POCKET
OB - GYN
1
Table of Contents
ANATOMY
MENARCHE AND MENSTRUATION
GENERALITIES
DIAGNOSIS OF PREGNANCY
MATERNAL ADAPTATIONS
PRE-NATAL CARE
PASSAGES
PASSENGER
FETAL ASSESSMENT
PARTURITION
CONDUCT OF NORMAL LABOR
PUERPERIUM
INTRAPARTUM ASSESSMENT
1ST TRIMESTER HEMORRHAGE
3RD TRIMESTER HEMORRHAGE
PLACENTAL DISORDERS
COMPLICATION OF PREGNANCY
DYSTOCIA
CESAREAN SECTION
ABNORMAL BLEEDING
ENDOMETRIOSIS
PELVIC SUPPORT
UROGYNECOLOGY
GENITAL TRACT INFECTIONS
BENIGN GYNECOLOGIC LESIONS
GYNECOLOGIC MALIGNANCIES
MENOPAUSE
INFERTILITY
POLYCYSTIC OVARIAN DISEASE
INTRAUTERINE GROWTH RESTRICTION
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ANATOMY
The female reproductive system contains two main parts: the vagina
and uterus, which act as the receptacle for the male’s sperm, the ovaries
which produce the female’s ova. The vagina meets the outside at the vulva,
which also includes the labia, clitoris and urethra. The vagina is attached to
the uterus through the cervix, while the uterus is attached to the ovaries via
the fallopian tubes.
Labia majora: Encloses and protect the other external reproductive organs.
They are relatively large and fleshy, and are comparable to the scrotum in males.
Labia minora: Can be very small or up to 2 inches wide. They lie just inside
the labia majora, and surround the openings to the vagina and urethra.
Bartholin’s glands: These glands are located next to the vaginal opening
and produce a fluid (mucus secretion.
Clitoris: The two labia minora meet at the clitoris, a small, sensitive protrusion that is comparable to the penis in males. The clitoris is covered
by a fold of skin, called the prepuce, which is similar to the foreskin at
the end of the penis.
The internal reproductive organs in the female include:
Vagina: A canal that joins the cervix to the outside of the body. It also is
known as the birth canal.
Uterus: A hollow, pear– shaped organ that is the home to a developing
fetus. It is divided into two parts: the cervix, which is the lower part
that opens into the vagina, and the main body of the uterus, called the
corpus. The corpus can easily expand to hold a developing baby. A
channel through the cervix allows sperm to enter and menstrual blood
to exit.
Ovaries: Oval-shaped glands that are located on either side of the uterus.
The ovaries produce eggs and hormones.
Fallopian tubes: These are narrow tubes that are attached to the upper part
of the uterus and serve as tunnels for the ova to travel from the ovaries to the uterus. Conception, the fertilization of an egg by a sperm,
normally occurs in the fallopian tubes. The fertilized egg then moves
to the uterus, where it implants to the uterine wall.
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MENARCHE AND MENSTRUATION
MENARCHE

First menstruation and usually occurs between 11 and 14 years of
age.

Follows thelarche (development of the breast buds) by 2 years.
MENSTRUATION

The periodic blood that flows as a discharge from the uterus

The menses occurs at approximately 4 week.

Intervals to compose the menstrual cycle.
HORMONAL ACTION AND THE MENSTRUAL CYCLE
GnRH

Source: Hypothalamus

Stimulates pituitary to secrete FSH and LH above a basal level.
FSH

Source: Pituitary

Stimulates ovaries to develop mature follicles (with ova); follicles produce increasingly high levels of estrogens
LH

Source: Pituitary

Surge of LH stimulates follicle to break open and discharge ovum and
follicular fluid (containing estrogens); follicle converted into corpus luteum, which secretes estrogen and gradually increasing amounts of progesterone.
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Estrogens

Source: Ovary (follicle)

Causes rapid growth of endometrium of uterus.

Causes the breast sensitivity that often accompanies menstrual
flow to disappear.

Rising level of estrogens have negative feedback effect on the hypothalamus and GnRH.
Progesterone

Source: Ovary ( corpus luteum)



Causes endometrium to become thick, spongy, glandular & receptive to fertilized ovum (zygote).
Causes breast engorgement.
Has negative feedback on pituitary.
GENERALITIES
DEFINITION OF TERMS
Age of Gestation: Measured from the 1st day of the last menstrual period
(LMP), in completed days or weeks.
Gravida: Woman who is/has been pregnant irrespective of the pregnancy
outcome
Primigravida– is or has been pregnant once
Multigravida– establishment of successive pregnancies
Nulligravida– is not and never has been pregnant
Parity: number of pregnancies reaching viability. Parity is same whether a
single or multiple fetuses were born alive/stillborn
Primipara– has never completed a pregnancy; may or may not
have aborted
Multipara– completed 2 or more pregnancies to viability
Nullipara– woman who has never completed a pregnancy beyond
the stage of viability or beyond as abortion
* a woman with her 1st triplets is also primipara
Obstetrical Score: Gravida_ Parity_ (T-P-A-L)
Full Term– Premature– Abortion-Live Birth
Parturient: Woman in labor
Parturition: Process of labor
Puerperium: 6-8 week period after delivery
Puerpera: Woman who had just given birth
Perinatal-period: Commences at 22 completed weeks of gestation and
ends 7 completed days after birth
Neonatal period: From birth to 28 days after birth
Pre-term: Less than 37 completed weeks
Term: From 37 to less than 42 completed weeks
Post term: 42 completed weeks or more
Low Birth Weight: Less than 2,500 g
Very Low Birth Weight: Less than 1,500 g
Extremely Low Birth Weight: Less than 1,000 g
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DIAGNOSIS OF PREGNANCY
PRESUMPTIVE SYMPTOMS OF PREGNANCY
1.
Nausea with or without vomiting → due to ↑HCG
2.
Disturbance in urination
3.
Fatigue– due to increase in metabolism
4.
Perception of fetal movement
* Quickening—awareness of first movement
º Primigravida: 18th to 20th week of AOG
ºMultigravida: 16th to 18th week of AOG
5.
Breast tenderness and tingling sensation
PRESUMPTIVE SIGNSOF PREGNANCY
1.
Amenorrhea (menses > 10 days late)
2.
Anatomic breast changes
* Darker areola, engorged breast, (+) tenderness
* Enlargement of Montgomery’s tubercles
3.
Changes in vaginal mucosa
* Chadwick’s sign– violaceous discoloration of the vagina due to ↑
vascularity at the 6th week AOG
4.
Skin pigmentation
* Chloasma– darkening of the skin over the forehead, nose bridge
or cheekbones
* Linea nigra– darkening of the linea alba, areola, nipples, axilla,
neck and groins
* Striae gravidarum or stretch marks– separation of underlying collagen which appears as irregular scars
* Spider telangiectasia– vascular, stellate marks from high levels of
circulating estrogen that blanch when compressed
5. Thermal signs
↑ temp by 0.3 to 0.5 for > 3 weeks due to progesterone
PROBABLE EVIDENCE OF PREGNANCY
1.
Enlargement of abdomen
2.
Changes in skin, shape and consistency of the uterus
* Hegar’s sign– softening of uterine isthmus– 6th to 8th week
* Goodell’s sign– softening of the cervix occurs at 4th week
3.
Anatomical changes in cervix
* Cervical mucus—”beaded” pattern due to progesterone
* Compared to “ferning” pattern characteristic of estrogen seen on
1st half of the cycle
4.
Braxton– Hick’s contraction that are painless and irregular
5.
Ballottment: feeling that something is something is floating/
”bouncing back” inside the abdomen by 20th week AOG
6.
Physical outlining of the fetus
7.
Positive pregnancy test β-HCG levels
POSITIVE EVIDENCE OF PREGNANCY
1.
Identification of fetal heart tones separately from mother
* Normal FHT—110 to 150 bpm (17th—19th weeks by auscultation)
* Ultrasound by 8th week
*Stethoscope by 18th week
* Doppler as early as 10th to 12th week
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2.
3.
* Other sounds that may be heard— funic or umbilical cord souffle,
uterine souffle; sound from movement of fetus; maternal pulse;
maternal bowel sounds
Perception of active fetal movement by the examiner
Ultrasound or radiologic evidence
RADIOGRAPHIC EVIDENCE OF FETAL DEATH
1.
Spalding’s sign– overlapping of fetal skull bones due to liquefaction of brain
2.
Exaggeration of fetal spine curvature
3.
Robert’s sign– gas bubbles in the fetus
MATERNAL ADAPTATIONS TO PREGNANCY
THE CARDIOVASCULAR SYSTEM

No actual enlargement but only slight dilatation and displacement
upwards and outwards due to gravid uterus

ECG may reveal slight axis deviation; occ. t waves; lowering of T
waves

↑ in heart rate maxima on the 7th– 8th month ~ 10 bpm

↑ in cardiac output by about 30-50%
THE RESPIRATORY SYSTEM
Structural and ventilator adaptation:

Increased maternal oxygen requirements

Chest expansion

Diaphragm elevation
THE GASTROINTESTINAL SYSTEM

Morning sickness common during first trimester

Hyperemesis:
Persistent and severe nausea and vomiting
 Can cause weight loss, fluid and electrolyte imbalance, ketonuria and dehydration
THE URINARY SYSTEM

↑ kidney size due to hypertrophy and ↑ renal blood flow causing as
↑ renal blood flow causing as ↑ renal vascular volume

“Physiologic Hydroureter of Pregnancy” - marked ↑ (25x) in
diameter of ureteral lumen, hypotonicity and hypomotility of its
musculature; more pronounced and frequent on the right side

Prone to UTI due to progesterone and pressure changes
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THE ENDOCRINE SYSTEM

Normal ovarian function suppressed - ↑ corpus luteum activity up to
12th week after which placenta takes over secretion of estrogen and
progesterone

Mild hyperthyroid state due to gland hyperplasia → slight elevation
of BMR and PBI

Hyperparathyroid state → ↑ calcium for fetus

Hyperadrenal state ← gland hyperplasia with ↑ corticosteroid

Diabetogenic due to placental degradation of insulin and anti– insulin effects of placental lactogen, estrogen, progesterone.
SKELETAL

Back pain due to lordosis

↑ mobility sacral joint
THE HEMATOLOGIC SYSTEM

Increased blood volume due to ↑↑ plasma, ↑ RBC → ↓ Hct

↑ reticulocyte and leukocyte count

Increased blood coagulation factors, increased fibrinogen levels, ↑
plasminogen and fibrin degradation products

↑ plasma iron binding capacity (transferring)
WEIGHT GAIN (average 24 lbs)
1st trimester– 2 lbs;
2nd trimester– 11 lbs;
3rd trimester– 11 lbs
PRE– NATAL CARE
I. ESTIMATION OF THE DURATION OF PREGNANCY
Last Menstrual Period (LMP)
 Count number of days since 1st day of last normal menses
 Add 280 days/ 40 weeks/ 9 ½ calendar months
II. EXPECTED DATE OF CONFINEMENT
(Naegele’s Rule)
9 months + 7 days from beginning of LMP
EDC= (1st day of LMP) + 7 days— 3 months + 1 year
E.g. LMP: 8 September 97
EDC: 15 June 98
III. LEOPOLD’S MANEUVER

First Maneuver (Upper pole)
 Examiner faces woman’s head
Palpate uterine fundus
Determine what fetal part is at uterine fundus
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
Second maneuver (Sides of maternal abdomen)
 Examiner faces woman’s head
Palpate with one hand on each side of abdomen
 Palpate fetus between two hands
 Assess which side is spine and which extremities

Third maneuver (Lower pole)
 Examiner faces woman’s feet
 Palpate just above symphysis pubis
 Palpate fetal presenting part between two hands
 Assess for Fetal Descent

