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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD

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OBSTETRICS SUPPLEMENT HANDOUT


VESTIBULE
• Functionally mature female structure of the urogenital
TABLE OF CONTENTS
sinus of the embryo. Extends from clitoris to forchette
Maternal Anatomy 1
Menstrual Physiology 5 STRUCTURES IN THE VESTIBULE
Fertilization 9 HYMEN Non keratinized Stratified squamous
Placenta 10 epithelium
Fetal Development 11 During first coitus, first that ruptures is
Maternal Physiology 13 usually at the 6 o’clock position
Prenatal Care 19 Caruncle Myrtiformes: Remnants of hymen
Postpartum Changes 22 in adult female
Postpartum hemorrhage 26 GLANDULAR Periurethral Glands “ Skene’s Glands”
Dystocia 27 STRUCTURES Vulvovaginal Glands “Bartholin’s Glands”
Other Important Obstetric Information 29 6 OPENINGS: Vaginal introitus
Important Gynecologic Concepts 32 Urethral opening
Paired Para urethral glands opening
MATERNAL ANATOMY Paired Bartholin ducts opening

GLANDULAR STRUCTURES
EXTERNAL GENITALIA
PERIURETHRAL VULVOVAGINAL
SURFACE ANATOMY
GLANDS GLANDS
“ Skene’s glands” “Bartholin’s glands”
Structure
Other name Lesser vestibular Greater vestibular glands
Mons Pubis escutheon glands
Labia Majora 7-8x2-3x1-1.5cm Male Prostate Bulbourethral gland
round ligaments terminate at their upper homology
borders
Type of Tubulo alveolar Compound alveolar/
Labia Minora connective tissue with many vessels, elastin gland compound acinar
fibers, and some smooth muscle fibers Location Adjacent to the 4 and 8 o clock of the
urethra vagina
Clitoris points downward and inward toward the Pathology Urethral Bartholins’s cyst/
vaginal opening; rarely exceeds 2 cm diverticulum abscess
Vestibule 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
Vestibular Glands Bartholin glands, paraurethral glands
(Skene glands diverticulum) minor
vestibular glands
Urethral opening lower two thirds of the urethra lie
immediately above the anterior vaginal
wall.
1 to 1.5 cm below the pubic arch
Vestibular bulbs lie beneath the bulbocavernosus muscle on
either side of the vestibule
vulvar hematoma.
Vaginal Hymenal caruncles
opening/hymen Impreforate hymen

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)

Continuous lies deep to the perineal membrane and


space with extends up into the pelvis
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 wedge-shaped spaces found on either side of


fossae the anal canal and comprise the bulk of the
posterior triangle
Continuous space

Clinical Significance PUDENDAL NERVE AND VESSELS


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:
Boundary Landmark
dorsal nerve of skin of the clitoris
Anterior pubic symphysis
the clitoris
Anterolateral ischiopubic rami and ischial tuberosities
perineal nerve muscles of the anterior triangle and labial
Posterolateral sacrotuberous ligaments skin

posterior coccyx inferior rectal external anal sphincter, the mucous


membrane of the anal canal, and the perianal
skin
Triangle
Landmark for Ischial spine
Anterior Urogenital triangle pudendal nerve
Superficial Boundaries: block
and deep Superrior- pubic rami
Lateral-ischial tuberosities Blood Supply internal pudendal artery
Posterior: superficial transverse perineal
muscle VAGINA
Posterior Anal triangle H-shaped
ischiorectal fossa, anal canal, anal sphincter lower portion of the vagina is constricted (urogenital hiatus
complex, and branches of the internal in the levator ani)
pudendal vessels and pudendal nerve Stratified squamous non keratinized epithelium without
glands
Upper part is more capacious
Urogenital (Anterior) Triangle: SUPERFICIAL SPACE
It extends from the vulva to the cervix.
Anterior Triangle (SUPERFICIAL SPACE) Ruggae that has an accordion like distensability
Vaginal length:
closed bounded deeply by the perineal – Anterior wall: 6-8 cm
compartment membrane and superficially by Colles – Posterior wall: 7-10 cm
fascia
Potential space: Lower third
ischiocavernosus, bulbocavernosus, and
superficial transverse perineal muscles;
Bartholin glands; vestibular bulbs; clitoral
body and crura; and branches of the
pudendal vessels and nerve

ischiocavernosus clitoral erection


muscle

bulbocavernosus Bartholin gland secretion


muscles Clitoral erection

superficial may be attenuated or even absent


transverse perineal Contributes to the perineal body
muscles

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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD
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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

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
Upper vaginal vaults o SCJ at the endocervical canal
– Subdivided into anterior, posterior, and two lateral o Formation of transformation zone with regrowth of
fornices by the uterine cervix the squamous epithelium
Internal pelvic organs usually can be palpated through their
thin walls
UTERUS
Posterior fornix provides surgical access to the peritoneal
cavity
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 Attaches at the cornua


tubes

Posterior Completely covered by visceral peritoneum


wall

Anterior wall Only upper portion with peritonem


vesicouterine pouch

CERVIX
ENDOMETRIUM STRATUM FUNCTIONALE Zona
• Shed during Spongiosa
ENDOCERVIX EXOCERVIX menstruation Zona
Supravaginal portion Portio vaginalis • Supplied by the Spiral compacta
Extends from the isthmus (Internal Extends from the Arteries
Os) to the ectocervix and contains the squamo columnar • Superficial 2/3
endocervical canal junction to the external STRATUM BASALE
orifice • Source of Stratum
Single layer of mucous secreting Non keratinized Functionale after
highly ciliated columnar epithelium stratified squamous menstruation
which is thrown into folds forming epithelium • Supplied by the Straight
complex glands and crypts Hormone Sensitive arteries
Extensive amount of nerves Few nerves only • Basal 1/3
• lympathics
Blood supply: Cervicovaginal branch of uterine artery located at
the lateral walls MYOMETRIUM Inner Longitudinal
Middle oblique
Outer longitudinal
SEROSA lymphatics

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LIGAMENTS OF THE UTERUS Ovaries: LAYERS
Broad • Two wing-like structure that extend from OUTER Innermost Primordial and Graafian follicles
ligament the lateral margins of the uterus to the pelvic CORTEX portion in various stages of
walls development
• Divide the pelvic cavity into anterior and Outermost Tunica Albuginea- dull and
posterior compartments portion whitish fibrous connective
Reproductive Fallopian tubes tissue covering the surface of
structures ovaries the ovary
Vessels: Ovarian arteries Germinal epithelium of
Uterine arteries Waldeyer- a single layer of
Ligaments: Ovarian ligament cuboidal epithelium over the
Round ligament of Tunica Albuginea
uterus INNER Composed of loose connective tissue that is
Cardinal • AKA Transverse Cervical Ligament or MEDULLA continuous with that of the mesovarium.
ligament Mackenrodt Ligament Smooth muscle fibers that are continuous with
• Originated form the densest portion of the those in the suspensory ligament.
broad ligament Contains the stroma and blood vessels of the
• Medially united to the supravaginal wall of ovary
the cervix
• Provide the major support of the uterus and PELVIS
cervix
• Maintain the anatomic position of the cervix Pelvic Organs: BLOOD SUPPLY
and upper part of the vagina MAJOR BLOOD SUPPLY TO THE FEMALE REPRODUCTIVE
Uterosacral • From posterolateral to the supravaginal SYSTEM
ligament portion of the cervix encircling the rectum Pudenda Internal Pudendal artery
• Insert into the fascia over S2 and S3 Vagina Vaginal Artery of the Uterine
Round • Extend from the lateral portion of the uterus, Artery
Ligament arising below and anterior to origin of the Cervix Cervicovaginal branch of
oviducts, that is continuous with the broad Uterine artery
ligament, outward and downward to the Uterus Uterine Artery
inguinal canal terminating at upper Fallopian tubes Ovarian Artery
portion of labium majus Ovaries
PARTICIPANTS IN THE COLLATERAL CIRCULATION OF THE
FALLOPIAN TUBES FEMALE PELVIS
single layer of columnar cells, some of them ciliated and Branches from the Ovarian artery
others secretory. Aorta Inferior mesenteric
No submucosa Lumbar and vertebral
supplied richly with elastic tissue, blood vessels, and Middle sacral arteries
lymphatics Branches from the Deep iliac circumflex
Sympathetic innervation External Iliac Artery Inferior epigastric artery
Diverticula Branches from the Medial femoral circumflex artery
Femoral Artery Lateral femoral circumflex artery
SEGMENTS OF THE FALLOPIAN TUBE
Intramural Embodied within 2% of ectopic pregnancy
False ANT: lower abdomen
Interstitial the muscular Ectopic pregnancy at this
wall of the uterus area result in severe POST: lumbar vertebra
maternal morbidity
Isthmus The narrow Most highly developed LATERAL: iliac fossa
portion of the musculature
tube that adjoins Narrowest portion L INEA TERMINALIS
the uterus, Preferred portion for
True SUPERIOR BOUNDARY: Pelvic inlet
passes gradually applying clips for female
into the wider, sterilization INFERIOR BOUNDARY: Pelvic outlet
lateral portion. Preferred portion for tubal
ligation ANTERIOR: Pubic Bones, Ascending Rami Of Ischial
12% of ectopic pregnancy Bones, Obturator Foramina
Ampulla Widest and most Site of fertilization
tortuous area 80% of ectopic pregnancy LATERAL: Ischial Bones and Sacrosciatic Notch
Infundibulum Fimbriated 5% of ectopic pregnancy
extremity
Tunnel shaped
opening of the
distal end of the
fallopian tube

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 PARAMESONEPHRIC Appendix of Hydatid of
• Anterior: symphysis pubis/arcuate ligament of the pubis DUCT testes Morgagni
• Posterior: sacroiliac Uterus and
• Hormonal changes during pregnancy cause laxity of these Cervix
joints Fallopian Tubes
• By 3-5 months POST PARTUM, laxity has regressed Upper ¼ of the
• Symphysis Pubis increase in width also Increase mobility vagina
and displacement of the sacroiliac joint
MESONEPHRIC DUCT Appendix of Appendix of
WHY THE DORSAL LITHOTOMY POSITION? epidydymis vesiculosis
• Upward gliding of sacroiliac joint is GREATEST in the Ductus of Duct of
DORSAL LITHOTOMY POSITION epididymis epoophoron
• Outlet increase by 1.5 -2.0 cm Ductus deferens Gartner’s Duct
Ejaculatory duct
Seminal Vesicle
METANEPHRIC DUCT Ureter
URETERIC BUD Renal Pelvis
Calyces
Collecting system
METANEPHRIC Glomerulus
MESENCHYME Renal Collecting Tubules
UNDIFFERENTIATED Testes Ovary
GONAD
CORTEX Seminiferous Ovarian Follicles
tubules
MEDULLA Rete Testis Rete Ovarii
GUBERNACULUM Gubernaculum Round ligament
testis of uterus
PELVIC TENDENCY AND TYPE
• Anterior – dictates the tendency of the pelvis
• Posterior – dictates the type or character of the pelvis MENSTRUAL PHYSIOLOGY
GYNE-
ANDROID
ANTHROPOI PLATY- Overview of Menstrual Cycle
COID D PELLOID Spontaneous, cyclical ovulation occurs at 25- to 35-day
FREQUENCY 50% 20% 25% 5% rarest intervals
INLET SHAPE Round
Heart Vertically Horizontally Cyclical ovulation continues for almost 40 years between
Shaped oriented oval oriented oval menarche and menopause
Divergent, Approximately 400 opportunities for pregnancy, which
Convergen
SIDEWALLS Straight Convergent then
t may occur with intercourse on any of 1,200 days (includes
convergent
Non
day of ovulation and its two preceding days) during the
ISCHIAL Non reproductive age of most women.
promine Prominent Prominent
SPINES prominent Menstrual cycle days 20 to 24 is the narrow window of
nt
Inclined endometrial receptivity to blastocyst implantation.
Forward
neither Straight = Mother and fetus coexist as two disctinct immunological
and Well curved
anteriorl pelvis deeper systems because of modifications on both fetal and
SACRUM straight and rotated
y nor than other 3 maternal tissues in a manner not seen elsewhere.
with little backward
posterior types
curvature Endometrium-decidua is the anatomical site of blastocyst
ly
Increased apposition, implantation, and placental development.
incidence
of Deep Increased Key Players:
Good Transvers incidence of 1. Anterior pituitary
Poor
prognosi e Arrest Face Delivery a. FSH
SIGNIFICANC prognosis for
s for Limited Good b. LH
E vaginal
vaginal posterior prognosis for 2. Ovarian follicle
delivery
delivery space for vaginal
a. Theca cells
fetal head, delivery
poor b. Granulosa cells
prognosis 3. Estrogen
4. Progesterone
EMBRYOLOGIC STRUCTURES AND DERIVATIVES 5. Endometrium
a. Basalis
b. Functionalis
EMBRYOLOGIC MALE FEMALE
STRUCTURES
OVARIAN CYCLE
LABIOSCROTAL Scrotum Labia Majora
SWELLING Average cycle duration is approximately 28 days, with a
UROGENITAL FOLDS Ventral portion Labia Minora range of 25 to 32 days.
of the penis Follicular phase (days 1 to 14) is characterized by:
PHALLUS (GENITAL Penis Clitoris o Rising levels of estrogen
TUBERCLE) o Thickening of the endometrium
UROGENITAL SINUS Urinary bladder Urinary bladder o Selection of dominant “ovulatory” follicle
Prostate gland Urethral and Luteal phase (days 14 to 21), the corpus luteum (CL)
Paraurethral produces estrogen and progesterone, which prepare the
glands endometrium for implantation. If implantation occurs, the
developing blastocysts will begin to produce hCG and
Prostatic Utricle Vagina
rescue the CL, thus maintaining progesterone production.
Bulbourethral Greater
glands vestibular glands
Seminal Hymen
colliculus
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A. Follicular or preovulatory ovarian phase
FOLLICLE PROFILE HORMONE PRODUCTION
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 Ovarian steroid production:
is fertilization 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

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
Oocyte transforming growth factors: one another and move outward from the oocyte along the
1. Growth differentiation factor 9 (GDF9) hyaluronan polymer.
2. Bone morphogenetic protein 15 (BMP-15) 8. LH induces remodelling of the ovarian extracellular matrix
to allow release of the mature oocyte.
Functions: 9. Activation of proteases on weakening of the follicular
1. Regulate proliferation & differentiation of granulosa cells basement membrane and ovulation.
(GC) as primary follicles grow
2. Stabilize and expand the cumulus oocyte complex in the C. Luteal or postovulatory ovarian phase
oviduct
CORPUS LUTEUM
FOLLICLE DEVELOPMENT Key events:
1. Recruitment of primordial follicles. 1. Constant at 12 to 14 days.
2. Cohort will grow GC. 2. Luteinization occurs after ovulation when the CL
3. Selection of dominant follicle. develops.
4. Dominant follicle increase GC. 3. Basement membrane separating the granulosa-lutein and
5. Follicle produce estradiol & initiate expression of LH theca-lutein cells breaks down
receptors. 4. Day 2 postovulation, blood vessels and capillaries
6. Appearance of LH receptors. invade the granulosa cell layer.
7. GC secrete progesterone which will cause LH release. 5. Increased capacity of granulosa-lutein cells to produce
8. GC produce inhibin B to inhibit FSH release. progesterone is due to increased access to steroidogenic
9. Increase estradiol & inhibin production causes drop of FSH precursors through blood-borne LDL-derived
10. Drop of FSH causes failure of other follicles to develop. cholesterol.
11. LH stimulates theca cells to produce androstenediol. 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)

