, salbutamol.
– Increase cyclic AMP levels in smooth muscle.
– Adverse effects of tachycardia, hypertension, hyperglycaemia.

28
Q

• Calcium channel blockers (and Magnesium Sulphate)

  • Examples
  • Mode of action
A

• Calcium channel blockers (and Magnesium Sulphate)
– Nifedipine (the current drug of choice for preterm labour)
– ^ Prevents intracellular calcium increase in smooth muscle

29
Q

• NSAIDs

  • Examples
  • Mode of action
A

• Non-steroidal anti-inflammatory drugs (NSAIDs)
– Indomethacin
– Inhibit prostaglandin biosynthesis

30
Q

• Oxytocin receptor antagonist

-Example

A

• Oxytocin receptor antagonist

-Example: Atosiban

31
Q

• Nitrates

  • Example
  • Mode of action
A

• Nitrates
– Nitric oxide (NO) donors
– Nitroglycerine patch

32
Q

Identify a potential cause of Dysmenorrhoea and Menorrhagia.

A

Prostaglandins may play a role

– Imbalance of prostaglandin E vs prostaglandin F in endometrium.

33
Q

Identify possible treatment options for Dysmenorrhoea and Menorrhagia.

A

• NSAIDs are effective for pain relief (unclear whether via uterine relaxation or central analgesic effect)
– Ibruprofen, naproxen, mefenamic acid

• Antifibrinolytics, i.e. tranexamic acid can help reduce blood loss by 50%