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Repro > pharmacology of the uterine > Flashcards

pharmacology of the uterine Flashcards

1
Q

what are the three layers of the myometrium

A
  • An outer layer of longitudinal fibres
  • A middle layer of figure of eight shaped fibres
  • Inner circular fibres
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2
Q

how is the organisation of smooth muscle adapted in myometrium

A

on contraction of the fibres = inc in uterine pressure = forces contents towards the cervix
myometrium fibre organisation acts as a a ligature (constricts) on blood vessels to prevent blood loss during birth.

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3
Q

general properties of myometrium

A

myogenic .’. can initiation own contractions

spontaneous contractions modulated by NT and hormones (oestrogen and progesterone)

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4
Q

effect of progesterone on myometrium

A

inhibits contraction of the myometrium

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5
Q

effect of oestrogen on myometrium

A

induces contraction of the myometrium

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6
Q

how are hormone levels changed at time of birth

A

oestrogen:progesterone ratio increases (oestrogen increases)
.’, uterus more stimulated to push baby out

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7
Q

describe contractions in nonpregnant uterus

A

weak contractions early in her menstrual cycle strong contractions during menstruation as there is a fall in progesterone and increase in prostaglandins.

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8
Q

describe contractions in pregnant uterus

A

early pregnancy -
weak uncoordinated contractions of myometrium (high progesterone)
parturition - strong and coordinated contractions (high oestrogen)

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9
Q

what is partutrition

A

at birth

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10
Q

what causes contraction of myometrium

A

is myogenic
BUT also innervated by ANS (sympathetic only)
contains alpha and beta adrenoceptors

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11
Q

what is the effect of stimulation of alpha adrenoreceptors of the myometrium

A

contraction

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12
Q

what is the effect of stimulation of beta adrenoreceptors of the myometrium

A

relaxation

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13
Q

what cells allow myometrium achieve synchronous contraction?

A

has pacemaker cells called interstitial cells of Cajal (ICCs) that initiate and coordinate contractions

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14
Q

what are ICCs

A

interstitial cells of Cajal (ICCs)
pacemaker cells of the uterus
(also found in gut)

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15
Q

How does the myometrium achieve synchronous contraction?

A
  1. ICG generated electrical activity -> passed to SMC junctions via gap junctions
  2. electrical activity passed from SMC to SMC via these gap junctions
    .’. electrical activty can quickly be passed on in synchronous and coordinated fashion. .’. coordinated contraction
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16
Q

what are gap junctions between SMC of uterus made of and how is this adaptive

A

gap junctions made of specialised proteins called connexins w/ low resistance pathways
.’. electrical easily passed from SMC to SMC .’. allows coordinated contractions.

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17
Q

how may hormones affect synchronous contractions of the uterus

A

hormones affect mechanism of synchronous contraction
eg oestrogen = inc expression of gap junctions = promote contraction. (inc gap junction = inc. ease of movement of electrical activity through cells)

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18
Q

how do ICCs cause contraction

A

they generate slow wave activity
-slow wave deloparisations generate action potentials
AP spreads from ICC to SM via gap junctions
electrical activity here
SMC depolarised, vgCa2+ activated .’. Ca2+ influx .’.contraction

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19
Q

oxytocin acts at what class of receptors in myometrium

A

GPCR

Gq/11 linked

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20
Q

mechanism of oxytocin binding in myometriyum

A

GPCR -Gq/11 linked

  1. oxytocin binds. stimulation of phospholipase C
  2. .’. PIP2 -> IP3 + DAG
  3. IP3 -> LGICR on SR .’.release of Ca2+ into cytosol
  4. DAG stimulates ion channels in sarcolemma .’. more depolarisation of cell membrane .’. activation of VGCC .’. influx of Ca2+
    * so inc intracellular Ca2+*
  5. Ca2+ binds to calmodulin .’. MLCK activated
  6. MLCK phosporylates MLC .’. formation f actin=myosin cross link
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21
Q

what is meant by graded contraction

A

in SM, force of contraction is proportional to Ca2+

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22
Q

how is the rise in Ca2+ reversed (to allow for next contraction)

A

mechanisms activated to lower intracellular Ca2+

inc. calcium extrusion back into SR

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23
Q

what may increase force of contraction in myometrium

A

stimulant concentration (eg oxytocin) is increased, it means there is a greater frequency of AP on top of the slow waves (i.e. higher peak in Ca2+), this will raise both the frequency and force of SMC contraction.

24
Q

what happens at maximal concentration of stimulants (eg oxytocin) on myometrium

A

result in hypertonus where there is incomplete relaxation as extrusion process cannot keep up and the Ca2+ extrusion process is no longer effective.
can be useful to stop haemorrhage but if baby still in uterus is bad bc wll have constant contraction .’. cut off blood supply to the foetus

25
Q

what releases oxytocin

A

synthesised in hypothalamus

released from post pituitary

26
Q

what stimulates release of oxytocin

A

response to suckling and cervical dilatation

27
Q

what are synthetic versions of oxytocin

A

Syntocinon/Pitocin

28
Q

what is oxytocins actions dependent on

A

oestrogen

29
Q

why is oxytocin action dependent on oestrogen

A

bc oestrogen produced:

  • inc in oxytocin release
  • inc in oxytocin receptors
  • inc in gap junction
30
Q

effect of low conc oxytocin analogues

A

increase both the frequency and force of myometrial contraction.