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10. CL is a transient endocrine organ that will rapidly
regress 9 to 11 days after ovulation.
LUTEOLYSIS A. Proliferative or preovulatory endometrial phase
Luteolysis may be due to the following: Features:
1. Decreased levels of circulating LH in the late luteal phase • Straight to slightly coiled, tubular glands are lined by
and pseudostratified columnar epithelium with scattered
2. Decrease LH sensitivity of luteal cells mitoses.
3. Apoptosis • Epithelial (glandular) cells, stromal (mesenchymal) cells
and blood vessels replicate cyclically.
Effects of luteolysis: • Functionalis layer is shed and regenerated from the deepest
1. Drop in circulating estradiol and progesterone levels. basalis layer almost 400 times during the reproductive
2. Allows follicular development and ovulation during the next lifetime of most women.
ovarian cycle • Day 5 of menses – the epithelial surface of the endometrium
3. Signals the endometrium to initiate molecular events that has been restored, and revascularization is in progress.
lead to menstruation.
Early proliferative phase:
D. Estrogen effects Endometrium is thin, usually < 2 mm thick
17B- estradiol is the most biologically potent naturally Glands are narrow, tubular structures that are almost a
occuring estrogen secreted by granulosa cells of the straight and parallel course from the basalis layer toward
dominant follicles and luteinized granulosa cells of the CL. the surface of the endometrial cavity.
Estrogen is the essential hormonal signal on which most Mitotic figures are identified by day 5 of cycle, and mitotic
events in the normal menstrual cycle depend. activity in both epithelium and stroma persists until day 16
Estrogen receptor (ER-alpha & ER-beta) interaction can to 17, or 2 to 3 days after ovulation.
promote synthesis of specfic m-RNAs and proteins (e.g. Epithelial cell growth is regulated in part by epidermal
estrogen and progesterone) growth factor (EGF) and transforming growth factor-alpha
Acts at endothelial cell surface to stimulate nitric oxide (TGF-a)
production, leading to its rapid vasoactive properties. Stromal cell proliferation appears to increase through
paracrine and autocrine action of estrogen and increased
E. Progesterone effects local production of VEGF, which causes angiogenesis
Progesterone enters cells by diffusion and in responsive through vessel elongation in the basalis.
tissues becomes associated with progesterone receptors ---
progesterone receptor type A (PR-A) and B (PR-B) Midproliferative phase:
PR-A can inhibit PR-B gene regulation. • Days 8-10
Both PR-A and PR-B are expressed in endometrial glands in • Columnar surface epithelium
the proliferative phase, such that both receptors are • Longer curving glands
involved with subnuclear vacuole formation. • Variable stromal edema
After ovulation, the glands continue to express only PR-B • Numerous mitotic figures
through the midluteal phase. In contrast, the stroma &
predecidual cells express only PR-A throughout the Late proliferative phase:
menstrual cycle. • Days 11-14
• Endometrium thickens from both glandular hyperplasia
and increased stromal ground substance.
ENDOMETRIAL CYCLE • Functionalis layer – glands are widely separated, loose
stroma is especially prominent.
LAYERS
• 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

B. Secretory or postovulatory endometrial phase


Early secretory phase:
Endometrial histologic features: • coiled glands with a slightly widened diameter
o Proliferative phase – straight to slightly coiled, tubular • lined by simple columnar epithelium that contains clear
glands are lined by pseudostratified columnar subnuclear vacuoles.
epithelium with scattered mitoses. • Luminal secretions are seen.
o Early secretory phase – coiled glands with a slightly Late secretory phase:
widened diameter are lined by simple columnar • serrated, dilated glands with intraluminal secretion are
epithelium that contains clear subnuclear vacuoles. lined by short columnar cells.
Luminal secretions are seen.
o Late secretory phase – serrated, dilated glands with Early secretory phase
intraluminal secretion are lined by short columnar cells. Dating based on glandular epithelium.
o Menstrual phase – fragmented endometrium with Day 17:
condensed stroma and glands with secretory vacuoles • glycogen accumulates in the basal portion of glandular
are seen in a background of blood. epithelium, creating subnuclear vaculoes and
Layers of endometrium pseudostratification (1st sign of ovulation)
o Basalis layer – supplied by straight artery Day 18:
o Functionalis layer – supplied by spiral artery • vacuoles move to the apical portion of the secretory
nonciliated cells
Day 19:
• cells begin to secrete glycoprotein and
mucopolysaccharide contents into the lumen;
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• glandular cell mitosis ceases with secretory activity.

Mid- to late-secretory phase Vasoactive peptides


Dating is based on endometrial stroma Endothelin-1 is a potent vasoconstrictor as a product of
Days 21 to 24: vascular endothelial cells.
• stroma becomes edematous o Degraded by enkephalinase, which is located in
• “window of implantation” endometrial stromal cells.
• epithelial surface cells show decreased microvilli and cilia o Increase in its activity parallels with the increase in
• appearance of pinopodes, luminal protrusions on the progesterone levels after ovulation
apical cell surface, in preparation for blastocyst o Enkephalinase activity is highest during the midluteal
implantation. phase and declines steadily thereafter as progesterone
Days 22 to 25: plasma levels decrease.
• stromal cells surrounding the spiral arterioles begin to
enlarge, and stromal mitosis becomes apparent. Activation of lytic mechanisms
• Predecidual transformation of upper 2/3 of functionalis Following vasoconstriction & endometrial cytokine
layer changes, activation of proteases (MMP-1 and MMP-3)
• Glands exhibit extensive coiling and luminal secretions within stromal cells and leukocyte invasion occurs to
become visible degrade the endometrial interstitial matrix.
Days 23 to 28:
• predecidual cells, which surround spiral arterioles Origin of menstrual blood
Spiral artery activity Arterial bleeding is appreciably greater than venous.
Endometrial bleeding appears to follow rupture of an
Arise from arcuate arteries, which are myometrial branches
arteriole of a coiled artery, with consequent hematoma
of the uterine vessels
formation.
Lengthen at a rate greater than the rate of increase in
With a hematoma, the superficial endometrium is distended
endometrial tissue height or thickness
and ruptures.
Rapid angiogenesis is regulated through estrogen- and
Fissures develop in the adjacent functionalis layer, and
progesterone-regulated synthesis of VEGF
blood, as well as tissue fragments of various sizes, are
Changes in blood flow through these vessels aid in
sloughed.
endometrial growth
Hemorrhage stops with arteriolar constriction as well as
Excessive coiling and stasis in blood flow coincide with
changes that accompany partial tissue necrosis.
regression of CL function and lead to a decline in
Endometrial surface is restored by growth of flanges, or
endometrial tissue volume
collars, that form the everted free ends of the endometrial
Coiling leads to endometrial hypoxia and necrosis
glands
Prior to endometrial bleeding, intense vasospasm occurs to
limit blood loss with menstruation
Interval between menses
Modal interval of menstruation is 28 days.
MENSTRUATION
Late premenstrual phase endometrium Decidua
• Stromal infiltration by neutrophils, giving a
Specialized, highly modified endometrium of pregnancy and
pseudoinflammatory appearance to the tissue
is a function of hemochorial placentation
• Endometrial stromal and epithelial cells produce IL-8,
which is a chemotactic activating factor for neutrophils, and Decidualization – transformation of secretory endometrium
serves to recruit neutrophils prior to menstruation to decidua; dependent on estrogen and progesterone and
• Invading leukocytes secrete enzymes that are members of factors secreted by the implanting blastocyst
the matrix metalloproteinase (MMP) family.
• Rising level of MMP’s tips the balance between proteases Structure
and protease inhibitors, effectively initiating matrix 3 parts
degradation. o Decidua basalis – directly beneath blastocyst
implantation, modified by trophoblast invasion
Anatomical events o Decidua capsularis – overlies the enlarging blastocyst,
and initially separates it from the uterine cavity.
Marked changes in endometrial blood flow
Prominent during the 2nd month of pregnancy.
Coiling of spiral arteries becomes sufficiently severe that
o Decidua parietalis – remainder of the uterine lining
resistance to blood flow increases strikingly, causing
o Decidua vera – when capsularis and parietalis are joined
hypoxia or the endometrium
later in pregnancy.
Resultant stasis is the primary cause of endometrial
By 14 to 16 weeks AOG – gestational sac completely fills the
ischemia and tissue degeneration.
uterine cavity and functionally obliterated.
Intense vasoconstriction & endometrial cytokine changes,
3 layers of decidua parietalis and basalis:
activation of proteases (MMP-1 & MMP-3)
o zona compacta – compact zone; part of zona functionalis
o zona spongiosa – spongy, middle portion, with
Prostaglandins & menstruation
remnants of glands and numerous small blood vessels;
Role of prostaglandin: part of zona functionalis
o Vasoconstriction o zona basalis – basal zone which remains after delivery
o Myometrial contractions and gives rise to new endometrium.
o Upregulation of pro-inflammatory responses
Progesterone withdrawal increases expression of inducible Reaction
COX-2 enzyme to synthesize prostaglandins and decrease Decidual reaction is completed only with blastocyst
expression of 15-hydroxyprostaglandin dehydrogenase implantation
(PGDH), which degrades prostaglandin Predecidual changes commence first during the midluteal
Increased prostaglandin production of stromal cells along phase in endometrial stromal cells adjacent to the spiral
with increased prostaglandin receptor density on blood arteries and arterioles.
vessels and surrounding cells. Endometrial stromal cells enlarge to form polygonal or
PGF2-alpha round decidual cells
o Vasoconstriction of spiral arteries, causing the Nuclei become round and vesicular, and the cytoplasm
uppermost endometrial zones to become hypoxic becomes clear, slightly basophilic and surrounded by a
o Potent inducer of angiogenesis and vascular pericellular membrane
permeability factors such as VEGF

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Pericellular matrix surrounding the decidual cells may
allow attachment of cytotrophoblasts through cellular
adhesion molecules.
Cell membrane also may provide decidual cell protection CLEAVAGE
against selected cytotrophoblastic proteases. Zygote cytoplasm is successively cleaved to form a blastula,
which consists of increasing smaller blastomeres
Blood supply At 32 -cell stage, the blastomeres form a morula, which
Spiral arteries in the decidua parietalis retain a smooth consists of an inner cell mass and outer cell mass
muscle wall and endothelium and thereby remain The morula enters the uterine cavity at about 3 days post
responsive to vasoactive agents that act on their smooth conception
muscle or endothelial cells.
Spiral arterioles and arteries are invaded by BLASTOCYST FORMATION
cytotrophoblasts. As a consequence, the walls of vessels in Occurs when fluid secreted within the morula forms the
the basalis are destroyed. These vascular conduits of blastocyst cavity
maternal blood, devoid of smooth muscle or endothelial Inner cell mass – future embryo, is now called the
cells, are not responsive to vasoactive agents. Embryoblast
The outer cell mass – future placenta, is now called the
FERTILIZATION Trophoblast

IMPLANTATION
EVENTS IN FERTILIZATION
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

TROPHOBLAST
Cytotrophoblast divide mitotically
Syncytiotrophoblast
o Does not divide mitotically
o Produces the HCG
o Continues its growth into the endometrium to make
1. The sperm binds to zona pellucida of the secondary oocyte contact with the endometrial blood vessels
and triggers the acrosome reaction, causing release of
acrosomal enzymes EMBRYO PERIOD: WEEK 3-8
2. Sperm penetrates the zona pellucida and unite with the
oocyte’s plasma membrane, eliciting the cortical reaction The beginning of the development of major organ systems
and rendering the secondary oocyte impermeable to other Coincides with the first missed menstrual period
sperm Period of high susceptibility to teratogen
3. Sperm and secondary oocyte cell membranes fuse and Gastrulation is a process that establishes the 3 primary
contents of the sperm enter the cytoplasm germ layers, forming a trilaminar embryonic disk
Male genetic material forms the male pronucleus o Ectoderm
Tail and mitochondria degenerate o Endoderm
4. Secondary oocyte completes meiosis II, forming a mature o Mesoderm
ovum. The nucleus of the ovum is the female pronucleus
5. The male and female pronuclei fuse to form a zygote DERIVATIVES
LAYER DERIVATIVES
POST CONCEPTION: WEEK 1 Ectoderm CNS and PNS
Sensory organs of seeing and hearing
1. Cleavage
Integument layer
2. Blastocyst formation
Endoderm Lining of the GIR and Respiratory tract
3. Implantation
Mesoderm Muscles
Cartilages
CVS
Urogenital System
RBC

EMBRYONIC PERIOD
Order of Formation
CNS First to develop and continues post natal
Heart Completed by 8 weeks
Upper limb Completed by 8 weeks
Lower limb Completed by 8 weeks
External genitalia Completed by 9 weeks

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o Fetal aspiration
o Exchange through skin and fetal membranes

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 Examples
Adequate and well-controlled human studies
have failed to demonstrate a risk to the fetus
A 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
B 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.
Fetal surface covered by amnion beneath which the fetal
Animal reproduction studies have shown an chorionic vessels course chorionic villi intervillous space
adverse effect on the fetus and there are no decidual plate myometrium
adequate and well-controlled studies in
C paroxetine
humans, but potential benefits may warrant FUNIS
use of the drug in pregnant women despite Umbilcal cord
potential risks. Two artery, one vein (left or right?)
There is positive evidence of human fetal risk Ave lenght: 55 cm
based on adverse reaction data from Wharton jelly- extracellular matrix of specialized connective
Phenytoin,
investigational or marketing experience or tissue
D tetracyclne,
studies in humans, but potential benefits may Anticlockwise spiral is present in 50 to 90 percent of
aspirin,
warrant use of the drug in pregnant women fetuses
despite potential risks.
Studies in animals or humans have PLACENTAL HORMONES
demonstrated fetal abnormalities and/or Trophoblast
there is positive evidence of human fetal risk Steroid hormones
based on adverse reaction data from Thalidomide, hPL, hCG, parathyroid hormone–related protein (PTH-rP),
X
investigational or marketing experience, and isotretinoin calcitonin, relaxin, inhibins, activins, and atrial natriuretic
the risks involved in use of the drug in peptide
pregnant women clearly outweigh potential hypothalamic-like releasing and inhibiting hormones:
benefits. thyrotropin-releasing hormone (TRH), gonadotropin-
releasing hormone (GnRH), corticotropin-releasing
PLACENTA hormone (CRH), somatostatin, and growth hormone–
FETAL TO MATERNAL MEMBRANES releasing hormone (GHRH).
Amnion
PLACENTAL STEROID HORMONES
o Avascular; provides tensile strenght; first identifiable
at 7th to 8th day of life; from fetal ectoderm Steroid Nonpregnant Pregnant
Chorion Estradiol-17 0.1–0.6 15–20
Decidua parietalis (endometrium) Estriol 0.02–0.1 50–150
Myometrium Progesterone 0.1–40 250–600
Serosa Aldosterone 0.05–0.1 0.250–0.600
Deoxycorticosterone 0.05–0.5 1–12
AMNIOTIC FLUID
Normal amniotic fluid volume Cortisol 10–30 10–20
o By 12 weeks = 60ml
o By 34-36 weeks = 1L hCG
o By term = 840 ml Almost exclusively produced by the placenta
o By 42 weeks = 540 ml Glycoprotein
Production of amniotic fluid Alpha and beta subunit
o Initially by amniotic epithelium Functions: rescue and maintenance of function of the
o Fetal kidneys and urine production corpus luteum, stimulates fetal testicular testosterone
*Amniotic fluid volume is also dependent on the extent of secretion, materanl thyroid gland stimulation (chorionic
maternal plasma expansion thyrotropins), promotion of relaxin secretion
Removal and regulation of amniotic fluid volume detectable in plasma of pregnant women 7 to 9 days after
o Fetal swallowing the midcycle surge of LH that precedes ovulation.
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Plasma levels increase rapidly, doubling every 2 days, with
maximal levels being attained at 8 to 10 weeks
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 Conditions that Affect Hormone Levels in Pregnancy


Source:
o First 6-7 weeks of pregnancy: Corpus luteum (ovary) Condition Findings
o After 8 weeks: Placenta (Syncytiotrophoblast)
Fetal Demise dec estrogen
Function:
o Affects tubal motility, the endometrium, uterine Fetal anencephaly Dec estrogen (estriol)
vasculature, and parturition
o Inhibits T lymphocyte–mediated tissue rejection Fetal adrenal hypoplasia absence of C19-precursors
Preferred precursor of progesterone biosynthesis by the
Trophoblast: Maternal plasma LDL cholesterol Fetal-Placental Sulfatase very low estrogen levels in
Deficiency otherwise normal pregnancies
ESTROGEN
Fetal-Placental Aromatase virilization of the mother and the
Pregnancy near term is hyperestrogenic
Deficiency female fetus
Produced exclusively by Syncytiotrophoblasts
Placenta produce all types of estrogen Trisomy 21—Down serum unconjugated estriol levels
Syndrome were low
ESTROGEN SOURCE
Estradiol Maternal ovaries for weeks 1 through 6 of Fetal Erythroblastosis Elevated
gestation Glucocorticoid Treatment Dec estrogen
After T1, the placenta is the major source of
circulating estradiol. Maternal Adrenal Dec estrogen
Estrone Maternal ovaries, adrenals, and peripheral Dysfunction
conversion in the first 4 to
6 weeks of pregnancy Gestational Trophoblastic placental estrogen formation is
The placenta subsequently secretes increasing Disease limited to the use of C19-steroids
quantities in the maternal plasma
Estriol Produced almost exclusively by the placental estrogen produced is principally
syncytiotrophoblast estradiol
Continued production depends on the living fetus
Marker of fetal well being
FETAL DEVELOPMENT

Terms
Perinatal Period beginning 20 weeks AOG and ending up to
period 28 completed days after birth
It is recommended that this period be defined as
commencing at BW of 500 grams

Neonatal Period after birth of an infant up to 28 completed


period days after birth

Fetal Begins from 8 weeks after fertilization or 10


period weeks after onset of last menses

Embryonic Commences beginning of the 3rd week after


period ovulation and fertilization and lasts up to 8 weeks
AOG
Placental Estrogen Production 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

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o Measures the actual age of the embryo from the time o Ductus venosus
of fertilization/ovulation o Foramen ovale
*A fetus that is 18 weeks AOG. What is the ovulation age? o Ductus arteriosus