Fourth maneuver (Presenting part evaluation)
 Examiner faces woman’s head
 Apply downward pressure on uterine fundus
 Hold presenting part between index finger and thumb
 Assess for cephalic versus Breech presentation
IV. PREGNANCY SCREENS
* Initial Work– Up– Hgb, blood group, Rh factor, Pap smear, rubella
titers, syphilis (VDRL), Hepa B screen
* Urine Test– if (+) bacteuria: treat even if asymptomatic
* Ultrasound
* At 16 weeks– Triple Screen (DOWN SYNDROME)
- AFP—hCG + estriol (if abnormal → amniocentesis)
* AFP elevated → open neural tube; multiple gestation; duodenal atresia
* AFP decreased → Down Syndrome
* Amniocentesis—offer to all women > 35 years; previous chromosomal abnormality, history of spontaneous abortions
* Chorionic Villi Sample
* 50 g OGCT, if > 130 mg/dL in 1 hr → Do 3 hr 100 g OGTT
V. FREQUENCY OF VISITS
* Every 4 weeks until 28 weeks
* Then every 2 weeks until 36 weeks
* Weekly thereafter
VI. HT of FUNDUS (in cm) = weeks AOG (18-32 weeks)
12th week– above the symphysis pubis
16th week– halfway between symphysis pubis and umbilicus
20th week– level of umbilicus
28th week– 6 cm above the umbilicus
36th week– 2 cm below the xiphoid process
40th week– 4 cm below the xiphoid process
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THE PASSAGES
I. INLET
A.
Anteroposterior diameters
1. True anatomic conjugate—11 cm (DC– 1.2 cm)
2. Obstetric conjugate– 10 cm (DC– 1.5 to 2 cm)
3. Diagonal conjugate– 12 cm (measure clinically)
B.
Transverse diameter– 13 cm
C.
Right and Left Oblique diameters– 13 cm each
II. MIDPELVIS
A.
Anteroposterior diameter
B.
Transverse diameter (Bispinous) - 10.5 cm
C.
Posterior sagittal– 4.5 cm
Clinical Assessment of an adequate midpelvis
1. Sacral promontory accessible
2. Ischial spines not prominent
3. Pelvic sidewalls not convergent
4. Sacrum curve
5. Sub– pubic arch wide
III. OUTLET
A.
Anteroposterior diameter– 9.5 to 11.5
B.
Transverse diameter (intertuberous)- 11 cm
C.
Posterior sagittal– 7 cm
IV. PLANE OF GREATEST DIAMETER
Anteroposterior diameters– 12.5 cm
FEATURES OF PATIENT PELVIC TYPES
(CALDWELL- MOLLOY CLASSIFICATION)
Shape
I
N
I
L
T
C
A
V
I
T
Y
Gynaecoid
Anthropod
Android
Platypelloid
Round
Anteroposteriorly oval
Triangular
Transversely
oval
Post segment
short;
Anterior
segment
narrow
Inclined
forward
and
straight
Anterior and
Post Segment
Almost
equal and
spacious
Both ↑ with
slight anterior narrowing
Sacrum
Well
curved
Long and
narrow
Sacro-sciatic
notch
Wide and
shallow
More wide
and shallow
Narrow
and deep
Side walls
Straight or
slight
divergent
Straight or
divergent
Convergent
10
Both reduced flat
Inclined
posteriorly and
straight
Slightly
narrow
and small
Divergent
O
U
T
L
E
T
Ischial spine
Not prominent
Not prominent
Prominent
Not prominent
Pubic arch
Curved
Long and
curved
Long and
straight
Short and
curved
Subpubic angle
Wide (86”)
Slightly narrow
Narrow
Very wide
(>90º)
Bituberous
diameter
Normal
Normal or
short
Short
Wide
No difficulty
More incidence of face
-to-pubis
delivery
Difficult
delivery
with ↑
chance of
perineal
injuries
No difficulty
Delivery
INDICATIONS FOR CLINICAL PELVIMETRY
1.
2.
3.
Previous injuries or disease likely to affect the pelvis
Breech for vaginal delivery
VBAC (Vaginal Birth After Caesarean)
SOFT PARTS OF THE PELVIS
Pelvic Floor– muscular part separating pelvic cavity from perineum; Levator
ani muscles (pubococcygeus, iliococcygeus, ischiococcygeus)
Pelvic diaphragm– helps in control of the external anal sphincter through the
puborectalis and ischiococcygeus and stabilize joints.
THE PASSENGER
FETAL ATTITUDE (Posture or Habitus)
* Relation of the fetal parts to one another
* Head is flexed; back becomes convex; thighs are flexed over the
abdomen; legs are bent at knees; and arches of the feet rest upon the
anterior surfaces of the legs
LIE OF THE FETUS
* Relation of long axis of the fetus to long axis of the mother
1. Longitudinal Lie (90%)
 Long axis of the fetus parallels the long axis of uterus
 Either fetal head or breech presenting
2. Transverse Lie
 Lies in transverse or one of oblique diameter of uterus
 Oblique lie– a variant of the transverse lie; unstable becoming
longitudinal or transvers lie during labor
 Shoulder is usually over the pelvic inlet
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PRESENTATION
* Part of fetus lying over the inlet
1. Cephalic Presentatin– 95% of cases
A. Vertex (occiput) presentation
 Most common because uterus is pyriform
 Occiput (posterior fontanel) is the presenting part
 With head fully flexed, the shortest AP diameter suboccipitobregmatic (~ 9.5 cm) is presented
B. Sinciput military attitude presentation
 Partially flexed; gradually changes to full flexion
 Bregma (anterior fontanel) is the presenting part
 Occipitofrontal (~12.5) is presented
C. Brow presentation
 Fetal head is partially extended
 Occipitomental plane (~ 13.5 cm),
the longest AP diameter is presented
 Converted into face presentation
by extension
D. Face presentation
 Fetal head may be sharply extended so that the occiput and the
back of the fetus comes in contact
Submentobregmatic(9.5 cm at
term) is presented
Vaginal delivery may result to cervical SC injury so is an indication for
cesarean delivery
2. Breech Presentation
A. Frank Breech
 Thighs are flexed on the abdomen & legs are
extended over the anterior surfaces of the body ,
thus the feet of fetus lie in proximity to the head
B. Complete Breech
Thighs are flexed on the abdomen, legs are
flexed upon the thighs & feet present at level of buttocks
C. Incomplete Breech
 1 or both thighs are extended so that the feet
and legs are below the level of the buttocks
Single footling : 1 leg extended & other flexed
Double footling: both legs extended
Complication: cord prolapse or entanglement
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3. Shoulder (Acromion Presentation)
4. Compound Presentation
 Prolapse of the fetal head along side the presenting vertex or
breech or foot alongside the head
POSITION
Relation of the point of direction to one of the 4 quadrants or to
the transverse diameter of the maternal pelvis
Points of direction: O (occiput) in cephalic ;
M (mentum/chin) in face
S (sacrum) in breech
A(acromion) in shoulder
ASSESSMENT OF FETAL WELL-BEING
CLINICAL ASSESSMENT OF FETAL WELL-BEING
1.
Serial Measurement of Maternal Weight
2.
Fundic Height in Determining Estimated Fetal Weight
ROUGH ESTIMATE at >32 weeks
Fundic height of 30 cm = estimate at 6 to 6 ½ lbs
31 cm = 6 ½ to 7 lbs
32 cm = 7 to 7 ½ lbs
McDONALD’S RULE
AOG in weeks = D x 8/7
Where D is distance in cm and K is 8/7
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JOHNSON’S RULE
FETAL WT in grams = 155 x (Fundic ht in cm—n)
N= 12 if station below ischial spines (engaged)
11 if above the Ischial spines (unengaged)
K is 155, constant
Note: if px > 200 lbs, “n” is raised by one
eg. Fundic ht of 30 cm whose vertex is at station +2
Fetal wt = 30 – 12 x 155 = 2790 g
3.
Fetal Heart Tones—n.v.: 110– 150 beats/min
4.
Fetal Activity Acceleration Determination
 Count fetal movements for 1 hour after meals
 Abnormal if < 3 fetal movements per hour
BIOPHYSICAL ASSESSMENT METHODS
1.
Ultrasonography
A. Real Time Sonography
 Biophysical Scoring System (BPS), see table below
2.
Electronic Fetal Monitoring
A. Contraction Stress Test/ Oxytocin Challenge Test
 Assess the uteroplacental circulation and umbilical artery of
the fetus
 Evaluates the reaction of heart rate to contractions induced
by nipple stimulation/ oxytocin administration
 Done when frequency is contractions/ 10 minutes
Interpretation
1.
Positive– consistent and persistent late decelerations (>
50%) of the fetal heart beat in the absence of uterine hypertonus or supine hypertension
2.
Negative– at least 3 contractions in 10 minutes, each lasting
40 seconds, without late deceleration
3.
Suspicious– inconstant late deceleration
4.
Hyperstimulation– uterine contractions occur more frequent
than 2 minutes or lasting longer than 90 seconds or presence of uterine hypertonus
5.
Unsatisfactory– frequency of contractions is less than 3 per
minute or the tracing is poor
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BIOPHYSICAL SCORING SYSTEM
Biophysical
Variable
Normal
Abnormal (Score = 0)
(Score = 2)
Fetal
Breathing
Movements
At least 1 episode of FBM
or at least 50s duration in
30 minutes
Absent FBM or no episodes of >30s in 30
minutes
Gross Body
Movement
At least 3 discrete body/limb 2 or fewer episodes of
movements in 30 minutes
body/limb movements in
30 secs
Fetal Tone
At least 1 episode of active
extension with return to
flexion of fetal limb/s or
trunk Opening and closing
of hand considered normal
tone
Reactive
FHR
At least 2 episodes of FHR Less than 2 episodes of
acceleration of > 15 bpm ad acceleration of FHR or
of at least 15s duration
acceleration of < 15 bpm
in 30 min
Qualitative
AFV
At least 1 pocket of AF that
measures at least 1 cm in 2
perpendicular planes
Either slow extension with
return of partial flexion or
movement of limb in full
extension or absent fetal
movement
Either no AF pockets or
pocket < 1 cm in 2 perpendicular planes
B. Non Stress Test
 Reactive: at least 2 FHR accelerations of at least 15 beats/min, lasting 15 secs, within a 20 minute period
As with a negative CST, a reactive NST, a reactive NST is also highly predictive of intrauterine survival
Non– reactive may imply that the fetus is acidotic, asleep, or drugs
was administered to the mother
15
ULTRASOUND IN PREGNANCY
Abdominal Ultrasound ( full bladder)
* Full bladder acts as a acoustic window, pushing the uterus out of
the pelvis, and displacing bowel superiorly
Vaginal Ultrasound (empty bladder)
* Small amount of urine pushes uterus posterior out of view
FIRST TRIMESTER ULTRASOUND
1.
Establishes uterine pregnancy, upon seeing
Gestational Sac (earliest 5 to 6 weeks) especially if ectopic pregnancy is suspected
2.
Detection of embryonic/ fetal life and number of fetuses
 Fetal heart motion by 7 weeks of gestation
3.
Evaluation of complicated early pregnancy such as retrochorionic
hemorrhage, incomplete abortion
 Hemorrhage volume > 60 cc is associated with abortion
4.
Early dating of pregnancy using
 Gestational sac (GS) diameter at 5-6 weeks
 Crown– rump length (CRL) at 12-14 weeks (most accurate)
 Biparietal diameter (BPD), femoral length (FL) onwards
5.
Evaluation of uterus and adnexa
SECOND AND THIRD TRIMESTER ULTRASOUND
1.
Fetal viability, number and presentation
 Presence of fetal cardiac activity and body movement
2.
Amount of amniotic fluid and Placental localization
 3 cm vertical pocket in 2nd and 3rd trim is normal
3.
Fetal age and growth by fetal biometry: (CRL, BPD, FL)
4.
Evaluation of fetal anatomic structures
 Reversal of fetal diastolic blood flow in the umbilical artery indicates a severely compromised fetus
PARTURITION
THE FOUR PHASES OF PARTURITION
PHASE 0 (Prelude to Parturition/ Quiescence)
* Before implantation until about 35– 38 weeks
* The smooth muscle of the uterus is tranquil and the cervix is rigid
from before implantation until late in gestation
* Progesterone: principal mediator
* Cervix: remains rigid and unyielding
16
PHASE 1 (Preparation to Labor)
* Uterus and cervix undergo anatomic and functional changes:
 ↑ oxytocin receptors in myometrial cells, ↑ number and size of
gap junctions, ↑ frequency of painless contractions
* Dependent on uterotorins or uterotropin-stimulating agents
* Cervix ripens: soften, yield and more readily dilatable
PHASE 2
*Active uterine contractions brings about cervical effacement and
dilatation, fetal descent and delivery
* STAGES OF LABOR
FIRST STAGE OF LABOR
* Average duration: 8 hours in nulliparous and 5 hours in multiparous
* Sufficient uterine contractions to bring about demonstrable cervical
effacement and dilatation up to full cervical dilatation
* No ↑ oxytocin levels in plasma but prostaglandin levels increase in
amniotic fluid and maternal blood
1.
Uterine Contractions
 Active phase of labor, contractions are moderate, every 2-3
minutes, lasting for 40-60 seconds
2.
Fetal Heart Tone Monitoring? Electronic Fetal Monitoring
 For cases of fetal compromise, preterm, induced, or augmented labor, meconium staining, abnormal fetal HR
 Records fetal heart rate by ultrasonic Doppler and uterine
contractions by tocodynamometers at fundus
3.
Attendance in Labor
 Subsequent vaginal examinations = 2 hour interval
 Cervical dilatation at 1-2 cm / hour
 Analgesia, IV fluids, bladder function
4.
Active Management of Labor
 Artificial amniotomy can be done at 4 cm dilatation to shorten
1st stage of labor and for early detection of meconium staining
Oxytocin infusion
- if dilatation did not progress at least 1 cm/hour
- started at 6 mU/min to ↑ at increments of 6 ml/min every 15
minutes but not to exceed a total of 60 mU/min
SECOND STAGE OF LABOR
* full cervical dilatation to expulsion of fetus
* average: 50 minutes nulliparas and 20 minutes multiparas
* contractions last for 90 seconds every 1-2 minutes
* maternal plasma oxytocin levels are increased
* dorsal lithotomy position: ↑ diameter of the pelvic outlet
17
1. Delivery of the head
 Crowning– fetal head is seen encircled b the vulvar ring;
episiotomy prevents perineal lacerations
2. Ritgen’s Maneuver
 Controls delivery of the head with extension so that smallest diameters of the head pass over the introitus
 When vulvar opening reaches a diameter of 5 cm, a towel
draped hand should be used to exert forward pressure on the
chin of the fetus through the perineum
