July 24, 2017 | Author: Eidette Lisondra | Category: Uterus, Luteinizing Hormone, Vagina, Ovary, Labia
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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] OBSTETRICS SUPPLEMENT HANDOUT TABLE OF CONTENTS Maternal Anatomy Menstrual Physiology Fertilization Placenta Fetal Development Maternal Physiology Prenatal Care Postpartum Changes Postpartum hemorrhage Dystocia Other Important Obstetric Information Important Gynecologic Concepts

1 5 9 10 11 13 19 22 26 27 29 32


Labia Minora

Clitoris Vestibule

Vestibular Glands

Urethral opening

Vestibular bulbs

Vaginal opening/hymen

escutheon 7-8x2-3x1-1.5cm round ligaments terminate at their upper borders connective tissue with many vessels, elastin fibers, and some smooth muscle fibers points downward and inward toward the vaginal opening; rarely exceeds 2 cm functionally mature female structure derived from the embryonic urogenital membrane perforated by six openings: urethra, the vagina, two Bartholin gland ducts, and two ducts of the Skene glands Bartholin glands, paraurethral glands (Skene glands diverticulum) minor vestibular glands lower two thirds of the urethra lie immediately above the anterior vaginal wall. 1 to 1.5 cm below the pubic arch lie beneath the bulbocavernosus muscle on either side of the vestibule vulvar hematoma. Hymenal caruncles Impreforate hymen

VESTIBULE • Functionally mature female structure of the urogenital sinus of the embryo. Extends from clitoris to forchette STRUCTURES IN THE VESTIBULE HYMEN  Non keratinized Stratified squamous epithelium  During first coitus, first that ruptures is usually at the 6 o’clock position  Caruncle Myrtiformes: Remnants of hymen in adult female GLANDULAR Periurethral Glands “ Skene’s Glands” STRUCTURES Vulvovaginal Glands “Bartholin’s Glands” 6 OPENINGS:  Vaginal introitus  Urethral opening  Paired Para urethral glands opening  Paired Bartholin ducts opening GLANDULAR STRUCTURES PERIURETHRAL GLANDS “ Skene’s glands” Other name Lesser vestibular glands Male Prostate homology Type of Tubulo alveolar gland Location Adjacent to the urethra Pathology Urethral diverticulum

VULVOVAGINAL GLANDS “Bartholin’s glands” Greater vestibular glands Bulbourethral gland Compound alveolar/ compound acinar 4 and 8 o clock of the vagina Bartholins’s cyst/ abscess

DIFFERENCE OF LABIA MAJORA AND LABIA MINORA LABIA MAJORA LABIA MINORA HOMOLOGY Scrotum Ventral portion of the penis Skin of the penis LINING Outer- KSSE NKSSE EPITHELIUM Inner- NKSSE NULLIPAROUS Lie in close Not visible behind WOMEN apposition the non separated Inner surface labia majora resembles the mucous membrane MULTIPAROUS Gape widely Project beyond the WOMEN Inner surface labia majora become skin like GLANDS (+) Hairfollicles No hair follicles (+) Sweat glands No sweat glands (+) Sebaceous (+) Sebaceous glands glands


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Urogenital (Anterior) Triangle: DEEP SPACE Anterior Triangle (DEEP SPACE)

Clinical Significance



pubic symphysis


ischiopubic rami and ischial tuberosities


sacrotuberous ligaments





Urogenital triangle Boundaries: Superrior- pubic rami Lateral-ischial tuberosities Posterior: superficial transverse perineal muscle Anal triangle ischiorectal fossa, anal canal, anal sphincter complex, and branches of the internal pudendal vessels and pudendal nerve

Urogenital (Anterior) Triangle: SUPERFICIAL SPACE Anterior Triangle (SUPERFICIAL SPACE) closed compartment

lies deep to the perineal membrane and extends up into the pelvis Contents: compressor urethrae and urethrovaginal sphincter muscles, external urethral sphincter, parts of urethra and vagina, branches of the internal pudendal artery, and the dorsal nerve and vein of the clitoris

Ishorectal fossae

wedge-shaped spaces found on either side of the anal canal and comprise the bulk of the posterior triangle Continuous space



Anterior  Superficial and deep

Continuous space with the pelvis

bounded deeply by the perineal membrane and superficially by Colles fascia ischiocavernosus, bulbocavernosus, and superficial transverse perineal muscles; Bartholin glands; vestibular bulbs; clitoral body and crura; and branches of the pudendal vessels and nerve

ischiocavernosus muscle

clitoral erection

bulbocavernosus muscles

Bartholin gland secretion Clitoral erection

superficial transverse perineal muscles

may be attenuated or even absent Contributes to the perineal body


Anterior rami of the 2nd to 4th sacral nerve


between the piriformis and coccygeus muscles and exits through the greater sciatic foramen in a location posteromedial to the ischial spine  obturator internus muscle  pudendal canal (Alcock Canal)  enter the perineum and divides into three terminal branches

Terminal Branches: dorsal nerve of the clitoris

skin of the clitoris

perineal nerve

muscles of the anterior triangle and labial skin

inferior rectal

external anal sphincter, the mucous membrane of the anal canal, and the perianal skin

Landmark for pudendal nerve block

Ischial spine

Blood Supply

internal pudendal artery

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VAGINA H-shaped lower portion of the vagina is constricted (urogenital hiatus in the levator ani) Stratified squamous non keratinized epithelium without glands Upper part is more capacious It extends from the vulva to the cervix. Ruggae that has an accordion like distensability Vaginal length: – Anterior wall: 6-8 cm – Posterior wall: 7-10 cm Potential space: Lower third


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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

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Upper vaginal vaults – Subdivided into anterior, posterior, and two lateral fornices by the uterine cervix Internal pelvic organs usually can be palpated through their thin walls Posterior fornix provides surgical access to the peritoneal cavity

CERVIX EXOCERVIX Portio vaginalis Extends from the squamo columnar junction to the external orifice Single layer of mucous secreting Non keratinized highly ciliated columnar epithelium stratified squamous which is thrown into folds forming epithelium complex glands and crypts Hormone Sensitive Extensive amount of nerves Few nerves only Blood supply: Cervicovaginal branch of uterine artery located at the lateral walls

Prepubertal women o Original SCJ at or near the exocervix Reproductive Age women o Eversion of endocervical epithelium and exposure of columnar cells to the vaginal environment o Relocation of SJC down the Exocervix Late adulthood / Post menopausal women o SCJ at the endocervical canal o Formation of transformation zone with regrowth of the squamous epithelium UTERUS


Nulliparous: 6 to 8 cm (fundus=cervix) , 50-70 g multiparous: 10 cm (cervix 1/3), 80 g or more


Lower uterine portion

Fallopian tubes

Attaches at the cornua

Posterior wall

Completely covered by visceral peritoneum

Anterior wall

Only upper portion with peritonem  vesicouterine pouch


ENDOCERVIX Supravaginal portion Extends from the isthmus (Internal Os) to the ectocervix and contains the endocervical canal



STRATUM FUNCTIONALE • Shed during menstruation • Supplied by the Spiral Arteries • Superficial 2/3 STRATUM BASALE • Source of Stratum Functionale after menstruation • Supplied by the Straight arteries • Basal 1/3 • lympathics Inner Longitudinal Middle oblique Outer longitudinal lymphatics


Zona Spongiosa Zona compacta

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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] LIGAMENTS OF THE UTERUS Broad • Two wing-like structure that extend from ligament the lateral margins of the uterus to the pelvic walls • Divide the pelvic cavity into anterior and posterior compartments Reproductive Fallopian tubes structures ovaries Vessels: Ovarian arteries Uterine arteries Ligaments: Ovarian ligament Round ligament of uterus Cardinal • AKA Transverse Cervical Ligament or ligament Mackenrodt Ligament • Originated form the densest portion of the broad ligament • Medially united to the supravaginal wall of the cervix • Provide the major support of the uterus and cervix • Maintain the anatomic position of the cervix and upper part of the vagina Uterosacral • From posterolateral to the supravaginal ligament portion of the cervix encircling the rectum • Insert into the fascia over S2 and S3 Round • Extend from the lateral portion of the uterus, Ligament arising below and anterior to origin of the oviducts, that is continuous with the broad ligament, outward and downward to the inguinal canal terminating at upper portion of labium majus

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FALLOPIAN TUBES single layer of columnar cells, some of them ciliated and others secretory. No submucosa supplied richly with elastic tissue, blood vessels, and lymphatics Sympathetic innervation Diverticula

SEGMENTS OF THE FALLOPIAN TUBE Intramural Embodied within 2% of ectopic pregnancy Interstitial the muscular Ectopic pregnancy at this wall of the uterus area result in severe maternal morbidity Isthmus The narrow Most highly developed portion of the musculature tube that adjoins Narrowest portion the uterus, Preferred portion for passes gradually applying clips for female into the wider, sterilization lateral portion. Preferred portion for tubal ligation 12% of ectopic pregnancy Ampulla Widest and most Site of fertilization tortuous area 80% of ectopic pregnancy Infundibulum Fimbriated 5% of ectopic pregnancy extremity Tunnel shaped opening of the distal end of the fallopian tube

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Ovaries: LAYERS OUTER Innermost CORTEX portion


Primordial and Graafian follicles in various stages of development Outermost  Tunica Albuginea- dull and portion whitish fibrous connective tissue covering the surface of the ovary  Germinal epithelium of Waldeyer- a single layer of cuboidal epithelium over the Tunica Albuginea  Composed of loose connective tissue that is continuous with that of the mesovarium.  Smooth muscle fibers that are continuous with those in the suspensory ligament.  Contains the stroma and blood vessels of the ovary 

PELVIS Pelvic Organs: BLOOD SUPPLY MAJOR BLOOD SUPPLY TO THE FEMALE REPRODUCTIVE SYSTEM Pudenda Internal Pudendal artery Vagina Vaginal Artery of the Uterine Artery Cervix Cervicovaginal branch of Uterine artery Uterus Uterine Artery Fallopian tubes Ovarian Artery Ovaries PARTICIPANTS IN THE COLLATERAL CIRCULATION OF THE FEMALE PELVIS Branches from the  Ovarian artery Aorta  Inferior mesenteric  Lumbar and vertebral  Middle sacral arteries Branches from the  Deep iliac circumflex External Iliac Artery  Inferior epigastric artery Branches from the  Medial femoral circumflex artery Femoral Artery  Lateral femoral circumflex artery False

ANT: lower abdomen POST: lumbar vertebra LATERAL: iliac fossa


SUPERIOR BOUNDARY: Pelvic inlet INFERIOR BOUNDARY: Pelvic outlet ANTERIOR: Pubic Bones, Ascending Rami Of Ischial Bones, Obturator Foramina LATERAL: Ischial Bones and Sacrosciatic Notch

OVARIES Lies on the posterior aspect of the broad ligament, in the ovarian fossa o lateral to the uterus in the pelvic sidewall where the common iliac artery bifurcates o ovarian fossa of Waldeyer Are attached to the broad ligament by the mesovarium. They are not covered by peritoneum.


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] PELVIC JOINTS • Anterior: symphysis pubis/arcuate ligament of the pubis • Posterior: sacroiliac • Hormonal changes during pregnancy cause laxity of these joints • By 3-5 months POST PARTUM, laxity has regressed • Symphysis Pubis increase in width also Increase mobility and displacement of the sacroiliac joint WHY THE DORSAL LITHOTOMY POSITION? • Upward gliding of sacroiliac joint is GREATEST in the DORSAL LITHOTOMY POSITION • Outlet increase by 1.5 -2.0 cm


Appendix of testes


Appendix of Appendix of epidydymis vesiculosis Ductus of Duct of epididymis epoophoron Ductus deferens Gartner’s Duct Ejaculatory duct Seminal Vesicle Ureter Renal Pelvis Calyces Collecting system Glomerulus Renal Collecting Tubules Testes Ovary










Non promine nt Inclined neither anteriorl y nor posterior ly

Good prognosi s for vaginal delivery




20% Heart Shaped

25% Vertically oriented oval

Convergen t


5% rarest Horizontally oriented oval Divergent, then convergent



Non prominent

Forward and straight with little curvature

Straight = pelvis deeper than other 3 types

Well curved and rotated backward

Increased incidence of Deep Transvers e Arrest Limited posterior space for fetal head, poor prognosis

Increased incidence of Face Delivery Good prognosis for vaginal delivery

Poor prognosis for vaginal delivery





Labia Majora

Ventral portion of the penis Penis

Labia Minora

Urinary bladder Prostate gland

Urinary bladder Urethral and Paraurethral glands Vagina Greater vestibular glands Hymen

Prostatic Utricle Bulbourethral glands Seminal colliculus

Seminiferous tubules Rete Testis Gubernaculum testis

Hydatid of Morgagni Uterus and Cervix Fallopian Tubes Upper ¼ of the vagina

Ovarian Follicles Rete Ovarii Round ligament of uterus

MENSTRUAL PHYSIOLOGY Overview of Menstrual Cycle  Spontaneous, cyclical ovulation occurs at 25- to 35-day intervals  Cyclical ovulation continues for almost 40 years between menarche and menopause  Approximately 400 opportunities for pregnancy, which may occur with intercourse on any of 1,200 days (includes day of ovulation and its two preceding days) during the reproductive age of most women.  Menstrual cycle days 20 to 24 is the narrow window of endometrial receptivity to blastocyst implantation.  Mother and fetus coexist as two disctinct immunological systems because of modifications on both fetal and maternal tissues in a manner not seen elsewhere.  Endometrium-decidua is the anatomical site of blastocyst apposition, implantation, and placental development. Key Players: 1. Anterior pituitary a. FSH b. LH 2. Ovarian follicle a. Theca cells b. Granulosa cells 3. Estrogen 4. Progesterone 5. Endometrium a. Basalis b. Functionalis

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Clitoris 

OVARIAN CYCLE Average cycle duration is approximately 28 days, with a range of 25 to 32 days. Follicular phase (days 1 to 14) is characterized by: o Rising levels of estrogen o Thickening of the endometrium o Selection of dominant “ovulatory” follicle Luteal phase (days 14 to 21), the corpus luteum (CL) produces estrogen and progesterone, which prepare the endometrium for implantation. If implantation occurs, the developing blastocysts will begin to produce hCG and rescue the CL, thus maintaining progesterone production.


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] A. Follicular or preovulatory ovarian phase FOLLICLE PROFILE Event Numbers At Birth 2 Million oocytes Puberty 400,000 follicles Depletion rate 1,000 follicles/month (puberty to 35y/o) Total follicles released during 400 follicles reproductive age Atresia (apoptosis) of follicles 99.9% OOCYTE CYCLE  Primary Oocyte o formed by 5th fetal month o Started their first meiotic division o Arrested in Prophase from 5th fetal month until the onset of puberty o Will complete the first meiotic division at the onset of puberty  Secondary Oocyte o Formed after completion of Meiotic I o Release of the first Polar Body During ovulation o Arrested in Metaphase II until fertilization o Completion of 2ND Meiotic Division only occurs if there is fertilization


Ovarian steroid production: 1. Estrogen levels rise in parallel to growth of a dominant follicle. 2. Increase in its number of granulosa cells. 3. GC are the exclusive site of FSH receptor expression. 4. Increase in FSH during the late luteal phase stimulates increase in FSH receptors & ability of cytochrome P450 to convert androstenedione into estradiol. B. Ovulation OVULATION

Oocyte transforming growth factors: 1. Growth differentiation factor 9 (GDF9) 2. Bone morphogenetic protein 15 (BMP-15) Functions: 1. Regulate proliferation & differentiation of granulosa cells (GC) as primary follicles grow 2. Stabilize and expand the cumulus oocyte complex in the oviduct FOLLICLE DEVELOPMENT 1. Recruitment of primordial follicles. 2. Cohort will grow GC. 3. Selection of dominant follicle. 4. Dominant follicle increase GC. 5. Follicle produce estradiol & initiate expression of LH receptors. 6. Appearance of LH receptors. 7. GC secrete progesterone which will cause LH release. 8. GC produce inhibin B to inhibit FSH release. 9. Increase estradiol & inhibin production causes drop of FSH 10. Drop of FSH causes failure of other follicles to develop. 11. LH stimulates theca cells to produce androstenediol.