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

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 Fetal Blood
of hair appear. HEMATOPOIESIS
external genitalia are beginning to show definitive signs o yolk sac – first site of hematopoiesis. embryonic
of male or female gender period
spontaneous movements. o Liver takes over up to near term
o Bone marrow starts at 4 mos AOG and remains as the
16 fetal crown-rump length is 12 major site of blood formation during adulthood
Gender can be determined by experienced observers by Erythrocytes – nucleated and have a shorter life span due
inspection of the external genitalia by 14 weeks. to their large volume and are more easily deformable
Quickening by multiparas Fetal blood volume (125 ml/kg)
20 fetus now weighs somewhat more than 300 g, and o Term infants = 80 ml/kg body weight
weight begins to increase in a linear manner. o Placenta = 45 ml/kg body weight
fetus moves about every minute and is active 10 to 30 Fetal Hemoglobin
percent of the time o Hemoglobin F
downy lanugo covers its entire body o Hemoglobin A (adult hgb)
o Hemoglobin A2
24 canalicular period of lung developmentis nearly
completed Fetal Circulation: CHANGES AFTER BIRTH
fat deposition begins Foramen ovale – functionally closed w/in several
fetus born at this time will attempt to breathe, but many minutes; anatomically fused 1 year after birth
will die because the terminal sacs have not yet formed Ductus arteriosus – functionally closed by 10-12 hours
after birth; anatomically closed by 2-3 weeks
28 crown-rump length is approximately 25 cm Ductus venosus constrict and becomes the ligamentum
skin is red and covered with vernix caseosa venosum
pupillary membrane has just disappeared from the eyes
born at this age has a 90-percent chance of survival Kleihauer-Betke test
Rationale:
36 CRL of 32
o Fetal RBC’s are resistant to denaturating effects of
deposition of subcutaneous fat
alkali.
40 average crown-rump length is about 36 cm o Mother’r RBC are sensitive, thus may hemolyze
weight is approximately 3400 g
FETAL PULMONARY SYSTEM
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
Presence of surfactant in the amnionic fluid is evidence of
FETAL CIRCULATION
fetal lung maturity (after 34 weeks)
3 vessels (AVA)
Surfactant is formed in the type II pneumocytes that line
o 2 arteries
the alveoli
o 1 vein
Starts to appear in the amniotic fluid at 28-32 weeks.
Three Shunts:
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90% lipid and 10% proteins
o Phosphatidylcholines (lecithin) account for 80% of the
glycerophospholipids
o Most active component – MATERNAL PHYSIOLOGY
dipalmitoylphosphatidylcholine (DPPC)
o 2nd most active - phosphatidylglycerol
CARDIOVASCULAR SYSTEM
Alveolar development = just before birth – 8 years old
Changes in cardiac function become apparent during the
SEXUAL DIFFERENTIATION 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.

A. 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.
Genetic/Chromosomal Sex
o XX or XY?
B. Cardiac Sounds
o Dependent on the presence of Y chromosome
Gonadal Sex Exaggerated splitting of the first heart sound with increased
o testes or ovaries? loudness of both components
o Dependent on the presence of SRY gene present on No definite changes in the aortic and pulmonary elements
the Y chromosome or the Testes Determining region of the second sound
Phenotypic Sex Loud, easily heard third sound
o Is it a penis or a vagina? Systolic murmur in 90% of pregnant patients which was
o Dependent on the hormones produced intensified during inspiration in some or expiration in
others, and disappeared shortly after delivery.

C. 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.

D. 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

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(angiotensinogen) is produced by both maternal and fetal compensated
liver. This increase in angiotensinogen results, in part, from respiratory alkalosis.
high levels of estrogen production during normal Residual
pregnancy. 1,000 800 Elevated diaphragm
volume
Expiratory
E. Cardiac natriuretic peptides reserve 700 550
Atrial natriuretic peptide (ANP) and B-type natriuretic volume
peptide (BNP) – are secreted by cardiomyocytes in Inspiratory
2,500 2,650
response to chamber-wall stretching. These peptides capacity
regulate blood volume by provoking natriuresis, dieresis, Inspiratory
and vascular smooth-muscle relaxation. reserve 2,050 2,050
During pregnancy, plasma ANP are maintained in the volume
nonpregnant range despite increased plasma volume. Functional
Median BNP levels are less than 20 pg/ml and are stable residual 1,700 1,350 Elevated diaphragm
across normal pregnancy. However, these levels are capacity
increased in severe preeclampsia. ANP-induced Vital
physiological adaptations participate in the expansion of 3,200 3,200
capacity
extracellular fluid volume and the increase in plasma
aldosterone concentrations characteristic of normal UNCHANGED
pregnancy. Respiratory rate is essentially unchanged.
C-type natriuretic peptide (CNP), is secreted by noncardiac Lung compliance is unaffected by pregnancy
tissues. This peptide appears to be a major regulator of fetal Maximum breathing capacity and forced or timed vital
bone growth. capacity are not altered appreciably

F. Prostaglandins INCREASED
Renal medullary prostaglandin E2 synthesis is increased Airway conductance is increased possibly as a result of
markedly during late pregnancy and is presumed to be progesterone
natriuretic. Amount of oxygen delivered into the lungs by the increased
Prostacyclin (PGI2), the principal prostaglandin of tidal volume clearly exceeds O2 requirements imposed by
endothelium, is increased during late pregnancy and pregnancy.
regulates blood pressure and platelet function. It also has Total haemoglobin mass, and in turn total oxygen-carrying
been implicated in the angiotensin resistance characteristic capacity, increases appreciably.
of normal pregnancy.

G. Endothelin DECREASED
Endothelin-1 is a potent vasoconstrictor in endothelial and Peak expiratory flow rates decline progressively as
vascular smooth muscle cells and regulates local vasomotor gestation advances.
tone. It stimulates secretion of ANP, aldosterone, and Total pulmonary resistance reduced possible as a result of
catecholamines. There are endothelin receptors in pregnant progesterone
and nonpregnant myometrium. They are also identified in Maternal arteriovenous oxygen difference is decreased due
the amnion, amniotic fluid, decidua, and placental tissue. to increased total oxygen carrying capacity.
Vascular sensitivity to endothelin-1 is not altered during
normal pregnancy. Vasodilating factors counterbalance the C. Acid-Base Equilibrium
endothelin-1 vasoconstrictor effects and produce reduced Blood Gas
peripheral vascular resistance. Non- First Second Third
pregnant trimester trimester trimester
H. Nitric Oxide HCO3 Not Not
22-26 16-22
It is a potent vasodilator released by endothelial cells and (mEq/L) reported reported
have important implication for modifying vascular PCO2 Not Not
resistance during pregnancy. 38-42 25-33
(mmHg) reported reported
PO2
PULMONARY SYSTEM 90-100 93-100 90-98 92-107
(mmHg)
A. Anatomic Changes 7.41 – 7.53
Diaphragm rises about 4 cm during pregnancy. 7.38 – 7.36 – 7.52 7.40 – 7.52 (v)
pH
Subcostal angle widens appreciably as the transverse 7.42 (a) (v) (v) 7.39 – 7.45
diameter of the thoracic cage increases approximately 2 cm. (a)
Thoracic circumference increases about 6 cm, but not (a) – arterial; (v) – venous
sufficiently to prevent a reduction in the residual lung
volume created by the elevated diaphragm Increased awareness of a desire to breathe early in
Diaphragmatic excursion is actually greater in pregnancy. pregnancy.
Physiologic dyspnea results from increased tidal volume
B. Pulmonary Function that lowers the blood PCO2 slightly, which paradoxically
causes dyspnea.
Lung Increased respiratory effort, and in turn the reduction in
Non- Term PCO2 is most likely induced in large part by progesterone
Volumes Etiology
pregnant Pregnancy and to a lesser degree by estrogen.
(ml)
Total lung Progesterone appears to act centrally, where it lowers the
4,200 4,000 threshold and increases the sensitivity of the
capacity
Resting minute chemoreflex response to CO2.
ventilation is also To compensate for resulting respiratory alkalosis, plasma
increased. Can be due bicarbonate levels decrease from 26 to approximately 22
to enhanced mmol/L
Tidal Although blood pH is increased only minimally, it does
450 600 respiratory drive due
volume shift the oxygen dissociation curve to the left. This shift
to stimulatory effects
of progesterone, low increases the affinity of maternal hemoglobin for oxygen,
expiratory reserve thereby decreasing the oxygen-releasing capacity of
volume and maternal blood.
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Slight pH increase also stimulates an increase in 2,3- Corpus luteum functions maximally during the first 6 – 7
diphosphoglycerate in maternal blood which shifts the weeks of pregnancy, produces progesterone.
curve back to the right. Reduced PCO2 from maternal Decidual reaction – elevated patches of tissue which bleed
hyperventilation aids CO2 (waste) transfer from the easily. Represents cellular detritus from the endometrium
fetus to the mother while also facilitating O2 release to that has passed through the fallopian tubes.
the fetus. Relaxin – protein hormone secreted by the corpus luteum,
deciduas and placenta. Remodelling of reproductive tract
REPRODUCTIVE SYSTEM connective tissue to accommodate pregnancy
A. Uterus
Non-pregnant weight of 70g to almost 1100 grams by term. D. Vagina & perineum
Non-pregnant capacity of 10 ml to a total volume of 5 to 20 Chadwick sign – increased vascularity affecting vagina and
liters by term results in violet discoloration
Uterine enlargement involves stretching and marked
hypertrophy of muscle cells, production of new myocytes SKIN
is limited. a. Abdominal wall
Accumulation of fibrous tissue, particularly in the external 1. Striae gravidarum or stretch marks
muscle layer, with an increase in elastic tissue to strengthen 2. Diastasis recti – rectus muscles separate in the midline
the uterine wall b. Hyperpigmentation – due elevated levels of melanocyte-
Uterine wall thins near term to only 1 to 2 cm. It becomes stimulating hormone; estrogen and progesterone have
soft and readily identable through which the fetus can be melanocyte-stimulating effects
palpated. Linea nigra
Uterine hypertrophy early in pregnancy probably is Chloasma or melasma gravidarum
stimulated by the action of estrogen and perhaps that of Pigmentation of areola and genital skin
progesterone. By 12 weeks, increase in size is related c. Vascular changes
predominantly to pressure exerted by the expanding Vascular spiders or angiomas – common on the face,
products of conception. neck, upper chest and arms
Uterine enlargement most marked in the fundus. Palmar erythema
Early months of pregnancy – fallopian tubes, ovarian and Increased cutaneous blood flow serves to dissipate
round ligaments attach slightly below the apex of the excess heat generated by increased metabolism
fundus
Later months of pregnancy – fallopian tubes, ovarian and METABOLIC CHANGES
round ligaments are located above the middle of the 3rd trimester – maternal basal metabolic rate is INCREASED
uterus by 10 to 20%
Portion of the uterus surrounding placental site enlarges WHO (2004) estimate of additional energy demands:
more rapidly. o 1st tri – 85 kcal/day
Arrangement of muscle cells: o 2nd tri – 285 kcal/day
o Outer hoodlike layer, which arches over the fundus o 3rd tri – 475 kcal/day
and extends into various ligaments
o Middle layer, dense network of muscle fibers a. Weight gain
perforated in all directions by blood vessels
Attributable to uterus and its contents, breasts, increase
o Internal layer, with sphincter-like fibers around the
blood volume and extracellular fluid
fallopian tube orifices and internal os of the cervix.
Accumulation of cellular water, fat and protein
o Main portion of the uterine wall is formed by the middle
Average weight gain is approx. 12.5 kg or 27.5 lbs
layer. Each cell in this layer has a double curve so that
the interlacing of any two gives approximately the form
b. Water metabolism
of a figure 8. When cells contract after delivery, they
constrict the penetrating blood vessels and act as 2. Increased water retention induced by resetting of osmotic
ligatures. thresholds for thirst and vasopressin secretion.
Pear shaped > globular form > spherical by 12 weeks > 3. Mimimum amount of extra water during normal pregnancy
ovoid shape (length more than width) = 6.5 liters
Displaces intestines laterally and superiorly o Amniotic fluid = 3.5 liters
o Maternal blood volume, uterus and breasts = 3.0 liters
Dextrorotation – uterus undergoes rotation to the right
4. Pitting edema of ankles and legs
because of the rectosigmoid on the left side of the pelvis.
o Increased venous pressure below the level of the uterus
There is tension exerted on the broad and round ligaments.
due to partial vena cava occlusion
Braxton Hicks contractions – unpredictable, sporadic and
o Decrease in interstitial colloid osmotic pressure
nonrhythmic contractons, every 10 to 20 minutes for some,
intensity between 5 and 25 mmHg.
c. Protein metabolism
Total uterine blood flow from uterine and ovarian arteries –
1. Fetus and placenta weigh about 4 kg and contain
450 to 650 mL/min
approximately 500 g of protein
2. Remaining 500 g is added to uterus, breasts primarily in the
B. Cervix
glands, and to hemoglobin and plasma proteins
Softening and cyanosis due to increased vascularity and 3. Nitrogen balance increased with gestational age
edema of the entire cervix, together with hypertrophy and 4. Maternal muscle breakdown is not required to meet
hyperplasia of cervical glands. metabolic demands.
Endocervical mucosal cells produce copious amounts of a
tenacious mucus that obstruct the cervical canal soon after d. Carbohydrate metabolism
conception.
Pregnancy is characterized by mild fasting hypoglycemia,
Cervical Mucus is rich in Ig and cytokines and may act as an
postprandial hyperglycemia, and hyperinsulinemia
immunological barrier to protect uterine contents against
Pregnancy-induced state of peripheral insulin resistance
infection.
occurs to ensure a sustained postprandial supply of glucose
Cervical mucus beading occurs as a result of progesterone.
to the fetus.
Arias-Stella reaction – endocervical gland hyperplasia and
o Progesterone and estrogen, may act, directly or
hypersecretory appearance
indirectly to mediate this insensitivity
o Placental lactogen may increase lipolysis and liberation
C. Ovaries
of free fatty acids. Increased free fatty acids may aid
Ovulation ceases and maturation of new follicles is increased tissue resistance to insulin
suspended.
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Pregnant women changes rapidly from a postrprandial state Hemoglobin & hematocrit DECREASE slightly
characterized by elevated and sustained glucose levels to a Whole blood viscosity DECREASES.
fasting state characterized by decreased plasma glucose and b. Iron metabolism
some amino acids 1. Storage
o Total iron content of normal adult women: 2.0 to 2.5
e. Fat metabolism grams. Most of this is incorporated in hemoglobin or
Lipids, lipoproteins and apolipoproteins increase myoglobin.
appreciably during pregnancy. o Iron stores of normal young women is approximately
Increased insulin resistance and estrogen stimulation are 300 mg
responsible for maternla hyperlipidemia
Increased lipid synthesis and food intake contribute to 2. Iron requirements
maternal fat accumulation during the first two trimesters. o Approximately 1,000 mg of iron is required for normal
During 3rd trimester, fat storage declines or ceases. This is pregnancy.
a consequence of enhanced lipolytic activity, and decreased a. 300 mg - actively transferred to the fetus and
lipoprotein lipase activity reduces circulating triglyceride placenta.
uptake into adipose tissue. This transition to a catabolic b. 200 mg – lost through normal excretion routes,
state favors maternal use of lipids as a source of energy and primarily in the GIT.
spares glucose and amino acids for the fetus. c. 500 mg – required for the increase in total
INCREASED levels during 3rd trimester: circulating erythrocyte volume (approx 450 ml)
o Triacylglycerol o The amount of dietary iron, together with that
o VLDL mobilized from stores, will be insufficient to meet the
o LDL average demands imposed by pregnancy.
o HDL
DECREASED levels after delivery: lipids, lipoproteins and 3. Puerperium
apolipoproteins o During vaginal delivery & the first postpartum days,
only approximately half of the added erythrocytes are
1. Leptin lost from most women.
o Primarily secreted by adipose tissue, some by placenta o Normal losses come from the following:
o Plays a role in body fat and energy expenditure a. Placental implantation site
regulation b. Episiotomy or lacerations
o May also help regulate fetal growth c. Lochia
o INCREASE and peak during the 2nd trimester and o Estimated blood loss:
plateau until term a. NSVD (singleton) – 500 to 600 ml
o Abnormally elevated leptin have been associated with b. CS or NSVD (Twin) – 1,000 ml
preeclampsia and gestational DM
c. Immunologic functions
2. Gherlin Suppression of various humoral and cell-mediated
o Secreted primarily by the stomach in response to immunological functions occur to accommodate the
hunger. “foreign” semiallogenic fetal graft.
o Cooperates with leptin in energy homeostasis Pregnancy is both a proinflammatory and antiinflammatory
modulation condition depending on the stage.
o Expressed also in placenta and likely has a role in fetal Three immunologic phases of pregnancy:
growth and cell proliferation. o Early pregnancy (pro-inflammatory)
Blastocyst must break through the uterine cavity
f. Electrolyte and mineral metabolism epithelial lining to invade endometrial tissue
Trophoblast must replace endometrium and
INCREASED DECREASED vascular smooth muscle of maternal blood
Iodine requirement Sodium vessels to secure adequate supply for the
Iron requirement Potassium placenta
Total serum calcium (ionized & Inflammatory environment is required to secure
non-ionized) cellular debris removal and adequate repair of
Serum magnesium the uterine epithelium
o Midpregnancy (anti-inflammatory)
HEMATOLOGIC CHANGES Period of rapid fetal growth and development
o Parturition (recrudescence of inflammatory process)
a. Blood volume
Influx of immune cells into the myometrium
Hypervolemia averages 40 to 45% above nonpregnant Suppressed activity:
blood volume after 32 to 34 weeks o T-helper (Th) 1 cells
Functions of hypervolemia: decreases secretion of IL-2, interferon-g, and
o Meets the metabolic demands of the enlarged uterus TNF-B
and its greatly hypertrophied vascular system suppressed Th1 response is requisite for
o Provides abundant nutrients and elements to support pregnancy continuation
the rapidly growing placenta and fetus suppressed Th1 during pregnancy results in
o Protects the mother and fetus against the deleterious remission of some autoimmune disorders such
effects of impaired venous return in the supine and as rheumatoid arthritis, multiple sclerosis, and
erect positions Hashimoto thyroiditis
o Safeguards the mother against the adverse effects of failure of Th1 suppression may be related ot
parturition-associated blood loss development of preeclampsia
Maternal blood volume expands most rapidly during the o T-cytotoxic (Tc) 1 cells
second trimester. Decreases secretion of IL-2, interferon-g, and
Blood volume expansion results from an increase in both TNF-B
plasma and erythrocytes. Upregulated activity:
Moderate erythroid hyperplasia is present in the bone o Th2 cells – increase secretion of IL-4, IL-6 and IL-13
marrow o IgA and IgG in cervical mucus increase
Reticulocyte count is elevated slightly. o IL-1B in cervical and vaginal mucus is increased during
Elevated maternal plasma erythropoietin levels – peaks the 1st trimester
early during the 3rd trimester and corresponds to maximal Vitamin K-dependent glycoprotein that inhibits activation
erythrocyte production. of factor X
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Low levels may prove to be a risk factor for otherwise b. Ureters
unexplained recurrent early pregnancy loss (Effraimidou Uterus rests upon ureters and laterally displaces it and
and associates, 2009) compresses them at the pelvic brim
Right ureter is dilated more than the left due to a
URINARY SYSTEM dextrorotated uterus and the right ovarian vein complex
a. Kidney lies obliquely over the right ureter.
Ureteral elongation and curvature formation occurs due to
RENAL CHANGES IN NORMAL PREGNANCY distention
Parameter Alteration Clinical relevance
Kidney size Approximately 1 cm Size returns to normal c. Bladder
longer of radiograph postpartum Bladder trigone is elevated by (>12 weeks):
Dilatation Resembles Can be confused with o Increased uterine size
hydronephrosis on obstructive uropathy; o Hyperemia
sonogram or IVP Retained urine leads o Hyperplasia of bladder’s muscle and connective tissue
(more marked on to collection errors; Note: Elevation of trigone causes thickening of posterior, or
right) Renal infections are intraureteric origin
more virulent;
May be responsible No mucosal changes
for “distention Increase in size and tortuosity of its blood vessels
syndrome”; Bladder pressure (primigravidas) increased from 8 cm H20
Elective pyelography (early pregnancy) to 20 cm H20 (at term).
should be deferred to Absolute and functional urethral lengths INCREASED
at least 12 weeks Maximal intraurethral pressure INCREASED from 70 to 93
postpartum cm H20, thus continence is maintained
Renal GFR & renal plasma Serum creatinine End of pregnancy changes:
function flow increase ≈ 50% decreases during o Entire base of blader is pusched forward and upward,
normal gestation converting normal convex surface to concave due to
(>0.8 mg/dl creatinine presenting part
already borderline); o Pressure of presenting part impairs drainage of blood
Protein, amino acid, and lymph from the bladder base which may lead to
and glucose excretion edema, and susceptibility to trauma and infections
all increase
Maintenance Decreased Serum bicarbonate GASTROINTESTINAL TRACT
of acid-base bicarbonate threshold; decreased by 4-5 Appendix displaced upward and laterally as the uterus
Progesterone mEq/L; enlarges, and it may reach the flank
stimulates respiratory PCO2 decreased 10 Gastric emptying time is UNCHANGED. During labor and
center mmHg; administration of analgesic agents, it becomes prolonged.
PCO2 or 40 mmHg General anesthesia may cause regurgitation and aspiration
already represents during delivery.
CO2 retention Pyrosis (heartburn) – reflux of acidic secretions into the
Plasma Osmoregulation Serum osmolality lower esophagus due to:
osmolality altered; decreases 10 mOsm/L o Altered position of of the stomach
Osmotic thresholds (serum Na ≈ 5 mEq/L) o Decreased LES tone
for vasopressin (AVP) during normal o Intraesophageal pressures are lower compared to
release and thirst gestation intragastric pressures
decrease Increased placental o Esophageal peristalsis has lower wave speed and lower
Hormonal disposal metabolism of AVP amplitude
rates increase may cause transient Gums may become hyperemic and softened and may bleed
diabetes insipidus when mildly traumatized as with a toothbrush
during pregnancy.
Epulis of pregnancy – focal, highly vascular swelling of the
gums but regresses spontaneously after delivery.
1. Loss of nutrients
Pregnancy DOES NOT incite tooth decay.
o Amino acids and water-soluble vitamins are lost in
Hemorrhoids are fairly common due to constipation and
urine in greater amounts
elevated pressure in veins below the level of the enlarged
uterus.
2. Tests of renal function
o Serum creatinine – DECREASED. Values above 0.9 mg/dl
a. Liver
suggest underlying renal disease and prompt
investigation NO INCREASE in liver size
o Creatinine clearance – INCREASED about 30% Hepatic blood flow and diameter of the portal vein is
INCREASED
3. Urinalysis Increased levels:
o Glucosuria – may NOT be abnormal. It can be due to o Total alkaline phosphatase – almost doubles
increase in GFR, together with impaired tubular o Total albumin
reabsorptive capacity for filtered glucose. About 1/6 of o Serum globin
pregnant women spill glucose, but the possibility of DM Decreased levels:
should not be ignored. o AST
o Proteinuria – NOT evident during pregnancy except o ALT
occasionally in slight amounts during or soon after o GGT
vigorous labor. o Bilirubin
o Albumin excretion is minimal and ranges from 5 to 30 o Serum albumin
mg/day Leucine aminopeptidase activity is markedly INCREASED.
o Hematuria is often a result of contamination during This is increased with liver disease.
collection. Common after difficult labor and delivery
because of trauma to the bladder and urethra. b. Gallbladder
Progesterone inhibits CCK-mediated smooth muscle
stimulation which impairs gallbladder contraction