 The other hand is placed on the occiput
 Prevents extension of episiotomy and fetal contamination
3. Nasopharyngeal toilette
 After delivery of the head, the face of the fetus is wiped and
the nares and throat quickly suctioned
 To prevent aspiration of amniotic fluid and blood
4. Nuchal cord care
THIRD STAGE OF LABOR
* Time from delivery of the infant to expulsion of the placenta
Mechanism of Placental Expulsion
1.
Schultze Mechanism
 Occurs initially at the central portion of the placenta
 Placenta descends by dragging the membranes along thus
forming some of an inverted sac
2.
Duncan Mechanism
 Occurs first at the periphery
 Placenta descends to the vagina sideways
Signs of Placental Separation
1.
Calkin’s sign– uterus becomes globular and firmer
2.
Sudden gush of blood
3.
Uterus rises in the abdomen as the detached placenta drops
to the lower segment and vagina
4.
Umbilical cords lengthens or protrudes out of the introitus
AFTER 3rd STAGE OF LABOR
* 1 hour after delivery of placenta in which it is critically to identify
postpartum hemorrhage 2 to a tony/ lacerations
* Management: uterine massage, ice packs, oxytoxics
18
PHASE 3 (Recovery Period)
* Uterine contraction and involution to prevent hemorrhage
* Initiation of lactation and milk ejection for breastfeeding
Regulators: uterotonins (oxytocin and endothelin-1)
Uterotropin– acts in myometrium and cervix to produce functional
elements that prepare the uterus for effective contraction and
cervical softening eg. gap junctions, oxytocin receptors
Uterotonins– causes smooth muscle contraction e.g. oxytocin,
prostaglandins and endothelin-1
EARLY SIGNS OF LABOR
1.
“Lightening” or “Baby Drop”
 ↓ fundic ht due to formation of lower uterine segment allowing fetal head to descend and ↓ in amount of AF
2.
“Show” or “Bloody Show”
 Small amount of blood-tinged mucus from vagina
 Considered a late sign because labor may ensue in the
next few hours or days or at times labor has begun
3.
False Labor
 Contractions of irregular interval, shorter duration, and
discomfort, confined to the lower abdomen or groin
 True vs False labor
Ferguson reflex– mechanical dilatation of cervix in the form of manipulation, “stripping” of fetal membranes or dilatation
Pathological Retraction Ring or Ring of Bandl– extreme thinning of lower
uterine segment as in obstructed labor; the ring becomes very
prominent; uterine rupture may ensue
DEGREE OF EFFACEMENT
* Synonyms to “obliteration” or “taking up” of the cervix
* Shortening of the cervical canal from length of about 2 cm to a
circular orifice of paper– thin edges (100% effaced)
* Upward pulling of muscular fibers of internal os while the external
os remains temporarily unchanged
* No fetal descent occurs but the presenting part descends
STATION
* Stations– measures in cm below level of ischial spine
* From the ischial spines up: Station –1 to –3
* Station 0 = engagement; Point of reference is ischial spine
* Station +1= presenting part 1 cm below ischial spine
* Station +2= presenting part 2 cm below ischial spine
* Progressive dilatation with no change in station in woman of low
parity may signify fetopelvic disproportion
19
CERVICAL DILATATION
* Degree of opening of the external os
* True indicator of labor
* Examining fingers are swept from one margin of the cervix to the
other: maximum diameter is 10 cms
Pattern of Cervical Dilatation
* Sigmoid curve
* Two Phases
1. Latent Phase– more variable; affected by factors such as
sedation
2. Active Phase (starts at 4 cm dilatation)
a. Acceleration Phase
- predictive of the outcome of a particular labor
b. Phase of Maximum slope
- measure of the overall efficiency
c. Deceleration Phase
FRIEDMAN’S CURVE
Pattern of Descent
* Hyperbolic curve
* Active descent takes place when the cervical dilatation has already advanced but the maximum slope of cervical dilatation
* Three functional divisions of labor
1. Preparatory division
- little cervical dilatation; affected by sedation
2. Dilatation division
-dilatation occurs at its most rapid rate
- unaffected by sedation or conduction/analgesia
20
3. Pelvic division
- starts at deceleration phase of cervical dilatation
- cardinal movements of the fetus takes place
WHO Principles of Partograph
A. Active phase of labor begins at 4 cm cervical dilatation
B. Latent phase of labor should not last > 8 hours
C. Rate of cervical dilatation during the active phase of labor should
not be slower than 1 cm/hr
D. 4– hour lag between slowing of labor and the need for intervention is unlikely to compromise the fetus
E. 4 hourly vaginal examinations is recommended
CARDINAL MOVEMENTS OF LABOR
1.
Engagement
 Entering of the biparietal diameter (measuring ear tip to ear tip
across the top of the baby’s head) into the pelvic inlet
2.
Descent
 The baby’s head moves deep into the pelvic cavity and is commonly called lightening
 The baby’s head becomes markedly molded when these distances are closely the same
 When the occiput is at the level of the ischial spines, assume
that the biparietal diameter is engaged and then descends into the
pelvic inlet.
3.
Flexion
 Occurs during descent and is brought about by the resistance
felt by the baby’s head against the soft tissues of the pelvis
 Resistance brings about a flexion in the baby’s head so that the
chin meets the chest
 The smallest diameter (suboccipitobregmatic plane) presents
into the pelvis
4.
Internal Rotation
 Occiput gradually move anteriorly towards the symphysis
5.
Extension
 Extension occurs as the head, face and chin are born
6.
External Rotation
 Head undergoes restitution (rotation of head back to its original
position in direction opposite that of internal rotation)
7.
Expulsion
 Immediately after external rotation, the anterior shoulder moves
out from under the pubic bone
 The perineum becomes distended by the posterior shoulder. The
rest of the baby’s body is then born
21
MAJOR STAGES IN BIRTH PROCESS
22
CHANGES IN THE SHAPE OF THE FETAL HEAD
Caput Succedaneum
* Located above periosteum and crosses the sagittal suture
* Unlike Cephal Hematoma, which is located below the periosteum
and does not cross the sagittal suture
Molding
* Bones of the fetal skull are not united and movement at the sutures may occur, so bones may overlap each other.
CONDUCT OF NORMAL LABOR AND DELIVERY
DIFFERENTIATION OF LABOR
Parameter
False Labor
True Labor
Contractions
Regularity
Irregular
Regular
Interval
Long may disappear
Increases gradually
Intensity
Unchanged
Increases gradually
Radiation of pain
Mostly hypogastric
Hypogastric to lumbosacral
Effect dilatation
Long and closed
Open and effacing
Effect effacement
Does not occur
Occurs and progresses
Effect of sedation
May stop contraction Not stopped
Lacerations of the Vagina and Perineum
1. 1” degree—involve the fourchette, perineal skin, vaginal mucosa but not
the underlying fascia and muscle
2. 2nd degree– involves fascia and the muscle of the perineal body but not
the anal sphincter
3. 3rd degree—extend from vaginal mucosa, perineal skin, and fascia up to
anal sphincter but not the rectal mucosa
4. 4th degree– extension– up to rectal mucosa; rectal mucosa is repaired
first before the vaginal mucosa
23
Two Types of Episiotomy
Advantages
MIDLINE
Disadvantages
Easier to repair, small
blood loss, minimal
post-op pain, heals
faster, rare
dyspareunia
MEDIOLA- More space for breech
TERAL
deliveries
May extend to anal sphincter
More difficult to repair,
greater blood loss, commonly postop pain,
dyspareunia
Suturing Technique
1.
Vaginal mucosa– interlocking sutures until lower end of hymenal
ring; repair 1 cm above angle of mucosal defect
2.
Subcutaneous and fascial layers– interrupted sutures
3.
Skin– interrupted or subcuticular sutures
PUERPERIUM
Time after delivery of placenta up to return of reproductive organs
to their normal non-pregnant condition; ~6-8 weeks
Clinical Aspect of Puerperium
* Uterine involution: Umbilicus– after delivery of the placenta, ↓ by
1-2 cm/day; Symphysis pubis– 10th—12th d
* Failure of the uterus to contract normally due to: Uterine atony,
clot formations at the thrombosed placental site, retained
placental cotyledons, inadequate drainage of tissues,
infection
* Slight fever: Due to vascular and lymphatic engorgement, and not
due to milk fever (<24 hours)
* Cardiac output returns to normally by the 2nd week
* Urinary retention first 24 hours due to:
1. Edema and congestion of vulva urethra, bladder trigone
2. Edema and reflex spasm of urethral sphincter
3. Bladder atony
* Diuresis is greatest from the 2nd to 5th day
24
* Lochia– discharge from the uterus during puerperium; odor is
heavy and fleshy but not offensive; lasts 4-8 weeks
Lochia Rubra– first 3-4 days, becomes reddish
Lochia Serosa– next 3-4 days, paler and pinkish
Lochia Alba– from the 10th day, consist of cervical mucous and
debris from healing tissues and leukocytes, thus becoming
lighter yellow and creamy in color
Foul lochia– 2 ‘ to poor healing, infection, retained secundines
* After Pains– contractions of the flaccid uterus to expel some of
the remaining fragments and blood clots esp. in multiparas;
more intense during breast feeding
* Constipation– due to patient’s inactivity, decrease intra-abdominal
pressure after delivery and painful perineum
* Weight loss
Ave weight loss of 5 kgs—immediately after delivery
Additional loss of 3 kgs—due to diuresis and skin loss
Normal pre-pregnant weight in attained in 6 months
* Postpartum blues
* Return of menses and ovulation
In 7 - 8 weeks if not lactating
Delayed with lactation due to prolactin’s inhibition of GnRH
* Post-partum check up in 4-6 weeks; Pap smear 6 months
INTRAPARTUM ASSESSMENT
CLASSIFICATION OF INTRAPARTUM TRACE
Normal Baseline rate 110– 150 bpm
Baseline variability 10 –25 bpm
2 accelerations in 20 minutes and no decelerations
Abnormal
Absence of accelerations and
Any of the following:
- Abnormal baseline rate <110 or > 150 bpm
- Abn. baseline variability < 5.10 bpm for 40 minutes
- Repetitive late/ Variable decelerations
3 Types of Fetal Heart Rate Pattern
EARLY DECELERATION
*Occurs with the onset of contraction and return to the baseline at
the end of the contraction with the nadir occurring at the peak of
each contraction
* Due to head compression, not hypoxia or acidosis
LATE DECELERATION
* Occurs after the onset of contraction (usually at the peak) and
return to the baseline after the contraction with the nadir occurring
after the peak of the contraction
* Connotes uteroplacental insufficiency
25
VARIABLE DECELERATION
* Most common type
* Occurs before, during, or after even without contraction
* Due to cord compression and cessation of umbilical blood flow
1ST TRIMESTER HEMORRHAGIC DISEASE
ABORTION
* Termination of pregnancy before 20 weeks AOG
* Delivery of a fetus < 500 grams
* Crown rump < 16 cm
Etiology/ Factors
1.
Fetal—abnormal zygote/ embryonic development
2.
Maternal- ↑ age, conception within 3 months of a live birth, chronic
infections (Herpes, etc.), chronic debilitating disease (DM, SLE),
malnutrition
3.
Anatomic– leiomyomas, incompetent cervix
4.
Environmental– tobacco, alcohol, caffeine
5.
Physical– radiation, anesthetic gases
COMPARATIVE ANALYSIS OF DIFFERENT TYPES OF ABORTION
Blee Cerviding cal
Dilata-
Uterine
size vs
AOG
Bag of Water
Other Findings
Mgt.
Threat +/ened
Closed Compatible
Intact
(+) FHT
CBR, progesterone,
Imminent
Open
Intact
(+) FHT
Watchful
expectancy
+
Compatible
Oxytocin
Inevitable
++
Open
Incompatible
Ruptured
Incompl
ete
++
Open
Complete
+/-
Misse
d
Habitual
Incompatible
Ruptured or Passage of
Not Appreci- meaty tissue
ated
Curettage
(ovum/ring
forceps)
Closed Incompatible
Not Appreci- Absent Signs
ated
of Pregnancy
Observation
Spot Closed Incomting
patible
Not Appreci- Retention of
ated
dead products
Prostaglandins; D and
+
+/-
Karyotyping
Cerclage Px
counselling
+
Compatible
(+) FHT
Curretage
Oxytocin
3 or more consecutive abortion
26
Causes of habitual abortion:
1.
Chromosomal abnormalities
2.
Defective zygote
3.
Cervical incompetence
4.
Infections
5.
Hormonal dysfunction
ECTOPIC PREGNANCY (Eccyesis)
* Implantation of the fertilized ovum outside the endometrium
* Heterotopic pregnancy– simultaneous intrauterine and ectopic
pregnancies
Pathology
1.
Salpingitis
2.
IUD
3.
Kinks
4.
Previous eccyesis
5.
Myomas and adnexal masses
6.
Failed bilateral tubal ligation
7.
Clomiphene citrate
8.
Progestin only contraceptives
9.
Idiopathic
Symptoms
1.
Colicky abdominal pain
2.
Amenorrhea of about 6 weeks followed by
3.
Minimal vaginal bleeding
Signs
1.
2.
* Wiggling tenderness– most common sign
Uterus smaller than AOG
Fullness of cul-de-sac due to hemoperitoneum
Ectopic Pregnancy
27
Diagnosis
* Lower HCG and progesterone levels
* Ultrasound diagnostic criteria
1. Detection of an adnexal mass
2. Absence of gestational sac using transvaginal transducer when
HCG > 2,500 mIU/ml at 5-6 weeks
3. Intrauterine gestational sac rules out an ectopic pregnancy
except in a heterotopic pregnancy
Management
Unruptured Ectopic Pregnancy
A.
Medical Management
1.
Methothrexate
2.
RU– 486– competes for progesterone binding sites
B.
Surgical Management
- Partial Salpingectomy, Salpingostomy, Salpingotomy
Ruptured Ectopic Pregnancy– primarily surgical
1.
Radical
A. Hysterectomy
B. Total salpingectomy with or without oophorectomy
2.
Conservative– segmental resection
GESTATIONAL TROPHOBLASTIC DISEASE (GTD)
I. Hydatidiform Mole
A. Partial Mole (PHM) 2– presence of some normal villi and some
cystic villi; mostly benign