Key events: 1. Preovulatory follicles increase estrogen secretion 34 to 36 hours before release of ovum with LH surge. 2. LH peaks 10 to 12 hours before ovulation. 3. Resumption of meiosis 1 in the ovum and release of first polar body. 4. Cumulus cell produces more progesterone and prostaglandin. 5. Oocyte growth factors (GDF9 and BMP-15) increases. 6. Increase formation of hyaluronan-rich ECM 7. Expansion occurs where cumulus cells lose contact with one another and move outward from the oocyte along the hyaluronan polymer. 8. LH induces remodelling of the ovarian extracellular matrix to allow release of the mature oocyte. 9. Activation of proteases on weakening of the follicular basement membrane and ovulation. C.

Luteal or postovulatory ovarian phase

CORPUS LUTEUM Key events: 1. Constant at 12 to 14 days. 2. Luteinization occurs after ovulation when the CL develops. 3. Basement membrane separating the granulosa-lutein and theca-lutein cells breaks down 4. Day 2 postovulation, blood vessels and capillaries invade the granulosa cell layer. 5. Increased capacity of granulosa-lutein cells to produce progesterone is due to increased access to steroidogenic precursors through blood-borne LDL-derived cholesterol. 6. Just after ovulation, estrogen levels decrease. 7. Mid-luteal phase is a secondary rise that reaches a peak production of 0.25 mg/day of 17B-estradiol. 8. Toward the end of the luteal phase, there is secondary decrease in estradiol production. 9. Ovarian progesterone peaks at 25 to 50 mg/day during the midluteal phase. (With pregnancy, CL continues progesterone production in response to embryonic hCG) 10. CL is a transient endocrine organ that will rapidly regress 9 to 11 days after ovulation.


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] LUTEOLYSIS Luteolysis may be due to the following: 1. Decreased levels of circulating LH in the late luteal phase and 2. Decrease LH sensitivity of luteal cells 3. Apoptosis Effects of luteolysis: 1. Drop in circulating estradiol and progesterone levels. 2. Allows follicular development and ovulation during the next ovarian cycle 3. Signals the endometrium to initiate molecular events that lead to menstruation. D.     E.    

Estrogen effects 17B- estradiol is the most biologically potent naturally occuring estrogen secreted by granulosa cells of the dominant follicles and luteinized granulosa cells of the CL. Estrogen is the essential hormonal signal on which most events in the normal menstrual cycle depend. Estrogen receptor (ER-alpha & ER-beta) interaction can promote synthesis of specfic m-RNAs and proteins (e.g. estrogen and progesterone) Acts at endothelial cell surface to stimulate nitric oxide production, leading to its rapid vasoactive properties. Progesterone effects Progesterone enters cells by diffusion and in responsive tissues becomes associated with progesterone receptors --progesterone receptor type A (PR-A) and B (PR-B) PR-A can inhibit PR-B gene regulation. Both PR-A and PR-B are expressed in endometrial glands in the proliferative phase, such that both receptors are involved with subnuclear vacuole formation. After ovulation, the glands continue to express only PR-B through the midluteal phase. In contrast, the stroma & predecidual cells express only PR-A throughout the menstrual cycle.


A. Proliferative or preovulatory endometrial phase Features: • Straight to slightly coiled, tubular glands are lined by pseudostratified columnar epithelium with scattered mitoses. • Epithelial (glandular) cells, stromal (mesenchymal) cells and blood vessels replicate cyclically. • Functionalis layer is shed and regenerated from the deepest basalis layer almost 400 times during the reproductive lifetime of most women. • Day 5 of menses – the epithelial surface of the endometrium has been restored, and revascularization is in progress. Early proliferative phase:  Endometrium is thin, usually < 2 mm thick  Glands are narrow, tubular structures that are almost a straight and parallel course from the basalis layer toward the surface of the endometrial cavity.  Mitotic figures are identified by day 5 of cycle, and mitotic activity in both epithelium and stroma persists until day 16 to 17, or 2 to 3 days after ovulation.  Epithelial cell growth is regulated in part by epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-a)  Stromal cell proliferation appears to increase through paracrine and autocrine action of estrogen and increased local production of VEGF, which causes angiogenesis through vessel elongation in the basalis. Midproliferative phase: • Days 8-10 • Columnar surface epithelium • Longer curving glands • Variable stromal edema • Numerous mitotic figures Late proliferative phase: • Days 11-14 • Endometrium thickens from both glandular hyperplasia and increased stromal ground substance. • Functionalis layer – glands are widely separated, loose stroma is especially prominent. • Basalis layer – glands are more crowded and stroma is denser. Midcycle (near ovulation): • Glandular epithelium becomes taller and pseudostratified. • Superficial epithelial cells acquire: 1. microvilli (increase epithelial surface area) and 2. cilia (aid in the movement of endometrial secretions during the secretory phase) • Ovulation is evidenced by presence of subnuclear vacuoles in 50% of glands

Endometrial histologic features: o Proliferative phase – straight to slightly coiled, tubular glands are lined by pseudostratified columnar epithelium with scattered mitoses. o Early secretory phase – coiled glands with a slightly widened diameter are lined by simple columnar epithelium that contains clear subnuclear vacuoles. Luminal secretions are seen. o Late secretory phase – serrated, dilated glands with intraluminal secretion are lined by short columnar cells. o Menstrual phase – fragmented endometrium with condensed stroma and glands with secretory vacuoles are seen in a background of blood. Layers of endometrium o Basalis layer – supplied by straight artery o Functionalis layer – supplied by spiral artery

B. Secretory or postovulatory endometrial phase Early secretory phase: • coiled glands with a slightly widened diameter • lined by simple columnar epithelium that contains clear subnuclear vacuoles. • Luminal secretions are seen. Late secretory phase: • serrated, dilated glands with intraluminal secretion are lined by short columnar cells. Early secretory phase Dating based on glandular epithelium. Day 17: • glycogen accumulates in the basal portion of glandular epithelium, creating subnuclear vaculoes and pseudostratification (1st sign of ovulation) Day 18: • vacuoles move to the apical portion of the secretory nonciliated cells Day 19: • cells begin to secrete glycoprotein and mucopolysaccharide contents into the lumen; • glandular cell mitosis ceases with secretory activity.


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] Mid- to late-secretory phase Dating is based on endometrial stroma Days 21 to 24: • stroma becomes edematous • “window of implantation” • epithelial surface cells show decreased microvilli and cilia • appearance of pinopodes, luminal protrusions on the apical cell surface, in preparation for blastocyst implantation. Days 22 to 25: • stromal cells surrounding the spiral arterioles begin to enlarge, and stromal mitosis becomes apparent. • Predecidual transformation of upper 2/3 of functionalis layer • Glands exhibit extensive coiling and luminal secretions become visible Days 23 to 28: • predecidual cells, which surround spiral arterioles Spiral artery activity  Arise from arcuate arteries, which are myometrial branches of the uterine vessels  Lengthen at a rate greater than the rate of increase in endometrial tissue height or thickness  Rapid angiogenesis is regulated through estrogen- and progesterone-regulated synthesis of VEGF  Changes in blood flow through these vessels aid in endometrial growth  Excessive coiling and stasis in blood flow coincide with regression of CL function and lead to a decline in endometrial tissue volume  Coiling leads to endometrial hypoxia and necrosis  Prior to endometrial bleeding, intense vasospasm occurs to limit blood loss with menstruation MENSTRUATION Late premenstrual phase endometrium • Stromal infiltration by neutrophils, giving a pseudoinflammatory appearance to the tissue • Endometrial stromal and epithelial cells produce IL-8, which is a chemotactic activating factor for neutrophils, and serves to recruit neutrophils prior to menstruation • Invading leukocytes secrete enzymes that are members of the matrix metalloproteinase (MMP) family. • Rising level of MMP’s tips the balance between proteases and protease inhibitors, effectively initiating matrix degradation. Anatomical events  Marked changes in endometrial blood flow  Coiling of spiral arteries becomes sufficiently severe that resistance to blood flow increases strikingly, causing hypoxia or the endometrium  Resultant stasis is the primary cause of endometrial ischemia and tissue degeneration.  Intense vasoconstriction & endometrial cytokine changes, activation of proteases (MMP-1 & MMP-3) Prostaglandins & menstruation  Role of prostaglandin: o Vasoconstriction o Myometrial contractions o Upregulation of pro-inflammatory responses  Progesterone withdrawal increases expression of inducible COX-2 enzyme to synthesize prostaglandins and decrease expression of 15-hydroxyprostaglandin dehydrogenase (PGDH), which degrades prostaglandin  Increased prostaglandin production of stromal cells along with increased prostaglandin receptor density on blood vessels and surrounding cells.  PGF2-alpha o Vasoconstriction of spiral arteries, causing the uppermost endometrial zones to become hypoxic o Potent inducer of angiogenesis and vascular permeability factors such as VEGF

Vasoactive peptides  Endothelin-1 is a potent vasoconstrictor as a product of vascular endothelial cells. o Degraded by enkephalinase, which is located in endometrial stromal cells. o Increase in its activity parallels with the increase in progesterone levels after ovulation o Enkephalinase activity is highest during the midluteal phase and declines steadily thereafter as progesterone plasma levels decrease. Activation of lytic mechanisms  Following vasoconstriction & endometrial cytokine changes, activation of proteases (MMP-1 and MMP-3) within stromal cells and leukocyte invasion occurs to degrade the endometrial interstitial matrix. Origin of menstrual blood  Arterial bleeding is appreciably greater than venous.  Endometrial bleeding appears to follow rupture of an arteriole of a coiled artery, with consequent hematoma formation.  With a hematoma, the superficial endometrium is distended and ruptures.  Fissures develop in the adjacent functionalis layer, and blood, as well as tissue fragments of various sizes, are sloughed.  Hemorrhage stops with arteriolar constriction as well as changes that accompany partial tissue necrosis.  Endometrial surface is restored by growth of flanges, or collars, that form the everted free ends of the endometrial glands Interval between menses  Modal interval of menstruation is 28 days. Decidua  Specialized, highly modified endometrium of pregnancy and is a function of hemochorial placentation  Decidualization – transformation of secretory endometrium to decidua; dependent on estrogen and progesterone and factors secreted by the implanting blastocyst Structure  3 parts o Decidua basalis – directly beneath blastocyst implantation, modified by trophoblast invasion o Decidua capsularis – overlies the enlarging blastocyst, and initially separates it from the uterine cavity. Prominent during the 2nd month of pregnancy. o Decidua parietalis – remainder of the uterine lining o Decidua vera – when capsularis and parietalis are joined later in pregnancy.  By 14 to 16 weeks AOG – gestational sac completely fills the uterine cavity and functionally obliterated.  3 layers of decidua parietalis and basalis: o zona compacta – compact zone; part of zona functionalis o zona spongiosa – spongy, middle portion, with remnants of glands and numerous small blood vessels; part of zona functionalis o zona basalis – basal zone which remains after delivery and gives rise to new endometrium. Reaction  Decidual reaction is completed only with blastocyst implantation  Predecidual changes commence first during the midluteal phase in endometrial stromal cells adjacent to the spiral arteries and arterioles.  Endometrial stromal cells enlarge to form polygonal or round decidual cells  Nuclei become round and vesicular, and the cytoplasm becomes clear, slightly basophilic and surrounded by a pericellular membrane  Pericellular matrix surrounding the decidual cells may allow attachment of cytotrophoblasts through cellular adhesion molecules.


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Cell membrane also may provide decidual cell protection against selected cytotrophoblastic proteases.

Blood supply  Spiral arteries in the decidua parietalis retain a smooth muscle wall and endothelium and thereby remain responsive to vasoactive agents that act on their smooth muscle or endothelial cells.  Spiral arterioles and arteries are invaded by cytotrophoblasts. As a consequence, the walls of vessels in the basalis are destroyed. These vascular conduits of maternal blood, devoid of smooth muscle or endothelial cells, are not responsive to vasoactive agents. FERTILIZATION EVENTS IN FERTILIZATION

CLEAVAGE  Zygote cytoplasm is successively cleaved to form a blastula, which consists of increasing smaller blastomeres  At 32 -cell stage, the blastomeres form a morula, which consists of an inner cell mass and outer cell mass  The morula enters the uterine cavity at about 3 days post conception BLASTOCYST FORMATION  Occurs when fluid secreted within the morula forms the blastocyst cavity  Inner cell mass – future embryo, is now called the Embryoblast  The outer cell mass – future placenta, is now called the Trophoblast IMPLANTATION  Blastocyst implants at around 7 days post conception within the posterior superior wall of the uterus  This is during the secretory phase of the menstrual cycle, so implantation occurs within the functional layer of endometrium. POST CONCEPTION: WEEK 2 EMBRYOBLAST  Differentiates into two distinct cell layers, the Epiblast and Hypoblast, forming a Bilaminar Embryonic Disk o Epiblast -clefts develop within the Epiblast to form the amniotic cavity o Hypoblast -form the yolk sac

1. 2.


4. 5.

The sperm binds to zona pellucida of the secondary oocyte and triggers the acrosome reaction, causing release of acrosomal enzymes Sperm penetrates the zona pellucida and unite with the oocyte’s plasma membrane, eliciting the cortical reaction and rendering the secondary oocyte impermeable to other sperm Sperm and secondary oocyte cell membranes fuse and contents of the sperm enter the cytoplasm  Male genetic material forms the male pronucleus  Tail and mitochondria degenerate Secondary oocyte completes meiosis II, forming a mature ovum. The nucleus of the ovum is the female pronucleus The male and female pronuclei fuse to form a zygote POST CONCEPTION: WEEK 1

1. 2. 3.

Cleavage Blastocyst formation Implantation

TROPHOBLAST  Cytotrophoblast divide mitotically  Syncytiotrophoblast o Does not divide mitotically o Produces the HCG o Continues its growth into the endometrium to make contact with the endometrial blood vessels

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EMBRYO PERIOD: WEEK 3-8 The beginning of the development of major organ systems Coincides with the first missed menstrual period Period of high susceptibility to teratogen Gastrulation is a process that establishes the 3 primary germ layers, forming a trilaminar embryonic disk o Ectoderm o Endoderm o Mesoderm

DERIVATIVES LAYER Ectoderm Endoderm Mesoderm

DERIVATIVES CNS and PNS Sensory organs of seeing and hearing Integument layer Lining of the GIR and Respiratory tract Muscles Cartilages CVS Urogenital System RBC

EMBRYONIC PERIOD Order of Formation CNS Heart Upper limb Lower limb External genitalia

First to develop and continues post natal Completed by 8 weeks Completed by 8 weeks Completed by 8 weeks Completed by 9 weeks


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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







Adequate and well-controlled human studies have failed to demonstrate a risk to the fetus Folic acid in the first trimester of pregnancy (and there is no evidence of risk in later trimesters). Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in Paracetamol, pregnant women OR Animal studies have amoxicillin, shown an adverse effect, but adequate and cephalexin, well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus in any trimester. Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in paroxetine humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks. There is positive evidence of human fetal risk based on adverse reaction data from Phenytoin, investigational or marketing experience or tetracyclne, studies in humans, but potential benefits may aspirin, warrant use of the drug in pregnant women despite potential risks. Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from Thalidomide, investigational or marketing experience, and isotretinoin the risks involved in use of the drug in pregnant women clearly outweigh potential benefits.