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Impaired/reduced gallbladder contraction leads to b. Thyroid gland
increased residual volume, and stasis with associated Thryroid hormone production INCREASED by 40 to 100%
increased bile cholesterol saturation of pregnancy to meet maternal and fetal needs
contributes to increased prevalence of gallstone in Thyroid gland undergoes moderate enlargement as a result
multiparous women. of glandular hyperplasia and increased vascularity. Volume
Intrahepatic cholestasis in pregnancy has been linked to increase from 12 ml (first trimester) to 15 ml (at term)
high circulating levels of estrogen, which inhibit intraductal Normal pregnancy does not typically cause significant
transport of bile acids. thyromegaly. Goiter should be investigated.
Pruritus gravidarum is due to retained bile salts. Thyroxin-binding globulin – increases in the first trimester
and reaches its zenith at about 20 weeks, and stabilizes at
ENDOCRINE SYSTEM approximately double baseline values for the remainder of
a. Pituitary gland pregnancy
Enlarges by approximately 135% but rarely cause visual Total serum thyroxine – INCREASE sharply between 6 and 9
disturbance from compression of optic chiasma weeks and reaches a plateau at 18 weeks
Not essential for maintenance of pregnancy Free serum T4 – rise slightly and peak along with hCG
levels, and return to normal
1. Growth Hormone (GH) Total triiodothyronine (T3) – INCREASE up to 18 weeks and
o First trimester – secreted predominantly from maternal plateaus.
pituitary gland; serum and amniotic fluid Thyroid-releasing hormone (TRH) – are NOT INCREASED,
concentrations are within nonpregnant values (0.5 to but CROSSES the placenta and may stimulate the fetal
7.5 ng.ml) pituitary to secrete thyrotropin
o At 8 weeks AOG – growth hormone secreted by placenta TSH and hCG has identical a-subunits, thus hCG has intrinsic
becomes detectable thyrotropic activity and cause thyroid stimulation.
o At 17 weeks AOG – placenta is the principal source of Thyroid-stimulating hormone (TSH) or thyrotropin
growth hormone secretion DECREASES in more than 80% of pregnant women, but
o Maternal serum levels plateau after 28 weeks at 14 remain normal for non-pregnant women.
ng/ml Normal suppression of TSH may lead to a misdiagnosis of
o Amniotic fluid levels peak at 14 to 15 weeks and slowly subclinical HYPERTHYROIDISM.
declines to reach baseline values after 36 weeks.
o Maternal GH c. Parathyroid glands
Correlate positively with birthweight and Regulation of calcium concentration is closely interrelated
negatively with fetal growth restriction & uterine to magnesium, phosphate, PTH, vitamin D, and calcitonin
artery resistance physiology
o Placental GH All markers of bone turnover INCREASED during normal
Differs from pituitary GH by 13 AA residues pregnancy and failed to reach baseline level by 12 months
Secreted by syncitiotrophoblasts in a nonpulsatile postpartum
fashion Calcium needed for fetal growth and lactation may be
Appears to have some influence on fetal growth drawn at least in part from the maternal skeleton.
as well as the development of preeclampsia Acute or chronic decreases in plasma calcium or acute
Major determinant of maternal insulin resistance decreases in magnesium stimulate the release of PTH, and
after midpregnancy vice versa.
Fetal growth progresses in the complete Action of PTH on bone resorption, intestinal absorption,
absence of placental GH and kidney reabsorption is to increase ECF calcium and
Not absolutely essential, but may act in concert decrease phosphate.
with human placental lactogen and other
somatolactogens to regulate fetal growth. 1. PTH and Calcium
o First trimester – plasma PTH decrease initially
2. Prolactin o Succeeding trimesters – INCREASE progressively
o INCREASE markedly and usually 10-fold greater at term Due to lower calcium concentrations in pregnancy
(150 ng/ml) as a result of increased plasma volume, increased
o DECREASES after delivery even in women who are GFR, and maternal-fetal transfer of calcium.
breast feeding. o Estrogen appears to BLOCK the action of PTH on bone
o There are pulsatile bursts of prolactin secretion in resorption, resulting in increase in PTH
response to suckling during early lactation. o Physiologic hyperparathyroidism of pregnancy occurs
o Increases prolactin level: to supply the fetus with adequate calcium.
Estrogen stimulation increases the number of
anterior pituitary lactotrophs and may stimulate 2. Calcitonin and Calcium
release of prolactin o Calcium and magnesium increase the biosynthesis and
TRH secretion of calcitonin
Serotonin o Food ingestion & various gastric hormones (e.g. gastrin,
o Dopamine (prolactin-inhibiting factor) – inhibits pentagastrin, glucagon, and pancreozymin) also
prolactin secretion INCREASE calcitonin levels.
o Functions of prolactin: o Calcitonin acts to OPPOSE PTH and Vitamin D to protect
Ensure lactation skeletal calcifications during times of calcium stress,
Initiate DNA synthesis and mitosis of glandular such as pregnancy and lactation.
epithelial cell and presecretory alveolar cells of the
breast (early pregnancy). 3. Vitamin D and Calcium
Increases the number of estrogen and prolactin o 1, 25-diOH Vitamin D3 – biologically active compound,
galactopoiesis, and production of casein, and stimulates resorption of calcium from bone and
lactalbumin, lactose, and lipids. absorption from the intestines
o Present in amniotic fluid in high concentrations. Up to o Conversion to active Vitamin D3
10,000 ng/ml at 20 to 26 weeks but decrease and reach Ingestion of Vit D or synthesis in the skin
a nadir after 34 weeks. Prolactin in amniotic fluid could LIVER – Vitamin D converted to 25-OH Vit D3
be produced by uterine decidua. Its function could be to KIDNEY, DECIDUA & PLACENTA – 25-OH Vit D3
prevent water transfer from fetus into the maternal converted to 1, 25 diOH Vit D3 (biologically active
compartment to prevent fetal dehydration. form) which is INCREASED in pregnancy.

