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module 4: REPRODUCTIVE SYSTEM/EMBRYOLOGY - Coggle Diagram
module 4: REPRODUCTIVE SYSTEM/EMBRYOLOGY
DEVELOPMENT AND DIFFERENTIATION OF REPRODUCTIVE SYSTEM
MALE
Sperms contain ether X or Y chromosome
Y (contains 80 genes) is believed to be derived from X (contains 1098 genes)
• Thus, in males – 1000 genes are only represented by a single allele from the X chromosome
• Leading to large # genetic diseases caused by X-linked genes (haemophilia, colour blindness, Duchenne muscular dystrophy)
TESTES FORMATION
• Y chromosome contains sexdetermining region Y (SRY) gene that produce TDF
• Testis-determining factor (TDF) causes conversion of the bipotential gonads to testes
• Testes produce testosterone
• Testosterone stimulates male sex organ development
Leydig cells begin secreting testosterone at 8 weeks of development and peak at 12-14th week
• This masculinizes embryonic structures
• Testosterone levels then decline to very low levels until puberty
Androgens masculinize the embryonic structures to form penis, male urethra, prostate, and scrotum
Testosterone production declines during 2nd trimester
Embryonic testes produce a lots of testosterone during
first trimester of pregnancy to masculinize foetus
Testes descend into scrotum shortly (~ 1 month) before birth
Because spermatogenesis requires temperature lower than abdominal core temperature
• Spermatogenesis doesn’t occur in cryptorchidism (undescended testes)
40 days after conception, testes are formed in XY fetus. Then, Sertoli & Leydig cells are formed, where Sertoli cells secrete MIF and Leydig cells secrete testosterone.
ACCESSORY SEX ORGAN
derived from Wolffian (mesonepheric) ducts
[Epididymis, vas deferens, seminal vesicles and ejaculatory duct]
At ~ day 60, Sertoli cells secrete Müllerian inhibiting factor (MIF) which causes Müllerian ducts to regress.
T from Leydig cells causes Wolffian ducts to give rise to male accessory organs
FACTORS IN SPERM MOTILITY
Factors that help sperm travel along the uterus and oviducts are:
contractions of uterus and uterine tubes
prostaglandins in seminal fluid
oxytocin produced by female’s posterior pituitary during orgasm
CAPACITATION
On coming in contact with female reproductive tract, sperm are activated for being able to fertilize the ovum
uterine & fallopian tube fluids wash away various inhibitory factors from the sperm
while travelling along female reproductive tract, the acrosome become weaker
membrane of sperm become much permeable to Ca2+
to increase the activity of flagellum
for acrosome to easily release the enzymes (hyaluronidase & protease) to penetrate granulosa cells and zona pellucida
FEMALE
Only 1 of two X chromosomes in females becomes active – X inactivation / lyonization
Other forms clump of inactive heterochromatin called
Barr body
not transcribed - used as test for chromosomal sex
All ova contain an X chromosome
In absence of TDF, ovaries develop -->> Ovarian follicles (functional units of ovary) don’t appear until day 105
In absence of T, clitoris forms instead of penis and labia instead of scrotum
ACCESSORY SEX ORGAN
derive from Müllerian (paramesonephric) ducts [Uterus and fallopian tubes]
BEGIN
First 40 days after conception, gonads of male and female are similar (bipotential gonads)
Cells that give rise to sperm and eggs migrate from yolk sac to develop gonads
• Gonads have the potential to become testes or ovaries
Chromosomal gender of zygote determined by the fertilising sperm
22 of these are autosomal chromosomes (chromosome 1 to 22). E.g. genes that code for height, eye colour, hair etc.
23rd pair are sex chromosomes
ABNORMALITY
GONADAL DYSGENESIS
• Definition:
incomplete differentiation of gonads and usually associated with sex chromosome abnormalities
• Errors in meiotic division – chromosomal non-disjunction, translocation, rearrangement or deletion
COMMONLY,
47, XXY – Klinefelter syndrome
is associated with small testes and infertility.
Patient with this syndrome is tall but have poor beard growth.
45, XO – Turner syndrome
is associated with short stature, amenorrhea
(infertile) and etc. as shown in the below figure.
IN NORMAL CHROM. NO.
