OBGYN Topic Titles

Question 1

Anatomy of the female pelvic

Answer 1

The bony Pelvis

 The bony pelvis consists of the paired innominate bones (each consisting of ilium, ischium and
pubis) and the sacrum and coccyx.

 The innominate bones are joined anteriorly at the symphysis pubis and each articulates
posteriorly with the sacrum in the sacroiliac joints.  All three joints are fixed in the non-pregnant state, but during pregnancy there is relaxation of
the joints to allow some mobility during labour and birth.

 The bony pelvis is divided into the false pelvis and the true pelvis by the pelvic.

o The true pelvis is divided into three sections:  the pelvic inlet (bounded anteriorly by the superior surface of the pubic
bones and posteriorly by the promontory and alae of the sacrum);

 the mid-pelvis (at the level of the ischial spines);  the pelvic outlet (bounded anteriorly by the lower border of the symphysis,
laterally by the ischial tuberosities and posteriorly by the tip of the sacrum).

The External Genitalia

 Vulva describe the female external genitalia which includes: mons pubis, labia majora, labia
minora, clitoris, external urinary meatus, vestibule of the vagina, vaginal orifice and hymen.

 Mons pubis composed of a fibrofatty pad of tissue that lies above the pubic symphysis an
Covered with dense pubic hair which begins to appear between the ages of 11 and 12 years.

 Labia majora consist of two longitudinal cutaneous folds that extend downwards and
posteriorly from the mons pubis anteriorly to the perineum posteriorly. Composed of an outer
surface covered by hair and sweat glands and an inner smooth layer containing sebaceous
follicles; Enclose the pudendal cleft into which the urethra and vagina open.

 Labia minora enclosed by the labia majora o Anteriorly divide to enclose the clitoris, the anterior fold forming the prepuce and
the posterior fold the frenulum; richly vascularized and innervated and are erectile.

o They do not contain hair but are rich in sebaceous glands.

 Clitoris is situated between the anterior ends of the labia minora. The consists of two corpora
cavernosa of erectile tissue enclosed in a fibrous sheath. The free end contains the glans,
composed of erectile tissue covered by skin and richly supplied with sensory nerve endings
and hence very sensitive- plays an important role in sexual stimulation and function.

 Vestibule consists of a shallow depression lying between the labia minora. The external
urethral orifice opens into the vestibule anteriorly and the vaginal orifice posteriorly.

o The ducts from Bartholin’s glands drain into the vestibule at the posterior margin.

o Skene’s ducts lie alongside the lower 1cm of the urethra and drain into the vestibule.

o The bulb of two erectile bodies that lie on either side of the vaginal orifice and are in
contact with the surface of the urogenital diaphragm.

 External urethral orifice lies 1.5–2 cm below the base of the clitoris and is covered by the labia
minora, which help to direct the urinary stream.

 The vaginal orifice opens into the lower part of the vestibule and is partly covered by the
hymenal membrane- The hymen is a thin fold of skin attached around the circumference of
the vaginal orifice. There are various types of opening within the hymen and the membrane
varies in consistency. Once the hymen has been penetrated, the remnants are represented by
the carunculae myrtiformes, which are nodules of fibrocutaneous material.

 Bartholin’s glands are a pair of glands located at either side of the vaginal introitus and
measuring 0.5-1.0 cm in diameter. The ducts are approximately 2 cm in length and open
between the labia minora and the vaginal orifice.

Their function is to secrete mucus during sexual arousal. o Cyst formation is relatively common but is the result of occlusion of the duct, with
fluid accumulation in the duct and not in the gland.

The Internal Genitalia
The vagina is a muscular tube some 6-7.5 cm long in the mature female, lined by non-cornified
squamous epithelium. It is capable of considerable distension, particularly during parturition when it
adapts to accommodate the passage of the fetal head.

 Separated from the anal canal by the perineal body. In the middle third, it lies in apposition to
the ampulla of the rectum and in the upper segment it is covered by the peritoneum of the
rectovaginal pouch (pouch of Douglas).  The uterine cervix protrudes into the vaginal vault. Four zones are described: the anterior
fornix; the posterior fornix; and the two lateral fornices.  The pH of the vagina in the sexually mature nonpregnant female is between 4.0 and 5.0- has
an important antibacterial function that reduces the risk of pelvic infection.

 The functions of the vagina are copulation, parturition and the drainage of menstrual loss.
The uterus is a hollow, muscular, pear-shaped organ situated in the pelvic cavity between the bladder
anteriorly and the rectum and pouch of Douglas posteriorly. The size depends on the hormonal status.

 In the sexually mature female, the uterus is approximately 7.5 cm long and 5 cm width.  The uterus normally lies in a position of anteversion such that the uterine fundus is anterior to
the uterine cervix. In about 10% of women, the uterus lies
in a position of retroversion.
The uterus may also be curved anteriorly in its longitudinal axis, a feature that is described as
anteflexion, or posteriorly, when it is described as retroflexion.

 It consists of a body or corpus, an isthmus and a cervix. The corpus uteri consist of a mass of
smooth muscle cells, the myometrium, arranged in three layers.

o The external layers: smooth muscle cells that pass transversely across the uterine
fundus into the lateral angles of the uterus; their fibres merge with the outer layers
of the smooth muscle of the Fallopian tubes and the ovarian and round ligaments. o The muscle fibres in the middle layer are arranged in a circular manner. o The inner layer contains a mixture of longitudinal, circular and oblique muscle fibres.

 The cavity of the uterus is triangular in shape and is flattened anteroposteriorly; total volume
of the cavity in the non-pregnant state is approximately 2 mL. It is lined by endometrium that
consists on the surface of mucus-secreting columnar epithelium. o The nature of the endometrium depends on the phase of the menstrual cycle.

The cervix is a barrel-shaped structure extending from the external cervical os to the internal cervical
os in its supravaginal portion. The internal os opens into the uterine cavity through the isthmus of the
uterus. In non-parous women the external os is round or oval, but it becomes transverse following
vaginal birth and this can be noted in clinical examination when a speculum is passed.

The cervical canal is fusiform in shape and is lined by ciliated columnar epithelium that is mucus-
secreting. The transition between this epithelium and vaginal ectocervix epithelium forms the
squamocolumnar junction. The exact site of this junction is related to the hormonal status of the
woman. If the cervical glands becomes obstructed- nabothian follicles may form.

The isthmus of the uterus joins the cervix to the corpus uteri and in the non-pregnant uterus is a
narrow, rather poorly defined, area some 2–3 mm in length.

In pregnancy, it enlarges and contributes to the formation of the lower segment of the uterus, which is
the normal site for the incision of caesarean section.
In labour it becomes a part of the birth canal but does not contribute significantly to the expulsion of
the fetus.

Supports and ligaments of the uterus  Broad ligament: connects the lateral uterus, fallopian tubes and ovaries with the lateral pelvic
wall; within it: ovarian artery and vein; round ligament; fallopian tubes and ovaries

 Round ligament: responsible for the anteroversion-anteflexion position of the uterus;
connects the uterine horn with the labia majora; contains the lymphatics of the uterine horn.

 Cardinal ligament: distal portion of the broad ligament; connects the cervix with the lateral
pelvic wall; contains the uterine artery and vein and the ureter.

The Fallopian tubes

 Fallopian tubes or uterine tubes found between the fundus of the uterus and the ovaries.  The tubes are approx. 10-12 cm long and lie on the posterior surface of the broad ligament.

 Enclosed in a mesosalpinx and contains the blood vessels and nerve supply to the tubes and
the ovaries.

 The tube is divided into four sections: o The interstitial portion opens into uterine cavity. o The isthmus is a constricted portion. The lumen of the tube is narrowest.

o The ampulla is a widened section of the tube and the muscle coat is much thinner.
(fertilization typically occurs at this section) .

o The infundibulum outermost part of the ampulla. surrounded by a fringe of fimbriae,
the longest of which is attached to the ovary.

 The tubes are lined by a single layer of ciliated columnar epithelium which serves to assist the
movement of the oocyte and are richly innervated.
The ovaries

 Paired almond-shaped organs that have both reproductive and endocrine functions. They are
approximately 2.5-5 cm in length and 1.5-3.0 cm in width; lie on the posterior surface of the
broad ligaments in a shallow depression known as the ovarian fossa.

 The anterior border is attached to the posterior layer of the broad ligament by a fold in the
peritoneum known as the mesovarium; contains the vessels and nerves supplying the ovary.

 The lower pole is attached to the lateral border of the uterus by a musculofibrous
condensation known as the ovarian ligament.  The surface of the ovary is covered by a cuboidal or low columnar type of germinal
epithelium; Beneath the germinal epithelium a layer of dense connective tissue- the tunica
albuginea.