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o PTH, low calcium and phosphate levels facilitates Attention and memory were improved in women with
conversion of 25-OH Vit D3 to 1, 25 diOHVit D3 preeclampsia receiving magnesium sulfate compared with
o Calcitonin OPPOSES conversion of Vit D to its active normal pregnant women (Rana and associates, 2006).
form. Mean blood flow in the middle and posterior cerebral
arteries decreased progressively from non-pregnant state
d. Adrenals – undergo little morphological change to late in the 3rd trimester. Unknown clinical significance
1. Cortisol – INCREASED (Zeeman and co-workers, 2003)
o Much of serum cortisol is bound by transcortin Pregnancy does not appear to impact cerebrovascular
(cortisol-binding globulin) autoregulation.
o Rate of adrneal cortisol secretion is not increased, and o Sleep
probably it is decreased compared with that of the Difficulty sleeping about 12 weeks to first 2
nonpregnant state. months postpartum with frequent awakening,
o Metabolic clearance rate is LOWER during pregnancy fewer hours of night sleep, and reduced sleep
because its half-life is nearly doubled. efficiency.
o During early pregnancy – ACTH levels are reduced Decreased frequency and duration of sleep apnea
strikingly episodes during pregnancy compared postpartum
o As pregnancy progresses, ACTH and free cortisol rises Supine position, average Pa)2 levels were lower
o Elevation in cortisol may be a result of “resetting” of the Greatest disruption of sleep is seen postpartum
maternal feedback mechanism to higher levels (Nolten and may contribute to postpartum blues or frank
and Rueckert, 1981) depression
o In response to elevated progesterone levels during
pregnancy, an elevated free cortisol is needed to PRENATAL CARE
maintain homeostasis (Keller-Wood and Wood, 2001)
2. Aldosterone – INCREASED Definition
o As early as 15 weeks, maternal adrenal glands secrete A comprehensive antepartum care program that involves a
more aldosterone coordinated approach to medical care and psychosocial
o Sodium intake restriction increases aldosterone support that optimally begins before conception and
secretion extends throughout the antepartum period. (AAP & ACOG,
o Increased aldosterone affords protection against the 2007)
natriuretic effect of progesterone and ANP. A planned program of medical evaluation and management,
observation, and education of the pregnant woman directed
3. Deoxycorticosterone – INCREASED toward making pregnancy, labor, delivery and the
o Due to increased kidney production from estrogen postpartum recovery, a safe and satisfying experience.
stimulation It should provide opportunities for the following:
o There is transfer of fetal deoxycorticosterone into the o Physician and patient to be better acquainted
maternal compartment due to high levels in fetal blood. o Physician to learn something about the patient’s
4. DHEA-S – DECREASED (serum and urine) emotional attitude toward pregnancy and labor
o Due to increased metabolic clearance through o Instruction for the patient and her husband in optimal
externsive maternal hepatic 16a-hydroxylation and care for herself and the coming baby
placental conversion to estrogen o Optimal instruction of the patient and her husband in a
5. Androstenedione and testosterone - INCREASED prepared childbirth program.
o Maternal plasma androstenedione and testosterone are
converted to estradiol in the placenta Components
o Increase in plasma SHBG retards testosterone clearance Preconceptional care, Diagnosis of pregnancy, Initial
prenatal evaluation, follow-up prenatal visits
OTHER SYSTEMS
1. Diagnosis of pregnancy
Musculoskeletal system
o Established through signs and symptoms,
Progressive lordosis is observed. The lordosis shifts the
chorionic gonadotropin, ultrasound
center of gravity back over the lower extremities.
recognition
Sacroiliac, sacrococcygeal and pubic joints have increased
Signs and symptoms of pregnancy
mobility during pregnancy.
Sign or Comments
Joint mobility may contribute to the alteration of maternal
symptom
posture and may cause discomfort in the lower back.
Occurs 10 days after expected menses
Pelvic joints normally relax, particularly the symphysis
One to two episodes of bloody discharge,
pubis. Most relaxation takes place in the first half of Cessation of
reminiscent of menstruation, can be due to
pregnancy. menses
blastocyst implantation or “implantation
Symphyseal separation greater than 1 cm may cause
bleeding”
significant pain. Regression begins immediately follwing
delivery, and it is usually complete within 3 to 5 months. Fern-like pattern – Day 7 to 18 of menses
due to increased NaCl when estrogen is
Eyes produced.
Cervical
Beaded pattern – Day 21 menses or
Intraocular pressure decreases during pregnancy, mucus
attributed to increased vitreous outflow. pregnancy due to decreased NaCl
Corneal sensitivity is decreased, particularly late in influenced by progesterone that prohibit
gestation ferning
Slight increase in corneal thickness due to edema. Breast tenderness and tingling
Krukenberg spindles – brownish-red opacities on the >2 months: increased breast size, delicate
posterior surface of the cornea – have been observed during veins becomes visible, nipples larger &
pregnancy. more pigmented, more erectile.
Breast
Colostrum can be expressed. Areola
Visual function is unaffected by pregnancy, except for changes
transient loss of accommodation. broader and deeply pigmented.
Glands of Montgomery which are
CNS hypertrophic sebaceous glands appear.
Women often report problems with attention, Breast striations may also appear
concentration, and memory throughout pregnancy and the Vaginal Chadwick’s sign. Vaginal mucosa becomes dark
early postpartum period. mucosa bluish or purplish red and congested.
Striae gravidarum or stretch marks
Skin changes
Diastasis recti. Rectus muscles separate in
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the midline.
Linea nigra. Brownish-black discoloration
of linea alba First 15-20 24-28 29-41
COMPONENT
Chloasma or melasma gravidarum (mask of visit weeks weeks weeks
pregnancy) History +
Angiomas or vascular spiders. Minute, red Complete PE +
elevations on the skin of the face, neck, Blood pressure + + + +
upper chest and arms. Often designated as Maternal weight + + + +
nevus, angioma or telangiectasia. Pelvic/cervical exam +
Palmar erythema Fundal height + + + +
First few weeks. Anteroposterior diameter FHT & position + + + +
is increased. Hemoglobin (Hgb) & + +
Changes in 12 weeks AOG: body of uterus becomes Hct
the uterus globular, average diameter is 8 cm. Blood type & Rh +
6 to 8 weeks AOG: Hegar’s sign is softening factor
of the isthmus. Antibody screen +
Goodell’s sign. Softening of the cervix. The Pap smear +
consistency of the cervical tissue Urine protein +
Changes in surrounding the external os is more similar Urine culture +
the cervix to that of the lips of the mouth. Rubella titer +
Cervical softening is also noted in women Syphillis test (VDRL) +
taking estrogen-progesterone pills. Hepatits B surface +
17 weeks: stethoscope Ag (HbsAg)
10 weeks: doppler equipment 50 grams +
5 weeks: transvaginal sonography OGCT/100g OGTT
Fetal heart rate: 110 to 160 bpm Gonococcal or * *
Other sounds heard in the pregnant Chlamydial culture
abdomen: HIV *
Fetal heart 1. Funic souffle – rush of blood *High-risk women
tone through the umbilical arteries.
Sharp, whistling sound, Components of Initial Prenatal Evaluation:
synchronous with fetal pulse. A. Prenatal Record
2. Uterine souffle – soft, blowing Terminologies for prenatal record:
sound, synchronous with maternal a. Nulligravida. Woman who is NOT now and never has
pulse. Heard at lower portion of been pregnant.
uterus produced by dilated b. Gravida. Woman who is or has been pregnant,
uterine arteries. irrespective of the pregnancy outcome. With the
18-20 weeks: Primigravid establishment of first pregnancy, she becomes
Fetal 16-18 weeks: Multigravid primigravida, and with successive pregnancies, a
movements 20 weeks: examiner can begin to detect multigravida.
fetal movements. c. Nullipara. Woman who has never completed a
pregnancy beyond 20 weeks gestation.
d. Primipara. Woman who has been delivered only once a
Presumptive Probable Positive
fetus or fetuses born alive or dead with an estimated
length of gestation 20 or more weeks.
Symptoms Symptoms
e. Multipara. Woman who has completed 2 or more
Nausea, vomiting Abdominal
prenancies to 20 weeks or more. Parity is determined
Bladder distention
by the number of pregnancies reaching 20 weeks and
frequency/urgency Braxton-Hicks
not by the number of fetuses delivered.
Perception of fetal
f. Gestational age or menstrual age is calculated from the
movement
first day of last menstrual period.
Breast
g. Ovulatory age or fertlization age, is 2 weeks shorter
enlargement
than gestational age. Used by embryologists and other
Signs Signs Signs reproductive biologists.
Secondary (+) Pregnancy test Fetal heart tone h. First trimester is from conception to 14 weeks
amenorrhea Abdominal Perception of fetal gestation. Second trimester is up to 28 weeks completed
Chadwick’s sign enlargement movement by gestation. Third trimester from 29th to 42nd week
Chloasma (face) Outlining of the examiner gestation.
Linea nigra, striae fetal parts Ultrasound
Spider Hegar’s sign evidence Normal pregnancy duration
telangiectasia Goodell’s sign 1. Non-viable pregnancy is less than or equal to 20 weeks
Breast changes Ballotment gestation (140 days)
Thermal changes 2. Viable pregnancy:
Preterm - >20 weeks to <37 weeks (141 to <259 days)
Pregnancy Test Term – 37 weeks to 42 weeks (259 – 294 days)
1. Chorionic gonadotrophin Post term - >42 weeks (294 days)
2. Ultrasound recognition (Transvaginal ultrasound) 3. Term Pregnancy Categories (ACOG/SMFM: Replace Phrase
'Term Pregnancy' With 4
2. Initial prenatal evaluation Categories. Medscape. Oct 22, 2013.)
Major goals: Early term: 37 weeks to 38 weeks, 6 days – has 7-fold
1. Define the health status of the mother and fetus. higher risk for neonatal morbidity
2. Estimate the gestational age. Full term: 39 weeks to 40 weeks, 6 days
3. Initiate a plan for continuing obstetrical care. Late term: 41 weeks to 41 weeks, 6 days
Components of routine prenatal care (Williams Post term: 42 weeks and beyond
Obstetrics, 23rd edition)
B. History
Menstrual history

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Psychosocial screening or glycosylated hemoglobin [HbA1c] or random
Nonbiomedical factors that affect mental and physical blood sugar [RBS])
well-being. o Diagnosis of OVERT DIABETES is given among
Screening for barriers to care: women with any of the following results in their
1. lack of transportation first visit.
2. child care or family support FBS > 126 mg/dl (7 mmol/L)
3. unstable housing RBS > 200 mg/dl (11.1 mmol/L)
4. unintended pregnancy HbA1c > 6.5%
5. communication barriers 2 hour 75 g OGTT > 200 mg/dl (11.1 mmol/L)
6. nutritional problems o Diagnosis of GDM is made if any one (1) of the
7. cigarette smoking, substance abuse following plasma values are exceeded:
8. depression FBS > 92 mg/dl (ADA/IADPSG/POGS
9. domestic violence 1 hour > 180 mg/dl
Cigarette Smoking: spontaneous abortion, low 2 hour > 153 mg/dl (ADA/IADPSG) or > 140
birthweight due to preterm delivery or fetal growth mg/dl (WHO/POGS)
restriction, infant and fetal deaths (SIDS), placental o For Filipino gravidas with no other risk factors
abruption, placenta previa, premature rupture of aside from race or ethnicity and the initial test
membranes (FBS, HbA1c or RBS) is normal, screening for GDM
Ethanol: potent teratogen and causes fetal alcohol should be done at 24-28 weeks using a 2 hour 75
syndrome, characterized by growth restriction, facial gram OGTT. If there are other risk factors
abnormalities and CNS dysfunction. identified, screening should proceed immediately
Illicit drugs include opium derivatives, barbiturates and to 2 hour 75 gram OGTT at first consult.
amphetamines which may cause fetal distress, low o If the OGTT at 24-28 weeks is normal, the woman
birthweight. should be re-tested at 32 weeks or earlier if
Domestic violence refers to violence against adolescent clinical signs and symptoms of hyperglycemia are
and adult females within the context of family or present both in the mother and the fetus (e.g.
intimate relationships. polyphagia, polyhdramnios, accelerated fetal
growth, etc)
C. Physical examination. Includes speculum and pap smear, o OGTT should be performed in the morning after an
digital pelvic examination and rectal exams. overnight fast of 8 hours following the general
D. Laboratory tests. Refer to table above. instructions for the test.
Iron status for women during pregnancy and the Observe and overnight fast (at least 8 hours,
postpartum period. (CPG on Iron Deficiency Anemia, but no more than 14 hours) prior to testing.
November 2009) Have an unrestricted diet (> 150 grams of
Iron carbohydrates per day) for at least 3 days
Iron prior to the testing
Iron deficiency
deficiency Remain seated and should not smoke during
sufficiency Without
anemia (IDA) the test.
anemia
Hgb 110 Hgb 110 Hgb <110
20 weeks g/L g/L g/L E. High Risk Pregnancies.
to delivery Ferritin 12 Ferritin <12 Ferritin <12
ugL ugL ugL 3. Subsequent prenatal visits
A. Prenatal Visits
Hgb 120 Hgb 120 Hgb <120
g/L g/L g/L Traditional: every 4 weeks until 28 weeks, every 2 weeks
6 months
until 36 weeks, every week until term. High-risk every week
postpartum Ferritin 15 Ferritin <15 Ferritin <15
or as indicated.
ugL ugL ugL
WHO Model consists of a mean of 5 visits: once in first
Criteria for anemia in pregnancy by WHO and US CDC
trimester to screen for risk factors, then at 26, 32 and 38
(CPG on Iron Deficiency Anemia, November 2009)
weeks.
Trimester Anemia if Hgb is less than
1st: 0-12 weeks 11.0 g/dl B. Prenatal Surveillance
2nd: 13-28 weeks 10.5 g/dl Fetal surveillance: heart rate, size (current & rate of
3rd: 29 weeks to term 11.0 g/dl change), amniotic fluid, presenting part and station (late in
pregnancy), activity
Severity of anemia by WHO (CPG on Iron Deficiency Maternal surveillance:
Anemia, November 2009) o Vital signs: BP, weight
Category Severity Hgb (g/dl) o Symptoms: headache, altered vision, abdominal pain,
1 Mild 9.5 – 10.5 nausea and vomiting, bleeding, vaginal fluid leakage,
2 Moderate 8.0 – 9.4 dysuria
3 Severe 6.9 – 7.9 o Abdominal Exam: fundal height
4 Very severe <6.9 o Vaginal exam: confirms presenting part & station,
pelvic capacity, and cervical consistency, effacement
Recommendations on Detection and Diagnosis of and dilatation
Diabetes Mellitus among Filipino Pregnant Women (CPG
on Diabetes Mellitus in Pregnancy, November 2011) LEOPOLD’S MANEUVER
o Diabetes mellitus recognized during pregnancy First maneuver answers the question:
should now be classified as either gestational “What fetal part occupies the fundus?”
diabetes mellitus (GDM) or over diabetes mellitus Second maneuver answers the question:
based on plasma glucose levels. “On what side is the fetal back?”
o Universal screening for GDM is recommended Third maneuver answers the question:
for Filipino gravidas. “What fetal part lies over the pelvic inlet?”
o At the first prenatal visit, determine if the gravid is Fourth maneuver answers the question:
high risk or not based on historical and pregnancy “On which side is the cephalic prominence?”
risk factors.
o ALL FILIPINO gravidas are considered “high risk” CHECK UTERINE SIZE
by race or ethnic group (Pacific Islander) and At 20-31 weeks, AOG correlates well with
should be screened for type 2 diabetes mellitus in Uterine size
the first prenatal visit (fasting blood sugar [FBS] At 12 weeks –palpable at level or just above of
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symphysis pubis a. Breast milk is clean and free of bacteria
At 16 weeks- midway between symphysis b. Contains antibodies (immunoglobulin) to many
pubis and umbilicus common infections, until he can make his own
At 20 weeks- at the level of umbilicus antibodies.
c. Contains white blood cells to help fight infection.
d. 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.
e. 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.
C. Assessment of Gestational Age 4. Breastfeeding helps to stop bleeding after delivery.
Fundal height – between 20 and 34 weeks, the height of the 5. Breastfeeding on demand helps to protect against another
uterine fundus measured in centimeters correlates closely pregnancy.
with gestational age in weeks. 6. It helps them to bond, become attached to each other and
Ancillary tests: Gestational diabetes, chlamydial infection, love each other.
gonococcal infection, fetal fibronectin (vaginal fluid), GBS 7. It is free. You don’t have to buy it.
infection, genetic diseases. 8. It is exclusively for your baby and cannot be served to
other adults.
Weight gain based on the BMI.
Protective Effects on Infants of Human Milk and Breast
BMI BMI
Category Kilograms Pounds Feeding (AAP, 1997)
(Asia-Pacific) (ACOG)
Decreased Incidence/Severity Possible protective effects
Underweight <18.5 <19.8 12.5 - 18 28 – 40
Normal 18.5 – 24.9 19.8 - 26 11.5 - 16 25 – 35 Diarrhea Sudden infant death
Lower respiratory infection syndrome
Overweight 25 – 29.9 26 - 29 7 – 11.5 15 – 25
Otitis media Type-1 Diabetes
Obese >30 >29 5 – 9.1 11 - 20
Bacteremia Inflammatory bowel disease
Bacterial meningitis Lymphoma
III. Nutrition
Botulism Allergies
2000 calories/day + 300 kcal/day (2nd & 3rd
Calories Necrotizing enterocolitis Chronic digestive diseases
trimester) Urinary infections
9 grams/day
Protein deficiency may lead to lowering of III. Composition of Human Breast Milk
hemoglobin-producing factors in the liver, Component Human milk Cow milk
which may result in hypochromic anemia.
Protein Water Enough (87.2% to More required
Absorption of calcium from intestinal tract
87.5%)
may be impaired.
Bacterial None Likely
Meats, mild and eggs are best sources of
contamination
protein.
Anti-infection Antibodies, Antibodies not
150 grams/day in the first trimester.
substances leucocytes, active, absent
225 grams/day at the end of pregnancy.
lactoferrin, bifidus lactoferrin
50-100 grams/day according to FNRI of the
factor
Philippines (1989) is sufficient to prevent
Carbohydrates Protein (Total) 1% 4% too much
ketosis and other symptoms of lack of dietary
Casein 0.5% 3% too much
carbohydrate.
lactalbumin 0.5% 0.5%
Adequate carbohydrates seem to lessen
nausea and vomiting Amino acids - Enough for growing Not enough
15-25 grams/day Cysteine brain Not present
Most concentrated sources of energy, Taurine Enough
Fats providing more than twice the energy value of Fats (Total) 4% average 4%
an equivalent weight of carbohydrates or Saturation Enough Too much
protein. UNsaturated saturated
No recommended level. Liberal intake of Fatty acids – Enough for growing Not enough
fruits, vegetables and whole grain cereals is linoleic acid brain Not enough
Dietary fiber highly recommended. (essential) Enough
Promoting normal bowel functions and bulk Cholesterol
or satiety value to meals. Lipase to digest fat Present None
Lactose (sugar) 7% (enough) 3% - 4% (not
POSTPARTUM CHANGES enough)
Salts (mEq/L) – 6.5 25 (too much)
Sodium 12 29 (too much)
BREASTS & LACTATION Chloride 14 35 (too much)
I. How breast milk protects babies against infection. (DOH, Potassium
1991) Iron – colostrum
0.5 – 0.8 mg/L
1. Breastfed babies have less diarrhea than artificially-fed Mature milk0.2 – 0.3 mg/L
babies.
2. Fewer respiratory and middle ear infection.
3. Fewer infections because of the following:
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IV. Some Myths about Breastfeeding: (Thomson Medical Frequent washing, especially with soap, removes the
Center, Singapore. 2004) natural oil from the nipple.
1. It is painful & difficult to learn. The skin becomes dry and is more easily damaged and
2. Breastfed babies cry more than bottle-fed babies. fissured.
3. Breastfeeding tends to isolate mother and baby from the
rest of the family members. FAMILY PLANNING
4. It is embarrassing. Fertility Awareness-based (FAB) Methods
5. Spoils a baby and weaning is difficult.
Family planning methods that attempt to identify fertile
6. Quality of breast milk depends on your mood.
time each cycle and then modify sexual behavior.
7. Breastfeeding mother may have to give up food she likes,
become tied down and be unable to work. Natural family planning (NFP) refers to sexual abstinence
8. Breastfed babies need more water. during the fertile time.
9. Breast milk lack iron. Fertility awareness-combined methods (FACM) refer to
using barrier method during the fertile time.
V. How should breastfeeding begin. (DOH, 1991) Various methods of periodic abstinence have pregnancy
1. First feed rates estimated from 5 to 40 per 100 woman years. The
First feed should be on the delivery table. unwanted pregnancy rate during the first year of use is
Cover both mother and baby to keep them warm. approximately 20%.
Let the mother hold the baby close and let him suck at
I. Standard Days Method
the breast.
Developed by the Institute for Reproductive Health at
Sucking stimulates the production of oxytocin which
Georgetown University
helps to deliver the placenta and stop hemorrhage.
Avoid unprotected intercourse during cycle days 8 through
Baby gets valuable colostrums.
19.
More likely to breastfeed for a long time. A delay of even
Women must have regular monthly cycles of 26 to 32 days.
a few hours will result in failure to breasfeed.
Cycle beads can be used to keep track of their cycle.
2. Rooming-in
II. Calendar Rhythm Method
There is no need for a mother and baby to rest
separately after a normal delivery. Requires counting the number of days in the shortest and
3. Demand feeding longest menstrual cycle during a 6- to 12-month span.
Let the mother pick up her baby and feed him whenever First fertile day – 18 days are subtracted from the shortest
he cries and she feels a need to feed him. cycle.
Frequent sucking stimulates the production of prolactin Last fertile day – 11 days are subtracted from the longest
which helps the milk to come in sooner. cycle.
It prevents engorgement of breasts. This is problematic because ovulation most often occurs 14
days before the onset of the next menses. This is not
4. Duration of feeds reliable.
More babies finish in 5-10 minutes, but some like to
III. Temperature Rhythm Method
take much longer, perhaps half an hour. It does not
matter. The first scientific NFP method developed which involves
measuring changes in body temperature after ovulation.
Slow feeders take the same total amount of milk as fast
feeders. Immediately after ovulation, basal body temperature, or the
body temperature at complete rest, dips slightly then rises
Sucking in the wrong position causes sore nipples.
by about 0.2 C to 0.5 C (0.4 F). It remains high until just
before the next period.
5. Feeding from both breasts
Follow a biphasic pattern, it remains low before ovulation
Let the baby finish the first breast to make sure that he
and higher after ovulation which is caused by progesterone.
gets the hindmilk. Let him take the second breast if he
wants to, but do not force him. The woman has to take her temperature everyday, upon
waking up in the morning, before getting out of bed, and
6. Prelacteal feeds after at least 3 hours of continuous sleep.
Prelacteal feeds (e.g. formula, glucose water, ampalaya She may take her temperature by mouth (under the tongue)
juice, diluted honey) are NOT necessary and they can be or by the axilla, but she has to use the same route
harmful. throughout the menstrual cycle. The thermometer must be
left in position for 5 minutes.
Small amount of colostrum is ALL that a normal baby
needs at this time. She must record it on a chart after taking it and include
other events like illness.
7. Extra water A coverline or baseline is drawn using the highest
Normal baby is born with a store of water which keeps temperature reading from day 6 to 10 of cycle and watch
him well hydrated until the milk comes in. He does not out for 3 consecutive temperature readings above the
need drinks of water, they interfere with breasfeeding. coverline which refers to the thermal or temperature shift
indicating that ovulation has taken place.
8. Night breastfeeds The woman must abstain from intercourse from the first
It is better if the mother breastfeeds the baby at night as day of menses through the 3rd day after the increase in
long as he wants to. temperature.
Night feeding helps to keep up the milk supply because With excellent compliance, the unwanted pregnancy is
the baby sucks more. approximately 2 percent the first year.
Night feeds are especially useful for working mothers.
IV. Cervical Mucus Rhythm Method
Night feeds are important for child spacing.
Also called “Billings method”, developed by John Billings,
depends on awareness of vaginal “dryness” and “wetness”.
9. Early weight changes
These are the consequences of changes in the amount and
A baby may lose weight for the first few days after
quality of cervical mucus at different times in the menstrual
delivery. He may lose up to 10% of his birth weight.
cycle.
When breastfeeding is started, the baby should regain
The fertile mucus is brought about byt increasing levels of
his birth weight in ten days.
estrogen and the infertile mucus by the increase in
progesterone.
10. Cleaning the breast

