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CAUSES AND ONSET OF LABOUR

PRESENTED BY : DR PAWAN JHALTA MODERATOR : DR GEETIKA

LABOUR
Labour is a physiologic process during which the products of conception (i.e., the fetus, membranes, umbilical cord and placenta) are expelled outside the uterus. Labour is achieved with changes in the biochemical connective tissue and with gradual effacement and dilatation of the uterine cervix as a result of rhythmic uterine contractions of sufficient frequency, intensity, and duration.

The following criteria should be present to call it normal labour:


Spontaneous expulsion, of a single, mature foetus, presented by vertex, through the birth canal, within a reasonable time (not less than 3 hours or more than 18 hours), without complications to the mother, or the foetus.

Onset of labour
Show (bloody show) - sign of the impending onset of active labor - extrusion of mucus plug of the cervical canal discharge of small amount of bloodtinged mucus from vagina
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Uterine contractions
Uterine Contractions Characteristic of Labor ; muscular contractions, those of uterine smooth muscle of labor are painful cause of pain (not known definitely) hypoxia of contracted myometrium compression of nerve ganglia in cervix & lower uterus by the tightly interlocking muscle bundles stretching of cervix during dilatation stretching of peritoneum overlying the fundus

Ferguson reflex : mechanical stretching of cervix enhances uterine activity : manipulation of the cervix and stripping the fetal membranes is associated with an increase in PGF2 metabolite in blood : exact mechanism : not clear Interval between contractions : 10 minutes at the onset of the first stage diminishes gradually 1 minute or less in the second stage

Periods of relaxation between contractions - essential to welfare of the fetus - unremitting contraction of uterus compromises uteroplacental blood flow, cause fetal hypoxia Duration of contraction : in active phase Duration 30-90 seconds (average 60 sec) Pressure 20-60 mmHg (average 40 mmHg)

Differentiation of Uterine Activity


: During active labor, uterus is transformed into 2 distinct parts (1) Upper segment actively contracting becomes thicker as labor advances quite firm or hard (2) Lower segment relatively passive develops into a much thinly walled passage for the fetus much less firm

Change in Uterine Shape


: each contraction produces elongation of uterus with decrease in horizontal diameter important effect on labor process decrease in horizontal diameter straightening of fetal vertebral column lengthening of uterus longitudinal fibers are drawn taut pulled upward the lower segment & cervix important factor in cervical dilatation

Ancillary Forces in Labor


: After the cervix is dilated fully, the most important force in the expulsion of the fetus is that produced by increased maternal intrabdominal pressure Pushing - increased intrabdominal pressure by contraction of abdominal muscles, simultaneously with forced respiratory efforts with glottis closed - important force in the expulsion of fetus - similar to that involved in defecation

Changes Induced in the Cervix with Labor


Effective force of the 1st stage of labor is uterine contraction As the result of the action of these forces, two fundamental changes take place in the already ripened cervix effacement & dilatation The cervix is said to be completely (fully) dilated : 10 cm

Cervical Effacement

obliteration or taking up of the cervix shortening of the cervical canal (2cm mere circular orifice with almost paper thin edge) muscular fibers at about the level of the internal os are pulled upward or taken up into the lower uterine segment external os remains temporarily unchanged

Cause of Onset of Labour


Mechanical factors Uterine distension theory:
Like any hollow organ in the body, when the uterus in distended to a certain limit, it starts to contract to evacuate its contents. This explains the preterm labour in case of multiple pregnancy and polyhydramnios.

Stretch of the lower uterine segment:


by the presenting part near term.

Biochemical and physiolgical processes


Current data favour uterotonins theory of labour initiation Increased number of uterotonin production would follow once phase 1 is suspended and uterine phase 2 processes are implemented

The phases of parturition

ANATOMICAL AND PHYSIOLOGICAL CONSIDERATIONS OF MYOMETRIUM

Smooth muscle cell shortening with contraction>striated muscle Forces can be exerted in multiple directions Plexiform arrangement aids greater shortening and force generating capacity Greater multidirectional force generation in fundus permits versatality in expulsive forces

Regulation of myometrial contraction and relaxation


Actin and myosin interaction Intracellular calcium :agents that increase intracellular calcium conc. Promote contraction e.g. oxytocin and PGF2 during labour and agents that decrease calcium conc. Promote uterine relaxation e.g.CRH,PGE2, 2 sympathomimetics Myometrial gap junnctions :increases in size and abundance during onset of labour Cell surface receptors

Uterine quiscence and cervical competence


Progesterone and oestrogen: administration of progesterone receptor antagonist will promote some or all key features of onset of labour like cervical ripening ,increased cervical distensibility and increased uterine sensitivity to uterotonins Steroid hormone regulation of myometrial cell to cell communication ; progeterone causes decreased expression of contraction associated proteins and is also known to inhibit expression ofgap junctional proteins

G-protein coupled receptors that promote myometrial relaxation


Beta Adrenreceptors:increases cAMP LH and hCG receptors :these receptors during pregnancy are greater before than during labour and activates sdenylyl cyclase by way of plasma membrane receptor Gs-linked system Relaxin ;relaxin family peptide receptor-1mediates activation of adenylyl cyclase and thus may promote uterine relaxation