 Graafian follicles are found in the highly vascular, central portion of the ovary: the medulla.
The blood vessels and nerve supply enter the ovary through the medulla.

The blood supply to the pelvic organs
Internal iliac arteries (hypogastric arteries):  Internal pudendal artery: perineum

 Umbilical artey: dome of the bladder (sup. Vesical artery).

 Vaginal artery: anterior and posterior wall of the vagina (can also arise from uterine artery)

 Middle rectal artery: lower rectum, upper anal canal and ureter.

 Uterine artery: superior branch: body and fundus of the uterus; vaginal branch: cervical
branch: cervix of the uterus and the vagina; anastomoses with ovarian artery becomes the
major vascular structure arising from this division during pregnancy, when there is a major
increase in uterine blood flow.

 Ovarian artery: arise from the abdominal aorta, crosses the proximal end of the external iliac
artery: supplies ovary through the suspensory ligament of the ovary.

The pelvic lymphatics system
Course along the internal iliac vessels and drain into the following lymph nodes:

 Inferior mesenteric and aortic lymph nodes: upper part of rectum

 Paraaortic lymph nodes: ovaries, fallopian tubes, uterus (fundus).  Internal and external iliac lymph nodes: uterus (body and cervix), bladder, rectum (internal
iliac nodes).
Nerves of the pelvis
Autonomic nerves:

 Superior and inferior hypogastric plexus; Hypogastric nerve; Sacral splanchnic nerves  Pelvic splanchnic nerves (S2-S4)

o Parasympathetic fibers o Form part of the pelvic plexus o Innervate the descending and sigmoid colon, and organs in the pelvis and perineum
(sexual organs)

Pudendal nerve (S2-S4):

 Provides motor innervation to external urethral sphincter, external anal sphincter, levator ani.

 Sensation to the perineum, clitoris, posterior labia, and the anal canal

 Sympathetic fibers to the clitoris.  Injury (e.g., pelvic trauma or surgery) can cause urinary and fecal incontinence.

 Used for pudendal nerve block during childbirth or during surgical procedures involving the
perineum; The ischial spine is used as a landmark for injection

The pelvic floor
 Diaphragm across the outlet of the true pelvis and some of the organs of the abdomen.

 Naturally breached by the vagina, the urethra and the rectum.

 These muscles play an important role in defecation, coughing, vomiting and parturition.

 The principal supports of the pelvic floor are the constituent parts of the levator ani muscles.
These are described in three sections:

o The iliococcygeus muscle
o The puborectalis muscle
o The pubococcygeus muscle

The perineum

 A region defined as the inferior aperture of the pelvis and consists of all the pelvic structures
that lie below the pelvic floor.

 Divided into anterior and posterior triangles by a line drawn between the two ischial
tuberosities.

o The anterior portion is known as the urogenital triangle and includes part of the
urethra; the urogenital diaphragm is a condensation of fascia below the level of the
pelvic floor muscles and is traversed by the vagina.

o The posterior or anal triangle includes the anus, the anal sphincter and the perineal
body.

 The pudendal nerve and internal pudendal vessels pass through the lateral aspect of the fossa
enclosed in the fascial layer of Alcock’s canal.

Question 2

Conception and nidation

Answer 2

Oogenesis
The germ cells form sex cords and become the cortex of the ovary which subsequently break up into
separate clumps of cells and by 16 weeks these clumped cells become primary follicles, which
incorporate central germ cells.
These cells undergo rapid mitotic activity, and by 20 weeks of intrauterine life, there are about 7
million cells, known as oogonia.
After this time, no further cell division occurs and no further ova are produced.
By birth, the oogonia have already begun the first meiotic division and have become primary oocytes.
The number of primary oocytes falls progressively and by birth is down to about 1 million and to about
0.4 million by puberty.

*watch Osmosis for menstrual cycle
Follicular development in the ovary

 The cortex of the ovary contains many oogonia surrounded by follicular cells that become
granulosa cells.

 The first stage is characterized by enlargement of the ovum with the aggregation of stromal
cells to form the thecal cells.

 A dominant follicle is selected at about day 6 of the cycle, the innermost layers of granulosa
cells adhere to the ovum and form the corona radiata.

 A fluid-filled space develops in the granulosa cells and a clear layer of gelatinous material
collects around the ovum, forming the zona pellucida.

 The ovum becomes eccentrically placed and the Graafian follicle assumes its classic mature
form. The mesenchymal cells around the follicle become differentiated into two layers,
forming the theca interna and the theca externa.

 The follicle bulges towards the surface of the ovary and the area under the germinal
epithelium thins out.

 The corpus luteum reaches its peak approximately 7 days after ovulation and thereafter
regresses unless implantation occurs, when β-hCG production by the implanting embryo
prolongs its function until the placenta takes over at about 10 weeks of gestation.

 This finally develops into a white scar known as the corpus albicans.

Hormonal events associated with ovulation
The maturation of oocytes, ovulation and the endometrial and tubal changes of the menstrual cycle
are all regulated by a series of interactive hormonal changes.

 The process is initiated by the release of the GnRH, resulting in the release of both FSH and LH
from the pituitary.

 GnRH is released in episodic fluctuations with an increase in the number of surges being
associated with the higher levels of plasma LH commencing just before midcycle and
continued ongoing GnRH action being required to initiate the huge oestrogen-induced LH
surge.

 Blood levels of FSH are slightly higher during menses and subsequently decline due to the
negative feedback effect of the oestrogen production by the dominant follicle.

 LH levels appear to remain at a relatively constant level in the first half of the cycle, however
there is a marked surge of LH 35–42 hours before ovulation and a smaller coincidental FSH
peak.

o The LH surge is, in fact, made up of two proximate surges and a peak in plasma
oestradiol precedes the LH surge.

o Plasma LH and FSH levels are slightly lower in the second half of the cycle than in the
pre-ovulatory phase, but continued LH release by the pituitary is necessary for
normal corpus luteum function.

 Oestrogen production increases in the first half of the cycle, falls to about 60% of its follicular
phase peak following ovulation and a second peak occurs in the luteal phase.

 Progesterone levels are low prior to ovulation but then become elevated throughout most of
the luteal phase.

 There are feedback mechanisms that regulate the release of FSH and LH by the pituitary. This
is principally achieved by the oestrogens and progesterone produced by the ovaries. In the
presence of ovarian failure, as seen in the menopause, the gonadotrophin levels become
markedly elevated because of the lack of ovarian oestrogen and progesterone production.
The action of gonadotrophins

 FSH stimulates follicular growth and development and binds exclusively to granulosa cells
in the growing follicle.

 Of the ~30 follicles that begin to mature in each cycle, one becomes pre-eminent and is
called the dominant follicle.

 The granulosa cells produce estrogen on the pituitary to suppress FSH release, with only
the dominant follicle then getting enough FSH to continue further development and
stimulates receptors for LH.

 LH stimulates the process of ovulation, the reactivation of meiosis I and sustains
development of the corpus luteum; receptors for LH are found in the theca and granulosa
cells and in the corpus luteum.

The endometrial cycle
The endometrium consists of three zones- the two outer zones that are shed during menstruation.
The basal zone (zona basalis) is the thin layer of the compact stroma that interdigitates with the
myometrium and shows little response to hormonal change. It is not shed at the time of menstruation.
The zona spongiosa contains the endometrial glands which are lined by columnar epithelial cells
surrounded by loosenstroma.

The zona compacta covers surface of the endometrium, surrounds the ostia of the endometrial glands.
The endometrial cycle is divided into four phases:

 Menstrual phase. This occupies the first 4 days of the cycle and results in shedding of the
outer two layers of the endometrium. The onset of menstruation is preceded by
segmental vasoconstriction of the spiral arterioles. This leads to necrosis and shedding of
the functional layers of the endometrium. The vascular changes are associated with a fall
in both oestrogen and progesterone.

 Phase of repair. This phase extends from day 4 to day 7 and is associated with the
formation of a new capillary bed arising from the arterial coils and with the regeneration
of the epithelial surface.

 Follicular or proliferative phase. This is the period of maximal growth of the endometrium
and is associated with elongation and expansion of the glands and with stromal
development. This phase extends from day 7 until the day of ovulation (generally day 14
of the cycle).

 Luteal or secretory phase. follows ovulation and continues until 14 days later when
menstruation starts again. The endometrial glands become convoluted and ‘saw-toothed’
in appearance, epithelial cells exhibit basal vacuolation and, by the mid-luteal phase
(about day 20), there is visible secretion in these cells. As menstruation approaches, there
is oedema of the stroma and a pseudodecidual reaction. Within 2 days of menstruation,
there is infiltration of the stroma by leukocytes.