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Dry days after the menses are the indicators of the dose changes within the cycle. Some formulations,
preovulatory phase or the first infertile phase, which are estrogen dose also varies.
relatively infertile days. ESTROGEN
Wet days signal the ovulatory phase and are therefore o Features:
fertile days. The fertile type mucus is more copious, Daily estrogen content varies from 10 to
slippery/lubricative, stretchy and wet. At times, it has the 50 ug of ethinyl estradiol, and most
appearance of raw egg white. This mucus makes it easy for contain 35 ug or less to minimize adverse
the sperm to travel through the cervix, uterus and the tubes effects.
to meet the egg. o Forms:
Last day of the wetness is called the peak day. Its timing is 1. Ethinyl estradiol – most common
around ovulation time. The 3 days after the peak day or the 2. Mestranol
post-peak days are still considered fertile days, giving 3. Estradiol valerate
allowance for the life span of the egg.
Ovulatory phase includes all days when the wet sensation is o Side effects:
first felt, including the Peak Day and the 3 post-Peak days. 1. Breast tenderness
Abstinence is required from the beginning of menses until 4 2. Fluid retention
days after slippery mucus is identified. 3. Weight gain
When used accurately, the first-year failure rate is 4. Nausea
approximately 3 percent. 5. Headache

V. Symptothermal Method PROGESTIN


Combines the use of changes in cervical mucus – onset of o Features:
fertile period, changes in basal body temperature – end of Structurally related to progesterone,
fertile period, and calculations to estimate the time of testosterone, or spironolactone
ovulation. Binds variably to progesterone,
One also has to look out for other bodily changes such as: androgen, estrogen, glucocorticoid, and
i. Feel and position of the cervix mineralocorticoid receptors which
1. Fertile: the cervix is far from the vaginal opening explain pill-related side effects
and is open and softer (consistency of the lips) Progestin related to testosterone may
2. Not fertile: cervix is closed, firm (tip of the nose) impart androgenic side effects such as
and close to the vulva acne and adverse HDL and LDL levels.
ii. Ovulation pain (Mittelschmerz) o Forms:
iii. Mid-cycle bleeding or spotting 1. Medroxyprogesterone acetate – mainly
iv. Breast sensitivity used in a progestin-only injectable form
v. Skin changes 2. Nomegestrol acetate – used in a COC
vi. Mood changes 3. Norethindrone acetate – used in a COC;
To avoid pregnancy, the couple abstains from vaginal non-acetate form used as progestin-only
intercourse on: 4. Norgestrel
i. Alternate preovulatory days of no mucus or dry 5. Norgestimate
mucus 6. Ethynodiol diacetate
ii. On all days of wet mucus 7. Levonorgestrel
iii. The four days after the last day of wet mucus, or the 8. Desogestrel
third day after temperature rise. 9. Dienogest
10. Drospirenone
Contraceptive Failure Rates During the First Year of Use Structurally similar to spironolactone
(Modified from Speroff and Darney, 2001, and Trussell, 2004) and have similar effects to 25 mg of
Method Perfect Use Typical Use this diuretic hormone.
None 85 85 Displays antiadrogenic activities
Calendar 9 20 Provides antialdosterone action to
Ovulation 3 - minimize water retention
Symptothermal 2 - Antimineralocorticoid properties that
may cause potassium retention and
Post-ovulation 1 -
hyperkalemia. Serum potassium level
Withdrawal 4 27
monitoring for the first month is
recommended. Likeswise for the
Hormonal Contraceptives
following drugs:
I. Combination hormonal contraceptives. NSAIDS, ACE inhibitors,
A. Mechanism of Action angiotensin II antagonists,
Prevent ovulation by suppression of hypothalamic herparin, aldosterone
gonodotropin releasing factors. Thus, prevents antagonists, and potassium-
pituitary secretion of FSH and LH. sparing diuretics.
Progestins action: Avoided in women with renal or
i. Prevent ovulation by suppressing LH adrenal insufficiency or with hepatic
ii. Thicken cervical mucus, thereby retarding dysfunction.
sperm passage. o PROGESTIN-ONLY side effects:
iii. Render the endometrium unfavourable for Irregular uterine bleeding, such as
implantation. metrorhhagia or menorrhagia (most
Estrogen action: frequently reported)
1. Prevents ovulation by suppressing FSH DO NOT significantly affect lipid
release. metabolism, glucose level, hemostatic
2. Stabilizes the endometrium, which factors, liver function, thyroid function,
prevents intermenstrual bleeding – also and blood pressure.
known as breakthrough bleeding. NOT shown to increase risk for
B. Composition thromboembolism, stroke, or CV disease.
Monophasic pills – progestin dose remains DMPA use shows increased LDL and
constant throughout the cycle. decreased HDL and may be less favorable
Multiphasic (bi-, tri- or quadriphasic) pills – dose with cardiac or vascular risks.
frequently varied depending on the number of DO NOT impair mild production
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NO increased risk of genital tract or o Nonsmoking women younger than 35 years
breast neoplasia old has and extremely low risk of ischemic and
Weight gain and bone mineral density hemorrhagic strokes.
loss are not prominent, except for DMPA o COCs may be considered for women with
Functional ovarian cysts develop with migraines that lack focal neurological signs if
greater frequency. they are otherwise healthy, normotensive
C. Administration nonsmkers younger than 35 years.
COC’s are taken daily some for 21 days with 7 pill- o VTE with COC use is only 3 to 4 per 10,000
free interval or placebo. woman-years and is lower than the incidence
Some provide 24 days of hormones followed by 4 of 5 to 6 per 10,000 woman-years estimated
pill-free days (e.g. Yaz). for pregnancy.
Ideally, women should begin on the first day of a o Clinical factors that increase VTE with COC
menstrual cycle. use:
There is a “quick start” method, wherein the pills Thrombophilias
are started on ANY DAY, regardless of cycle timing. Hypertension
A back-up method is used during the first week. If Obesity
the woman is already pregnant during Quick Start Diabetes
initiation, COC’s ARE NOT TERATOGENIC. Smoking
For maximum efficiency, pills should be taken at Sedentary lifestyle
the same time each day. o COCs are NOT recommended for women
Spotting or bleeding is common with initiation of within the first 4 weeks after delivery.
COCs. It does not reflect contraceptive failure and o For all women, VTE risk with drospirenone-
typically resolves within one to three cycles. containing COCs has been shown.

D. Method-specific effects Neoplasia


Altered Drug Efficacy o Overall, COCs are not associated with an
o Three (3) groups of drugs that decrease COC increased risk for cancer.
effectiveness: o Protective effect against ovarian and
1. Anti-TB drugs: rifampin and rifabutin endometrial cancer
2. Anti-HIV drugs: efavirenz and ritonavir- o Relative risk of cervical dysplasia and cervical
boosted protease inhibitors cancer is increased in current COC users, but
3. Anticonvulsants: phytoin (Dilantin), following 10 or more years of disuse, risk
carbamazepine (Tegretol), oxcarbazepine returns to that of never users.
(Trileptal), barbiturates, primidone, and o No evidence for increased risk of
topiramate (Topamax) hepatocellular cancer.
o Women with known tumores, COCs are
Metabolic changes
AVOIDED in those with benign hepatic
o COCs increase serum levels of triglycerides and
adenoma and hepatocellular carcinoma.
total cholesterol.
o Women who are carriers of the BRCA1 and
o Estrogen decreases LDL
BRCA2 gene mutation, risks for breast cancer
o Estrogen increases HDL and VLDL
are NOT INCREASED by COC use.
o OCP are NOT atherogenic
o COCs appear to lower rates of benign breast
o Women with LDL >160 mg/dl or with multiple
disease.
additional risk factors for CV disease,
alternative methods are recommended.
E. Non-contraceptive benefits of COCs
o Estrogen use related to increase in fibrinogen
1. Increased bone density
and may of the clotting factor levels and may
2. Reduced menstrual blood loss and anemia
lead to thrombosis.
3. Decreased risk for ectopic pregnancy
o COCs augment angiotensinogen production
4. Improved dysmenorrhea from endometriosis
and its conversion by renin to angiotensin I
5. Fewer premenstrual complaints
which may be associated with “pill-induced
6. Decreased risk of endometrial and ovarian cancer
hypertension”
7. Reduction in various benign breast diseases
o COCs increase SHBG which decrease
8. Inhibition of hirsutism progression
bioavailable testosterone concentrations and
9. Improvement of acne
improve androgenic side effects.
10. Prevention of atherogenesis
o Risk of developing diabetes is NOT increased.
11. Decreased incidence and severity of acute salpingitis
o NO connection beteween COCs and weight
12. Decreased activity of rheumatoid arthritis
gain.
o OCP use related to elevated total plasma
II. Injectable Progestin Contraceptives
thyroxine (T4) and thyroid-binding proteins
Intramuscular depot medroxyprogesteron acetate
(Depo-Provera or Depo-Trust), 150 mg every 3 months,
Cardiovascular effects
injected into the deltoid or gluteus muscle.
o Women using low-dose COCs formulations
rarely develop clinically significant Mechanisms of action: ovulation inhibition, increased
hypertension. cervical mucus viscosity, and creation of an
o Patients are advised to return 8 to 12 weeks endometrium unfavourable for ovum implantation.
after COC initiation for evaluation of blood Initial injection should begin within the first 5 days
pressure and other symptoms. following menses onset. No back-up contraceptive is
o COCs are permissible in women with well- required if initiated within 5 days of menses onset.
controlled uncomplicated hypertension who
are non-smokers, otherwise healthy, and III. Implants
younger than 35. Etonogestrel implant
o COCs use are NOT advisable for those with o Thin, pliable progestin-containing cylinders that are
severe forms of hypertension, especially with implanted subdermally and release hormone over
end-organ involvement. many years.
o Women with prior stroke or myocardial o Implanon
infaction, COCs should NOT be considered. 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 Problems with the above definitions:
surface of the upper arm 8 to 10 cm from the 1. Clinical estimation of blood loss is frequently inaccurate
elbow in the biceps groove and aligned with the and the brisk nature of blood loss during delivery or the
long axis of the arm. presence of amniotic fluid can make this more difficult.
Provides contraception for 3 years and then 2. Delay in obtaining laboratory results. Information from
replaced at the same site or in the opposite arm. laboratory tests would not reflect the patient’s current
hemodynamic status.
Method-specific adverse effects 3. Any definition based on the need for transfusion is difficult
o Branches of the medial antebrachial cutaneous as there are differences in provider practice patterns
nerve can be injured if the implant or insertion regarding transfusion.
needle is placed too deeply or if exploration for a
lost implant is aggressive. Definition of obstetric hemorrhage combining clinical and
o Numbness and paresthesia over the anteromedial objective data (Bonnar, 2000)
aspect of the forearm Blood Systolic
EBL Heart
o Nonpalpable devices may require radiological volume BP Signs & symptoms
(ml) rate
imaging for localization (%) (mmHg)
500-
10-15 <100 Normal None
Insertion timing 1000
o Etonogestrel implant: Ideally inserted within 5 days 1000 - 100- Slight Vasoconstriction,
15-25
of menses. If inserted later in the cycle, alternative 1500 120 decrease weakness, sweating
contraception is recommended for 7 days following 1500 - 120- Restlessness, pallor,
25-35 80-100
placement. 2000 140 oliguria
o Levonogestrel implant: Contraception is established 2000- Anuria, altered
35-45 >140 60-80
within 24 hours if inserted within the first 7 days of 3000 consciousness
the menstrual cycle.
o Transitioning methods: Etiology and Risk Factors
On the day of the first placebo COC pill Etiology Pathophysiology Risk Factors
On the day of the next DMPA injection Multiple gestation
Within 24 hours of taking the last POP Overdistended uterus Polyhydramnios
o Inserted before discharge following delivery, Macrosomia
miscarriage, or abortion Prolonged labor
TONE Uterine muscle fatigue Augmented labor
Intrauterine devices (IUD) (Abnormal Prior PPH
IUD are “use and forget” effective reversible contraceptive uterine Prolonged rupture of
methods that do not have to be replaced for 5 or 10 years, Chorioamnionitis
contractility) membranes (ROM)
depending on the brand. Uterine Fibroids (myoma),
It is now better established that the major actions of IUDs distortion/abnormality placenta previa
are contraceptive, NOT abortifacient. B-mimetics, MgSO4,
Risk of pelvic infections is markedly reduced with the Uterine relaxing drugs
anesthetic drugs
currently used monofilament string and with techniques to Prior uterine surgery
ensure safer insertion. Accreta/Increta/Percre
Placenta previa
Risk of an associated ectopic pregnancy has been clarified. TISSUE ta
Multiparity
Specifically, the contraceptive effect decreases the absolute (Retained
Manual placenta
number of ectopic pregnancies by approximately 50% products of
Retained removal
compared with that of women not using contraception. conception)
placenta/membranes Succinturiate/accesso
With failure, pregnancy is more likely to be ectopic. ry lobe
Within the uterus, an intense local endometrial Precipitous delivery
inflammatory response in induced, especially by copper- Macrosomia
containing devices. Cellular and humoral components of Laceration of the
Shoulder dystocia
this inflammation are expressed in endometrial tissue and cervix, vagina or
Operative delivery
in fluid filling the uterine cavity and fallopian tubes. These perineum
Episiotomy (e.g.
lead to decreased sperm and egg viability. mediolateral)
With the LBG-IUS, in addition to an inflammatory reaction, TRAUMA
Deep engagement
progestin release in long-term users causes glandular (Genital tract Extension/laceration at
Malposition
atrophy and stromal decidualization. Progestins create trauma) CS
Malpresentation
scant viscous cervical mucus that hinders sperm motility. Uterine rupture Prior uterine surgery
Fundal placenta
Barrier Methods Grand multiparity
Male Condoms Uterine inversion
Excessive traction on
Diaphragm umbilical cord
Preexisting clotting History of
Surgical Methods abnormalities (e.g. Coagulopathy or liver
Tubal ligation hemophilia, disease
Vasectomy THROMBIN vonWillebrands
(Abnormaliti disease,
POST-PARTUM HEMORRHAGE (PPH) es of hypofibrinogenemia)
coagulation)
DIC Sepsis
Definition HELLP Intrauterine demise
The following are suggested definitions but there is a lack of Anticoagulation Hemorrhage
agreement on what constitutes excessive blood loss:
1. Blood loss >500 ml for vaginal delivery and 1,000 ml for
cesarean section (CS). General Management of PPH:
2. Blood loss >500 ml in the first 24 hours following delivery. 1. Initial management approach to obstetric hemorrhage:
3. Ten percent (10%) decrease in hemoglobin or hematocrit a. Assessment: constant awareness of the hemodynamic
level. status as well as evaluation to determine the cause of
4. Need for transfusion. bleeding.
b. Breathing: administration of oxygen