PLACENTA FETAL TO MATERNAL MEMBRANES  Amnion o Avascular; provides tensile strenght; first identifiable at 7th to 8th day of life; from fetal ectoderm  Chorion  Decidua parietalis (endometrium)  Myometrium  Serosa AMNIOTIC FLUID  Normal amniotic fluid volume o By 12 weeks = 60ml o By 34-36 weeks = 1L o By term = 840 ml o By 42 weeks = 540 ml  Production of amniotic fluid o Initially by amniotic epithelium o Fetal kidneys and urine production *Amniotic fluid volume is also dependent on the extent of maternal plasma expansion  Removal and regulation of amniotic fluid volume o Fetal swallowing o Fetal aspiration o Exchange through skin and fetal membranes

Fetal surface covered by amnion beneath which the fetal chorionic vessels course chorionic villi intervillous space decidual plate  myometrium

FUNIS  Umbilcal cord  Two artery, one vein (left or right?)  Ave lenght: 55 cm  Wharton jelly- extracellular matrix of specialized connective tissue  Anticlockwise spiral is present in 50 to 90 percent of fetuses PLACENTAL HORMONES  Trophoblast  Steroid hormones  hPL, hCG, parathyroid hormone–related protein (PTH-rP), calcitonin, relaxin, inhibins, activins, and atrial natriuretic peptide  hypothalamic-like releasing and inhibiting hormones: thyrotropin-releasing hormone (TRH), gonadotropinreleasing hormone (GnRH), corticotropin-releasing hormone (CRH), somatostatin, and growth hormone– releasing hormone (GHRH). PLACENTAL STEROID HORMONES Steroid Nonpregnant Estradiol-17 0.1–0.6 Estriol 0.02–0.1 Progesterone 0.1–40 Aldosterone 0.05–0.1 Deoxycorticosterone 0.05–0.5 Cortisol 10–30 hCG    

 

Pregnant 15–20 50–150 250–600 0.250–0.600 1–12 10–20

Almost exclusively produced by the placenta Glycoprotein Alpha and beta subunit Functions: rescue and maintenance of function of the corpus luteum, stimulates fetal testicular testosterone secretion, materanl thyroid gland stimulation (chorionic thyrotropins), promotion of relaxin secretion detectable in plasma of pregnant women 7 to 9 days after the midcycle surge of LH that precedes ovulation. Plasma levels increase rapidly, doubling every 2 days, with maximal levels being attained at 8 to 10 weeks


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At 10 to 12 weeks, plasma levels begin to decline, and a nadir is reached by about 16 weeks Clearance: mainly hepatic, renal (30%)

hPL  Similar to hGH  detected in maternal serum as early as 3 weeks  Maternal plasma concentrations are linked to placental mass, and they rise steadily until 34 to 36 weeks  production rate near term: approximately 1 g/day  Functions: Maternal lipolysis , anti-insulin or "diabetogenic”, potent angiogenic PROGESTERONE  Source: o First 6-7 weeks of pregnancy: Corpus luteum (ovary) o After 8 weeks: Placenta (Syncytiotrophoblast)  Function: o Affects tubal motility, the endometrium, uterine vasculature, and parturition o Inhibits T lymphocyte–mediated tissue rejection  Preferred precursor of progesterone biosynthesis by the Trophoblast: Maternal plasma LDL cholesterol ESTROGEN  Pregnancy near term is hyperestrogenic  Produced exclusively by Syncytiotrophoblasts  Placenta produce all types of estrogen ESTROGEN Estradiol



SOURCE Maternal ovaries for weeks 1 through 6 of gestation After T1, the placenta is the major source of circulating estradiol. Maternal ovaries, adrenals, and peripheral conversion in the first 4 to 6 weeks of pregnancy The placenta subsequently secretes increasing quantities Produced almost exclusively by the placental syncytiotrophoblast Continued production depends on the living fetus Marker of fetal well being

Placental Estrogen Production

Conditions that Affect Hormone Levels in Pregnancy Condition


Fetal Demise

dec estrogen

Fetal anencephaly

Dec estrogen (estriol)

Fetal adrenal hypoplasia

absence of C19-precursors

Fetal-Placental Sulfatase Deficiency

very low estrogen levels in otherwise normal pregnancies

Fetal-Placental Aromatase Deficiency

virilization of the mother and the female fetus

Trisomy 21—Down Syndrome

serum unconjugated estriol levels were low

Fetal Erythroblastosis


Glucocorticoid Treatment

Dec estrogen

Maternal Adrenal Dysfunction

Dec estrogen

Gestational Trophoblastic Disease

placental estrogen formation is limited to the use of C19-steroids in the maternal plasma estrogen produced is principally estradiol

FETAL DEVELOPMENT Terms Perinatal period

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

Neonatal period

Period after birth of an infant up to 28 completed days after birth

Fetal period

Begins from 8 weeks after fertilization or 10 weeks after onset of last menses

Embryonic period

Commences beginning of the 3rd week after ovulation and fertilization and lasts up to 8 weeks AOG 8 weeks period from the time of fertilization 10 weeks period from the time of the last menstrual cycle/Ovulation


Fetus or embryo removed or expelled fro uterus during the first half of gestation 20 weeks or less, or in the absence of accurate dating criteria, born weighing less than 500 grams

GESTATIONAL AGE vs. OVULATION AGE  Gestational age/menstrual age o The time elapsed since the last menstruation o Precedes fertilization/ovulation by 2 weeks  Ovulation age/post conceptional age o Measures the actual age of the embryo from the time of fertilization/ovulation *A fetus that is 18 weeks AOG. What is the ovulation age? DETERMINING THE AGE OF THE FETUS  Naegele’s Rule  Crown Rump Length (CRL) o Measured from the superior to inferior pole of the fetus preferably in extended position o Used for First trimester  Biparietal Diameter (BPD) o Measured at the outer to outer aspect of the skull at the level of the occipitofrontal plane o Used during the second and third trimester


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The uterus usually is just palpable above the symphysis pubis, crown-rump length is 6 to 7 cm. Centers of ossification have appeared in most of the fetal bones fingers and toes have become differentiated Skin and nails have developed and scattered rudiments of hair appear. external genitalia are beginning to show definitive signs of male or female gender spontaneous movements.


fetal crown-rump length is 12 Gender can be determined by experienced observers by inspection of the external genitalia by 14 weeks. Quickening by multiparas


fetus now weighs somewhat more than 300 g, and weight begins to increase in a linear manner. fetus moves about every minute and is active 10 to 30 percent of the time downy lanugo covers its entire body


canalicular period of lung developmentis nearly completed fat deposition begins fetus born at this time will attempt to breathe, but many will die because the terminal sacs have not yet formed


crown-rump length is approximately 25 cm skin is red and covered with vernix caseosa pupillary membrane has just disappeared from the eyes born at this age has a 90-percent chance of survival


CRL of 32 deposition of subcutaneous fat


average crown-rump length is about 36 cm weight is approximately 3400 g

HEAD DIAMETERS  Bitemporal diameter (8.0cm) o Greatest TRANSVERSE diameter of the head  Biparietal diameter (9.5 cm)  Occipitomental ( 12.5 cms)  Occipitofrontal (11.5 cms) o The plane that corresponds to the greatest CIRCUMFERENCE o 34.5 cm  Suboccipitobregmatic ( 9.5 cms) o The plane that corresponds to the smallest circumference of the head o 32 cm

Fetal Blood  HEMATOPOIESIS o yolk sac – first site of hematopoiesis. embryonic period o Liver takes over up to near term o Bone marrow starts at 4 mos AOG and remains as the major site of blood formation during adulthood  Erythrocytes – nucleated and have a shorter life span due to their large volume and are more easily deformable  Fetal blood volume (125 ml/kg) o Term infants = 80 ml/kg body weight o Placenta = 45 ml/kg body weight  Fetal Hemoglobin o Hemoglobin F o Hemoglobin A (adult hgb) o Hemoglobin A2 Fetal Circulation: CHANGES AFTER BIRTH  Foramen ovale – functionally closed w/in several minutes; anatomically fused 1 year after birth  Ductus arteriosus – functionally closed by 10-12 hours after birth; anatomically closed by 2-3 weeks  Ductus venosus constrict and becomes the ligamentum venosum Kleihauer-Betke test  Rationale: o Fetal RBC’s are resistant to denaturating effects of alkali. o Mother’r RBC are sensitive, thus may hemolyze FETAL PULMONARY SYSTEM

FETAL CIRCULATION  3 vessels (AVA) o 2 arteries o 1 vein  Three Shunts: o Ductus venosus o Foramen ovale o Ductus arteriosus

   

Presence of surfactant in the amnionic fluid is evidence of fetal lung maturity (after 34 weeks) Surfactant is formed in the type II pneumocytes that line the alveoli Starts to appear in the amniotic fluid at 28-32 weeks. 90% lipid and 10% proteins o Phosphatidylcholines (lecithin) account for 80% of the glycerophospholipids


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] Most active component – dipalmitoylphosphatidylcholine (DPPC) o 2nd most active - phosphatidylglycerol Alveolar development = just before birth – 8 years old o



    

A. 

   

Genetic/Chromosomal Sex o XX or XY? o Dependent on the presence of Y chromosome Gonadal Sex o testes or ovaries? o Dependent on the presence of SRY gene present on the Y chromosome or the Testes Determining region Phenotypic Sex o Is it a penis or a vagina? o Dependent on the hormones produced

B.    

C.  

D.    

CARDIOVASCULAR SYSTEM Changes in cardiac function become apparent during the first 8 weeks of pregnancy. Cardiac output is increased as early as the fifth week and reflects a reduced systemic vascular resistance and an increased heart rate. Resting pulse rate increases about 10 bpm. Between 10 and 20 weeks, plasma volume expansion begins and preload is increased. Ventricular performance is influenced by both the decrease in systemic vascular resistance and changes in pulsatile arterial flow. Heart Heart is displaced to the left and upward and rotated somewhat on its long axis. The apex is moved somewhat laterally from its usual position, causing a larger cardiac silhouette on chest radiograph. Pregnant women normally have some degree of benign pericardial effusion, which may increase the cardiac silhouette. Normal pregnancy induces NO characteristic ECG changes other than slight left-axis deviation as a result of the altered heart position. Cardiac Sounds Exaggerated splitting of the first heart sound with increased loudness of both components No definite changes in the aortic and pulmonary elements of the second sound Loud, easily heard third sound Systolic murmur in 90% of pregnant patients which was intensified during inspiration in some or expiration in others, and disappeared shortly after delivery. Cardiac output Mean arterial pressure and vascular resistance decrease, while blood volume and basal metabolic rate increase. Cardiac output at rest, when measured in lateral recumbent position, increases significantly beginning in early pregnancy. It continues to increase and remain elevated during the remainder of pregnancy. During late pregnancy with a woman in SUPINE position, the large pregnant uterus compresses venous return from the lower body. It may compress the aorta and cardiac filling may be reduced with dimished cardiac output. Fetal oxygen saturation is approximately 10% higher when a labouring woman is in a lateral recumbent position compared with supine. Upon standing, cardiac output fall to the same degree as in the non-pregnant woman. During the 1st stage of labor, cardiac output increases moderately. During the 2md stage, with vigorous expulsive efforts, it is appreciably greater. The pregnancy-induced increase is lost after delivery. Circulation and blood pressure Brachial artery pressure when sitting is lower than that when in the lateral recumbent supine position. Arterial pressure usually decreases to a nadir at 24 to 26 weeks and rises thereafter. Diastolic pressure decreases more than systolic. In about 10% of women, supine compression of the great vessels by the uterus causes significantly arterial hypotension, referred to as the supine hypotensive syndrome. This may directly affect fetal heart rate patterns. This also occurs with hemorrhage or with spinal analgesia. The components of the rennin-angiotensin-aldosterone axis are increased in normal pregnancy. These components are involved in renal control of blood pressure via sodium and water balance. Renin is produced by both the maternal kidney and placenta, and increased renin substrate (angiotensinogen) is produced by both maternal and fetal liver. This increase in angiotensinogen results, in part, from


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] high levels of pregnancy. E. 

F.  

G. 

H. 



during normal

Cardiac natriuretic peptides Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) – are secreted by cardiomyocytes in response to chamber-wall stretching. These peptides regulate blood volume by provoking natriuresis, dieresis, and vascular smooth-muscle relaxation. During pregnancy, plasma ANP are maintained in the nonpregnant range despite increased plasma volume. Median BNP levels are less than 20 pg/ml and are stable across normal pregnancy. However, these levels are increased in severe preeclampsia. ANP-induced physiological adaptations participate in the expansion of extracellular fluid volume and the increase in plasma aldosterone concentrations characteristic of normal pregnancy. C-type natriuretic peptide (CNP), is secreted by noncardiac tissues. This peptide appears to be a major regulator of fetal bone growth.












Elevated diaphragm

Elevated diaphragm

UNCHANGED  Respiratory rate is essentially unchanged.  Lung compliance is unaffected by pregnancy  Maximum breathing capacity and forced or timed vital capacity are not altered appreciably INCREASED  Airway conductance is increased possibly as a result of progesterone  Amount of oxygen delivered into the lungs by the increased tidal volume clearly exceeds O2 requirements imposed by pregnancy.  Total haemoglobin mass, and in turn total oxygen-carrying capacity, increases appreciably.

Endothelin Endothelin-1 is a potent vasoconstrictor in endothelial and vascular smooth muscle cells and regulates local vasomotor tone. It stimulates secretion of ANP, aldosterone, and catecholamines. There are endothelin receptors in pregnant and nonpregnant myometrium. They are also identified in the amnion, amniotic fluid, decidua, and placental tissue. Vascular sensitivity to endothelin-1 is not altered during normal pregnancy. Vasodilating factors counterbalance the endothelin-1 vasoconstrictor effects and produce reduced peripheral vascular resistance.

DECREASED  Peak expiratory flow rates decline progressively as gestation advances.  Total pulmonary resistance reduced possible as a result of progesterone  Maternal arteriovenous oxygen difference is decreased due to increased total oxygen carrying capacity.

Nitric Oxide It is a potent vasodilator released by endothelial cells and have important implication for modifying vascular resistance during pregnancy.

 B.

Pulmonary Function


Prostaglandins Renal medullary prostaglandin E2 synthesis is increased markedly during late pregnancy and is presumed to be natriuretic. Prostacyclin (PGI2), the principal prostaglandin of endothelium, is increased during late pregnancy and regulates blood pressure and platelet function. It also has been implicated in the angiotensin resistance characteristic of normal pregnancy.