Fertilization
The process of fertilization involves the fusion of the male and female gametes to produce the diploid
genetic complement from the genes of both partners.

 Sperm transport: following the deposition of semen near the cervical os, migration occurs
rapidly into the cervical mucus. The speed of this migration depends on the presence of
receptive mucus in mid-cycle. During the luteal phase, the mucus is not receptive to sperm
invasion and therefore very few spermatozoa reach the uterine cavity. Under favorable
circumstances, sperm migrate at a rate of 6 mm/min.

 Capacitation: During their passage through the Fallopian tubes, the sperm undergo the final
stage in maturation (capacitation), which enables penetration of the zona pellucida.

 Fertilization and implantation: The adherence of the sperm to the oocyte initiates the
acrosome reaction, which involves the loss of plasma membrane over the acrosomal cap this
allows the release of lytic enzymes, which facilitates penetration of the oocyte membrane.

The sperm head fuses with the oocyte plasma membrane and by phagocytosis the sperm
head and midpiece are engulfed into the oocyte. The sperm head decondenses in the female
egg to form the zygote.

o During the 36 hours after fertilization, the conceptus is transported through the tube
by muscular peristaltic action. The zygote undergoes cleavage and at the 16-cell
stage, becomes a solid ball of cells known as a morula.

o A fluid-filled cavity develops within the morula to form the blastocyst. Six days after ovulation, the embryonic pole of the blastocyst attaches itself to the
endometrium, usually near to the mid-portion of the uterine cavity.

o By the seventh post-ovulatory day, the blastocyst has penetrated deeply into the
endometrium.

Endometrial cells are destroyed by the cytotrophoblast and the cells
are incorporated by fusion and phagocytosis into the trophoblast. The endometrial
stromal cells become large and pale; known as the decidual reaction.

Question 3

Physiological changes in pregnancy: uterus, vagina,
cardiovascular system, blood, respiratory function

Answer 3

Question 4

Physiological changes in pregnancy: renal function,
alimentary system, nutrients in blood, skin, breasts.
Maternal weight gain, endocrine changes.

Answer 4

Question 5

Placental growth, development and function

Answer 5

(Last page) Uteroplacental blood flow

1. Formation of the intervillous space begins with small lacunas of blood dispersed between the decidual cells and eventually are dispersed between the syncytiotrophoblasts.

They are supplied by maternal spiral arteries. Growing of the lacunas is due to their fusion with adjacent lacunasuntil the maternal blood “baths” the blastocyst allowing for further growth of the villi and until the formation of the cotyledon.

8. Trophoblastic invasion to maternal spiral arterioles leads to destruction of smooth muscle and formation of sinusoids which makes the blood circulation more efficient.
9. Uterine blood flow is between 500-750mL/min.
10. Factors influencing uterine blood flowa. Catecholaminesb. Mechanical forcec. Hemorrhagesd. RAASe. Vasodilators
11. Transfer of material is by simple diffusion, facilitated diffusion (passive and active) and pinocytosis.

Placental functions

1. Gas exchange
   a. Simple diffusion of oxygen.
   b. What favors O2 uptake by the fetus and placenta?

(right shift in the oxygen dissociation curve – Bohr’s effect)

i. PO2 of maternal is 90-100mmHg which is higher than the fetal PO2.

ii. The period of high fetal metabolism produces high CO2 levels that promote O2 uptake from the mother.

iii. Fetal hemoglobin has higher affinity for oxygen.

c. The placenta utilizes high amount of oxygen and remaining goes to the fetus.

2. Nutrition and excretiona.

Maternal glucose crosses the placenta and provides 90% of fetal energy.

b. Hormones regulating glucose metabolism do not cross the placenta – insulin, glucagon, human placental lactogen and growth hormone.

c. Glycogen is stored in the placenta and also in the fetal liver which serves as energy source for the period after pregnancy and for asphyxiated fetus.

d. Free fatty acids cross the placenta.e. Proteins are synthesized by the fetus and can cross the placenta via active transporters.

f. Immunoglobulin are synthesized by the fetus and IgM appears first in the fetus by week 20.3.

g. IgG is the only one who can cross the placenta.

Hormones synthesisa.

hCG produced by trophoblasts similar to (LH). It maintains corpus callosum which is responsible for progesterone until the placenta is able to produce it by itself.

b. hPL produced by syncytiotrophoblasts.

It increases free fatty acids and insulin levels. Used to assess placental function (low levels indicate placental failure).

c. Progesterone is formed by the placenta by week 17. About 350mg are formed by full term.

d. Estrogen is mainly formed by the placenta and to lesser extent by the ovaries.

Question 6

Fetal development

Answer 6

Question 7

Amniotic fluid, amniocentesis

Answer 7

iv. Treatmentb.

• • Polyhydramnios

Hydration
Amnioinfusioni.

Definition: excessive volume of amniotic fluidii.

Associated with:
* Anencephaly
* Esophageal atresia
* Hydrocephaly
* Chorioangioma of placenta – very large placenta
* Diaphragmatic hernia
* Diabetes mellitusiii.

Complications:
* Premature rupture of membranes (PROM)
* Intrauterine fetal anoxia
* Weak labor activity
* Umbilical cord prolapseiv.

Symptoms:
* Nausea
* Dyspnea
* Vomiting
* Weak sensation of fetal movementsv.

Treatment
* Amniocentesis
* Indomethacin – reduces fetal urine production (crosses the placenta)

Amniocentesis

1. Definition: procedure where amniotic fluid is obtained by a needle through anterior abdomen under local anesthesia and with ultrasound guidance.
2. Usage:
   a. Diagnostici. Chromosomal abnormalities – karyotype determination of

• Sex-linked disorders –turner syndrome, thalassemia, hemophilia, Duchene’s muscular dystrophy
• Down syndromeii. Metabolic disorders – e.g. Tay-Sachs

iii. Lung maturity – sampling of amount of surfactant (lechitin/sphingomyelin ratio) originating in the pulmonary secretions into the amniotic fluid.

b. Therapeutici. Drainage of polyhydramnios

Question 8

Perinatal mortality

Answer 8

Question 9

Maternal mortality

Answer 9

Question 10

History taking in obstetrics

Answer 10

Question 11

Physical examination in obstetrics

Answer 11

There are 2 tables in the note (diameter) check.

8. Pelvisa.

b. c. d. Vulvar lesions
Speculum examination – used during gynecological examination (for complaints about bleedings, abnormal vaginal discharge, Pap test, during labor in cases of bleeding or cervical assessment.

Digital vaginal examination – contraindicated in later pregnancy due to the risk of introducing infection, artificial rupture of membranes.

However, used during labor for evaluation of cervical effacement and assessment of fetal presentation.

Pelvimetry – not a routine anymore but used in cases ofi.

Delayed labor progressionii. Previous fractures

iii. Abnormal development of bony pelvisiv. Includes the following measurements:

• Transverse diameter – line between widest iliopectineal points
• True conjugate – line between the sacral promontory and superior

Inlet*
* pubic symphysis
Obstetric conjugate – line between the sacral promontory and midlinepubic symphysis

Diagonal conjugate diameter – line between inferior margin of the pubic symphysis to sacral promontory (most clinically important)

Midline * Mid-cavity – line between ischial spines

Outlet
* Anteroposterior diameter (least pelvic diameter) - sacrococcygeal joint and the inferior margin of pubic symphysisIntertuberous diameter – line between ischial tuberosities

Anatomy remindersi. Pelvic girdle is a single hip boneii. Bony pelvis is 2 hips + sacrum + coccyxiii.

Pelvic brim (pelvic inlet) is bordered by pubic symphysis, iliopectineal line, margin of ala and sacral promontoryiv.

True pelvis is below pelvic inlet and false pelvis is above pelvic inlet

Palpation of fetal parts
1. Features:
* Head is firm
* Buttocks are soft
* Breech is not ballotable
* Normal fetal altitude is flexion

2. Liea.
   b. Definition: relationship of long axis of fetus to the long axis of uterus

Types:
i. ii. iii. Transverse - poles of fetus palpable in the lumber regions

Oblique - presenting part is palpable in iliac fossa

Longitudinal - presenting part (head or breech) palpable over pelvic inlet

Presentationa.

Definition: the leading body part of the fetus through the birth canal (dilated cervix and vagina)

b. Types:

i. ii. Cephalic presentation (head) – longitudinal lie* * * *

BreechVertex (occipito-) – hyperflexed (most common)
Brow (eyebrows) – partially extended
Forehead – partially flexed
Face (mento-) – hyperextended
* Buttocks (sacro-)
* Feet (podalic-)
iii. iv. Shoulder - transverse or oblique lie

Compound presentation – more than >1 presenting part (e.g. cephalic and an extremity)

c. Positiona.
Diagnosis – vaginal examination in established labor

Definition: relationship of the denominator (the prominent part of the presenting part) to the maternal pelvis (direction the fetus is facing in relation to the mother’s spine.
b. Examples:

c. Stationa.

