Hi-yield Notes in Ob-gyne
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HI-YIELD FACTS IN OBSTETRICS [from USMLE CLERKSHIP-OB & handy notes] GENERALITIES Keyterms Ovulation /postconception Gravida Parity Puerperium Perinatal period Neonatal period Embryonic period Previable period Viable period Preterm Term Post-term Low birth weight Very low birth weight Extremely low birthweight Puerperium
It is 2 wks < gestational age Woman who is, or has been pregnant irrespective of the outcome Number of pregnancies reaching viability 6-8 wks period after delivery Commences at 22 completed wks of gestation & ends 7 completed days after birth From birth to 28 days after birth 3rd wk to 7th wk after fertilization, when major structures are formed Lasts from 11-20 AOG Lasts from 21-40 AOG Less than 37 completed wks From 37-42 completed wks 42 completed wks or more Less than 2500 gms Less than 1500 gms Less than 1000 gms Time after delivery of placenta up to return of reproductive organs to their normal non-pregnant state [usually occur at 6-8 wks]
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Chapter 3: Physiology of Normal Mensrual cycle Menstruation Average thelarche = 10 y/o [↑ estradiol], estradiol], pubarche = 11 y/ o [↑ adrenal hormones], hormones], menarche = 12 y/o [↑ estradiol] estradiol ] Causes of precocious puberty and manifestations: Idiopathic – Idiopathic – MC cause Thelarche/pubarche/menarche Thelarche/pubarche/menarche Tumors of hypothalamic-pituitary stalk Thelarche/pubarche/menarche Thelarche/pubarche/menarche Inflammation of the hypothalamus Thelarche/pubarche/menarche Thelarche/pubarche/menarche 21-hydroxylase deficiency Pubarche Excess estrogen Thelarche and menarche
PHYSIOLOGIC OBSTETRICS Chapter 2: Anatomy of F emale Reproductive Tract Functional components: Placental arm Paracrine arm Nutritive, endocrine, Pregnancy maintenance, immunologic acceptance, immunologic AFV & hemostasis, hemostasis, physical protection of fetus fetus
Communication system: Placental arm Maternal blood to placental intervillous s pace, fetal blood confined to capillaries
Embryology Paramesonephric Paramesonephric or mullerian ducts
Paracrine arm Chroion leave, maternal deciduas parietalis, amnion
Urogenital sinus Mesonephric system or wolffian duct Germinal epithelium
Forms uterine tubes [cranial], uterus [caudal], and upper part of vagina Forms lower part of vagina & vestibule Forms the epoophoron & paroophorron Forms the ovary
6 openings of vestibule: o Urethra, vagina, bartholin’s ducts [2], paraurethral/ skenes ducts [2] Vagina: o pH = 4-5 o blood supply: Upper 1/3 Cervicovaginal branch of uterine A. Middle 1/3 Inferior vesical A. Lower 1/3 Middle rectal and internal puddendal A. o
lymphatics: Upper 1/3 Middle 1/3 Lower 1/3 & vulva
Oviducts:
Average menses menses = 3-6 days Blood loss in menstruation averages 30-50 ml, should not form clots. > 80 ml is abnormal amount of blood loss. Phases of menstrual cycle: st o Menstruation: days 1-4 [1 part of follicular phase] o Follicular phase [proliferative phase]: days 1-14 o Ovulation; day 14 o Luteal phase: days 14-28 Main events of menstruation: absence of progesterone causes endometrial sloughing. 2 main events in follicular phase: o FSH causes follicle maturation and estrogen secretion. o Estrogen causes endometrial proliferation. Main event of ovulation: o LH surge causes oocyte to be released. Main events of luteal phase: corpus luteum secretes progesterone w/c causes endometrial maturation [↓FSH, ↓LH].
Chapter 4: Endometrium and Decidua Endometrial cycle and histology: Early proliferative Glands are tubular and short, nuclei are basally located w/ phase abundant mitotic figures Late proliferative Glands become tortuous w/ cells lining the gland undergoing phase pseudostratification Early secretory Glycogen-rich subnuclear vacuoles appear at base of cells Mid-late secretory Endometrium rich in glycogen, decidualization of stromal cells Premenstrual Intense coiling of spiral arteries w/ PMN infiltration of stroma
Sex-steroid hormone induced proliferation: Pre-ovulatory or follicular phase Estradiol 17-β 17-β is secreted by follicles Post-ovulatory or follicular phase Progesterone secreted by corpus luteum, at 7-8 days after ovulation progest + estrogen declines Proliferative phase Estrogen is the predominant hormone, ↑ PTH rp, vasodilatation occurs Late ssecretory phase + menses Progesterone withdrawal + TGF-β TGF- β, increase endothelin-1, vasoconstriction occurs
Iliac nodes Internal iliac nodes Inguinal nodes
Perineum: o Blood supply: internal pudendal and its branches [inferior rectal + posterior labial A.] o Innervation: pudendal nerve o Muscles: Pelvic diaphragm Levator ani and coccygeus muscles Urogenital diaphragm Deep transverse perineal, constrictor urethrae, internal and external fascial coverings Perineal body: body: on w/c converge the bulbocavernosus M., superficial transverse perineal M., and external anal sphincter Uterus: o Wall: endometrium, myometrium and serosa o Lymphatics: hypogastric nodes [cervix], internal iliac, nodes to ovarian region and periaortic nodes [body] o Ligaments: Uterosacral lig. O superior part of cervix encircling the rectum, insert over S2-3 Cardinal lig. Aka: transverse cerviacal lig. Or Mackenrodt lig. United firmly to the supravaginal wall of cervix Round lig. Continuous w/ broad lig. to inguinal canal terminatinng at upper part of labium majus, holds the ovary in pl ace
Parts [from uterus to lateral wall]: interstitial part, isthmus, ampulla, fimbrial end / infundibulum]
3 portions of deciduas Decidua basalis Decidua capsularis Decidua parietalis
Directly beneath site of blastocyst implantation Overlies the enlarging blastocyst & is most prominent during 2nd month of pregnancy Joins decidua capsularis at 14-16 wks of pregnancy
Blood supply of endometrium: Basal 1/3 Straight arteries Superficial 1/3 Coiled or spiral arteries
Important facts At 6 days post-fertilization, post-fertilization, blastocyst establishes cell to cell contact contact w/ endometrium. Restoration of epithelial surface of endometrium is complete by 5 days of endometrial cycle. Subnuclear vacuolization is the 1st histologic indication of progesterone effect. Decidua is the source of prolactin in amniotic fluid. Nitabuch’s layer is where invading trophoblast meet the decidua, a zone of fibrinoid degeneration.
Chapter 5: Placenta and Fetal membranes Structures: Amnion Tough and tenacious tenacious bu pliable membrane, membrane, innermost vascular fetal membrane, contiguous w/ amniotic fluid. Amnion layer continuos w/ chorion leave is the acellular zona spongiosa. The amnion develops about 7th-8th day of blastocysts development. It has no muscles, nerves, lymphatics, and is avascular. It also provides all the tensile strength of fetal membranes.
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Umbilical cord
Amniotic fluid
30-100 cm [ave. [ave. 55] 55] length, w/ 2 arteries and 1 vein, vein, 0.8-2.0 cm in diameter, average of 55 cm. Exracellular matrix of umbilical cord is composed of specialized specialized tissue [Wharton’s jelly]. Average vol: 1,000 1,000 cc at term, 400 cc at at midpregnancy, 50 cc at 12 wks
Important facts Zona pellucida disappears prior to implantation & blastocyst adheres to endometrial surface [apposition]. Leafy chorion/chorion frondosum [fetal part] while chorion leave/bald chorion contains the ghost villi. As emdryo grows further, the decidua capsularis capsularis & parietalis form the decidua decidua Vera. The impetus for implantation invasion is provided by trophoblasts. Human placenta is of hemochorioendothelial type. Mainstem villi & its ramififications constitute a placental cotyledon. Chorionic villi can be seen in human placenta by 12th day post-fertilization. MC vascular anomaly in humans is absence of 1 umbilical Artery.
10th wk 3rd lunar month 4th lunar month 24 or more wks 24-26 wks 28 wks
Spontaneous Spontaneous movement noted Histological evidence of taste buds Complete finger closure Ability o suck Fetus hears sounds in uterus Eye sensitive to light, responsive to vibrations in taste
Chapter 6: Placental hormones Important facts ANP is produced in atrial myocytes & is synthesized synthesized in placenta. It causes natriuresis, natriuresis, diuresis and vasorelaxation of uterus during pregnancy. Inhibin acts to inhibit FSH release by the pituitary. Highest carbohydrate content of any human hormone is in HCG [pregnancy hormone]. A glycoprotein produced by syncitiotrophoblasts. It is secreted maximally at 8-10 wks AOG. It also acts to rescue or maintain corpus luteum to promote continued estrogen stimulation. T ½ of HCG is 24 hrs while LH is 2 hrs. GH releasing hormaone is also known as somatocrinin. DHEAS is the principal circulating precursor of placental estrone & estradiol. Adrenal cortex is the largest organ in fetus, fetus, a principal source of estrogen precursors. precursors. The primary placental estrogen that enters maternal compartment is estradiol. Pregnanediol Pregnanediol is the principal urinary metabolite of progesterone. Maternal plasma LDL cholesterol is the principal precursor of progesterone biosynthesis in placenta. 5 alpha-reduction of progesterone is the major pathway of progesterone metabolism. Major role of relaxin is r emodeling of CT of reproductive tract allowing pregnancy accommodation & successful parturition.