PULMONARY SYSTEM Anatomic Changes Diaphragm rises about 4 cm during pregnancy. Subcostal angle widens appreciably as the transverse diameter of the thoracic cage increases approximately 2 cm. Thoracic circumference increases about 6 cm, but not sufficiently to prevent a reduction in the residual lung volume created by the elevated diaphragm Diaphragmatic excursion is actually greater in pregnancy.

A.  

Residual volume Expiratory reserve volume Inspiratory capacity Inspiratory reserve volume Functional residual capacity Vital capacity

Lung Volumes (ml) Total lung capacity


Term Pregnancy



C. Acid-Base Equilibrium Blood Gas NonFirst pregnant trimester HCO3 Not 22-26 (mEq/L) reported PCO2 Not 38-42 (mmHg) reported PO2 90-100 93-100 (mmHg) pH

7.38 – 7.42 (a)

7.36 – 7.52 (v)

Second trimester Not reported Not reported

Third trimester



7.40 – 7.52 (v)

7.41 – 7.53 (v) 7.39 – 7.45 (a)

16-22 25-33

(a) – arterial; (v) – venous   

Etiology 

Increased awareness of a desire to breathe early in pregnancy. Physiologic dyspnea results from increased tidal volume that lowers the blood PCO2 slightly, which paradoxically causes dyspnea. Increased respiratory effort, and in turn the reduction in PCO2 is most likely induced in large part by progesterone and to a lesser degree by estrogen. Progesterone appears to act centrally, where it lowers the threshold and increases the sensitivity of the chemoreflex response to CO2. To compensate for resulting respiratory alkalosis, plasma bicarbonate levels decrease from 26 to approximately 22 mmol/L Although blood pH is increased only minimally, it does shift the oxygen dissociation curve to the left. This shift increases the affinity of maternal hemoglobin for oxygen, thereby decreasing the oxygen-releasing capacity of maternal blood. Slight pH increase also stimulates an increase in 2,3diphosphoglycerate in maternal blood which shifts the

Resting minute  ventilation is also increased. Can be due to enhanced  respiratory drive due Tidal 450 600 to stimulatory effects volume of progesterone, low expiratory reserve volume and  compensated respiratory alkalosis. TOPNOTCH MEDICAL BOARD PREP OBSTETRICS HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected]

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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] curve back to the right. Reduced PCO2 from maternal hyperventilation aids CO2 (waste) transfer from the fetus to the mother while also facilitating O2 release to the fetus.

A.      

    

      B.      C. 

REPRODUCTIVE SYSTEM Uterus Non-pregnant weight of 70g to almost 1100 grams by term. Non-pregnant capacity of 10 ml to a total volume of 5 to 20 liters by term Uterine enlargement involves stretching and marked hypertrophy of muscle cells, production of new myocytes is limited. Accumulation of fibrous tissue, particularly in the external muscle layer, with an increase in elastic tissue to strengthen the uterine wall Uterine wall thins near term to only 1 to 2 cm. It becomes soft and readily identable through which the fetus can be palpated. Uterine hypertrophy early in pregnancy probably is stimulated by the action of estrogen and perhaps that of progesterone. By 12 weeks, increase in size is related predominantly to pressure exerted by the expanding products of conception. Uterine enlargement most marked in the fundus. Early months of pregnancy – fallopian tubes, ovarian and round ligaments attach slightly below the apex of the fundus Later months of pregnancy – fallopian tubes, ovarian and round ligaments are located above the middle of the uterus Portion of the uterus surrounding placental site enlarges more rapidly. Arrangement of muscle cells: o Outer hoodlike layer, which arches over the fundus and extends into various ligaments o Middle layer, dense network of muscle fibers perforated in all directions by blood vessels o Internal layer, with sphincter-like fibers around the fallopian tube orifices and internal os of the cervix. o Main portion of the uterine wall is formed by the middle layer. Each cell in this layer has a double curve so that the interlacing of any two gives approximately the form of a figure 8. When cells contract after delivery, they constrict the penetrating blood vessels and act as ligatures. Pear shaped > globular form > spherical by 12 weeks > ovoid shape (length more than width) Displaces intestines laterally and superiorly Dextrorotation – uterus undergoes rotation to the right because of the rectosigmoid on the left side of the pelvis. There is tension exerted on the broad and round ligaments. Braxton Hicks contractions – unpredictable, sporadic and nonrhythmic contractons, every 10 to 20 minutes for some, intensity between 5 and 25 mmHg. Total uterine blood flow from uterine and ovarian arteries – 450 to 650 mL/min Cervix Softening and cyanosis due to increased vascularity and edema of the entire cervix, together with hypertrophy and hyperplasia of cervical glands. Endocervical mucosal cells produce copious amounts of a tenacious mucus that obstruct the cervical canal soon after conception. Cervical Mucus is rich in Ig and cytokines and may act as an immunological barrier to protect uterine contents against infection. Cervical mucus beading occurs as a result of progesterone. Arias-Stella reaction – endocervical gland hyperplasia and hypersecretory appearance

 

D. 

Decidual reaction – elevated patches of tissue which bleed easily. Represents cellular detritus from the endometrium that has passed through the fallopian tubes. Relaxin – protein hormone secreted by the corpus luteum, deciduas and placenta. Remodelling of reproductive tract connective tissue to accommodate pregnancy Vagina & perineum Chadwick sign – increased vascularity affecting vagina and results in violet discoloration

SKIN Abdominal wall 1. Striae gravidarum or stretch marks 2. Diastasis recti – rectus muscles separate in the midline b. Hyperpigmentation – due elevated levels of melanocytestimulating hormone; estrogen and progesterone have melanocyte-stimulating effects  Linea nigra  Chloasma or melasma gravidarum  Pigmentation of areola and genital skin c. Vascular changes  Vascular spiders or angiomas – common on the face, neck, upper chest and arms  Palmar erythema  Increased cutaneous blood flow serves to dissipate excess heat generated by increased metabolism a.

 

a.   

METABOLIC CHANGES 3rd trimester – maternal basal metabolic rate is INCREASED by 10 to 20% WHO (2004) estimate of additional energy demands: o 1st tri – 85 kcal/day o 2nd tri – 285 kcal/day o 3rd tri – 475 kcal/day Weight gain Attributable to uterus and its contents, breasts, increase blood volume and extracellular fluid Accumulation of cellular water, fat and protein Average weight gain is approx. 12.5 kg or 27.5 lbs

b. 2.

Water metabolism Increased water retention induced by resetting of osmotic thresholds for thirst and vasopressin secretion. 3. Mimimum amount of extra water during normal pregnancy = 6.5 liters o Amniotic fluid = 3.5 liters o Maternal blood volume, uterus and breasts = 3.0 liters 4. Pitting edema of ankles and legs o Increased venous pressure below the level of the uterus due to partial vena cava occlusion o Decrease in interstitial colloid osmotic pressure c. 1. 2. 3. 4. d.  

Protein metabolism Fetus and placenta weigh about 4 kg and contain approximately 500 g of protein Remaining 500 g is added to uterus, breasts primarily in the glands, and to hemoglobin and plasma proteins Nitrogen balance increased with gestational age Maternal muscle breakdown is not required to meet metabolic demands. Carbohydrate metabolism Pregnancy is characterized by mild fasting hypoglycemia, postprandial hyperglycemia, and hyperinsulinemia Pregnancy-induced state of peripheral insulin resistance occurs to ensure a sustained postprandial supply of glucose to the fetus. o Progesterone and estrogen, may act, directly or indirectly to mediate this insensitivity o Placental lactogen may increase lipolysis and liberation of free fatty acids. Increased free fatty acids may aid increased tissue resistance to insulin Pregnant women changes rapidly from a postrprandial state characterized by elevated and sustained glucose levels to a

Ovaries Ovulation ceases and maturation of new follicles is suspended.   Corpus luteum functions maximally during the first 6 – 7 weeks of pregnancy, produces progesterone. TOPNOTCH MEDICAL BOARD PREP OBSTETRICS HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected]

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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] fasting state characterized by decreased plasma glucose and some amino acids e.    

Fat metabolism Lipids, lipoproteins and apolipoproteins increase appreciably during pregnancy. Increased insulin resistance and estrogen stimulation are responsible for maternla hyperlipidemia Increased lipid synthesis and food intake contribute to maternal fat accumulation during the first two trimesters. During 3rd trimester, fat storage declines or ceases. This is a consequence of enhanced lipolytic activity, and decreased lipoprotein lipase activity reduces circulating triglyceride uptake into adipose tissue. This transition to a catabolic state favors maternal use of lipids as a source of energy and spares glucose and amino acids for the fetus. INCREASED levels during 3rd trimester: o Triacylglycerol o VLDL o LDL o HDL DECREASED levels after delivery: lipids, lipoproteins and apolipoproteins


Leptin o Primarily secreted by adipose tissue, some by placenta o Plays a role in body fat and energy expenditure regulation o May also help regulate fetal growth o INCREASE and peak during the 2nd trimester and plateau until term o Abnormally elevated leptin have been associated with preeclampsia and gestational DM


Gherlin o Secreted primarily by the stomach in response to hunger. o Cooperates with leptin in energy homeostasis modulation o Expressed also in placenta and likely has a role in fetal growth and cell proliferation.


      

Iron metabolism Storage o Total iron content of normal adult women: 2.0 to 2.5 grams. Most of this is incorporated in hemoglobin or myoglobin. o Iron stores of normal young women is approximately 300 mg


Iron requirements o Approximately 1,000 mg of iron is required for normal pregnancy. a. 300 mg - actively transferred to the fetus and placenta. b. 200 mg – lost through normal excretion routes, primarily in the GIT. c. 500 mg – required for the increase in total circulating erythrocyte volume (approx 450 ml) o The amount of dietary iron, together with that mobilized from stores, will be insufficient to meet the average demands imposed by pregnancy.


Puerperium o During vaginal delivery & the first postpartum days, only approximately half of the added erythrocytes are lost from most women. o Normal losses come from the following: a. Placental implantation site b. Episiotomy or lacerations c. Lochia o Estimated blood loss: a. NSVD (singleton) – 500 to 600 ml b. CS or NSVD (Twin) – 1,000 ml

c. 

Immunologic functions Suppression of various humoral and cell-mediated immunological functions occur to accommodate the “foreign” semiallogenic fetal graft. Pregnancy is both a proinflammatory and antiinflammatory condition depending on the stage. Three immunologic phases of pregnancy: o Early pregnancy (pro-inflammatory)  Blastocyst must break through the uterine cavity epithelial lining to invade endometrial tissue  Trophoblast must replace endometrium and vascular smooth muscle of maternal blood vessels to secure adequate supply for the placenta  Inflammatory environment is required to secure cellular debris removal and adequate repair of the uterine epithelium o Midpregnancy (anti-inflammatory)  Period of rapid fetal growth and development o Parturition (recrudescence of inflammatory process)  Influx of immune cells into the myometrium Suppressed activity: o T-helper (Th) 1 cells  decreases secretion of IL-2, interferon-g, and TNF-B  suppressed Th1 response is requisite for pregnancy continuation  suppressed Th1 during pregnancy results in remission of some autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, and Hashimoto thyroiditis  failure of Th1 suppression may be related ot development of preeclampsia o T-cytotoxic (Tc) 1 cells  Decreases secretion of IL-2, interferon-g, and TNF-B Upregulated activity: o Th2 cells – increase secretion of IL-4, IL-6 and IL-13 o IgA and IgG in cervical mucus increase o IL-1B in cervical and vaginal mucus is increased during the 1st trimester Vitamin K-dependent glycoprotein that inhibits activation of factor X

 

Electrolyte and mineral metabolism

INCREASED Iodine requirement Iron requirement

a. 

b. 1.

DECREASED Sodium Potassium Total serum calcium (ionized & non-ionized) Serum magnesium

HEMATOLOGIC CHANGES Blood volume Hypervolemia averages 40 to 45% above nonpregnant blood volume after 32 to 34 weeks Functions of hypervolemia: o Meets the metabolic demands of the enlarged uterus and its greatly hypertrophied vascular system o Provides abundant nutrients and elements to support the rapidly growing placenta and fetus o Protects the mother and fetus against the deleterious effects of impaired venous return in the supine and erect positions o Safeguards the mother against the adverse effects of parturition-associated blood loss Maternal blood volume expands most rapidly during the second trimester. Blood volume expansion results from an increase in both plasma and erythrocytes. Moderate erythroid hyperplasia is present in the bone marrow Reticulocyte count is elevated slightly. Elevated maternal plasma erythropoietin levels – peaks early during the 3rd trimester and corresponds to maximal erythrocyte production. Hemoglobin & hematocrit DECREASE slightly Whole blood viscosity DECREASES.


Page 16 of 36


Low levels may prove to be a risk factor for otherwise unexplained recurrent early pregnancy loss (Effraimidou and associates, 2009) URINARY SYSTEM



RENAL CHANGES IN NORMAL PREGNANCY Parameter Alteration Clinical relevance Kidney size Approximately 1 cm Size returns to normal longer of radiograph postpartum Dilatation Resembles Can be confused with hydronephrosis on obstructive uropathy; sonogram or IVP Retained urine leads (more marked on to collection errors; right) Renal infections are more virulent; May be responsible for “distention syndrome”; Elective pyelography should be deferred to at least 12 weeks postpartum Renal GFR & renal plasma Serum creatinine function flow increase ≈ 50% decreases during normal gestation (>0.8 mg/dl creatinine already borderline); Protein, amino acid, and glucose excretion all increase Maintenance Decreased Serum bicarbonate of acid-base bicarbonate threshold; decreased by 4-5 Progesterone mEq/L; stimulates respiratory PCO2 decreased 10 center mmHg; PCO2 or 40 mmHg already represents CO2 retention Plasma Osmoregulation Serum osmolality osmolality altered; decreases 10 mOsm/L Osmotic thresholds (serum Na ≈ 5 mEq/L) for vasopressin (AVP) during normal release and thirst gestation decrease Increased placental Hormonal disposal metabolism of AVP rates increase may cause transient diabetes insipidus during pregnancy. 1.

Loss of nutrients o Amino acids and water-soluble vitamins are lost in urine in greater amounts


Tests of renal function o Serum creatinine – DECREASED. Values above 0.9 mg/dl suggest underlying renal disease and prompt investigation o Creatinine clearance – INCREASED about 30%


Urinalysis o Glucosuria – may NOT be abnormal. It can be due to increase in GFR, together with impaired tubular reabsorptive capacity for filtered glucose. About 1/6 of pregnant women spill glucose, but the possibility of DM should not be ignored. o Proteinuria – NOT evident during pregnancy except occasionally in slight amounts during or soon after vigorous labor. o Albumin excretion is minimal and ranges from 5 to 30 mg/day o Hematuria is often a result of contamination during collection. Common after difficult labor and delivery because of trauma to the bladder and urethra.

b.   

Ureters Uterus rests upon ureters and laterally displaces it and compresses them at the pelvic brim Right ureter is dilated more than the left due to a dextrorotated uterus and the right ovarian vein complex lies obliquely over the right ureter. Ureteral elongation and curvature formation occurs due to distention

c. 

Bladder Bladder trigone is elevated by (>12 weeks): o Increased uterine size o Hyperemia o Hyperplasia of bladder’s muscle and connective tissue Note: Elevation of trigone causes thickening of posterior, or intraureteric origin      

 

   

a.   

 b. 

