TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD
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OBSTETRICS SUPPLEMENT HANDOUT
TABLE OF CONTENTS
Maternal Anatomy
Menstrual Physiology
Fertilization
Placenta
Fetal Development
Maternal Physiology
Prenatal Care
Postpartum Changes
Postpartum hemorrhage
Dystocia
Other Important Obstetric Information
Important Gynecologic Concepts
1
5
9
10
11
13
19
22
26
27
29
32
MATERNAL ANATOMY
EXTERNAL GENITALIA
SURFACE ANATOMY
Structure
Mons Pubis
Labia Majora
Labia Minora
Clitoris
Vestibule
Vestibular Glands
Urethral opening
Vestibular bulbs
Vaginal
opening/hymen
escutheon
7-8x2-3x1-1.5cm
round ligaments terminate at their upper
borders
connective tissue with many vessels, elastin
fibers, and some smooth muscle fibers
points downward and inward toward the
vaginal opening; rarely exceeds 2 cm
functionally mature female structure
derived from the embryonic urogenital
membrane
perforated by six openings: urethra, the
vagina, two Bartholin gland ducts, and two
ducts of the Skene glands
Bartholin glands, paraurethral glands
(Skene glands diverticulum) minor
vestibular glands
lower two thirds of the urethra lie
immediately above the anterior vaginal
wall.
1 to 1.5 cm below the pubic arch
lie beneath the bulbocavernosus muscle on
either side of the vestibule
vulvar hematoma.
Hymenal caruncles
Impreforate hymen
VESTIBULE
•
Functionally mature female structure of the urogenital
sinus of the embryo. Extends from clitoris to forchette
STRUCTURES IN THE VESTIBULE
HYMEN

Non keratinized Stratified squamous
epithelium

During first coitus, first that ruptures is
usually at the 6 o’clock position

Caruncle Myrtiformes: Remnants of hymen
in adult female
GLANDULAR
Periurethral Glands “ Skene’s Glands”
STRUCTURES Vulvovaginal Glands “Bartholin’s Glands”
6 OPENINGS: 
Vaginal introitus

Urethral opening

Paired Para urethral glands opening

Paired Bartholin ducts opening
GLANDULAR STRUCTURES
PERIURETHRAL
GLANDS
“ Skene’s glands”
Other name Lesser vestibular
glands
Male
Prostate
homology
Type of
Tubulo alveolar
gland
Location
Adjacent to the
urethra
Pathology
Urethral
diverticulum
VULVOVAGINAL
GLANDS
“Bartholin’s glands”
Greater vestibular glands
Bulbourethral gland
Compound alveolar/
compound acinar
4 and 8 o clock of the
vagina
Bartholins’s cyst/
abscess
DIFFERENCE OF LABIA MAJORA AND LABIA MINORA
LABIA MAJORA
LABIA MINORA
HOMOLOGY
Scrotum
Ventral portion of
the penis
Skin of the penis
LINING
Outer- KSSE
NKSSE
EPITHELIUM
Inner- NKSSE
NULLIPAROUS
Lie in close
Not visible behind
WOMEN
apposition
the non separated
Inner surface
labia majora
resembles the
mucous membrane
MULTIPAROUS
Gape widely
Project beyond the
WOMEN
Inner surface
labia majora
become skin like
GLANDS
(+) Hairfollicles
No hair follicles
(+) Sweat glands
No sweat glands
(+) Sebaceous
(+) Sebaceous
glands
glands
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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD
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PERINEUM
Urogenital (Anterior) Triangle: DEEP SPACE
Anterior Triangle (DEEP SPACE)
Clinical Significance
Landmark
Anterior
pubic symphysis
Anterolateral
ischiopubic rami and ischial tuberosities
Posterolateral
sacrotuberous ligaments
posterior
coccyx
Triangle
Posterior
Urogenital triangle
Boundaries:
Superrior- pubic rami
Lateral-ischial tuberosities
Posterior: superficial transverse perineal
muscle
Anal triangle
ischiorectal fossa, anal canal, anal sphincter
complex, and branches of the internal
pudendal vessels and pudendal nerve
Urogenital (Anterior) Triangle: SUPERFICIAL SPACE
Anterior Triangle (SUPERFICIAL SPACE)
closed
compartment
lies deep to the perineal membrane and
extends up into the pelvis
Contents: compressor urethrae and
urethrovaginal sphincter muscles, external
urethral sphincter, parts of urethra and vagina,
branches of the internal pudendal artery, and
the dorsal nerve and vein of the clitoris
Ishorectal
fossae
wedge-shaped spaces found on either side of
the anal canal and comprise the bulk of the
posterior triangle
Continuous space
PUDENDAL NERVE AND VESSELS
Boundary
Anterior
 Superficial
and deep
Continuous
space with
the pelvis
bounded deeply by the perineal
membrane and superficially by Colles
fascia
ischiocavernosus, bulbocavernosus, and
superficial transverse perineal muscles;
Bartholin glands; vestibular bulbs; clitoral
body and crura; and branches of the
pudendal vessels and nerve
ischiocavernosus
muscle
clitoral erection
bulbocavernosus
muscles
Bartholin gland secretion
Clitoral erection
superficial
transverse perineal
muscles
may be attenuated or even absent
Contributes to the perineal body
Roots
Anterior rami of the 2nd to 4th sacral nerve
Course
between the piriformis and coccygeus
muscles and exits through the greater sciatic
foramen in a location posteromedial to the
ischial spine
 obturator internus muscle  pudendal
canal (Alcock Canal)  enter the perineum
and divides into three terminal branches
Terminal Branches:
dorsal nerve of
the clitoris
skin of the clitoris
perineal nerve
muscles of the anterior triangle and labial
skin
inferior rectal
external anal sphincter, the mucous
membrane of the anal canal, and the perianal
skin
Landmark for
pudendal nerve
block
Ischial spine
Blood Supply
internal pudendal artery








VAGINA
H-shaped
lower portion of the vagina is constricted (urogenital hiatus
in the levator ani)
Stratified squamous non keratinized epithelium without
glands
Upper part is more capacious
It extends from the vulva to the cervix.
Ruggae that has an accordion like distensability
Vaginal length:
– Anterior wall: 6-8 cm
– Posterior wall: 7-10 cm
Potential space: Lower third
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Cervix: SQUAMO-COLUMNAR JUNCTION



Vesicovaginal septum
– Separates the vagina from the bladder and urethra
Rectovaginal septum
– Separates the lower portion of the vagina from the
rectum
Rectouterine pouch of Douglas
– Separates the upper fourth of the vagina from the
rectum





Upper vaginal vaults
– Subdivided into anterior, posterior, and two lateral
fornices by the uterine cervix
Internal pelvic organs usually can be palpated through their
thin walls
Posterior fornix provides surgical access to the peritoneal
cavity
CERVIX
EXOCERVIX
Portio vaginalis
Extends from the
squamo columnar
junction to the external
orifice
Single layer of mucous secreting
Non keratinized
highly ciliated columnar epithelium
stratified squamous
which is thrown into folds forming
epithelium
complex glands and crypts
Hormone Sensitive
Extensive amount of nerves
Few nerves only
Blood supply: Cervicovaginal branch of uterine artery located at
the lateral walls

Prepubertal women
o Original SCJ at or near the exocervix
Reproductive Age women
o Eversion of endocervical epithelium and exposure of
columnar cells to the vaginal environment
o Relocation of SJC down the Exocervix
Late adulthood / Post menopausal women
o SCJ at the endocervical canal
o Formation of transformation zone with regrowth of
the squamous epithelium
UTERUS
SIZE
Nulliparous: 6 to 8 cm (fundus=cervix) , 50-70 g
multiparous: 10 cm (cervix 1/3), 80 g or more
Isthmus
Lower uterine portion
Fallopian
tubes
Attaches at the cornua
Posterior
wall
Completely covered by visceral peritoneum
Anterior wall
Only upper portion with peritonem 
vesicouterine pouch
ENDOMETRIUM
ENDOCERVIX
Supravaginal portion
Extends from the isthmus (Internal
Os) to the ectocervix and contains the
endocervical canal
MYOMETRIUM
SEROSA
STRATUM FUNCTIONALE
•
Shed during
menstruation
•
Supplied by the Spiral
Arteries
•
Superficial 2/3
STRATUM BASALE
•
Source of Stratum
Functionale after
menstruation
•
Supplied by the Straight
arteries
•
Basal 1/3
•
lympathics
Inner Longitudinal
Middle oblique
Outer longitudinal
lymphatics
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Zona
Spongiosa
Zona
compacta
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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD
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LIGAMENTS OF THE UTERUS
Broad
•
Two wing-like structure that extend from
ligament
the lateral margins of the uterus to the pelvic
walls
•
Divide the pelvic cavity into anterior and
posterior compartments
Reproductive
Fallopian tubes
structures
ovaries
Vessels:
Ovarian arteries
Uterine arteries
Ligaments:
Ovarian ligament
Round ligament of
uterus
Cardinal
•
AKA Transverse Cervical Ligament or
ligament
Mackenrodt Ligament
•
Originated form the densest portion of the
broad ligament
•
Medially united to the supravaginal wall of
the cervix
•
Provide the major support of the uterus and
cervix
•
Maintain the anatomic position of the cervix
and upper part of the vagina
Uterosacral •
From posterolateral to the supravaginal
ligament
portion of the cervix encircling the rectum
•
Insert into the fascia over S2 and S3
Round
•
Extend from the lateral portion of the uterus,
Ligament
arising below and anterior to origin of the
oviducts, that is continuous with the broad
ligament, outward and downward to the
inguinal canal
terminating at upper
portion of labium majus





FALLOPIAN TUBES
single layer of columnar cells, some of them ciliated and
others secretory.
No submucosa
supplied richly with elastic tissue, blood vessels, and
lymphatics
Sympathetic innervation
Diverticula
SEGMENTS OF THE FALLOPIAN TUBE
Intramural
Embodied within 2% of ectopic pregnancy
Interstitial
the muscular
Ectopic pregnancy at this
wall of the uterus area result in severe
maternal morbidity
Isthmus
The narrow
Most highly developed
portion of the
musculature
tube that adjoins
Narrowest portion
the uterus,
Preferred portion for
passes gradually
applying clips for female
into the wider,
sterilization
lateral portion.
Preferred portion for tubal
ligation
12% of ectopic pregnancy
Ampulla
Widest and most
Site of fertilization
tortuous area
80% of ectopic pregnancy
Infundibulum Fimbriated
5% of ectopic pregnancy
extremity
Tunnel shaped
opening of the
distal end of the
fallopian tube



Ovaries: LAYERS
OUTER
Innermost
CORTEX
portion
INNER
MEDULLA
Primordial and Graafian follicles
in various stages of
development
Outermost

Tunica Albuginea- dull and
portion
whitish fibrous connective
tissue covering the surface of
the ovary

Germinal epithelium of
Waldeyer- a single layer of
cuboidal epithelium over the
Tunica Albuginea

Composed of loose connective tissue that is
continuous with that of the mesovarium.

Smooth muscle fibers that are continuous with
those in the suspensory ligament.

Contains the stroma and blood vessels of the
ovary

PELVIS
Pelvic Organs: BLOOD SUPPLY
MAJOR BLOOD SUPPLY TO THE FEMALE REPRODUCTIVE
SYSTEM
Pudenda
Internal Pudendal artery
Vagina
Vaginal Artery of the Uterine
Artery
Cervix
Cervicovaginal branch of
Uterine artery
Uterus
Uterine Artery
Fallopian tubes
Ovarian Artery
Ovaries
PARTICIPANTS IN THE COLLATERAL CIRCULATION OF THE
FEMALE PELVIS
Branches from the

Ovarian artery
Aorta

Inferior mesenteric

Lumbar and vertebral

Middle sacral arteries
Branches from the

Deep iliac circumflex
External Iliac Artery

Inferior epigastric artery
Branches from the

Medial femoral circumflex artery
Femoral Artery

Lateral femoral circumflex artery
False
ANT: lower abdomen
POST: lumbar vertebra
LATERAL: iliac fossa
L INEA TERMINALIS
True
SUPERIOR BOUNDARY: Pelvic inlet
INFERIOR BOUNDARY: Pelvic outlet
ANTERIOR: Pubic Bones, Ascending Rami Of Ischial
Bones, Obturator Foramina
LATERAL: Ischial Bones and Sacrosciatic Notch
OVARIES
Lies on the posterior aspect of the broad ligament, in the
ovarian fossa
o lateral to the uterus in the pelvic sidewall where the
common iliac artery bifurcates
o ovarian fossa of Waldeyer
Are attached to the broad ligament by the mesovarium.
They are not covered by peritoneum.
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PELVIC JOINTS
•
Anterior: symphysis pubis/arcuate ligament of the pubis
•
Posterior: sacroiliac
•
Hormonal changes during pregnancy cause laxity of these
joints
•
By 3-5 months POST PARTUM, laxity has regressed
•
Symphysis Pubis increase in width also Increase mobility
and displacement of the sacroiliac joint
WHY THE DORSAL LITHOTOMY POSITION?
•
Upward gliding of sacroiliac joint is GREATEST in the
DORSAL LITHOTOMY POSITION
•
Outlet increase by 1.5 -2.0 cm
PARAMESONEPHRIC
DUCT
Appendix of
testes
MESONEPHRIC DUCT
Appendix of
Appendix of
epidydymis
vesiculosis
Ductus of
Duct of
epididymis
epoophoron
Ductus deferens
Gartner’s Duct
Ejaculatory duct
Seminal Vesicle
Ureter
Renal Pelvis
Calyces
Collecting system
Glomerulus
Renal Collecting Tubules
Testes
Ovary
METANEPHRIC DUCT
URETERIC BUD
METANEPHRIC
MESENCHYME
UNDIFFERENTIATED
GONAD
CORTEX
MEDULLA
GUBERNACULUM
PELVIC TENDENCY AND TYPE
•
Anterior – dictates the tendency of the pelvis
•
Posterior – dictates the type or character of the pelvis
GYNECOID
FREQUENCY
50%
INLET SHAPE
Round
SIDEWALLS
Straight
ISCHIAL
SPINES
SACRUM
SIGNIFICANC
E
Non
promine
nt
Inclined
neither
anteriorl
y nor
posterior
ly
Good
prognosi
s for
vaginal
delivery
ANDROID
ANTHROPOI
D
PLATYPELLOID
20%
Heart
Shaped
25%
Vertically
oriented oval
Convergen
t
Convergent
5% rarest
Horizontally
oriented oval
Divergent,
then
convergent
Prominent
Prominent
Non
prominent
Forward
and
straight
with little
curvature
Straight =
pelvis deeper
than other 3
types
Well curved
and rotated
backward
Increased
incidence
of Deep
Transvers
e Arrest
Limited
posterior
space for
fetal head,
poor
prognosis
Increased
incidence of
Face Delivery
Good
prognosis for
vaginal
delivery
Poor
prognosis for
vaginal
delivery
EMBRYOLOGIC STRUCTURES AND DERIVATIVES
EMBRYOLOGIC
STRUCTURES
LABIOSCROTAL
SWELLING
UROGENITAL FOLDS
PHALLUS (GENITAL
TUBERCLE)
UROGENITAL SINUS
MALE
FEMALE
Scrotum
Labia Majora
Ventral portion
of the penis
Penis
Labia Minora
Urinary bladder
Prostate gland
Urinary bladder
Urethral and
Paraurethral
glands
Vagina
Greater
vestibular glands
Hymen
Prostatic Utricle
Bulbourethral
glands
Seminal
colliculus
Seminiferous
tubules
Rete Testis
Gubernaculum
testis
Hydatid of
Morgagni
Uterus and
Cervix
Fallopian Tubes
Upper ¼ of the
vagina
Ovarian Follicles
Rete Ovarii
Round ligament
of uterus
MENSTRUAL PHYSIOLOGY
Overview of Menstrual Cycle

Spontaneous, cyclical ovulation occurs at 25- to 35-day
intervals

Cyclical ovulation continues for almost 40 years between
menarche and menopause

Approximately 400 opportunities for pregnancy, which
may occur with intercourse on any of 1,200 days (includes
day of ovulation and its two preceding days) during the
reproductive age of most women.

Menstrual cycle days 20 to 24 is the narrow window of
endometrial receptivity to blastocyst implantation.

Mother and fetus coexist as two disctinct immunological
systems because of modifications on both fetal and
maternal tissues in a manner not seen elsewhere.

Endometrium-decidua is the anatomical site of blastocyst
apposition, implantation, and placental development.
Key Players:
1. Anterior pituitary
a. FSH
b. LH
2. Ovarian follicle
a. Theca cells
b. Granulosa cells
3. Estrogen
4. Progesterone
5. Endometrium
a. Basalis
b. Functionalis


Clitoris

OVARIAN CYCLE
Average cycle duration is approximately 28 days, with a
range of 25 to 32 days.
Follicular phase (days 1 to 14) is characterized by:
o Rising levels of estrogen
o Thickening of the endometrium
o Selection of dominant “ovulatory” follicle
Luteal phase (days 14 to 21), the corpus luteum (CL)
produces estrogen and progesterone, which prepare the
endometrium for implantation. If implantation occurs, the
developing blastocysts will begin to produce hCG and
rescue the CL, thus maintaining progesterone production.
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A. Follicular or preovulatory ovarian phase
FOLLICLE PROFILE
Event
Numbers
At Birth
2 Million oocytes
Puberty
400,000 follicles
Depletion rate
1,000 follicles/month
(puberty to 35y/o)
Total follicles released during
400 follicles
reproductive age
Atresia (apoptosis) of follicles
99.9%
OOCYTE CYCLE

Primary Oocyte
o formed by 5th fetal month
o Started their first meiotic division
o Arrested in Prophase from 5th fetal month until the
onset of puberty
o Will complete the first meiotic division at the onset of
puberty

Secondary Oocyte
o Formed after completion of Meiotic I
o Release of the first Polar Body During ovulation
o Arrested in Metaphase II until fertilization
o Completion of 2ND Meiotic Division only occurs if there
is fertilization
HORMONE PRODUCTION
Ovarian steroid production:
1. Estrogen levels rise in parallel to growth of a dominant
follicle.
2. Increase in its number of granulosa cells.
3. GC are the exclusive site of FSH receptor expression.
4. Increase in FSH during the late luteal phase stimulates
increase in FSH receptors & ability of cytochrome P450 to
convert androstenedione into estradiol.
B. Ovulation
OVULATION
Oocyte transforming growth factors:
1. Growth differentiation factor 9 (GDF9)
2. Bone morphogenetic protein 15 (BMP-15)
Functions:
1. Regulate proliferation & differentiation of granulosa cells
(GC) as primary follicles grow
2. Stabilize and expand the cumulus oocyte complex in the
oviduct
FOLLICLE DEVELOPMENT
1. Recruitment of primordial follicles.
2. Cohort will grow GC.
3. Selection of dominant follicle.
4. Dominant follicle increase GC.
5. Follicle produce estradiol & initiate expression of LH
receptors.
6. Appearance of LH receptors.
7. GC secrete progesterone which will cause LH release.
8. GC produce inhibin B to inhibit FSH release.
9. Increase estradiol & inhibin production causes drop of FSH
10. Drop of FSH causes failure of other follicles to develop.
11. LH stimulates theca cells to produce androstenediol.
Key events:
1. Preovulatory follicles increase estrogen secretion 34 to
36 hours before release of ovum with LH surge.
2. LH peaks 10 to 12 hours before ovulation.
3. Resumption of meiosis 1 in the ovum and release of first
polar body.
4. Cumulus cell produces more progesterone and
prostaglandin.
5. Oocyte growth factors (GDF9 and BMP-15) increases.
6. Increase formation of hyaluronan-rich ECM
7. Expansion occurs where cumulus cells lose contact with
one another and move outward from the oocyte along the
hyaluronan polymer.
8. LH induces remodelling of the ovarian extracellular matrix
to allow release of the mature oocyte.
9. Activation of proteases on weakening of the follicular
basement membrane and ovulation.
C.
Luteal or postovulatory ovarian phase
CORPUS LUTEUM
Key events:
1. Constant at 12 to 14 days.
2. Luteinization occurs after ovulation when the CL
develops.
3. Basement membrane separating the granulosa-lutein and
theca-lutein cells breaks down
4. Day 2 postovulation, blood vessels and capillaries
invade the granulosa cell layer.
5. Increased capacity of granulosa-lutein cells to produce
progesterone is due to increased access to steroidogenic
precursors through blood-borne LDL-derived
cholesterol.
6. Just after ovulation, estrogen levels decrease.
7. Mid-luteal phase is a secondary rise that reaches a peak
production of 0.25 mg/day of 17B-estradiol.
8. Toward the end of the luteal phase, there is secondary
decrease in estradiol production.
9. Ovarian progesterone peaks at 25 to 50 mg/day during
the midluteal phase. (With pregnancy, CL continues
progesterone production in response to embryonic hCG)
10. CL is a transient endocrine organ that will rapidly
regress 9 to 11 days after ovulation.
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LUTEOLYSIS
Luteolysis may be due to the following:
1. Decreased levels of circulating LH in the late luteal phase
and
2. Decrease LH sensitivity of luteal cells
3. Apoptosis
Effects of luteolysis:
1. Drop in circulating estradiol and progesterone levels.
2. Allows follicular development and ovulation during the next
ovarian cycle
3. Signals the endometrium to initiate molecular events that
lead to menstruation.
D.