Respiratory system Glycerophospholipid composition of mature surfactant: i. Phosphatidylcholine = 78% ii. Phosphatidylglycerol = 9% Hormone regulation of surfactant: Cortisol Natural stimulus for augmented surfactant synthesis Prolactin Accelerate rate of synthesis of phosphatidylcholine by lungs Estrogen Promote prolactin release Thyroxine Accelerate fetal lung maturation EGF Promote surfactant secretion and increase SP-A [major apoprotein surfactant]
Urinary system Fetal kidneys star producing urine by 12 wks Metanephros Metanephros is the definitive urinary system. Lecithin is principal surface active c omponent of surfactant. Phospholipid is the primary surface tension-lowering component of surfactant. Surface apoproteins serves to facilitate serve to facilitate forming & reforming of surface film in alveoli during respiration. Cortisol is the natural stimlus for augmented surfactant surfactant synthesis. Urine production = 10 ml/hr at 30 wks, 27 ml/hr at term Amniotic fluid volume: volume: - Term fetus is able to swallow as much as 450 ml/24 hrs of amniotic fluid - At 16-18 wks, fetal urine becomes an important important source of amniotic fluid 12 wks 50 ml Midpregnancy 400 ml 36-38 wks 1000 ml
Chapter 7: Morphological and Functional development of f etus Most frequently used diameters of fetal head: Occipitofrontal 11.5 cm From root of nose to occipital bone Biparietal 9.5 cm Greatest transverse diameter of the head Bitemporal 8.0 cm Greatest distance btw 2 temporal sutures Occipitomental 12.5 cm Greatest diameter of fetal head Suboccipitobregmatic Suboccipitobregmatic 9.5 cm From large fontanelle to occipital bone
Plane of occipitofrontal diameter: 34.5 cm [greatest head circumference] Plane of suboccipitobregmatic: 32 cm [smallest head circumference]
Respiration Respiratory movements are seen at 4 mos. Endocrine system Neurohypophysis secretes oxytocin & AVP by 10-12 wks. Gonads Fetal testis secretes testosterone and pregnenolone by 10 wks. Genetic sex is established at time of fertilization Sexual development of male and female embryo is identical up to 8 wks. Maleness: testosterone and MIF, its absence i n Femaleness
Chapter 8: Maternal adaptations to pregnancy Cardiovascular system Heart is displaced upwards and outwards due to gravid uterus Maximal increase in heart rate during 7-8 th mos. w/ average of 10 bpm CO peaks during 25 th-32nd wks [highest at 28 th wks] = 30-40% 4 periods of increased CO: 1. on 28 wks AOG [highest peak] 2. during labor 3. immediately postpartum 4. 1st wk of puerperium ↑ Plasma volume [50-60%] [50-60%] w/c peaks by 7 mos. → dilutional anemia ↑ Pulse pressure maximum on the 7-8 7 -8th mos. ↓ DBP [note that presence of diastolic murmur in pregnancy is never normal] Elevated venous pressure in lower extremities Respiratory system Upward displacement of diaphragm by 4 cm ↑ in RR, TV, respiratory minute volume, and airway conductance ↓ FRC, RV, TPR, and broncho-motor broncho -motor tone [progesterone effect] Lung compliance is unaffected Gastrointestinal system Px may have GERD/heartburn [progesterone effect] Decreased responsiveness to CCK Liver of pregnancy – pregnancy – swelling swelling of kuppfer cells Urinary system Kidneys hypertrophy due to ↑ renal blood flow Physiologic hydroureter evident at 1st trimester Estrogen stimulates hypertrophy and elongation of muscles whil e progesterone promotes generalized atony Prone to UTI due to progesterone and pressure changes Endocrine system ↑ corpus luteum activity up to 12 wks Mild hyperthyroid state due to gland hyperplasia
Cardiovascular system Remnants of the following will become: Umbilical vein Ligamentum teres Umbilical artery Medial umbilical ligament Urachus Median umbilical ligament Tongue remnant [thyroid] Foramen cecum Vitelline duct Meckel’s diverticulum Ductus venosus Ligamentum venosum Ductus arteriosus [closes at 10-96 hrs] Ligamentum arteriosus Foramen ovale [closes after several mins] Anatomical fusion at 1 yr. Fetal coagulation factors ↓ factors 2,6,9,10,11,12,13 2,6, 9,10,11,12,13,, fibrinogen & plasminogen, ↑ thrombin, thrombin , normal platelet count
Immunocompetence Immunocompetence of fetus 13 wks: fetus is immunologically competent IgG Transported btw mother to fetus at 16 wks IgM Produced by fetus in response o infections, adult levels at 9 mos. B lymphocytes Appear in liver at 9 wks, in blood and spleen at 12 12 wks T lymphocytes Produced by thymus at 14 wks
Gastrointestinal tract Glucagon identified by 8 wks, insulin detectable by 12 wks Fetal pancreas noted at 9-10 wks Swallowing begins at 10-12 wks Peristalsis a 11 wks AOG
Nervous system and sensory organs 8th wk Flexion of fetal neck and trunk
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Pituitary gland hypertrophy and hyperplasia Diabetogenic due to placental degradation of insulin and insulin effects of placental lactogen, estrogen, and progeterone Increase oxytocin production near term Placenta HCG is detected in maternal plasma or urine by 8-9 days after ovulation, reaches nadir at 100-130 days, peaks at 60-70 days hPl detected as early as 2 nd-3rd wk after fertilization, rises steadily at 34-36th wks of pregnancy progesterone synthesis is accomplished by syncitiotrophoblasts after 6-8 wks of pregnancy Hematologic system ↑ retic count and RC volume due to erythroid hyperplasia ↓ Hct due o increase plasma volume Total iron requirement = 1 gm or 6-7 mg/day [RDA] 300 mg Fetus and placenta 200 mg Excreted 500 mg Erythrocyte production
Fetal blood hematopoiesis Mesoblastic In yolk sac during embryonic period Hepatic Liver up to near term Myeloid BM starts at 4 mos. fetal age, major site in adults Skeletal system Progressive lordosis Increased mobility of pelvis joints Immunologic system Immuosupressive mechanism by progesterone, estrogen and HCG Production of suppressor T cells and AFP by fetus Maternal metabolism Weight gain: at least 25 lbs weight gain 1st trimester 2 lbs 2nd trimester 11 lbs 3rd trimester 11 lbs
Carbohydrate metabolism – pregnancy is diabetogenic due to: o hPl has anti-insulin effect o estrogen, progesterone and cortisol induce insulin resistance o placenta secretes insulinase w/c cause insulin degeneration Protein metabolism th o + nitrogen balance at 29 wks Fat metabolism – lipemia occurs
Acid-base balance Pregnant women normally hyperventilate to reduce arterial PCO2 Partial renal compensation: increase HCO3 secretion
Chapter 9: Diagnosis of pregnancy Presumptive Nausea with or w/o vomiting [due to increased HCG levels] Sx Urinary disturbances Fatigue [due to increased metabolism] Perception of fetal movement [quickening] = 18- 20 th wks AOG [primigravida] and 16-18th wks [multigraviida]. Presumptive Amenorrhea, breast changes [dark areola, erected nipple, signs engorged breast], skin pigmentation [choalasma/mask of pregnancy, striae gravidarum, spider telangiectasia (estrogen effect), linea nigra], changes in vaginal mucosa, thermal signs [↑ temp by 0.3-0.5 for > 3 wks due t o progesterone effect] Probable Abdominal enlargement, changes in skin, shape, and consistency signs of uterus, anatomical cervical changes, Braxton-hicks contractions, ballotment, physical outlining of fetus, (+) preg test Positive Identification of FHT separate from mother, perception of active evidence fetal movement by physician, UTZ or radiologic evidence
NAV occurs in 50% 0f pregnancies, most notably at 6 wks AOG and disappears 6-12 wks later. Braxton-Hicks contraction: painless, irregular contractions at 28th wks. Quickening – awareness of 1 st movement of the baby Ballottement noted at 20 th wks. Anatomical changes in cervix: o Beaded pattern of cervical mucus due to progesterone st o Ferning pattern due to estrogen seen on 1 half of the cycle Fetal heart tones: o Normal FHT = 110-150 bpm th o UTZ by 8 wks th o Stethoscope by 17-19 wk th o Doppler as early as 10-12 wks
Changes in cervical mucus: beading [progesterone], ferning [estrogen] Perception of fetal movement [quickening]: 16-18 wks [multi], 18-20 wks [primi] Different signs of pregnancy: Presumptive Chadwick sign [6 wks] Discoloration of vaginal mucosa Probable Hegars [6-8 wks] Soft compressible isthmus Probable Goodell’s [4-8 wks] Cyanosis and softening of cervix HCG: o Detected in maternal plasma or urine by 8-9 days after ovulation o Peak levels at 60-70 days, Nadir reached at 100-130 days o Urine HCG – preferred method to recognize normal pregnancy [25 mU/ml by 1 wk after LMP] Radiographic evidence of fetal death: o Spalding sign: overlapping of fetal skull bones due to brain liquefaction o Robert’s sign: gas bubble in fetus o Exaggeration of fetal spine curvature Cranial signs of spina bifida on UTZ: o Small BPD o Ventriculomegaly o Frontal bone scalloping [lemon sign] o Abnormal curvature of cerebellum [banana sign] o Effacement/obliteration of c isterna magna Scan dating is useful up to 20 wks AOG when menstrual data is unreliable or conflicts with clinical findings. Ideal weight gain: ST o 1 trimester: 1.5-3 lbs nd rd o 2 and 3 trimester: 0.8 lbs/wk Pregnancy is an anabolic state. The optimal time to screen for glucose intolerance/DM in the pregnant female is at 26 -28 AOG. By midpregnancy, fat is the primary source of maternal energy. Normal pregnancy is a hyperlipemic as well as glucosuric state. Diastolic murmurs in pregnancy are never normal. Chadwick’s sign: bluish discoloration of vagina and cervix due to congestion of pelvic vasculature. Constipation may occur secondary to progesterone, w/c relaxes the intestinal smooth muscle and slows peristalsis. Asymptomatic bacteriuria occurs in 5-8% of pregnant women. OCPs and HRT [combinations of estrogen and progesterone] are the MC cause of melasma or “mask of pregnancy”. TSH, PTH and calcitonin do not cross the placenta. HCG is detectable in maternal serum after implantation has taken place at 8-11 days after conception. Trophoblasts [rophoecoderm] are the precursor cells for the placenta and membranes. Placenta is the primary producer of steroid hormones after 7 weeks AOG. HCG maintains the corpus luteum and stimulates adrenal and placental steroidogenesis. MSAFP peaks btw 10-13 wks AOG then declines thereafter. After 1st trimester, placenta is the major source of ci rculating estradiol. Progesterone concentrations of < 5 ng/ml are diagnostic of fetal death in 1 st trimester. Progesterone concentrations are si gnificantly elevated in: women w/ hydatidiform mole complications of Rh isoimmunization.