B. Complete mole (CHM)- universal avascular villi
II. Gestational Trophoblastic Tumor (GTT)
A. Invasive Mole (IM)
B. Choriocarcinoma (CCA)- most malignant
C. Placental Site Trophoblastic Tumor (PSTT)- mainly cytotrophoblast
D. Residual or Persistent Trophoblastic Disease– clinically manifest
sequelae of molar pregnancies
H-mole
Choriocarcinoma
Diffuse hydropic villi
Proliferation of cytotrophoblast
Hyperplastic trophoblasts
Proliferation of syncytiotrophoblast
Invasive mole: Invades myometrium
No villi present
Vaginal bleeding
Following molar pregnancy
Uterine size greater than date
Following spontaneous abortion
Hyperemesis
Following term pregnancy
High B-hCG
High B-hCG
28
Signs and Symptoms
* Abnormal bleeding and lower abdominal pain
* Toxemia before 24 weeks of gestation– complete mole
* Hyperemesis gravidarum and hyperthyroidism
* Uterus large for dates (50%) - complete moles
* Enlargement of ovaries (20%)
* Absent fetal heart tones and fetal heart tones and fetal parts–
complete moles
* Snow storm appearance on ultrasound
Management of Hydatidiform Mole
1.
Replacement of blood loss
2.
Combat infection
3.
Termination of pregnancy either by suction curettage or hysterectomy (if complete family size or age > 35)
4.
Prophylactic chemotherapy
5.
Follow– up signs of persistent disease:
A. weekly hCG serum determination until normal for 2 values, then
every 2 weeks for 3 months, monthly for 6-12 months, every
6 months for 1-2 years, then annually
B. Chest X-ray examination initially and repeat if abnormal or if
hCG plateaus or rises
C. Contraception for 1 year because pregnancy will ↑ hCG
D. Pelvic exam q2 weeks until normal then q3 months
E. Initiate chemotherapy if:
hCG levels increases or plateaus; metastatic disease is
present; choriocarcinoma is diagnosed on tissue
hCG level still ↑ 6 months after molar evacuation
↑ hCG is detected after normal levels are reached
COMPLETE VERSUS PARTIAL HYDATIDIFORM
Complete Mole
Partial Mole
More common higher hCG titer (> 100,000
IU/liter)
Karyotype: 46 XX or 46 XY
Karyotype: normal or trisomic
Uterus usually large for date
Diagnosis: before expulsion of uterine contents
Diagnosis: after expulsion of
uterine contents
Gross: all villi are dilated like a bunch of
grapes without gestational sac
Gross: not all villi are dilated
with or without a gestational
Microscopic: all villi are cystic, avascular
with a central cistern in the stroma. Theca
lutein cysts– result of bombardment of follicle theca cells by high titer hCG
Microscopic: not all villi are
cystic with blood vessels with
nucleated RBC
High malignant potential
Low malignant potential
29
FIGO STAGING FOR TROPHOBLASTIC TUMORS
Stage
Characteristics
Stage I
Disease confined to the uterus
Stage II
Disease extending outside the uterus but limited to the
genital structures (adnexa, vagina, broad ligament)
Stage III
Disease extending to the lungs with or without known
genital tract involvement
Stage IV
Disease at other metastatic sites
SUBSTAGE A No risk fx
B 1 risk fx
C 2 risk fx
Risk Factors affecting prognosis including the following
1.
HCG > 100, 000 mIU/ml
2.
Duration of disease >6 months from end of antecedent oregnancy
GESTATIONAL TROPHOBLASTIC TUMOR (GTT)
INVASIVE MOLE
* Invasion of H-mole deep into uterine wall
Irregular bleeding within 6 months of molar evacuation
* Treatment:
A. single– agent chemotx with methotrexate 5-day: 0.4– 0.5 mg/kg,
IM or IV daily Weekly: 50 mg/m2, IM or IV
CHORIOCARCINOMA
* Pure epithelial tumor: syncitiotrophoblast and cytotrophoblast
* Grossly: necrotic hemorrhagic masses or nodules
* Microscopic: exuberant trophoblastic growth without the characteristic villous pattern
* Treatment:
A. Chemotherapy– single agent or drug combinations
B. Surgery– hysterectomy
30
PROGNOSTIC SCORING SYSTEM FOR GIT
Score
Factor
1
2
< 39
> 39
Antecedent pregnancy
H mole
Abortion
Term
Interval b/n end
of pregnancy and
start of chemotherapy
< 4 months
4-6
7-12
> 12
hCG (IU/L)
< 103
103-104
104-105
> 10 5
ABO groups
<3
O or A
B or AB
Largest tumor,
incl. uterine (cm)
3-5
>5
Site of metastases
Spleen,
kidney
GI tract, liver
Brain
4-8
>8
1 drug
> 2 drugs
Age (years)
Number of metastases
Prior chemotherapy
1-3
3
Low risk < 4; Medium risk 5-7; High risk > 8
* Score of 7 or less: good response to triple therapy, MAC
(Methotrexate, Actinomycin D, Cyclophosphamide)
* Score of > 8: has 46% survival with MAC
31
4
THIRD TRIMESTER BLEEDING
PLACENTA PREVIA
The placenta is lying unusually low in the uterus, next to or covering the cervix. The placenta supplies the baby with nutrients through the
umbilical cord.
It is not usually a problem early in pregnancy. But if it persists into
later pregnancy, it can cause bleeding, which may require delivering early
and can lead to other complications.
Types:
1.
Total– placenta covers cervical os completely
2.
Partial– Internal os partially covered by placenta
3.
Marginal– edge of the placenta is at margin of internal os
4.
Low– lying– placenta is implanted in lower uterine segment in close
proximity but not reaching the placental edge
Etiology:
1.
Multiparity
2.
Multiple induced abortions
3.
Puerperal endometritis
4.
Previous CS
5.
Large placenta
6.
Advancing age
Diagnosis:
* Painless third trimester bleeding
* Ultrasound for placental localization
* Placental migration– placental close to the internal os during 2 nd
trimester migrate to fundus as pregnancy advances
32
ABRUPTIO PLACENTA
* Separation of a normally implanted after the 20 th week of pregnancy and before birth of fetus
Since the round, flat placenta is a “lifeline” that supplies nutrients
and oxygen to a fetus from the mother, an abruption can be life– threatening for the fetus, and sometimes for the mother as well.
It can lead to preterm birth, low birth wt, and major maternal blood
loss. In rare cases, severe placenta abruptio leads to fetal or newborn
death.
Etiology
1. Pre– eclampsia
2. Chronic HPN
3. External trauma
4. Short umbilical cord
5. Sudden uterine decompression
Clinical Classification of Abruptio Placenta
Mild
Moderate
Severe
Mother
Normal CVP
↑ pulse, ↓ CVP, hypotension
Shock
Fetus
Normal FHT
Alive but signs of
fetal distress are
Fetal distress or fetal
death
Complications
None; Good
output
None; urine output
may be marginal
Renal failure, coagulopathy
Uterus
Irritability, pain
tenderness
Irritability, pain, severe tenderness
Severe pain and tenderness, tetanic con-
500– 1000 ml
> 1000 ml
Bleeding < 500 ml
Placenta <1/6 separation 1/6 to 2/3
33
> 2/3 separation
DIFFERENT B/N PLACENTA PREVIA AND ABRUPTIO PLACENTA
Abruptio Placenta
History
Frequent association of preeclampsia or HPN from any
cause
A single attack of vaginal
bleeding, which continues
until delivery
Placenta Previa
No association with preeclampsia
Repeated “warning” hemorrhages, often occurring
over a period weeks
Usually no abdominal pain
Abdominal pain
Abdominal
Exam
Local uterine tenderness
hypertonic “woody” uterus in
a concealed abruption
Px usually in labor
Presenting part often engaged
Normal uterine tone and
usually no tenderness
Patient rarely in labor
Presenting part above brim,
malpresentation is frequently found
Fetal parts may be difficult to Fetal psrts usually palpable
palpate
Fetal heart tones usually
Fetal heart tones often abpresent
Ancillary Aids Placenta demonstrated in
upper uterine segment by
UTZ
Placenta demonstrated in
lower uterine segment by
ultrasound
Vaginal Exam
Double set– up reveals no
Double set– up reveals
placenta within 5 cm of inter- placenta implanted in lower
nal os
uterine segment
MGT
No place for expectant treat- If bleeding stops and fetus
ment when this diagnosis is is < 36 weeks old, exmade
pectant tx may be indicated
PLACENTAL DISORDERS
ABNORMALITIES OF PLACENTAL FETAL MEMBRANES
Placentomegaly: > 600 grams
Placenta succenturiata: accessory lobe outside main disc
Extrachorial placentas: membranes do not insert at disc
1.
Circummarginate– membranes without thickening
2.
Circumvallate– membranes arise from a cup
34
Placenta accrete: villi contiguous with myometrium
Placenta increta: villi invade myometrium
Placenta percreta: villi penetrate serosal surface of myometrium
CHORIOAMIONITIS Criteria (at least 2)
1.
Fever . 38º C
2.
Tachycardia (fetal and maternal)
3.
Maternal leukocytosis
ABNORMALITIES OF AMNIOTIC FLUID
Hydramnios
* amniotic fluid of more than 2000 ml at any time in gestation
* Clinical correlates: GI tract abnormalities, DM, anencephaly/
spina bifida, erythroblastosis fetalis
* Diagnosis: measure largest pocket of AF on US
Mild hydramnios– 8 to 11 cm
Moderate– 12 to 15 cm
Severe– 16 cm and over
* Amniotic fluid index (AFI)- ∑ of the largest vertical pockets of 4
quadrants of uterus (AFI > 24 cm)
Oligohydramnios
* Paucity of amniotic fluid at term (<500 ml)
* Clinical correlates: IUGR, dysmaturity syndromes, renal agenesis,
and obstruction to urinary tract
* AFI < 4
COMPLICATIONS OF PREGNANCY
HYPERTENSION
Hypertension: BP 140/90 or ↑ of 30/15 mmHg
Proteinuria: 300 mg/24 hr urine sample or 1,000 mg/random urine sample
or +2 to +4 dipstick
Pathologic edema: pretibial pitting edema after 12 hours of bed rest or
weight gain of 5 lbs per week
Preeclampsia: HPN + proteinuria + edema after 20th week AOG
Severe Preeclampsia: presence of > 1 of the following:
A. Systolic BP or 160 mmHg or diastolic BP of 110 mmHg
B. Proteinuria of at least 4g/day or 2+ with renal involvement
C. Oliguria of < 400 cc/day
D. Severe headache or visual disturbances
E. Pulmonary edema or cyanosis: IUGR
Ü HELLP syndrome Hemolysis, Elevated liver enzymes and Low Platelet count
Eclampsia: presence of convulsions with underlying preeclampsia
35
Classification of Hypertensive Disorders
Gestational HPN - > 140/90 dx for the first time during pregnancy
(↓ BP at middle of preg - 20th week - due to hemodilution, pulling of
blood to the lower portion of the gravid uterus)
Pre-eclampsia - dx after 20th week AOG
- with proteinuria and/or edema
Eclampsia - with convulsions and proteinuria, with or without edema
Superimposed Pre - Eclampsia - preeclampsia that develop with
chronic hypertension or renal disease
Chronic Hypertensive Vascular Disease - persistent before 20th week
Treatment
1.
Control Convulsions
Magnesium Sulfate: drug of choice
Loading dose = 4 g/IV bolus + 10 g/IM (5 g per buttock)
Maintenance = 1-2 h/hour/IV drip or 5g/IM q6
Monitor toxicity using: DTR’s, RR > 12, UO > 30cc/hr
(Antidote: Calcium Gluconate)
2.
Control Hypertension
Hydralazine (Apresoline): 5 mg IV bolus following by 5 mg increments q30 minutes up to a total dose of 20 mg
Calcium Channel Blockers: Nifedipine or Nicardipine Beta Blockers
3.
Optimum Time and Mode of Delivery
DIABETES MELLITUS
* Pregnancy is diabetogenic due to impairment of peripheral insulin
action as a consequence of the action of placental lactogens, estrogens and progesterone
* Insulin does not cross the placenta → fetal hyperglycemia
* Diabetes screening - 24th to 28th week
Ü using 50g OGCT, if >130 mg/dL in 1 hour then proceed with 3
hour 100g OGTT after an overnight fast
Above - normal results for the oral glucose tolerance test*
Fasting
95 or higher
At 1 hour
180 or higher
At 2 hours
155 or higher
At 3 hours
140 or higher
Note: Some labs use other numbers for this test
*Using a drink with 100g of glucose
36
Fetal Effects of Diabetes
1.
Perinatal death
2.
Preterm delivery - ↑ 2-3x
3.
Congenital anomalies - ↑ 3x
4.
Birth injury due to macrosomia
5.
Metabolic impairment - hypoglycemia and hypocalcemia
6.
Cardiomyopathy
Maternal Effects of Diabetes
1.
Preeclempsia - ↑ 4x
2.
Difficult delivery
3.
Bacterial infection
4.
Hydramnios
MULTIFETAL PREGNANCY
Factors race, heredity, age > 35, parity > 4, maternal size and nutrition,
use of ovulating drugs (clomiphene, gonadotropins)
Types:
Double ovum with 2 chorions, 2 amnions, 2 placentas
Double ovum with 2 chorions, 2 amnions but 1 placenta
Single ovum with 2 chorions, 1 amnion, 1 placenta
Single ovum with 1 chorion, amnion, and placenta
Maternal Complications:
1.
Greater discomfort and difficulty in locomotion
2.
↑ severity of nausea/vomiting and anemia
3.
↑ risk for previa, abruption placenta, malpresentation, postpartum
hemorrhage, PIH, pre-term labor
Fetal complications
1.
IUGR
2.
Anomalous anastomotic vascular connections → “twin-twin transfusion” → discordant twins with the larger twin the larger twin developing hydramnios and polycythemia and the smaller twin oligohydramnios and anemia
3.
Intertwining of umbilical cords
4.
Consumptive coagulopathy following death of a twin
5.
Collision (both twins in cephalic presentation) and interlocking (chin
to chin lock)
PRETERM LABOR
Preterm - <37 weeks AOG but > 20 weeks AOG
Premature - infants born before term and who have suffered subnormal
growth in utero
Low birth weight
1.
LBW - <2,500 grams
2.
Very LBW - <1,500 grams
37
3.
Extremely LBW - <1,000 grams
Ü Average birth weight for Filipinos: 2,275 grams
Ü Survival feasible at 26-27 weeks AOG
Causes of Preterm Birth:
1.
Medical and Obstetrical Complications (placental hemorrhage, hypertensive disorders, multifetal pregnancy)
2.
Lifestyle factors (smoking, poor nutrition, drugs)
3.
Amniotic fluid infection, chorioamnionitis
4.
Bacterial vaginosis, Chlamydia, Candida vaginitis
5.
Genetics factors: preterm delivery is a condition that runs in the
family
Management
* Patient education; restriction of physical and sexual activity
* Bed rest, hydration and sedation
* Correction of infection if present
* Repair of Incompetent cervix
* Tocolytic agents: greatest benefit if given 32-34 weeks AOG