No mucosal changes Increase in size and tortuosity of its blood vessels Bladder pressure (primigravidas) increased from 8 cm H20 (early pregnancy) to 20 cm H20 (at term). Absolute and functional urethral lengths INCREASED Maximal intraurethral pressure INCREASED from 70 to 93 cm H20, thus continence is maintained End of pregnancy changes: o Entire base of blader is pusched forward and upward, converting normal convex surface to concave due to presenting part o Pressure of presenting part impairs drainage of blood and lymph from the bladder base which may lead to edema, and susceptibility to trauma and infections GASTROINTESTINAL TRACT Appendix displaced upward and laterally as the uterus enlarges, and it may reach the flank Gastric emptying time is UNCHANGED. During labor and administration of analgesic agents, it becomes prolonged. General anesthesia may cause regurgitation and aspiration during delivery. Pyrosis (heartburn) – reflux of acidic secretions into the lower esophagus due to: o Altered position of of the stomach o Decreased LES tone o Intraesophageal pressures are lower compared to intragastric pressures o Esophageal peristalsis has lower wave speed and lower amplitude Gums may become hyperemic and softened and may bleed when mildly traumatized as with a toothbrush Epulis of pregnancy – focal, highly vascular swelling of the gums but regresses spontaneously after delivery. Pregnancy DOES NOT incite tooth decay. Hemorrhoids are fairly common due to constipation and elevated pressure in veins below the level of the enlarged uterus. Liver NO INCREASE in liver size Hepatic blood flow and diameter of the portal vein is INCREASED Increased levels: o Total alkaline phosphatase – almost doubles o Total albumin o Serum globin Decreased levels: o AST o ALT o GGT o Bilirubin o Serum albumin Leucine aminopeptidase activity is markedly INCREASED. This is increased with liver disease. Gallbladder Progesterone inhibits CCK-mediated smooth muscle stimulation which impairs gallbladder contraction


Page 17 of 36


 

a.   1.


Impaired/reduced gallbladder contraction leads to increased residual volume, and stasis with associated increased bile cholesterol saturation of pregnancy contributes to increased prevalence of gallstone in multiparous women. Intrahepatic cholestasis in pregnancy has been linked to high circulating levels of estrogen, which inhibit intraductal transport of bile acids. Pruritus gravidarum is due to retained bile salts. ENDOCRINE SYSTEM Pituitary gland Enlarges by approximately 135% but rarely cause visual disturbance from compression of optic chiasma Not essential for maintenance of pregnancy Growth Hormone (GH) o First trimester – secreted predominantly from maternal pituitary gland; serum and amniotic fluid concentrations are within nonpregnant values (0.5 to 7.5 o At 8 weeks AOG – growth hormone secreted by placenta becomes detectable o At 17 weeks AOG – placenta is the principal source of growth hormone secretion o Maternal serum levels plateau after 28 weeks at 14 ng/ml o Amniotic fluid levels peak at 14 to 15 weeks and slowly declines to reach baseline values after 36 weeks. o Maternal GH  Correlate positively with birthweight and negatively with fetal growth restriction & uterine artery resistance o Placental GH  Differs from pituitary GH by 13 AA residues  Secreted by syncitiotrophoblasts in a nonpulsatile fashion  Appears to have some influence on fetal growth as well as the development of preeclampsia  Major determinant of maternal insulin resistance after midpregnancy  Fetal growth progresses in the complete absence of placental GH  Not absolutely essential, but may act in concert with human placental lactogen and other somatolactogens to regulate fetal growth. Prolactin o INCREASE markedly and usually 10-fold greater at term (150 ng/ml) o DECREASES after delivery even in women who are breast feeding. o There are pulsatile bursts of prolactin secretion in response to suckling during early lactation. o Increases prolactin level:  Estrogen stimulation increases the number of anterior pituitary lactotrophs and may stimulate release of prolactin  TRH  Serotonin o Dopamine (prolactin-inhibiting factor) – inhibits prolactin secretion o Functions of prolactin:  Ensure lactation  Initiate DNA synthesis and mitosis of glandular epithelial cell and presecretory alveolar cells of the breast (early pregnancy).  Increases the number of estrogen and prolactin galactopoiesis, and production of casein, lactalbumin, lactose, and lipids. o Present in amniotic fluid in high concentrations. Up to 10,000 ng/ml at 20 to 26 weeks but decrease and reach a nadir after 34 weeks. Prolactin in amniotic fluid could be produced by uterine decidua. Its function could be to prevent water transfer from fetus into the maternal compartment to prevent fetal dehydration.

b.    

       c.     

Thyroid gland Thryroid hormone production INCREASED by 40 to 100% to meet maternal and fetal needs Thyroid gland undergoes moderate enlargement as a result of glandular hyperplasia and increased vascularity. Volume increase from 12 ml (first trimester) to 15 ml (at term) Normal pregnancy does not typically cause significant thyromegaly. Goiter should be investigated. Thyroxin-binding globulin – increases in the first trimester and reaches its zenith at about 20 weeks, and stabilizes at approximately double baseline values for the remainder of pregnancy Total serum thyroxine – INCREASE sharply between 6 and 9 weeks and reaches a plateau at 18 weeks Free serum T4 – rise slightly and peak along with hCG levels, and return to normal Total triiodothyronine (T3) – INCREASE up to 18 weeks and plateaus. Thyroid-releasing hormone (TRH) – are NOT INCREASED, but CROSSES the placenta and may stimulate the fetal pituitary to secrete thyrotropin TSH and hCG has identical a-subunits, thus hCG has intrinsic thyrotropic activity and cause thyroid stimulation. Thyroid-stimulating hormone (TSH) or thyrotropin DECREASES in more than 80% of pregnant women, but remain normal for non-pregnant women. Normal suppression of TSH may lead to a misdiagnosis of subclinical HYPERTHYROIDISM. Parathyroid glands Regulation of calcium concentration is closely interrelated to magnesium, phosphate, PTH, vitamin D, and calcitonin physiology All markers of bone turnover INCREASED during normal pregnancy and failed to reach baseline level by 12 months postpartum Calcium needed for fetal growth and lactation may be drawn at least in part from the maternal skeleton. Acute or chronic decreases in plasma calcium or acute decreases in magnesium stimulate the release of PTH, and vice versa. Action of PTH on bone resorption, intestinal absorption, and kidney reabsorption is to increase ECF calcium and decrease phosphate.


PTH and Calcium o First trimester – plasma PTH decrease initially o Succeeding trimesters – INCREASE progressively  Due to lower calcium concentrations in pregnancy as a result of increased plasma volume, increased GFR, and maternal-fetal transfer of calcium. o Estrogen appears to BLOCK the action of PTH on bone resorption, resulting in increase in PTH o Physiologic hyperparathyroidism of pregnancy occurs to supply the fetus with adequate calcium.


Calcitonin and Calcium o Calcium and magnesium increase the biosynthesis and secretion of calcitonin o Food ingestion & various gastric hormones (e.g. gastrin, pentagastrin, glucagon, and pancreozymin) also INCREASE calcitonin levels. o Calcitonin acts to OPPOSE PTH and Vitamin D to protect skeletal calcifications during times of calcium stress, such as pregnancy and lactation.


Vitamin D and Calcium o 1, 25-diOH Vitamin D3 – biologically active compound, and stimulates resorption of calcium from bone and absorption from the intestines o Conversion to active Vitamin D3  Ingestion of Vit D or synthesis in the skin  LIVER – Vitamin D converted to 25-OH Vit D3  KIDNEY, DECIDUA & PLACENTA – 25-OH Vit D3 converted to 1, 25 diOH Vit D3 (biologically active form) which is INCREASED in pregnancy.


Page 18 of 36


PTH, low calcium and phosphate levels facilitates conversion of 25-OH Vit D3 to 1, 25 diOHVit D3 Calcitonin OPPOSES conversion of Vit D to its active form.

d. 1.

Adrenals – undergo little morphological change Cortisol – INCREASED o Much of serum cortisol is bound by transcortin (cortisol-binding globulin) o Rate of adrneal cortisol secretion is not increased, and probably it is decreased compared with that of the nonpregnant state. o Metabolic clearance rate is LOWER during pregnancy because its half-life is nearly doubled. o During early pregnancy – ACTH levels are reduced strikingly o As pregnancy progresses, ACTH and free cortisol rises o Elevation in cortisol may be a result of “resetting” of the maternal feedback mechanism to higher levels (Nolten and Rueckert, 1981) o In response to elevated progesterone levels during pregnancy, an elevated free cortisol is needed to maintain homeostasis (Keller-Wood and Wood, 2001) 2. Aldosterone – INCREASED o As early as 15 weeks, maternal adrenal glands secrete more aldosterone o Sodium intake restriction increases aldosterone secretion o Increased aldosterone affords protection against the natriuretic effect of progesterone and ANP. 3.

Deoxycorticosterone – INCREASED o Due to increased kidney production from estrogen stimulation o There is transfer of fetal deoxycorticosterone into the maternal compartment due to high levels in fetal blood. 4. DHEA-S – DECREASED (serum and urine) o Due to increased metabolic clearance through externsive maternal hepatic 16a-hydroxylation and placental conversion to estrogen 5. Androstenedione and testosterone - INCREASED o Maternal plasma androstenedione and testosterone are converted to estradiol in the placenta o Increase in plasma SHBG retards testosterone clearance OTHER SYSTEMS Musculoskeletal system  Progressive lordosis is observed. The lordosis shifts the center of gravity back over the lower extremities.  Sacroiliac, sacrococcygeal and pubic joints have increased mobility during pregnancy.  Joint mobility may contribute to the alteration of maternal posture and may cause discomfort in the lower back.  Pelvic joints normally relax, particularly the symphysis pubis. Most relaxation takes place in the first half of pregnancy.  Symphyseal separation greater than 1 cm may cause significant pain. Regression begins immediately follwing delivery, and it is usually complete within 3 to 5 months.

 

Attention and memory were improved in women with preeclampsia receiving magnesium sulfate compared with normal pregnant women (Rana and associates, 2006). Mean blood flow in the middle and posterior cerebral arteries decreased progressively from non-pregnant state to late in the 3rd trimester. Unknown clinical significance (Zeeman and co-workers, 2003) Pregnancy does not appear to impact cerebrovascular autoregulation. o Sleep  Difficulty sleeping about 12 weeks to first 2 months postpartum with frequent awakening, fewer hours of night sleep, and reduced sleep efficiency.  Decreased frequency and duration of sleep apnea episodes during pregnancy compared postpartum  Supine position, average Pa)2 levels were lower  Greatest disruption of sleep is seen postpartum and may contribute to postpartum blues or frank depression

PRENATAL CARE Definition  A comprehensive antepartum care program that involves a coordinated approach to medical care and psychosocial support that optimally begins before conception and extends throughout the antepartum period. (AAP & ACOG, 2007)  A planned program of medical evaluation and management, observation, and education of the pregnant woman directed toward making pregnancy, labor, delivery and the postpartum recovery, a safe and satisfying experience.  It should provide opportunities for the following: o Physician and patient to be better acquainted o Physician to learn something about the patient’s emotional attitude toward pregnancy and labor o Instruction for the patient and her husband in optimal care for herself and the coming baby o Optimal instruction of the patient and her husband in a prepared childbirth program. Components  Preconceptional care, Diagnosis of pregnancy, Initial prenatal evaluation, follow-up prenatal visits

1. Diagnosis of pregnancy o Established through signs and symptoms, chorionic gonadotropin, ultrasound recognition  Signs and symptoms of pregnancy Sign or Comments symptom  Occurs 10 days after expected menses  One to two episodes of bloody discharge, Cessation of reminiscent of menstruation, can be due to menses blastocyst implantation or “implantation bleeding”  Fern-like pattern – Day 7 to 18 of menses due to increased NaCl when estrogen is produced. Eyes Cervical  Beaded pattern – Day 21 menses or  Intraocular pressure decreases during pregnancy, mucus pregnancy due to decreased NaCl attributed to increased vitreous outflow. influenced by progesterone that prohibit  Corneal sensitivity is decreased, particularly late in ferning gestation  Breast tenderness and tingling  Slight increase in corneal thickness due to edema.  >2 months: increased breast size, delicate  Krukenberg spindles – brownish-red opacities on the veins becomes visible, nipples larger & posterior surface of the cornea – have been observed during more pigmented, more erectile. pregnancy. Breast  Colostrum can be expressed. Areola  Visual function is unaffected by pregnancy, except for changes broader and deeply pigmented. transient loss of accommodation.  Glands of Montgomery which are hypertrophic sebaceous glands appear. CNS  Breast striations may also appear  Women often report problems with attention, Vaginal Chadwick’s sign. Vaginal mucosa becomes dark concentration, and memory throughout pregnancy and the mucosa bluish or purplish red and congested. early postpartum period.  Striae gravidarum or stretch marks Skin changes  Diastasis recti. Rectus muscles separate in TOPNOTCH MEDICAL BOARD PREP OBSTETRICS HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD Page 19 of 36 For inquiries visit or email us at [email protected]


  Changes in the uterus

  

Changes in the cervix       Fetal heart tone

Fetal movements

  

the midline. Linea nigra. Brownish-black discoloration of linea alba Chloasma or melasma gravidarum (mask of pregnancy) Angiomas or vascular spiders. Minute, red elevations on the skin of the face, neck, upper chest and arms. Often designated as nevus, angioma or telangiectasia. Palmar erythema First few weeks. Anteroposterior diameter is increased. 12 weeks AOG: body of uterus becomes globular, average diameter is 8 cm. 6 to 8 weeks AOG: Hegar’s sign is softening of the isthmus. Goodell’s sign. Softening of the cervix. The consistency of the cervical tissue surrounding the external os is more similar to that of the lips of the mouth. Cervical softening is also noted in women taking estrogen-progesterone pills. 17 weeks: stethoscope 10 weeks: doppler equipment 5 weeks: transvaginal sonography Fetal heart rate: 110 to 160 bpm Other sounds heard in the pregnant abdomen: 1. Funic souffle – rush of blood through the umbilical arteries. Sharp, whistling sound, synchronous with fetal pulse. 2. Uterine souffle – soft, blowing sound, synchronous with maternal pulse. Heard at lower portion of uterus produced by dilated uterine arteries. 18-20 weeks: Primigravid 16-18 weeks: Multigravid 20 weeks: examiner can begin to detect fetal movements.