ANTEPARTUM Frequency of visits: < 28 wks – every month, 28-36 wks – every 2-3 wks, 36 wks to delivery – once per week until delivery Triple screen: serum AFP, estriol, beta-HCG at 16-18 wks Important hallmarks in prenatal visits: st o Pap smear: 1 visit st o Rh screen – 1 visit st o Gonorrhea and Chlamydia – 1 visit st o 1 sonogram – week 16-18 o Amniocentesis – week 16-18 o Triple screen – week 16-18 o Diabetes screen – week 16-18 o Group B strep culture – week 36. An inaccurate gestational age is the most common reason for an abnormal screen. After Rh sensitization, a Kleihauer-Bettke test is done to determine the amount of fetal RBCs in the maternal circulation. RhoGAM administered to Rh-mothers exposed to fetal blood. Anti-D titers of > 1:16 require amniocentesis and analysis of amniotic fluid bilirubin]. Intrauterine pregnancy seen via vaginal UTZ when beta-HCG > 1,500 Intrauterine pregnancy seen via abdominal UTZ when beta-HCG > 6,000. Anti-D titers of > 1:16 require amniocentesis and analysis of amniotic fluid [bilirubin]. Oligohydramnios [AFI < 5], may suggest possible fetal compromise due to umbilical cord compression. Polyhydramnios [AFI>20] may signify poor control in a diabeti pregnancy or a diabetic pregnancy or a fetal anomaly. The average woman must consume an additional 300 kcal/day beyond baseline needs.
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Vaccines safe in pregnancy: hep B, oral polio, tetanus, yellow fever, dipheria Vaccines unsafe in pregnancy: measles, mumps and rubella Give immune globulin in pregnancy for exposure to: heap A and B, tetanus, chickenpox and rabies.
Chaper 10: Prenatal care Estimation of pregnancy duration st o LMP = count number of days since 1 day of last normal menses o 280 days or 40 wks or 9 ½ calendar months EDC = [1 st day of LMP] + 7 days – 3 mos. + 1 year [ex. LMP= 7/10/93, EDC = 4/17/94] Height of fundus [in cm] = wks AOG [18-32 wks] Fetal weight in gms = 155 x [ fundic ht in cm – n] o n = 12 if sation below i schial spines [engaged], 11 if above the ischial spines [unengaged] o k = 155, constant Fundal height during pregnancy Weeks Fundal height 12 Above pubic symphysis 16 Midpoint btw pubic symphysis and umbilicus 20 At umbilicus 28 6 cm above umbilicus 36 2 cm below xiphoid process 40 4 cm below xiphoid process
Iron
Calcium + phosphorus Zinc Iodine
Magnesium
Leopolds maneuver: LM1 Fundal grip LM2 Umbilical grip LM3 Pawlick’s grip LM4 Pelvic grip
Findings: LM1 LM2 LM3 LM4
Chapter 11: Identification of high-risk pregnancy Maternal age < 18 y.o or nullipara > 30 y.o Maternal height 60 inches or < 153 cm Maternal weight > 20% of standard weight for height Obstetric hx If [+] medical illness Chapter 15: Immunizations during pregnancy Contraindicated vaccines: measles, mumps and varizella-zoster Vaccines given similar o non-pregnant women: rabies, pneumococcal, meningococcal, tetanus, hepa A and B Requested only after 1 st trimester: influenza Given only as post-exposure prophylaxis: hepa A and B, rabies, tetanus, VZV, measles
What fetal pole occupies the fundus? Which side is the back? What fetal part lies above pelvic inlet? Which side is the cephalic prominence?
Irregular nodular [breech] Linear, convex, bony ridge [back] Round, ballotable [unengaged] Cephalic prominence on same side as fetal parts [flexion]
Round [cephalic] Numerous nodulations [small parts] Fixed, knoblike part [engaged] Cephalic prominence on same side as fetal back [extension]
Visit intervals: q 4wks until 28 wks, then q 2-3 wks until 36 wks then weekly thereafter Lab examinations: Time [wks] Assessment Initially [ASAP] CBC, U/A, blood group & Rh type, PAP smear, Hepa B screen] 8-18 wks UTZ, amniocentesis, chorionic villous sampling 15-20 wks MSAFP screening 26-28 wks Screen for GDM if indicated, repeat CBC [esp. Hb and Hct] 28 wks Test D-negative women for antibodies 32-36 wks UTZ, repeat CBC, test for STD 3rd trimester Hepa B screening
Note: Give hepa B Ig & vaccine to infans of HBsAg [+] mothers 50 g OGCT, if > 130 mg/dl in 1 hr then proceed to 3 hr 100 g OGCT Triple screen for Down’s syndrome: ↓AFP, ↑ HCG, ↓ unconjugaed estriol Chapter 14: Ultrasound in pregnancy Abdominal UTZ [full bladder] Full bladder acts as acoustic window, pushing uterus out of pelvis & displacing bowel superiorly Vaginal UTZ [empty bladder] Small amount of urine pushes the uterus posteriorly out of view Indications for 1st trimester UTZ o Establishes uterine pregnancy upon seeing gestational sac [earliest at 5-6 wks] o Detection of fetal life and number of fetuses [FHT by 7 wks AOG] o Evaluates for retrochorionic hemorrhage, incomplete/complete abortion [if > 600 cc] o Early dating of pregnancy using: Gestational sac diameter At 5-6 wks CRL At 12-14 wks [most accurate] BPD, femoral length Onwards
Evaluation of uterus and adnexa Indications for 2nd and 3rd trimester UTZ o Fetal viability, number and presentation rd o Amount of AFV & placental localization [3 cm VFP in 3 trimester is normal] o Fetal age and growth by fetal biometry [CRL, BPD, FL] o Evaluation of fetal amniotic structures [reversal of fetal diastolic blood flow in umbilical artery indicates a severely compromised fetus] o
30 mg/day 60-100 mg for large built, twin fetuses, late pregnancy 200 mg for overly anemic women 15 mg/day for nonpregaant and lactating women 1200 mg/day for nonpregnant, pregnant and lactating women 15 mg/day for pregnant women, 12-19 mg/day for nonpregnant, pregnant and lactating women 175 ug/day for pregnant women 150-200 ug/day for nonpregnant and lactating women Pregnancy = 320 mg/day Nonpregnant = 280 mg/day Lactation = 355 mg/day
Chapter 16: The Pelvis [Passages] Pelvic inlet: o Diameters of inlet: 1. Anteroposterior diameters Diagonal conjugate True or anatomic conjugate Obstetric conjugate 2. Transverse diameter of inlet 3. Posterior sagittal of inlet
12 cm 11 cm 10 cm 13 cm 4 cm
Only APD measured clinically DC – 1.2 cm DC -1.5-2 cm R and L oblique diameters
Plane of greatest diameter: 12.5 cm – anteroposterior diameter Plane of midpelvis: o Landmarks of areas of assessment of midpelvis: 1. prominence of ischial spines 2. convergent pelvic sidewalls 3. shallow concavity of sacrum 4. bi-ischial diameter of outlet: < 8 cm o Diameters of midpelvis: Anteroposterior diameter ? Transverse diameter [bispinous] 10.5 cm Posterior sagittal of midpelvis 4.5 ccm Pelvic outlet: Anteroposterior diameter of outlet Transverse diameter [intertuberous] Posterior sagittal of outlet
9.5-11.5 cm 11 cm 7 cm
Indications for clinical pelvimetry: o Previous injuries or disease affecting the pelvis o Breech for vaginal delivery, VBAC Soft parts of the pelvis: pelvic floor and pelvic diaphragm Forceps delivery is usually indicated in pxs w/ antrophoid pelvis. Different pelvic types: [refer to OB-GYNE handy notes p. 11]
Chapter 18: Parturition 4 phases of parturition: Phase 0 Prelude to parturition or quiescence Phase 1 Preparation to labor
Phase 2 Phase 3
Active labor Recovery period
Time of contractility and uterine unresposiveness, occurs before implantation until 35-38 wks, mediaed by progesterone, cervix remains rigid & unyielding Uterus & cervix undergo anatomic and functional changes, ↑ oxytocin in myometrial cells, dependent on uterotonins or uterotropin, cervix ripens & dilates Active uterine contractions occur, 3 stages of labor occur Uterine contraction & involution to prevent hemorrhage, initiation of lactation and milk ejection for breastfeeding, uterotonins present
Uterotropin vs. uterotonins Uterotropin [ex. gap junctions Acts in myometrium & cervix to produce functional elements to & oxytocin receptors] prepare uterus for effective contraction & cervical softening Uterotonins [ex. oxytocin, Causes smooth muscle contraction
Chapter 13: Nutrition during pregnancy Calories Daily increase of 300 kcal/day Protein Increase to 5-6 gm/day
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prostaglandin, endothelin] INTRAPARTUM Early signs of labor: Lightening or ↓ fundic height due to formation of LUS allowing fetal head to “baby drop” descend & ↓ AFV Bloody show Blood-tinged mucus from vagina, considered a late sign False labor Irregular interval of contractions, shorter duration, and discomfort confined to lower abdomen or groin
Ferguson’s reflex: mechanical stretching of cervi x that enhances uterine contractions Pathologic retraction ring [Bandl ring]: extreme thinning of LUS as in obstructed labor Patterns of cervical dilatation [active phase]: maximum diameter is 10 cm Latent phase More variable, affected by sedation Active phase Starts at 4cm dilatation Acceleration phase Predictive of outcome of labor Phase of maximum slope A good measure of the overall efficiency of the uterus Deceleration phase Reflective of fetopelvic relationship
Chapter 21: Intrapartum assessment 3 types of FHR pattern: Type Characteristics Early deceleration Occurs w/ onset of contraction Late deceleration Occurs after onset of contraction Variable MC type, occurs before, during or deceleration after & even w/o contraction
Progressive dilatation w/ no change in station in woman of low parity may signify fetopelvic disproportion. Pattern of descent: hyperbolic curve 3 functional divisions of labor: Preparatory Affected by sedation & analgesia Dilatational Rapid rate, unaffected by sedation or analgesia Pelvic Commences ww/ deceleration phase of cervical dilatation, cardinal movements of labor take place
1. 2. 3. 4. 5.