E.




Estrogen effects
17B- estradiol is the most biologically potent naturally
occuring estrogen secreted by granulosa cells of the
dominant follicles and luteinized granulosa cells of the CL.
Estrogen is the essential hormonal signal on which most
events in the normal menstrual cycle depend.
Estrogen receptor (ER-alpha & ER-beta) interaction can
promote synthesis of specfic m-RNAs and proteins (e.g.
estrogen and progesterone)
Acts at endothelial cell surface to stimulate nitric oxide
production, leading to its rapid vasoactive properties.
Progesterone effects
Progesterone enters cells by diffusion and in responsive
tissues becomes associated with progesterone receptors --progesterone receptor type A (PR-A) and B (PR-B)
PR-A can inhibit PR-B gene regulation.
Both PR-A and PR-B are expressed in endometrial glands in
the proliferative phase, such that both receptors are
involved with subnuclear vacuole formation.
After ovulation, the glands continue to express only PR-B
through the midluteal phase. In contrast, the stroma &
predecidual cells express only PR-A throughout the
menstrual cycle.
ENDOMETRIAL CYCLE
LAYERS
A. Proliferative or preovulatory endometrial phase
Features:
•
Straight to slightly coiled, tubular glands are lined by
pseudostratified columnar epithelium with scattered
mitoses.
•
Epithelial (glandular) cells, stromal (mesenchymal) cells
and blood vessels replicate cyclically.
•
Functionalis layer is shed and regenerated from the deepest
basalis layer almost 400 times during the reproductive
lifetime of most women.
•
Day 5 of menses – the epithelial surface of the endometrium
has been restored, and revascularization is in progress.
Early proliferative phase:

Endometrium is thin, usually < 2 mm thick

Glands are narrow, tubular structures that are almost a
straight and parallel course from the basalis layer toward
the surface of the endometrial cavity.

Mitotic figures are identified by day 5 of cycle, and mitotic
activity in both epithelium and stroma persists until day 16
to 17, or 2 to 3 days after ovulation.

Epithelial cell growth is regulated in part by epidermal
growth factor (EGF) and transforming growth factor-alpha
(TGF-a)

Stromal cell proliferation appears to increase through
paracrine and autocrine action of estrogen and increased
local production of VEGF, which causes angiogenesis
through vessel elongation in the basalis.
Midproliferative phase:
•
Days 8-10
•
Columnar surface epithelium
•
Longer curving glands
•
Variable stromal edema
•
Numerous mitotic figures
Late proliferative phase:
•
Days 11-14
•
Endometrium thickens from both glandular hyperplasia
and increased stromal ground substance.
•
Functionalis layer – glands are widely separated, loose
stroma is especially prominent.
•
Basalis layer – glands are more crowded and stroma is
denser.
Midcycle (near ovulation):
•
Glandular epithelium becomes taller and pseudostratified.
•
Superficial epithelial cells acquire:
1. microvilli (increase epithelial surface area) and
2. cilia (aid in the movement of endometrial secretions
during the secretory phase)
•
Ovulation is evidenced by presence of subnuclear vacuoles
in 50% of glands


Endometrial histologic features:
o Proliferative phase – straight to slightly coiled, tubular
glands are lined by pseudostratified columnar
epithelium with scattered mitoses.
o Early secretory phase – coiled glands with a slightly
widened diameter are lined by simple columnar
epithelium that contains clear subnuclear vacuoles.
Luminal secretions are seen.
o Late secretory phase – serrated, dilated glands with
intraluminal secretion are lined by short columnar cells.
o Menstrual phase – fragmented endometrium with
condensed stroma and glands with secretory vacuoles
are seen in a background of blood.
Layers of endometrium
o Basalis layer – supplied by straight artery
o Functionalis layer – supplied by spiral artery
B. Secretory or postovulatory endometrial phase
Early secretory phase:
•
coiled glands with a slightly widened diameter
•
lined by simple columnar epithelium that contains clear
subnuclear vacuoles.
•
Luminal secretions are seen.
Late secretory phase:
•
serrated, dilated glands with intraluminal secretion are
lined by short columnar cells.
Early secretory phase
Dating based on glandular epithelium.
Day 17:
•
glycogen accumulates in the basal portion of glandular
epithelium, creating subnuclear vaculoes and
pseudostratification (1st sign of ovulation)
Day 18:
•
vacuoles move to the apical portion of the secretory
nonciliated cells
Day 19:
•
cells begin to secrete glycoprotein and
mucopolysaccharide contents into the lumen;
•
glandular cell mitosis ceases with secretory activity.
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Mid- to late-secretory phase
Dating is based on endometrial stroma
Days 21 to 24:
•
stroma becomes edematous
•
“window of implantation”
•
epithelial surface cells show decreased microvilli and cilia
•
appearance of pinopodes, luminal protrusions on the
apical cell surface, in preparation for blastocyst
implantation.
Days 22 to 25:
•
stromal cells surrounding the spiral arterioles begin to
enlarge, and stromal mitosis becomes apparent.
•
Predecidual transformation of upper 2/3 of functionalis
layer
•
Glands exhibit extensive coiling and luminal secretions
become visible
Days 23 to 28:
•
predecidual cells, which surround spiral arterioles
Spiral artery activity

Arise from arcuate arteries, which are myometrial branches
of the uterine vessels

Lengthen at a rate greater than the rate of increase in
endometrial tissue height or thickness

Rapid angiogenesis is regulated through estrogen- and
progesterone-regulated synthesis of VEGF

Changes in blood flow through these vessels aid in
endometrial growth

Excessive coiling and stasis in blood flow coincide with
regression of CL function and lead to a decline in
endometrial tissue volume

Coiling leads to endometrial hypoxia and necrosis

Prior to endometrial bleeding, intense vasospasm occurs to
limit blood loss with menstruation
MENSTRUATION
Late premenstrual phase endometrium
•
Stromal infiltration by neutrophils, giving a
pseudoinflammatory appearance to the tissue
•
Endometrial stromal and epithelial cells produce IL-8,
which is a chemotactic activating factor for neutrophils, and
serves to recruit neutrophils prior to menstruation
•
Invading leukocytes secrete enzymes that are members of
the matrix metalloproteinase (MMP) family.
•
Rising level of MMP’s tips the balance between proteases
and protease inhibitors, effectively initiating matrix
degradation.
Anatomical events

Marked changes in endometrial blood flow

Coiling of spiral arteries becomes sufficiently severe that
resistance to blood flow increases strikingly, causing
hypoxia or the endometrium

Resultant stasis is the primary cause of endometrial
ischemia and tissue degeneration.

Intense vasoconstriction & endometrial cytokine changes,
activation of proteases (MMP-1 & MMP-3)
Prostaglandins & menstruation

Role of prostaglandin:
o Vasoconstriction
o Myometrial contractions
o Upregulation of pro-inflammatory responses

Progesterone withdrawal increases expression of inducible
COX-2 enzyme to synthesize prostaglandins and decrease
expression of 15-hydroxyprostaglandin dehydrogenase
(PGDH), which degrades prostaglandin

Increased prostaglandin production of stromal cells along
with increased prostaglandin receptor density on blood
vessels and surrounding cells.

PGF2-alpha
o Vasoconstriction of spiral arteries, causing the
uppermost endometrial zones to become hypoxic
o Potent inducer of angiogenesis and vascular
permeability factors such as VEGF
Vasoactive peptides

Endothelin-1 is a potent vasoconstrictor as a product of
vascular endothelial cells.
o Degraded by enkephalinase, which is located in
endometrial stromal cells.
o Increase in its activity parallels with the increase in
progesterone levels after ovulation
o Enkephalinase activity is highest during the midluteal
phase and declines steadily thereafter as progesterone
plasma levels decrease.
Activation of lytic mechanisms

Following vasoconstriction & endometrial cytokine
changes, activation of proteases (MMP-1 and MMP-3)
within stromal cells and leukocyte invasion occurs to
degrade the endometrial interstitial matrix.
Origin of menstrual blood

Arterial bleeding is appreciably greater than venous.

Endometrial bleeding appears to follow rupture of an
arteriole of a coiled artery, with consequent hematoma
formation.

With a hematoma, the superficial endometrium is distended
and ruptures.

Fissures develop in the adjacent functionalis layer, and
blood, as well as tissue fragments of various sizes, are
sloughed.

Hemorrhage stops with arteriolar constriction as well as
changes that accompany partial tissue necrosis.

Endometrial surface is restored by growth of flanges, or
collars, that form the everted free ends of the endometrial
glands
Interval between menses

Modal interval of menstruation is 28 days.
Decidua

Specialized, highly modified endometrium of pregnancy and
is a function of hemochorial placentation

Decidualization – transformation of secretory endometrium
to decidua; dependent on estrogen and progesterone and
factors secreted by the implanting blastocyst
Structure

3 parts
o Decidua basalis – directly beneath blastocyst
implantation, modified by trophoblast invasion
o Decidua capsularis – overlies the enlarging blastocyst,
and initially separates it from the uterine cavity.
Prominent during the 2nd month of pregnancy.
o Decidua parietalis – remainder of the uterine lining
o Decidua vera – when capsularis and parietalis are joined
later in pregnancy.

By 14 to 16 weeks AOG – gestational sac completely fills the
uterine cavity and functionally obliterated.

3 layers of decidua parietalis and basalis:
o zona compacta – compact zone; part of zona functionalis
o zona spongiosa – spongy, middle portion, with
remnants of glands and numerous small blood vessels;
part of zona functionalis
o zona basalis – basal zone which remains after delivery
and gives rise to new endometrium.
Reaction

Decidual reaction is completed only with blastocyst
implantation

Predecidual changes commence first during the midluteal
phase in endometrial stromal cells adjacent to the spiral
arteries and arterioles.

Endometrial stromal cells enlarge to form polygonal or
round decidual cells

Nuclei become round and vesicular, and the cytoplasm
becomes clear, slightly basophilic and surrounded by a
pericellular membrane

Pericellular matrix surrounding the decidual cells may
allow attachment of cytotrophoblasts through cellular
adhesion molecules.
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
Cell membrane also may provide decidual cell protection
against selected cytotrophoblastic proteases.
Blood supply

Spiral arteries in the decidua parietalis retain a smooth
muscle wall and endothelium and thereby remain
responsive to vasoactive agents that act on their smooth
muscle or endothelial cells.

Spiral arterioles and arteries are invaded by
cytotrophoblasts. As a consequence, the walls of vessels in
the basalis are destroyed. These vascular conduits of
maternal blood, devoid of smooth muscle or endothelial
cells, are not responsive to vasoactive agents.
FERTILIZATION
EVENTS IN FERTILIZATION
CLEAVAGE

Zygote cytoplasm is successively cleaved to form a blastula,
which consists of increasing smaller blastomeres

At 32 -cell stage, the blastomeres form a morula, which
consists of an inner cell mass and outer cell mass

The morula enters the uterine cavity at about 3 days post
conception
BLASTOCYST FORMATION

Occurs when fluid secreted within the morula forms the
blastocyst cavity

Inner cell mass – future embryo, is now called the
Embryoblast

The outer cell mass – future placenta, is now called the
Trophoblast
IMPLANTATION

Blastocyst implants at around 7 days post conception
within the posterior superior wall of the uterus

This is during the secretory phase of the menstrual cycle, so
implantation occurs within the functional layer of
endometrium.
POST CONCEPTION: WEEK 2
EMBRYOBLAST

Differentiates into two distinct cell layers, the Epiblast and
Hypoblast, forming a Bilaminar Embryonic Disk
o Epiblast -clefts develop within the Epiblast to form the
amniotic cavity
o Hypoblast -form the yolk sac
1.
2.
3.
4.
5.
The sperm binds to zona pellucida of the secondary oocyte
and triggers the acrosome reaction, causing release of
acrosomal enzymes
Sperm penetrates the zona pellucida and unite with the
oocyte’s plasma membrane, eliciting the cortical reaction
and rendering the secondary oocyte impermeable to other
sperm
Sperm and secondary oocyte cell membranes fuse and
contents of the sperm enter the cytoplasm
 Male genetic material forms the male pronucleus
 Tail and mitochondria degenerate
Secondary oocyte completes meiosis II, forming a mature
ovum. The nucleus of the ovum is the female pronucleus
The male and female pronuclei fuse to form a zygote
POST CONCEPTION: WEEK 1
1.
2.
3.
Cleavage
Blastocyst formation
Implantation
TROPHOBLAST

Cytotrophoblast divide mitotically

Syncytiotrophoblast
o Does not divide mitotically
o Produces the HCG
o Continues its growth into the endometrium to make
contact with the endometrial blood vessels




EMBRYO PERIOD: WEEK 3-8
The beginning of the development of major organ systems
Coincides with the first missed menstrual period
Period of high susceptibility to teratogen
Gastrulation is a process that establishes the 3 primary
germ layers, forming a trilaminar embryonic disk
o Ectoderm
o Endoderm
o Mesoderm
DERIVATIVES
LAYER
Ectoderm
Endoderm
Mesoderm
DERIVATIVES
CNS and PNS
Sensory organs of seeing and hearing
Integument layer
Lining of the GIR and Respiratory tract
Muscles
Cartilages
CVS
Urogenital System
RBC
EMBRYONIC PERIOD
Order of Formation
CNS
Heart
Upper limb
Lower limb
External genitalia
First to develop and continues post natal
Completed by 8 weeks
Completed by 8 weeks
Completed by 8 weeks
Completed by 9 weeks
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PERIOD OF TERATOGENICITY
THE PLACENTA AT TERM

Volume 497 Ml

Weight 508 grams (450-500 grams)

Surfaces
o Fetal

Covered with amniotic membrane giving it
white, glistening appearance

Where the umbilical cord arises
o Maternal

Attached to the decidua

Deep, bloody appearance arranged into 15-20
irregular lobes, cotyledons

Hofbauer cells
Circulation in the Mature Placenta
DRUGS IN PREGNANCY
Category
A
B
C
D
X
Examples
Adequate and well-controlled human studies
have failed to demonstrate a risk to the fetus
Folic acid
in the first trimester of pregnancy (and there
is no evidence of risk in later trimesters).
Animal reproduction studies have failed to
demonstrate a risk to the fetus and there are
no adequate and well-controlled studies in
Paracetamol,
pregnant women OR Animal studies have
amoxicillin,
shown an adverse effect, but adequate and
cephalexin,
well-controlled studies in pregnant women
have failed to demonstrate a risk to the fetus
in any trimester.
Animal reproduction studies have shown an
adverse effect on the fetus and there are no
adequate and well-controlled studies in
paroxetine
humans, but potential benefits may warrant
use of the drug in pregnant women despite
potential risks.
There is positive evidence of human fetal risk
based on adverse reaction data from
Phenytoin,
investigational or marketing experience or
tetracyclne,
studies in humans, but potential benefits may
aspirin,
warrant use of the drug in pregnant women
despite potential risks.
Studies in animals or humans have
demonstrated fetal abnormalities and/or
there is positive evidence of human fetal risk
based on adverse reaction data from
Thalidomide,
investigational or marketing experience, and isotretinoin
the risks involved in use of the drug in
pregnant women clearly outweigh potential
benefits.
PLACENTA
FETAL TO MATERNAL MEMBRANES

Amnion
o Avascular; provides tensile strenght; first identifiable
at 7th to 8th day of life; from fetal ectoderm

Chorion

Decidua parietalis (endometrium)

Myometrium

Serosa
AMNIOTIC FLUID

Normal amniotic fluid volume
o By 12 weeks = 60ml
o By 34-36 weeks = 1L
o By term = 840 ml
o By 42 weeks = 540 ml

Production of amniotic fluid
o Initially by amniotic epithelium
o Fetal kidneys and urine production
*Amniotic fluid volume is also dependent on the extent of
maternal plasma expansion

Removal and regulation of amniotic fluid volume
o Fetal swallowing
o Fetal aspiration
o Exchange through skin and fetal membranes

Fetal surface covered by amnion beneath which the fetal
chorionic vessels course chorionic villi intervillous space
decidual plate  myometrium
FUNIS

Umbilcal cord

Two artery, one vein (left or right?)