• 46, XX – female pseudohermaphrodite
have normal ovaries but external genitalia is
inappropriate
• Individual develops very female appearance but is infertile
• Due to exposure of foetus or mother to androgens (congenital adrenal hyperplasia, maternal androgen excess)
46, XY – male pseudohermaphrodite, testicular feminisation syndrome (Xlinked recessive)
have testes but accessory organs and external
genitalia are incompletely developed or inappropriate
Deficient in testosterone secretion due to testicular dysgenesis; impaired secretion of testosterone (congenital 17α-hydroxylase deficiency) or MIF; failure of target tissue response to androgen (androgen resistance) or MIF or failure of testosterone conversion to dihydrotestosterone (DHT) [5α -reductase deficiency]
TRUE HERMAPHRODITISM
Ovotestis
• Uterus is usually present
REPRODUCTIVE SYSTEM
MALE
SPERMATOGENESIS
HORMONAL CONTROL
Spermatogonia mature into primary spermatocytes begins during
adolescence
stages from spermatogonia to spermatids is androgen-independent
testosterone (T) and its metabolites are required for completion of meiosis and spermatid maturation
Follicle-stimulating hormone (FSH) roles in spermatogenesis
it enhances T-stimulated spermatogenesis for maximal sperm production
and at puberty FSH acts with T to stimulate proliferation of Sertoli cells
TEMPERATIRE
Testes are maintained at ~2oC below abdominal temperature.
Hot baths for 30 minutes a day, tight cloth may reduce sperm count
Testosterone production is not affected
BEGIN
Germ cells that migrate from yolk sac during development become spermatogonia (stem cells)
◦ spermatogonia replicate throughout life by mitosis
◦ spermatocytes differentiate to form haploid sperm by meiosis
Occurs in wall of seminiferous tubules (ST)
Spermatogonia and 1o spermatocytes are located in outer part of ST
At end of 2nd meiotic division, 4 spermatids are still interconnected
Maturation and separation of spermatids into mature spermatozoa
Requires participation of Sertoli cells
Spermatids and mature spermatozoa are located toward lumen
At end of spermiogenesis, spermatozoa are released into the lumen
During spermiogenesis, proteins called protamines replace the DNA-associated histones
◦ cause extreme compaction of chromatin, changing nuclear shape
◦ Sertoli cells phagocytize cytoplasm of developing sperm
◦ a flagellum and acrosome (cap of digestive enzymes) develop
NEGATIVE FEEDBACK
T inhibits LH and GnRH secretion but not FSH
Inhibin from Sertoli cells provides negative feedback on FSH secretion
SEMEN CONTENT
Normal volume of ejaculate is 1-5 ml with 60-150 million sperm/ml
◦ Average sperm count: 100 million/mL
◦ < 20% abnormal sperm
Sperm count of < 20 million/ml constitutes oligospermia (<50 million/ejaculation)
◦ associated with decreased fertility
◦ caused by heat, lead or arsenic poisoning, and drugs including marijuana, cocaine, and anabolic steroids
INFERTILITY
Presence of many morphologically abnormal or immotile spermatozoa
ABNORMAL
TESTICULAR FUNCTION
Hypergonadotrophic hypogonadism
– if testicular disease causing high gonadotrophins level.
Cryptorchidism
Undescended testes – occur in 10% of newborns.
• Testes remain in the abdominal cavity or inguinal canal.
Early Rx is required : gonadotropic hormone (speeds descent) or surgery
Androgen-secreting tumours
Androgen-secreting Leydig cell tumours are rare and cause endocrine symptoms in prepubertal boys – pseudopuberty develops
Hypogonadotrophic hypogonadism
– if disorders of pituitary or hypothalamus (Kallmann syndrome) causing low gonadotrophin level.
If the endocrine fx of testes lost during adulthood, the 2nd sex
characteristics will regress slowly.
(eunuchoidism)
If in childhood, Leydig cell deficiency – low testosterone.
the person is tall as the epiphyses remain open, narrow shoulder, small muscle & body configuration resembling females.