WHO principles of partograph [study Friedman’s curve on OB-GYN handy notes p. 20] active phase of labor begins at 4 cm cervical dilatation latent phase of labor should not last longer than 8 hrs rate of cervical dilatation during active phase of l abor & should not be slower than 1 cm/hr 4 hr lag btw slowing of l abor and the need for intervention is unlikely t o compromise he fetus 4 hourly vaginal examinations is recommended
Cardinal movements of labor; Engagement Head enters the brim in transverse biparietal diameter Asynclitism – slight deflection either anteriorly towards symphysis or posteriorly towards promontory Fismanns obliquity [sagittal suture lies anteriorly], Naegeles’ obliquity [sagittal suture lies posteriorly] Descent 1st requisite for normal spontaneous delivery, facilitated by amniotic fluid pressure, fundal pressure, and abdominal muscle contraction Flexion As head meets resistance of birth canal Internal rotation Occiput gradually moves anteriorly towards symphysis Extension Delivery of fetal head occurs External rotation Head undergoes restitution [rotation of head back o its original position] Expulsion
Mechanism of placental extrusion: Schultze mechanism Central type of placental separation Fetal surface of placenta
Abnormalities of the 2nd stage of labor may be either protraction or arrest of descent [fetal head descends < 1 cm/hr in nulliparous and < 2 cm/hr in multiparous] If 30 mins have passed w/o placental extrusion, manual removal of the placenta may be required. Normal blood flow to nonpregnant uterus – 100 cc/min Normal blood loss for normal vaginal delivery – 300 to 500 ml Normal blood loss for normal CS – 800-1000 ml False [+] nitrazine test may be cause by vaginal infections w/ trichomonas vaginalis, blood and semen. A score of > 8 in bishop’s score indicates that the probability of vaginal delivery after labor induction is similar to that after spontaneous labor. Vaginal prostaglandins are inserted for ripening of cervix. Anterior fontanelle: bigger, diamond-shape Posterior fontanelle: smaller, triangle-shape Vaginal delivery is possible only if fetus is mentum anterior. Engagement is measured by palpation of the presenting part of the occiput. Ferguson’s reflex: mechanical sretching or stripping of the cervix The anterior shoulder is the one closest to the s uperior portions of the vagina, while the posterior shoulder is losest to the perineum and anus. Modified ritgen’s maneuver: allows for delivery of fetal head w/ smallest diameter passing thru the introitus and over the perineum. Maneuver’s for placental separation: o Brandt-andrews maneuver: o Crede’s maneuver: manual extraction of placenta [after > 30 mins of not being expelled] MC indication for primary CS: dystocia Montevideo units are calculated by increases in uterine pressure above baseline [8-12 mmHg] multiplied by contraction frequency per 10 minutes. Uterine pressure increases and stages of labor: 1st stage 25-50% mmHg ↑ by 3-5 contractions/10 mins 2nd stage 80-100 mmHg ↑ by 5-6 contractions/10 mins Vaginal exams: VE q 4 hrs in latent phase and q 2 hrs in active phase FHT monitoring: q 30 mins [1 st stage], and q 15 [2 nd stage] Electronic fetal monitoring: q 15 mins [1 st stage], and q 5 mins [2 nd stage] Non-stress test: normally there is acceleration i n FHR of > 15 bpm above baseline for at least 15 secs. o If at least 2 such acceleration occurs in a 20 mins interval, the fetus is deemed healthy and the test is reactive. o A non-reactive test may imply that fetus is acidotic, asleep, or drugs administered to mother. Contraction stress test / Oxytocin Challenge test: measure of the uteroplacental function o Evaluates reaction of heart rate to contractions induced by nipple stimulation or oxytocin administration. o Done when frequency is 3 contractions/10 mins o Interpretation: Positive Consistent & persistent late decelerations of FHT in absence of uterine hypertonus or supine hypertension Negative At least 3 contrations in 10 mins, each lasting 40 secs, without late deceleration Suspicious Inconstant late deceleration Hyperstimulation Uterine contractions occur more frequent than 2 mins or lasting longer than 90 secs or presence of uterine hypertonus Unsatisfactory Frequency of contractions is < 3 per minutes or tracing is poor
Duncan mechanism Peripheral type of separation Dirty maternal surface
Uterine phases of parturition: Phase 1 Prelude to parturition, phase of myometrial smooth muscle unresponsiveness and cervical rigidity Phase 2 Morphological and functional changes in myometrium and cervix occur in preparation of labor Uterine changes: 1. ↑ myometrial oxytocin receptors 2. ↑ gap junctions btw myometrial cells 3. uterine irritability 4. ↑ responsiveness to uterotonics 5. formation of LUS Cervical changes 1. collagen breakdown and rearrangement 2. ↑ hyaluronic acid and ↓ dermatan su lfate Phase 2 Period of uterine contractions w/c causes: 1. cervical dilatation and effacement 2. fetal descent 3. delivery of conceptus Phase 3 Events of puerperium 1. maternal recovery from childbirth 2. maternal contribution to infant survival 3. restoration of fertility
Cause Head compression Uteroplacental insufficiency Cord compression & cessation of umbilical blood flow
5 parameters in BPP [read p. 15 of OB-GYN handy notes]: fetal breathing movements [chest wall], fetal activity [trunk/limb], amniotic fluid index, fetal tone [flexion/extension of lower extremities], reactivity NST] The physiologic basis for using BPP lies i n the fact that coordinated fetal activities require an intact, non-hypoxic CNS. Reactivity and the normal FHR: normal FHR = 110-160 bpm, baseline refers to a heart rate lasting > 10 mins. A fetus < 28 wks GA is neurologically immature and thus is not expected to have a “reactive” FHR. Early decelerations: are normal and due to head compressionduring contractions.
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Late decelerations: are abnormal and due to uteroplacental insufficiency during contractions. The lateral recumbent position [either side] is best for maximizing c ardiac output and uterine blood flow [in supine position, the vena cava and aortic vess els may be compressed by the gravid uterus] Variable decelerations are abnormal and can be mild or severe and are due to compression and sometimes head c ompression. Classification of variable decelerations: Mild variability < 30 secs and depth > 70-80 bpm Moderate variability 30-60 secs and depth < 70-80 bpm Severe variability > 60 secs and depth < 70 bpm Amnioinfusion: infuse normal saline into the uterus thru the intrauterine pressure catheter to alleviate cord compression. Fetal tachycardia: mild = 161-180 bpm, severe > 181 w/c may indicate intrauterine infection, severe fetal hypoxia, CHD, or maternal fever. Beat-to-beat variability: single most important characteristic of the baseline FHR. At < 28 wks GA, the fetus is neurologically immature, thus decreased variability is expected. Long-term variability = 3-6 cycles/min. If an FHR of 160 bpm lasts for > mins, then tachycardia is present. Beat-to-beat variability can be reliably determined only w/ internal FHR monitoring. Prolonged decelerations: isolated decelerations that last 2-10 mins. Short-term variability is thought to be the most important predictor of fetal outcome. If deceleration has occurred w/o recovery after 2 mins, an emergency C-section i s required. Scalp deceleration is done between decelerations to elicit a reactive acceleration and rule out metabolic acidosis. Fetal lung maturity must be confirmed before elective induction at < 39 wks AOG, unless lung maturity can be inferred from other maturity criteria. Candidates for VBAC: 1 or2 prior LTCS, clinically adequate pelvis, no other uterine scars or previous rupture. Contraindications for VBAC: prior classical or T-shaped incision or other transfundal uterine surgery, contracted pelvis, medical/obstetric complication that precludes vaginal delivery. Prerequisites for forceps delivery: a fully dilated cervix, ROM, engaged fetal head, > +2 station, no cephalopelvic disproportion, empty bladder, and vertex presentation. If delivery occurs w/in 1 hour of analgesia, neonatal depression may occur. Prophylactic measures against aspiration include fasting for at least 6 hrs prior to anesthesia and antacid administration before induction.