Diagnosis – vaginal examination in established labor (dilated cervix and palpable fontanelles)

Definition: measurement (cm) of the presenting part above and below the maternal ischial spine.

6. Engagementa.

Definition: when the widest diameter (usually biparietal diameter [BPD]) passed through the pelvic inlet to the true pelvis.

Measurement is described in fifths. “Engaged head” is when ≤ 2/5 of the head is palpable in the abdomen. Palpable head is usually not engaged.

7. Synclitismb.

Definition: parallelism between pelvic inlet plane and fetal plane. Sagittal suture is the in line with the pubic symphysis and sacral promontory.

c. Asynclitism: sagittal suture is in the transverse diameter of the pelvic inlet.

Question 12

Normal pregnancy and antenatal care

Answer 12

a. Some are needed to be stopped or replaced.

7. Fetal anomalya.

Trisomy 21 (Down’s syndrome)

i. Positive results end with either termination of pregnancy or continuation of pregnancy that allows for better preparation for birth by the parents (for those who want to keep the baby)

ii. Ultrasound examination of nuchal translucency and biochemical tests

Risk factors
1. Smokinga. CO has higher affinity for Hemoglobin (200 times greater than oxygen) and shifts dissociation curve to the left

2. b. Nicotine is vasoconstrictor causing narrowing of capillaries of placentac. Placental structure shows thickening of trophoblastic membraned.

Reduces birth weight of infant and crown-heel length.Alcohol abusea.

Fetal alcohol syndromei. Growth retardationii. Structural defects (facial, cardiac and joint anomalies)

b. 3. Drugsa. Interferes also with recommended dietary intake (alcohol is only energy and not a source for proteins, vitamins etc.)

Heroine, amphetamine, cocaine cause:i. IUGRii. Miscarriageb. iii. Placental abruptioniv. Developmental anomaliesv. Cardiac arrhythmiasMarijuana showed to be teratogenic in animal studies

4. Maternal age (both extremes are bad)

Question 13

Hypertensive disorders of pregnancy

Answer 13

Gestational HTN and Pre-eclampsia

Assessment status (fetal and maternal) and necessity for hospitalization and deliver by:

laboratoy values, fetal ultrasound, non-stress test (NTS) – 20-40 minutes of CTG recording fetal movements in relation to heart rate (different from contraction test that is used to assess heart rate in relation to hypoxia).

Depending on results, either monitor or hospitalize with delivery:

Monitor – 1-2 times a week (blood pressure, urine analysis and lab tests), educate patient for identifying symptoms (mentioned above, reduced fetal movements, vaginal bleeding) and start antihypertensive therapy (labetalol, hydralazine, methyldopa, NO ACE inhibitors they are teratogenic)Hospitalize and delivery if: >37 week, suspected placental abruption, oligohydramnios, abnormal lab

Severe pre-eclampsia

Delivery is the only treatment.Delivery if >34 week or <34 week with maternal or fetal instability.Immediate delivery if pulmonary edema, eclampsia, DIC, placental abruptionDelayed (24h – 48h) delivery if HELLP, PROM,

HELLP
Stabilization - blood transfusion and IV fluids. Antihypertensives - methyldopa, hydralazine, alpha and beta blockers, nifedipineDeliveryIf before <34 week or at any gestational age with presence of deteriorating maternal or fetal status → deliver.If no maternal of fetal stress and stabilization has calmed give corticosteroids for 24-48 hours and then deliver

5. Diagnosis:

a. 4-hour monitoring until blood pressure has returned to normal.
b. Urine checks for proteinuria

c. Maternal

d. Blood count (particular platelets)
Renal and liver functions

e. Uric acid

f. Clottingg.
Catecholamines (to rule out pheochromocytoma)

h. Serial ultrasounds (measure fetal growth every 2 weeks and CSF volume twice a week)

j. Fetali.
k. Doppler ultrasound – umbilical and uterine arteries (check absence or reverse of flow)

Cardiotocography – fetal heart rate and uterine contractionUltrasound – fetal growth in relation to gestational age, placental implantation and amniotic fluid

6. Prevention:a. Ca2+ (may reduce risk)b. Low-dose aspirin (COX inhibitor)

Eclampsia

1. Definition: pre-eclampsia and convulsions (fast relaxing and contracting muscles→seizures). It is secondary to pre-eclampsia
2. Featuresa. Manifests when pre-eclampsia is not recognizedb. Can be preventedc. Can occur in pre-, intra- and post-partum periods.
3. Management:

d. Pre-termi. Control seizures* Ensure airway* MgSu (drug of choice) - 4g solution over 20 minutes + maintenance dose 1 g/h.

ii. Control blood pressure* Labetalol 20mg followed by 40mg, 80mg to total of 200mg* Epidural analgesia - to relief pain and cause vasodilation in lower extremities.

iii. Fetus delivery – after controlling blood pressure, oxytocin induced labor or Csection are followed.

b. Post-term – continues up to 7 days after delivery. In case seizures continue, epilepsy or cortical thrombus need to be considered.

i. Constant patient observationii. Maintain levels of sedationiii. Antihypertensive therapy (until returned to normal)

iv. Fluid balance

Question 14

Antepartum haemorrhage

Answer 14

Complications:
1. Fetal hypoxia
2. Maldevelopmenta.
Placenta accerta – attached to myometrium)b. Placenta increta – invades myometrium)c. Placenta precreta – invades parametriumPlacental abruption

Definition:Hemorrhage from premature separation of the placenta from the uterus.

Risk factors:
1. Dietary deficiency (especially folic acid)
2. Smoking
3. HTN
4. Thrombophilia
5. Trauma
Classification (clinically unimportant):
1. Revealed
2. Concealed
3. Mixed

DD from placenta previa

Symptoms:

Painful vaginal bleeding

Increased uterine contractions

Longitudinal lie of fetus

Pathogenesis:

Blood in the uterine wall causes increase in resting tone and onset of contractions as well as clot formation (consumption of maternal clotting factors which promotes further bleeding).

Clinical presentation example:

1. Pregnant woman with sudden onset of abdominal pain with uterine contraction with or without bleeding → might suffer from placental abruption.
2. Assessment of oxygenation and blood pressure. If pulse measure is higher than systolic measure it is suggestive for serious blood loss (e.g pulse 110 and systole 80)
3. Required IV fluids, CTG and ultrasound assessment of fetus4. Prognosis is dependent on extent of placental separation.

Management:
1. General approacha. Blood transfusion and IV fluidsb. Monitor vital signsc. Clotting factorsd. Maintain airwaye. Anti-D Ig antibodies in Rh(-) motherf. Ultrasound – assess fetal growth and placental site

2. Normal findings:a. <34 weeksi. Observe and monitorii. Use corticosteroids and tocolytics to aim for normal deliveryb. >34 weeks

i. If active uterine contractions attempt vaginal delivery ii. If no contractions and no fetal distress and no bleeding → conservative treatment (as in placental previa)

3. Acute symptoms and live fetus:
   a. Induction of labor with syntocinon and vaginal delivery – only when close to termb.

Otherwise, emergency C-section regardless of gestational age4. Acute symptoms and dead fetus:

a. Induction of delivery or emergency C-section in case of maternal risk due to bleeding or slow labor progression.

Complications1. Afibrinogenemia –thromboplastin released to mother circulation resulting in DIC.

2. Hypovolemia
3. Renal tubular necrosis
4. Couvelaire uterus - when blood penetrates the wall causing bruised appearance to the uterus or may reach the peritoneum.

Uterine rupture

Definition: life-threatening obstetric condition with tearing lesion in the uterus. Presents with sudden onset or more commonly during labor.

Symptoms:
1. Severe painful abdominal pain
2. Sudden pause of contractions
3. Fetal distress
4. Vaginal bleeding

Risk factors:1. Previous C-section or other uterine surgery2. Placental abruption

Question 15

Multiple pregnancy

Answer 15

Related to zygosity

Complications:
1. Nausea and vomiting – higher incidence than singlet.
2. Anemia – due to extra metabolic demands
3. Miscarriage – “vanishing twin syndrome”
4. Antepartum hemorrhage – placenta previa and placental abruption.
5. Pre-eclampsia
6. Intra uterine growth restriction (IUGR) – one fetus is smaller than the other
7.
8. Related to zygosity
9. Pre-term labor – due to over distension of uterus (two fetuses and higher amniotic fluid)

Twin-to-twin transfusion syndrome (TTTS) – blood shunting; one fetus (donor) transfuses blood to the other fetus (recipient) via common vascular channels.