STEROIDOGENESIS
Vas deferens carries sperm into pelvic cavity
Fluid becomes semen when prostate adds secretions containing citric acid, Ca2+ and coagulation proteins (which coagulate semen during ejaculation)
Seminal vesicles add fluid (constituting 60% of ejaculate) to that coming from epididymis
◦ contains fructose for energy for sperm
Spermatozoa from STs are non-motile and cannot fertilize the ovum [ Partly due to low pH ]
Spermatozoa mature and become motile in epididymis [ More resistant to changes in pH and temperature ]
• Prostatic fluid (which is alkaline) neutralizes pH during ejaculation
• Sperm become fully motile and capable of fertilizing an ovum
Sertoli cells
of STs contain receptors for follicle stimulating hormone (FSH) [FSH stimulates spermatogenesis]
--> CREATE blood-testes barrier
--> NURTURE Spermatogonia and developing spermatozoa
--> secrete androgen-binding protein (ABP) into lumen of STs [ABP binds testosterone, concentrating it in tubules]
--> Contains FSH receptors [FSH stimulates ABP & inhibin production and secretion]
--> provide negative feedback on FSH via production of inhibin
Leydig cells
contain luteinizing hormone (LH) receptors [LH stimulates production & secretion of T]
REGULATION
GnRH
Pulsatile pattern of GnRH release is important for physiologic function of the testes
--> [Pulsatile release of GnRH is under negative feedback regulation by gonadal hormones]
Continuous exposure of gonadotrophs to GnRH cause desensitization of GnRH receptors
This will result in reduced LH and FSH secretion hence testicular fx
BODY CHANGES
T develop and maintain male secondary sex characteristics, stimulate growth of larynx, bone, and Hb levels & stimulate muscle growth along with FSH, maintain spermatogenesis
IN BRAIN
T in brain are mediated by its derivatives --> It is converted to oestradiol (E) by aromatase o E mediates negative feedback effects of T --> T is converted to dihydrotestosterone (DHT) by 5α-reductase in some target tissues
FEMALE
INTRO
Extensions of fallopian tubes called fimbriae partially cover each ovary --> the cilia of its lining draw in ovulated eggs
3 LAYERS UTERUS
Perimetrium is outer layer of connective tissue
Myometrium is middle layer of smooth muscle
Endometrium is hormonally responsive inner epithelial layer that is shed during menstruation
Between uterus and vagina is cervix
PRODUCTION OF OOCYTES
Germ cells that migrate into ovaries from yolk sac multiply so that at 5 month-gestation, ovaries contain 6-7 million primordial germ cells or oogonia
Toward the end of gestation, oogonia (now 1o oocytes) begin meiosis but arrest in prophase I
About 400 oocytes are ovulated during reproductive years; the rest undergo apoptosis
There is a continual loss of 1o oocytes throughout life
at birth are 2 million left
at puberty 400,000 are left
FUNCTION OVARIAN HORMONE
ESTROGEN
change the vaginal epithelium from cuboidal into stratified type
cause proliferation of endometrial stroma and increase development of endometrial glands
cause proliferation of glandular tissues & increase the ciliated epithelial cells in the fallopian tubes
cause cervical mucus to become thin and watery to allow sperm penetration
E initiate growth of the breasts at puberty
Development of the stromal tissues of the breasts
Growth of ductile system
Deposition of fat
PROGESTRONE
Promotes secretory changes in endometrium
Promotes increased secretion in fallopian tubes, for nutrition of the fertilized ovum
Promotes development of lobules and alveoli of the breasts
CONTRACEPTIVE
Oral contraceptive pills usually contain synthetic E and P
taken daily for 3 weeks after menstrual period
mimic CL so that negative feedback inhibits ovulation
placebo pills are taken in 4th week to permit menstruation
MENSTRUAL CYCLE
Is ~month-long cycle of ovarian activity
-Characterized by shedding of endometrial lining and bleeding (menstruation)
Results from interaction of hypothalamus-pituitary-ovaries
Other animals have estrous cycles in which there is no shedding of endometrium and sexual receptivity is limited
HUMAN
Day 1 is taken to be first day of menstruation
Days 1 thru ovulation constitute the follicular phase of ovarian cycle (variable in duration)
Time from ovulation to menstruation is luteal phase of ovarian cycle (relatively constant; 14 + 2 days)
Normal menstrual bleeding occurs every 25-35 days
Endometrial changes are divided into menstrual, proliferative, and secretory phases
OVARIAN CYCLE
FOLLICULAR PHASE
1 o oocytes are contained in 1o follicles consisting of oocyte + follicle cells
In response to FSH some follicles enter ovarian cycle and grow, producing layers of granulosa cells
Some 1o follicles (preantral follicles) continue to grow, developing vesicles and becoming 2o follicles (antral follicles)
The cells of theca interna are the primary source of circulating oestrogens
One of the follicles grows rapidly and becomes dominant follicle
→ vesicles fuse, forming fluid-filled cavity called an antrum
→ mature follicle is now called a Graafian follicle
Others regress forming atretic follicles
As Graafian follicle develops, 1 o oocyte completes meiosis I
This is an asymmetric division because 1 daughter cell (the 2o oocyte) gets all cytoplasm
other daughter becomes a small polar body which will degenerate
2 o oocyte arrests at metaphase II → only fertilized eggs complete meiosis II
2o oocyte is part of Graafian follicle