Ave lenght: 55 cm

Wharton jelly- extracellular matrix of specialized connective
tissue

Anticlockwise spiral is present in 50 to 90 percent of
fetuses
PLACENTAL HORMONES

Trophoblast

Steroid hormones

hPL, hCG, parathyroid hormone–related protein (PTH-rP),
calcitonin, relaxin, inhibins, activins, and atrial natriuretic
peptide

hypothalamic-like releasing and inhibiting hormones:
thyrotropin-releasing hormone (TRH), gonadotropinreleasing hormone (GnRH), corticotropin-releasing
hormone (CRH), somatostatin, and growth hormone–
releasing hormone (GHRH).
PLACENTAL STEROID HORMONES
Steroid
Nonpregnant
Estradiol-17
0.1–0.6
Estriol
0.02–0.1
Progesterone
0.1–40
Aldosterone
0.05–0.1
Deoxycorticosterone
0.05–0.5
Cortisol
10–30
hCG






Pregnant
15–20
50–150
250–600
0.250–0.600
1–12
10–20
Almost exclusively produced by the placenta
Glycoprotein
Alpha and beta subunit
Functions: rescue and maintenance of function of the
corpus luteum, stimulates fetal testicular testosterone
secretion, materanl thyroid gland stimulation (chorionic
thyrotropins), promotion of relaxin secretion
detectable in plasma of pregnant women 7 to 9 days after
the midcycle surge of LH that precedes ovulation.
Plasma levels increase rapidly, doubling every 2 days, with
maximal levels being attained at 8 to 10 weeks
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

At 10 to 12 weeks, plasma levels begin to decline, and a
nadir is reached by about 16 weeks
Clearance: mainly hepatic, renal (30%)
hPL

Similar to hGH

detected in maternal serum as early as 3 weeks

Maternal plasma concentrations are linked to placental
mass, and they rise steadily until 34 to 36 weeks

production rate near term: approximately 1 g/day

Functions: Maternal lipolysis , anti-insulin or
"diabetogenic”, potent angiogenic
PROGESTERONE

Source:
o First 6-7 weeks of pregnancy: Corpus luteum (ovary)
o After 8 weeks: Placenta (Syncytiotrophoblast)

Function:
o Affects tubal motility, the endometrium, uterine
vasculature, and parturition
o Inhibits T lymphocyte–mediated tissue rejection

Preferred precursor of progesterone biosynthesis by the
Trophoblast: Maternal plasma LDL cholesterol
ESTROGEN

Pregnancy near term is hyperestrogenic

Produced exclusively by Syncytiotrophoblasts

Placenta produce all types of estrogen
ESTROGEN
Estradiol
Estrone
Estriol
SOURCE
Maternal ovaries for weeks 1 through 6 of
gestation
After T1, the placenta is the major source of
circulating estradiol.
Maternal ovaries, adrenals, and peripheral
conversion in the first 4 to
6 weeks of pregnancy
The placenta subsequently secretes increasing
quantities
Produced almost exclusively by the placental
syncytiotrophoblast
Continued production depends on the living fetus
Marker of fetal well being
Placental Estrogen Production
Conditions that Affect Hormone Levels in Pregnancy
Condition
Findings
Fetal Demise
dec estrogen
Fetal anencephaly
Dec estrogen (estriol)
Fetal adrenal hypoplasia
absence of C19-precursors
Fetal-Placental Sulfatase
Deficiency
very low estrogen levels in
otherwise normal pregnancies
Fetal-Placental Aromatase
Deficiency
virilization of the mother and the
female fetus
Trisomy 21—Down
Syndrome
serum unconjugated estriol levels
were low
Fetal Erythroblastosis
Elevated
Glucocorticoid Treatment
Dec estrogen
Maternal Adrenal
Dysfunction
Dec estrogen
Gestational Trophoblastic
Disease
placental estrogen formation is
limited to the use of C19-steroids
in the maternal plasma
estrogen produced is principally
estradiol
FETAL DEVELOPMENT
Terms
Perinatal
period
Period beginning 20 weeks AOG and ending up to
28 completed days after birth
It is recommended that this period be defined as
commencing at BW of 500 grams
Neonatal
period
Period after birth of an infant up to 28 completed
days after birth
Fetal
period
Begins from 8 weeks after fertilization or 10
weeks after onset of last menses
Embryonic
period
Commences beginning of the 3rd week after
ovulation and fertilization and lasts up to 8 weeks
AOG
8 weeks period from the time of fertilization
10 weeks period from the time of the last
menstrual cycle/Ovulation
Abortus
Fetus or embryo removed or expelled fro uterus
during the first half of gestation
20 weeks or less, or in the absence of accurate
dating criteria, born weighing less than 500 grams
GESTATIONAL AGE vs. OVULATION AGE

Gestational age/menstrual age
o The time elapsed since the last menstruation
o Precedes fertilization/ovulation by 2 weeks

Ovulation age/post conceptional age
o Measures the actual age of the embryo from the time
of fertilization/ovulation
*A fetus that is 18 weeks AOG. What is the ovulation age?
DETERMINING THE AGE OF THE FETUS

Naegele’s Rule

Crown Rump Length (CRL)
o Measured from the superior to inferior pole of the
fetus preferably in extended position
o Used for First trimester

Biparietal Diameter (BPD)
o Measured at the outer to outer aspect of the skull at
the level of the occipitofrontal plane
o Used during the second and third trimester
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FETAL PERIOD
AOG
12
The uterus usually is just palpable above the symphysis
pubis,
crown-rump length is 6 to 7 cm.
Centers of ossification have appeared in most of the
fetal bones
fingers and toes have become differentiated
Skin and nails have developed and scattered rudiments
of hair appear.
external genitalia are beginning to show definitive signs
of male or female gender
spontaneous movements.
16
fetal crown-rump length is 12
Gender can be determined by experienced observers by
inspection of the external genitalia by 14 weeks.
Quickening by multiparas
20
fetus now weighs somewhat more than 300 g, and
weight begins to increase in a linear manner.
fetus moves about every minute and is active 10 to 30
percent of the time
downy lanugo covers its entire body
24
canalicular period of lung developmentis nearly
completed
fat deposition begins
fetus born at this time will attempt to breathe, but many
will die because the terminal sacs have not yet formed
28
crown-rump length is approximately 25 cm
skin is red and covered with vernix caseosa
pupillary membrane has just disappeared from the eyes
born at this age has a 90-percent chance of survival
36
CRL of 32
deposition of subcutaneous fat
40
average crown-rump length is about 36 cm
weight is approximately 3400 g
HEAD DIAMETERS

Bitemporal diameter (8.0cm)
o Greatest TRANSVERSE diameter of the head

Biparietal diameter (9.5 cm)

Occipitomental ( 12.5 cms)

Occipitofrontal (11.5 cms)
o The plane that corresponds to the greatest
CIRCUMFERENCE
o 34.5 cm

Suboccipitobregmatic ( 9.5 cms)
o
The plane that corresponds to the smallest
circumference of the head
o 32 cm
Fetal Blood

HEMATOPOIESIS
o yolk sac – first site of hematopoiesis. embryonic
period
o Liver takes over up to near term
o Bone marrow starts at 4 mos AOG and remains as the
major site of blood formation during adulthood

Erythrocytes – nucleated and have a shorter life span due
to their large volume and are more easily deformable

Fetal blood volume (125 ml/kg)
o Term infants = 80 ml/kg body weight
o Placenta = 45 ml/kg body weight

Fetal Hemoglobin
o Hemoglobin F
o Hemoglobin A (adult hgb)
o Hemoglobin A2
Fetal Circulation: CHANGES AFTER BIRTH

Foramen ovale – functionally closed w/in several
minutes; anatomically fused 1 year after birth

Ductus arteriosus – functionally closed by 10-12 hours
after birth; anatomically closed by 2-3 weeks

Ductus venosus constrict and becomes the ligamentum
venosum
Kleihauer-Betke test

Rationale:
o Fetal RBC’s are resistant to denaturating effects of
alkali.
o Mother’r RBC are sensitive, thus may hemolyze
FETAL PULMONARY SYSTEM
FETAL CIRCULATION

3 vessels (AVA)
o 2 arteries
o 1 vein

Three Shunts:
o Ductus venosus
o Foramen ovale
o Ductus arteriosus




Presence of surfactant in the amnionic fluid is evidence of
fetal lung maturity (after 34 weeks)
Surfactant is formed in the type II pneumocytes that line
the alveoli
Starts to appear in the amniotic fluid at 28-32 weeks.
90% lipid and 10% proteins
o Phosphatidylcholines (lecithin) account for 80% of the
glycerophospholipids
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Most active component –
dipalmitoylphosphatidylcholine (DPPC)
o 2nd most active - phosphatidylglycerol
Alveolar development = just before birth – 8 years old
o

SEXUAL DIFFERENTIATION
MATERNAL PHYSIOLOGY

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A.
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Genetic/Chromosomal Sex
o XX or XY?
o Dependent on the presence of Y chromosome
Gonadal Sex
o testes or ovaries?
o Dependent on the presence of SRY gene present on
the Y chromosome or the Testes Determining region
Phenotypic Sex
o Is it a penis or a vagina?
o Dependent on the hormones produced
B.
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C.
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D.
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CARDIOVASCULAR SYSTEM
Changes in cardiac function become apparent during the
first 8 weeks of pregnancy.
Cardiac output is increased as early as the fifth week and
reflects a reduced systemic vascular resistance and an
increased heart rate.
Resting pulse rate increases about 10 bpm.
Between 10 and 20 weeks, plasma volume expansion
begins and preload is increased.
Ventricular performance is influenced by both the decrease
in systemic vascular resistance and changes in pulsatile
arterial flow.
Heart
Heart is displaced to the left and upward and rotated
somewhat on its long axis. The apex is moved somewhat
laterally from its usual position, causing a larger cardiac
silhouette on chest radiograph.
Pregnant women normally have some degree of benign
pericardial effusion, which may increase the cardiac
silhouette.
Normal pregnancy induces NO characteristic ECG changes
other than slight left-axis deviation as a result of the altered
heart position.
Cardiac Sounds
Exaggerated splitting of the first heart sound with increased
loudness of both components
No definite changes in the aortic and pulmonary elements
of the second sound
Loud, easily heard third sound
Systolic murmur in 90% of pregnant patients which was
intensified during inspiration in some or expiration in
others, and disappeared shortly after delivery.
Cardiac output
Mean arterial pressure and vascular resistance decrease,
while blood volume and basal metabolic rate increase.
Cardiac output at rest, when measured in lateral recumbent
position, increases significantly beginning in early
pregnancy. It continues to increase and remain elevated
during the remainder of pregnancy.
During late pregnancy with a woman in SUPINE position,
the large pregnant uterus compresses venous return from
the lower body. It may compress the aorta and cardiac
filling may be reduced with dimished cardiac output. Fetal
oxygen saturation is approximately 10% higher when a
labouring woman is in a lateral recumbent position
compared with supine. Upon standing, cardiac output fall to
the same degree as in the non-pregnant woman.
During the 1st stage of labor, cardiac output increases
moderately. During the 2md stage, with vigorous expulsive
efforts, it is appreciably greater. The pregnancy-induced
increase is lost after delivery.
Circulation and blood pressure
Brachial artery pressure when sitting is lower than that
when in the lateral recumbent supine position.
Arterial pressure usually decreases to a nadir at 24 to 26
weeks and rises thereafter.
Diastolic pressure decreases more than systolic.
In about 10% of women, supine compression of the great
vessels by the uterus causes significantly arterial
hypotension, referred to as the supine hypotensive
syndrome. This may directly affect fetal heart rate patterns.
This also occurs with hemorrhage or with spinal analgesia.
The components of the rennin-angiotensin-aldosterone axis
are increased in normal pregnancy. These components are
involved in renal control of blood pressure via sodium and
water balance. Renin is produced by both the maternal
kidney and placenta, and increased renin substrate
(angiotensinogen) is produced by both maternal and fetal
liver. This increase in angiotensinogen results, in part, from
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high levels of
pregnancy.
E.
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F.
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G.
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H.
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estrogen
production
during normal
Cardiac natriuretic peptides
Atrial natriuretic peptide (ANP) and B-type natriuretic
peptide (BNP) – are secreted by cardiomyocytes in
response to chamber-wall stretching. These peptides
regulate blood volume by provoking natriuresis, dieresis,
and vascular smooth-muscle relaxation.
During pregnancy, plasma ANP are maintained in the
nonpregnant range despite increased plasma volume.
Median BNP levels are less than 20 pg/ml and are stable
across normal pregnancy. However, these levels are
increased
in
severe
preeclampsia.
ANP-induced
physiological adaptations participate in the expansion of
extracellular fluid volume and the increase in plasma
aldosterone concentrations characteristic of normal
pregnancy.
C-type natriuretic peptide (CNP), is secreted by noncardiac
tissues. This peptide appears to be a major regulator of fetal
bone growth.
800
700
550
2,500
2,650
2,050
2,050
1,700
1,350
3,200
3,200
Elevated diaphragm
Elevated diaphragm
UNCHANGED
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Respiratory rate is essentially unchanged.
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Lung compliance is unaffected by pregnancy
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Maximum breathing capacity and forced or timed vital
capacity are not altered appreciably
INCREASED
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Airway conductance is increased possibly as a result of
progesterone
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Amount of oxygen delivered into the lungs by the increased
tidal volume clearly exceeds O2 requirements imposed by
pregnancy.

Total haemoglobin mass, and in turn total oxygen-carrying
capacity, increases appreciably.
Endothelin
Endothelin-1 is a potent vasoconstrictor in endothelial and
vascular smooth muscle cells and regulates local vasomotor
tone. It stimulates secretion of ANP, aldosterone, and
catecholamines. There are endothelin receptors in pregnant
and nonpregnant myometrium. They are also identified in
the amnion, amniotic fluid, decidua, and placental tissue.
Vascular sensitivity to endothelin-1 is not altered during
normal pregnancy. Vasodilating factors counterbalance the
endothelin-1 vasoconstrictor effects and produce reduced
peripheral vascular resistance.
DECREASED
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Peak expiratory flow rates decline progressively as
gestation advances.

Total pulmonary resistance reduced possible as a result of
progesterone
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Maternal arteriovenous oxygen difference is decreased due
to increased total oxygen carrying capacity.
Nitric Oxide
It is a potent vasodilator released by endothelial cells and
have important implication for modifying vascular
resistance during pregnancy.
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B.
Pulmonary Function
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1,000
Prostaglandins
Renal medullary prostaglandin E2 synthesis is increased
markedly during late pregnancy and is presumed to be
natriuretic.
Prostacyclin (PGI2), the principal prostaglandin of
endothelium, is increased during late pregnancy and
regulates blood pressure and platelet function. It also has
been implicated in the angiotensin resistance characteristic
of normal pregnancy.
PULMONARY SYSTEM
Anatomic Changes
Diaphragm rises about 4 cm during pregnancy.
Subcostal angle widens appreciably as the transverse
diameter of the thoracic cage increases approximately 2 cm.
Thoracic circumference increases about 6 cm, but not
sufficiently to prevent a reduction in the residual lung
volume created by the elevated diaphragm
Diaphragmatic excursion is actually greater in pregnancy.
A.
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Residual
volume
Expiratory
reserve
volume
Inspiratory
capacity
Inspiratory
reserve
volume
Functional
residual
capacity
Vital
capacity
Lung
Volumes
(ml)
Total lung
capacity
Nonpregnant
Term
Pregnancy
4,200
4,000
C. Acid-Base Equilibrium
Blood Gas
NonFirst
pregnant
trimester
HCO3
Not
22-26
(mEq/L)
reported
PCO2
Not
38-42
(mmHg)
reported
PO2
90-100
93-100
(mmHg)
pH
7.38 –
7.42 (a)
7.36 – 7.52
(v)
Second
trimester
Not
reported
Not
reported
Third
trimester
90-98
92-107
7.40 – 7.52
(v)
7.41 – 7.53
(v)
7.39 – 7.45
(a)
16-22
25-33
(a) – arterial; (v) – venous
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Etiology
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Increased awareness of a desire to breathe early in
pregnancy.
Physiologic dyspnea results from increased tidal volume
that lowers the blood PCO2 slightly, which paradoxically
causes dyspnea.
Increased respiratory effort, and in turn the reduction in
PCO2 is most likely induced in large part by progesterone
and to a lesser degree by estrogen.
Progesterone appears to act centrally, where it lowers the
threshold and increases the sensitivity of the
chemoreflex response to CO2.
To compensate for resulting respiratory alkalosis, plasma
bicarbonate levels decrease from 26 to approximately 22
mmol/L
Although blood pH is increased only minimally, it does
shift the oxygen dissociation curve to the left. This shift
increases the affinity of maternal hemoglobin for oxygen,
thereby decreasing the oxygen-releasing capacity of
maternal blood.
Slight pH increase also stimulates an increase in 2,3diphosphoglycerate in maternal blood which shifts the
Resting minute

ventilation is also
increased. Can be due
to enhanced

respiratory drive due
Tidal
450
600
to stimulatory effects
volume
of progesterone, low
expiratory reserve
volume and

compensated
respiratory alkalosis.
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curve back to the right. Reduced PCO2 from maternal
hyperventilation aids CO2 (waste) transfer from the
fetus to the mother while also facilitating O2 release to
the fetus.
A.
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B.
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C.
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REPRODUCTIVE SYSTEM
Uterus
Non-pregnant weight of 70g to almost 1100 grams by term.
Non-pregnant capacity of 10 ml to a total volume of 5 to 20
liters by term
Uterine enlargement involves stretching and marked
hypertrophy of muscle cells, production of new myocytes
is limited.
Accumulation of fibrous tissue, particularly in the external
muscle layer, with an increase in elastic tissue to strengthen
the uterine wall
Uterine wall thins near term to only 1 to 2 cm. It becomes
soft and readily identable through which the fetus can be
palpated.
Uterine hypertrophy early in pregnancy probably is
stimulated by the action of estrogen and perhaps that of
progesterone. By 12 weeks, increase in size is related
predominantly to pressure exerted by the expanding
products of conception.
Uterine enlargement most marked in the fundus.
Early months of pregnancy – fallopian tubes, ovarian and
round ligaments attach slightly below the apex of the
fundus
Later months of pregnancy – fallopian tubes, ovarian and
round ligaments are located above the middle of the
uterus
Portion of the uterus surrounding placental site enlarges
more rapidly.
Arrangement of muscle cells:
o Outer hoodlike layer, which arches over the fundus
and extends into various ligaments
o Middle layer, dense network of muscle fibers
perforated in all directions by blood vessels
o Internal layer, with sphincter-like fibers around the
fallopian tube orifices and internal os of the cervix.
o Main portion of the uterine wall is formed by the middle
layer. Each cell in this layer has a double curve so that
the interlacing of any two gives approximately the form
of a figure 8. When cells contract after delivery, they
constrict the penetrating blood vessels and act as
ligatures.
Pear shaped > globular form > spherical by 12 weeks >
ovoid shape (length more than width)
Displaces intestines laterally and superiorly
Dextrorotation – uterus undergoes rotation to the right
because of the rectosigmoid on the left side of the pelvis.
There is tension exerted on the broad and round ligaments.
Braxton Hicks contractions – unpredictable, sporadic and
nonrhythmic contractons, every 10 to 20 minutes for some,
intensity between 5 and 25 mmHg.
Total uterine blood flow from uterine and ovarian arteries –
450 to 650 mL/min
Cervix
Softening and cyanosis due to increased vascularity and
edema of the entire cervix, together with hypertrophy and
hyperplasia of cervical glands.
Endocervical mucosal cells produce copious amounts of a
tenacious mucus that obstruct the cervical canal soon after
conception.
Cervical Mucus is rich in Ig and cytokines and may act as an
immunological barrier to protect uterine contents against
infection.
Cervical mucus beading occurs as a result of progesterone.
Arias-Stella reaction – endocervical gland hyperplasia and
hypersecretory appearance
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D.
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Decidual reaction – elevated patches of tissue which bleed
easily. Represents cellular detritus from the endometrium
that has passed through the fallopian tubes.
Relaxin – protein hormone secreted by the corpus luteum,
deciduas and placenta. Remodelling of reproductive tract
connective tissue to accommodate pregnancy
Vagina & perineum
Chadwick sign – increased vascularity affecting vagina and
results in violet discoloration
SKIN
Abdominal wall
1. Striae gravidarum or stretch marks
2. Diastasis recti – rectus muscles separate in the midline
b. Hyperpigmentation – due elevated levels of melanocytestimulating hormone; estrogen and progesterone have
melanocyte-stimulating effects

Linea nigra

Chloasma or melasma gravidarum

Pigmentation of areola and genital skin
c. Vascular changes

Vascular spiders or angiomas – common on the face,
neck, upper chest and arms
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Palmar erythema

Increased cutaneous blood flow serves to dissipate
excess heat generated by increased metabolism
a.
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a.
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METABOLIC CHANGES
3rd trimester – maternal basal metabolic rate is INCREASED
by 10 to 20%
WHO (2004) estimate of additional energy demands:
o 1st tri – 85 kcal/day
o 2nd tri – 285 kcal/day
o 3rd tri – 475 kcal/day
Weight gain
Attributable to uterus and its contents, breasts, increase
blood volume and extracellular fluid
Accumulation of cellular water, fat and protein
Average weight gain is approx. 12.5 kg or 27.5 lbs
b.
2.
Water metabolism
Increased water retention induced by resetting of osmotic
thresholds for thirst and vasopressin secretion.
3. Mimimum amount of extra water during normal pregnancy
= 6.5 liters
o Amniotic fluid = 3.5 liters
o Maternal blood volume, uterus and breasts = 3.0 liters
4. Pitting edema of ankles and legs
o Increased venous pressure below the level of the uterus
due to partial vena cava occlusion
o Decrease in interstitial colloid osmotic pressure
c.
1.
2.
3.
4.
d.
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Protein metabolism
Fetus and placenta weigh about 4 kg and contain
approximately 500 g of protein
Remaining 500 g is added to uterus, breasts primarily in the
glands, and to hemoglobin and plasma proteins
Nitrogen balance increased with gestational age
Maternal muscle breakdown is not required to meet
metabolic demands.
Carbohydrate metabolism
Pregnancy is characterized by mild fasting hypoglycemia,
postprandial hyperglycemia, and hyperinsulinemia
Pregnancy-induced state of peripheral insulin resistance
occurs to ensure a sustained postprandial supply of glucose
to the fetus.
o Progesterone and estrogen, may act, directly or
indirectly to mediate this insensitivity
o Placental lactogen may increase lipolysis and liberation
of free fatty acids. Increased free fatty acids may aid
increased tissue resistance to insulin
Pregnant women changes rapidly from a postrprandial state
characterized by elevated and sustained glucose levels to a
Ovaries
Ovulation ceases and maturation of new follicles is
suspended.


