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PHYSIOLOGY
OF LABOR
AND
LACTATION
Ermin Rachmawati, MD
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LABOR
Process by which the fetus is expelled
from uterus through vagina
D e f i n i t i o n
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Mechanism of LABOR
Determined by complex interaction of several
placental and fetal hormones
Dilatation of the cervix and uterine
contraction
Progressive hormonal changes and progressive
mechanical changes
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Female hormonal system
Consists of three hierarchies of hormones, as follows:
1. A hypothalamic releasing hormone, gonadotropin-releasing hormone(GnRH)
2. The anterior pituitary sex hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), both of which are secreted in response to the release of GnRHfrom the hypothalamus
3. The ovarian hormones, estrogen and progesterone, whichare secreted by the ovaries in response to the two femalesex hormones from the anterior pituitary gland
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GLANDS AND HORMONS
• Ovaries• Estrogens Promotes growth and development of female Steroid,
reproductive system, female breasts, and female secondary sexualcharacteristics
• Progesterone Stimulates secretion of “uterine milk” by the uterine
Steroid endometrial glands and promotes development of secretoryapparatus of breasts
• Placenta• Human chorionic gonadotropin (HCG) Promotes growth of corpus
luteum and secretion of Peptide
estrogens and progesterone by corpus luteum• Human somatomammotropin Probably helps promote development
of some Peptidefetal tissues as well as the mother’s breasts
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HORMONAL CHANGES
•RATIO OF ESTROGEN TO PROGESTERON INCREASE
• FETAL HORMONS
• EFFECT OF OXYTOCIN
• EFFECT OF PROSTAGLANDIN
• EFFECT OF RELAXIN
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The primary hormones produced by the placentaare human chorionic gonadotropin (hCG),corticotropin-releasing hormone (CRH),estrogens, progesterone, human placental lactogen (hPL), and proopiomelanocortin
(POMC)• Maternal conc. of hPL and CRH-controlled
estrogens rise sharply during the third trimester • Placental hormones are distributed to mother
and fetus. Because of the close connectionbetween maternal, fetal and placental hormonesynthesis, they are jointly referred to as thefetoplacental unit
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LEVEL OF ESTROGEN IN THE
MOTHER’S BLOOD RISE
SHARPLY
INCREASING SECRETION BY
THE PLACENTA OF CRH
STIMULATES THE FETAL
ANTERIOR PITUITARY TO
SECRETE ACTH
ACTH STIMULATES THE FETAL
ADRENAL GLAND TO SECRETE
CORTISOL AND DHEA
PLACENTA CONVERTS DHEA
INTO ESTROGEN
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Toward the end of pregnancy, the daily production of placental estrogens increases to about 30 times themother’s normal level of production. However, thesecretion of estrogens by the placenta is quite differentfrom secretion by the ovaries. Most important, the
estrogens secreted by the placenta are not synthesizedde novo from basic substrates in the placenta. Instead,they are formed almost entirely from androgenic steroidcompounds, dehydroepiandroster one and 16-hydroxydehydroepiandrosterone, which are formed both
in the mother’s adrenal glands and in the adrenal glandsof the fetus. These weak androgens are transported bythe blood to the placenta and converted by the trophoblastcells into estradiol, estrone, and estriol
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Placental CRH stimulates the release of
ACTH by the fetal pituitary, resulting in
increased
cortisol production in the adult zone
of FAC; this again stimulates the release of CRH
(positive feedback). CRH also stimulates
lung
development and the production of DHEA
and
DHEA-S in the fetal zone of FAC
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HIGH LEVEL OF ESTROGEN
cause uterine muscle fiber to display receptor
for oxytocin
Increase the number of gap junction between the
adjacent cells of smooth muscle
stimulate the placenta to release prostaglandin
HIGH LEVEL OF ESTROGEN
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O X Y T O C I N and P G
• Release by posterior pituitary stimulates
uterine contraction
• Prostaglandin induce production of
enzymes that digest collagen fibers in the
cervix causing it soften
Function IN labor
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Mechanical
• Stretch of uterine
muscle
• Irritation of the cervix
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Cervical changes
During most of the pregnancy, The cervix
must remain unyielding and reasonably rigid.