The donor is oligouric, anemic,oligohydramnionic and growth restricted compared to the recipient which
is polyhydramnionic and polycythemic.

Types of anastomoses are artery to artery, vein to vein or artery to vein (most dangerous).

Monoamniotic and conjoined twinning

10. Undiagnosed twins – oxytocic drugs are administered after delivery leading for entrapment of the second twin (irreversible even with using tocolytics drugs)
11. Malpresentation (especially transverse lie)
12. Locked twins – twins lock chin to chin

Presentation:

Management:
1. Antenatal ultrasound to detect anomalies (defect growth, TTTS, IUGR)
2. C-section (same indications for singlet pregnancy but when additional complications exist it is chosen – diabetes, pre-eclampsia, subfertility, pervious scar, preterm labor 28-34 weeks)

3. Vaginal delivery

a. Indication – cephalocephalic or cephalobreech.b. Establish IV linec. Monitor both fetusesd. Deliver first fetus. For second fetus delivery, lie and presentation are needed to be verified along with continuous monitoring of heart rate and uterine contractionsi.

In case of transverse lie or other abnormal position – internal podalic version orexternal cephalic version may be attempted.

ii. If contractions are not present – use oxytocin (wait 30 minutes for normal contraction before administration of oxytocin)

TTTS

4.Amniocenteses – removal of amniotic fluid from the recipient

5 Selective feticide
6 Laster ablation of communicating vessels (if one twin dies the other often dies as well due to hemodynamic changes)

Question 16

Prolonged pregnancy

Answer 16

Question 17

Breech presentation

Answer 17

https://www.youtube.com/watch?v=d9pU_6LDVUM

C sectiona.

Indications:

i. Estimated birth weight <1.5 kg or >4 kg (especially in breech presentation)

ii. Severe pre-eclampsiaiii. Placental abruptioniv. Placental previav.

Previous C sectionb.

Techniques:

i. Transverse lower segment (Pfannensteil incision) – most common

ii. Longitudinal midline incision (in case lower segment was not formed –usually early gestation)

iii. EXIT procedure – when fetus airways are obstructed, first exposure of the head after C section and intubation followed by taking out the baby.

iv. Misgav Ladach – modified C section (faster and with better healing)

Question 18

Unstable lie, transverse lie and shoulder presentation

Question 19

Minor complaints of pregnancy

Answer 19

Pelvic girdle dysfunction (symphyseal pelvic dysfunction)1.
Causes:
a. Relaxin – hormone produced by corpus luteum (mostly) and causes increase in joint mobility by tissue softening

2. Management:
   a. Physiotherapy
   b. Analgesics

Question 20

Medical problems arising in pregnancy

Answer 20

. 75g dose is given and glucose levels are measured 2 hours later

6. Symptoms:

a. Asymptomatic

7. Complications:

a. Maternal:
i. Pre-eclampsiaii.
b. iii. iv. v. vi.
Fetus:i. Recurrent infections

Polyhydramnios
Induced labor

If vaginal birth occurs → shoulder dystocia and extended perineal tears.

Develop type 2 diabetes post-gestational

Neonatal unit admissionii.

Hypoglycemia (due to increased fetal pancreas activity to oppose the uncontrolled maternal glucose that crosses the placenta. Maternal insulin does not cross so fetus is dependent on its own supply.)

iii. IRDSiv.

Jaundicev. Macrosomia8. vi. Management:Increased risk for diabetes and obesity in childhooda.

During pregnancy – control blood glucose levels.

i. Low glycemic index foodsii. Medication – metformin, glibenclamide and insulinb. During labor – fetal blood glucose monitoring.

c. Post labor – stop treatment and continue monitoringi. If values are normalized → true gestational diabetesii.

If values remain elevated → masked (prior to pregnancy) or developed diabetesInfections1. Diseases:a. Chicken poxi. Pathogen: varicella zoster.

ii. Disease: pneumonia (fetal and maternal), congenital varicella syndrome (eye defects, limb hypoplasia and neurological defects)

iii. Management: IgG prophylaxis (for non-immune women) or acyclovir (for infected women)

. Parvovirus 19

i. Pathogen: parvovirus 19

ii. Disease: erythema infectiosum / fifth disease / slapped cheek syndrome, fever, rash, arthropathy, fetal anemia (aplastic anemia), miscarriage, fetal hydrops (heart failure → edema, ascites, pleural effusion, pericardial effusion).

iii. Management:* Maternal: analgesics and antipyretics* Fetal: infection after week 20 → Doppler US of middle cerebral artery can detect fetal anemia → if so utero blood transfusionsc. Influenza H1N1

i. Disease: fever, cough, respiratory failure, secondary infections, preterm birth, stillbirth, neonatal death.

ii. Management: vaccine or antiviral medication (oseltamivir, zanamivir) for infected women.d. HIVi.

ii. Disease: AIDS, secondary infection, cancer development, vertical transmission (transplacental or vaginal birth or breast feeding), miscarriage, stillbirth.

Management: HAART (highly active anti-retroviral therapy), C-section (in women who do not take HAART) and avoid breast feeding.

e. Viral hepatitisi.

Pathogen: Hepatitis A, B, C, D and E

ii. Transmission: A (fecal-oral), B&C (blood)iii. Disease: preterm birth, vertical transmission (perinatally)

iv. Management:
* Prvention (hygiene – Hep. A, vaccine – Hep. B)
* Screening – to reduce vertical transmission and exclude co-infection with HIV

• Vaginal delivery with avoidance of interventions that may increase bleeding (C-section and lack of breast feeding do NOT reduce vertical transmission).

f. * Tuberculosis:Fetal immunization with IgG and vaccinei.

Pathogen: Mycobacterium tuberculosisii. Disease: miscarriage and same as in non-pregnantiii.

Diagnosis: Tuberculin test (in suspected women) → x-ray chest (in positive tests)

iv. Management: RIPE antibiotics (streptomycin is contraindicated as it causes deafness)UTI1.

Features:a. 2-10% of all sexually active women2. b. Causes:30% out of this group develops ascending infections

a. E. coli (most common)
Complications:

a. Pyelonephritis → bacteremia and septic shock

b. Preterm

4. Management: antibioticsThromboembolic disease (VTE)
5. Features:
   a. 10 times more common in pregnancy than non-pregnant
6. b. Causes:a.

b. c. Leading cause of maternal mortality
Increased coagulation factors

Suppressed anticoagulants and fibrinolysisVenous stasis due to compression on pelvic vessels

Prothrombotic pregnancy state

3. Risk factors:a. Family history of VTEb.

Thrombophiliac.

Obesity

d. Smokinge. Sickle cells diseasef. Immobilityg. Operative deliveryh. Multiple pregnanciesi. Pre-eclampsiaj.

Contraceptives (estrogen containing)

4. Diagnosisa. Doppler USb. MRI

c. CT (with caution to fetus)

5. Clinically:

a. DVT: swelling and tenderness of the legi. Compression of left common iliac vein by the right common iliac artery lead to stasis and thrombus formation most commonly in the iliac or femoral veins.

b. PE: dyspnea and pleuritic chest pain

6. Management:

a. Prophylaxis for high risk – elastic compression stock and LMWH.i. LMWH – does not cross placenta

ii. Warfarin – crosses placenta causing abnormalities if used in 1st trimester

iii. Stop treatment briefly perinatally to reduce postpartum hemorrhage but continue again for 6 weeks after delivery.

b. In acute case – heparin therapy

Liver disease

1. Obstetric cholestasisa.

Definition: static bile acids flow commonly in 3rd trimester

b. Risk factors:i.

Genetics

ii. Hormonal pregnancy state (influencing bile acids flow)

iii. Ethnicityc.

Clinically:

i. Itching (especially palms and soles) → cholestatic pruritis (irritation of nerve endings)

ii. Pale stool

iii. Dark urineiv. Jaundiced.

Diagnosis:

i. High serum bile acids

ii. High liver enzymes

iii. Serology – rule out hepatitis and autoimmune hepatitis (anti-SM and antimitochondrial antibodies)

e. Complication:

i. Preterm birth

ii. Still birth

iii. Impaired liver function (prolonged bleeding time)

iv. Recurrence in following pregnancies

f. Management:

i. Medication: ursodeoxycholic acid (for itching and liver function), vitamin K (for bleeding), cholestyramine

2. Acute fatty liver of pregnancy (AFLP)a. Definition: rare disease most common in the third trimester characterized by extensive fatty infiltration of the liver, which can result in acute liver failureb.