Corpus luteum functions maximally during the first 6 – 7
weeks of pregnancy, produces progesterone.
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fasting state characterized by decreased plasma glucose and
some amino acids
e.
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Fat metabolism
Lipids, lipoproteins and apolipoproteins increase
appreciably during pregnancy.
Increased insulin resistance and estrogen stimulation are
responsible for maternla hyperlipidemia
Increased lipid synthesis and food intake contribute to
maternal fat accumulation during the first two trimesters.
During 3rd trimester, fat storage declines or ceases. This is
a consequence of enhanced lipolytic activity, and decreased
lipoprotein lipase activity reduces circulating triglyceride
uptake into adipose tissue. This transition to a catabolic
state favors maternal use of lipids as a source of energy and
spares glucose and amino acids for the fetus.
INCREASED levels during 3rd trimester:
o Triacylglycerol
o VLDL
o LDL
o
HDL
DECREASED levels after delivery: lipids, lipoproteins and
apolipoproteins
1.
Leptin
o Primarily secreted by adipose tissue, some by placenta
o Plays a role in body fat and energy expenditure
regulation
o May also help regulate fetal growth
o INCREASE and peak during the 2nd trimester and
plateau until term
o Abnormally elevated leptin have been associated with
preeclampsia and gestational DM
2.
Gherlin
o Secreted primarily by the stomach in response to
hunger.
o Cooperates with leptin in energy homeostasis
modulation
o Expressed also in placenta and likely has a role in fetal
growth and cell proliferation.
f.
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Iron metabolism
Storage
o Total iron content of normal adult women: 2.0 to 2.5
grams. Most of this is incorporated in hemoglobin or
myoglobin.
o Iron stores of normal young women is approximately
300 mg
2.
Iron requirements
o Approximately 1,000 mg of iron is required for normal
pregnancy.
a. 300 mg - actively transferred to the fetus and
placenta.
b. 200 mg – lost through normal excretion routes,
primarily in the GIT.
c. 500 mg – required for the increase in total
circulating erythrocyte volume (approx 450 ml)
o The amount of dietary iron, together with that
mobilized from stores, will be insufficient to meet the
average demands imposed by pregnancy.
3.
Puerperium
o During vaginal delivery & the first postpartum days,
only approximately half of the added erythrocytes are
lost from most women.
o Normal losses come from the following:
a. Placental implantation site
b. Episiotomy or lacerations
c. Lochia
o Estimated blood loss:
a. NSVD (singleton) – 500 to 600 ml
b. CS or NSVD (Twin) – 1,000 ml
c.

Immunologic functions
Suppression of various humoral and cell-mediated
immunological functions occur to accommodate the
“foreign” semiallogenic fetal graft.
Pregnancy is both a proinflammatory and antiinflammatory
condition depending on the stage.
Three immunologic phases of pregnancy:
o Early pregnancy (pro-inflammatory)

Blastocyst must break through the uterine cavity
epithelial lining to invade endometrial tissue

Trophoblast must replace endometrium and
vascular smooth muscle of maternal blood
vessels to secure adequate supply for the
placenta

Inflammatory environment is required to secure
cellular debris removal and adequate repair of
the uterine epithelium
o Midpregnancy (anti-inflammatory)

Period of rapid fetal growth and development
o Parturition (recrudescence of inflammatory process)

Influx of immune cells into the myometrium
Suppressed activity:
o T-helper (Th) 1 cells

decreases secretion of IL-2, interferon-g, and
TNF-B

suppressed Th1 response is requisite for
pregnancy continuation

suppressed Th1 during pregnancy results in
remission of some autoimmune disorders such
as rheumatoid arthritis, multiple sclerosis, and
Hashimoto thyroiditis

failure of Th1 suppression may be related ot
development of preeclampsia
o T-cytotoxic (Tc) 1 cells

Decreases secretion of IL-2, interferon-g, and
TNF-B
Upregulated activity:
o Th2 cells – increase secretion of IL-4, IL-6 and IL-13
o IgA and IgG in cervical mucus increase
o IL-1B in cervical and vaginal mucus is increased during
the 1st trimester
Vitamin K-dependent glycoprotein that inhibits activation
of factor X

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Electrolyte and mineral metabolism
INCREASED
Iodine requirement
Iron requirement
a.

b.
1.
DECREASED
Sodium
Potassium
Total serum calcium (ionized &
non-ionized)
Serum magnesium
HEMATOLOGIC CHANGES
Blood volume
Hypervolemia averages 40 to 45% above nonpregnant
blood volume after 32 to 34 weeks
Functions of hypervolemia:
o Meets the metabolic demands of the enlarged uterus
and its greatly hypertrophied vascular system
o Provides abundant nutrients and elements to support
the rapidly growing placenta and fetus
o Protects the mother and fetus against the deleterious
effects of impaired venous return in the supine and
erect positions
o Safeguards the mother against the adverse effects of
parturition-associated blood loss
Maternal blood volume expands most rapidly during the
second trimester.
Blood volume expansion results from an increase in both
plasma and erythrocytes.
Moderate erythroid hyperplasia is present in the bone
marrow
Reticulocyte count is elevated slightly.
Elevated maternal plasma erythropoietin levels – peaks
early during the 3rd trimester and corresponds to maximal
erythrocyte production.
Hemoglobin & hematocrit DECREASE slightly
Whole blood viscosity DECREASES.
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
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
Low levels may prove to be a risk factor for otherwise
unexplained recurrent early pregnancy loss (Effraimidou
and associates, 2009)
URINARY SYSTEM
a.
Kidney
RENAL CHANGES IN NORMAL PREGNANCY
Parameter
Alteration
Clinical relevance
Kidney size
Approximately 1 cm
Size returns to normal
longer of radiograph
postpartum
Dilatation
Resembles
Can be confused with
hydronephrosis on
obstructive uropathy;
sonogram or IVP
Retained urine leads
(more marked on
to collection errors;
right)
Renal infections are
more virulent;
May be responsible
for “distention
syndrome”;
Elective pyelography
should be deferred to
at least 12 weeks
postpartum
Renal
GFR & renal plasma
Serum creatinine
function
flow increase ≈ 50%
decreases during
normal gestation
(>0.8 mg/dl creatinine
already borderline);
Protein, amino acid,
and glucose excretion
all increase
Maintenance
Decreased
Serum bicarbonate
of acid-base
bicarbonate threshold; decreased by 4-5
Progesterone
mEq/L;
stimulates respiratory PCO2 decreased 10
center
mmHg;
PCO2 or 40 mmHg
already represents
CO2 retention
Plasma
Osmoregulation
Serum osmolality
osmolality
altered;
decreases 10 mOsm/L
Osmotic thresholds
(serum Na ≈ 5 mEq/L)
for vasopressin (AVP)
during normal
release and thirst
gestation
decrease
Increased placental
Hormonal disposal
metabolism of AVP
rates increase
may cause transient
diabetes insipidus
during pregnancy.
1.
Loss of nutrients
o Amino acids and water-soluble vitamins are lost in
urine in greater amounts
2.
Tests of renal function
o Serum creatinine – DECREASED. Values above 0.9 mg/dl
suggest underlying renal disease and prompt
investigation
o Creatinine clearance – INCREASED about 30%
3.
Urinalysis
o Glucosuria – may NOT be abnormal. It can be due to
increase in GFR, together with impaired tubular
reabsorptive capacity for filtered glucose. About 1/6 of
pregnant women spill glucose, but the possibility of DM
should not be ignored.
o Proteinuria – NOT evident during pregnancy except
occasionally in slight amounts during or soon after
vigorous labor.
o Albumin excretion is minimal and ranges from 5 to 30
mg/day
o Hematuria is often a result of contamination during
collection. Common after difficult labor and delivery
because of trauma to the bladder and urethra.
b.



Ureters
Uterus rests upon ureters and laterally displaces it and
compresses them at the pelvic brim
Right ureter is dilated more than the left due to a
dextrorotated uterus and the right ovarian vein complex
lies obliquely over the right ureter.
Ureteral elongation and curvature formation occurs due to
distention
c.

Bladder
Bladder trigone is elevated by (>12 weeks):
o Increased uterine size
o Hyperemia
o Hyperplasia of bladder’s muscle and connective tissue
Note: Elevation of trigone causes thickening of posterior, or
intraureteric origin
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
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
a.

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

b.

No mucosal changes
Increase in size and tortuosity of its blood vessels
Bladder pressure (primigravidas) increased from 8 cm H20
(early pregnancy) to 20 cm H20 (at term).
Absolute and functional urethral lengths INCREASED
Maximal intraurethral pressure INCREASED from 70 to 93
cm H20, thus continence is maintained
End of pregnancy changes:
o Entire base of blader is pusched forward and upward,
converting normal convex surface to concave due to
presenting part
o Pressure of presenting part impairs drainage of blood
and lymph from the bladder base which may lead to
edema, and susceptibility to trauma and infections
GASTROINTESTINAL TRACT
Appendix displaced upward and laterally as the uterus
enlarges, and it may reach the flank
Gastric emptying time is UNCHANGED. During labor and
administration of analgesic agents, it becomes prolonged.
General anesthesia may cause regurgitation and aspiration
during delivery.
Pyrosis (heartburn) – reflux of acidic secretions into the
lower esophagus due to:
o Altered position of of the stomach
o Decreased LES tone
o Intraesophageal pressures are lower compared to
intragastric pressures
o Esophageal peristalsis has lower wave speed and lower
amplitude
Gums may become hyperemic and softened and may bleed
when mildly traumatized as with a toothbrush
Epulis of pregnancy – focal, highly vascular swelling of the
gums but regresses spontaneously after delivery.
Pregnancy DOES NOT incite tooth decay.
Hemorrhoids are fairly common due to constipation and
elevated pressure in veins below the level of the enlarged
uterus.
Liver
NO INCREASE in liver size
Hepatic blood flow and diameter of the portal vein is
INCREASED
Increased levels:
o Total alkaline phosphatase – almost doubles
o Total albumin
o Serum globin
Decreased levels:
o AST
o ALT
o GGT
o Bilirubin
o Serum albumin
Leucine aminopeptidase activity is markedly INCREASED.
This is increased with liver disease.
Gallbladder
Progesterone inhibits CCK-mediated smooth muscle
stimulation which impairs gallbladder contraction
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


a.


1.
2.
Impaired/reduced gallbladder contraction leads to
increased residual volume, and stasis with associated
increased bile cholesterol saturation of pregnancy
contributes to increased prevalence of gallstone in
multiparous women.
Intrahepatic cholestasis in pregnancy has been linked to
high circulating levels of estrogen, which inhibit intraductal
transport of bile acids.
Pruritus gravidarum is due to retained bile salts.
ENDOCRINE SYSTEM
Pituitary gland
Enlarges by approximately 135% but rarely cause visual
disturbance from compression of optic chiasma
Not essential for maintenance of pregnancy
Growth Hormone (GH)
o First trimester – secreted predominantly from maternal
pituitary gland; serum and amniotic fluid
concentrations are within nonpregnant values (0.5 to
7.5 ng.ml)
o At 8 weeks AOG – growth hormone secreted by placenta
becomes detectable
o At 17 weeks AOG – placenta is the principal source of
growth hormone secretion
o Maternal serum levels plateau after 28 weeks at 14
ng/ml
o Amniotic fluid levels peak at 14 to 15 weeks and slowly
declines to reach baseline values after 36 weeks.
o Maternal GH
 Correlate positively with birthweight and
negatively with fetal growth restriction & uterine
artery resistance
o Placental GH
 Differs from pituitary GH by 13 AA residues
 Secreted by syncitiotrophoblasts in a nonpulsatile
fashion
 Appears to have some influence on fetal growth
as well as the development of preeclampsia
 Major determinant of maternal insulin resistance
after midpregnancy
 Fetal growth progresses in the complete
absence of placental GH
 Not absolutely essential, but may act in concert
with human placental lactogen and other
somatolactogens to regulate fetal growth.
Prolactin
o INCREASE markedly and usually 10-fold greater at term
(150 ng/ml)
o DECREASES after delivery even in women who are
breast feeding.
o There are pulsatile bursts of prolactin secretion in
response to suckling during early lactation.
o Increases prolactin level:
 Estrogen stimulation increases the number of
anterior pituitary lactotrophs and may stimulate
release of prolactin
 TRH
 Serotonin
o Dopamine (prolactin-inhibiting factor) – inhibits
prolactin secretion
o Functions of prolactin:
 Ensure lactation
 Initiate DNA synthesis and mitosis of glandular
epithelial cell and presecretory alveolar cells of the
breast (early pregnancy).
 Increases the number of estrogen and prolactin
galactopoiesis, and production of casein,
lactalbumin, lactose, and lipids.
o Present in amniotic fluid in high concentrations. Up to
10,000 ng/ml at 20 to 26 weeks but decrease and reach
a nadir after 34 weeks. Prolactin in amniotic fluid could
be produced by uterine decidua. Its function could be to
prevent water transfer from fetus into the maternal
compartment to prevent fetal dehydration.
b.











c.





Thyroid gland
Thryroid hormone production INCREASED by 40 to 100%
to meet maternal and fetal needs
Thyroid gland undergoes moderate enlargement as a result
of glandular hyperplasia and increased vascularity. Volume
increase from 12 ml (first trimester) to 15 ml (at term)
Normal pregnancy does not typically cause significant
thyromegaly. Goiter should be investigated.
Thyroxin-binding globulin – increases in the first trimester
and reaches its zenith at about 20 weeks, and stabilizes at
approximately double baseline values for the remainder of
pregnancy
Total serum thyroxine – INCREASE sharply between 6 and 9
weeks and reaches a plateau at 18 weeks
Free serum T4 – rise slightly and peak along with hCG
levels, and return to normal
Total triiodothyronine (T3) – INCREASE up to 18 weeks and
plateaus.
Thyroid-releasing hormone (TRH) – are NOT INCREASED,
but CROSSES the placenta and may stimulate the fetal
pituitary to secrete thyrotropin
TSH and hCG has identical a-subunits, thus hCG has intrinsic
thyrotropic activity and cause thyroid stimulation.
Thyroid-stimulating hormone (TSH) or thyrotropin
DECREASES in more than 80% of pregnant women, but
remain normal for non-pregnant women.
Normal suppression of TSH may lead to a misdiagnosis of
subclinical HYPERTHYROIDISM.
Parathyroid glands
Regulation of calcium concentration is closely interrelated
to magnesium, phosphate, PTH, vitamin D, and calcitonin
physiology
All markers of bone turnover INCREASED during normal
pregnancy and failed to reach baseline level by 12 months
postpartum
Calcium needed for fetal growth and lactation may be
drawn at least in part from the maternal skeleton.
Acute or chronic decreases in plasma calcium or acute
decreases in magnesium stimulate the release of PTH, and
vice versa.
Action of PTH on bone resorption, intestinal absorption,
and kidney reabsorption is to increase ECF calcium and
decrease phosphate.
1.
PTH and Calcium
o First trimester – plasma PTH decrease initially
o Succeeding trimesters – INCREASE progressively
 Due to lower calcium concentrations in pregnancy
as a result of increased plasma volume, increased
GFR, and maternal-fetal transfer of calcium.
o Estrogen appears to BLOCK the action of PTH on bone
resorption, resulting in increase in PTH
o Physiologic hyperparathyroidism of pregnancy occurs
to supply the fetus with adequate calcium.
2.
Calcitonin and Calcium
o Calcium and magnesium increase the biosynthesis and
secretion of calcitonin
o Food ingestion & various gastric hormones (e.g. gastrin,
pentagastrin, glucagon, and pancreozymin) also
INCREASE calcitonin levels.
o Calcitonin acts to OPPOSE PTH and Vitamin D to protect
skeletal calcifications during times of calcium stress,
such as pregnancy and lactation.
3.
Vitamin D and Calcium
o 1, 25-diOH Vitamin D3 – biologically active compound,
and stimulates resorption of calcium from bone and
absorption from the intestines
o Conversion to active Vitamin D3
 Ingestion of Vit D or synthesis in the skin
 LIVER – Vitamin D converted to 25-OH Vit D3
 KIDNEY, DECIDUA & PLACENTA – 25-OH Vit D3
converted to 1, 25 diOH Vit D3 (biologically active
form) which is INCREASED in pregnancy.
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o
o
PTH, low calcium and phosphate levels facilitates
conversion of 25-OH Vit D3 to 1, 25 diOHVit D3
Calcitonin OPPOSES conversion of Vit D to its active
form.
d.
1.
Adrenals – undergo little morphological change
Cortisol – INCREASED
o Much of serum cortisol is bound by transcortin
(cortisol-binding globulin)
o Rate of adrneal cortisol secretion is not increased, and
probably it is decreased compared with that of the
nonpregnant state.
o Metabolic clearance rate is LOWER during pregnancy
because its half-life is nearly doubled.
o During early pregnancy – ACTH levels are reduced
strikingly
o As pregnancy progresses, ACTH and free cortisol rises
o Elevation in cortisol may be a result of “resetting” of the
maternal feedback mechanism to higher levels (Nolten
and Rueckert, 1981)
o In response to elevated progesterone levels during
pregnancy, an elevated free cortisol is needed to
maintain homeostasis (Keller-Wood and Wood, 2001)
2. Aldosterone – INCREASED
o As early as 15 weeks, maternal adrenal glands secrete
more aldosterone
o Sodium intake restriction increases aldosterone
secretion
o Increased aldosterone affords protection against the
natriuretic effect of progesterone and ANP.
3.
Deoxycorticosterone – INCREASED
o Due to increased kidney production from estrogen
stimulation
o There is transfer of fetal deoxycorticosterone into the
maternal compartment due to high levels in fetal blood.
4. DHEA-S – DECREASED (serum and urine)
o Due to increased metabolic clearance through
externsive maternal hepatic 16a-hydroxylation and
placental conversion to estrogen
5. Androstenedione and testosterone - INCREASED
o Maternal plasma androstenedione and testosterone are
converted to estradiol in the placenta
o Increase in plasma SHBG retards testosterone clearance
OTHER SYSTEMS
Musculoskeletal system

Progressive lordosis is observed. The lordosis shifts the
center of gravity back over the lower extremities.

Sacroiliac, sacrococcygeal and pubic joints have increased
mobility during pregnancy.

Joint mobility may contribute to the alteration of maternal
posture and may cause discomfort in the lower back.

Pelvic joints normally relax, particularly the symphysis
pubis. Most relaxation takes place in the first half of
pregnancy.