With initiation of parturition, the cervix mustsoften, yield and more readily dilatable.
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• The process by which the cervix becomessoft, compliant and partially dilated istermed ‘cervical ripening’ .
• Cervical ripening is due to a combinationof biochemical, endocrine, mechanical and
possibly inflammatory events. It is believedthat the increasing myometrial contractility,in the form of Braxton Hicks contractions,seen with advancing gestation plays a vital
role in the effacement of the cervix, prior to the actual commencement of labour.
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• Structurally, the cervix is mainly composed of collagen, predominantly type I and III.
• In the cervix, the main glycosaminoglycans aredermatan sulphate and chondroitin sulphate whichare hydrophobic and are responsible for thefirmness of the cervix. Towards term, the
glycosaminoglycan concentration of the cervixalters and the dermatan and chondroitin sulphatesare replaced by hyaluronic acid, which ishydrophilic and imbibes water, destablishing thecollagen fibrils contributing to cervical ripening.Collagenase produced by fibroblasts andleucocytes is an enzyme which breaks downcollagen types I, II, III.
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• Leukocyte elastase produced by macrophages, neutrophils
and eosinophils is an enzyme that breaks down elastin,collagen and proteoglycans. The level of both these enzymes
are found to increase with advancing gestation and are
associated with progressive decline in concentration of
cervical collagen.
• Prostaglandins has a direct effect on the production of
procollagenase, which is a precursor of collagenase. This
explains why the administration of intracervical
prostaglandins both PGE2 and PGF2a produces cervical
changes in women without inducing uterine contractions.
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• Process of cervical remodeling takes place with
advancing gestation. The mature collagen is replaced
by immature collagen with few cross links which isweaker and is easily broken down during labour. Sex
steroids, estrogen and progesterone play opposing
roles with regard to cervix during labour.
Progesterone prevents cervical ripening during
pregnancy . Progesterone antagonist, mifepristone
has been found to cause cervical ripening in women
undergoing termination of pregnancy. Estrogen promotes cervical ripening . Concentration of relaxin
increases towards late pregnancy and induces
cervical ripening. It increases production and
secretion of collagenases from the aminon.
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Myometrial changes.
• The myometrium undergoes a series of changes phase I toprepare it for labour. There is transition from a contractile statecharacterized predominantly by occasional painless contractionsto one in which more frequent contractions develop. This is dueto alteration in the expression of contraction associated proteins
(CAPs). There is increase in myometrial oxytocin receptors.There are increased numbers and surface areas of myometrialcell gap junction proteins such as connexin-43. these changesresult in increased uterine irritability and responsiveness touterotonins.
• Another change that occurs in phase I is formation of lower uterine segment with the development of well formed lower segment, the fetal head descends to or even through the pelvicinlet- an event referred to as lightening.
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POSITIVE FEED BACK
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Estrogen
Mendorong janin
menekan serviks
Ketanggapan uterus thdp
oksitosin dlm darah
Kontraksi uterus
Reseptor oksitosin di miometrium
Melalui refleks neuroendokrin
Sekresi oksitosin
Berperan dlm
kemajuan
persalinan
Memicu awitan
atau persalinan
(teori utama)
Pembentukanprostaglandin
++
++
UMPAN BALIK HORMONAL POSITIF SELAMA PERSALINAN
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1. STAGE OF DILATATION
2. STAGE OF EXPULSION
3. PLACENTAL STAGE
a period of progressive cervical dilatio
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CRITICAL FACTORS IN LABOR
Primary forces of labor – The frequency, duration, and intensity of uterine contractions as
the fetus moves through the firth passage – The effectiveness of maternal pushing effort – The duration of labor
The birth passage – size of pelvis – type of pelvis – Ability of cervix to dilate and efface and vaginal canal to distend
The fetus – Fetal head, Fetal attitude, Fetal lie, Fetal presentation, Fetal
position, Size of fetus, Placenta implantation site
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LACTATION
Breast feeding
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D e f I n I t I o n
The secretion and ejection of milk from themammary gland
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During pregnancy
• high estrogen level causes the extensivedevelopment of ductus
• high progesteron level stimulate formation of alveoli lobule
• Prolactin, secreted from pituitary anterior stimulated by the increase level of estrogen,have an important role in the development of mammary glands by secretion of enzymes thatis already needed to milk formation
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P R O L AC T I N
• This hormone is secreted by the mother’s
anterior pituitary gland, and itsconcentration in her blood rises steadily
from the fifth week of pregnancy until birth
of the baby, at which time it has risen to10 to 20 times the normal nonpregnant
level
P R O L AC T I N
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Immediately after the baby is born,
the sudden loss of both estrogenand progesterone secretion fromthe placenta allows the lactogeniceffect of prolactin from the mother’spituitary gland to assume its naturalmilkpromoting role, and over thenext 1 to 7 days, the breasts begin
to secrete copious quantities of milk instead of colostrum.