1.
β adrenergic agonists - Ritodrine and Terbutaline
Side Effects: maternal tachycardia, hypotension, pulmonary edema
2.
Magnesium sulfate - MOA: Calcium antagonist
Side Effects: pulmonary edema and respiratory depression
3.
Prostaglandin inhibitors - Indomethacin, Aspirin, Naproxen
Side Effects: closure of the ductus arteriosus, necrotizing enterocolitis and intracranial hemorrhage
4.
Calcium channel blockers - Nifedipine
Side Effects: may cause maternal hypotension
***when given with MgSO4, can enhance the Mg toxicity → neuromuscular blockade causing pulmonary and cardiac compromise
5.
Atosiban - MOA: competitive oxytocin
6.
Nitrous Oxide drugs - Nitroglycerine
A potent endogenous smooth muscle relaxant in blood vessels, GUT and uterus
POSTTERM PREGNANCIES
* Prolonged: 42 completed weeks (295 days) AOG
* ACOG: A pregnancy lasting > 2 weeks beyond EDD
* Post Mature: Used to describe the infant with recognizable clinical
features indicating a pathologically prolonged pregnancy
* Maternal risks: operative deliveries: postpartum hemorrhage and
infection, failed induction of labor, prolonged labor with cephalopelvic disproportion and pregnancy hypertension
* Fetal and neonatal risks: antepartum and intrapartum stillbirths;
IUGR; fetal distress and hypoxia; meconium aspiration; shoulder
dystocia and birth injuries due to macrosomia; specific congenital
malformations: anencephaly and adrenal hypoplasia
38
* 3 stages of Postmaturity:
1. The amniotic fluid is clear
2. The skin is stained green
3. The skin discoloration is yellow–green
Management
1.
Assessment of true gestational age
2.
Patient counselling regarding induction of labor vs. conservative
management
3.
Antepartum surveillance tests conducted twice weekly: fetal movement counting, non-stress test, contraction stress test, fetal acoustic stimulation test, biophysical profile scoring and NST + AFI
Precautions regarding possible difficult deliveries in post term:
1.
Fetal estimated weight >4.5 kg
2.
Prolonged 1st stage especially at the arrest of dilatation
3.
Prolonged 2nd stage with marked caput and molding
URINARY TRACT INFECTIONS IN PREGNANCY
Asymptomatic Bacteriuria in Pregnancy
Diagnosis
* > 100,000 cfu/ml with 1 or more organisms in 2 consecutive midstream specimens or 1 catheterized specimen
* Screening should be done on 1st prenatal visit, especially for diabetics and those with previous history of UTI
* Test of choice: urine culture, clean catch midstream
* Urinalysis alone is not recommended
Treatment: Antibiotics for 7 days with following-up culture after 1 week
Antibiotics Used In Pregnancy
Safe
With Caution
Contraindicated
Amoxicillin
Nitofurantonin
Cephalosporins
Co-amoxyclav
Ampicillin-Sulbactam
Azutreonam
Aminogylcoside
TMP/SMX
(1st and 2nd trimester)
Tetracycline Fluoroquinolone TMP/
SMX (3rd trimester)
Acute Cystitis in Pregnancy
Diagnosis
* Urinary frequency, dysuria and bacteriuria
* Pyuria of > 8 pus cells/mm3 (uncentrifugated) or > 5 pus cells/hpf
(centrifugated) OR (+) leukocyte esterase and nitrate test
Treatment: 7 day antibiotics, see above table
39
Acute Pyelonephritis in Pregnancy
Diagnosis:
* Chills, fever, flank pain, nausea and vomiting with or without signs
of lower UTI, CVA tenderness
* Pyuria (> 5 wbc/hpf centrifugated urine) and bacteriuria (> 10,000
cfu of a uropathogen/ml)
* Gram stain, urine C&S, blood cultures
Treatment:
* Admit. Immediate antibiotic therapy for a duration of 14 days
DYSTOCIA
Difficult labor: Most common indication for Primary CS
DYSTOCIA DUE TO ABNORMALITIES OF POWER
I. Disorder of Preparatory Division of Labor
Prolonged Latent Phase
Nulliparas - latent phase duration of > 20 hours
Multiparas - latent phase duration of > 14 hours
II. Disorders of Dilatation Division of Labor
Protracted Active Phase of Dilatation
Nulliparas - max. slope of dilatation of <1.2 cm/hr
Multiparas - max. slope of dilatation of <1.5 cm/hr
III. Disorders of Pelvic Division of Labor
Prolonged Deceleration Phase
Nulliparas - deceleration phase duration of > 3 hours
Multiparas - deceleration phase duration of > 1 hour
2º Arrest of Dilatation - cessation of active phase progression for 2
hours or more
Arrest of Descent - cessation of descent progression > 1 hour
Failure of Descent - lack of expected descent during deceleration
phase and second stage
IV. Precipitate Labor Disorders
Precipitate Dilatation
Nulliparas - max. slope of dilatation of >5 cm/hr
Multiparas - max. slope of dilatation of > 10 cm/hr
Precipitate Descent
Nulliparas - maximum slope of descent of > 5 cm/hr
Multiparas - maximum slope of descent of > 5 cm/hr
DYSTOCIA DUE TO ABNORMALITIES OF THE FETUS
I. Different Presentations
* Breech, face, transverse lie, compound, persistent occiput posterior, deep transvers arrest, shoulder
40
II. Fetal Developmental Abnormalities
√ Macrosomia: > 4000 grams possibly due to DM, multiparity, large
parents/genetic or postdatism
√ Hydrocephalus: consider cephalocentesis and CS delivery
√ Large Abdomen: for transabdominal decompression
√ Conjoined twins
DYSTOCIA DUE TO ABNORMALITIES OF THE PELVIS
Bony Dystocia: Contracted inlet, midpelvis, outlet
Soft Tissue Dystocia: uterine myomas or prolapse, cervical stenosis,
transverse septum of vagina, cystocoele, rectocoele
ACOG Classification of Forcep’s Delivery
Procedure
Outlet Forceps
Characteristics
1.
Scalp is visible at the introitus without separating the labia
2.
Fetal skull has reached the pelvic floor
3.
Sagittal is in the antero-posterior diameter or
right or LOA or posterior position
4.
Fetal head is at or on perineum
5.
Rotation does not reach 45º
Low Forceps
Leading portion of the fetal skull is at station +2 or
below and not on the pelvic floor
Mid Forceps
Station above +2 but head engaged
High Forceps
Not included in this classification
Elective Forceps
Generally, outlet forceps with general anes
Used for academic training purpose
Prerequisites
1.
Head must be engaged
2.
Fully dilated cervix
3.
Known position of vertex
4. Ruptured membranes
5. No CPD
6. Vertex/Mentum anterior
41
INSTRUMENTAL VAGINAL DELIVERY
Obstetric Forceps
* Composed of a blade, shank, lock and handle
* Types: Simpson forceps, Barton (for transverse arrest), Piper (for
after coming head in breech)
* Maternal Indications: heart disease pulmonary edema, maternal
exhaustion, some intrapartum infections, neurologic conditions,
prolonged 2nd stage of labor, effect of anesthesia
* Fetal indications: cord prolapse, abruption, worrisome FHR
CESAREAN SECTION
* Delivery of a fetus through an abdominal incision (laparotomy)
followed by incision of the uterine wall (hysterotomy)
Indications:
Repeat cesarean, Multiple pregnancies, CPD, post-term pregnancy, breech in a primigravid, fetal distress, uterine dysfunctions, cord
complications, uncontrolled hypertension, malpresentation, hemorrhagic complications (Placenta previa/abruption placenta)
Technique of Cesarean Section
A. Types of Abdominal Incision
1. Median Infraumbilical Longitudinal Incision
2. Transverse Suprapubic (Pfannenstiel/Bikini) Incision
* more difficult but it is stronger and with less dehiscence
B. Types of Uterine Incision
1. Classical Cesarean Section
* longitudinal incision above the lower tendency to rupture
* rarely done - strong tendency to rupture
2. Low Segmental Incision
* preferred method due to low tendency to rupture
A. Low Transverse (Kerr Incision)
- preferred method due to only moderate dissection of the bladder
however, offers little space for extension
- ↓ blood loss and adhesions,, faster and easier to repair
B. Low Longitudinal Incision (Kronig Technique)
- more bladder dissection but can be extended
VAGINAL BIRTH AFTER A CAESAREAN SECTION (VBAC)
* Allow a trial of labor under double set-up for all previous Cesareans of one low segment incision after excluding an inadequate pelvis and unless a new indication arises
42
ABNORMAL UTERINE BLEEDING
Normal Uterine Bleeding
* Mean interval between menses: 28 days ( + 7 days)
* Mean duration of menstrual flow: 4 days
Oligomenorrhea - infrequent uterine bleeding with intervals from 35 days
to 6 months
Amenorrhea - no menses for at least 6 months
Menorrhagia - prolonged (> 7 days) or excessive (80 ml) uterine bleeding
occurring at regular intervals
Metrorrhagia - uterine bleeding occurring at irregular but frequent intervals, the amount being variable
Menometrorrhagia - prolonged and irregular uterine bleeding
Intermenstrual bleeding - bleeding of variable amounts occurring between
regular menstrual periods
Etiology of Bleeding
A.
Organic (ovulatory cycles in reproductive age group)
1.
Systemic - coagulation defects, hypothyroidism, cirrhosis
2.
Reproductive Tract Disease - abortion, GTD, malignancies, infection, myomas, polyps, foreign bodies
B. Dysfunctional (in extremes of ages)
1.
Anovulatory
* Alterations in neuroendocrinologic function
* Continuous estradiol production without corpus luteum formation
and progesterone production leading to a continuously proliferating
endometrium and ↓ prostaglandin (PGF 2) vasoconstrictor
2.
Ovulatory
* Common after adolescence or before perimenopause
Management
Medical Management:
1.
Estrogens - for rapid endometrial growth
2.
Progestins - does not stop an acute episode but instead produces
a normal bleeding episode after estrogen is withdrawn; 10 mg OD
for 10d each month
3.
NSAIDS– prostaglandin synthetase inhibitors
4.
Antifibrinolytic agents – Tranexamic acid (AMCA)
5.
Androgenic Steroids (Danazol) - 200-400 mg/d x 12 weeks
6.
GnRH agonists
Surgical Management: D and C, Ablation, Hysterectomy
AMENORRHEA
Physiologic - during pregnancy and postpartum
Pathologic - produced by endocrinologic and anatomic d/o
Primary Amenorrhea - Amenorrhea indicates a failure of the hypothalamicpituitary-gonadal axis. It is primary if menarche has not occurred by
age 16 years.
43
Causes of Primary Amenorrhea
1.
Turner –XO
2.
Testicular Feminization - XY
3.
Mulerian dysgenesis - absence of tubes, uterus, cervix, upper vagina
4.
Stein– Leventhal (polycystic ovaries) - infertility, hirsutism, endometrial hyperplasia; high LH, androgens, estrogens; low or normal
FSH
5.
Kallman syndrome - anosmia; lack of GnRH
6.
Imperforate Hymen - monthly abdominal pain but no menses
Classification (1º Amenorrhea with normal woman external genitalia)
I. Absent breast development; uterus present
A. Gonadak failure - 45X (Turner syndrome); 46X, abnormal X;
Mosaicism; Pure gonadal dysgenesis; 17 α-hydroxylase deficiency
with 46 XX
B. Hypothalamic failure secondary to inadequate GnRH release Neurotransmitter defect, Kallman syndrome, congenital CNS defect
or neoplasm
C. Pituitary failure
II. Breast development; uterus absent
A. Androgen resistance (testicular feminization)
B. COngenoital absence of uterus
III. Absent breast development; uterus absent
A. 17, 20 desmolase deficiency
B. Agonadism
C. 17 α-hydroxylase deficiency with 46 XY karyotype
IV. Breast development; uterus present
A. Hypothalamic etiology
B. Pituitary etiology
C. Ovarian etiology
D. Uterine etiology
Presumptions:
* Breast present means estrogen is being produced
* Uterus present means Y chromosome is not present
Diagnosis:
* FSH and LH levels to check HPO function; Testosterone, Prolcatin and TSH levels; Karyotyping, Progesterone Challenge Test;
Gonadal Biopsy
Secondary Amenorrhea - No menses for 3 or more months
In women who menstruated previously. You must rule out pregnancy (MC cause of 2º amenorrhea).
Chronic anovulation is the 2nd MC cause: get progesterone challenge test
Causes of Secondary Amenorrhea
1.
Stress/ Exercise - leads to reduced GnRH levels
2.
Anorexia Nervosa - leads to reduced GnRH levels
3.
Post-pill - should last not longer than 6 months
4.
Drugs - Antipsychotics, Tricyclic antidepressants, benzodiazepines,
reserpine
44
5.
Sheehan’s Syndrome - low FSH and LH; postpartum pituitary necrosis
6.
Pituitary Neoplasms - increased prolactin
Asherman syndrome - post-traumatic/post-curettage intrauterine adhesions
Simmond syndrome - pituitary hemorrhage not related to pregnancy
PROGESTERONE CHALLENGE TEST
A.
Positive if bleeding occurs
- Patient is anovulatory (no corpus luteum, no secretory transformation of endometrium)
B.
Negative if no bleeding within 2 weeks
- determine FSH levels; get CT scan of sella turcica
ENDOMETRIOSIS
* Presence and growth of endometrial glands and stroma in an
aberrant or heterotropic location i.e.: outside the uterus
Etiology
1.
Retrograde menstruation
5. Immunologic defect
2.
Coelomic metaplasia
6. Genetic predisposition
3.
Activation of embryonic nests
4.
Iatrogenic dissemination
Common Sites
* Ovaries, pelvic peritoneum, uterine ligaments, cervix, sigmoid,
appendix, pelvic nodes, vagina, fallopian tubes
Signs and Symptoms
* Classic Symptom - cyclic pelvic pain (2º dysmenorrhea/
dyspareunia), infertility, abnormal bleeding
* Classic Sign - fixed retroverted uterus with scarring and tenderness posterior to the uterus; nodularity of the uterosacral ligaments
and cul-de-sac of Douglas or rectovaginal examination
Management
* Medical therapy - to create a state of pseudopregnancy or pseudomenopause e.g. Danazol, GnRH agonists, Oral contraceptives
* Surgical therapy - indicated for acute rupture of endometriomas,
ureteral/bowel obstruction, ovarian endometriomas > 2 cm or adnexal enlargments > 8 cm
 Laparoscopy
 Conservative surgery - removal of all macroscopic, visible
areas with preservation of ovaries
 Definitive surgery - TAHBSO; of far-advanced and no desire
for future fertility