Symptoms Nausea, vomiting Bladder frequency/urgency Perception of fetal movement Breast enlargement

Symptoms Abdominal distention Braxton-Hicks

Signs Secondary amenorrhea Chadwick’s sign Chloasma (face) Linea nigra, striae Spider telangiectasia Breast changes Thermal changes

Signs (+) Pregnancy test Abdominal enlargement Outlining of the fetal parts Hegar’s sign Goodell’s sign Ballotment


Signs Fetal heart tone Perception of fetal movement by examiner Ultrasound evidence

Pregnancy Test 1. Chorionic gonadotrophin 2. Ultrasound recognition (Transvaginal ultrasound)

2. Initial prenatal evaluation  Major goals: 1. Define the health status of the mother and fetus. 2. Estimate the gestational age. 3. Initiate a plan for continuing obstetrical care.  Components of routine prenatal care (Williams Obstetrics, 23rd edition)

COMPONENT History Complete PE Blood pressure Maternal weight Pelvic/cervical exam Fundal height FHT & position Hemoglobin (Hgb) & Hct Blood type & Rh factor Antibody screen Pap smear Urine protein Urine culture Rubella titer Syphillis test (VDRL) Hepatits B surface Ag (HbsAg) 50 grams OGCT/100g OGTT Gonococcal or Chlamydial culture HIV *High-risk women

First visit + + + + + + + +

15-20 weeks

24-28 weeks

29-41 weeks

+ +

+ +

+ +

+ +

+ + +

+ +

+ + + + + + + + + *



Components of Initial Prenatal Evaluation: A. Prenatal Record Terminologies for prenatal record: a. Nulligravida. Woman who is NOT now and never has been pregnant. b. Gravida. Woman who is or has been pregnant, irrespective of the pregnancy outcome. With the establishment of first pregnancy, she becomes primigravida, and with successive pregnancies, a multigravida. c. Nullipara. Woman who has never completed a pregnancy beyond 20 weeks gestation. d. Primipara. Woman who has been delivered only once a fetus or fetuses born alive or dead with an estimated length of gestation 20 or more weeks. e. Multipara. Woman who has completed 2 or more prenancies to 20 weeks or more. Parity is determined by the number of pregnancies reaching 20 weeks and not by the number of fetuses delivered. f. Gestational age or menstrual age is calculated from the first day of last menstrual period. g. Ovulatory age or fertlization age, is 2 weeks shorter than gestational age. Used by embryologists and other reproductive biologists. h. First trimester is from conception to 14 weeks gestation. Second trimester is up to 28 weeks completed gestation. Third trimester from 29th to 42nd week gestation. Normal pregnancy duration 1. Non-viable pregnancy is less than or equal to 20 weeks gestation (140 days) 2. Viable pregnancy:  Preterm - >20 weeks to 140 mg/dl (WHO/POGS) For Filipino gravidas with no other risk factors aside from race or ethnicity and the initial test (FBS, HbA1c or RBS) is normal, screening for GDM should be done at 24-28 weeks using a 2 hour 75 gram OGTT. If there are other risk factors identified, screening should proceed immediately to 2 hour 75 gram OGTT at first consult. If the OGTT at 24-28 weeks is normal, the woman should be re-tested at 32 weeks or earlier if clinical signs and symptoms of hyperglycemia are present both in the mother and the fetus (e.g. polyphagia, polyhdramnios, accelerated fetal growth, etc) OGTT should be performed in the morning after an overnight fast of 8 hours following the general instructions for the test.  Observe and overnight fast (at least 8 hours, but no more than 14 hours) prior to testing.  Have an unrestricted diet (> 150 grams of carbohydrates per day) for at least 3 days prior to the testing  Remain seated and should not smoke during the test.

High Risk Pregnancies.

3. Subsequent prenatal visits A. Prenatal Visits  Traditional: every 4 weeks until 28 weeks, every 2 weeks until 36 weeks, every week until term. High-risk every week or as indicated.  WHO Model consists of a mean of 5 visits: once in first trimester to screen for risk factors, then at 26, 32 and 38 weeks. B. Prenatal Surveillance  Fetal surveillance: heart rate, size (current & rate of change), amniotic fluid, presenting part and station (late in pregnancy), activity  Maternal surveillance: o Vital signs: BP, weight o Symptoms: headache, altered vision, abdominal pain, nausea and vomiting, bleeding, vaginal fluid leakage, dysuria o Abdominal Exam: fundal height o Vaginal exam: confirms presenting part & station, pelvic capacity, and cervical consistency, effacement and dilatation LEOPOLD’S MANEUVER  First maneuver answers the question: “What fetal part occupies the fundus?”  Second maneuver answers the question: “On what side is the fetal back?”  Third maneuver answers the question: “What fetal part lies over the pelvic inlet?”  Fourth maneuver answers the question: “On which side is the cephalic prominence?” CHECK UTERINE SIZE  At 20-31 weeks, AOG correlates well with Uterine size  At 12 weeks –palpable at level or just above of


Page 21 of 36

TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] symphysis pubis At 16 weeks- midway between symphysis pubis and umbilicus At 20 weeks- at the level of umbilicus

 

a. b. c. d.


C. Assessment of Gestational Age  Fundal height – between 20 and 34 weeks, the height of the uterine fundus measured in centimeters correlates closely with gestational age in weeks.  Ancillary tests: Gestational diabetes, chlamydial infection, gonococcal infection, fetal fibronectin (vaginal fluid), GBS infection, genetic diseases.  Weight gain based on the BMI. Category Underweight Normal Overweight Obese

BMI (Asia-Pacific) 30




12.5 - 18 11.5 - 16 7 – 11.5 5 – 9.1

28 – 40 25 – 35 15 – 25 11 - 20

III. Nutrition Calories




Dietary fiber

2000 calories/day + 300 kcal/day (2nd & 3rd trimester) 9 grams/day Protein deficiency may lead to lowering of hemoglobin-producing factors in the liver, which may result in hypochromic anemia. Absorption of calcium from intestinal tract may be impaired. Meats, mild and eggs are best sources of protein. 150 grams/day in the first trimester. 225 grams/day at the end of pregnancy. 50-100 grams/day according to FNRI of the Philippines (1989) is sufficient to prevent ketosis and other symptoms of lack of dietary carbohydrate. Adequate carbohydrates seem to lessen nausea and vomiting 15-25 grams/day Most concentrated sources of energy, providing more than twice the energy value of an equivalent weight of carbohydrates or protein. No recommended level. Liberal intake of fruits, vegetables and whole grain cereals is highly recommended. Promoting normal bowel functions and bulk or satiety value to meals. POSTPARTUM CHANGES

BREASTS & LACTATION I. How breast milk protects babies against infection. (DOH, 1991) 1. Breastfed babies have less diarrhea than artificially-fed babies. 2. Fewer respiratory and middle ear infection. 3. Fewer infections because of the following:

Breast milk is clean and free of bacteria Contains antibodies (immunoglobulin) to many common infections, until he can make his own antibodies. Contains white blood cells to help fight infection. Contains bifidus factor which helps special bacteria called Lactobacillus bifidus to grow in the baby’s intestine. Lactobacillus bifidus prevents other harmful bacteria from growing and causing diarrhea. Contains lactoferrin which binds iron. Prevents the growth of some harmful bacteria which need iron.

II. Other advantages of breastfeeding. (DOH, 1991) 1. Breast milk contains lipase which digests fat. Breast milk is quickly and easily digested and a breastfed baby may want to feed again more quickly than an artificially-fed baby. 2. Breast milk is always ready to feed to the baby and it needs no preparation. 3. Breast milk never goes sour or bad in the breast even if a woman does not feed her baby for some days. 4. Breastfeeding helps to stop bleeding after delivery. 5. Breastfeeding on demand helps to protect against another pregnancy. 6. It helps them to bond, become attached to each other and love each other. 7. It is free. You don’t have to buy it. 8. It is exclusively for your baby and cannot be served to other adults. Protective Effects on Infants of Human Milk and Breast Feeding (AAP, 1997) Decreased Incidence/Severity Possible protective effects Diarrhea Sudden infant death Lower respiratory infection syndrome Otitis media Type-1 Diabetes Bacteremia Inflammatory bowel disease Bacterial meningitis Lymphoma Botulism Allergies Necrotizing enterocolitis Chronic digestive diseases Urinary infections III. Composition of Human Breast Milk Component Human milk Water Enough (87.2% to 87.5%) Bacterial None contamination Anti-infection Antibodies, substances leucocytes, lactoferrin, bifidus factor Protein (Total) 1% 0.5%  Casein 0.5%  lactalbumin Amino acids Enough for growing Cysteine brain Enough  Taurine Fats (Total) 4% average  Saturation Enough UNsaturated Fatty acids – Enough for growing linoleic acid brain (essential) Enough  Cholesterol Lipase to digest fat Present Lactose (sugar) 7% (enough) Salts (mEq/L) – Sodium  Chloride  Potassium Iron – colostrum  Mature milk

6.5 12 14

Cow milk More required Likely Antibodies not active, absent lactoferrin 4% too much 3% too much 0.5% Not enough Not present 4% Too much saturated Not enough Not enough None 3% - 4% (not enough) 25 (too much) 29 (too much) 35 (too much)

0.5 – 0.8 mg/L 0.2 – 0.3 mg/L


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] IV. Some Myths about Breastfeeding: (Thomson Medical Center, Singapore. 2004) 1. It is painful & difficult to learn. 2. Breastfed babies cry more than bottle-fed babies. 3. Breastfeeding tends to isolate mother and baby from the rest of the family members. 4. It is embarrassing. 5. Spoils a baby and weaning is difficult. 6. Quality of breast milk depends on your mood. 7. Breastfeeding mother may have to give up food she likes, become tied down and be unable to work. 8. Breastfed babies need more water. 9. Breast milk lack iron. V. How should breastfeeding begin. (DOH, 1991) 1. First feed  First feed should be on the delivery table.  Cover both mother and baby to keep them warm.  Let the mother hold the baby close and let him suck at the breast.  Sucking stimulates the production of oxytocin which helps to deliver the placenta and stop hemorrhage.  Baby gets valuable colostrums.  More likely to breastfeed for a long time. A delay of even a few hours will result in failure to breasfeed. 2.

Rooming-in There is no need for a mother and baby to rest separately after a normal delivery. 3. Demand feeding  Let the mother pick up her baby and feed him whenever he cries and she feels a need to feed him.  Frequent sucking stimulates the production of prolactin which helps the milk to come in sooner.  It prevents engorgement of breasts. 


Duration of feeds More babies finish in 5-10 minutes, but some like to take much longer, perhaps half an hour. It does not matter.  Slow feeders take the same total amount of milk as fast feeders.  Sucking in the wrong position causes sore nipples. 

5. 


 

FAMILY PLANNING Fertility Awareness-based (FAB) Methods  Family planning methods that attempt to identify fertile time each cycle and then modify sexual behavior.  Natural family planning (NFP) refers to sexual abstinence during the fertile time.  Fertility awareness-combined methods (FACM) refer to using barrier method during the fertile time.  Various methods of periodic abstinence have pregnancy rates estimated from 5 to 40 per 100 woman years. The unwanted pregnancy rate during the first year of use is approximately 20%. I.     II.    

III.  

Feeding from both breasts Let the baby finish the first breast to make sure that he gets the hindmilk. Let him take the second breast if he wants to, but do not force him.

 

Prelacteal feeds Prelacteal feeds (e.g. formula, glucose water, ampalaya juice, diluted honey) are NOT necessary and they can be harmful.  Small amount of colostrum is ALL that a normal baby needs at this time.



   


 

Extra water  Normal baby is born with a store of water which keeps him well hydrated until the milk comes in. He does not need drinks of water, they interfere with breasfeeding. Night breastfeeds It is better if the mother breastfeeds the baby at night as long as he wants to. Night feeding helps to keep up the milk supply because the baby sucks more. Night feeds are especially useful for working mothers. Night feeds are important for child spacing.

Early weight changes A baby may lose weight for the first few days after delivery. He may lose up to 10% of his birth weight.  When breastfeeding is started, the baby should regain his birth weight in ten days. 

10. Cleaning the breast

Frequent washing, especially with soap, removes the natural oil from the nipple. The skin becomes dry and is more easily damaged and fissured.

  IV.

  

Standard Days Method Developed by the Institute for Reproductive Health at Georgetown University Avoid unprotected intercourse during cycle days 8 through 19. Women must have regular monthly cycles of 26 to 32 days. Cycle beads can be used to keep track of their cycle. Calendar Rhythm Method Requires counting the number of days in the shortest and longest menstrual cycle during a 6- to 12-month span. First fertile day – 18 days are subtracted from the shortest cycle. Last fertile day – 11 days are subtracted from the longest cycle. This is problematic because ovulation most often occurs 14 days before the onset of the next menses. This is not reliable. Temperature Rhythm Method The first scientific NFP method developed which involves measuring changes in body temperature after ovulation. Immediately after ovulation, basal body temperature, or the body temperature at complete rest, dips slightly then rises by about 0.2 C to 0.5 C (0.4 F). It remains high until just before the next period. Follow a biphasic pattern, it remains low before ovulation and higher after ovulation which is caused by progesterone. The woman has to take her temperature everyday, upon waking up in the morning, before getting out of bed, and after at least 3 hours of continuous sleep. She may take her temperature by mouth (under the tongue) or by the axilla, but she has to use the same route throughout the menstrual cycle. The thermometer must be left in position for 5 minutes. She must record it on a chart after taking it and include other events like illness. A coverline or baseline is drawn using the highest temperature reading from day 6 to 10 of cycle and watch out for 3 consecutive temperature readings above the coverline which refers to the thermal or temperature shift indicating that ovulation has taken place. The woman must abstain from intercourse from the first day of menses through the 3rd day after the increase in temperature. With excellent compliance, the unwanted pregnancy is approximately 2 percent the first year. Cervical Mucus Rhythm Method Also called “Billings method”, developed by John Billings, depends on awareness of vaginal “dryness” and “wetness”. These are the consequences of changes in the amount and quality of cervical mucus at different times in the menstrual cycle. The fertile mucus is brought about byt increasing levels of estrogen and the infertile mucus by the increase in progesterone.


Page 23 of 36


  

Dry days after the menses are the indicators of the preovulatory phase or the first infertile phase, which are relatively infertile days. Wet days signal the ovulatory phase and are therefore fertile days. The fertile type mucus is more copious, slippery/lubricative, stretchy and wet. At times, it has the appearance of raw egg white. This mucus makes it easy for the sperm to travel through the cervix, uterus and the tubes to meet the egg. Last day of the wetness is called the peak day. Its timing is around ovulation time. The 3 days after the peak day or the post-peak days are still considered fertile days, giving allowance for the life span of the egg. Ovulatory phase includes all days when the wet sensation is first felt, including the Peak Day and the 3 post-Peak days. Abstinence is required from the beginning of menses until 4 days after slippery mucus is identified. When used accurately, the first-year failure rate is approximately 3 percent.

V. 

Symptothermal Method Combines the use of changes in cervical mucus – onset of fertile period, changes in basal body temperature – end of fertile period, and calculations to estimate the time of ovulation.  One also has to look out for other bodily changes such as: i. Feel and position of the cervix 1. Fertile: the cervix is far from the vaginal opening and is open and softer (consistency of the lips) 2. Not fertile: cervix is closed, firm (tip of the nose) and close to the vulva ii. Ovulation pain (Mittelschmerz) iii. Mid-cycle bleeding or spotting iv. Breast sensitivity v. Skin changes vi. Mood changes  To avoid pregnancy, the couple abstains from vaginal intercourse on: i. Alternate preovulatory days of no mucus or dry mucus ii. On all days of wet mucus iii. The four days after the last day of wet mucus, or the third day after temperature rise.