Chapter 19: Mechanism of labor in Occiput or Vertex presentation Fetal lie - - relation of long axis of fetus to long axis of mother Longitudinal lie [99%] Long axis of fetus parallels to long axis of uterus Transverse lie [< 1%] Lies in transverse to 1 of the oblique diameters of uterus Oblique lie – a variant, unstable
Stages Stage 1
Stage 2
Stage 3
Stage 4
1. 2. 3. 4.
1. 2. 3. 4. 5.
Presentation – part of fetus lying over the inlet o Cephalic [95% of cases]: Type Presenting diameter Vertex/occiput Suboccipitobragmatic = 9.5 cm Sinciput/mliary Occipiofrontal = 12.5 cm Brow Occipitomenal = 13.5 cm Face Submentobregmatic = 9.5 cm
Nullipara 8 hrs
Multipara 5 hrs
50 mins
20 mins
Signs of placental separation: calkin’s sign – uterus becomes globular and firmer sudden gush of blood uterus rises in abdomen as deched placena drops to lower segment & vagina lengthening of umbilical cord & protrudes out of the introitus Indications for CS hysterectomy: arrest hemorrhage from uterine atony lower segment bleeding laceration of major uterine vessel large myoma cervical dysplasia /CIS
Types of lacerations of vagina & perineum: 1st degree Fourchette, perineal skin, vaginal mucosa [not underlying fascia & muscle] 2nd degree Involve fascia & muscle of perineal body but not the anal sphincter 3rd degree From vaginal mucosa, perineal skin, fascia, up to anal sphincter [not rectum] 4th degree Extension up to rectal mucosa [repaire first before the vaginal mucoosa]
Features Cervical effacement & dilatation to full dilatation a. Uterine contractions q 2-3 mins x 40-60 secs b. FHT q 15 mins c. I.E q 2 hrs [ dilatation should be 1-2 cm/hr] d. artificial amniotomy can be done at 4 cm From full dilatation to fetal expulsion Contractions are q 1-2 mins x 90 s ecs Dorsal lithotomy position [to ↑ p elvic diameter] Crowning occurs, fetal head delivery by Ritgen’s maneuver, suctioning and cord care From delivery to placental expulsion Schultze – at central placental part, Duncan – occurs at the periphery & descends sideways Occurs 1 hr after placental delivery, critical to identify postpartum hemorrhage sec. to atony, mg by massage, ice packs, and oxytoxics
Types of incisions; Kronig’s incision Kerr incision Transverse/Pfannenstiel Maylard incision
Vertical incision at LUS Transverse incision at LUS Curvilinear incision Transverse incision w/ the rectus divided
Types of episiotomies: Median type Less painful, easy to repair, heals faster but may extend to rectum if perineal body is short Mediolateral type Used more often
Chapter 22: Analgesia and anesthesia For painless labor o Meperidine: 50-100 mg [Demerol] – readily crosses placenta o Promethazine: 100 mg [Phenergan] o Butorphanol: 1-2 mg – neonatal depression is lesser o Nalbuphine; 15-20 mg, no neonatal depression o Fentanyl: 50-100 ug o Naloxone: reverses respiratory depression Measures important for effective prophylaxis: o Fasting from solids at least 8 hrs and preferably longer before anesthesia o Use of agents to reduce gastric acidity during induction and maintenance of general anesthesia o Skillful tracheal incubation, accompanied by pressure on cricoid cartilage to occlude esophagus [Sellick maneuver] o After intubation and during surgery, passage of NGT to empty stomach of all contents o Awake extubation w/ protective airway reflexes intact o Use of regional techniques when appropriate Regional anesthesia Uterine innervation – pain during 1 st stage of labor generated largely from uterus → pain of uterine contractions thru 11 th-12th thoracic nerves Lower genital tract innervation – pain transmitted thru pudendal nerve w/c posterior surface of sacrospinous ligament as it attaches to the ischial spine I. Local infiltration Lidocaine - most commonly used local anesthetic II. Pudendal block [S2-4] Goal: to block the pudendal nerve distal to its formation by anterior division of S2-S4 but proximal to its terminal branches Maternal complications are uncommon MC used anesthetic is lidocaine Complication: hematoma formation, convulsion, infection III. Paracervical block
Features Occiput [posterior fontanelle] =PF Bregma [anterior fontanelle] =PF Converted to face by extension CS due to ↑ risk of SC injury
Breech [5% of cases] – complication is cord prol apse or entanglement Frank Thighs are flexed on abdomen, legs are extended over anterior breech surface of the body, thus feet of fetus lies cl ose to the head Complete Thighs are flexed on abdomen, legs are flexed on thighs and feet breech presents a level of the buttocks Incomplete 1 or both thighs are extended so that fee and legs are below the breech level of the buttocks o Shoulder or acromion presentation o Compound presentation: prolapse of fetal hand alongside the presenting vertex or breech or foot alongside the head. o
Position – relation of point of direction to 1 of the 4 quadrants or to transverse diameter of maternal pelvis. Points of direction: occiput in cephalic, mentum/chin in face, sacrum in breech, acromion in shoulder [LOT is the most common presentation]. Fetal Attitude [posture/habitus] – relation of fetal parts to 1 another
Chapter 13; Conduct of normal labor and delivery Difference between false and true labor [read p. 21 of OB-GYN handy notes] Duration of the stages of labor in nulliparas and multiparas 3 stages of labor:
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Provides pain relief during 1 st stage of labor Complication: fetal bradycardia IV. Spinal [subarachnoid] block [T8] Low spinal block is popular form of analgesia for forceps or vacuum delivery V: Epidural anesthesia [T10-S5] Complete analgesia for pain of labor & vaginal delivery necessitates block from T10-S5
POSTPARTUM Within 2 weeks, the uterus has descended into the cavity of the true pelvis. When involution is defective, late puerperal hemorrhage may occur. Rugae reappear by 3 rd week. Colostrum can be expressed from the nipple by 2 nd postpartum day and is secreted by breasts for 5 days postpartum. Colostrum is then onverted to mature milk by 4 weeks postpartum. All vitamins except vitamin K are found in human milk. Women w/ extensive pituitary necrosis [Sheehan syndrome], cannot lactate due to absence of prolactin. Episiotomy incision is typically well -healed and asymptomatic by week 3 of the puerperium. Ensure that postpartum woman has voided w/in 4 hrs of delivery. Continue iron until 3 mos. postpartum. After 6 weeks, coitus may be resumed based on pxs desire and comfort.
Outlet contraction: o Interischial tuberous diameter of < 8 cm
Active phase disorders Before diagnosis is made during 1 st stage of labor, both of this criteria should be met: o Latent phase has been completed, w/ cervix dilated 4 cm or more o Uterine contraction pattern of 200 montevideo units or more in 1-10 minute period has been present for 2 hours w/o cervical change Precipitate labor Effects: Maternal effects Fetal effects Uterine rupture, exensive Hypoxia, intracranial trauma, Erblaceration, AFE Duchenne palsy
Nulliparas Multiparas
Chapter 24: Puerperium Urinary retention in the 1 st 24 hrs is due to: 1. edema & congestion of vulva, urethra, bladder trigone 2. edema & reflex spasm of urethral sphincter 3. bladder atony diuresis is greatest from 2 nd to 5th day Types of lochia [discharge from uterus after delivery lasting 4 -8 wks]: Lochia rubra 1st 3-4 d Reddish discharge Lochia serosa Next 3-4 days Paler & pinkish discharge Lochia alba From 10th day Lighter yellow & creamy color
After pains – due to uterne contraction, more intense during breastfeeding Constipation due to pxs inactivity, decrease intraabdominal pressure after delivery & painful perineum Weight loss: normal non-pregnant weight is attained in 6 mos. Average loss of 5 kgs Immediately after delivery Additional loss of 3 kgs Due to diuresis and skin loss
Cervical dilatation 5m/hr or faster Cervical dilatation 10 cm/hr
Chapter 44: Dystocia due to abnormal presentation, position nd development of fetus Face presentation – w/ head hyperextended so occiput is in contact w/ fetal back Brow presentation – the portion of fetal head btw he orbital ri dge and anterior fontanelle presents at the pelvic inlet Transverse lie/shoulder/acromion presentation – long axis of fetus is perpendicular to that of mother Compound presentation – an extremity prolapses alongside the presenting in the pelvis simultaneously Persistent occiput posterior position – may be due to transverse narrowing of the midpelvis Deep transverse arrest of the head – associated w/ platypelloid and android pelvis, caused by hypotonic uterine dysfunction Shoulder dystocia management: McRobert’s ‘exagerrated lithotomy”, involves flexing thigh upon her own abdomen Wood-Corkscrew Progressively rotating the posterior shoulder 180 degrees in maneuver corkscrew fashion Rubin maneuver Fetal shoulders rocked from side to side applying force on m other’s abdomen Hibbard maneuver Pressured is applied to infant’s jaw and neck i n the direction of mothers rectum Zavanelli Cephalic replacement into the pelvis followed by cesarean delivery
Fetal developmental anomalies Fetal macrosomnia – defined as fetal weight > 4,000 gms, possibly due to DM, multiparity, large parents/genetic, or postdatism Hydrocephalus – consider cephalocentesis & CS delivery; prognosis: uterine rupture Large abdomen – for transabdominal decompression Conjoined twins
Postpartum check-up in 4-8 wks, PAPsmear at 6 mos. Other events after delivery: 2 wks Uterus descends into the umbilicus, CO returns to normal 3 wks Entire endometrium is restored 4 wks Uterus regains non-pregnant size 6 wks Complete extrusion of placental site 2-8 wks Dilaed ureters and pelvis return at prepregnant state 6 mos. May approach prepregnant weight 2 wks Coitus may be resumed depending on px desire 6-8 wks Return of menstruation and ovulation