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c. Circulation: obtaining intravenous (IV) access and o Unstable lie
adequate circulating blood volume through infusion of Manipulation of the fetus through the maternal abdomen to
crystalloid and blood products. Second large-bore IV a cephalic presentation.
catheter is needed Use of tocolysis with beta sympathomimetics may increase
2. Notify the blood bank. success rate of ECV
3. Simultaneous, coordinated, multi-disciplinary management
(OB-GYN, anesthesiologist, hematologists, radiologists, 3. POP, OT
nurses, laboratory and blood bank technicians) to concur Factors for incomplete rotation of fetal head:
timely management in the presence of obstetric hemorrhage. o Poor contractions
4. Preoperative preparedness is important especially for o Faulty flexion of head
patients identified as high risk. o Epidural anesthesia – diminishes abdominal muscular
pushing & relaxes pelvic floor
Important Causes of PPH: Digital rotation of the fetus in the OP position.
1. Uterine atony
2. Retained placenta 4. Brow and Face
3. Uterine rupture
Brow
4. Genital tract trauma
Expectant management, as long as FHR remains reassuring and
5. Uterine inversion
dilatation and descent are progressing normally.

Face
DYSTOCIA Continuous EFM is mandatory because of increased
incidence of abnormal FHR patterns and/or fetal
DYSTOCIA: PROBLEMS IN PASSENGER compromise
Fetal Presentations and Conditions Oxytocin can be used to augment labor using the same
1. Breech precautions
2. External cephalic version Forceps, using Kielland forceps, may be used if the mentum
3. POP, OT is anterior.
4. Brow and Face
5. Transverse/Oblique 5. Transverse/Oblique
6. Compound Both will benefit from a trial of version to cephalic presentation
7. Macrosomia following the criteria & recommendation of ECV for breech.
8. Shoulder dystocia
6. Compound
1. Breech If the hand has not prolapsed beyond the presenting part,
Planned CS has reduced risk for perinatal or neonatal causing the hand to retract often is accomplished. It can be
death/morbidity ignored as long as labor is progressing normally
Planned vaginal breech criteria: If the hand or arm has prolapsed past the presenting part,
o Skilled OB CS delivery is wise.
o Facilities for possible CS available
o Woman is informed of risks 7. Macrosomia
o EFW: 2500g to 4000g Macrosomia: 4000 g (8 lb 13 oz) or 4500 g (9 lb 4 oz)
o Continuous EFM Labor & vaginal delivery is NOT CONTRAINDICATED for
o Induction is NOT recommended. Oxytocin women with EFW up to 5 kg in the absence of maternal DM
augmentation if with hypotonic uterine dysfunction. Indication for CS:
o Passive 2nd stage without active pushing for 90 min o >4,500 g, and
allowing breech to descend into pelvis o prolonged 2nd stage or arrest of descent in 2nd stage
o Once active pusching commences and delivery not Prophylactic CS:
imminent after 60 min, CS is recommended. o EFW > 5,000 g (w/o maternal DM)
Delivery of the aftercoming head: o EFW > 4,500 g (w/ maternal DM)
o assistant should apply suprapubic pressure to favor Suspected macrosomia is NOT a contraindication to
flexion and engagement of fetal head attempted VBAC
o Mauriceau-Smellie-Veit maneuver, or
o Use of Piper forceps
Spontaneous or assisted breech delivery is acceptable. Fetal 8. Shoulder Dystocia
manipulation applied after spontaneous delivery to the Shouder Dystocia Drill:
level of umbilicus. 1. Call for HELP!
Nuchal arms may be reduced by Lovset maneuver. 2. Generous EPISIOTOMY
3. SUPRAPUBIC pressure
Suspected breech 4. McRoberts maneuver
o Pre- or early labor ultrasound to assess type of breech,
fetal growth, EFW, attitude of fetal head. If the “Drill” fails, attempt the following:
o If ultrasound is not available, CS is recommended. 1. Delivery of posterior arm
2. Woods screw maneuver
2. External cephalic version 3. Rubin maneuver
ABSOLUTE Contraindications 4. Zavanelli maneuver
o Where CS is required 5. Cleidotomy
o Anterpartum bleeding within the last 7 days 6. Symphysiotomy
o Abnormal CTG
o Major uterine anomaly (supplementary)
o Ruptured membranes “Shoulder dystocia drill” to better organize emergency
o Multiple pregnancy (except delivery of the 2nd twin) management:
RELATIVE Contraindications
o SGA fetus with abnormal Doppler 1. Call for help—mobilize assistants and anesthesia and
o Proteinuric preeclampsia pediat- ric personnel. Initially, a gentle attempt at traction is
o Oligohydramnios made. Drain the bladder if it is distended.
o Major fetal anomalies 2. A generous episiotomy may be desired to afford room
o Scarred uterus posteriorly. 

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3. Suprapubic pressure is used initially by most practitioners CS performed for those with history of complete
because it has the advantage of simplicity. Only one assis- transverse vaginal septum and vaginal agenesis due to
tant is needed to provide suprapubic pressure, while normal risk of vaginal soft tissue dystocia and lateral vault
downward traction is applied to the fetal head. 
 laceration
4. The McRoberts maneuver requires two assistants. Each
assistant grasps a leg and sharply flexes the maternal thigh 3. Abnormalities of the placenta, cord, membranes and
against the abdomen. This is the
 single most effective amniotic fluid
intervention and performed first. Vasa previa
These maneuvers will resolve most cases of shoulder dystocia. If o Elective CS between 35-37 weeks AOG
the above listed steps fail, the following steps may be attempted, o Emergency CS for bleeding vasa previa
and any of the maneuvers may be repeated: Placenta previa
5. Delivery of the posterior arm is attempted. With a fully o Any degree of placental overlap (>0 mm) at the
extended arm, however, this is usually difficult to internal os after 35 weeks is an indication for CS
accomplish.
 o Previa within 1 cm of the internal os is an indication
6. Woods screw maneuver is applied. 
 Progressively rotating for CS
the posterior shoulder 180 degrees in a corkscrew fashion, o Elective CS for asymptomatic woman with previa >37
the impacted anterior shoulder could be released. weeks and for suspected accreta >36 weeks
7. Rubin maneuver is attempted. 
 Abruptio placenta
First, the fetal shoulders are rocked from side to side by o Emergency CS for abruptio placenta with fetal
applying force to the maternal abdomen. compromise, severe uterine hyprtonus, life
If this is not successful, the pelvic hand reaches the most threatening bleeding or DIC, and remote from vaginal
easily accessible fetal shoulder, which is then pushed delivery.
toward the anterior surface of the chest. This maneuver Cord prolapse
most often abducts both shoulders, which in turn produces o Emergency CS for cord prolapse
a smaller shoulder-to-shoulder diameter. This permits o Cord prolapse with poor chances of viability, vaginal
displacement of the anterior shoulder from behind the delivery may be tried with informed consent
symphysis. o Ultrasound finding suggestive of forelying cord or
Other maneuvers: funic presentation is NOT an absolute indication for
o Zavanelli maneuver – replaces or flexes the fetal CS
head back into the vagina, then CS is performed. o Digital diagnosis of funic/cord presentation in labor is
o Cleidotomy – deliberate fracture of the anterior an indication for CS
clavicle to fee the shoulder impaction. Chorioamnionitis or intra-amniotic infection
o Symphysiotomy – intervening symphyseal cartilage o Presence of clinical chorioamnionitis or intra-amniotic
and much of its ligamentous support is cut to widen infection is NOT an absolute indication for CS.
the symphysis pubis Oligohydramnios
o Uncomplicated oligohydramnios is NOT an absolute
GUIDELINES FOR CESAREAN SECTION indication for CS
Indications
1. Previous uterine scar 4. Infection in pregnancy
2. Abnormalities of the reproductive tract Herpes simplex virus
3. Abnormalities of placenta, cord, membranes & AF o CS for those who develop primary genital herpes
4. Infection in pregnancy within 6 weeks of delivery
5. Maternal medical conditions o CS for those with active genital lesions or prodromal
6. IUGR/FGR symptoms (e.g. vulvar pain or burning) at the time of
7. Fetal congenital anomalies delivery
8. CDMR (Maternal request) Hepatitis B virus
o Scheduled CS at 39 weeks with HBV profile as follows:
1. Previous uterine scar HbeAg positive
In the presence of scarred uterus, the following are HBV DNA copies >1,000,000
ABSOLUTE INDICATIONS for elective CS: (Level III, Grade C) Not received oral antiretroviral therapy
o Previous classical or inverted T-uterine scar Human papilloma virus
o Uncertainty of type of previous CS scar o Only for those with very large genital warts causing
o Previous multiple low transverse segment uterine pelvic outlet obstruction or potential for excessive
scars bleeding during vaginal delivery
o Previous hysterotomy or myomectomy entering the HIV
uterine cavity or extensive transfundal uterine o Elective CS at 39 weeks to reduce risk of MTCT
surgery provided:
o Previous uterine rupture Currently on highly active antiretroviral therapy
o Presence of a contraindication to labor, such as (HAART)
placenta previa/accreta, or malpresentation Viral load <400 copies/ml
o No informed consent for VBAC On any ARV with viral load <50 copies/ml
Failed trial of labor during VBAC.
5.
Maternal medical conditions
2. Abnormalities of the reproductive tract Hypertensive complications
Presence of gynecologic tumors in pregnancy, such as o Maternal indications
uterine myoma and/or adnexal masses, are NOT ABSOLUTE Deteriorating maternal condition
indications for CS, unless they cause dystocia Uncontrolled hypertension despite drug therapy
CS performed for those with a history of surgical repair of HELLP syndrome
obstetric and anal sphincters, urinary incontinence and Placental abruptio
pelvic organ prolapse because of risk of recurrences o Fetal indications
Genital warts and genital cancers may be an indication Severe IUGR/FGR
for CS if it obstructs the birth canal, or if it is excessively Non-reassuring FHR pattern, repeated Category
bleeding, or in order to prevent profuse bleeding II or III, refractory with resuscitation, remote
Presence of cervical stenosis is NOT A from delivery
CONTRAINDICATION to attempted vaginal delivery. There BPP <4, done 6 hours apart
is increased risk for CS. Doppler studies: ARED
Vaginal delivery for corrected imperforate hymen. Severe bronchial asthma
o CS is rarely needed.
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Cardiac disease Uncomplicated elective CS may have modest amounts of
o CS reserved for high-risk cardiac patients. clear liquids up to 2 hours prior to induction of anesthesia
Gestational DM Patient undergoing elective surgery should have a fasting
Obesity period for solids at least 6-8 hours prior to induction.
o Increased risk for CS Aspiration prophylaxis: non-particulate antacids, H2
Macrosomia receptor antagonists, metoclopramide
Post-CS care
6. IUGR/FGR No evidence to recommend a policy of delaying oral fluids
Deterioration in the fetal condition or when there is an and food after CS
unripe cervix or when there are indications of additional Remove the dressing 24 hours after the CS.
fetal compromise during labor No evidence of adverse outcomes associated with early
Viable fetus with IUGR when there is: postnatal discharge (3-4 days)
o deterioration in the BPP Sexual intercourse may be resumed as early as 2 weeks
o loss of variability on NST postpartum for as long as the patient feels comfortable.
o severe oligohydramnios, and
o failure to grow on serial biometry in the presence of OTHER IMPORTNANT OBSTETRIC INFORMATION
abnormal umbilical artery or venous Doppler studies.
DERMATOSES IN PREGNANCY
7. 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

8. 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. PITUITARY DESTRUCTION
Damage or necrosis of the pituitary gland caused by anoxia,
9. Multiple pregnancy thrombosis, or hemorrhage. It is called Sheehan’s syndrome
10. Fetal malpresentation (Refer to Section III) when related to pregnancy and Simmonds’ disease when
11. Abnormal labor patterns (Refer to Section II) unrelated to pregnancy.
12. Abnormal FHR patterns (Refer to Section I)
OBSTETRICAL HEMORRHAGE
Operative Recommendations
Timing of planned CS
Scheduled at 39 weeks
Pre-operative preparation for CS
Hemoglobin determination
Antimicrobial prophylaxis within 60 minutes pre-
operatively 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

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

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
Uterine Atony o Soft tissue abnormalities of the reproductive
The most frequent cause of obstetrical hemorrhage is failure of tract may form an obstacle to fetal descent
the uterus to contract sufficiently after delivery and to arrest
bleeding from vessels at the placental implantation site

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

Late onset sequelae include hearing


loss, neurological deficits, chorioretinitis,
psychomotor
retardation, and learning disabilities
Group A Remains the most common
Streptococcus cause of severe maternal postpartum
infection and death
worldwide
Group B May cause preterm labor, prematurely
Streptococcus ruptured membranes, clinical
and subclinical chorioamnionitis, and fetal
infections.

GBS can also cause maternal bacteriuria,


pyelonephritis, osteomyelitis,
postpartum mastitis, and puerperal
infections.

MRSA Skin and soft tissue infections are the most


common presentation of MRSA in
pregnant women
Listeriosis Discolored, brownish, or meconium-
stained amnionic fluid is common with
fetal infection, even preterm gestations

Diagnosis Effects Maternal listeriosis causes fetal infection


Varicella Congenital varicella syndrome- that characteristically produces
chorioretinitis, microphthalmia, cerebral disseminated granulomatous lesions with
cortical atrophy, growth restriction, microabscesses
hydronephrosis, limb hypoplasia,
and cicatricial skin lesions Chorioamnionitis is common with
Influenza No firm evidence that it causes congenital maternal infection, and placental lesions
malformations include multiple, well-demarcated
Mumps Women who develop mumps in the first macroabscesses.
trimester may have an increased risk of Toxoplasmosis Clinically affected neonates
spontaneous abortion usually have generalized disease
Measles/Rubeola The virus does not appear to be expressed as low birthweight,
teratogenic. hepatosplenomegaly, jaundice, and
However, an increased frequency of anemia. Some primarily
abortion, preterm delivery, have neurological disease with
and low-birthweight neonates is noted intracranial calcifications and
with maternal measles with hydrocephaly or microcephaly. Many
German Rubella infection in eventually develop
Measles/ Rubella the first trimester, however, poses chorioretinitis and exhibit learning
significant risk for abortion and disabilities.
severe congenital malformations.
TRIAD: Chorioretinitis, intracranial
Rubella is one of the most complete calcifications and hydrocephalus
teratogens, and sequelae
of fetal infection are worst during APPENDICITIS IN PREGNANCY
organogenesis. - Suspected appendicitis is one of the most common
indications for abdominal exploration during
Congenital Rubella Syndrome pregnancy
• Eye defects—cataracts and congenital
- When appendicitis is suspected, treatment is prompt
glaucoma
• Congenital heart defects—patent ductus
surgical exploration.
arteriosus and - Although diagnostic errors may lead to removal of a
pulmonary artery stenosis normal appendix, surgical evaluation is preferable to
• Sensorineural deafness—the most postponed intervention and generalized peritonitis
common single defect o Appendicitis increases the likelihood of
• Central nervous system defects— abortion or preterm labor, especially if there
microcephaly, developmental is peritonitis
delay, mental retardation, and
meningoencephalitis PANCREATITIS IN PREGNANCY
• Pigmentary retinopathy - Medical treatment is the same as that for nonpregnant
• Neonatal purpura patients and includes analgesics, intravenous hydration,
• Hepatosplenomegaly and jaundice and measures to decrease pancreatic secretion by
• Radiolucent bone disease interdiction of oral intake.