Contraceptive Failure Rates During the First Year of Use (Modified from Speroff and Darney, 2001, and Trussell, 2004) Method Perfect Use Typical Use None 85 85 Calendar 9 20 Ovulation 3 Symptothermal 2 Post-ovulation 1 Withdrawal 4 27 Hormonal Contraceptives I. Combination hormonal contraceptives. A. Mechanism of Action  Prevent ovulation by suppression of hypothalamic gonodotropin releasing factors. Thus, prevents pituitary secretion of FSH and LH.  Progestins action: i. Prevent ovulation by suppressing LH ii. Thicken cervical mucus, thereby retarding sperm passage. iii. Render the endometrium unfavourable for implantation.  Estrogen action: 1. Prevents ovulation by suppressing FSH release. 2. Stabilizes the endometrium, which prevents intermenstrual bleeding – also known as breakthrough bleeding. B. Composition  Monophasic pills – progestin dose remains constant throughout the cycle.  Multiphasic (bi-, tri- or quadriphasic) pills – dose frequently varied depending on the number of

dose changes within the cycle. Some formulations, estrogen dose also varies. ESTROGEN o Features:  Daily estrogen content varies from 10 to 50 ug of ethinyl estradiol, and most contain 35 ug or less to minimize adverse effects. o Forms: 1. Ethinyl estradiol – most common 2. Mestranol 3. Estradiol valerate o

Side effects: 1. Breast tenderness 2. Fluid retention 3. Weight gain 4. Nausea 5. Headache

PROGESTIN o Features:  Structurally related to progesterone, testosterone, or spironolactone  Binds variably to progesterone, androgen, estrogen, glucocorticoid, and mineralocorticoid receptors which explain pill-related side effects  Progestin related to testosterone may impart androgenic side effects such as acne and adverse HDL and LDL levels. o Forms: 1. Medroxyprogesterone acetate – mainly used in a progestin-only injectable form 2. Nomegestrol acetate – used in a COC 3. Norethindrone acetate – used in a COC; non-acetate form used as progestin-only 4. Norgestrel 5. Norgestimate 6. Ethynodiol diacetate 7. Levonorgestrel 8. Desogestrel 9. Dienogest 10. Drospirenone  Structurally similar to spironolactone and have similar effects to 25 mg of this diuretic hormone.  Displays antiadrogenic activities  Provides antialdosterone action to minimize water retention  Antimineralocorticoid properties that may cause potassium retention and hyperkalemia. Serum potassium level monitoring for the first month is recommended. Likeswise for the following drugs:  NSAIDS, ACE inhibitors, angiotensin II antagonists, herparin, aldosterone antagonists, and potassiumsparing diuretics.  Avoided in women with renal or adrenal insufficiency or with hepatic dysfunction. o PROGESTIN-ONLY side effects:  Irregular uterine bleeding, such as metrorhhagia or menorrhagia (most frequently reported)  DO NOT significantly affect lipid metabolism, glucose level, hemostatic factors, liver function, thyroid function, and blood pressure.  NOT shown to increase risk for thromboembolism, stroke, or CV disease.  DMPA use shows increased LDL and decreased HDL and may be less favorable with cardiac or vascular risks.  DO NOT impair mild production


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NO increased risk of genital tract or breast neoplasia  Weight gain and bone mineral density loss are not prominent, except for DMPA  Functional ovarian cysts develop with greater frequency. Administration  COC’s are taken daily some for 21 days with 7 pillfree interval or placebo.  Some provide 24 days of hormones followed by 4 pill-free days (e.g. Yaz).  Ideally, women should begin on the first day of a menstrual cycle.  There is a “quick start” method, wherein the pills are started on ANY DAY, regardless of cycle timing. A back-up method is used during the first week. If the woman is already pregnant during Quick Start initiation, COC’s ARE NOT TERATOGENIC.  For maximum efficiency, pills should be taken at the same time each day.  Spotting or bleeding is common with initiation of COCs. It does not reflect contraceptive failure and typically resolves within one to three cycles. Method-specific effects  Altered Drug Efficacy o Three (3) groups of drugs that decrease COC effectiveness: 1. Anti-TB drugs: rifampin and rifabutin 2. Anti-HIV drugs: efavirenz and ritonavirboosted protease inhibitors 3. Anticonvulsants: phytoin (Dilantin), carbamazepine (Tegretol), oxcarbazepine (Trileptal), barbiturates, primidone, and topiramate (Topamax)  Metabolic changes o COCs increase serum levels of triglycerides and total cholesterol. o Estrogen decreases LDL o Estrogen increases HDL and VLDL o OCP are NOT atherogenic o Women with LDL >160 mg/dl or with multiple additional risk factors for CV disease, alternative methods are recommended. o Estrogen use related to increase in fibrinogen and may of the clotting factor levels and may lead to thrombosis. o COCs augment angiotensinogen production and its conversion by renin to angiotensin I which may be associated with “pill-induced hypertension” o COCs increase SHBG which decrease bioavailable testosterone concentrations and improve androgenic side effects. o Risk of developing diabetes is NOT increased. o NO connection beteween COCs and weight gain. o OCP use related to elevated total plasma thyroxine (T4) and thyroid-binding proteins 

Cardiovascular effects o Women using low-dose COCs formulations rarely develop clinically significant hypertension. o Patients are advised to return 8 to 12 weeks after COC initiation for evaluation of blood pressure and other symptoms. o COCs are permissible in women with wellcontrolled uncomplicated hypertension who are non-smokers, otherwise healthy, and younger than 35. o COCs use are NOT advisable for those with severe forms of hypertension, especially with end-organ involvement. o Women with prior stroke or myocardial infaction, COCs should NOT be considered.

o o



o o 


Nonsmoking women younger than 35 years old has and extremely low risk of ischemic and hemorrhagic strokes. COCs may be considered for women with migraines that lack focal neurological signs if they are otherwise healthy, normotensive nonsmkers younger than 35 years. VTE with COC use is only 3 to 4 per 10,000 woman-years and is lower than the incidence of 5 to 6 per 10,000 woman-years estimated for pregnancy. Clinical factors that increase VTE with COC use:  Thrombophilias  Hypertension  Obesity  Diabetes  Smoking  Sedentary lifestyle COCs are NOT recommended for women within the first 4 weeks after delivery. For all women, VTE risk with drospirenonecontaining COCs has been shown.

Neoplasia o Overall, COCs are not associated with an increased risk for cancer. o Protective effect against ovarian and endometrial cancer o Relative risk of cervical dysplasia and cervical cancer is increased in current COC users, but following 10 or more years of disuse, risk returns to that of never users. o No evidence for increased risk of hepatocellular cancer. o Women with known tumores, COCs are AVOIDED in those with benign hepatic adenoma and hepatocellular carcinoma. o Women who are carriers of the BRCA1 and BRCA2 gene mutation, risks for breast cancer are NOT INCREASED by COC use. o COCs appear to lower rates of benign breast disease.

Non-contraceptive benefits of COCs 1. Increased bone density 2. Reduced menstrual blood loss and anemia 3. Decreased risk for ectopic pregnancy 4. Improved dysmenorrhea from endometriosis 5. Fewer premenstrual complaints 6. Decreased risk of endometrial and ovarian cancer 7. Reduction in various benign breast diseases 8. Inhibition of hirsutism progression 9. Improvement of acne 10. Prevention of atherogenesis 11. Decreased incidence and severity of acute salpingitis 12. Decreased activity of rheumatoid arthritis


Injectable Progestin Contraceptives  Intramuscular depot medroxyprogesteron acetate (Depo-Provera or Depo-Trust), 150 mg every 3 months, injected into the deltoid or gluteus muscle.  Mechanisms of action: ovulation inhibition, increased cervical mucus viscosity, and creation of an endometrium unfavourable for ovum implantation.  Initial injection should begin within the first 5 days following menses onset. No back-up contraceptive is required if initiated within 5 days of menses onset.


Implants  Etonogestrel implant o Thin, pliable progestin-containing cylinders that are implanted subdermally and release hormone over many years. o Implanon  Single-rod implant with 68 mg of etonogestrel covered by an ethylene vinyl acetate copolymer cover.


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 

Implant is placed subdermally on the medial surface of the upper arm 8 to 10 cm from the elbow in the biceps groove and aligned with the long axis of the arm. Provides contraception for 3 years and then replaced at the same site or in the opposite arm.

Method-specific adverse effects o Branches of the medial antebrachial cutaneous nerve can be injured if the implant or insertion needle is placed too deeply or if exploration for a lost implant is aggressive. o Numbness and paresthesia over the anteromedial aspect of the forearm o Nonpalpable devices may require radiological imaging for localization Insertion timing o Etonogestrel implant: Ideally inserted within 5 days of menses. If inserted later in the cycle, alternative contraception is recommended for 7 days following placement. o Levonogestrel implant: Contraception is established within 24 hours if inserted within the first 7 days of the menstrual cycle. o Transitioning methods:  On the day of the first placebo COC pill  On the day of the next DMPA injection  Within 24 hours of taking the last POP o Inserted before discharge following delivery, miscarriage, or abortion

Intrauterine devices (IUD)  IUD are “use and forget” effective reversible contraceptive methods that do not have to be replaced for 5 or 10 years, depending on the brand.  It is now better established that the major actions of IUDs are contraceptive, NOT abortifacient.  Risk of pelvic infections is markedly reduced with the currently used monofilament string and with techniques to ensure safer insertion.  Risk of an associated ectopic pregnancy has been clarified. Specifically, the contraceptive effect decreases the absolute number of ectopic pregnancies by approximately 50% compared with that of women not using contraception. With failure, pregnancy is more likely to be ectopic.  Within the uterus, an intense local endometrial inflammatory response in induced, especially by coppercontaining devices. Cellular and humoral components of this inflammation are expressed in endometrial tissue and in fluid filling the uterine cavity and fallopian tubes. These lead to decreased sperm and egg viability.  With the LBG-IUS, in addition to an inflammatory reaction, progestin release in long-term users causes glandular atrophy and stromal decidualization. Progestins create scant viscous cervical mucus that hinders sperm motility.

Problems with the above definitions: 1. Clinical estimation of blood loss is frequently inaccurate and the brisk nature of blood loss during delivery or the presence of amniotic fluid can make this more difficult. 2. Delay in obtaining laboratory results. Information from laboratory tests would not reflect the patient’s current hemodynamic status. 3. Any definition based on the need for transfusion is difficult as there are differences in provider practice patterns regarding transfusion. Definition of obstetric hemorrhage combining clinical and objective data (Bonnar, 2000) Blood Systolic EBL Heart volume BP Signs & symptoms (ml) rate (%) (mmHg) 50010-15 140 60-80 3000 consciousness Etiology and Risk Factors Etiology Pathophysiology Overdistended uterus TONE (Abnormal uterine contractility)

POST-PARTUM HEMORRHAGE (PPH) Definition The following are suggested definitions but there is a lack of agreement on what constitutes excessive blood loss: 1. Blood loss >500 ml for vaginal delivery and 1,000 ml for cesarean section (CS). 2. Blood loss >500 ml in the first 24 hours following delivery. 3. Ten percent (10%) decrease in hemoglobin or hematocrit level. 4. Need for transfusion.

Chorioamnionitis Uterine distortion/abnormality Uterine relaxing drugs

TISSUE (Retained products of conception)

Accreta/Increta/Percre ta Retained placenta/membranes

Laceration of the cervix, vagina or perineum TRAUMA (Genital tract trauma)

Extension/laceration at CS Uterine rupture

Barrier Methods  Male Condoms  Diaphragm Surgical Methods  Tubal ligation  Vasectomy

Uterine muscle fatigue

Uterine inversion

THROMBIN (Abnormaliti es of coagulation)

Preexisting clotting abnormalities (e.g. hemophilia, vonWillebrands disease, hypofibrinogenemia) DIC HELLP Anticoagulation

Risk Factors Multiple gestation Polyhydramnios Macrosomia Prolonged labor Augmented labor Prior PPH Prolonged rupture of membranes (ROM) Fibroids (myoma), placenta previa B-mimetics, MgSO4, anesthetic drugs Prior uterine surgery Placenta previa Multiparity Manual placenta removal Succinturiate/accesso ry lobe Precipitous delivery Macrosomia Shoulder dystocia Operative delivery Episiotomy (e.g. mediolateral) Deep engagement Malposition Malpresentation Prior uterine surgery Fundal placenta Grand multiparity Excessive traction on umbilical cord History of Coagulopathy or liver disease

Sepsis Intrauterine demise Hemorrhage

General Management of PPH: 1. Initial management approach to obstetric hemorrhage: a. Assessment: constant awareness of the hemodynamic status as well as evaluation to determine the cause of bleeding. b. Breathing: administration of oxygen


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2. 3.


Circulation: obtaining intravenous (IV) access and adequate circulating blood volume through infusion of crystalloid and blood products. Second large-bore IV catheter is needed Notify the blood bank. Simultaneous, coordinated, multi-disciplinary management (OB-GYN, anesthesiologist, hematologists, radiologists, nurses, laboratory and blood bank technicians) to concur timely management in the presence of obstetric hemorrhage. Preoperative preparedness is important especially for patients identified as high risk.

Important Causes of PPH: 1. Uterine atony 2. Retained placenta 3. Uterine rupture 4. Genital tract trauma 5. Uterine inversion

DYSTOCIA DYSTOCIA: PROBLEMS IN PASSENGER Fetal Presentations and Conditions 1. Breech 2. External cephalic version 3. POP, OT 4. Brow and Face 5. Transverse/Oblique 6. Compound 7. Macrosomia 8. Shoulder dystocia 1. Breech  Planned CS has reduced risk for perinatal or neonatal death/morbidity  Planned vaginal breech criteria: o Skilled OB o Facilities for possible CS available o Woman is informed of risks o EFW: 2500g to 4000g o Continuous EFM o Induction is NOT recommended. Oxytocin augmentation if with hypotonic uterine dysfunction. o Passive 2nd stage without active pushing for 90 min allowing breech to descend into pelvis o Once active pusching commences and delivery not imminent after 60 min, CS is recommended.  Delivery of the aftercoming head: o assistant should apply suprapubic pressure to favor flexion and engagement of fetal head o Mauriceau-Smellie-Veit maneuver, or o Use of Piper forceps  Spontaneous or assisted breech delivery is acceptable. Fetal manipulation applied after spontaneous delivery to the level of umbilicus.  Nuchal arms may be reduced by Lovset maneuver. Suspected breech o Pre- or early labor ultrasound to assess type of breech, fetal growth, EFW, attitude of fetal head. o If ultrasound is not available, CS is recommended. 2. External cephalic version  ABSOLUTE Contraindications o Where CS is required o Anterpartum bleeding within the last 7 days o Abnormal CTG o Major uterine anomaly o Ruptured membranes o Multiple pregnancy (except delivery of the 2nd twin)  RELATIVE Contraindications o SGA fetus with abnormal Doppler o Proteinuric preeclampsia o Oligohydramnios o Major fetal anomalies o Scarred uterus

 

o Unstable lie Manipulation of the fetus through the maternal abdomen to a cephalic presentation. Use of tocolysis with beta sympathomimetics may increase success rate of ECV

3. POP, OT  Factors for incomplete rotation of fetal head: o Poor contractions o Faulty flexion of head o Epidural anesthesia – diminishes abdominal muscular pushing & relaxes pelvic floor  Digital rotation of the fetus in the OP position. 4. Brow and Face Brow Expectant management, as long as FHR remains reassuring and dilatation and descent are progressing normally. Face  Continuous EFM is mandatory because of increased incidence of abnormal FHR patterns and/or fetal compromise  Oxytocin can be used to augment labor using the same precautions  Forceps, using Kielland forceps, may be used if the mentum is anterior. 5. Transverse/Oblique Both will benefit from a trial of version to cephalic presentation following the criteria & recommendation of ECV for breech. 6. Compound  If the hand has not prolapsed beyond the presenting part, causing the hand to retract often is accomplished. It can be ignored as long as labor is progressing normally  If the hand or arm has prolapsed past the presenting part, CS delivery is wise. 7. Macrosomia  Macrosomia: 4000 g (8 lb 13 oz) or 4500 g (9 lb 4 oz)  Labor & vaginal delivery is NOT CONTRAINDICATED for women with EFW up to 5 kg in the absence of maternal DM  Indication for CS: o >4,500 g, and o prolonged 2nd stage or arrest of descent in 2nd stage  Prophylactic CS: o EFW > 5,000 g (w/o maternal DM) o EFW > 4,500 g (w/ maternal DM)  Suspected macrosomia is NOT a contraindication to attempted VBAC 8. Shoulder Dystocia Shouder Dystocia Drill: 1. Call for HELP! 2. Generous EPISIOTOMY 3. SUPRAPUBIC pressure 4. McRoberts maneuver If the “Drill” fails, attempt the following: 1. Delivery of posterior arm 2. Woods screw maneuver 3. Rubin maneuver 4. Zavanelli maneuver 5. Cleidotomy 6. Symphysiotomy (supplementary) “Shoulder dystocia drill” to better organize emergency management: 1. 2.