Granulosa cells form layer around outside of follicle → high oestrogen in follicular fluid comes from granulosa cells
as follicles grow, secrete larger amounts of E reaching peak about day 12
Oocyte sits on mound in this layer called cumulus oophorus
2 o oocyte is enclosed by ring of granulosa cells called corona radiata
Between oocyte and radiata is gelatinous layer called zona pellucida (forms barrier to sperm penetration)
LUTEAL PHASE
LH causes empty follicle to become corpus luteum (CL)
→ which secretes progesterone (P) and E after 2 weeks if no fertilization,
CL becomes corpus albicans (nonfunctional remnant)
P levels rise and peak about a week after ovulation
Development of new follicles and another ovulation are inhibited by
→ high P and E exert strong negative feedback on LH and FSH
→ inhibin from CL further suppresses FSH
With no fertilization, CL regresses consequently E and P levels decline → causing menstruation and allowing new c
OVULATION
By 10-14 days after menstruation begins, only 1 follicle survives
Surviving Graafian follicle forms bulge on surface of ovary
→ secretes increasing levels of E
At about day-14 of cycle, follicle ruptures and the ovum is extruded into the abdominal cavity
The ovum is picked up by fimbriated ends of oviducts
If fertilized, ovum completes meiosis II with formation of another polar body
Ovum degenerates in 2 days if not fertilized
INDICATION
cervical mucus thinner and more alkaline [E]
--> promote the survival and transport of sperm
--> ferning results from crystallization of inorganic salts
its elasticity or spinnbarkeit increases
--> in midcycle, a drop of cervical mucus can be stretched into a long, thin thread (8-12 cm or more)
cervical mucus thick, tenacious and cellular [P]
thermometer with wide gradations
--> temperature (oral or rectal) is taken in the morning before getting out of bed
Rhythm method involves daily measurement of oral basal body temperature (BT) upon awakening
--> because ovarian steroids cause BT changes
--> E begins to decline on day of LH surge causes a slight drop in BT
--> rising P on day after LH peak causes elevated BT for the rest of luteal phase
UTERINE CYCLE [endometrium]
Are driven by cyclic changes in E and P levels
Proliferative phase occurs during follicular phase when menstrual flow ceases.
E levels increase
→ E stimulates growth of endometrial lining
→ Epithelial cells proliferate [ glands are straight, short & narrow spiral arteries develop ]
→ E increases receptors for P in endometrium
Secretory phase occurs during luteal phase → endometrium becomes ready for implantation
P and E cause endometrium to become thick, vascular, and spongy
HIGH P
→ P causes cervical mucus to thicken and become sticky
→ P causes enlargement of myometrium but reduces the excitability of the cells.
→ P stimulates development of uterine glands (rich in glycoprotein, sugars & amino acids)
Menstrual phase results from drop in P and E following CL degeneration
→ low P causes constriction of spiral arteries
→ functional layer of stroma begins to shrink
→ blood flow stops, causing necrosis and sloughing of endometrium
FACTORS
Release of GnRH is regulated not only by hormonal feedback but also by input from higher brain centers
olfactory system (sense of smell) can send activity to
hypothalamus in response to pheromones
--> can cause the “dormitory effect” in which cycles of roommates become synchronized
Limbic system (involved in emotions) input to the hypothalamus in times of stress can cause functional amenorrhea (cessation of menstruation)
also occurs in thin or athletic females with low body weight
--> appears to be related to reduced leptin secretion by small adipocytes
ABNORMALITIES
ANOVULATORY CYCLE
Ovulation fails to occur during menstrual cycle BUT common for the first 12-18 months after menarche (first occurrence of menstruation) and before the onset of menopause
There is no CL, so the effects of P on the endometrium are absent
E continue to cause growth of endometrium
--> becomes thick enough to break down and begins to slough
--> usually menstrual cycle occurs in less than 28 days
Cervical mucus smear shows fern-like pattern
AMENORRHOEA
absence of menstrual periods
1 o amenorrhoea – menstrual bleeding has never occurred
2 o amenorrhea – cessation of cycles in a woman with previously normal periods [MOST COMMON]
Hypomenorrhoea (short or scanty menses),
menorrhagia (heavy menses),
metrorrhagia (irregular menses),
oligomenorrhoea (infrequent menses),
dysmenorrhoea (painful menses)
HYPOGONADOTROPHIC HYPOGONADISM
deficiency of GnRH results in reduced gonadotropin & E levels
and failure of ovulation with oligomenorrhoea or amenorrhoea
GERMINAL LAYERS
GASTRULATION
EMBRYO
1ST WEEK
1 layer: inner cell mass @ embryoblast
2ND WEEK
2 layer (bilaminar germ disc): epiblast & hypoblast
3RD WEEK
3 layers (trigeminal germ disc): ectoderm, mesoderm, endoderm. - ALL ARE PRECURSOR off embryonic tissue
formation of notochord
ESTABLISHMENT OF BODY AXES
INVOLVe
movement & cell migration,
extensive cell shape changes,
rearrangement,
changes in adhesive properties
begins w/ formation of primitive streak on surface of epiblast,
cephalic end of streak = primitive node,
primitive groove = narrow groove in primitive streak,
primitive node = slightly elevated are at the cephalic end of primitive streak,
primiive pit = small depression in primitive node
cell of epiblast migrate & invaginate toward primitive streak.