Risk factors:

c. i. Multiple pregnancies

ii. Obesity

Pathomechanism:

i. Mutated mitochondrial enzyme (of the fetus) leads to unoxidized fatty acids that enter the maternal circulation and accumulate in her liver.

d. Clinically:

i. Non-specific symptoms – nausea, vomiting, abdominal pain

ii. Jaundicee.

iii. Coagulopathy with risk for DICiv. Hypoalbuminemia and ascites

Diagnosis:i. Symptoms

ii. Exclude other causes

• Pre-eclampsia
• HELLP syndrome (hemolysis, elevated liver enzymes and low platelets).
• Viral hepatitis

iii. iv. v. Hypoglycemia
Elevated liver enzymes
Biopsy

f. Management:

i. Immediate C-sectiong.

Complications:
i. Acute liver failure
ii. Hemorrhage
iii. Hepatic encephalopathy (nitrogen-containing compounds are not excreted because urea cycle is impaired.

These compounds go to the circulation cross the BBB and are consumed by astrocytes that use them to produce glutamate. Glutamate causes increased osmotic pressure and astrocytes are swollen).

Question 21

Pre-existing medical conditions and pregnancy

Answer 21

(Another table in note)

iv. Ophthalmic assessment each semester for diabetic retinopathy

Fetal assessmenti. Chromosomal problems (1st trimester) and routine anatomy check (week 20).

ii. Additional cardiac anatomy scan.

f. Give birth in hospital with neonatal facilities.

Thyroid diseases

1. Features:

a. Estrogen increases TBP (thyroid binding proteins) that reduce levels of T4 and T3 in the

b. c. blood → resulting in increased production by the thyroid to maintain normal levels.

Iodine levels fall due to increased renal loss leading to enlarged thyroid.

TSH levels drop due to hCG.

2. Hyperthyroidism:

a. Causes:

i. Grave’s disease (laboratory shows high T4 and T3 with low TSH)

b. Implications:

i. Pregnancy over disease – increases thyroxine demand so it has less significance in pregnancy, unless there is untreated thyrotoxicosis.

ii. Disease over pregnancy: pre-eclampsia, fetal growth restriction, still birth, fetal thyrotoxicosisc.

Management:

i. Thyroid function tests
ii. Anti-thyroid therapy (methimazole and propylthiouracil)
iii. Assessment of fetal growth and heart rate

3. Hypothyroidism:

a. Causes:

b.
i. Autoimmune (autoantibodies, Hashimoto disease).
ii. Iatrogenic (thyroidectomy, anti-thyroid drugs)

Implications:

i. Pregnancy over disease – few effects.

ii. Disease over pregnancy – spontaneous abortion, pre-eclampsia, low birth weight, reduced IQ, congenital iodine deficiency syndrome (cretinism)

c. Management:

i. Thyroid function test (T4) and TSH levels every trimester.

ii. Iodine supplementation or dietary.

Obesity

1. 2. 3. Definition: BMI > 25 (weight / (height^2)

Features:

a. Co-morbidities of HTN, sleep apnea, cardiovascular disease

Implications:

a. Pregnancy over disease – increased weight gainb. Disease over pregnancy

i. Increased miscarriage and congenital abnormalities (1st trimester)

ii. Pre-eclampsia and gestational diabetes (2nd trimester)

iii. Fetal macrosomiaiv.

Childhood obesity and juvenile diabetes.
v. Induction of labor and C-section.

4. Management:

a. Pre-counseling

b. Diet support.

c. Folic acid (until week 12 due to increased neural defects)

d. Assessment for co-morbidities.e. Low dose aspirin for pre-eclampsia and thromboprophylaxis.

f. OGTT throughout pregnancy.g. Fetal screening – poor ultrasound visualization because of mother

Thrombophilia

1. Features – pregnancy is a prothrombotic state.
2. Implications:

a. Disease over pregnancy:i. Thromboembolism

ii. Factor V Leiden mutation leads to fetal loss

iii. Pre-eclampsia

iv. Placental abruptionv. Growth restriction

vi. Miscarriage

vii. Premature birth

3. Management:

a. Screening for thrombophilia (family history, recurrent miscarriage, early onset of preeclampsia)

b. Obstetrician and hematologist assessmentsc. Prophylactic LMWH (safer in pregnancy) – around time of birth to avoid bleeding

d. Compression stockingse. Hydrationf. Antiphospholipid syndrome

i. Recurrent pregnancy loss before week 10 and the presence of lupus anticoagulant and/or anticardiolipin antibodies.

ii. Therapy with aspirin combined with heparin reduces pregnancy loss.

Epilepsy

1. Definition: neurological disorder in which brain activity is abnormal, causing seizures or periods of unusual behavior and sometimes loss of awareness
2. Implications:

a. Pregnancy over disease – variable. Seizures frequency can increase, decrease or stay the b. same.Disease over pregnancy:

i. Congenital abnormalities (due to anti-epileptic drugs)

ii. Tonic-clonic seizures (muscle contractions and relaxations) associated with fetal loss.

iii. Increased chance for child with epilepsy

3. Management:

a. Pre-counseling to discuss risk and review of taken medications.

b. Risk of uncontrolled epilepsy is greater than risk of taken medications.

c. Aim is to avoid seizures during pregnancy.

Cardiac diseases

1. Features:
2. a. b. Causes:

a. Most common cause for indirect maternal death.

Mostly Acquired
Valvular lesions

b. Congenital heart disease

c. Cardiomyopathies

d. Arrhythmiase. Ischemic heart disease.

3. Implications:

a. Pregnancy over disease:

i. Deterioration of conditions (aortic stenosis, regurgitations etc.) due to increased cardiac demand in pregnancy.

ii. Mimic of normal pregnancy symptoms such as dizziness, syncope, palpitations

iii. Risk for: CHF, hypoxia, bacterial endocarditis, VTE, aortic dissection, angina and ischemia

4. Disease over pregnancy

:a. Depends in the cardiac problem

.b. Increased risk in general: pre-eclampsia, intrauterine growth, preterm birth

5. Management:

a. Pre-counseling as sometimes pregnancy may not be advisable.

Eisenmenger’s syndrome - left-to-right cardiac shunt caused by a congenital heart defect (ventricular septal defect, atrial septal defect or patent ductus arteriosus) causes pulmonary hypertension

b. Medications (may be required)i. Anticoagulants

c. Fetal assessments

i. Growth scans

ii. Cardiac abnormalities

d. Special attention to postpartum period as it is most risky due the hemodynamic changes

Respiratory disorders

1. Asthmaa.

Implications:

i. Pregnancy over disease – variable.
ii. Disease of pregnancy – if well controlled no adverse effects, else, premature birth, pre-eclampsia and growth restrictions.

b. Management:
i. Medications (safe for pregnancies)ii. Avoid triggering agents.

2. iii. Cystic fibrosis:In acute case the treatment is the same as in non-pregnant.

a. Implications:

i. Pregnancy over disease – pregnancy can be tolerated well but risk relate to degree of pulmonary dysfunction which can deteriorate.

ii. Disease of pregnancy – fetal inheritance, gestational diabetes, preterm birth

b. Management

:i. Genetic counseling

ii. Treatment of GI and lung dysfunctions.

iii. Pulmonary function tests at prior and during pregnancy.

iv. High dose folate (5mg/day)v. Nutritional supportvi.

Treat chest infections immediately.

vii. OGTT

Autoimmune

1. Features:

a. b. Some diseases may “benefit” from the suppressed immune state of pregnancy such as Crohn’s disease and RA.

Other diseases include: SLE, APS, scleroderma etc.

2. SLE
   a.
   b. Diagnosis:i. At least 4/11 clinical criteria + serology (positive ANA)

Implications

:i. Pregnancy over disease: increased relapses and deterioration of kidney function.

ii. Disease over pregnancy:

1. Miscarriage
2. Stillbirth
3. Pre-eclampsia
4. Preterm birthc.
   5.
5. Management:If co-existence with APS → increased VTE riskIncreased neonatal lupus and congenital heart block

i. Avoid pregnancy at least 6 months after flare.

ii. Medications:

1. Low dose aspirin for pre-eclampsia
2. LMWH for APS co-existenceiii.
3. Steroids in severe lupus cases (but only non-teratogenic)

Induced labor at weeks 37-38 to avoid thrombotic events.
Hemoglobinopathies

1. Sickle cells anemia:

a. Definition: autosomal recessive disorder of a gene mutation of glutamic acid to valine on the beta-globin subunit.

Polymerization of hemoglobin ensues resulting in sickling of erythrocytes.