Call for help—mobilize assistants and anesthesia and pediat- ric personnel. Initially, a gentle attempt at traction is made. Drain the bladder if it is distended. A generous episiotomy may be desired to afford room posteriorly. 


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Suprapubic pressure is used initially by most practitioners because it has the advantage of simplicity. Only one assistant is needed to provide suprapubic pressure, while normal downward traction is applied to the fetal head. 
 4. The McRoberts maneuver requires two assistants. Each assistant grasps a leg and sharply flexes the maternal thigh against the abdomen. This is the
 single most effective intervention and performed first. These maneuvers will resolve most cases of shoulder dystocia. If the above listed steps fail, the following steps may be attempted, and any of the maneuvers may be repeated: 5. Delivery of the posterior arm is attempted. With a fully extended arm, however, this is usually difficult to accomplish.
 6. Woods screw maneuver is applied. 
 Progressively rotating the posterior shoulder 180 degrees in a corkscrew fashion, the impacted anterior shoulder could be released. 7. Rubin maneuver is attempted. 
  First, the fetal shoulders are rocked from side to side by applying force to the maternal abdomen.  If this is not successful, the pelvic hand reaches the most easily accessible fetal shoulder, which is then pushed toward the anterior surface of the chest. This maneuver most often abducts both shoulders, which in turn produces a smaller shoulder-to-shoulder diameter. This permits displacement of the anterior shoulder from behind the symphysis.  Other maneuvers: o Zavanelli maneuver – replaces or flexes the fetal head back into the vagina, then CS is performed. o Cleidotomy – deliberate fracture of the anterior clavicle to fee the shoulder impaction. o Symphysiotomy – intervening symphyseal cartilage and much of its ligamentous support is cut to widen the symphysis pubis GUIDELINES FOR CESAREAN SECTION Indications 1. Previous uterine scar 2. Abnormalities of the reproductive tract 3. Abnormalities of placenta, cord, membranes & AF 4. Infection in pregnancy 5. Maternal medical conditions 6. IUGR/FGR 7. Fetal congenital anomalies 8. CDMR (Maternal request) 1. 

Previous uterine scar In the presence of scarred uterus, the following are ABSOLUTE INDICATIONS for elective CS: (Level III, Grade C) o Previous classical or inverted T-uterine scar o Uncertainty of type of previous CS scar o Previous multiple low transverse segment uterine scars o Previous hysterotomy or myomectomy entering the uterine cavity or extensive transfundal uterine surgery o Previous uterine rupture o Presence of a contraindication to labor, such as placenta previa/accreta, or malpresentation o No informed consent for VBAC Failed trial of labor during VBAC.

CS performed for those with history of complete transverse vaginal septum and vaginal agenesis due to risk of vaginal soft tissue dystocia and lateral vault laceration


Abnormalities of the placenta, cord, membranes and amniotic fluid Vasa previa o Elective CS between 35-37 weeks AOG o Emergency CS for bleeding vasa previa Placenta previa o Any degree of placental overlap (>0 mm) at the internal os after 35 weeks is an indication for CS o Previa within 1 cm of the internal os is an indication for CS o Elective CS for asymptomatic woman with previa >37 weeks and for suspected accreta >36 weeks Abruptio placenta o Emergency CS for abruptio placenta with fetal compromise, severe uterine hyprtonus, life threatening bleeding or DIC, and remote from vaginal delivery. Cord prolapse o Emergency CS for cord prolapse o Cord prolapse with poor chances of viability, vaginal delivery may be tried with informed consent o Ultrasound finding suggestive of forelying cord or funic presentation is NOT an absolute indication for CS o Digital diagnosis of funic/cord presentation in labor is an indication for CS Chorioamnionitis or intra-amniotic infection o Presence of clinical chorioamnionitis or intra-amniotic infection is NOT an absolute indication for CS. Oligohydramnios o Uncomplicated oligohydramnios is NOT an absolute indication for CS

 

 

4. 

Maternal medical conditions Hypertensive complications o Maternal indications  Deteriorating maternal condition  Uncontrolled hypertension despite drug therapy  HELLP syndrome   Placental abruptio o Fetal indications  Severe IUGR/FGR   Non-reassuring FHR pattern, repeated Category II or III, refractory with resuscitation, remote from delivery   BPP 1,000,000  Not received oral antiretroviral therapy Human papilloma virus o Only for those with very large genital warts causing pelvic outlet obstruction or potential for excessive bleeding during vaginal delivery HIV o Elective CS at 39 weeks to reduce risk of MTCT provided:  Currently on highly active antiretroviral therapy (HAART)  Viral load 5 cm o Hydrocephalus with BPD >10 cm or HC >36 cm Elective CS o Fetus with hypoplastic left heart syndrome o Transposition of great arteries with intact intraventricular septum that require urgent neonatal atrial septostomy Maternal request (CDMR) If without clear indication or there is fear of childbirth, the OB should provide counseling to the patient. Well-written informed consent with proper approval by the hospital’s ethics committee should be secured before performing the CS. Should be performed >39 weeks AOG, unless there is documentation of fetal lung maturity. Multiple pregnancy Fetal malpresentation (Refer to Section III) Abnormal labor patterns (Refer to Section II) Abnormal FHR patterns (Refer to Section I)

Operative Recommendations Timing of planned CS  Scheduled at 39 weeks Pre-operative preparation for CS  Hemoglobin determination  Antimicrobial prophylaxis within 60 minutes preoperatively with either penicillins or cephalosporins (1st or 2nd gen) – Cefazolin 2g/IV (1st gen), Cefuroxime 1.5 g/IV (2nd gen)  Alternative (if allergic): Clindamycin 600 mg/SIV  Morbid obese (BMI>35): double dose of antibiotic  Routine shaving not recommended. Clippers are recommended than razors for excessive hair. Techniques of CS  Transverse abdominal incision or Joel-Cohen incision is preferred.  Placental delivery by controlled cord traction rather than manual extraction  Blunt dissection of uterus was associated with reduced mean blood loss compared to sharp dissection.  Single layer closure was associated with significant reduction in mean blood loss, duration of operative time, post-operative pain but more likely to result in uterine rupture.  Closure of both visceral and parietal peritoneum after CS lead to LESS adhesions  Closure of subcutaneous tissue for >2 cm subcutaneous fat.  Indwelling FC may be removed 4 weeks post evacuation 1. 20,000 IU/I - serum 2. 30,000 IU/I- urine 2. Histological evidence of choriocarcinoma at any site, or any evidence of metastasis 3. Progressive increase in hCG at any time after the evacuation GESTATIONAL TROPHOBLASTIC NEOPLASIA • Also called malignant gestational trophoblastic disease • Refers to: • Invasive mole • Choriocarcinoma • Placental site trophoblastic tumor PERSISTENT/ INVASIVE MOLE


Placental Site Trophoblastic Tumor

 75% of all GTD’s  Usually follow a molar pregnancy  Excessive trophoblastic overgrowth and extensive penetration including the whole villi, myometrium, and adjacents tructures  Very sensitive to chemotherapy  Extremely malignant form of trophoblastic tumor of the chorionic epithelium  Metastasize most of the time (lung)  Extremely hemorrhagic and necrotic with absence of villous pattern, chorionic villi, and cellular atypia  Very sensitive to chemotherapy  Extremely rare  Arises from placental implantation following either a nomal pregnancy or abortion  Predominantly cytotrophoblast and cells secreting prolactin and gonadotropin  Low hCG level  Hysterectormy is the treatment of choice

GTN Diagnosis  Recognition of the possibility of GTN is the most important factor in the diagnosis  Any unusual bleeding after term pregnancy should be investigated by curettage and measurements of serum hCG MANAGEMENT OF AMENORRHEA  The most important elements in the diagnosis of amenorrhea include physical examination for secondary sexual characteristics and anatomic abnormalities,  Measurement of: o human chorionic gonadotropin (hCG) to rule out pregnancy o serum prolactin and thyroid stimulating hormone (TSH) levels o assessment of follicle-stimulating hormone (FSH) levels to differentiate between

Management  Laboratory o Pregnancy test, CBC, Prothrombin time, PTT, VWF  Imaging o Ultrasound  Endometrial Sampling o Performed for women at risk for endometrial pathology (polyps, hyperplasia or carcinoma)  Management o Mefenamic Acid and other NSAIDs o Tranexamic Acid o Mild bleeding: combination low-dose oral contraceptive o Acute moderate bleeding: combination monophasic oral contraceptives every 6 hours for 4-7 days o Emergency management:  Hormonal therapy: Estrogenprogestin therapy 1-2 pills 2x/day for 7 days effective for 12-24 hours OR conjugated estrogens 25-40 mg IV every 6 hrs or 2.5 mg oral every 6 hours  If intrauterine clots are detected D&C is indicated GENITOURINARY INFECTIONS and STDs Diagnosis Bacterial Vaginosis

Description Most common cause of vaginitis in the US

Treatment Metronidazole Clindamycin

Women with BV are at risk for PID, Pregnant women are at risk for PROM, preterm labor and delivery, chorioamnionitis


Diagnosis: fishy vaginal odor; clue cells in histology Profuse, purulent, malodorous vaginal discharge with pruritus; Strawberry cervix may be observed


Women with this infection


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Atrophic vaginitis Cervicitis

Pelvic Inflammatory Disease

should also be tested for other STDs 75% of women may experience this in their lifetime. Predisposing factors: pregnancy, diabetes, antibiotic use. Discharge may be varied from watery to thick Common in menopausal women Presents with purulent cervical discharge

Diagnosis implies that the patient has upper genital tract infection and inflammation (ascended to the endometrium and fallopian tubes) Commonly caused by N. gonorrhoeae and C. trachomatis Triad: pelvic pain, cervical motion and adnexal tenderness and fever

pathogen for acute cystitis Topical azoles (Butoconazole, Clotrimazole, Miconazole, Tioconazole, Nystatin, Fluconazole) Estrogen cream Treatment – for lower genital tract infection with both chlamydia and gonorrhea Cefexime, Azithromycin, Doxycycline, Ofloxacin, Levofloxacin Outpatient treatment: Cefoxitin or Ceftriaxone PLUS Doxycycline or Azithromycin

TMP-SMX, Nitrofurantoin Pyelonephritis: TMP-SMX, Levofloxacin, Cetriazone, Ampicillin, Gentamicin



Characterized by a combination of hyperandrogenism (either clinical or biochemical), chronic anovulation, and polycystic ovaries. It is frequently associated with insulin resistance and obesity It is the most common cause of hyperandrogenism, hirsutism, and anovulatory infertility in developed countries Criteria: o Oligoovulation or anovulation o Clinical and/or biochemical signs of hyperandrogenism o Polycystic ovaries and exclusion of other etiologies (congenital adrenal hyperplasia, androgen-secreting tumors, Cushing’s syndrome)

Inpatient treatment: Cefoxitin or Cefotan PLUS Doxycline Or

Tubo-ovarian Abscess

End stage process of PID

Genital Ulcers

Those with genital ulcers may have HSV or syphilis or chancroid

Clindamycin PLUS Cefrtriaxone or Gentamicin Medical treatment or Abscess Drainage Chancroid: Azithromycin, Ceftriaxone, Ciprofloxacin, Erythromycin HSV: Acyclovir, Famciclovir, Valacyclovir

Genital warts

Manifestation of HPV 51 (external) Non-oncogenic HPV 6 and 11 also cause external genital warts

Syphillis: Pen G Goal of treatment is to remove the warts but it is not possible to eradicate the infection


Highly contagious


E.coli is the most common

Cryotherapy, Imiquimod cream, Podophyllin, Podofilox, Trichloroacetic acid, Cautery, Laser, Interferon Acute Cystitis:


Metabolic Syndrome Diagnostic Criteria o Female waist >35 inches o Triglycerides >150 mg/dL o HDL 130/85 mmHg o Fasting glucose: 110–126 mg/dL o Two-hour glucose (75 gm OGTT): 140–199 mg/dL Treatment o Hormonal contraception or ovulation induction o Hirsutism: Weight loss, Oral contraceptives, medroxyprogesterone, GnRH analogues, glucorticoids, ketoconazole, finasteride, spironolactone, flutamide, metformin


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TOPNOTCH MEDICAL BOARD PREP OB SUPPLEMENT HANDOUT BY CHRISTOPHER JOSEPH SORIANO, MD For inquiries visit or email us at [email protected] AMBIGUOUS GENITALIA AND CONGENITAL ADRENAL HYPERPLASIA Ambiguous genitalia will be found in 1 in 14,000 newborns Females with masculinized external genitalia will be identified as female pseudohermaphrodites Most common cause is Congenital Adrenal Hyperplasia You may see clitoral enlargement and labial fusion

CONGENITAL ADRENAL HYPERPLASIA (CAH) May be demonstrated at birth by the presence of ambiguous genitalia in genetic females or present later in childhood Significant proportions of newborns with this




condition are also at risk for the development of life-threatening neonatal adrenal crises as a result of sodium loss because of absent aldosterone. In milder disease, delayed diagnosis may result in abnormalities of accelerated bone maturation, leading to short stature. The development of premature secondary sexual characteristics in males and further virilization in females may also occur Treatment and Management o Replacement of cortisol – suppresses ACTH output and decreases the stimulation of the cortisol producing pathways in the adrenal cortex o For females at risk – dexamethasone o Corrective surgery o Psychosocial support and counseling

IMPERFORATE HYMEN Hypen should establish a connection between the lumen of the vaginal canal and the vestibule May result to primary amenorrhea May cause hydrocolpos or mucocolpos- caused by collection of secretions behind the hymen, and in rare cases may build up to form a mass that obstructs the urinary tract May develop hematocolpos and hematometrium overtime Fallopian tubes can also be distended because the menstrual flow may back up through the tubes VAGINAL AGENESIS Also called Mullerian agenesis or Mullerian aplasia Usually associated with the Mayer-Rokitansky-KusterHauser (MRKH) syndrome o congenital absence of the vagina and uterus (in 75% of patients), although small masses of smooth muscular material resembling a rudimentary bicornuate uterus are not uncommon o Some patients have rudimentary uterine horns o 50% have concurrent urinary tract anomalies o Presents with primary amenorrhea o PE findings shows a short vaginal pouch and inability to palpare a uterus


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