cell become flasked-shaped, detach from epiblast and slip through beneath epiblast and hypoblast
some cell displace hypoblast --> endoderm.
some cell lie btw epiblast and endoder --> mesoderm.
some cell remain in epiblast layer --> ectoderm
when complete, primitive streak disappears [end of 4th week].
after that, body axes of embryo appear: ant-post, dorsal-ventral, left-right
DERIVATIVES
ECTODERM
skin [epidermis], sensory epithelium of eye, ear, nose, central & peripheral nervous sytem
MESODERM
muscle, cartilage, bone, dermis of skin
ENDODER
epithelial lining of GI tract, respiratory tract, urinary bladder, and other organs
DIFFERENTIATION OF INTRAEMBRYONIC MESODERM
mesoderm lies on either side of notochord (axis skeleton), buccopharyngeal mem. (future oral cavity), cloacal mem (future anus)
PARAXIAL
INTERMEDIAT
LATERAL PLATE
craniofacial DEFECT
Treacher Collins Syndrome
Treacher Collins syndrome is a genetic disorder characterized by deformities of the ears, eyes, cheekbones, and chin
A change in the gene TCOF1 causes up to 93 per cent of cases of Treacher Collins syndrome. This gene, located on chromosome 5, is responsible for facial development. In about half of all cases, TCOF1 spontaneously changes at conception but what triggers the gene change is unknown.
PREGNANCY & PARTURITION
FERTILISATION
Once sperm had entered the ovum, ovum completed meiosis 2 to form mature ovum and a second polar body
Female pronucleus and male pronucleus then combine to form a complete complement of 46 chromosomes
3-4 days are required to transport fertillised ovum (zygote) to uterine cavity which is aided by:
fluid current from epithelial secretion
cilia of oviductal epithelium that beating toward uterus
weak contractions of oviducts
progesterone relaxes the isthmus of oviducts to allow the entry
HORMONAL FACTOR
Syncytial trophoblast cells secrete human chorionic gonadotropin (hCG)
serum hCG levels can first be measured 8-9 days after ovulation
The rate of hCG secretion rises rapidly & reaches maximum at ~10-12 weeks of pregnancy
hCG levels drop & remain low after 16-20 weeks
hCG
It has a molecular structure and fx similar to LH
It prevents involution (shrinking size) & stimulates growth of corpus luteum (CL) to about twice its initial size
It causes CL to secrete large quantities of estrogens & progesterone (E & P) for the 1st trimester
It also stimulates testes of male fetus to secrete testosterone
IMPLANTATION
At the same time, fertilized ovum divides few times to form blastocyst (~100 cells)
Fertilized ovum gets its nutrition from fallopian tube secretion
~7 days after ovulation, fertilized ovum implants in uterine wall
blastocyst gets its nutrition from endometrial secretion (‘uterine milk’)
PARTURITION
Parturition is the process of the birth of the baby
Its due to: progressive hormonal changes that increase excitability of uterine musculature & progressive mechanical changes
INCREASE UTERINE CONTRACTILITY
Increased E:P ratio
From 7th month of gestation, E secretion continues to increase while P remains constant or slightly decreases
E increase the no. of gap junctions hence increase the degree of uterine contractility
E increase the no. oxytocin receptors in the myometrium & decidua
OXYTOCIN
secreted by posterior hypothalamus causes uterine contraction
Oxytocin secretion at the time of labour increased in positive feedback manner
At the time of labour, fetus also secretes increasing amount of hormones to increase the intensity of uterine contractions
pituitary gland secretes oxytocin adrenal glands secrete cortisol fetal membranes release prostaglandins
MECHANICAL FACTORS
Stretching of uterine smooth muscles increases their contractility
Stretching or irritation of uterine cervix initiates uterine contractions
As pregnancy progress, uterus undergoes periodic episodes of weak & slow rhythmic contractions
Uterine contractions become progressively stronger toward the end of pregnancy
STAGES
1ST
period of progressive cervical dilation
toward the end of pregnancy, cervix becomes soft and stretched
when labour contractions begin this stage lasts for 8 – 24 hours in first pregnancy
2ND
once the cervix dilated fully, the fetal membranes rupture and amniotic fluid is lost through vagina
fetal head moves into birth canal
it last for 1 to 30 min
PREGNANCY
PLACENTA
secretes human chorionic somatomammotropin (hCS) at ~5th week of gestation.