31
Q

effect of high dose oxytocin analogue

A

cause hypertonus and this can cause foetal distress.

32
Q

what are some uses of oxytocin

A
  • induce labour at term (inc contraction of uterus)

- combination of oxytocin +ergot used to treat/prevent post-partum haemorrhage.

33
Q

why may oxytocin analogue be given at term

A

induce labour

inc. contraction of uterus
- oxytocin DOES NOT soften cervix. f cervix not adequately softened, is not as helpful

34
Q

why may combinatio oxytocin/ergot be given

A

treat/prevent post-partum haemorrhage.
contracts the uterus and ligature the vessels to prevent/reduce bleeding.
oxytocin =rapid action
ergot =prolonged contractile action.

35
Q

where are prostoglandins in uterus produced

A

Prostaglandins PGE2 (a vasodilator) and PGF2a (a vasoconstrictor) are synthesised in the myometrium and endometrium.

36
Q

what promotes synthesis of prostoglandins

A

Prostaglandins PGE2 (a vasodilator) and PGF2a (a vasoconstrictor) are synthesised in the myometrium and endometrium.

37
Q

why are NSAIDS used to treat menstrual pain

A

Prostaglandins thought to be involved in dysmenorrhea and menorrhagia
.’. used to treat as NSAIDS inhibit COX and stop production of prostaglandins.

38
Q

actions of prostoglandings

A

PGE2 =vasodilator, PGF2a = vasoconstrictor
act together to coordinate inc in frequency in frequency and force of uterine contraction
inc presence of gap junctions
inc sythesis of oxytocin
soften the cervix

39
Q

PG analogues used clinically include

A

Dinoprostone (PGE2)
Carboprost (PGF2a)
Mistoprotol (PGE1)

40
Q

when/why may PG analogues be used clinically

A
  • Induction of labour before term, oxytocin would be unlikely to do this as the no. of receptors would not be high enough
  • Induce an abortion
  • Postpartum bleeding
  • Softening the cervix
41
Q

side effects of PG analogues

A

can be problematic if they get into circulation

  • cause systemic vasodilatation .’. drop in BP .’. cardiovascular collapse
  • hypertonus
  • fetal distress
42
Q

how are are PG analogues administered to pregnant women

A

as a cervical gel/vaginal insert so that they only act locally.

43
Q

what is ergometrine

A

a medication used to cause contractions of the uterus
contains an array of potent agents inc:
ergometrine, ergotamine, histamine, tyramine and Ach.

44
Q

side effect of ergot

A

gangrene (due to vasoconstriction)
convulsions
abortion

45
Q

clinical use for ergot

A

produce powerful &prolonged uterine contractions.
.’. treating/preventing post-partum bleeding
NOT TO INDUCE LABOUR

46
Q

mechanism of ergot

A

thrugh stimulation of a-adrenoreceptors .’. contraction of the uterus

47
Q

when may we use myometrial relaxants

A

in premature labour

delay delivery by 48hrs

48
Q

types of myometrial relaxants

A

b2-adrenoceptor agonists
Ca2+ channel antagonists
oxytocin receptor antagonists
COX inhibitors

49
Q

why may we use b2-adrenoreceptor agonists in pregnancy

A

induce relaxation
relax uterine contractions by direct action on the myometrium and used to reduce the strength of contractions in premature labour.

50
Q

why may we use Ca2+channel antagonists in pregnancy

A

nifedipine (used in hypertension) or magnesium sulfate (a membrane stabiliser, prevents membrane depolarisation) would be useful as it is Ca2+ influx that causes contraction of the smooth muscle.

51
Q

why may we use oxytocin receptor antagonists in pregnancy

A

compete with oxytocin for their receptors and block them and this would reduce the effect of oxytocin at birth.

52
Q

why may we use COX inhibitors in pregnancy

A

reduce levels of PGs, this is why they are useful to treat dysmenorrhea and menorrhagia.

53
Q

risk of NSAID use in pregnancy

A

can get into the foetal circulation and this can cause fetal renal dysfunction.

54
Q

what would we use to induce labour at term

A

oxytocin

as high oestrogen .’. lots of oxytocin receptors and gap junctions

55
Q

what would we use to induce labour before term/termination

A

PG as no oxytocin receptors yet

56
Q

what would we used to reduce or prevent post-partum bleeding

A

PG
oxtocin/ergot
to liature the vessels

57
Q

what would we use to prevent a premature birth

A

b2-adrenoceptor agonist, Ca2+ blockers, Mg sulfate or oxytocin inhibitors!

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