PHYSIOLOGY OF LABOR AND LACTATION

Ermin Rachmawati, MD

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LABOR Definition

Process by which the fetus is expelled from uterus through vagina

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Mechanism of LABOR
Progressive hormonal changes and progressive mechanical changes Determined by complex interaction of several placental and fetal hormones Dilatation of the cervix and uterine contraction
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Female hormonal system

Consists of three hierarchies of hormones, as follows: 1. A hypothalamic releasing hormone, gonadotropinreleasing 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 GnRH from the hypothalamus 3. The ovarian hormones, estrogen and progesterone, which are secreted by the ovaries in response to the two female sex 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 sexual characteristics Progesterone Stimulates secretion of uterine milk by the uterine Steroid endometrial glands and promotes development of secretory apparatus 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 mothers 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 placenta are 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 connection between maternal, fetal and placental hormone synthesis, they are jointly referred to as the fetoplacental unit
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STIMULATES THE FETAL ANTERIOR PITUITARY TO SECRETE ACTH

ACTH STIMULATES THE FETAL ADRENAL GLAND TO SECRETE CORTISOL AND DHEA

PLACENTA CONVERTS DHEA INTO ESTROGEN

INCREASING SECRETION BY THE PLACENTA OF CRH

LEVEL OF ESTROGEN IN THE MOTHERS BLOOD RISE SHARPLY

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Toward the end of pregnancy, the daily production of placental estrogens increases to about 30 times the mothers normal level of production. However, the secretion of estrogens by the placenta is quite different from secretion by the ovaries. Most important, the estrogens secreted by the placenta are not synthesized de novo from basic substrates in the placenta. Instead, they are formed almost entirely from androgenic steroid compounds, dehydroepiandrosterone and 16hydroxydehydroepiandrosterone, which are formed both in the mothers adrenal glands and in the adrenal glands of the fetus. These weak androgens are transported by the blood to the placenta and converted by the trophoblast cells 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 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

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O X Y T O C I N and P G
Function IN labor Release by posterior pituitary stimulates uterine contraction Prostaglandin induce production of enzymes that digest collagen fibers in the cervix causing it soften

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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 must soften, yield and more readily dilatable.

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 The process by which the cervix becomes soft, compliant and partially dilated is termed cervical ripening. Cervical ripening is due to a combination of biochemical, endocrine, mechanical and possibly inflammatory events. It is believed that 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 are dermatan sulphate and chondroitin sulphate which are hydrophobic and are responsible for the firmness of the cervix. Towards term, the glycosaminoglycan concentration of the cervix alters and the dermatan and chondroitin sulphates are replaced by hyaluronic acid, which is hydrophilic and imbibes water, destablishing the collagen fibrils contributing to cervical ripening. Collagenase produced by fibroblasts and leucocytes is an enzyme which breaks down collagen 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 is weaker 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 Ermin's doc/block life cycle/2010 18 secretion of collagenases from the aminon.

Myometrial changes.
The myometrium undergoes a series of changes phase I to prepare it for labour. There is transition from a contractile state characterized predominantly by occasional painless contractions to one in which more frequent contractions develop. This is due to alteration in the expression of contraction associated proteins (CAPs). There is increase in myometrial oxytocin receptors. There are increased numbers and surface areas of myometrial cell gap junction proteins such as connexin-43. these changes result in increased uterine irritability and responsiveness to uterotonins. 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 pelvic inlet- an event referred to as lightening.
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POSITIVE FEED BACK

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UMPAN BALIK HORMONAL POSITIF SELAMA PERSALINAN Estrogen Memicu awitan atau persalinan (teori utama)

Reseptor oksitosin di miometrium Ketanggapan uterus thdp oksitosin dlm darah

+
Kontraksi uterus

Berperan dlm kemajuan persalinan

Mendorong janin menekan serviks

Melalui refleks neuroendokrin

+
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Sekresi oksitosin

Pembentukan21 prostaglandin

1. STAGE OF DILATATION

a period of progressive cervical dilation

2. STAGE OF EXPULSION

3. PLACENTAL STAGE

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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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DefInItIon

The secretion and ejection of milk from the mammary gland

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During pregnancy
high estrogen level causes the extensive development 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 that is already needed to milk formation
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P R O L AC T I N
P R O L AC T I N

This hormone is secreted by the mothers anterior pituitary gland, and its concentration in her blood rises steadily from the fifth week of pregnancy until birth of the baby, at which time it has risen to 10 to 20 times the normal nonpregnant level
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Immediately after the baby is born, the sudden loss of both estrogen and progesterone secretion from the placenta allows the lactogenic effect of prolactin from the mothers pituitary gland to assume its natural milkpromoting role, and over the next 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 adequate background secretion of most of the mothers other hormones as well, but most important are growth hormone, cortisol, parathyroid hormone, and insulin. These hormones are necessary to provide the amino acids, fatty acids, glucose, and calcium required for milk formation.
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 After birth of the baby, the basal level of prolactin secretion returns to the nonpregnant level over the next few weeks each time the mother nurses her baby, nervous signals from the nipples to the hypothalamus cause a 10- to 20-fold surge in prolactin secretion that lasts for about 1 hour This prolactin acts on the mothers breasts to keep the mammary glands secreting milk into the alveoli for the subsequent nursing periods.
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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 the alveoli of the breasts, but milk does not flow easily from the alveoli into the ductal system and, therefore, does not continually 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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When the baby suckles, it receives virtually no milk for the first half minute or so. Sensory impulses must first be transmitted through somatic nerves from the nipples to the mothers 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 the blood 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 Suckling on one breast causes milk flow not only in that 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. Ermin's doc/block life cycle/2010

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Suckling of baby on nipple causes Increasing Touch sensation

THE MILK EJECTION REFLEX, A POSITIVE FEEDBACK CYCLE

Receptors Touch sensitive sensory neurons in nipple Output Nerve pulse Control centres Hypothalamus and posterior pituitary input Increase oxytocin in blood
Positive feedback : milk availability encourages continued suckling, so touch sensaitions on nipple and oxytosin release continue

Effectors Contraction of myoepithelial cells in mammary glands

Milk injection
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Baby ceases to suckle, thus breaking the positive feedback cycle

Grabowski., Tortora. (2003). Principles of Anatomy and Physiology.10th edition.USA. John Wiley&Sons, Inc. ISBN 0-47122934-2. 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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