CRH ;synthesized in placenta and hypothalamus ,found to have dual role during pregnancy and labour, During pregnancy it binds the receptor CRHR1 production of cAMP and subseqent inhibition of myometrial activity At term CRH can activate the Gq prtein pathway which favours myometrial contraction

Prostaglandins ;most commonly considered as uterotonins however they have diverse effects and some acts as smooth muscle relaxants Both PGE2 and PGI2 could potentially act to maintain uterine quiscence by increasing cAMP signaling yet PGE2 can promote uterine contractility through binding to EP1 and EP2 receptors Thus either the generation of specific prostaglandins or relative expression of the various prostaglandins receptors may determine myometrial response to prostaglandins

Atrial and brain natriuretic peptide and cGMP Accelarated uterotonin degradation e.g.by oxyticinase and PGDH

Uterine activation and cervical ripening


Progesterone functional withdrawl:this can be mediated through several mechanisms Changes in the relative expression of of nuclear progesterone receptor isoforms,PRA,PR-B and PR-c Changes in relative expression of membrane bound progesterone receptors

Posttranslational modifications of progesterone receptor Alterations in progesterone receptor activity through changes in in the expression of coactivators or co-repressors that directly influence receptor function Local inactivation of progesterone by steroidmetabolizing enzymes or synthesis of a natural antagonist.

Oxytocin receptors
There is an increase in myometrial oxytocin receptors and there activation results in increased phospholipase C activity and subsequent increase in cytosolic calcium and uterine contractility

Relaxin
Causes remodeling of extracellular matrix of uterus,cervix,vagina, breast and pubic symphysis as well as promoting cell proliferation and inhibiting apoptosis.

Fetal contribution to initiation of labour


Uterine stretch and parturition is required for induction of contraction associated proteins. Stretch increases expression of gap junction protein-connexin 43,as well as oxytocin receptors.

Fetal endocrine cascade


At term the fetal adrenal glands weigh same as those in the adults and similar in size The daily production of steroid by adrenal glands near term is 100 to 200mg/day higher than 30 to 40mg/dayseen in adult glandsat rest Fetal cortisol levels increase during the last weeks of gestation during the same period levels of DHEA-S also increases significantly leading to increase in maternal oestrogens particularly estriol.

Placental CRH production


A CRH hormone identical to maternal and fetal hypothalamic CRH is synthesized by placenta in relatively large amounts. One important difference is that,unlike hypothalamic CRH which is under glucocorticoid negative feedback , cortisol has been shown to stimulate placental CRH production.

This ability makes it possible to create a feed forward endocrine cascade that does not end untill separation of fetus from placenta at delivery. Resulting high levels of CRH may modulate myometrial cotractility via interaction with the CRH receptor isoform CRH-R1d this isoform is known to enhance myometrial contractile response

It has also been proposed that cortisol affects the myometrium indirectly by stimulating the fetal membranes to increase PG synthesis Finally CRH has been shown to stimulate fetal adrenal C19- steroid synthesis thereby increasing substrate for placental aromatization and increased levels of oestrogen

Fetal lung surfactant


Pulmonary surfactant and its components such as PAF when secreted into amniotic fluid have been reported to stimulate PG synthesis anduterine contractility

Onset of labour
Uterotonins that are candidates for labour induction include,oxytocin,PGs,serotonin;histamine,PAF,ang iotensin II and many others All have been shown to stimulate smooth muscle contraction through G-protein coupling

Oxytocin
It was first uterotonin to be implicated in parturition initiation following observations provide support for this theory The number of oxytocin receptors strikingly increases in myometrial and decidual tissues near end of gestation Oxytocin acts on decidual tissue to promote prostaglandin release Oxytocin is synthesized directly in decidual and extraembryonic fetal tissues and in the placenta.

Prostaglandins
Evidence supportive of trhis theory includes; Levels of prostaglandins or their metabolites in amniotic fluid ,maternal plasma and maternal urine are increased during labour Treatment of pregnant women with PGs by any of several routes of administration,causes abortion or labour at all stages of gestation. Administration of PGHS type 2 inhibitors to pregnant women will delay spontaneous onset of labour and sometimes arrest preterm labour.

Platelet activating factor


The PAF receptor is a member of the Gprotein- coupled receptor family of transmembrane receptors. Its stimulation by PAF increases myometrial cell calcium levels and promotes uterine contractions. Levels of PAF in amnionic fluid are increased during labor PAF treatment of myometrial tissue promotes contraction.

Endothelin-1
The endothelins are a family of 21-amino acid peptides that powerfully induce myometrial contraction. It is produced in myometrium and its potential contribution to phase 3 of parturition is not defined.

Angiotensin-II
There are two G-protein-linked angioteneism II receptors in the uterus - AT1 and AT2. In non pregnant women the AT2 receptors is predominant, but the AT1 receptor is preferentially expressed in pregnant. Angiotenism II is binding to the plasmmembrane receptor evokes contraction.

Crticotropin-Releasing Hormone(CRH)
Late in pregnancy phase 2 or 3 of parturition modification in the CRH receptor favours a switch cAMP formation to increased myometrial cell calcium levels via protein kinase C activation. Oxytocin acts attentuate CRH-stimulated accumulation of cAMP myometrial tissue and CRH augments the contraction-inducing potency of a given dose of oxytocin n human myometrial strips. Finally CRH acts to increase myometrial contractile force in response to PGF2.