Symphyseal separation greater than 1 cm may cause
significant pain. Regression begins immediately follwing
delivery, and it is usually complete within 3 to 5 months.



Attention and memory were improved in women with
preeclampsia receiving magnesium sulfate compared with
normal pregnant women (Rana and associates, 2006).
Mean blood flow in the middle and posterior cerebral
arteries decreased progressively from non-pregnant state
to late in the 3rd trimester. Unknown clinical significance
(Zeeman and co-workers, 2003)
Pregnancy does not appear to impact cerebrovascular
autoregulation.
o Sleep
 Difficulty sleeping about 12 weeks to first 2
months postpartum with frequent awakening,
fewer hours of night sleep, and reduced sleep
efficiency.
 Decreased frequency and duration of sleep apnea
episodes during pregnancy compared postpartum
 Supine position, average Pa)2 levels were lower
 Greatest disruption of sleep is seen postpartum
and may contribute to postpartum blues or frank
depression
PRENATAL CARE
Definition

A comprehensive antepartum care program that involves a
coordinated approach to medical care and psychosocial
support that optimally begins before conception and
extends throughout the antepartum period. (AAP & ACOG,
2007)

A planned program of medical evaluation and management,
observation, and education of the pregnant woman directed
toward making pregnancy, labor, delivery and the
postpartum recovery, a safe and satisfying experience.

It should provide opportunities for the following:
o Physician and patient to be better acquainted
o Physician to learn something about the patient’s
emotional attitude toward pregnancy and labor
o Instruction for the patient and her husband in optimal
care for herself and the coming baby
o Optimal instruction of the patient and her husband in a
prepared childbirth program.
Components

Preconceptional care, Diagnosis of pregnancy, Initial
prenatal evaluation, follow-up prenatal visits
1. Diagnosis of pregnancy
o Established through signs and symptoms,
chorionic gonadotropin, ultrasound
recognition

Signs and symptoms of pregnancy
Sign or
Comments
symptom

Occurs 10 days after expected menses

One to two episodes of bloody discharge,
Cessation of
reminiscent of menstruation, can be due to
menses
blastocyst implantation or “implantation
bleeding”

Fern-like pattern – Day 7 to 18 of menses
due to increased NaCl when estrogen is
produced.
Eyes
Cervical

Beaded pattern – Day 21 menses or

Intraocular pressure decreases during pregnancy,
mucus
pregnancy due to decreased NaCl
attributed to increased vitreous outflow.
influenced by progesterone that prohibit

Corneal sensitivity is decreased, particularly late in
ferning
gestation

Breast tenderness and tingling

Slight increase in corneal thickness due to edema.

>2 months: increased breast size, delicate

Krukenberg spindles – brownish-red opacities on the
veins becomes visible, nipples larger &
posterior surface of the cornea – have been observed during
more pigmented, more erectile.
pregnancy.
Breast

Colostrum can be expressed. Areola

Visual function is unaffected by pregnancy, except for
changes
broader and deeply pigmented.
transient loss of accommodation.

Glands of Montgomery which are
hypertrophic sebaceous glands appear.
CNS

Breast striations may also appear

Women often report problems with attention,
Vaginal
Chadwick’s sign. Vaginal mucosa becomes dark
concentration, and memory throughout pregnancy and the
mucosa
bluish or purplish red and congested.
early postpartum period.

Striae gravidarum or stretch marks
Skin changes

Diastasis recti. Rectus muscles separate in
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




Changes in
the uterus



Changes in
the cervix






Fetal heart
tone
Fetal
movements



the midline.
Linea nigra. Brownish-black discoloration
of linea alba
Chloasma or melasma gravidarum (mask of
pregnancy)
Angiomas or vascular spiders. Minute, red
elevations on the skin of the face, neck,
upper chest and arms. Often designated as
nevus, angioma or telangiectasia.
Palmar erythema
First few weeks. Anteroposterior diameter
is increased.
12 weeks AOG: body of uterus becomes
globular, average diameter is 8 cm.
6 to 8 weeks AOG: Hegar’s sign is softening
of the isthmus.
Goodell’s sign. Softening of the cervix. The
consistency of the cervical tissue
surrounding the external os is more similar
to that of the lips of the mouth.
Cervical softening is also noted in women
taking estrogen-progesterone pills.
17 weeks: stethoscope
10 weeks: doppler equipment
5 weeks: transvaginal sonography
Fetal heart rate: 110 to 160 bpm
Other sounds heard in the pregnant
abdomen:
1. Funic souffle – rush of blood
through the umbilical arteries.
Sharp, whistling sound,
synchronous with fetal pulse.
2. Uterine souffle – soft, blowing
sound, synchronous with maternal
pulse. Heard at lower portion of
uterus produced by dilated
uterine arteries.
18-20 weeks: Primigravid
16-18 weeks: Multigravid
20 weeks: examiner can begin to detect
fetal movements.
Presumptive
Probable
Symptoms
Nausea, vomiting
Bladder
frequency/urgency
Perception of fetal
movement
Breast
enlargement
Symptoms
Abdominal
distention
Braxton-Hicks
Signs
Secondary
amenorrhea
Chadwick’s sign
Chloasma (face)
Linea nigra, striae
Spider
telangiectasia
Breast changes
Thermal changes
Signs
(+) Pregnancy test
Abdominal
enlargement
Outlining of the
fetal parts
Hegar’s sign
Goodell’s sign
Ballotment

Positive
Signs
Fetal heart tone
Perception of fetal
movement by
examiner
Ultrasound
evidence
Pregnancy Test
1. Chorionic gonadotrophin
2. Ultrasound recognition (Transvaginal ultrasound)
2. Initial prenatal evaluation

Major goals:
1. Define the health status of the mother and fetus.
2. Estimate the gestational age.
3. Initiate a plan for continuing obstetrical care.

Components of routine prenatal care (Williams
Obstetrics, 23rd edition)
COMPONENT
History
Complete PE
Blood pressure
Maternal weight
Pelvic/cervical exam
Fundal height
FHT & position
Hemoglobin (Hgb) &
Hct
Blood type & Rh
factor
Antibody screen
Pap smear
Urine protein
Urine culture
Rubella titer
Syphillis test (VDRL)
Hepatits B surface
Ag (HbsAg)
50 grams
OGCT/100g OGTT
Gonococcal or
Chlamydial culture
HIV
*High-risk women
First
visit
+
+
+
+
+
+
+
+
15-20
weeks
24-28
weeks
29-41
weeks
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
*
*
*
Components of Initial Prenatal Evaluation:
A. Prenatal Record
Terminologies for prenatal record:
a. Nulligravida. Woman who is NOT now and never has
been pregnant.
b. Gravida. Woman who is or has been pregnant,
irrespective of the pregnancy outcome. With the
establishment of first pregnancy, she becomes
primigravida, and with successive pregnancies, a
multigravida.
c. Nullipara. Woman who has never completed a
pregnancy beyond 20 weeks gestation.
d. Primipara. Woman who has been delivered only once a
fetus or fetuses born alive or dead with an estimated
length of gestation 20 or more weeks.
e. Multipara. Woman who has completed 2 or more
prenancies to 20 weeks or more. Parity is determined
by the number of pregnancies reaching 20 weeks and
not by the number of fetuses delivered.
f. Gestational age or menstrual age is calculated from the
first day of last menstrual period.
g. Ovulatory age or fertlization age, is 2 weeks shorter
than gestational age. Used by embryologists and other
reproductive biologists.
h. First trimester is from conception to 14 weeks
gestation. Second trimester is up to 28 weeks completed
gestation. Third trimester from 29th to 42nd week
gestation.
Normal pregnancy duration
1. Non-viable pregnancy is less than or equal to 20 weeks
gestation (140 days)
2. Viable pregnancy:

Preterm - >20 weeks to <37 weeks (141 to <259 days)

Term – 37 weeks to 42 weeks (259 – 294 days)

Post term - >42 weeks (294 days)
3. Term Pregnancy Categories (ACOG/SMFM: Replace Phrase
'Term Pregnancy' With 4
Categories. Medscape. Oct 22, 2013.)

Early term: 37 weeks to 38 weeks, 6 days – has 7-fold
higher risk for neonatal morbidity

Full term: 39 weeks to 40 weeks, 6 days

Late term: 41 weeks to 41 weeks, 6 days

Post term: 42 weeks and beyond
B.
History

Menstrual history

Psychosocial screening
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



Nonbiomedical factors that affect mental and physical
well-being.
Screening for barriers to care:
1. lack of transportation
2. child care or family support
3. unstable housing
4. unintended pregnancy
5. communication barriers
6. nutritional problems
7. cigarette smoking, substance abuse
8. depression
9. domestic violence
Cigarette Smoking: spontaneous abortion, low
birthweight due to preterm delivery or fetal growth
restriction, infant and fetal deaths (SIDS), placental
abruption, placenta previa, premature rupture of
membranes
Ethanol: potent teratogen and causes fetal alcohol
syndrome, characterized by growth restriction, facial
abnormalities and CNS dysfunction.
Illicit drugs include opium derivatives, barbiturates and
amphetamines which may cause fetal distress, low
birthweight.
Domestic violence refers to violence against adolescent
and adult females within the context of family or
intimate relationships.
Physical examination. Includes speculum and pap smear,
digital pelvic examination and rectal exams.
D. Laboratory tests. Refer to table above.

Iron status for women during pregnancy and the
postpartum period. (CPG on Iron Deficiency Anemia,
November 2009)
Iron
Iron
Iron
deficiency
deficiency
sufficiency
Without
anemia (IDA)
anemia
Hgb
110 Hgb
110 Hgb
<110
g/L
g/L
g/L
20 weeks
to delivery
Ferritin 12
Ferritin <12 Ferritin <12
ugL
ugL
ugL
Hgb
120 Hgb
120 Hgb
<120
g/L
g/L
g/L
6 months
postpartum Ferritin 15
Ferritin <15 Ferritin <15
ugL
ugL
ugL

Criteria for anemia in pregnancy by WHO and US CDC
(CPG on Iron Deficiency Anemia, November 2009)
Trimester
Anemia if Hgb is less than
1st: 0-12 weeks
11.0 g/dl
2nd: 13-28 weeks
10.5 g/dl
3rd: 29 weeks to term
11.0 g/dl
o
o
o
o
C.

Severity of anemia by WHO (CPG on Iron Deficiency
Anemia, November 2009)
Category
Severity
Hgb (g/dl)
1
Mild
9.5 – 10.5
2
Moderate
8.0 – 9.4
3
Severe
6.9 – 7.9
4
Very severe <6.9

Recommendations on Detection and Diagnosis of
Diabetes Mellitus among Filipino Pregnant Women (CPG
on Diabetes Mellitus in Pregnancy, November 2011)
o Diabetes mellitus recognized during pregnancy
should now be classified as either gestational
diabetes mellitus (GDM) or over diabetes mellitus
based on plasma glucose levels.
o Universal screening for GDM is recommended
for Filipino gravidas.
o At the first prenatal visit, determine if the gravid is
high risk or not based on historical and pregnancy
risk factors.
o ALL FILIPINO gravidas are considered “high risk”
by race or ethnic group (Pacific Islander) and
should be screened for type 2 diabetes mellitus in
the first prenatal visit (fasting blood sugar [FBS]
o
E.
or glycosylated hemoglobin [HbA1c] or random
blood sugar [RBS])
Diagnosis of OVERT DIABETES is given among
women with any of the following results in their
first visit.

FBS > 126 mg/dl (7 mmol/L)

RBS > 200 mg/dl (11.1 mmol/L)

HbA1c > 6.5%

2 hour 75 g OGTT > 200 mg/dl (11.1 mmol/L)
Diagnosis of GDM is made if any one (1) of the
following plasma values are exceeded:

FBS > 92 mg/dl (ADA/IADPSG/POGS

1 hour > 180 mg/dl

2 hour > 153 mg/dl (ADA/IADPSG) or > 140
mg/dl (WHO/POGS)
For Filipino gravidas with no other risk factors
aside from race or ethnicity and the initial test
(FBS, HbA1c or RBS) is normal, screening for GDM
should be done at 24-28 weeks using a 2 hour 75
gram OGTT. If there are other risk factors
identified, screening should proceed immediately
to 2 hour 75 gram OGTT at first consult.
If the OGTT at 24-28 weeks is normal, the woman
should be re-tested at 32 weeks or earlier if
clinical signs and symptoms of hyperglycemia are
present both in the mother and the fetus (e.g.
polyphagia, polyhdramnios, accelerated fetal
growth, etc)
OGTT should be performed in the morning after an
overnight fast of 8 hours following the general
instructions for the test.

Observe and overnight fast (at least 8 hours,
but no more than 14 hours) prior to testing.

Have an unrestricted diet (> 150 grams of
carbohydrates per day) for at least 3 days
prior to the testing

Remain seated and should not smoke during
the test.
High Risk Pregnancies.
3. Subsequent prenatal visits
A. Prenatal Visits

Traditional: every 4 weeks until 28 weeks, every 2 weeks
until 36 weeks, every week until term. High-risk every week
or as indicated.

WHO Model consists of a mean of 5 visits: once in first
trimester to screen for risk factors, then at 26, 32 and 38
weeks.
B. Prenatal Surveillance

Fetal surveillance: heart rate, size (current & rate of
change), amniotic fluid, presenting part and station (late in
pregnancy), activity

Maternal surveillance:
o Vital signs: BP, weight
o Symptoms: headache, altered vision, abdominal pain,
nausea and vomiting, bleeding, vaginal fluid leakage,
dysuria
o Abdominal Exam: fundal height
o Vaginal exam: confirms presenting part & station,
pelvic capacity, and cervical consistency, effacement
and dilatation
LEOPOLD’S MANEUVER

First maneuver answers the question:
“What fetal part occupies the fundus?”

Second maneuver answers the question:
“On what side is the fetal back?”

Third maneuver answers the question:
“What fetal part lies over the pelvic inlet?”

Fourth maneuver answers the question:
“On which side is the cephalic prominence?”
CHECK UTERINE SIZE

At 20-31 weeks, AOG correlates well with
Uterine size

At 12 weeks –palpable at level or just above of
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symphysis pubis
At 16 weeks- midway between symphysis
pubis and umbilicus
At 20 weeks- at the level of umbilicus


a.
b.
c.
d.
e.
C. Assessment of Gestational Age

Fundal height – between 20 and 34 weeks, the height of the
uterine fundus measured in centimeters correlates closely
with gestational age in weeks.

Ancillary tests: Gestational diabetes, chlamydial infection,
gonococcal infection, fetal fibronectin (vaginal fluid), GBS
infection, genetic diseases.

Weight gain based on the BMI.
Category
Underweight
Normal
Overweight
Obese
BMI
(Asia-Pacific)
<18.5
18.5 – 24.9
25 – 29.9
>30
BMI
(ACOG)
<19.8
19.8 - 26
26 - 29
>29
Kilograms
Pounds
12.5 - 18
11.5 - 16
7 – 11.5
5 – 9.1
28 – 40
25 – 35
15 – 25
11 - 20
III. Nutrition
Calories
Protein
Carbohydrates
Fats
Dietary fiber
2000 calories/day + 300 kcal/day (2nd & 3rd
trimester)
9 grams/day
Protein deficiency may lead to lowering of
hemoglobin-producing factors in the liver,
which may result in hypochromic anemia.
Absorption of calcium from intestinal tract
may be impaired.
Meats, mild and eggs are best sources of
protein.
150 grams/day in the first trimester.
225 grams/day at the end of pregnancy.
50-100 grams/day according to FNRI of the
Philippines (1989) is sufficient to prevent
ketosis and other symptoms of lack of dietary
carbohydrate.
Adequate carbohydrates seem to lessen
nausea and vomiting
15-25 grams/day
Most concentrated sources of energy,
providing more than twice the energy value of
an equivalent weight of carbohydrates or
protein.
No recommended level. Liberal intake of
fruits, vegetables and whole grain cereals is
highly recommended.
Promoting normal bowel functions and bulk
or satiety value to meals.
POSTPARTUM CHANGES
BREASTS & LACTATION
I. How breast milk protects babies against infection. (DOH,
1991)
1. Breastfed babies have less diarrhea than artificially-fed
babies.
2. Fewer respiratory and middle ear infection.
3. Fewer infections because of the following:
Breast milk is clean and free of bacteria
Contains antibodies (immunoglobulin) to many
common infections, until he can make his own
antibodies.
Contains white blood cells to help fight infection.
Contains bifidus factor which helps special bacteria
called Lactobacillus bifidus to grow in the baby’s
intestine. Lactobacillus bifidus prevents other
harmful bacteria from growing and causing
diarrhea.
Contains lactoferrin which binds iron. Prevents the
growth of some harmful bacteria which need iron.
II. Other advantages of breastfeeding. (DOH, 1991)
1. Breast milk contains lipase which digests fat. Breast milk
is quickly and easily digested and a breastfed baby may
want to feed again more quickly than an artificially-fed
baby.
2. Breast milk is always ready to feed to the baby and it
needs no preparation.
3. Breast milk never goes sour or bad in the breast even if a
woman does not feed her baby for some days.
4. Breastfeeding helps to stop bleeding after delivery.
5. Breastfeeding on demand helps to protect against another
pregnancy.
6. It helps them to bond, become attached to each other and
love each other.
7. It is free. You don’t have to buy it.
8. It is exclusively for your baby and cannot be served to
other adults.
Protective Effects on Infants of Human Milk and Breast
Feeding (AAP, 1997)
Decreased Incidence/Severity
Possible protective effects
Diarrhea
Sudden infant death
Lower respiratory infection
syndrome
Otitis media
Type-1 Diabetes
Bacteremia
Inflammatory bowel disease
Bacterial meningitis
Lymphoma
Botulism
Allergies
Necrotizing enterocolitis
Chronic digestive diseases
Urinary infections
III. Composition of Human Breast Milk
Component
Human milk
Water
Enough (87.2% to
87.5%)
Bacterial
None
contamination
Anti-infection
Antibodies,
substances
leucocytes,
lactoferrin, bifidus
factor
Protein (Total)
1%
0.5%

Casein
0.5%

lactalbumin
Amino acids Enough for growing
Cysteine
brain
Enough

Taurine
Fats (Total)
4% average

Saturation Enough
UNsaturated
Fatty acids –
Enough for growing
linoleic acid
brain
(essential)
Enough

Cholesterol
Lipase to digest fat
Present
Lactose (sugar)
7% (enough)
Salts (mEq/L) –
Sodium

Chloride

Potassium
Iron – colostrum

Mature milk
6.5
12
14
Cow milk
More required
Likely
Antibodies not
active, absent
lactoferrin
4% too much
3% too much
0.5%
Not enough
Not present
4%
Too much
saturated
Not enough
Not enough
None
3% - 4% (not
enough)
25 (too much)
29 (too much)
35 (too much)
0.5 – 0.8 mg/L
0.2 – 0.3 mg/L
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IV. Some Myths about Breastfeeding: (Thomson Medical
Center, Singapore. 2004)
1. It is painful & difficult to learn.
2. Breastfed babies cry more than bottle-fed babies.
3. Breastfeeding tends to isolate mother and baby from the
rest of the family members.
4. It is embarrassing.
5. Spoils a baby and weaning is difficult.
6. Quality of breast milk depends on your mood.
7. Breastfeeding mother may have to give up food she likes,
become tied down and be unable to work.
8. Breastfed babies need more water.
9. Breast milk lack iron.
V. How should breastfeeding begin. (DOH, 1991)
1. First feed
 First feed should be on the delivery table.
 Cover both mother and baby to keep them warm.
 Let the mother hold the baby close and let him suck at
the breast.
 Sucking stimulates the production of oxytocin which
helps to deliver the placenta and stop hemorrhage.
 Baby gets valuable colostrums.
 More likely to breastfeed for a long time. A delay of even
a few hours will result in failure to breasfeed.
2.
Rooming-in
There is no need for a mother and baby to rest
separately after a normal delivery.
3. Demand feeding
 Let the mother pick up her baby and feed him whenever
he cries and she feels a need to feed him.
 Frequent sucking stimulates the production of prolactin
which helps the milk to come in sooner.
 It prevents engorgement of breasts.