PATHOLOGIC OBSTETRICS Chapter 45: Dystocia, abnormal labor and feto-pelvic disproportion Types of uterine dysfunction: Hypotonic uterine dysfunction Hypertonic uterine dysfunction No basal hypertonus and uterine Incoordinated uterine dysfunction contraction have a normal gradient Either basal tone is elevated or pressure Occurs during active phase of labor gradient is distorted Responds to x w/ oxytocin Occurs during latent phase Usually responds w/ sedation
Estimation of fetal head size [Mueller-Hillis maneuver] o W/ internal examining fingers note the fetal presenting part in relation of the ischial spines [station] while thumb is placed over the symphysis pubis to note the degree of overlapping. Pelvic inlet contraction: o If diagonal conjugate is < 11.5 cm o Borderline if AP diameter of inlet is 10 cm o Severe if AP diameter is < 9 c m Midpelvic contraction: o If sum of interischial spinous diameter [10.5 cm] and posterosagital diameter of midpelvis [5 cm] falls to 13.5 cm and below o Interischial diameters is < 10 cm o Prominent ischial spines, convergent sidewalls, narrow sacrosciatic notch on vaginal exam
Dystocia due to abnormalities of Pelvis Bony dystocia: contracted inlet, outlet and midpelvis [see clinical pelvimetry] Soft tissue dystocia: uterine myomas or prolapse, cervical stenosis, transverse septum or vagina, cystocele, rectocele
Chaptter 43: Dystocia due to Abnormality of Powers Dystocia/difficult labor is the MC indication for primary CS Classification: A. disorder of preparatory division Nullipara Prolonged latent phase > 20 hrs B. protracted active phase of dilatation < 1.2 cm/hr C. disorders of pelvic division Prolonged deceleration phase > 3 hrs Secondary arrest of dilatation > 2 hrs Arrest of descent > 1 hr Failure of descent No descent D. precipitate labor disorders Precipitate dilatation > 5 cm/hr Precipitate descent > 5 cm/hr
Multipara > 14 hrs < 1.5 cm/hr > 1 hr > 2 hrs > 1 hr No descent > 10 cm/hr > 10 cm/hr
Chapter 47: Forceps Delivery and Vacuum Extraction Obstetric forceps Types of obstetric forceps Molded Simpson’s forceps Rounded Tucker’s forceps For aftercoming head Piper’s forceps For transverse arrest Barton’s forceps [Refer to p. 45 of OB-GYN handy notes f or ACOG classification of Forceps delivery] Prerequisites: 1. head must be engaged 2. fully dilated cervix
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3. 4. 5. 6.
known position of vertex ruptured membranes no CPD vertex or mentum anterior
Chapter 46: Breech presentation and delivery Methods of vaginal breech delivery Spontaneous Infant is expelled entirely spontaneously w/o any traction or breech delivery manipulation other than support of the infant Partial breech Infant is delivered spontaneously as far as the umbilicus, but the extraction remainder of the body is extracted/delivered w/ operator traction Total breech Entire body of the infant is extracted by the obstetrician extraction
Mechanism of breech delivery: Lovesets Delivery of posterior shoulder ahead of the anterior Kristeller’s The head may be delivered by suprapubic pressure
Methods of delivery of the head: Piper’s forceps Preferred method, the head well engaged, occiput diretly anterior, blades of head MauriceauThe body of the baby is placed on arm of the operator w/ index and the smellie-veit middle fingers over malar bones Bracht Breech is allowed to deliver spontaneously to navel Prague Body is swung over the mother’s abdomen Pinnard Hand is introduced inside the uterus to reach for popliteal fossa
Entrapment of the aftercoming head: Durhssen’s incision Cervix should be made 7 cm dilated, 3 i ncisions made 2,6 and 10 o’ clock positions Abdominal rescue Replacement of fetus higher into the vagina and uterus, followed by CS delivery
Chapter 48: Cessarean section Delivery of fetus thru abdominal incision [laparotomy], followed by incision of uterine wall [hysterotomy]. [Refer to p. 46 of OB-GYN handy notes f or indications of CS delivery] Techniques in CS: o Types of abdominal incision: Median infraumbilicallongitudinal incision Transverse suprapubic incision More difficult but is stronger & w/ Or Pfannenstiel/Bikini type less dehiscence
o Types of uterine incision: Classical CS Longitudinal incision above LUS, strong tendency to rupture Low-segment incision Low tendency to rupture Low transverse/ kerr Preferred due to only moderate dissection of the bladder Low longitudinal/kronig More bladder dissection but can be extended
Vaginal birth after a CS/VBAC: allow a trial of labor under double set-up for all previous CS of 1 low segment incision after excluding in adequate pelvis & unless new indication arises.
Chapter 35: Hypertensive disorders Classification: Hypertension A BP of at least 140 mmHg or 90 mmHg diastolic, previously defined by an increase of 30 mmHg systolic or 15 mmHg diastolic over baseline values Gestational HPN w/o proteinuria occurring after 20 wks AOG or postpartum, BP HPN returns to normal < 12 wks postpartum Preeclampsia Presence of HPN + proteinuria [300 mg/24 hr or +2 dipstick] occurring after 20 wks AOG except in cases of extensive trophoblastic proliferation Superimposed ↑ of at least 15 mmHg diastolic or 30 mmHg systolic over baseline preeclampsia hypertensive BP levels Eclampsia Presence of convulsions in a woman w/ preeclampsia Superimposed Convulsions + superimposed preeclampsia ecclampsia Chronic HPN Presence of 140/90 mmHg or greater prior o pregnancy or is detected before the 20 th wk of pregnancy and persists long after delivery
1. 2. 3. 4. 5. 6.
Severe preeclampsia – presence of one or more of the ffg: SBP of 160 mmHg or DBP of 110 mmHg proteinuria of at least 4 g/d or +2, w/ renal involvement oliguria of < 400 cc/day severe headache or visual disturbance pulmonary edema or cyanosis; IUGR HELLP syndrome – hemolysis, elevated liver enzymes & l ow platelet count
Classification of hypertensive disorders [refer to p. 37 of OB-GYN handy notes] Pathophysiology: o Trophoblastic hypoperfusion, w/ ibgrowth of trophoblastic cells into tunica media of spiral arterioles results in denervation & loss of muscular and elastic components causing thinning of walls, dilation & elongation to a “ corkscrew or saw-toothed configuration o Prostacyclin deficiency + abnormal arterioles result in a st ate of relative vasoconstriction Changes in preeclampsia: o ↓ antithrombin 3 and ↑ fibronectin o ↓ pasma levels of rennin, angioensin 2, and aldosterone, ↑ ADH o ANP is released upon arterial wall distention o Glomerular capillary wall distention o Periporal hemorrhagic necrosis – pahognomonic of preeclampsia o Subcapsular hematoma w/ epigastric or RUQ pain o Principal cerebral lesions: amaurosis and retinal detachment Roll-over test: increase of at least 20 mmHg in DBP from a left lateral decubitus position to supine is a positive test MAP test = DBP + 1/3 SBP or 1/3 [SBP + 2DBP] nd rd o MAP 2 trimester = > 90 mmHg, or MAP 3 trimester = > 105 mmHg predict future PIH. Management: Control of HPN: o Hydralazine [apresoline] = 5 mg IV bolus w/ increments of 5 mg q 30 mins if DBP does not improve up o total of 20 mg dose o Beta-blockers and Ca+ channel blockers: nifedipine or nicardipine o ACE inhibitors are not recommended in pregnancy. Control of convusion: o Magnesium sulfate [DOC] = loading dose of 4 g IV bolus + 10 g IM [5g per buttock]; maintenance dose = 1-2 g/hr IV drip or 5 g IM q 6 hrs [monitor toxicity using DTR, RR > 12, UO >100 cc/4 hrs] Optimum time & mode of delivery Prevention: low dose aspirin, high dose Ca+
Chapter 26: Obstetrical hemorrhage Placenta previa: bleeding due to separation of placenta implanted in the immediate vicinity of cervical canal. rd o Bleeding is proportionate to blood loss, usually painless & occurs at 3 trimester o [Refer to page 35 of OB-GYN handy notes for differentiation btw placenta previa and abruption placenta]. o Dx; double set-up, UTZ, MRI o Types of placenta previa: Total placenta previa Internal os is completely covered by placenta Partial placenta previa Internal os is partially covered by placenta Marginal placenta Edge of placenta is at the margin of internal os Low-lying placenta Placenta implanted at the LUS such that the placental edge actually does not reach the internal os but is in close proximity to it
Abruption placenta: bleeding may come from separation of placenta located elsewhere in the uterine cavity, occurs after 20 th wk of pregnancy and before birth of fetus o MC etiology is preeclampsia. o Bleeding is proportionate to placental separation. o Types of abruption: External Bleeding passes btw membranes and uterus and escapes thru the cervix Concealed If it extravasates into amniotic cavity after breaking the membranes, placenta is completely separated yet membranes retain their attachment to uterine wall Marginal Placental separation is limited to the margin w/ minimal bleeding but w/o uterine tenderness and pain Vasa previa: bleeding may be the consequence of velamentous insertion of umbilical cord w/ rupture and hemorrhage from a fetal blood vessel at the time of rupture of the membranes. [Read on Handy notes OB-GYNE for classification of abruption placenta p. 34] Complications of abruption placenta: o Couvelaire uterus/uterine apoplexy: in w/c the entire uterus may undergo bluish, purple or copper discoloration due to blood extravasation into myometrium and uterine serosa. o Acute renal failure: due to reduced CO and intrarenal vasospasm due to massive hemorrhage. o DIC Complications of placenta previa: o Placenta accrete o Postpartum hemorrhage o IUGR o Congenital abnormalities IUFD o Absence of fetal movement o Confirmed by: 1. spalding’s sign [7 days after fetal death] – opening of the fontanelles 2. hyperflexion of spine
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3. 4.
crowding of rib shadow robert’s sign o Mgt: delivery o Compication: DIC Uterine rupture o Complete rupture: uterus may communicate directly w/ the peritoneal cavity o Incomplete rupture: may be separated from peritoneal cavity by visceral peritoneum over the uterus or of broad ligament.