ADENOMYOSIS
* Growth of endometrial glands and stroma in the uterine myometrium at a depth of at least 2.5 mm from the basalis layer of the endometrium
45
DISORDERS OF PELVIC SUPPORT
URETHROCOELE AND CYSTOCOELE
* Descent of the urethra (urethrocoele), bladder neck, bladder
(cystocoele) into vaginal canal due to rupture or attenuation of the
pubovesicle fascia
* Signs and symptoms: sensation of fullness/pressure; feeling of
organs falling out; stress incontinence; urgency, incomplete voiding; soft, bulging, non-tender mass of the anterior vaginal wall
which may be manually reducible
* Diagnosis: patient in lithotomy position is asked to strain
* Differential Diagnosis: Inflamed Skene’s glands (tender and purulent), urethral diverticula (sensation of a mass), Bladder tumors
* Treatment:
Non-operative - Pessaries (Smith-Hodge or Inflatable), Kegel exercises (isometric contractions of the pubococcygeus muscle), estrogen cream
Operative - Anterior wall repair (colporrhaphy) usually in conjuncttion with a posterior wall repair
RECTOCOELE
* Heaviness; feeling of “falling out” in the vagina with constipation
or incomplete emptying of rectal vault
* Tx: Non-operative - same as urethrocoele
Operative - Posterior colporrhaphy with perineorraphy (for
weakness of the perineal body)
ENTEROCOELE
* Due to a weakened support of the Pouch of Douglas (uterosacral
and cardinal ligaments) as in post abdominal or vaginal hysterectomy
* Seen as separate bulge above rectocoele which on transillumination shows small bowel shadows in the sac
* Tx: reduced transabdominally as a 1º procedure
UTERINE PROLAPSE
* Due to injury to endopelvic fascia, cardinal and uterosacral ligaments and pelvic floor (levator ani muscles)
* Due to ↑ pressure/tension on pelvic musculature such as in
chronic constipation, tumors, chronic respiratory disease (asthma,
COPD), multiparity, old age, sacral nerve disorders (diabetic neuropathy, S1-S4 injuries)
* Classification
A. 1st degree - prolapse into the upper barrel of the vagina
B. 2nd degree - prolapse thru vaginal barrel into introitus
C. 3rd degree or Total - prolapse out through the introitus which
predisposes to dryness and thickening of vaginal epithelium and
stasis ulcers
* S/Sx: perineal heaviness or fullness or sensation of mass with
symptoms of cystocoele and rectocoele
46
* Treatment:
Non-operative (for minutes prolapse) - pessaries, estrogen
Operative - vaginal hysterectomy with anterior and posterior repair
with a perineorrhaphy to reinforce the introitus
UROGYNECOLOGY
Innervation of Bladder and Urethra
Continence
Bladder
Micturition
Sympathetic (NE)
Relaxation → prevents
micturition
Sphincter
Sympathetic (NE) Contraction → prevents mic-
Parasympathetic (ACh)
Relaxation → prevents
micturition
Parasympathetic (ACh)
Risk factors for incontinence
1.
Immobility
10. Cognitive
2.
Medication Use
11. History of fecal impaction
3.
Smoking
12. History of low fluid intake
4.
Delirium
13. DM, Obesity
5.
Racial status
14. Stroke
6.
Pregnancy
15. Hypoestrogen state
7.
Childhood nocturnal eneuresis
8.
High impact activities
9.
Pelvic muscle weakness
Diagnostic procedures
1.
Urinalysis and culture - especially for chronic infections
2.
Test for residual urine - catheterization within 10-15 minutes of
voiding; residual urine should be < 50 cc
3.
Office cystometrics - sterile saline given through a urinary catheter
measures volume that causes urge to void (150-200 ml) and functional capacity (400-500 ml) while maintaining incontinence
4.
Stress (Bonney Test) - instill 250 cc sterile saline and ask patient to
cough
 If urine spurts out immediately → stress incontinence
 If urine spurts out after a delay → detrusor instability
5.
Urethroscopy - for visualization of urethra
6.
Cystoscopy and Cystometry - best used for diagnosis of detrusor
hyperactivity
47
TYPES OF INCOTINENCE
1.
Genuine Stress Incontinence
 Urine loss due to sphincter incompetence without demonstrable contraction of bladder detrusor muscles
 Urine loss with ↑ intra-abdominal pressure (coughing, sneezing, laughing, lifting)
 Loss of PUV angle (Normally <120º)
 Able to stop stream when voiding
 Incontinence disappears during the night
2.
Detrusor dyssynergia/irritabilty/instability
 Involuntary contraction of the bladder during distension with
urine or other fluids
 Chronic with an urgency-frequency problem, painless urine
loss, inability to stop their stream and nocturia
 Urge incontinence - involuntary loss of urine associated with a
sudden and strong urge to void
 Detrusor hyperreflexia - if a neurologic disorder is present
(Stroke, Parkinson’s or other CNS pathology)
 Diagnosis: electronic urethrocystometry
 Treatment: bladder retraining; anti-cholinergic or beta– adrenergic stimulation/drugs (propantheline, Oxybutinin, Imipramine,
Ephedrine)
3.
True incontinence
 Loss of urine without abnormal bladder function due to fistulas
or other damage to the urinary tract
4.
Overflow incontinence
 Neurologic disorder or partial obstruction of the urethra → inability to empty (residual urine) → overdistended bladder → overflow
INFECTIONS OF THE GENITAL TRACT
INFECTIONS OF THE VULVA
A.
Infection of Bartholin’s gland: obstruction of ducts at 5 and 7 o’clock
position complicated by abscess formation
B.
Pediculosis pubis and scabies
C.
Molluscum contagiosum: “water wart” caused by poxvirus
D.
Condyloma accuminata
 Most common viral STD due to HPV
 Premalignant serotypes: 16, 18, 31, 45
 Treatment: 10% Podophylline, TCA, 5– FU, Cautery
E.
Genital ulcers: see next page
48
CLINICAL FEATURES OF GENITAL ULCERS
Syphillis
Incubation 2-4 weeks
Herpes
2-7 days 1-14 days 3 days—6
weeks
Vesicle
Usually
Chancroid Lymphgran- Donovanosis
uloma Venereum
Papule or
pustule
1-4 weeks
(up to 6
mos)
Papule, pus- Pustule
tule or vesicle
Multiple Usually
may
multiple,
coalesoe may coalesce
Usually one
Variable
1-2 mm
2-20 mm
2-10 mm
Variable
Edge
Sharp, ele- EryUndervated
themato mined,
round/oval us
ragged,
irregular
Elevated,
round or
oval
Elevated,
irregular
Depth
Superficial
or deep
Superficial
Base
Smooth,
nonpurulent
Serous
Purulent
erythemato
us
Variable
Red and
rough
(“beefy”)
Firm
None
Soft
Occ. Firm
Firm
Unusual
Common
Very tender
Variable
Uncommon
Firm,
tender,
often
bilateral
Tender,
may suppurate,
usually
unilateral
Tender, may Pseudoadesuppurate,
nopathy
usually unilateral
Diameter
Pain
Lymphade- Firm, nonnopathy
tender,
bilateral
Excavated Superficial
or deep
49
Elevated
VAGINITIS: Appearance of Vaginal Discharge
Candidiasis or
Monillasis
Trichomonas
vaginalis
pH
< 4.5
> 5.0
> 5.0
Vaginal Discharge
Curdlike, floccular, viacious
and adheres to
anterior and
lateral vagina
Thin, foamy,
profuse, yellow
-gray and foul
smelling
Homogenous,
gray, rotten fish
odor after adding 10% KOH
(Whiff test)
Vaginal epithe- Severe pruritus
lium and cervix and burning
sensation, redness, excoriation
Small punctuate, red areas,
Strawberry
cervix
Diagnosis
KOH smear
Yeast cells and
pseudohyphae
Wet: flagellated Wet smear:
orgs; (+) Whiff clue cells; (+)
test
Whiff test
Treatment
Miconazole,
Metronidazole
TMP-SMX, Nys-
Metronidazole
Normal vaginal discharge should be white, floccular, odorless with pH of
3.8-4.2
PELVIC INFLAMMATORY DISEASE
* May include infection of any or all of the following: endometrium
(endometritis), oviducts (salpingitis), ovary (oophoritis), uterine wall
(myometritis), uterine serosa and broad ligament (parametritis) and
the pelvic peritoneum
* Organisms ascending from the vagina and cervix during menses;
usually polymicrobial (N. gonorrhea, C. trachomatis, endogenous
aerobic and anaerobic bacteria)
* Risk Factors: teenager with multiple sex partners, use of IUD
(OCP) decreases the risk due to progestins which thickens the
cervical mucus making it impenetrable to organism)
* Gold Standard - Laparoscopy
50
* Pathophysiology
99 % ascending infection from vagina and cervix → spread through
mucosal surface → colonize endometrium and fallopian tubes →
may extend to ovaries → inflammation
(may produce suppuration) → tuboovarian abscess
Different Diagnosis - ectopic pregnancy, torsion of adnexal mass,
ruptured ovarian cyst
CDC Guidelines For Diagnosis of Acute PID
Minimum Criteria
Empiric treatment of PID should be instituted based on the presence
of all of the following three minimum clinical criteria:
Lower abdominal tenderness
Adnexal tenderness
Cervical motion tenderness
Routine Criteria for Diagnosing PID
Oral Temperature > 38.3º C
Abnormal cervical or vaginal discharge
Elevated ESR and C-reactive protein
Lab evidence: N. Gonorrhea or C. trachomatis
Elaborate Criteria for Diagnosing PID
Histopathologic evidence of endometritis on biopsy
Tuboovarian abscess on sonography or radiologic tests
Laparoscopic abnormalities consistent with PID
Salphingitis: most characteristic
Fitz Hugh-Curtis Syndrome: perihepatic inflammation develops from transperitoneal or vascular dissemination with “ violin string” adhesions to the
parietal peritoneum beneath the diaphragm
CERVICITIS
* Endocervitis - N. gonorrhea and C. trachomatis
* Ectocervitis - Trichomonas vaginalis
* Mucopurulent cervicitis
Criteria: visualization of yellow mucopurulent material; PMNs > 10 on
endocervial smears; erythema and edema in area of cervical ectopy
and/or bleeding 2º to endocervical ulceration
Treatment for Gonorrhea: Ceftriaxone 125 mg/IM single dose or Cefixime 400 mg/PO single dose or Ofloxacin 400 mg/PO single dose +
Doxycycline 100 mg/PO BID x 6 days if with C. trachomatis
51
BENIGN GYNECOLOGIC LESIONS
BREAST
Breast cancer is the most common CA in women.
Fibrocystic change is very common and benign
Fibrocystic Change
* Often bilateral, multiple nodules, menstrual variation, may regress
during pregnancy
* Does not increase risk of breast cancer but makes detection more
difficult
Breast Cancer
* Often unilateral, single mass, no cyclic variations
Perhaps
Benign
PE: Discrete, smooth, movanle, tender
Perhaps
Malignant
PE: Ill-defines, non-movable, edema
Mammography: round, ovoid, smooth, clearly defined margins, may contain calcifications
Mammography: distinct, irregular tumor mass, projection of
dense spicules, may contain calcifications
VULVA
Cysts
* MC large cyst: Bartholin’s duct obstruction
* MC small cyst: Epidermal inclusion cyst or Sebaceous cyst
(located right beneath the epidermis on the anterior half of the labia
majora, non-tender and slow growing)
* Most require treatment with heat or I and D, only if infected
Hemangioma
* Malformations of blood vessels discovered in childhood
Types:
1.
Cavernous/Strawberry
3. Angiokeratoma
2.
Cherry/Senile
4. Pyogenic granuloma
Fibroma
* Most common benign solid tumor of the vulva
Vulvodynia
* “Itch-Scratch Cycle” → Chronic discomfort: burning and rawness
52
VAGINA
Urethral diverticulum
* Epithelialized saclike projection from the posterior urethra I reproductive females in their 40’s with chronic UTI
* 3 D’s: dysuria, dyspareunia, dribbling
* Treatment: Excision or Marsupialization
Inclusion cyst
* Most common
* Usually in posterior or lateral walls of lower third of vagina
CERVIX
Polyp
* Most common in multiparous women (40-50’s y.o.)
* Endocervix –pedunculated, smooth, reddish-purple to cherry red,
fragile, 2 º to inflammation or hormonal stimulation
* Ectocervix - grayish-white with a short broad base usually in post
menopausal women
* Classic symptom - intermenstrual bleeding especially after contact
Treatment: grasp base of polyp and avulse with a twisting motion,
cauterize if with bleeding and send for histopathology
Stenosis
* May be congenital or acquired (operation such as cautery or biopsy, infection, neoplasia, atrophy, radiation)
* Premenopausal Symptoms: dysmenorrhea, abnormal bleeding,
amenorrhea, infertility
* Postmenopausal Symptoms: asymptomatic for a long time before
developing hematometra, hydrometra, or pyometra
* Treatment: dilation with dilators or luminaria (fungus that absorbs
water like a sponge and expands acting as a dilator)
Nabothian cysts
* Translucent or opaque-white retention cysts occurring where a
tunnel of cleft was covered by squamous metaplasia
* Considered normal feature of adult cervix; no treatment
UTERUS
Polyp
* Localized overgrowths of endometrial glands and stroma
* Soft and pliable; 40-50 years; mostly associated with endometrial
hyperplasia due to unopposed estrogen
* Most are asymptomatic but when symptomatic appear as pre
menstrual and postmenstrual staining or spotting
* Removed by curettage or via hysteroscopy
53
Hematomera
* Distention with blood due to obstruction of any part of the lower genital tract most common causes are:
Congenital - imperforate hymen, transverse vaginal septum
Acquired - cervical stenosis, senile atrophy, synechiae
* Diagnosis: amenorrhea with cyclic abdominal pain
* Treatment: operative relief of obstruction
Leimyoma
* Also called myomas, fibromayomas, fibroids
* Most frequent pelvic tumors
* Types:
1. Subserous - just beneath the serosa of the uterus
2. Intramural
3. Submucous - just beneath endometrium; most troublesome;
causes AUB
4. Parasitic - outgrows its uterine blood supply and obtains 2º blood
supply form another organ like the perineum
5. Broad ligament - growth of myoma into the broad ligament which
may cause hydroureter and be difficult to differentiate from a solid
ovarian tumor
* Pathogenesis: somatic mutation of normal myometrium influence
by estrogen, progesterone and growth factors
* Grossly, lighter in color than normal myometrium; on cut surface,
has a glistening , pearl-white appearance with smooth muscle in