4.
Duration of feeds
More babies finish in 5-10 minutes, but some like to
take much longer, perhaps half an hour. It does not
matter.
 Slow feeders take the same total amount of milk as fast
feeders.
 Sucking in the wrong position causes sore nipples.

5.

6.


FAMILY PLANNING
Fertility Awareness-based (FAB) Methods

Family planning methods that attempt to identify fertile
time each cycle and then modify sexual behavior.

Natural family planning (NFP) refers to sexual abstinence
during the fertile time.

Fertility awareness-combined methods (FACM) refer to
using barrier method during the fertile time.

Various methods of periodic abstinence have pregnancy
rates estimated from 5 to 40 per 100 woman years. The
unwanted pregnancy rate during the first year of use is
approximately 20%.
I.




II.




III.


Feeding from both breasts
Let the baby finish the first breast to make sure that he
gets the hindmilk. Let him take the second breast if he
wants to, but do not force him.


Prelacteal feeds
Prelacteal feeds (e.g. formula, glucose water, ampalaya
juice, diluted honey) are NOT necessary and they can be
harmful.
 Small amount of colostrum is ALL that a normal baby
needs at this time.


7.
8.




9.


Extra water
 Normal baby is born with a store of water which keeps
him well hydrated until the milk comes in. He does not
need drinks of water, they interfere with breasfeeding.
Night breastfeeds
It is better if the mother breastfeeds the baby at night as
long as he wants to.
Night feeding helps to keep up the milk supply because
the baby sucks more.
Night feeds are especially useful for working mothers.
Night feeds are important for child spacing.
Early weight changes
A baby may lose weight for the first few days after
delivery. He may lose up to 10% of his birth weight.
 When breastfeeding is started, the baby should regain
his birth weight in ten days.

10. Cleaning the breast
Frequent washing, especially with soap, removes the
natural oil from the nipple.
The skin becomes dry and is more easily damaged and
fissured.


IV.



Standard Days Method
Developed by the Institute for Reproductive Health at
Georgetown University
Avoid unprotected intercourse during cycle days 8 through
19.
Women must have regular monthly cycles of 26 to 32 days.
Cycle beads can be used to keep track of their cycle.
Calendar Rhythm Method
Requires counting the number of days in the shortest and
longest menstrual cycle during a 6- to 12-month span.
First fertile day – 18 days are subtracted from the shortest
cycle.
Last fertile day – 11 days are subtracted from the longest
cycle.
This is problematic because ovulation most often occurs 14
days before the onset of the next menses. This is not
reliable.
Temperature Rhythm Method
The first scientific NFP method developed which involves
measuring changes in body temperature after ovulation.
Immediately after ovulation, basal body temperature, or the
body temperature at complete rest, dips slightly then rises
by about 0.2 C to 0.5 C (0.4 F). It remains high until just
before the next period.
Follow a biphasic pattern, it remains low before ovulation
and higher after ovulation which is caused by progesterone.
The woman has to take her temperature everyday, upon
waking up in the morning, before getting out of bed, and
after at least 3 hours of continuous sleep.
She may take her temperature by mouth (under the tongue)
or by the axilla, but she has to use the same route
throughout the menstrual cycle. The thermometer must be
left in position for 5 minutes.
She must record it on a chart after taking it and include
other events like illness.
A coverline or baseline is drawn using the highest
temperature reading from day 6 to 10 of cycle and watch
out for 3 consecutive temperature readings above the
coverline which refers to the thermal or temperature shift
indicating that ovulation has taken place.
The woman must abstain from intercourse from the first
day of menses through the 3rd day after the increase in
temperature.
With excellent compliance, the unwanted pregnancy is
approximately 2 percent the first year.
Cervical Mucus Rhythm Method
Also called “Billings method”, developed by John Billings,
depends on awareness of vaginal “dryness” and “wetness”.
These are the consequences of changes in the amount and
quality of cervical mucus at different times in the menstrual
cycle.
The fertile mucus is brought about byt increasing levels of
estrogen and the infertile mucus by the increase in
progesterone.
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





Dry days after the menses are the indicators of the
preovulatory phase or the first infertile phase, which are
relatively infertile days.
Wet days signal the ovulatory phase and are therefore
fertile days. The fertile type mucus is more copious,
slippery/lubricative, stretchy and wet. At times, it has the
appearance of raw egg white. This mucus makes it easy for
the sperm to travel through the cervix, uterus and the tubes
to meet the egg.
Last day of the wetness is called the peak day. Its timing is
around ovulation time. The 3 days after the peak day or the
post-peak days are still considered fertile days, giving
allowance for the life span of the egg.
Ovulatory phase includes all days when the wet sensation is
first felt, including the Peak Day and the 3 post-Peak days.
Abstinence is required from the beginning of menses until 4
days after slippery mucus is identified.
When used accurately, the first-year failure rate is
approximately 3 percent.
V.

Symptothermal Method
Combines the use of changes in cervical mucus – onset of
fertile period, changes in basal body temperature – end of
fertile period, and calculations to estimate the time of
ovulation.

One also has to look out for other bodily changes such as:
i.
Feel and position of the cervix
1. Fertile: the cervix is far from the vaginal opening
and is open and softer (consistency of the lips)
2. Not fertile: cervix is closed, firm (tip of the nose)
and close to the vulva
ii.
Ovulation pain (Mittelschmerz)
iii.
Mid-cycle bleeding or spotting
iv.
Breast sensitivity
v.
Skin changes
vi.
Mood changes

To avoid pregnancy, the couple abstains from vaginal
intercourse on:
i.
Alternate preovulatory days of no mucus or dry
mucus
ii.
On all days of wet mucus
iii.
The four days after the last day of wet mucus, or the
third day after temperature rise.
Contraceptive Failure Rates During the First Year of Use
(Modified from Speroff and Darney, 2001, and Trussell, 2004)
Method
Perfect Use
Typical Use
None
85
85
Calendar
9
20
Ovulation
3
Symptothermal
2
Post-ovulation
1
Withdrawal
4
27
Hormonal Contraceptives
I.
Combination hormonal contraceptives.
A. Mechanism of Action

Prevent ovulation by suppression of hypothalamic
gonodotropin releasing factors. Thus, prevents
pituitary secretion of FSH and LH.

Progestins action:
i.
Prevent ovulation by suppressing LH
ii.
Thicken cervical mucus, thereby retarding
sperm passage.
iii.
Render the endometrium unfavourable for
implantation.

Estrogen action:
1. Prevents ovulation by suppressing FSH
release.
2. Stabilizes the endometrium, which
prevents intermenstrual bleeding – also
known as breakthrough bleeding.
B. Composition

Monophasic pills – progestin dose remains
constant throughout the cycle.

Multiphasic (bi-, tri- or quadriphasic) pills – dose
frequently varied depending on the number of

dose changes within the cycle. Some formulations,
estrogen dose also varies.
ESTROGEN
o Features:

Daily estrogen content varies from 10 to
50 ug of ethinyl estradiol, and most
contain 35 ug or less to minimize adverse
effects.
o Forms:
1. Ethinyl estradiol – most common
2. Mestranol
3. Estradiol valerate
o

Side effects:
1. Breast tenderness
2. Fluid retention
3. Weight gain
4. Nausea
5. Headache
PROGESTIN
o Features:

Structurally related to progesterone,
testosterone, or spironolactone

Binds variably to progesterone,
androgen, estrogen, glucocorticoid, and
mineralocorticoid receptors which
explain pill-related side effects

Progestin related to testosterone may
impart androgenic side effects such as
acne and adverse HDL and LDL levels.
o Forms:
1. Medroxyprogesterone acetate – mainly
used in a progestin-only injectable form
2. Nomegestrol acetate – used in a COC
3. Norethindrone acetate – used in a COC;
non-acetate form used as progestin-only
4. Norgestrel
5. Norgestimate
6. Ethynodiol diacetate
7. Levonorgestrel
8. Desogestrel
9. Dienogest
10. Drospirenone

Structurally similar to spironolactone
and have similar effects to 25 mg of
this diuretic hormone.

Displays antiadrogenic activities

Provides antialdosterone action to
minimize water retention

Antimineralocorticoid properties that
may cause potassium retention and
hyperkalemia. Serum potassium level
monitoring for the first month is
recommended. Likeswise for the
following drugs:
 NSAIDS, ACE inhibitors,
angiotensin II antagonists,
herparin, aldosterone
antagonists, and potassiumsparing diuretics.

Avoided in women with renal or
adrenal insufficiency or with hepatic
dysfunction.
o PROGESTIN-ONLY side effects:

Irregular uterine bleeding, such as
metrorhhagia or menorrhagia (most
frequently reported)

DO NOT significantly affect lipid
metabolism, glucose level, hemostatic
factors, liver function, thyroid function,
and blood pressure.

NOT shown to increase risk for
thromboembolism, stroke, or CV disease.

DMPA use shows increased LDL and
decreased HDL and may be less favorable
with cardiac or vascular risks.

DO NOT impair mild production
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
C.
D.
NO increased risk of genital tract or
breast neoplasia

Weight gain and bone mineral density
loss are not prominent, except for DMPA

Functional ovarian cysts develop with
greater frequency.
Administration

COC’s are taken daily some for 21 days with 7 pillfree interval or placebo.

Some provide 24 days of hormones followed by 4
pill-free days (e.g. Yaz).

Ideally, women should begin on the first day of a
menstrual cycle.

There is a “quick start” method, wherein the pills
are started on ANY DAY, regardless of cycle timing.
A back-up method is used during the first week. If
the woman is already pregnant during Quick Start
initiation, COC’s ARE NOT TERATOGENIC.

For maximum efficiency, pills should be taken at
the same time each day.

Spotting or bleeding is common with initiation of
COCs. It does not reflect contraceptive failure and
typically resolves within one to three cycles.
Method-specific effects

Altered Drug Efficacy
o Three (3) groups of drugs that decrease COC
effectiveness:
1. Anti-TB drugs: rifampin and rifabutin
2. Anti-HIV drugs: efavirenz and ritonavirboosted protease inhibitors
3. Anticonvulsants: phytoin (Dilantin),
carbamazepine (Tegretol), oxcarbazepine
(Trileptal), barbiturates, primidone, and
topiramate (Topamax)

Metabolic changes
o COCs increase serum levels of triglycerides and
total cholesterol.
o Estrogen decreases LDL
o Estrogen increases HDL and VLDL
o OCP are NOT atherogenic
o Women with LDL >160 mg/dl or with multiple
additional risk factors for CV disease,
alternative methods are recommended.
o Estrogen use related to increase in fibrinogen
and may of the clotting factor levels and may
lead to thrombosis.
o COCs augment angiotensinogen production
and its conversion by renin to angiotensin I
which may be associated with “pill-induced
hypertension”
o COCs increase SHBG which decrease
bioavailable testosterone concentrations and
improve androgenic side effects.
o Risk of developing diabetes is NOT increased.
o NO connection beteween COCs and weight
gain.
o OCP use related to elevated total plasma
thyroxine (T4) and thyroid-binding proteins

Cardiovascular effects
o Women using low-dose COCs formulations
rarely develop clinically significant
hypertension.
o Patients are advised to return 8 to 12 weeks
after COC initiation for evaluation of blood
pressure and other symptoms.
o COCs are permissible in women with wellcontrolled uncomplicated hypertension who
are non-smokers, otherwise healthy, and
younger than 35.
o COCs use are NOT advisable for those with
severe forms of hypertension, especially with
end-organ involvement.
o Women with prior stroke or myocardial
infaction, COCs should NOT be considered.
o
o
o
o
o
o

E.
Nonsmoking women younger than 35 years
old has and extremely low risk of ischemic and
hemorrhagic strokes.
COCs may be considered for women with
migraines that lack focal neurological signs if
they are otherwise healthy, normotensive
nonsmkers younger than 35 years.
VTE with COC use is only 3 to 4 per 10,000
woman-years and is lower than the incidence
of 5 to 6 per 10,000 woman-years estimated
for pregnancy.
Clinical factors that increase VTE with COC
use:

Thrombophilias

Hypertension

Obesity

Diabetes

Smoking

Sedentary lifestyle
COCs are NOT recommended for women
within the first 4 weeks after delivery.
For all women, VTE risk with drospirenonecontaining COCs has been shown.
Neoplasia
o Overall, COCs are not associated with an
increased risk for cancer.
o Protective effect against ovarian and
endometrial cancer
o Relative risk of cervical dysplasia and cervical
cancer is increased in current COC users, but
following 10 or more years of disuse, risk
returns to that of never users.
o No evidence for increased risk of
hepatocellular cancer.
o Women with known tumores, COCs are
AVOIDED in those with benign hepatic
adenoma and hepatocellular carcinoma.
o Women who are carriers of the BRCA1 and
BRCA2 gene mutation, risks for breast cancer
are NOT INCREASED by COC use.
o COCs appear to lower rates of benign breast
disease.
Non-contraceptive benefits of COCs
1. Increased bone density
2. Reduced menstrual blood loss and anemia
3. Decreased risk for ectopic pregnancy
4. Improved dysmenorrhea from endometriosis
5. Fewer premenstrual complaints
6. Decreased risk of endometrial and ovarian cancer
7. Reduction in various benign breast diseases
8. Inhibition of hirsutism progression
9. Improvement of acne
10. Prevention of atherogenesis
11. Decreased incidence and severity of acute salpingitis
12. Decreased activity of rheumatoid arthritis
II.
Injectable Progestin Contraceptives

Intramuscular depot medroxyprogesteron acetate
(Depo-Provera or Depo-Trust), 150 mg every 3 months,
injected into the deltoid or gluteus muscle.

Mechanisms of action: ovulation inhibition, increased
cervical mucus viscosity, and creation of an
endometrium unfavourable for ovum implantation.

Initial injection should begin within the first 5 days
following menses onset. No back-up contraceptive is
required if initiated within 5 days of menses onset.
III.
Implants

Etonogestrel implant
o Thin, pliable progestin-containing cylinders that are
implanted subdermally and release hormone over
many years.
o Implanon

Single-rod implant with 68 mg of etonogestrel
covered by an ethylene vinyl acetate copolymer
cover.
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



Implant is placed subdermally on the medial
surface of the upper arm 8 to 10 cm from the
elbow in the biceps groove and aligned with the
long axis of the arm.
Provides contraception for 3 years and then
replaced at the same site or in the opposite arm.
Method-specific adverse effects
o Branches of the medial antebrachial cutaneous
nerve can be injured if the implant or insertion
needle is placed too deeply or if exploration for a
lost implant is aggressive.
o Numbness and paresthesia over the anteromedial
aspect of the forearm
o Nonpalpable devices may require radiological
imaging for localization
Insertion timing
o Etonogestrel implant: Ideally inserted within 5 days
of menses. If inserted later in the cycle, alternative
contraception is recommended for 7 days following
placement.
o Levonogestrel implant: Contraception is established
within 24 hours if inserted within the first 7 days of
the menstrual cycle.
o Transitioning methods:

On the day of the first placebo COC pill

On the day of the next DMPA injection

Within 24 hours of taking the last POP
o Inserted before discharge following delivery,
miscarriage, or abortion
Intrauterine devices (IUD)

IUD are “use and forget” effective reversible contraceptive
methods that do not have to be replaced for 5 or 10 years,
depending on the brand.

It is now better established that the major actions of IUDs
are contraceptive, NOT abortifacient.

Risk of pelvic infections is markedly reduced with the
currently used monofilament string and with techniques to
ensure safer insertion.

Risk of an associated ectopic pregnancy has been clarified.
Specifically, the contraceptive effect decreases the absolute
number of ectopic pregnancies by approximately 50%
compared with that of women not using contraception.
With failure, pregnancy is more likely to be ectopic.

Within the uterus, an intense local endometrial
inflammatory response in induced, especially by coppercontaining devices. Cellular and humoral components of
this inflammation are expressed in endometrial tissue and
in fluid filling the uterine cavity and fallopian tubes. These
lead to decreased sperm and egg viability.

With the LBG-IUS, in addition to an inflammatory reaction,
progestin release in long-term users causes glandular
atrophy and stromal decidualization. Progestins create
scant viscous cervical mucus that hinders sperm motility.
Problems with the above definitions:
1. Clinical estimation of blood loss is frequently inaccurate
and the brisk nature of blood loss during delivery or the
presence of amniotic fluid can make this more difficult.
2. Delay in obtaining laboratory results. Information from
laboratory tests would not reflect the patient’s current
hemodynamic status.
3. Any definition based on the need for transfusion is difficult
as there are differences in provider practice patterns
regarding transfusion.
Definition of obstetric hemorrhage combining clinical and
objective data (Bonnar, 2000)
Blood
Systolic
EBL
Heart
volume
BP
Signs & symptoms
(ml)
rate
(%)
(mmHg)
50010-15
<100
Normal
None
1000
1000 100Slight
Vasoconstriction,
15-25
1500
120
decrease
weakness, sweating
1500 120Restlessness, pallor,
25-35
80-100
2000
140
oliguria
2000Anuria, altered
35-45
>140
60-80
3000
consciousness
Etiology and Risk Factors
Etiology
Pathophysiology
Overdistended uterus
TONE
(Abnormal
uterine
contractility)
POST-PARTUM HEMORRHAGE (PPH)
Definition
The following are suggested definitions but there is a lack of
agreement on what constitutes excessive blood loss:
1. Blood loss >500 ml for vaginal delivery and 1,000 ml for
cesarean section (CS).
2. Blood loss >500 ml in the first 24 hours following delivery.
3. Ten percent (10%) decrease in hemoglobin or hematocrit
level.
4. Need for transfusion.
Chorioamnionitis
Uterine
distortion/abnormality
Uterine relaxing drugs
TISSUE
(Retained
products of
conception)
Accreta/Increta/Percre
ta
Retained
placenta/membranes
Laceration of the
cervix, vagina or
perineum
TRAUMA
(Genital tract
trauma)
Extension/laceration at
CS
Uterine rupture
Barrier Methods

Male Condoms

Diaphragm
Surgical Methods

Tubal ligation

Vasectomy
Uterine muscle fatigue
Uterine inversion
THROMBIN
(Abnormaliti
es of
coagulation)
Preexisting clotting
abnormalities (e.g.
hemophilia,
vonWillebrands
disease,
hypofibrinogenemia)
DIC
HELLP
Anticoagulation
Risk Factors
Multiple gestation
Polyhydramnios
Macrosomia
Prolonged labor
Augmented labor
Prior PPH
Prolonged rupture of
membranes (ROM)
Fibroids (myoma),
placenta previa
B-mimetics, MgSO4,
anesthetic drugs
Prior uterine surgery
Placenta previa
Multiparity
Manual placenta
removal
Succinturiate/accesso
ry lobe
Precipitous delivery
Macrosomia
Shoulder dystocia
Operative delivery
Episiotomy (e.g.
mediolateral)
Deep engagement
Malposition
Malpresentation
Prior uterine surgery
Fundal placenta
Grand multiparity
Excessive traction on
umbilical cord
History of
Coagulopathy or liver
disease
Sepsis
Intrauterine demise
Hemorrhage
General Management of PPH:
1. Initial management approach to obstetric hemorrhage:
a. Assessment: constant awareness of the hemodynamic
status as well as evaluation to determine the cause of
bleeding.
b. Breathing: administration of oxygen
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c.
2.
3.
4.
Circulation: obtaining intravenous (IV) access and
adequate circulating blood volume through infusion of
crystalloid and blood products. Second large-bore IV
catheter is needed
Notify the blood bank.
Simultaneous, coordinated, multi-disciplinary management
(OB-GYN, anesthesiologist, hematologists, radiologists,
nurses, laboratory and blood bank technicians) to concur
timely management in the presence of obstetric hemorrhage.
Preoperative preparedness is important especially for
patients identified as high risk.
Important Causes of PPH:
1. Uterine atony
2. Retained placenta
3. Uterine rupture
4. Genital tract trauma
5. Uterine inversion
DYSTOCIA
DYSTOCIA: PROBLEMS IN PASSENGER
Fetal Presentations and Conditions
1. Breech
2. External cephalic version
3. POP, OT
4. Brow and Face
5. Transverse/Oblique
6. Compound
7. Macrosomia
8. Shoulder dystocia
1. Breech

Planned CS has reduced risk for perinatal or neonatal
death/morbidity

Planned vaginal breech criteria:
o Skilled OB
o Facilities for possible CS available
o Woman is informed of risks
o EFW: 2500g to 4000g
o Continuous EFM
o Induction is NOT recommended. Oxytocin
augmentation if with hypotonic uterine dysfunction.
o Passive 2nd stage without active pushing for 90 min
allowing breech to descend into pelvis
o Once active pusching commences and delivery not
imminent after 60 min, CS is recommended.