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• This secretion of milk requires adequatebackground secretion of most of themother’s other hormones as well, but most
important are growth hormone, cortisol , parathyroid hormone, and insulin.
• These hormones are necessary to providethe amino acids, fatty acids, glucose, andcalcium required for milk formation.
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• After birth of the baby, the basal level of prolactin secretion returns to the nonpregnantlevel over the next few weeks
• each time the mother nurses her baby,nervous signals from the nipples to thehypothalamus cause a 10- to 20-fold surge inprolactin secretion that lasts for about 1 hour This prolactin acts on the mother’s breasts to
keep the mammary glands secreting milk intothe alveoli for the subsequent nursingperiods.
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• The hypothalamus mainly stimulates production of all the other hormones, but it mainly inhibits prolactin production.
• anterior pituitary secretion• of prolactin is controlled either entirely or almost• entirely by an inhibitory factor formed in the hypothalamus
• and transported through the hypothalamichypophysial• portal system to the anterior pituitary• gland. This factor is called prolactin inhibitory • hormone. It is almost certainly the same as the catecholamine• dopamine, which is known to be secreted
• by the arcuate nuclei of the hypothalamus and can• decrease prolactin secretion as much as 10-fold.
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• Milk is secreted continuously into thealveoli of the breasts, but milk does not
flow easily from the alveoli into the ductal
system and, therefore, does notcontinually leak from the breast nipples.
Instead, the milk must be ejected from the
alveoli into the ducts before the baby can
obtain it.
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Suckling on one breast causes milk flow not only inthat breast but also in the opposite breast. It is especially
interesting that fondling of the baby by the
mother or hearing the baby crying often gives enough
of an emotional signal to the hypothalamus to cause
milk ejection.
When the baby suckles, it receives virtually no milkfor the first half minute or so. Sensory impulses must
first be transmitted through somatic nerves from the
nipples to the mother’s spinal cord and then to her
hypothalamus, where they cause nerve signals that
promote oxytocin secretion at the same time that they
cause prolactin secretion.The oxytocin is carried in theblood to the breasts, where it causes myoepithelial cells
(which surround the outer walls of the alveoli) to contract,
thereby expressing the milk from the alveoli into
the ducts at a pressure of +10 to 20 mm Hg
THE MILK EJECTION REFLEX, A
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Suckling of baby on nipple causes
Effectors
Contraction of myoepithelial cells in mammary glands
Receptors
Touch sensitive sensory neurons in nipple
Control centresHypothalamus and posterior pituitary
Touch sensation
Milk injection
Interruption of cycleBaby ceases to suckle, thus breaking the positive feedback cycle
Positive feedback : milk availability
encourages continued suckling,
so touch sensaitions on nippleand oxytosin release continue
Increasing
Nerve pulseOutput
Increase oxytocin in bloodinput
,
POSITIVE FEEDBACK CYCLE
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• Grabowski., Tortora. (2003). “Principles of Anatomy and
Physiology”.10th edition.USA. John Wiley&Sons, Inc. ISBN 0-471-
22934-2.
• Hall, Guyton.(1997). “Buku Ajar Fisiologi Kedokteran”.Edisi :9.
Jakarta. EGC. ISBN 979-448-357-5
• Sherwood. (2005). “Physiology from Cellular to Cell”.10th
edition.USA. John Wiley&Sons,Inc. ISBN 0-471-29301-2
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