trabeculated or whorled pattern
* *With continued growth, degeneration occurs because the tumors
outgrows its blood supply
Extent of degeneration: hyaline (mildest), myxomatous, calcific,
cystic, fatty, or red degeneration
* Red or Carneous infarction - most acute degeneration occurs
during pregnancy
* Most are asymptomatic but most common complaint is acquired
dysmenorrhea with abnormal uterine bleeding
* Pelvic pressure/pain felt as myoma enlarges
* Leimyosarcoma - suspected with rapid growth of a myoma after
menopause
* Different dx: pregnancy, adenomyosis, ovarian CA
* Indications of Myomectomy
Rapidly enlarging mass, persistent abn. Bleeding, pain or pressure,
enlargement of an asymptomatic myoma to > 8 cm in a woman
who hasn’t completed childbearing
* Contraindication to a Myomectomy:
Pregnancy, advanced adnexal disease, malignancy, if myomectomy will result in a severe reduction of endometrial surface
* Indications for hysterectomy:
Uterine size reaching 12-14 week size, and again rapid growth of
myoma after menopause
* Medical treatment r-GnRH agonists, medroxyprogesterone acetate (DepoProvera), danazol, antiprogesterone RU 486
54
OVARY
I. FUNCTIONAL CYSTS
A.
Follicular Cysts
 Most frequent cystic structure in normal ovary ~ 2.5-3 cm
 Most common in young menstruating women
 Usually asymptomatic, discovered on routine imaging
 Treatment: conservative observation as majority disappear spontaneously due to reabsorption/silent rupture in 4-8 weeks
B.
Corpus luteum Cysts
 Corpora lutea with a minimum diameter of 3 cm
 Hemorrhagic corpus luteum - 2 to 4 days after ovulation, thin-
C.
walled capillaries invade granulose cells which may cause spontaneous bleeding (if excessive, may cause rupture)
 Triad: delayed menses and followed by spotting, unilateral pelvic
pain, and a small tender adnexal mass
 Different diagnosis if ruptured: ectopic pregnancy, ruptured endometrioma, ovarian torsion
Theca Lutein Cysts
 Almost always bilateral with moderate to massive enlargement
due to excessive gonadotropin stimulation or sensitivity
Assisted with molar pregnancies and hypothyroidism
 Treatment is conservative because they regress spontaneously
II. BENIGN NEOPLASMS OF THE OVARY
A.
Benign Cystic Teratoma (dermoid cyst, mature teratoma)
 Most common slow-growing ovarian tumor usually in prepubertal and teenage girls
 Contains elements from all 3 germ layers (i.e. skin, hair, teeth ,
GI and respiratory epithelium, sebaceous fluid)
55
 Solid elements are in a protrusion or nipple in the cyst wall
termed prominence or tubercle of Rokitansky
 50-60% are asymptomatic, discovered on routine exam
 Symptoms: pain, dysmenorrhea, pelvic pressure
 Complications: torsion (most frequent), rupture (most serious
due to chemical peritonitis), infection, hemorrhage and malignant
degeneration (immature teratoma)
 3 associated medical diseases: Thyrotoxicosis, Carcinoid syndrome, Autoimmune hemolytic anemia
 Kustner’s sign - dermoid floats upward in the abdomen, elongating the ovarian pedicle and causing them to lie anterior and superior to the uterus, in contrast to other ovarian tumors which are found
posterior to the uterus
 Struma ovarii - teratoma in which thyroid tissue has overgrown
other elements
 Treatment: Pelvic Lap with Frozen section, Cystectomy
B.
Endometriomas
 Associated with endometriosis
 Usually hemorrhagic appearing as chocolate cysts
 Ovaries are tender and immobile secondary to inflammation and
adhesions, only 5% with ovarian enlargement
 Medical therapy rarely successful while surgical therapy is complicated by formation of de novo and recurrent adhesions
C.
Fibroma
 Most common benign, solid ovarian tumor
 Extremely slow-growing, usually postmenopausal
 Meig’s syndrome– association of fibroma with ascites and hydrothorax which resolve after removal of tumor
 Ascites due to transudation of fluid from the fibroma while hydrothorax is due to flow of ascetic fluid into the pleura space
 Treatment: excision
D.
Brenner Tumors
 Rare, small, smooth, solid, fibroepithelial ovarian tumors that
are generally asymptomatic in women aged 40-60
 Treatment: excision
E. Adenofibroma and Cystadenofibroma
 Benign, firm, rare solid variants of serous cystadenomas
 Treatment: bilateral salphingo-oophorectomy and total abdominal hysterectomy because they occur in post-menopausal
women
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MALIGNANT GYNECOLOGIC LESIONS
BENIGN vs. MALIGNANT LESIONS
Benign
Malignant
Occurrence
Unilateral
Bilateral
Consistency
Cystic
Solid
Surface
Smooth
Irregular
Mobility
Mobile
Fixed
Weight Loss, Ascites, Absent
Color Flow
Present
CERVICAL INTRAEPITHELIAL NEOPLASIA
* Premalignant changes in the cervical epithelium usually in the
squamo-columnar junction that can progress to cervical carcinoma
* The change from mild to severe is described as CIN I to III dependent on extent of dysplasia
Potential Risk Factors For Cervical Neoplasm
Epidemiologic Characteristics
1.
Early intercourse
5. Early Childbearing
2.
Multiple sex partners
6. STD infevtion, HIV
3.
Early marriage
7. Prostitution
4.
Socioeconomic status, race 8. male factors
Other Potential Factors
1.
Oral contraceptives
4. Prior radiation
2.
Cigarrete smoking
5. DES exposure
3.
Vitamin A,C,E and folate
6. Lupus erythematous
Viral Relations
Papillomavirus, Herpes virus, Cytomegalovirus
Diagnosis:
1.
Cytology
 Papanicalaou smear (PAP smear) - samples taken from endocervix, ectocervix and lateral vaginal wall
2.
Biopsy/ Colposcopy
 Colposcopically directed biopsy and endocervical curettage
 Abnormal colposcopic findings:
P– punctuation/red stipping
A– acetowhite epithelium
L- Lleukoplakia
M– mosaic pattern of sharp-bordered lesions
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Treatment:
1. Ablative therapy-eryotherapy, laser therapy, cautery
2. Excisional therapy
A. Conization– cold-knife, laser, LEEP (loop electrosurgical
excision procedure)
B. Hysterectomy
TRADITIONAL CLASSIFICATION vs (MODIFIED)
BETHESDA CLASSIFICATIO OF PAP SMEAR
Bethesda Classification (Modified)
A. Benign Cellular Changes
1.
Infections - Trichomonas, Candida
2.
Reactive Changes - Inflmmation, atrophic vaginitis
B. Epithelial Cell Abnormalities
1.
Atypical squamous cells of undetermined significance (borderline
between severe reactive change and mild dysplasia)
2.
Low-grade intraepithelial lesions - HPV, CIN 1
3.
High-grade intraepithelial lesions - CIN 2 and 3, CA in situ
4.
Squamous cell CA
A pap smear is a medical procedure in which a sample of cells
from a woman’s cervix is collected and spread on a microscope slide. The
cells are examined under a microscope in order to look for pre-malignant
or malignant changes
DEGREE’S OF DYSPLASIA/CERVICAL NEOPLASIA
Low Grade Squamous
Intraepithelial Lesion
High Grade Squamous
Intraepithelial Lesion
Koilocytosis
CIN I
CIN II
Perinuclear
cavitation and
nuclear atypicality, associated with Papillo-
Mild Dysplasia
abnormal cells
up to 1/3 of
basal epithelium
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CIN III
Moderate dys- Severe Dysplaplasia abnormal sia abnormal
cells up to 2/3 cells involving
of basal epithe- full thickness
lium
CERVICAL CARCINOMA
Major Categories of Cervical Carcinoma
Squamous Cell Carcinoma (85-90%)
Small Cell
Verrucous
Large cell (keratinizing or non-keratinizing)
Adenocarcinoma (10-15%)
Typical (endocervical)
Clear cell
Endometriod
Adenoma malignum
Adenoid cystic
(basaloid cylindroma)
Mixed Carcinomas
Adenosquamous
Glassy cell
Natural History and Spread
* Presents with abnormal bleeding or brownish discharge noted
after douching or intercourse and between menses
* Exophytic growth - cauliflower-like extruding from the cervix usually producing bleeding
* Endophytic- initially asymptomatic; deeply invasive
* “Barrel-shaped appearance” of adenoCA starts at the endocervix
then fills the cervix and lower uterine segment
* Spreads locally then to primary pelvic nodes (pericervical, hypogastric and external iliac nodes)
CLINICAL STAGES OF CERVICAL CANCER
Cervical CA is the only gynecologic malignancy staged clinically, the rest
are staged surgically.
Stage I
Carcinoma limited to cervix
Stage II
Involvement of upper 2/3 vagina or involvement of parametria
Stage III
Involvement of lower 1/3 vagina or involvement of pelvic sidewall
Stage IV
Involvement of bladder or rectum or distant
metastases
Treatment
* Stage I: Total Abdominal Hysterectomy (TAH)
* Stage II: Radical Hysterectomy with BLND
Cervical CA in pregnancy
* < 20 weeks - immediate treatment
* > 20 weeks - delayed treatment until fetal viability
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ENDOMETRIAL HYPERPLASIA
Classification of Endometrial Hyperplasia
Traditional
World Health Organization
Cystic hyperplasia
Adenomatous hyperplasia
Atypical adenomatous
Architectural atypia (mild,
moderate, severe)
Cytologic atypia (mild, moderate, severe)
Simple hyperplasia
Complex hyperplasia
(adenomatous hyperplasia without cytologic atypia)
Atypical hyperplasia
(adenomatous hyperplasia with
cytologic atypia)
Treatment
1.
In young women without atypia → D and C
2.
Progrestin (Provera) 10 mg daily for 10 days
3.
Estrogen-Progestin combinations (oral contraceptives)
ENDOMETRIAL CARCINOMA
* Most common malignancy of the genital tract
* Most affecting perimenopausal/postmenopausal years
* Most frequent symptom: abnormal uterine bleeding
Risk Factors:
1.
Unopposed estrogen stimulation; Nulliparity (2-3x)
2.
Use of estrogen replacement tx (4-8x)
3.
Menopause after 52 years (2.4x)
4.
Obesity (3-10x); Diabetes (2.8x)
5.
Feminizing ovarian tumors; PCOS
6.
Tamoxifen therapy for breast cancer (>2 years)
CLASSIFICATION OF ENDOMETRIAL CANCER
Stage I
Limited to endometrium
Stage II
Involves endocervical glands or stroma
Stage III
Invades serosa or involves vagina or pelvic and/or paraaortic
lymph nodes
Stage IV
Involves rectum or bladder or distant mets
60
OVARIAN CARCINOMA
* 2nd MC (endometrial > ovarian > cervix)
* Highest mortality because of late detection
* Increased risk of breast and endometrial CA
* Cystic adnexal mass in menstruating ovary < 8 cm: functional
* Postmenopausal ovary atrophies to 1.5-2 cm
Risk Factors:
1.
Family history of CA
4. Infertility
2.
Nulliparity
5. Diet rich in animal fats
3.
Late child bearing
6. Late menopause
Ultrasound Findings that Correlate with Malignancy
* Septations and loculations
* Solid lesions or cystic lesions with solid components
* Internal papillations - echogenic structures protruding into mass
* Smaller cyst adjacent to or part of the wall of larger cysts
Color Flow Doppler
* Low resistance = malignancy
* High resistance = normal or benign
SASSONE CRITERIA IN DIAGNOSIS OF OVARIAN MALIGNANCY
Inner Wall
Thickness
Wall Thickness
Septa (mm)
Echogenicity
1
Smooth
Thin < 3 mm
No septa
Sonoluscent
2
Irregular < 3
mm
Thick > 3 mm
< 3 mm
Low
3
Papillaries > 3
mm
Mostly solid
> 3 mm
Low; echogenic core
4
Mostly solid
Mixed
5
High
TUMOR MARKERS
1.
CA-125: Epithelial Ovarian Tumors
2.
Serum LDH: Dysgerminoma
3.
Alpha-Feto Protein: Endodermal Sinus Tumor
4.
hCG: Choriocarcinoma
61
STAGING OF OVARIAN CA (2nd MC Malignancy)
Stage I
Confined to 1 or 2 ovaries
Stage II
Pelvic spread
Stage III
Intra-abdominal spread
Stage IV
Distant spread
VULVAR CARCINOMA
* Most common squamous cell CA, women > 60 y/o
* Spread: femoral-inguinal nodes = deep pelvic, iliac and obturator
Staging of Vulvar Carcinoma
Stage
Characteristics
0
CA in situ/intra-epithelial carcinoma
I
< 2 cm and confined to the vulva and/or perineum
II
> 2 cm and confined to the vulva and/or perineum
III
Extends to the anus, vagina, and/or lower urethra, and/or
unilateral inguinal lymph node metastases
IV
Spreads to the bladder or rectum or pelvic bone or upper
urethra or non vulvar sites, or bilateral node metastases
MENOPAUSE
*Complete or permanent cessation of menstruation indicated by the
final menstrual period, often during the climacteric
* Interval of 6 to 12 months of amenorrhea
* Usual age: 45 to 55 years
* Follicles become less sensitive to gonadotropins
* Estrogen decreases
* LH and FSH increase (up to 20 fold)
* Vaginal bleeding due to unopposed estrogen normal for up to 12
months
* If vaginal bleeding continues > 12 months: rule out endometrial
pathology
Climacteric
* Phase of the aging process of women during which they make the
transition from reproductive to the non reproductive stage
* Period declining ovarian function, clinically apparent over 2 to 5
years around menopause
Premature Menopause - menopause at 40 years or less
62
Ovarian Changes
* Depletion of primordial follicles - irregular ovulation failure of progesterone - follicle activity completely ceases - lack of estrogen
with total cessation of menstrual function - atrophic ovaries
Endocrine Changes
* Several years before menopause there is
1. Gradual increase in FSH
2. Concomitant decrease in estradiol
3. No significant change in LH
4. Slight decrease in progesterone
* Increase resistance of remaining follicles to gonadotropins plus
smaller ovaries - ↓ estrogen
Effects of Reduced Estrogen
1.
Brain - hot flushes, depression, sleep disturbances, inability to concentrate, memory lapses
2.
Heart and vessel - coronary heart disease, arteriosclerosis
3.
Bone - mineral mass, fractures
4.
Skin - thinning, slow healing
5.
Vagina - vaginal atrophy, atrophic vaginitis
Treatment
1.
Estrogen
2.
Increase Calcium intake
3.
Weight bearing exercises
Estrogen Replacement Therapy
Advantages
Relief of menopausal symptoms