Delivery of the aftercoming head:
o assistant should apply suprapubic pressure to favor
flexion and engagement of fetal head
o Mauriceau-Smellie-Veit maneuver, or
o Use of Piper forceps

Spontaneous or assisted breech delivery is acceptable. Fetal
manipulation applied after spontaneous delivery to the
level of umbilicus.

Nuchal arms may be reduced by Lovset maneuver.
Suspected breech
o Pre- or early labor ultrasound to assess type of breech,
fetal growth, EFW, attitude of fetal head.
o If ultrasound is not available, CS is recommended.
2. External cephalic version

ABSOLUTE Contraindications
o Where CS is required
o Anterpartum bleeding within the last 7 days
o Abnormal CTG
o Major uterine anomaly
o Ruptured membranes
o Multiple pregnancy (except delivery of the 2nd twin)

RELATIVE Contraindications
o SGA fetus with abnormal Doppler
o Proteinuric preeclampsia
o Oligohydramnios
o Major fetal anomalies
o Scarred uterus


o Unstable lie
Manipulation of the fetus through the maternal abdomen to
a cephalic presentation.
Use of tocolysis with beta sympathomimetics may increase
success rate of ECV
3. POP, OT

Factors for incomplete rotation of fetal head:
o Poor contractions
o Faulty flexion of head
o Epidural anesthesia – diminishes abdominal muscular
pushing & relaxes pelvic floor

Digital rotation of the fetus in the OP position.
4. Brow and Face
Brow
Expectant management, as long as FHR remains reassuring and
dilatation and descent are progressing normally.
Face

Continuous EFM is mandatory because of increased
incidence of abnormal FHR patterns and/or fetal
compromise

Oxytocin can be used to augment labor using the same
precautions

Forceps, using Kielland forceps, may be used if the mentum
is anterior.
5. Transverse/Oblique
Both will benefit from a trial of version to cephalic presentation
following the criteria & recommendation of ECV for breech.
6. Compound

If the hand has not prolapsed beyond the presenting part,
causing the hand to retract often is accomplished. It can be
ignored as long as labor is progressing normally

If the hand or arm has prolapsed past the presenting part,
CS delivery is wise.
7. Macrosomia

Macrosomia: 4000 g (8 lb 13 oz) or 4500 g (9 lb 4 oz)

Labor & vaginal delivery is NOT CONTRAINDICATED for
women with EFW up to 5 kg in the absence of maternal DM

Indication for CS:
o >4,500 g, and
o prolonged 2nd stage or arrest of descent in 2nd stage

Prophylactic CS:
o EFW > 5,000 g (w/o maternal DM)
o EFW > 4,500 g (w/ maternal DM)

Suspected macrosomia is NOT a contraindication to
attempted VBAC
8. Shoulder Dystocia
Shouder Dystocia Drill:
1. Call for HELP!
2. Generous EPISIOTOMY
3. SUPRAPUBIC pressure
4. McRoberts maneuver
If the “Drill” fails, attempt the following:
1. Delivery of posterior arm
2. Woods screw maneuver
3. Rubin maneuver
4. Zavanelli maneuver
5. Cleidotomy
6. Symphysiotomy
(supplementary)
“Shoulder dystocia drill” to better organize emergency
management:
1.
2.
Call for help—mobilize assistants and anesthesia and
pediat- ric personnel. Initially, a gentle attempt at traction is
made. Drain the bladder if it is distended.
A generous episiotomy may be desired to afford room
posteriorly.
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3.
Suprapubic pressure is used initially by most practitioners
because it has the advantage of simplicity. Only one assistant is needed to provide suprapubic pressure, while normal
downward traction is applied to the fetal head.
4. The McRoberts maneuver requires two assistants. Each
assistant grasps a leg and sharply flexes the maternal thigh
against the abdomen. This is the single most effective
intervention and performed first.
These maneuvers will resolve most cases of shoulder dystocia. If
the above listed steps fail, the following steps may be attempted,
and any of the maneuvers may be repeated:
5. Delivery of the posterior arm is attempted. With a fully
extended arm, however, this is usually difficult to
accomplish.
6. Woods screw maneuver is applied. Progressively rotating
the posterior shoulder 180 degrees in a corkscrew fashion,
the impacted anterior shoulder could be released.
7. Rubin maneuver is attempted.

First, the fetal shoulders are rocked from side to side by
applying force to the maternal abdomen.

If this is not successful, the pelvic hand reaches the most
easily accessible fetal shoulder, which is then pushed
toward the anterior surface of the chest. This maneuver
most often abducts both shoulders, which in turn produces
a smaller shoulder-to-shoulder diameter. This permits
displacement of the anterior shoulder from behind the
symphysis.

Other maneuvers:
o Zavanelli maneuver – replaces or flexes the fetal
head back into the vagina, then CS is performed.
o Cleidotomy – deliberate fracture of the anterior
clavicle to fee the shoulder impaction.
o Symphysiotomy – intervening symphyseal cartilage
and much of its ligamentous support is cut to widen
the symphysis pubis
GUIDELINES FOR CESAREAN SECTION
Indications
1. Previous uterine scar
2. Abnormalities of the reproductive tract
3. Abnormalities of placenta, cord, membranes & AF
4. Infection in pregnancy
5. Maternal medical conditions
6. IUGR/FGR
7. Fetal congenital anomalies
8. CDMR (Maternal request)
1.


Previous uterine scar
In the presence of scarred uterus, the following are
ABSOLUTE INDICATIONS for elective CS: (Level III, Grade C)
o Previous classical or inverted T-uterine scar
o Uncertainty of type of previous CS scar
o Previous multiple low transverse segment uterine
scars
o Previous hysterotomy or myomectomy entering the
uterine cavity or extensive transfundal uterine
surgery
o Previous uterine rupture
o Presence of a contraindication to labor, such as
placenta previa/accreta, or malpresentation
o No informed consent for VBAC
Failed trial of labor during VBAC.

CS performed for those with history of complete
transverse vaginal septum and vaginal agenesis due to
risk of vaginal soft tissue dystocia and lateral vault
laceration
3.
Abnormalities of the placenta, cord, membranes and
amniotic fluid
Vasa previa
o Elective CS between 35-37 weeks AOG
o Emergency CS for bleeding vasa previa
Placenta previa
o Any degree of placental overlap (>0 mm) at the
internal os after 35 weeks is an indication for CS
o Previa within 1 cm of the internal os is an indication
for CS
o Elective CS for asymptomatic woman with previa >37
weeks and for suspected accreta >36 weeks
Abruptio placenta
o Emergency CS for abruptio placenta with fetal
compromise, severe uterine hyprtonus, life
threatening bleeding or DIC, and remote from vaginal
delivery.
Cord prolapse
o Emergency CS for cord prolapse
o Cord prolapse with poor chances of viability, vaginal
delivery may be tried with informed consent
o Ultrasound finding suggestive of forelying cord or
funic presentation is NOT an absolute indication for
CS
o Digital diagnosis of funic/cord presentation in labor is
an indication for CS
Chorioamnionitis or intra-amniotic infection
o Presence of clinical chorioamnionitis or intra-amniotic
infection is NOT an absolute indication for CS.
Oligohydramnios
o Uncomplicated oligohydramnios is NOT an absolute
indication for CS






4.




Maternal medical conditions
Hypertensive complications
o Maternal indications

Deteriorating maternal condition

Uncontrolled hypertension despite drug therapy

HELLP syndrome


Placental abruptio
o Fetal indications

Severe IUGR/FGR


Non-reassuring FHR pattern, repeated Category
II or III, refractory with resuscitation, remote
from delivery


BPP <4, done 6 hours apart

Doppler studies: ARED


Severe bronchial asthma
o CS is rarely needed.
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2.

Abnormalities of the reproductive tract
Presence of gynecologic tumors in pregnancy, such as
uterine myoma and/or adnexal masses, are NOT ABSOLUTE
indications for CS, unless they cause dystocia
CS performed for those with a history of surgical repair of
obstetric and anal sphincters, urinary incontinence and
pelvic organ prolapse because of risk of recurrences
Genital warts and genital cancers may be an indication
for CS if it obstructs the birth canal, or if it is excessively
bleeding, or in order to prevent profuse bleeding
Presence of cervical stenosis is NOT A
CONTRAINDICATION to attempted vaginal delivery. There
is increased risk for CS.
Vaginal delivery for corrected imperforate hymen.
5.

Infection in pregnancy
Herpes simplex virus
o CS for those who develop primary genital herpes
within 6 weeks of delivery
o CS for those with active genital lesions or prodromal
symptoms (e.g. vulvar pain or burning) at the time of
delivery
Hepatitis B virus
o Scheduled CS at 39 weeks with HBV profile as follows:

HbeAg positive

HBV DNA copies >1,000,000

Not received oral antiretroviral therapy
Human papilloma virus
o Only for those with very large genital warts causing
pelvic outlet obstruction or potential for excessive
bleeding during vaginal delivery
HIV
o Elective CS at 39 weeks to reduce risk of MTCT
provided:

Currently on highly active antiretroviral therapy
(HAART)

Viral load <400 copies/ml

On any ARV with viral load <50 copies/ml
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



6.


7.


8.



9.
10.
11.
12.
Cardiac disease
o CS reserved for high-risk cardiac patients.
Gestational DM
Obesity
o Increased risk for CS
Macrosomia
IUGR/FGR
Deterioration in the fetal condition or when there is an
unripe cervix or when there are indications of additional
fetal compromise during labor
Viable fetus with IUGR when there is:
o deterioration in the BPP
o loss of variability on NST
o severe oligohydramnios, and
o failure to grow on serial biometry in the presence of
abnormal umbilical artery or venous Doppler studies.
Fetal congenital anomalies
Fetuses with the following anomalies may benefit from CS:
o Neural tube defects with fetus in breech
o Neural tube defects with sac >6 cm
o Cystic hygromas
o Sacrococcygeal teratomas >5 cm
o Hydrocephalus with BPD >10 cm or HC >36 cm
Elective CS
o Fetus with hypoplastic left heart syndrome
o Transposition of great arteries with intact
intraventricular septum that require urgent neonatal
atrial septostomy
Maternal request (CDMR)
If without clear indication or there is fear of childbirth, the
OB should provide counseling to the patient.
Well-written informed consent with proper approval by
the hospital’s ethics committee should be secured before
performing the CS.
Should be performed >39 weeks AOG, unless there is
documentation of fetal lung maturity.
Multiple pregnancy
Fetal malpresentation (Refer to Section III)
Abnormal labor patterns (Refer to Section II)
Abnormal FHR patterns (Refer to Section I)
Operative Recommendations
Timing of planned CS

Scheduled at 39 weeks
Pre-operative preparation for CS

Hemoglobin determination

Antimicrobial prophylaxis within 60 minutes preoperatively with either penicillins or cephalosporins (1st or
2nd gen) – Cefazolin 2g/IV (1st gen), Cefuroxime 1.5 g/IV
(2nd gen)

Alternative (if allergic): Clindamycin 600 mg/SIV

Morbid obese (BMI>35): double dose of antibiotic

Routine shaving not recommended. Clippers are
recommended than razors for excessive hair.
Techniques of CS

Transverse abdominal incision or Joel-Cohen incision is
preferred.

Placental delivery by controlled cord traction rather than
manual extraction

Blunt dissection of uterus was associated with reduced
mean blood loss compared to sharp dissection.

Single layer closure was associated with significant
reduction in mean blood loss, duration of operative time,
post-operative pain but more likely to result in uterine
rupture.

Closure of both visceral and parietal peritoneum after
CS lead to LESS adhesions

Closure of subcutaneous tissue for >2 cm subcutaneous
fat.

Indwelling FC may be removed <24 hours after CS

Uncomplicated elective CS may have modest amounts of
clear liquids up to 2 hours prior to induction of anesthesia

Patient undergoing elective surgery should have a fasting
period for solids at least 6-8 hours prior to induction.

Aspiration prophylaxis: non-particulate antacids, H2
receptor antagonists, metoclopramide
Post-CS care

No evidence to recommend a policy of delaying oral fluids
and food after CS

Remove the dressing 24 hours after the CS.

No evidence of adverse outcomes associated with early
postnatal discharge (3-4 days)

Sexual intercourse may be resumed as early as 2 weeks
postpartum for as long as the patient feels comfortable.
OTHER IMPORTNANT OBSTETRIC INFORMATION
DERMATOSES IN PREGNANCY
PITUITARY DESTRUCTION
Damage or necrosis of the pituitary gland caused by anoxia,
thrombosis, or hemorrhage. It is called Sheehan’s syndrome
when related to pregnancy and Simmonds’ disease when
unrelated to pregnancy.
OBSTETRICAL HEMORRHAGE
Anesthesia in CS
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o
Associated with exposure to drugs that block
the renin-angiotensin system (ACE inhibitors
and NSAIDs)
Pregnancy Outcomes
Increased risk of adverse pregnancy outcomes
o More likely to have malformations
o Higher levels of fetal stillbirth, growth
restriction, non-reassuring heart rate pattern,
meconium aspiration syndrome were aslo
noted
o Increased spontaneous/medically indicated
preterm birth
o Increased risk for CS for fetal distress and risk
for APGAR <7
o Pulmonary hypoplasia
Management
Target the underlying etiology
o Evaluate fetal abnormalities and growth
o Close fetal surveillance
o Amnioinfusion – may be used intrapartum in
the setting of variable fetal heart rate
decelerations, NOT considered a treatment or
a standard of care
Uterine Atony
The most frequent cause of obstetrical hemorrhage is failure of
the uterus to contract sufficiently after delivery and to arrest
bleeding from vessels at the placental implantation site
DYSTOCIA
Difficult labor, characterized by abnormally slow labor
progress
o Expulsive forces may be abnormal

Contractions are insufficiently strong
or inappropriately coordinated to
efface and dilate the cervix

Inadequate voluntary maternal
muscle effort
o Fetal abnormalities of presentation, position
or development may slow labor
o Abnormalities of the maternal body pelvis may
create a contracted pelvis
o Soft tissue abnormalities of the reproductive
tract may form an obstacle to fetal descent
Uterine Inversion
Puerperal inversion of the uterus is considered to be one of the
classic hemorrhagic disasters encountered in obstetrics. Unless
promptly recognized and managed appropriately, associated
bleeding often is massive. Risk factors include alone or in
combination:
1. Fundal placental implantation,
2. Delayed-onset or inadequate uterine contractility after
delivery of the fetus, that is, uterine atony,
3. Cord traction applied before placental separation, and
4. Abnormally adhered placentation such as with the accrete
syndromes
OLIGOHYDRAMNIOS
Causes of Oligohydramnios

Fetal abnormality
o Congenital abnormalities

By 18 weeks the fetal kidneys are the
main contributor to amniotic fluid
volume

Severely decreased amniotic fluid
volume beginning in early in
gestation are secondary to
genitourinary abnormalties

Other organ system anomalies can
also indirectly cause
oligohydramnios

Uteroplacental insufficiency

Post term pregnancies (most common)

Exposure to medications
INFECTIOUS DISEASES IN PREGNANCY
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mental and motor retardation,
sensorineural deficits,
hepatosplenomegaly, jaundice, hemolytic
anemia, and thrombocytopenic purpura
Group A
Streptococcus
Group B
Streptococcus
Late onset sequelae include hearing
loss, neurological deficits, chorioretinitis,
psychomotor
retardation, and learning disabilities
Remains the most common
cause of severe maternal postpartum
infection and death
worldwide
May cause preterm labor, prematurely
ruptured membranes, clinical
and subclinical chorioamnionitis, and fetal
infections.
GBS can also cause maternal bacteriuria,
pyelonephritis, osteomyelitis,
postpartum mastitis, and puerperal
infections.
MRSA
Listeriosis
Diagnosis
Varicella
Influenza
Mumps
Measles/Rubeola
German
Measles/ Rubella
Effects
Congenital varicella syndromechorioretinitis, microphthalmia, cerebral
cortical atrophy, growth restriction,
hydronephrosis, limb hypoplasia,
and cicatricial skin lesions
No firm evidence that it causes congenital
malformations
Women who develop mumps in the first
trimester may have an increased risk of
spontaneous abortion
The virus does not appear to be
teratogenic.
However, an increased frequency of
abortion, preterm delivery,
and low-birthweight neonates is noted
with maternal measles
Rubella infection in
the first trimester, however, poses
significant risk for abortion and
severe congenital malformations.
Rubella is one of the most complete
teratogens, and sequelae
of fetal infection are worst during
organogenesis.
Congenital Rubella Syndrome
• Eye defects—cataracts and congenital
glaucoma
• Congenital heart defects—patent ductus
arteriosus and
pulmonary artery stenosis
• Sensorineural deafness—the most
common single defect
• Central nervous system defects—
microcephaly, developmental
delay, mental retardation, and
meningoencephalitis
• Pigmentary retinopathy
• Neonatal purpura
• Hepatosplenomegaly and jaundice
• Radiolucent bone disease
Parvovirus B19
Cytomegalovirus
Associated with abortion, nonimmune
hydrops and still birth
Growth restriction, microcephaly,
intracranial calcifications, chorioretinitis,
Skin and soft tissue infections are the most
common presentation of MRSA in
pregnant women
Discolored, brownish, or meconiumstained amnionic fluid is common with
fetal infection, even preterm gestations
Maternal listeriosis causes fetal infection
that characteristically produces
disseminated granulomatous lesions with
microabscesses
Toxoplasmosis
Chorioamnionitis is common with
maternal infection, and placental lesions
include multiple, well-demarcated
macroabscesses.
Clinically affected neonates
usually have generalized disease
expressed as low birthweight,
hepatosplenomegaly, jaundice, and
anemia. Some primarily
have neurological disease with
intracranial calcifications and
with hydrocephaly or microcephaly. Many
eventually develop
chorioretinitis and exhibit learning
disabilities.
TRIAD: Chorioretinitis, intracranial
calcifications and hydrocephalus
APPENDICITIS IN PREGNANCY
-
Suspected appendicitis is one of the most common
indications for abdominal exploration during
pregnancy
When appendicitis is suspected, treatment is prompt
surgical exploration.
Although diagnostic errors may lead to removal of a
normal appendix, surgical evaluation is preferable to
postponed intervention and generalized peritonitis
o Appendicitis increases the likelihood of
abortion or preterm labor, especially if there
is peritonitis
PANCREATITIS IN PREGNANCY
Medical treatment is the same as that for nonpregnant
patients and includes analgesics, intravenous hydration,
and measures to decrease pancreatic secretion by
interdiction of oral intake.
LEIOMYOMAS IN PREGNANCY
Can regress after pregnancy
May cause pain or pressure
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-
May outgrow their blood supply and hemorrhagic
infarct follows- Red or Carneous Degeneration
Treatment is analgesic medication, myomectomy has
resulted in good outcomes
Pedunculated subserosal myosmas will undergo
torsion—can be managed with laparoscopy or
laparotomy
Complications
o Preter labor
o Placental abruption
o Fetal malpresentation
o Obstructed labor
o Cesarian delivery
o Postpartum hemorrhage
IMPORTANT GYNECOLOGIC CONCEPTS
BENIGN GYNECOLOGIC LESIONS BASED ON LOCATION
Vulva

Urethral Caruncles – small, single, sessile but may be
pedunculated, 1-2 cm in diameter. Occurs frequently in postmenopausal women, and may be secondary to infection or
chronic irritation

Cysts- the most common large cyst of the vulva is a cystic
dilatation of an obstructed Bartholin’s duct. The most
common small vulvar cysts are epidermal inclusion cysts or
sebacious cysts.