Chapter 37: Preterm Birth Preterm = < 37 wks AOG but > 20 wks AOG Average birthweight for Filipinos is 2,275 gms Survival is feasible at 26-27 wks AOG Dx: o Regular uterine contractions 5-8 mins or less apart accompanied by 1 of the ffg. 1. progressive change in cervix 2. cervical dilatation of 2 cm or more 3. cervical effacement of 80% or more o Passage of cervical mucus; low back pains, pelvic pressure, menstrual-like or intestinal cramps Mgt: repair of incompetent cervix, combat infection, tocolytics Tocolytic agents are of greater benefit if given 32-34 wks AOG, includes: o Beta-adrenergic agonists – reduce myometrial contractility by decreasing intracellular Ca+ & reducing effect of Ca+ on myometrial activation [ex. i soxuprine/duvadilan] o Magenesium sulfate o Prostaglandin inhibitors – indomethacin o Ca+ channel blockers
Amnionic cysts Amnion nodosum Amnionic bands
Chapter 39: Fetal Growth Disorders Intrauterine Growth Retardation Types: Symmetric IUGR / Insult early in gestation w/ equal decrease in HC, weight & l ength type 1 such as in chromosomal anomalies Asymmetric IUGR Insult of later onset such as maternal disease, presents w/ a / type 2 characteristic “head sparing”
1. 2.
Dx: UTZ measurement of increase in biparietal diameter < 2 mm/wk from 13 th-34th wk < 1 mm/wk from 35 th wk to term
Chapter 36: Multifetal Pregnancy Classification: Dizygotic twins Results from maturation and fertilization of 2 separate ova during [fraternal twins] a single ovulatory cycle Monozygotic twins Results from twins that may arise from a single fertilized ovum
1. 2. 3. 4.
1. 2. 3. 4. 5.
Factors: race, heredity, age > 35, parity > 4, maternal size & nutrition, use of ovulating drugs [clmiphene, gonadotropins] Types: double ovum w/ 2 chorions, 2 amnions & 2 placenta double ovum w/ 2 chorions, 2 amnions & 1 placenta single ovum w/ 2 chorions, 1 amnion & 1 placenta single ovum w/ 1 chorion, amnion & placenta Presentation and incidence: o Cephalic-cephalic: 42% o Cephalic-breech: 27% o Cephalic-transverse: 18% o Breech-breech; 5% Fetal complications: IUGR Intertwining of umbilical cords DIC following deah of a twin collision [both twins in cephalic presentation] & interlocking [chin to chin lock] anomalous anastomotic vascular connections → “twin -twin transfusion syndrome” – discordant twins w/ larger twin developing hydramnios + polycythemia while smaller twin develops oligohydramnios + anemia Anesthesia and analgesia: epidural anesthesia – preferred Route of delivery: CS – preferred
Chapter 29: Abnormalities of the Placenta, F etal Membranes & Amniotic fluid Meconium staining Stained amniotic membranes w/in 1-3 h after meconium passage Chorioamnionitis Associated w/ prolonged membrane rupture w/ long membranes Criteria: Fever > 38, tachycardia [fetal/maternal], maternal leukocytosis
Normal Amniotic fluid volumes: o Maximum amniotic fluid is at 28 wks; 800 ml o After 28 wks, amniotic fluid decreases. o At 40 wks, amniotic fluid is at 500 ml. Abnormal amniotic fluid volumes: o Normal vertical fluid pocket [VFP]= 2-8 cm o Oligohydramnios: < 4-5 AFI [VFP = < 2 cm] MC cause; rupture of membranes Clinical correlates: IUGR, dysmaturiy syndromes, renal agenesis, urinary tract obstruction, pulmonary hypoplasia o Polyhydramnios: > 20-24 AFI or 2 L [VFP = > 8 cm] Clinical correlates: GI abnormalities, anencephaly, spina bifida, DM, erytroblastosis fetalis, TEF, esophageal aresia Classification: Mild 8-11 cm Moderate 12-15 cm Severe > 16
Chapter 38: Post-term Pregnancy [> 42 wks] Mgt: 1. assessment of true gestational age 2. px counseling regarding induction of labor vs. conservative mgt. 3. antepartum surveillance tests: fetal movement counting, NST/CST, FAST, BPP + AFI
Results from fusion of amnionic fold, w/ fluid retention Made up of fetal ectodermal debris including vernix caseosa w hair, squames and sebum May adhere to fetus and impair growth and development of involved structure
Aniotic fluid index [AFI] – summation of the largest vertical pockets of 4 quadrans of uterus. Placentomegaly > 600 gms Types of placental abnormalities: Placenta succenturiata w/ accessory lobe outside main disc Extrachorial placenta Membranes do not insert at disc 1. circummarginate Membranes w/o thickening 2. circumvallate Membranes arise from a cup Placenta accreta Villi contiguous w/ myometrium Placenta increta Villi invade the myometrium Placent percreta Villi penetrates serosal surface of myometrium
Abnormal shapes: Succenturiate 1 or more small accessory lobes developed in he membranes at a placenta distance from the periphery of the main placenta Ring-shaped Because of atrophy of the tissue of the ring placenta Membranaceous Placenta develops into a thin membranous structure Placenta Fenestrated The central portion of discoidal plaenta is missing Circumvallate Placenta presents a central depression surrounded by a thickened, grayish white ring Circummarginate Ring coincides w/ placental margin
Abnormal adherence: Accreta Placental villi attached to myometrium Increta Placental villi invade the myometrium Percreta Placental villi penetrate the myometrium A consequence of partial or total absence of the decidua basalis and imperfect development of fibrinoid layer [Nitabuch’s layer] Dx: UTZ = lack of usual subplacental sonolucent space or “hypoehoic retroplacental zone” Safest treatment is prompt hysterectomy.
Abnormalities of Umbilical Cord Mean length of umbilical cord: 55-60 cm, >70 [long cord], < 32 [short cord] Marginal insertion Cord insertion at placental margin , aka Battledore placenta Velamentous insertion Umbilical vessels separate in the membranes at a distance from the placental margin Vasa previa Associated w/ velamentous insertion when some of the fetal vessels in membranes cross the region of the internal os and occupy a position ahead of the presenting part
Cord abnormalities impending blood flow: False knots – due to kinking of vessels to accommodate the length of the cord True knots – due to active fetal movements Torsion As a result of fetal movements, the cord becomes twisted, fetal circulation becomes compromised Stricture Associated w/ extreme focal deficiency in Wharton jelly, usually assoc. w/ torsion Hematoma Result from rupture of varix [ umbilical vein], w/ effusion of blood into the cord Cysts True cysts – from remnants of umbilical vesicle or of allantois False cysts – from liquefaction of Wharton jelly Edema Associated w/ edema of fetus, common w/ macerated fetus
Knots
9
Chapter 30: Gestational Trophoblastic Disease Refers to proliferative abnormalities of trophoblast w/c retains its ability to secrete HCG. Classification of GTD [refer to p. 29 of OB-GYN handy notes] Complete vs. partial H. mole [refer to p. 30 of OB-GYN handy notes] FIGO staging for trophoblastic disease [refer to p. 30-31 of OB-GYN handy notes] Most malignant type of GTT is choriocarcinoma Classic S/sx for complete H. mole: toxemia before 24 wks AOG, uterus large for dates, absent FHT and fetal parts Histological structure of complete H. mole: o Hydrophic degeneration and swelling of the villous stroma o Absence of blood vessels in the swollen vili o Proliferation of trophoblastic epithelium to a varying degree o Absence of fetus and amnion Classic UTZ finding; ‘snow-storm pattern” Mgt: o Replacement of blood loss o Combat infection if present o Termination of pregnancy either by suction curettage or hysterectomy o Prophylactic chemotherapy [Contraindicated if: hb , 10 gml, WBC < 3 x 10 9/l, platelets < 100, 000 m3, and if w/ [+] l iver or renal fxn test impairment o Follow-up for signs of persistent disease: HCG Weekly until normal x 2 val ues, then q 2 wks x 3 mos, then q determination monthly x 6-12 mos, then q 6 mos x 1-2 yrs, hen annually CXR Initially then repeat if abnormal or if HCG plateus or rises Contraception For 1 yr because pregnany will increase HCG levels Pelvic exam Q 2 wks until normal then q 3 mos Chapter 31: Gestational Trophoblastic Tumors Hammonds classification of GTT [refer to p. 33 of OB-GYN handy notes] Chemotherapeutic drugs used [refer to p. 33 of OB-GYN handy notes] Type Features Treatment Invasive Invasion of H. mole deep into uterine wall Single-agent chemotherapy mole S/Sx: irregular bleeding w/in 6 mos. of [methotrexate] or molar evacuation hysterectomy ChorioSyncitiotrophoblast + cytotrophoblast, hx: Chemotherapy – single/multi carcinoma exuberant rophoblastic growth w/o villi Hysterectomy
1. 2.