Eliminates hot flushes

Prevents atrophic vagina
Prevention of cardiovascular disease

decreases LDL; increases HDL
Prevention of osteoporosis
Disadvantages
Slightly increased cancer risk

endometrial CA: 4-8 fold

Breast CA
Increased risk of thrombosis
May cause cholestasis
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INFERTILITY
* Inability of couples of reproductive age to establish a pregnancy
after 1 year of unprotected intercourse
* Primary– woman has never been pregnant
* Secondary - occurs after one or more pregnancies
Fecundability - probability of conception occurring in a population of couples in a given period of time, usually 1 month
Hypofertile - those with low fecundability who are eventually able to conceive without treatment
Sterile - those who never without therapy
Causes of Infertility
1.
Anovulation
- Abn. androgen, gonadotropin, prolactin, secretion
- Dx: basal body temperature and progesterone level
- Tx: Clomiphene, hMG, pure follicle stimulating hormone, GnRh,
bromocriptine (if due to hyperprolactinemia), corticosteroids (if due
to adrenal hyperplasia)
2.
Male Factor
- Semen Analysis
- at least 2-3 specimens, examined within 2 to 4 hours
- collected after at least 3 or 4 days of abstinence from ejaculation but preferably after 4 to 6 days
A. Volume normally 2.5 to 5 ml, alkaline pH, viscid
B. Liquefaction - complete within 10-30 minutes
C. Motility - at least 50% active motile sperm at 4 hours
D. Cell count - 20 to 150 million per ml
- Oligospermia - less than 20 million per ml
- Azospermia - zero sperm; i.e. Klinefelter
E. Cell Morphology - 60– to 80% sperm heads with normal morphology
3.
Uterine Factor
- Adhesions, leiomyoma, tuberculosis
4.
Tubal Factor
- Salpingitis, adhesions, congenital
Dx: Hysterosalphingography and Laparoscopy
5.
Cervical Factor
- Diagnosis:
Post-coital Cervical Mucus Test - normal: 5-20 motile sperm/hpf at
2 to 6 hours after coitus
Sperm Hamster Ova Penetration Assay - normal: 10% of hamster
eggs are penetrated
6. Endometriosis
- Oviduct adhesions interfere with normal motility
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POLYCYSTIC OVARIAN DISEASE
* Characterized by enlarged ovaries with multiple small cysts, an
abnormally high number of follicles at various states of maturation,
and a thick, scarred capsule surrounding each ovary.
Causes, incidence, and risk factors
* An endocrine disorder, which means normal hormone cycles are
interrupted.
* Under-developed follicles accumulate in the ovaries,
Follicles are sacs within the ovaries that contain eggs. The eggs in
these follicles do not mature and, therefore, cannot be released
from the ovaries
* Insulin resistance also seems to be a key feature in polycystic
ovarian syndrome
* Women are usually diagnosed when in their 20s or 30s
* Many women with polycystic ovary disease have irregular periods
and may have very little menstruation (oligomenorrhea) or no period at all
Symptoms
* Abnormal, irregular, or scanty (very light or infrequent) menstrual
periods
* Absent periods, usually (but not always) after having one or more
normal menstrual periods during puberty (secondary amenorrhea)
* Weight gain, even obesity
* Insulin resistance and diabetes
* Infertility
* Increased hair growth; distribution of body hair may be in a male
pattern
* Virilization– development of male sex characteristics in a female.
This may include an increase in body hair, facial hair, a deepening
of the voice, male-pattern baldness, and clitoral enlargement.
* Decreased breast size
* Aggravation of acne
65
Signs and Tests
* FSH levels– low or normal
* LH levels - generally high
* Androgen (testosterone) levels - high
* Estrogen (primarily estrone and estradiol) levels - relatively high
* Urine 17-ketosteroids - possibly high
* Vaginal ultrasound and, possibly, abdominal UTZ
* Laparoscopy
* Ovarian biopsy
* Other blood tests that may be done include:
Serum HCG (pregnancy test) negative
Thyroid functional tests
Prolactin levels
Treatment
Weight loss, Birth control pills, spironolactone, flutamide, and clomiphene citrate; Metformin or one of the thiazolidione medications, such as
piogitiazone or rosiglitazone.
Complications
√ Sterility
√ Obesity-related conditions
√ High blood pressure and diabetes
√ Increased the risk of endometrial cancer - this is because the endometrium (lining of the uterine wall that sheds when you menstruate) can get thicker and thicker (hyperplasia) due to the lack of
ovulation
√ Possible increased risk of breast cancer
INTRAUTERINE GROWTH RESTRICTION
* Normal Fetal Growth - characterized by sequential patterns of tissue and growth, differentiation and maturation
* Fetal growth rates: 5g/day—15 weeks
15-20g/day - 24 weeks
30-35 g/day – 34 weeks
100-200 g/week in the 3rd trimester
* IUGR (Runting) - small for gestational age:
* infants with wts below the 10th percentile for AOG
* increased risk for neonatal death
* incidence 3-10%
* chronic placental insufficiency → 1/3 low birth wt infants
Type I (Symmetric IUGR)
* Insult early in gestation with equal decrease in HC, wt and length
such as in chromosomal anomalies
* ↑ morbidity, lower BW, late catch-up
66
Type II
* Insult of later onset such as maternal disease
* Presents with characteristic “sparing of the head”
Metabolic Anomalies
* Fetal Hypoxia
* Hypertriglyceridemia
* Thrombocytopenia
* Elevated adenosine concentrations
Risk Factors:
1.
Constitutionally small mothers
2.
Social deprivation - smoking, alcohol, drugs
3.
Poor maternal weight gain and nutrition
4.
Fetal infections
5.
Congenital malformations
6.
Primary disorders of cartilage and bone - osteogenesis imperfecta
and chondrodystrophies
7.
Chemical teratogens
8.
Chronic renal disease and chronic hypoxia
9.
Maternal anemia - sickle cell/inherited anemias
10.
Placental and cord abnormalities
11.
Multiple fetuses, Extrauterine pregnancy
12.
Anti-phospholipid Antibody Syndrome
* Screening of IUGR: Uterine fundal height, ultrasonic measurement and
Doppler velocimetry
* Management - Growth restriction near term:
- Prompt delivery: best outcome for the fetus near term
- Presence of oligohydramnios and > 34 weeks → deliver
- If FHR is reassuring: vaginal delivery
- (+) fetal compromise: cesarean section
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