Its secretion increases progressively throughout pregnancy
Previously it was known as human placental lactogen (hPL)
hCS
SIMILAR TO GH.
promotes proteins formation & enhances active amino acid transfer across the placenta
It decreases insulin sensitivity & decreases glucose utilised by mother
--> so that larger amount of glucose available to fetus
It promotes release of free fatty acids from maternal fat stores as alternative source of energy for mother’s metabolism
Stimulates the growth & dev of the breast
After 13th-17th week of gestation, CL involutes slowly
Secretions of E & P are taken over by placenta
--> E secretion increases to ~30x the normal level
-->E is derived from weak androgens [Dehydroepiandrosterone (DHEA) & 16-hydroxyDHEA] which are formed from both maternal & fetal adrenal glands
-->P secretion increases ~10 folds
HORMONE
Pituitary gland enlarges by 50% and increases production of adrenocorticotropic hormone (
ACTH
), thyroid stimulating hormone (
TSH
) &
prolactin
Glucocorticoids
is moderately increased --> helps to mobilize amino acids to be used for fetal tissue synthesis
Increased
thyroxine
to increase metabolism
Increased parathyroid hormone (
PTH
) to maintain maternal Ca2+ concentration --> fetus uses Ca2+ to form bone
Relaxin
softens the cervix at time of delivery
MATERNAL ADAPTATION
Increased ventilation by 30-40% at 27th week of gestation
Increased respiratory rate to maintain extra ventilation
--> due to increased metabolic rate, O2 use, CO2 formation & restricted lung expansion
Increased blood volume by 30% during latter half of pregnancy
--> due to androgen & E effects, fluid retention and increased RBC formation in bone marrow
Glomerular filtration rate (GFR) & renal tubules’ reabsorptive capacity for Na+ , Cl- & H2O increase by 50%
--> hence rate of urine formation slightly increased
LACTATION
MAMMARY GLAND
Made up of lobules which contain alveoli lined by epithelial cells
Myoepithelial cells lie in between.
Ducts arise from each alveoli and converge to form lactiferous duct which open on the nipple.
HORMONE
High estrogen – promotes extensive ductal development
High progesterone – stimulates abundant alveolar-lobular formation
Prolactin – lactogenic hormone responsible for milk secretion
Oxytocin – causes milk ejection (let down)
human chorionic somatomammotropin, hCS – placenta lactogen - induces the synthesis of enzymes needed for milk production in mammary glands
PROCESS
In first half of gestation –Growth of glandular tissue occurs. --> Mammary glands are fully capable to produce milk by the middle of pregnancy.
In the last half of gestation – High E & P prevent lactation by blocking prolactin’s stimulatory action on milk secretion. .
At parturition, sudden fall of E & P initiates lactation.
Involution – After normal period of lactation (7-9 months), alveolar epithelium undergoes apoptosis & glands revert back to non-pregnant state
Suckling reflex release oxytocin which causes milk ejection, --> it also increases prolactin secretion to maintain milk secretion.
Other stimuli: crying of infant can stimulate milk flow (condition reflex)
Adrenaline inhibits contraction of myoepithelial cells. --> Therefore, emotional disturbances will inhibit milk ejection.