Parvovirus B19 Associated with abortion, nonimmune LEIOMYOMAS IN PREGNANCY


hydrops and still birth - Can regress after pregnancy
Cytomegalovirus Growth restriction, microcephaly, - May cause pain or pressure
intracranial calcifications, chorioretinitis,
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- May outgrow their blood supply and hemorrhagic symptomatic to nulliparous women, highest occuring in 5th
infarct follows- Red or Carneous Degeneration decade. May cause miscarriage.
- Treatment is analgesic medication, myomectomy has o Types
resulted in good outcomes Intramural
- Pedunculated subserosal myosmas will undergo Subserous- just beneath the serosa
torsion—can be managed with laparoscopy or Submucosal- just below the
laparotomy endometrium, may be associated
- Complications with abnormal bleeding and
o Preter labor distortion of the uterine cavity that
o Placental abruption may produce infertility or abortion
o Fetal malpresentation Broad ligaement
o Obstructed labor Parastic
o Cesarian delivery o Myomas often enlarge during pregnancy
o Postpartum hemorrhage o Most common symptoms
Pelvic pain or pressure
IMPORTANT GYNECOLOGIC CONCEPTS Enlarging pelvic mass
Abnormal uterine bleeding (30%)
BENIGN GYNECOLOGIC LESIONS BASED ON LOCATION o Management
Judicious observation- for small
Vulva asymptomatic myomas
Urethral Caruncles – small, single, sessile but may be Myomectomy
pedunculated, 1-2 cm in diameter. Occurs frequently in post- Persistent pain/pressure
menopausal women, and may be secondary to infection or Enlargement to more than
chronic irritation 8 cm to a woman who has
Cysts- the most common large cyst of the vulva is a cystic not completed childbearing
dilatation of an obstructed Bartholin’s duct. The most CONTRAINDICATION:
common small vulvar cysts are epidermal inclusion cysts or Pregnancy
sebacious cysts. Hysterectomy
Nevus- vulvar nevi are one of the most common benign Persistent pain/pressure
neoplasms in females; generally asymptomatic Size reached the size of a
Hemangioma- rare malformations of blood vessesls than 14-16 week gestation
true neoplasms. Usually discovered intitially during Medical Management – decrease the
childhood. It is usually single, 1-2 cm in diameter, flat, soft circulating level of estrogen and
and colors range from brown, red or purple. These tumors progesterone
range in size and not encapsulated Adenomyosis – from aberrant glands of the basalis layer
Fibroma- the most common benign solid tumors of the vulva. of endometrium. 50% are asymptomatic, but those who
It occurs in all age groups and commonly found in the labia are symptomatic present with dysmentorrhea,
majora. Majority are 1-10 cm in diameter. menorrhagia ages 35-50
Lipoma- Benign, slow-growing, circumscribed tumors or fat
cells arising from the sub cutaneous tissue of the vulva Oviduct
Leiomyomas
Vagina Angiomyomas
Urethral diverticulum- permanent, epithelialized, sac-like Paratubal cysts – if pedunculated and near the fimbrial end
projection that arises from the posterior urethra, present at of the oviduct, they are called hydatid cysts of Morgagni
a mass of the anterior vaginal wall. It is a common problem
discovered in 1-3% of women Ovary
Inclusion cysts- the most common cystic structures of the Fuctional cysts – All are benign and usually does not cause
vagina symptoms or require surgical management
Dysontogenic cysts- thin walled, soft cysts of embryonic o Follicular cysts- most frequent cystic
origin structures in normal ovaries. Mostly
o Gartner’s duct cysts – from the mesonephros asymptomatic
o Mullerian cysts – from the o Corpus luteum cysts- minimum of 3 cm in
paramesonephricum diameter, associated with normal, delayed
o Vestibular cysts – fromt he urogenital sinus menses or amenorrhea. It may cause
intraperitoneal bleeding
Cervix o Theca lutein cysts- least common of the 3
Endocervical and Cervical Polyps – Most common benign physiologic ovarian cyts, almost always found
neoplastic growth of the cervix. It is most common in bilaterally, and can produce enlargement of
multiparous women in their 40s-50s. Majority are smooth, the ovaries. It is caused by prolonged or
soft, reddish purple to cherry red. They are fragile and excessive stimulation of the ovaries to
readily bleed when touched. It may arise to endocervical gonadotropins. USUALLY OCCUR WITH
canal or ectocervix PREGNANCY, INCLUDING MOLAR
Nabothian cysts- retention cysts that are very common that PREGNANCY.
they are considered a normal feature of the adult cervix.
Aymptomatic and no treatment is necessary Benign neoplams
Cervical myoma- usually a solitary growth, small and most o Benign cystic teratoma (Dermoid cyst)- cystic
are asymptomatic structures that on histologic examination
contain elemetns of the three germ cell layers.
Uterus Benign teratomas are among the most
Endometrial polyps – localized overgrowths of endometrial common ovarian neoplasms, and are the most
glands and stroma beyond the surface of the endometrium. common neoplasms in prepubertal females
Majority are asymptomatic, but those who are symptomatic and teenagers. When opened, sebacous fluid
are associated with a wide range of bleeding patterns along with hair, cartilage and teeth can be
found
Hematometra – uterus distended with blood and secondary
o Endometriomas (Chocolate cyst) – usually
to gynatresia. Common symptoms include amennorrhea and
associated with endometriosis, and one of the
cyclic lower abdominal pain
most common causes of the enlargement of
Leiomyomas/Myomas – most frequent pelvic tumor and the
the ovary. It range to small (1-5 mm) to 5-10
most common tumor in women. More prone to grow and
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cm in diameter hemorrhagic cysts. Symptoms COMPLETE/CLASSI PARTIAL/INCOMPLETE
include pelvic pain, dyspareunia and infertility C MOLE MOLE
o Fibromas- most common benign, solid
neoplasms of the ovary. Associated with GENETICS
Meig’s syndome (Ovarian fibroma + ascites MC 46, XX 69, XXY
+ hydrothrorax) karyotype
o Brenner tumors (Transitional cell tumor)- Chromosom All paternally Extra paternal set
rare, small, smooth, fibroepithelial ovarian al Origin derived
tumors that are generally asymptomatic. 1-2%
undergo malignant changes. Histologically, it is CLINICAL PRESENTATION
composed of solid masses/nests of epithelial Signs and Abnormal vaginal Missed abortion
cells (similar to transition cells of the urinary Symptoms bleeding
bladder) and surrounding fibrous stroma Classic Common Rare
o Adenofibroma and Cystadenofibroma – symptoms
benign, firm tumors, consists of fibrous and Uterine size 50% large for Size equals date or
epithelial components Gestational Age smaller
Theca Present in 25% Rare
In relation to pregnancy: Lutein Cyst
The most frequent types of ovarian masses are corpus hCG levels High ( >100,000) Slightly elevated
luteum cysts, endometriomas, benign cystadenomas, and Malignant 15-25% <5%
mature cystic teratomas (dermoids) Potential
Weeks to 14 weeks 8 weeks
normal hCG
TUMOR MARKERS

Marker Description
Serum CA125 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

Serum CA125 levels are useful in


distinguishing malignant from benign pelvic
masses
Alfafetoprotein Both α -fetoprotein (AFP) and human chorionic
and hCG gonadotropin (hCG) are secreted by some
germ cell malignancies
CLINICAL DIAGNOSTIC FEATURES IN COMPLETE MOLE
Most endodermal sinus tumor (EST) lesions • Vaginal bleeding before 12 weeks
secrete AFP • Most common symptom
• Uterine enlargement out of proportion to AOG
The mixed germ cell lesions may secrete either • Most common finding
AFP, hCG, or both or neither of these markers, • Absence of fetal parts or fetal heart sounds
depending on the components • Classic signs and symptoms related to high level of hCG
Inhibin Inhibin is secreted by some granulosa cell (>100,000)
tumors • Pre-eclampsia/ eclampsia developing before
20 weeks
• Hyperemesis gravidarum
GESTATIONAL TROPOBLASTIC DISEASES • Thyrotoxicosis
• Presence of Theca Lutein Cysts
• Refers to the pregnancy related trophoblastic
proliferative abnormalities DIAGNOSIS
• Classification: • The measurement of HCG is an integral part of the
• Benign GTD diagnosis and evaluation of the patient suspected of
• Complete mole having GTD.
• Incomplete mole • Ultrasonography is the criterion standard for
• Malignant GTD identifying both complete and partial molar
• Persistent/ Invasive mole pregnancies.
• Choriocarcinoma • Complete Mole
• Placental Site Tumor • Snow storm pattern
• Homogenous intrauterine echoes
COMPLETE/CLASSI PARTIAL/INCOMPLETE without a gestational sac or fetal
C MOLE MOLE parts
• Incomplete Mole
PATHOLOGY • Swiss cheese pattern
Cause Dyspermic Dyspermic fertilization • CXR
fertilization of an of a normal egg by 2 • Once a molar pregnancy is diagnosed get CXR
empty egg by one normal sperms • If with lung mets, CANNON BALL EXUDATES
normal sperm
Coexistent Absent Present BASIC APPROACH TO GTD
Fetus Pre- B- hCG titer • Baseline for future
Chorionic Hydropic (swollen) Focal hydropic treatment comparison
Villi evaluation CXR • To rule out lung metastasis
Trophoblast Severe hyperplasia Minimal or none Phases of Suction D&C 1. Immediate evacuation of

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treatment mole hypergonadotropic and hypogonadotropic
2. Treatment of choice is forms of hypogonadism
Suction D&C Treatment:
3. Hysterectomy is preferred o Individuals with primary amenorrhea
if more than 35 YO or has associated with all forms of gonadal
no desire for future ailure and hypergonadotropic hypogonadism
pregnancy need cyclic estrogen and progestogen therapy
Subsequent • Measure hCG every 2 to initiate, mature, and maintain secondary
Follow up and weeks until 3 consecutive sexual characteristics.
evaluation negative values
• Once negative value, test MANAGEMENT OF AUB/DUB
monthly for 6 months and
then every 2 months for a Dysfunctional Uterine Bleeding
total of 1 year - Describes abnormal bleeding for which no specific
• A rise or plateau of hCG cause was found; often a diagnosis of exclusion
demands evaluation
Prevention of • 1 year of OCP to prevent Causes of Bleeding Per Age Group
pregnancy pregnancy

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 Management
• Placental site trophoblastic tumor Laboratory
o Pregnancy test, CBC, Prothrombin time, PTT,
PERSISTENT/ 75% of all GTD’s VWF
INVASIVE Usually follow a molar pregnancy Imaging
MOLE Excessive trophoblastic overgrowth o Ultrasound
and extensive penetration including Endometrial Sampling
the whole villi, myometrium, and o Performed for women at risk for endometrial
adjacents tructures pathology (polyps, hyperplasia or carcinoma)
Very sensitive to chemotherapy Management
CHORIOCARCINOMA Extremely malignant form of o Mefenamic Acid and other NSAIDs
trophoblastic tumor of the chorionic o Tranexamic Acid
epithelium o Mild bleeding: combination low-dose oral
Metastasize most of the time (lung) contraceptive
Extremely hemorrhagic and o Acute moderate bleeding: combination
necrotic with absence of villous monophasic oral contraceptives every 6 hours
pattern, chorionic villi, and cellular for 4-7 days
atypia o Emergency management:
Very sensitive to chemotherapy Hormonal therapy: Estrogen-
Placental Site Extremely rare progestin therapy 1-2 pills 2x/day
Trophoblastic Tumor Arises from placental implantation for 7 days effective for 12-24 hours
following either a nomal pregnancy OR conjugated estrogens 25-40 mg
or abortion IV every 6 hrs or 2.5 mg oral every 6
Predominantly cytotrophoblast and hours
cells secreting prolactin and If intrauterine clots are detected D&C
gonadotropin is indicated
Low hCG level
Hysterectormy is the treatment of
choice GENITOURINARY INFECTIONS and STDs

GTN Diagnosis Diagnosis Description Treatment


Recognition of the possibility of GTN is the most important Bacterial Most common cause of Metronidazole
factor in the diagnosis Vaginosis vaginitis in the US Clindamycin
Any unusual bleeding after term pregnancy should be
investigated by curettage and measurements of serum hCG Women with BV are at risk for
PID, Pregnant women are at
MANAGEMENT OF AMENORRHEA risk for PROM, preterm labor
The most important elements in the diagnosis of and delivery, chorioamnionitis
amenorrhea include physical examination for secondary
sexual characteristics and anatomic abnormalities, Diagnosis: fishy vaginal odor;
Measurement of: clue cells in histology
o human chorionic gonadotropin (hCG) to rule Trichomonas Profuse, purulent, malodorous Metronidazole
out pregnancy vaginal discharge with
o serum prolactin and thyroid stimulating pruritus; Strawberry cervix
hormone (TSH) levels may be observed
o assessment of follicle-stimulating hormone
(FSH) levels to differentiate between Women with this infection

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should also be tested for other pathogen for acute cystitis TMP-SMX,
STDs Nitrofurantoin
Candidiasis 75% of women may Topical azoles
experience this in their (Butoconazole, Pyelonephritis:
lifetime. Predisposing factors: Clotrimazole, TMP-SMX,
pregnancy, diabetes, antibiotic Miconazole, Levofloxacin,
use. Discharge may be varied Tioconazole, Cetriazone,
from watery to thick Nystatin, Ampicillin,
Fluconazole) Gentamicin
Atrophic Common in menopausal Estrogen
vaginitis women cream
Cervicitis Presents with purulent Treatment –
cervical discharge for lower
genital tract POLYCYSTIC OVARY SYNDROME
infection with
both - Characterized by a combination of hyperandrogenism
chlamydia and (either clinical or biochemical), chronic anovulation,
gonorrhea and polycystic ovaries. It is frequently associated with
insulin resistance and obesity
Cefexime, - It is the most common cause of hyperandrogenism,
Azithromycin, hirsutism, and anovulatory infertility in developed
Doxycycline, countries
Ofloxacin, - Criteria:
Levofloxacin o Oligoovulation or anovulation
Pelvic Diagnosis implies that the Outpatient o Clinical and/or biochemical signs of
Inflammatory patient has upper genital tract treatment: hyperandrogenism
Disease infection and inflammation Cefoxitin or o Polycystic ovaries and exclusion of other
(ascended to the endometrium Ceftriaxone etiologies (congenital adrenal hyperplasia,
and fallopian tubes) PLUS androgen-secreting tumors, Cushing’s
Doxycycline or syndrome)
Commonly caused by N. Azithromycin
gonorrhoeae and C.
trachomatis Inpatient
treatment:
Triad: pelvic pain, cervical Cefoxitin or
motion and adnexal Cefotan PLUS
tenderness and fever Doxycline

Or

Clindamycin
PLUS
Cefrtriaxone or
Gentamicin
Tubo-ovarian End stage process of PID Medical
Abscess treatment or
Abscess
Drainage
Genital Those with genital ulcers may Chancroid:
Ulcers have HSV or syphilis or Azithromycin,
chancroid Ceftriaxone,
Ciprofloxacin,
Erythromycin

HSV: Acyclovir,
Famciclovir,
Valacyclovir

Syphillis: Pen
G
Genital warts Manifestation of HPV 51 Goal of
(external) treatment is to - Metabolic Syndrome Diagnostic Criteria
remove the o Female waist >35 inches
Non-oncogenic HPV 6 and 11 warts but it is o Triglycerides >150 mg/dL
also cause external genital not possible to o HDL <50 mg/dL
warts eradicate the o Blood pressure >130/85 mmHg
infection o Fasting glucose: 110–126 mg/dL
Highly contagious o Two-hour glucose (75 gm OGTT): 140–199
Cryotherapy, mg/dL
Imiquimod - Treatment
cream, o Hormonal contraception or ovulation
Podophyllin, induction
Podofilox, o Hirsutism: Weight loss, Oral contraceptives,
Trichloroacetic medroxyprogesterone, GnRH analogues,
acid, Cautery, glucorticoids, ketoconazole, finasteride,
Laser, spironolactone, flutamide, metformin
Interferon
UTI E.coli is the most common Acute Cystitis:
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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 IMPERFORATE HYMEN
females may also occur - Hypen should establish a connection between the
- Treatment and Management lumen of the vaginal canal and the vestibule
o Replacement of cortisol – suppresses - May result to primary amenorrhea
ACTH output and decreases the - May cause hydrocolpos or mucocolpos- caused by
stimulation of the cortisol producing collection of secretions behind the hymen, and in rare
pathways in the adrenal cortex cases may build up to form a mass that obstructs the
o For females at risk – dexamethasone urinary tract
- May develop hematocolpos and hematometrium
o Corrective surgery
overtime
o Psychosocial support and counseling
- 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-Kuster-
Hauser (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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