2. Implications:

a. Pregnancy over disease – variable according to severity of disease (heterozygous or homozygous).

i. Sickle cell crisis - acute conditions leading most commonly to vaso-occlusive crisis and splenic crisis with splenomegaly presenting with severe pain and limb swelling.

b. Disease over pregnancy:

i. Anemia and infections

ii. Preterm birth
iii. Miscarriage,
iv. VTE
v. Growth restrictions

c. Management:
i. Prenatal diagnosis (of both partners)
ii. High dose folate due to increased hemolysis

. Low dose aspirin for pre-eclampsia.

iv. Prophylactic antibiotics
v. Fetal assessments (growth scans)vi. Blood transfusions if necessary

vii. VTE prophylaxis

Question 22

Congenital abnormalities

Answer 22

g. Tetralogy of Fallot - pulmonary stenosis, ventricular septal defect, right ventricular hypertrophy, overriding aorta (blood from both ventricles enter the aorta)

2. Diagnosis:

a. Ultrasound – 18th-20th weeks using several views:

i. Four chamber view
ii. iii. iv. Abdominal wall defects
Left ventricular outflow view

Right ventricular outflow view

Transverse abdominal view standard fetal echocardiogram consists of several specific views which can be obtained to optimize visualization of different cardiac abnormalities

1. Types:

a. b. Gastroschisis – herniation through rectus abdominis muscle (usually below and to the right from the umbilical cord) and without peritoneal covering.

Size of the hole is variable so sometimes other organs can be seen but mostly only intestines.

Exomphalos (Omphalocele) – large hernia of the umbilical cord with peritoneal covering

Abdominal wall defects
Left ventricular outflow view
Right ventricular outflow view

Transverse abdominal view standard fetal echocardiogram consists of several specific views which can be obtained to optimize visualization of different cardiac abnormalities

1. Types:

a. b. Gastroschisis – herniation through rectus abdominis muscle (usually below and to the right from the umbilical cord) and without peritoneal covering.

Size of the hole is variable so sometimes other organs can be seen but mostly only intestines.

Exomphalos (Omphalocele) – large hernia of the umbilical cord with peritoneal covering

2. Complications:

a. Intrauterine growth restrictions
b. Intestinal atresiac.
Premature birth

3. Management:

a. Postpartum surgery
Chromosomal abnormalities

1. Definition: Structural or numerical abnormality of the chromosomes.

Normal human karyotype is diploid (2 copies of each chromosome) with 22 somatic pairs and 1 sex pair of chromosomes.

Chromosomal abnormalities identified from the culture and karyotyping of fetal or placental cells in the amniotic fluid or from the chorionic plate.

2. Types

a. Down’s syndrome (trisomy 21)

i. Clinically:

• Mental retardation and progressive IQ decline
• Congenital heart diseases
• Flat face and occiput with low flat nose, epicanthal folds
• Short ribs, pelvis, extremities and hands exhibiting simian crease.
• Duodenal stenosis
• Infertilityii.
• Types:*
• High risk for leukemiaNondisjunction (95%) - before conception (all cells are triploid) or after conception (variable severity depending when the nondisjunction occurred – leading to mosaic pattern)Robertsonian translocation (5%)

– between chromosome 14 and 21.

iii. Diagnosis:

• Amniocentesis or chorionic villus sampling
• Nuchal translucency:

o Describes the sonographic appearance of fluid collection under the skin behind the neck.

o Done in weeks 11-13o Measure higher than >3mm is abnormalo

Criteria: sagittal section with certain structures that are needed to be visible, neutral position of fetal head (not hyperflexed or extended), widest thickness is measured (higher value higher risk), depends on crown-rump length (CRL)*

• In case of increased risk additional finding at weeks 14-20 may include no or small nasal bone, large ventricles

Quad test – maternal blood measurements of hCG, AFP, Estriol and Inhibin-Ab.

c. d.

• Post birth – physical appearance and karyotyping

Turner syndrome – sex chromosome monosomy (X0) and fetus usually undergo spontaneous abortion.

Klinefelter syndrome – sex chromosome trisomy (XXY) due to nondisjunction of first meiotic division.

Edward’s syndrome (Trisomy 18) – most infants die postnatally.

Question 23

Assessment of fetal wellbeing

Answer 23

h. Biometry (BPD, OFD, HC, AC, FL) – IUGRWeeks 36-37 (+6 days)i. Fetal presentation

j. Biometry

k. Amniotic fluid volume

l. Placental localization and maturitym.

Previous C-section scar (with full bladder)Blood tests and amniocentesis (screening for Down’s syndrome)

1. Sampling is done by

a. Chorionic villus sampling (CVS)
b. Amniocentesis

2. Combined screening testa. Between weeks 11-13

b. Nuchal translucency (NT) – see criteria for measurement and also needed CRL measures are 45-84mm

c. Biochemical markers hCG and pregnancy-associated plasma protein A (PPPA)

3. Quad test

a. Between weeks 14-20

b. Biochemical markers – hCG, inhibin-A, AFP and unconjugated estradiol (uE3)

Doppler examinations

1. Normal fetal recording (A)
2. Absent end-diastolic velocity (AEDV) is a typical type UPVD.

Usually fatal but early recognition and monitoring until elective term can be performed at 34 weeks (B).

3. Reverse end diastolic velocity (REDV) – leads to fetal death but elective pre-term at 26 weeks or more may be done

(C)
Fetal growth

1. Definition: ultrasound measurements of the head (HC) and abdominal (AC) circumferences.
2. Small fetus – suboptimal fetal growth with values below the lowest centile range.
3. Typical – not high risk for complications and seen usually in short or Asian ethnicity woman.
4. Atypical asymmetric – tends to occur at later pregnancy and associated and associated with UPVD.
5. Atypical symmetric – tends to occur in early pregnancy and associated with severe early onset of pre-eclampsia.
6. Large fetus
7. Typical – usually seen in tall women or Afro-Caribbean ethnicity.
8. Atypical – accelerated growth above the upper limit of the central range.

Mostly seen in diabetic women.Amniotic fluid volume (AFV)

1. Accurate measurement is done with US and two method are used:

a. Single deepest pocket – normal range is 2-8 cm. The deepest longest vertical diameter of echo-free pocket between the fetus and uterus.

Less than 2 is oligohydramnios and more than 8 is polyhydramnios.

b. Amniotic fluid index (AFI) – sum of measurements of the largest pocket in each of the four quadrants. Normal range is 6-24.

Biophysical profile scoring (BPS)

1. Definition:

prenatal evaluation of the fetal well-being involving a scoring system.

Normal score is a fetus presenting at least 4 of the following parameters in a period of 40 minutes.

Parameters are:a. b. c. d. e. Fetal heart rate (FHR) – recorded with cardiotocograph (CTG) maximum recording of 40 minutes.

At least 2 accelerations of 15 bpm lasting for at least 15 seconds.

Normal FHR is 110-160 bpm.

Fetal movements – maximum of 40 minutes fetal observation in ultrasound.

At least 3 separate distinct movementsFetal tone – one of the fetal movements demonstrates full 90-degree flexion-extension flexion cycle of the limb or opening and closing of the hand.

Fetal breathing – maximum of 40 minutes fetal observation in ultrasound. At least one episode of 30 seconds regular fetal breathing movements.AFV - at least 1 vertical measurement between 2 – 8 cm.

Management1. When fetal risk is proven real by fetal surveillance methods mentioned above, there are only two intervention that are in value:

2. Elective deliverya. ≥34 weeks elected delivery is performed.b. <34 weeks if acute measures of health are abnormal then delivery is performed. If normal continuous monitoring to gain time.
3. Maternal steroidsa. In case of elective delivery is set in a high-risk pregnancy and the chronic fetal measures are abnormal then betamethasone is given

Question 24

Normal labour

Answer 24

Uterine activity in labor

1. The 3 P’s of birth progression (power, passages and passenger)

a. Poweri.

Infrequent, low-intensity contraction throughout pregnancy are replaced by the activity of contractions that show an increase in frequency, duration and strength as full-term approaches.

ii. Identification of these contractions by palpitation or tocography and intrauterine pressure by a measuring catheter (normal resting tone is around 10-20mmHg)

iii. Establishment of labor is likely when 2 contractions last >20 seconds in a period of 10 minutes.

iv. Retraction - progressive contractions lead to effacement and dilatation of cervix due to shortening of myometrial fiber in the upper segment and stretching and thinning of lower segment.

As uterus and round ligaments contract the longitudinal axis are pulled towards the abdominal wall and the realignment if the axis is what promotes the descent of the presenting part.

vi. Obstructed labor – an abnormal junction between the upper and lower segments may become visible at the level of the umbilicus called retraction ring (Bandl’s ring)

b. Passagesvii. Structure of bony pelvis (described in earlier chapters)viii. Size and shape of the pelvis varies and effects the outcome of labor.

ix. Softening of sacroiliac ligaments and pubic symphysis allow expansion of pelvic cavity.