BENEFIT
TO INFANT
Milk contains colostrum for the first 2 or 3 days
--> it contains antibodies that protect infant against infections until its own immune system fully functional
Breast milk also contains water, proteins, amino acids, lipids, sugars and salts
Lysozyme in milk is an enzyme with antibiotic properties
TO MOTHER
Women who breastfeed their child regularly & continuously have amenorrhea for 25-30 week
Women who do not breastfeed usually have their first menses 6 weeks after delivery
Breastfeeding stimulates prolactin secretion
--> Prolactin inhibits GnRH secretion, reduced gonadotropins effect on ovaries
--> So, ovaries are inactive & ovulation is inhibited E & P remain at low levels
PELVIS & PERINEUM
PELVIC REGION
PELVIC GIRDLE
FX
. 1. Bear the weight of the upper body when sitting & standing
Transmits body weight from the vertebral column to the femurs 3. Contains, supports, and protects the pelvic viscera & provides attachment for trunk and lower limb muscles
PELVIC CAVITY
Enclosed by bony, ligamentous & muscular wall
Contains urinary bladder, ureters, pelvic genital organs, rectum, blood vessels, lymphatics & nerves
Pelvic outlet (inferior pelvic aperture)
Pelvic inlet [sup pelvic aperture]
INLET
Posteriorly – sacral promontory (superior portion of sacrum) & sacral wings (ala)
Laterally – iliopectineal lines (arcuate line on the inner surface of the ilium & the pectineal line on the superior pubic ramus)
Anteriorly – pubic symphysis
OUTLET
Posteriorly – coccyx
Anterolaterally – ischiopubic ramus
Posterolaterally – Sacrotuberous ligament
Anteriorly – pubic symphysis
division
FALSE/ greater
Located superiorly
Provide support of the lower abdominal viscera (ilium & sigmoid colon)
Little obstetric relevance
Bounded by:
Posteriorly – lumbar vertebrae
Laterally – iliac fossae & the iliacus
Anteriorly – lower part of the anterior abdominal wall
TRUE
Located inferiorly
Resides the pelvic cavity and pelvic viscera
It has an inlet and an outlet
PELVIC AXIS
is an imaginary line that curves through true pelvis from the central point of the pelvic inlet (pelvic brim) plane to the central point of the pelvic outlet plane
• Route for baby’s head during birth
PELVIC SHAPE
ROUNDED
TRIANGULAR [HEART]
TRANSVERSALLY OVAL
OVAL SHAPE
PELVIC WALL
MUSCLE
OBTIRATOR INTERNUS
O: Anterolateral wall of true pelvis (deep surface of obturator membrane and surrounding bone)
I: Medial surface of greater trochanter of femur
N: Nerve to obturator internus L5, SI
FX: Lateral rotation of the extended hip joint; abduction of flexed hip
PIRIFORMIS
O: Anterior surface of sacrum between anterior sacral foramina
I: Medial side of superior border of greater trochanter of femur
N: Branches from SI, and S2 -
FX: Lateral rotation of the extended hip joint; abduction of flexed hip
LIGAMENT
SACROSPINOUS
Apex attached to ischial spine.
Base attached to related margins of sacrum and coccyx
SACROTUBEROUS
Apex is attached to the medial margin of the ischial tuberosity.
Base has broad attachment. Extends from the posterior superior iliac spine, along the dorsal and the lateral margin of sacrum and onto the dorsolateral of coccyx
FX: o Stabilize the sacrum on the pelvic bones --> resisting the upward tilting of the inferior aspect of the sacrum
o convert the greater & lesser sciatic notches of the pelvic bone into foramina
Acetabulum + femoral head = hip joint
PELVIC FLOOR
FX
seal inferior outlet of the pelvis
Support pelvic floor and elevate it to release faeces
Resist increased intraabdominal pressure [DEFECATION, MICTURITION, PARTURITION]
INTRO
Pelvic floor is formed by the funnel shaped pelvic diaphragm
Inferior to the pelvic diaphragm is the perineal membrane & perineal body à pelvic floor
pierced by: rectum urethra, vagina
completed posteriorly by coccygeus muscle
MUSCLE
LEVATOR ANI
PUBORECTALIS
Puborectalis pulls the anorectal junction forward & maintain rectal
continence. Relax during defecation.