Nevus- vulvar nevi are one of the most common benign
neoplasms in females; generally asymptomatic

Hemangioma- rare malformations of blood vessesls than
true neoplasms. Usually discovered intitially during
childhood. It is usually single, 1-2 cm in diameter, flat, soft
and colors range from brown, red or purple. These tumors
range in size and not encapsulated

Fibroma- the most common benign solid tumors of the vulva.
It occurs in all age groups and commonly found in the labia
majora. Majority are 1-10 cm in diameter.

Lipoma- Benign, slow-growing, circumscribed tumors or fat
cells arising from the sub cutaneous tissue of the vulva
Vagina

Urethral diverticulum- permanent, epithelialized, sac-like
projection that arises from the posterior urethra, present at
a mass of the anterior vaginal wall. It is a common problem
discovered in 1-3% of women

Inclusion cysts- the most common cystic structures of the
vagina

Dysontogenic cysts- thin walled, soft cysts of embryonic
origin
o Gartner’s duct cysts – from the mesonephros
o Mullerian cysts – from the
paramesonephricum
o Vestibular cysts – fromt he urogenital sinus
Cervix

Endocervical and Cervical Polyps – Most common benign
neoplastic growth of the cervix. It is most common in
multiparous women in their 40s-50s. Majority are smooth,
soft, reddish purple to cherry red. They are fragile and
readily bleed when touched. It may arise to endocervical
canal or ectocervix

Nabothian cysts- retention cysts that are very common that
they are considered a normal feature of the adult cervix.
Aymptomatic and no treatment is necessary

Cervical myoma- usually a solitary growth, small and most
are asymptomatic
symptomatic to nulliparous women, highest occuring in 5th
decade. May cause miscarriage.
o Types

Intramural

Subserous- just beneath the serosa

Submucosal- just below the
endometrium, may be associated
with abnormal bleeding and
distortion of the uterine cavity that
may produce infertility or abortion

Broad ligaement

Parastic
o Myomas often enlarge during pregnancy
o Most common symptoms

Pelvic pain or pressure

Enlarging pelvic mass

Abnormal uterine bleeding (30%)
o Management

Judicious observation- for small
asymptomatic myomas

Myomectomy

Persistent pain/pressure

Enlargement to more than
8 cm to a woman who has
not completed childbearing

CONTRAINDICATION:
Pregnancy

Hysterectomy

Persistent pain/pressure

Size reached the size of a
14-16 week gestation

Medical Management – decrease the
circulating level of estrogen and
progesterone

Adenomyosis – from aberrant glands of the basalis layer
of endometrium. 50% are asymptomatic, but those who
are symptomatic present with dysmentorrhea,
menorrhagia ages 35-50
Oviduct

Leiomyomas

Angiomyomas

Paratubal cysts – if pedunculated and near the fimbrial end
of the oviduct, they are called hydatid cysts of Morgagni
Ovary

Fuctional cysts – All are benign and usually does not cause
symptoms or require surgical management
o Follicular cysts- most frequent cystic
structures in normal ovaries. Mostly
asymptomatic
o Corpus luteum cysts- minimum of 3 cm in
diameter, associated with normal, delayed
menses or amenorrhea. It may cause
intraperitoneal bleeding
o Theca lutein cysts- least common of the 3
physiologic ovarian cyts, almost always found
bilaterally, and can produce enlargement of
the ovaries. It is caused by prolonged or
excessive stimulation of the ovaries to
gonadotropins. USUALLY OCCUR WITH
PREGNANCY, INCLUDING MOLAR
PREGNANCY.

Benign neoplams
o Benign cystic teratoma (Dermoid cyst)- cystic
structures that on histologic examination
contain elemetns of the three germ cell layers.
Benign teratomas are among the most
common ovarian neoplasms, and are the most
common neoplasms in prepubertal females
and teenagers. When opened, sebacous fluid
along with hair, cartilage and teeth can be
found
o Endometriomas (Chocolate cyst) – usually
associated with endometriosis, and one of the
most common causes of the enlargement of
the ovary. It range to small (1-5 mm) to 5-10
Uterus

Endometrial polyps – localized overgrowths of endometrial
glands and stroma beyond the surface of the endometrium.
Majority are asymptomatic, but those who are symptomatic
are associated with a wide range of bleeding patterns

Hematometra – uterus distended with blood and secondary
to gynatresia. Common symptoms include amennorrhea and
cyclic lower abdominal pain

Leiomyomas/Myomas – most frequent pelvic tumor and the
most common tumor in women. More prone to grow and
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o
cm in diameter hemorrhagic cysts. Symptoms
include pelvic pain, dyspareunia and infertility
Fibromas- most common benign, solid
neoplasms of the ovary. Associated with
Meig’s syndome (Ovarian fibroma + ascites
+ hydrothrorax)
Brenner tumors (Transitional cell tumor)rare, small, smooth, fibroepithelial ovarian
tumors that are generally asymptomatic. 1-2%
undergo malignant changes. Histologically, it is
composed of solid masses/nests of epithelial
cells (similar to transition cells of the urinary
bladder) and surrounding fibrous stroma
Adenofibroma and Cystadenofibroma –
benign, firm tumors, consists of fibrous and
epithelial components
o
o
In relation to pregnancy:
The most frequent types of ovarian masses are corpus
luteum cysts, endometriomas, benign cystadenomas, and
mature cystic teratomas (dermoids)
TUMOR MARKERS
Marker
Serum CA125
GENETICS
MC
karyotype
Chromosom
al Origin
COMPLETE/CLASSI
C MOLE
PARTIAL/INCOMPLETE
MOLE
46, XX
69, XXY
All paternally
derived
Extra paternal set
CLINICAL PRESENTATION
Signs and
Abnormal vaginal
Symptoms
bleeding
Classic
Common
symptoms
Uterine size
50% large for
Gestational Age
Theca
Present in 25%
Lutein Cyst
hCG levels
High ( >100,000)
Malignant
15-25%
Potential
Weeks to
14 weeks
normal hCG
Missed abortion
Rare
Size equals date or
smaller
Rare
Slightly elevated
<5%
8 weeks
Description
Antigenic determinant, elevated in 80% of
patients with advanced epithelial ovarian
cancers, is elevated in most patients with
advanced or metastatic endometrial cancers
Also useful for monitoring epithelial ovarian
cancer. Seen in 50% with stage 1 ovarian
cancer
Alfafetoprotein
and hCG
Serum CA125 levels are useful in
distinguishing malignant from benign pelvic
masses
Both α -fetoprotein (AFP) and human chorionic
gonadotropin (hCG) are secreted by some
germ cell malignancies
Most endodermal sinus tumor (EST) lesions
secrete AFP
The mixed germ cell lesions may secrete either
AFP, hCG, or both or neither of these markers,
depending on the components
Inhibin is secreted by some granulosa cell
tumors
Inhibin
GESTATIONAL TROPOBLASTIC DISEASES
•
•
Refers to the pregnancy related trophoblastic
proliferative abnormalities
Classification:
•
Benign GTD
•
Complete mole
•
Incomplete mole
•
Malignant GTD
•
Persistent/ Invasive mole
•
Choriocarcinoma
•
Placental Site Tumor
COMPLETE/CLASSI
C MOLE
PATHOLOGY
Cause
Dyspermic
fertilization of an
empty egg by one
normal sperm
Coexistent
Absent
Fetus
Chorionic
Villi
Trophoblast
PARTIAL/INCOMPLETE
MOLE
Dyspermic fertilization
of a normal egg by 2
normal sperms
Present
Hydropic (swollen)
Focal hydropic
Severe hyperplasia
Minimal or none
CLINICAL DIAGNOSTIC FEATURES IN COMPLETE MOLE
•
Vaginal bleeding before 12 weeks
•
Most common symptom
•
Uterine enlargement out of proportion to AOG
•
Most common finding
•
Absence of fetal parts or fetal heart sounds
•
Classic signs and symptoms related to high level of hCG
(>100,000)
•
Pre-eclampsia/ eclampsia developing before
20 weeks
•
Hyperemesis gravidarum
•
Thyrotoxicosis
•
Presence of Theca Lutein Cysts
DIAGNOSIS
•
The measurement of HCG is an integral part of the
diagnosis and evaluation of the patient suspected of
having GTD.
•
Ultrasonography is the criterion standard for
identifying both complete and partial molar
pregnancies.
•
Complete Mole
•
Snow storm pattern
•
Homogenous intrauterine echoes
without a gestational sac or fetal
parts
•
Incomplete Mole
•
Swiss cheese pattern
•
CXR
•
Once a molar pregnancy is diagnosed get CXR
•
If with lung mets, CANNON BALL EXUDATES
BASIC APPROACH TO GTD
PreB- hCG titer
treatment
evaluation
CXR
Phases of
Suction D&C
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• Baseline for future
comparison
• To rule out lung metastasis
1. Immediate evacuation of
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treatment
Subsequent
Follow up and
evaluation
Prevention of
pregnancy
mole
2. Treatment of choice is
Suction D&C
3. Hysterectomy is preferred
if more than 35 YO or has
no desire for future
pregnancy
• Measure hCG every 2
weeks until 3 consecutive
negative values
• Once negative value, test
monthly for 6 months and
then every 2 months for a
total of 1 year
• A rise or plateau of hCG
demands evaluation
• 1 year of OCP to prevent
pregnancy

hypergonadotropic and hypogonadotropic
forms of hypogonadism
Treatment:
o Individuals with primary amenorrhea
associated with all forms of gonadal
ailure and hypergonadotropic hypogonadism
need cyclic estrogen and progestogen therapy
to initiate, mature, and maintain secondary
sexual characteristics.
MANAGEMENT OF AUB/DUB
Dysfunctional Uterine Bleeding
Describes abnormal bleeding for which no specific
cause was found; often a diagnosis of exclusion
Causes of Bleeding Per Age Group
ACTIVE THERAPY FOR H.MOLE
1. High levels > 4 weeks post evacuation
1. 20,000 IU/I - serum
2. 30,000 IU/I- urine
2. Histological evidence of choriocarcinoma at any site, or any
evidence of metastasis
3. Progressive increase in hCG at any time after the evacuation
GESTATIONAL TROPHOBLASTIC NEOPLASIA
•
Also called malignant gestational trophoblastic disease
•
Refers to:
•
Invasive mole
•
Choriocarcinoma
•
Placental site trophoblastic tumor
PERSISTENT/
INVASIVE
MOLE
CHORIOCARCINOMA
Placental Site
Trophoblastic Tumor
 75% of all GTD’s
 Usually follow a molar pregnancy
 Excessive trophoblastic overgrowth
and extensive penetration including
the whole villi, myometrium, and
adjacents tructures
 Very sensitive to chemotherapy
 Extremely malignant form of
trophoblastic tumor of the chorionic
epithelium
 Metastasize most of the time (lung)
 Extremely hemorrhagic and
necrotic with absence of villous
pattern, chorionic villi, and cellular
atypia
 Very sensitive to chemotherapy
 Extremely rare
 Arises from placental implantation
following either a nomal pregnancy
or abortion
 Predominantly cytotrophoblast and
cells secreting prolactin and
gonadotropin
 Low hCG level
 Hysterectormy is the treatment of
choice
GTN Diagnosis

Recognition of the possibility of GTN is the most important
factor in the diagnosis

Any unusual bleeding after term pregnancy should be
investigated by curettage and measurements of serum hCG
MANAGEMENT OF AMENORRHEA

The most important elements in the diagnosis of
amenorrhea include physical examination for secondary
sexual characteristics and anatomic abnormalities,

Measurement of:
o
human chorionic gonadotropin (hCG) to rule
out pregnancy
o serum prolactin and thyroid stimulating
hormone (TSH) levels
o assessment of follicle-stimulating hormone
(FSH) levels to differentiate between
Management

Laboratory
o Pregnancy test, CBC, Prothrombin time, PTT,
VWF

Imaging
o Ultrasound

Endometrial Sampling
o Performed for women at risk for endometrial
pathology (polyps, hyperplasia or carcinoma)

Management
o Mefenamic Acid and other NSAIDs
o Tranexamic Acid
o Mild bleeding: combination low-dose oral
contraceptive
o Acute moderate bleeding: combination
monophasic oral contraceptives every 6 hours
for 4-7 days
o Emergency management:

Hormonal therapy: Estrogenprogestin therapy 1-2 pills 2x/day
for 7 days effective for 12-24 hours
OR conjugated estrogens 25-40 mg
IV every 6 hrs or 2.5 mg oral every 6
hours

If intrauterine clots are detected D&C
is indicated
GENITOURINARY INFECTIONS and STDs
Diagnosis
Bacterial
Vaginosis
Description
Most common cause of
vaginitis in the US
Treatment
Metronidazole
Clindamycin
Women with BV are at risk for
PID, Pregnant women are at
risk for PROM, preterm labor
and delivery, chorioamnionitis
Trichomonas
Diagnosis: fishy vaginal odor;
clue cells in histology
Profuse, purulent, malodorous
vaginal discharge with
pruritus; Strawberry cervix
may be observed
Metronidazole
Women with this infection
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Candidiasis
Atrophic
vaginitis
Cervicitis
Pelvic
Inflammatory
Disease
should also be tested for other
STDs
75% of women may
experience this in their
lifetime. Predisposing factors:
pregnancy, diabetes, antibiotic
use. Discharge may be varied
from watery to thick
Common in menopausal
women
Presents with purulent
cervical discharge
Diagnosis implies that the
patient has upper genital tract
infection and inflammation
(ascended to the endometrium
and fallopian tubes)
Commonly caused by N.
gonorrhoeae and C.
trachomatis
Triad: pelvic pain, cervical
motion and adnexal
tenderness and fever
pathogen for acute cystitis
Topical azoles
(Butoconazole,
Clotrimazole,
Miconazole,
Tioconazole,
Nystatin,
Fluconazole)
Estrogen
cream
Treatment –
for lower
genital tract
infection with
both
chlamydia and
gonorrhea
Cefexime,
Azithromycin,
Doxycycline,
Ofloxacin,
Levofloxacin
Outpatient
treatment:
Cefoxitin or
Ceftriaxone
PLUS
Doxycycline or
Azithromycin
TMP-SMX,
Nitrofurantoin
Pyelonephritis:
TMP-SMX,
Levofloxacin,
Cetriazone,
Ampicillin,
Gentamicin
POLYCYSTIC OVARY SYNDROME
-
-
Characterized by a combination of hyperandrogenism
(either clinical or biochemical), chronic anovulation,
and polycystic ovaries. It is frequently associated with
insulin resistance and obesity
It is the most common cause of hyperandrogenism,
hirsutism, and anovulatory infertility in developed
countries
Criteria:
o Oligoovulation or anovulation
o Clinical and/or biochemical signs of
hyperandrogenism
o
Polycystic ovaries and exclusion of other
etiologies (congenital adrenal hyperplasia,
androgen-secreting tumors, Cushing’s
syndrome)
Inpatient
treatment:
Cefoxitin or
Cefotan PLUS
Doxycline
Or
Tubo-ovarian
Abscess
End stage process of PID
Genital
Ulcers
Those with genital ulcers may
have HSV or syphilis or
chancroid
Clindamycin
PLUS
Cefrtriaxone or
Gentamicin
Medical
treatment or
Abscess
Drainage
Chancroid:
Azithromycin,
Ceftriaxone,
Ciprofloxacin,
Erythromycin
HSV: Acyclovir,
Famciclovir,
Valacyclovir
Genital warts
Manifestation of HPV 51
(external)
Non-oncogenic HPV 6 and 11
also cause external genital
warts
Syphillis: Pen
G
Goal of
treatment is to
remove the
warts but it is
not possible to
eradicate the
infection
-
Highly contagious
UTI
E.coli is the most common
Cryotherapy,
Imiquimod
cream,
Podophyllin,
Podofilox,
Trichloroacetic
acid, Cautery,
Laser,
Interferon
Acute Cystitis:
-
Metabolic Syndrome Diagnostic Criteria
o Female waist >35 inches
o Triglycerides >150 mg/dL
o HDL <50 mg/dL
o Blood pressure >130/85 mmHg
o Fasting glucose: 110–126 mg/dL
o Two-hour glucose (75 gm OGTT): 140–199
mg/dL
Treatment
o Hormonal contraception or ovulation
induction
o Hirsutism: Weight loss, Oral contraceptives,
medroxyprogesterone, GnRH analogues,
glucorticoids, ketoconazole, finasteride,
spironolactone, flutamide, metformin
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AMBIGUOUS GENITALIA AND CONGENITAL ADRENAL
HYPERPLASIA
Ambiguous genitalia will be found in 1 in 14,000
newborns
Females with masculinized external genitalia will be
identified as female pseudohermaphrodites
Most common cause is Congenital Adrenal Hyperplasia
You may see clitoral enlargement and labial fusion
CONGENITAL ADRENAL HYPERPLASIA (CAH)
May be demonstrated at birth by the presence of
ambiguous genitalia in genetic females or present later
in childhood
Significant proportions of newborns with this
-
-
-
condition are also at risk for the development of
life-threatening neonatal adrenal crises as a result
of sodium loss because of absent aldosterone.
In milder disease, delayed diagnosis may result in
abnormalities of accelerated bone maturation,
leading to short stature.
The development of premature secondary sexual
characteristics in males and further virilization in
females may also occur
Treatment and Management
o Replacement of cortisol – suppresses
ACTH output and decreases the
stimulation of the cortisol producing
pathways in the adrenal cortex
o For females at risk – dexamethasone
o Corrective surgery
o Psychosocial support and counseling
IMPERFORATE HYMEN
Hypen should establish a connection between the
lumen of the vaginal canal and the vestibule
May result to primary amenorrhea
May cause hydrocolpos or mucocolpos- caused by
collection of secretions behind the hymen, and in rare
cases may build up to form a mass that obstructs the
urinary tract
May develop hematocolpos and hematometrium
overtime
Fallopian tubes can also be distended because the
menstrual flow may back up through the tubes
VAGINAL AGENESIS
Also called Mullerian agenesis or Mullerian aplasia
Usually associated with the Mayer-Rokitansky-KusterHauser (MRKH) syndrome
o congenital absence of the vagina and uterus
(in 75% of patients), although small masses of
smooth muscular material resembling a
rudimentary bicornuate uterus are not
uncommon
o Some patients have rudimentary uterine horns
o 50% have concurrent urinary tract anomalies
o Presents with primary amenorrhea
o PE findings shows a short vaginal pouch and
inability to palpare a uterus
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