Passenger

x.Fetal size, lie and position (described in earlier chapters)

Mechanism of labor
1. Descent – occurs throughout labor.

Engagement of head occurs before onset of labor in the majority of primigravid but not multipara. Provides measure of the progress of labor.

2. Flexion – head flexes towards the chest which reduces the diameter of presentation.

Begins from deflexed occipito-frontal diameter to suboccipitobregmatic diameter which is fully flexed.

3. Internal rotation – head rotates when it reaches pelvic floor and the occiput is facing anteriorly towards the pubic symphysis in most cases but also face-to-pubis delivery may occur.
4. Extension – head extends until it is delivered. The occiput comes in contact with the inferior rami of the pubis.
5. Restitution – after delivery the head, it rotates back to its normal relationship with the shoulders.
6. External rotation – shoulders reach pelvic floor and rotate antero-posteriorly.
7. Delivery of shoulders – final expulsion of trunk occurs after shoulders are delivered.

Question 25

Management of normal labour

Answer 25

. After 6 hours if delivery is not imminent then intravenous fluids should be given.

Signs for dehydration include:

i. Tachycardia
ii. Pyrexia (fever)

iii. Loss of tissue turgor

Question 26

Pain relief in labour

Question 27

Fetal monitoring during labour

Answer 27

• The nadir is after the peak of the uterine contraction.

Variable decelerations

• Vary in time, amplitude, shape and size.
• Due to cord compression or prolapse accompanied by uterine contractions.
• Usually fall by more than ≥40 bpm
• Increase in the depth and duration might suggest hypoxia.

Fetal acid-base balance

1. In case of fetal heart rate abnormalities acidosis might occur and the acid-base balance is examined.
2. Amnioscope inserted through cervix (at least 2 cm dilated) while the mother lies on lateral position.

A small incision is made in the scalp and blood is collected to a tube.

a. Normal pH is 7.25-7.35
b. If pH is <7.20 delivery is recommended.

3. This method is rarely used because of false-positive results that alter the pH values:

c. Cerebral edema mixing with the bloodd. Amniotic fluid mixed with the blood sample

Question 28

Preterm delivery

Answer 28

Method of delivery

a. It is rare to inhibit labor when gestation is over 34 weeks because the benefits of intervention overcome those of inhibition.

b. Head/vertex presentation – preferred is gentle vaginal delivery and only if necessary,the use of forceps.

c. Breech presentation – C-section (unless gestation is over 34 weeks) because the head is bigger than the trunk and it might get stuck if the cervix is not dilated enough and cause compression of head leading to intracranial hemorrhage.

Question 29

Prelabour rupture of the membranes

Answer 29

Question 30

Induction of labour

Answer 30

Question 31

Precipitate labour

Answer 31

Question 32

Delay in progress in labour

Answer 32

Question 33

Insufficient uterine activity

Question 34

Cephalopelvic disproportion

Question 35

Cord presentation and cord prolapse

Answer 35

Question 36

Normal vaginal delivery

Answer 36

Question 37

Repair of episiotomy or perineal injury

Answer 37

Question 38

Malpresentation

Answer 38

Question 39

Malposition of the fetal head

Answer 39

Question 40

Instrumental delivery

Answer 40

Question 41

Caesarean section

Answer 41

3. Available anesthesia and personnel for emergency c-section
4. There is a higher success rate when the woman has had at least one vaginal birth in the past
5. Complications uterine dehiscence of old scar or uterine rupture.
6. If first pregnancy was C-section due to CPD than it is likely for second pregnancy to be done with C-section.

If first pregnancy was C-section due to macrosomia of the fetus than it is possible for second pregnancy to be done by vaginal delivery as the fetus might not be as large.

Question 42

Shoulder dystocia

Answer 42

Question 43

Abnormalities of the third stage labour

Answer 43

• Hysterectomy (last resort)Vaginal wall hematoma

1. Causes:
2. a. Vaginal and perineal lacerations by assisted delivery

Symptoms

a. Anemia
b. Pelvic pain
c. Urine retention

3. Diagnosis

a. Visible bleeding
b. Vaginal examination – in deep bleedings where bleeding is not visible a bulge can be felt
c. Ultrasound

4. Management

a. Venous bleeding controlled by compressionb. Arterial bleedingi.

Superficial – drainage and ligature of vessels.

ii. Deep – incision, drainage, suturing and antibiotics.

Amniotic fluid embolism (AFE)

1. Diagnosisa. Sudden development of ARDS and shock in patients in labor or recently delivered
2. Pathomechanism

a. Amniotic fluid enters maternal circulation via tears in the placental membrane →triggers anaphylaxis shock like response → DIC is followed bleeding to massive bleeding

3. Managementa. Supportive (oxygenation)

Question 44

Postpartum problems

Answer 44

i. Dehiscence

ii. Necrotizing fasciitis

5. Thromboembolisma.

Thrombophlebitis

i. 3-5 days post-delivery

ii. Superficial venous inflammation of the legs

iii. No severe manifestations

iv. Anti-inflammatory drugs

b. Phlebothrombosis (DVT)

i. 7-10 days post-delivery

ii. Risk factors:

• Immobilization

iii. Symptoms
* Chest pain
* Dyspnea
* Hemoptysis

iv. Diagnosis
* Ronchi and pleural rub
* Chest CT

6. Maternal collapse

a. Definition: involving cardiorespiratory system with decreased consciousness up to 6 weeks following pregnancy.

b. Causes: 4 T’s4 H’s

Thromboembolism
Tamponade (cardiac)
Tension pneumothorax
Toxicity (drugs)
Hypoxia
Hypovolemia
Hypothermia
Hypo- or hyperkalemia

Question 45

Psychiatric disorders of childbirth

Answer 45

Screening

1. History taking

a. Family history

b. Drug abuse (substance misuse)

c. Current mental health (early pregnancy and also on later occasions)

d. Whooley questions

i. During the past month have you often been botheredby feeling down, hopeless or depressed?

ii. During the past month have you often been botheredby having little interest or pleasure in doing things?

iii. Do you feel you need or want help with this?

2. Edinburgh Postnatal Depression Scale (EPDS)

a. Management

10 screening questions that can indicate whether mother has symptoms that are common in depression and anxiety.

1. Principles

a. Mild disorders may improve as pregnancy progresses

b. Serious disorders who have not shown relapse in more than 2 years are not consideredto be for high-risk antenatal recurrence (the opposite is also true)

c. Serious disorders who have not shown relapse in more than 2 years are considered to be for high-risk postnatal illnessd.

Women under medications are considered for high-risk of both antenatal and postpartum relapsee. For new-onset symptomatic disorders “watch-and-wait” approach (for 2 weeks)

f. Relapse is common after recent illness or stopping medication intake

g. Some medications are safe to use while others should be stopped before conception or reduced and slowly withdrawn

2. Non-medication

a. Psychological treatment

b. Counselling

c. Cognitive behavior therapy

d. Family and other health professional care providers involvement

e. Lifestyle change

3. Medications

a. Antidepressants

i. Monoamine oxidase inhibitors (MAOIs)

• Not used due to risk of drug and food interactions

ii. Tricyclic antidepressants (TCAs) – amitriptyline, imipramine, clomipramine, doxepin

• No risk for fetal abnormalities (except for clomipramine)

iii. Selective serotonin reuptake inhibitors (SSRIs) – fluoxetine, paroxetine, sertaline

• Risk for cardiac abnormalities (ventricular septal defects)Antipsychotic - for schizophrenia and bipolar illness

i. Typical “older” drugs (chlorpromazine, trifluoperazine)

• No risk for fetal abnormality but associated with poor obstetric outcome (e.g. early delivery and increased C-section rate)

ii. Atypical “newer” drugs (olanzapine, quetiapine, risperidone)

• No risk for fetal abnormality but associated with gestational diabetes, venous emboli and weight gain

c. Mood stabilizers and anti-epileptics – for bipolar disorders

i. Valporate (lithium containing agents)

ii. Risk for cardiac abnormalities, neural tube defects, fetal hypothyroidism and polyhydramnios.

iii. If no evident relapse for the last 2 years medication should not be used. Otherwise it can be used but alternatives should be explored.

Prevention

1. Counsel women with chronic severe mental illness about pregnancy
2. Bipolar illness: consider restarting treatment after delivery
3. Maintain chronic schizophrenic medication throughout pregnancy
4. Previous history of serious mental illness or puerperal psychosis/severe postnatal depression: close contact first weeks
5. Consider prophylaxis after delivery
6. Assess all women at

6 weeks postnatal check for postnatal depression