Originates from the pubic, passes inferiorly on each side to form a sling around the terminal part of GI tract 2)
This sling maintains an angle called perineal flexure at the anorectal junction 3)
Function: keeps the end of the GI system closed except during defecation (“pinch valve”)
PUBOCOCCYGEUS
1) Gives stability & support to abdominal and pelvic organs
2) Originates from the pelvis’ posterior surface
3) Prone for damage during childbirth
ILLIOCOCCYGEUS
1) Elevates the pelvic floor & anorectal canal
2) Originates from ischial spines & posterior tendinous arch of the internal obturator fascia
3) Inserts onto coccyx, perineal body & anococcygeal ligament
COCCYGEUS
1) Triangular muscle posterior to the levator ani
2) Supports pelvic viscera
3) Flexes the coccyx
PERINEUM
INTRO
DIAMOND SHAPE.
Boundaries (bony):
Anterior: lower border pubic symphysis
Posterior: tip of coccyx
Antero-laterally: ischiopubic rami, ischial tuberosities
Postero-laterally: sacrotuberous ligament
DIVISION
UROGENITAL TRIANGLE
ANAL TRIANGLE
PERINEAL MEM.
i. A thick fascial
ii. Triangular structure
iii. Attached to the bony framework of pubic arch
iv. Horizontal plane
v. Has a free posterior margin
vi. Anterior: small gap between membrane and inferior pubic ligament
vii. The membrane anchors the roots
of the external genitalia
POUCHES
DEEP
Closed space deep to the perineal membrane
Contains membranous urethra passing through the perineal membrane + sphincter urethrae + deep transverse perineal muscles
SUPERFICIAL
A space superior to perineal membrane
Contains erectile tissues of the penis & clitoris + continuation of urethra & vagina + muscles
MUSCLE [SUPERFICIAL]
ISCHIOCAVERNOUS
O: Ischial tuberosity & ramus
I: Crus of penis & clitoris
N: Pudendal nerve
FX: Move blood from crura into the body of the erect penis and clitoris
BULBOSPONGIOSUS
WOMAN
O: perineal body,
I: bulb of vestibule, perineal membrane, body of clitoris, and corpus cavernosum
N: Pudendal nerve
FX: Move blood from attached parts of the clitoris and penis into the glans
MAN
O: perineal body, midline raphe.
I: bulbospongiosus, perineal membrane, corpus cavernosum.
N: Pudendal nerve
FX: removal of residual urine from urethra after urination; pulsatile emission of semen during ejaculation
SUP TRANSVERSE PERINEAL
O: Ischial tuberosity and ramus
I: Perineal body
N: Pudendal nerve
FX: Stabilize the perineal body
MUSCLE [DEEP]
EXTERNAL URETHRAL SPHINCTER
O: From the inferior ramus of the pubis on each side and adjacent walls of the deep perineal pouch
I: Surrounds membranous part of urethra
N: pudendal n
FX: Compresses the membranous urethra; relaxes during micturition
DEEP TRANSVERSE PERINEAL
O: Medial aspect of ischial ramus
I: Perineal body
N: pudendal n
FX: Stabilizes the position of the perineal body
COMPRESSOR URETHRAE
O: Ischiopubic ramus on each side
I: Blends with partner on other side anterior to the URETHRA
N: pudendal n
FX: Functions as an accessory sphincter of the urethra
SPHINCTER URETHROVAGINALIS
ARTERY
COMMON ILIAC ARTERY
INTERNAL I A
ANT
supply pelvic viscera, perineum, gluteal region, adductor thigh region, fetus, PLACENTA
TRUNK
UMBILICAL [The first branch]
SUP VESICLE [Originates from the root of umbilical artery]
OBTURATOR
INF VESICLE/VAGINAL
MIDDLE RECTAL
INT PUDENDAL [The main artery for perineum]
INF GLUTEAL [The large terminal branch of anterior trunk]
UTERINE [Major blood supply to the uterus IN PREGNANCY]
POST
supply lower posterior abdominal wall, posterior pelvic wall, gluteal region
ILIOLUMBAR A
LUMBAR
ILIAC
LATERAL SACRAL A
Its branches passed into anterior sacral foramina
SUP GLUTEAL A
Terminal continuation of posterior trunk [LARGEST]
NERVE
SACRAL PLEXUS
from L4-L5 & S1-S4
L4 and anterior ramus of L5 = lumbosacral trunk
lies lateral to anterior sacral foramina
COCCYGEUS PLEXUS
from S4 & anterior rami S5 and C0
penetrate the muscle and the overlying sacrospinous and sacrotuberous ligaments and pass superficially to innervate skin in the anal triangle of the perineum
GROWTH
FACE
TONGUE
THYROID