Chapter 27: Abortion Refers to termination of pregnancy before 20 wks AOG, or delivery of fetus < 500 gms Comparative analysis of different types of abortion [refer to p. 27 of OB-GYN handy notes] Etiologic agents for septic abortion: Anaerobic B. fragilis, strep, clostridium weichii, tetanus Aerobic e. coli, klebsiella, staph, pseudomonas
+ cervical glands opposite the placental attachment whole part of the placenta must be situated below the entrance of uterine vessels or below the entrance of uterine vessels 3. attachment of placenta to cervix must be intimate 4. fetal elements must not be present in corpus uteri Ovarian pregnancy o Spiegelberg criteria: 1. tube including fimbria ovarica is intact 2. gestational sac is in normal anatomic location of ovary 3. the sac is connected to uterus by ovarian li gament 4. definitive ovarian tissue is histologically demonstrated in sac wall Abdominal pregnancy o Sonographic criteria: 1. visualization of fetus separate from uterus 2. failure to visualize the uterine wall between the fetus and urinary bladder 3. close approximation of fetal parts to the maternal abdominal wall 4. eccentric position or abnormal fetal attitude and visualization of extrauterine placental tissue o Studdiford criteria: 1. Tubes appear to normal w/ no evidence of recent or past injury 2. There is no uteroplacental fistula or evidence of uterine rupture 3. The pregnancy is exclusively attached to peritoneal surfaces and is early enough to eliminate the possibility of secondary implantation following tubal nidation
Chapter 41: Congenital Anomalies & Abnormalities of Reproductive tract [read APMC] Imperforate hymen o Primary amenorrhea [cryptomenorrhea] w/ cyclic, crampy pain at puberty o Sx: hematocopos → hematometra → hematosalpinx → endometriosis/endometritis o Bulging membrane at introitus is tx w/ hymenotomy. Transverse vaginal septum o Associated w/ intrauterine DES exposure rd o Site: upper 3 and lower 2/3 of vagina o Same Sx w/ imperforate hymen, tx by excision Mullerain fusion anomalies Complete duplication Asymptomatic Non-communicating uterine horn Cyclic pelvic pains, pelvic mass & ectopic pregnancy Septate/bicornuate uterus Reproductive wastage, uterine dysfunction, abnormal fetal presentation
60% of spontaneous abortions in the 1 st trimester are a result of chromosomal abnormalities. 94% of abortions occur in 1 st trimester. Women w/ hx of recurrent abortion have 23% chance of abortion in subsequent pregnancies that are detectable by UTZ. MC cause ofhabitual or recurrent abortion is Antiphospholipid antibody syndrome/APAS Presence of blighted ovum is seen in Inevitable abortion.
Chapter 28: Ectopic pregnancy Refers to implantation of fertilized ovum outside endometrium. Ectopic pregnancy is the leading cause of pregnancy-related death during 1 st trimester. Heterotopic pregnancy – simultaneous intrauterine & ectopic pregnancies. MC cause is salpingitis or PID. Classic triad of Sx: colicky abdominal pain [MC], amenorrhea for 6 wks followed minimal vaginal bleeding Classic signs: wiggling tenderness [MC], uterus smaller than AOG, fullness of cul-de sac [due to hemoperitoneum] Dx: HCG & progesterone Low levels UTZ criteria [+] adnexal mass, no gestational sac when HCG levels > 2,500 mIU/ml at 5-6 wks
The presence of intrauterine gestational sac rules out ectopic except in heterotopic pregnancy. Mgt: Unruptured Medical – methotrexate [for rapid absorption of placental tissue], RU486 [competes for progesterone binding sites], Surgical – partial salpi ngectomy, salpingostomy, salpingotomy Ruptured Radical hysterectomy, total salpingectomy with or w/o oophorectomy, Conservative – segmental resection
Cervical pregnancy o Rubin’s criteria:
Chapter 15: Teratology, Drugs, and Medications Category A Controlled studies in humans have been demonstrated no fetal risk Category B Animal studies indicate no fetal risk, but there are no human studies or adverse effects have been demonstrated in animals, but not in well-controlled Human studies Category C No adequate studies, either animal or human, or there are adverse effects in animal studies but no available human data Category D Evidence of fetal risk, benefits outweigh the risks Category X Proven fetal risks clearly outweigh any benefits MEDICAL CONDITIONS AND PREGNANCY MC medical complication in pregnancy: diabetes Gestational DM probably results from placental lactogen secreted during pregnancy; w/c has large glucagons-like effects. Insulin does no cross the placenta → feal hyperglycemia [Refer to p. 39 of OB-GYN h andy notes for Criteria in Dx of GDM] The CNS anomaly most specific to DM is caudal regression. Grave’s disease is the MC cause of thyrotoxicosis in pregnancy. Tx is PTU [drug of choice] and methimazole. Sheehan’s syndrome: pituitary ischemia and necrosis associated w/ obstetrical blood loss leading to hypopituitarism. Pxs do not lactate due low levels of prolactin. MC serious medical complication of pregnancy and occurs in 1-2% of pregnant women: acute pyelonephritis MC surgical condition in pregnancy: appendicitis The 2 MC causes of anemia during pregnancy and puerperium are IDA and acute blood loss.
URINARY TRACT IFECTIONS AND PREGNANCY Asymptomatic bacteriuria o Dx: 1. absence of Sx 2. > 100,000 cfu/ml w/ 1 or more organisms in 2 c onsecutive midstream specimens or 1 cathetherized specimen 3. screening should be done at 1 st prenatal visit esp. for diabetics & those w/ previous hx of UTI 4. test of choice: urine culture [clean catch midstream] 5. U/A alone is not recommended o Tx:antibiotics x 7 days w/ follow-up culture after 1 wk Acute cystitis in pregnancy o S/Sx: urinary frequency, dysuria & bacteriuria
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Dx: pyuria > 8 pus c ells/mm3 [uncentrifuged], or > 5 pus cells/hpf [centrifuged] or [+] leukocyte esterase & nitrate test o Tx: 7 days antibiotics Acute pyelonephritis in pregnancy o Dx: pyuria [> 5 wbc/hpf centrifuged urine] & bacteriuria [> 10,000 cfu of uropathogen], gm stain, urine C & S, blood cultures o Tx: admit, immediate antibiotic therapy for a duration of 14 days
Parous
o
o
o o
o
Note: Antibiotics in pregnancy Safe antibiotics Amoxicillin, nitrofurantoin, cephaalosporins, coamoxiclav, ampicillin-sulbactam, aztreonam
Use w/ caution Aminoglycosides TMP/SMX at 1 st & 2nd trimester
Contraindicated Tetracycline, fluorioquinolones, TM/SMX at 3 rd trimester
COMPLICATIONS OF PREGNANCY Magnesium toxicity [7-10 mEq/L] is associated w/ loss of patellar reflexes. Tx w/ calcium gluconate 10% solution 1 g IV. Magnesium levels and toxicity: 4-7 mg Uterine contractions decreased 6-12 mg ECG changes, hyporeflexia 10 mg Loss of deep tendon reflex 15 mg Respiratory paralysis, cardiac depression
External os has fishmouth appearance
In normal nonpregnant state, uterus is approximately 6 cm x 4 cm & weighs about 70 gms [ovary is 3cm x 2 cm] Lymphatics: aortic, lumbar and pelvic nodes Nerve supply: hypogastric and ovarian plexus [sympathetic], pelvic N. + S2-4 [parasympathetic]. Blood supply: Uterine A. Large branch of hypogastric A. Ovarian A. Directly from aorta
Fallopian tube/oviducts Blood supply: Uterine A. From hypogastric A. Ovarian A. From aorta
o
Hydration often stops contractions during preterm labor. L:S ratio is normally > 2.0 PROM is the MC dx associated w/ preterm delivery. Oxytocin should never be given as undiluted bolus [due to serious hypotension] Antibiotics for endometritis: clindamycin + gentamicin
o
REPRODUCTIVE ANATOMY Key terms: Canal of Nuck – tubular process of peritoneum accompanying round ligament into inguinal canal, generally obliterated in adults. Carunculae myrtiformes – small nodules of fibrous tissue at v aginal orifice w/c are remnants of hymen. Cornu – where oviducts enter uterine cavity. Cul-de-sac of Douglas – separates uterus from large intestine Fimbria ovarica – finger-like projections of distal end of oviducts, attaches oviducts to ovary. Frankenhauser’s plexus – concentration of both my elinated and non-myelinated nerve fibers in uterosacral lligament supplying primarily the uterus and cervix. Space of Retzius – area btw bladder and symphysis pubis bounded laterally by obliterated hypogastric A.
Lymphatics: aortic and iliac nodes nerve supply: ovarian, hypogastric and aortic plexuses Internal pudendal A. – terminal branch of internal iliac A. Cardinal ligaments/Mackenrodt’s ligament – provides the major support of uterus & cervix. Uterosacral ligament – last to cut in hysterectomy. o o
HI-YIELD FACTS IN GYNECOLOGY [from GYNE-MISCHELLE & handy notes]
Lymphatics; internal iliac and aortic nodes Innervation: uterine & ovarian plexus, sensory nerves from T11-12, L1 Ovaries: o Blood supply: ovarian A. [from aorta] o Venous drainage: L ovarian V. Drains to L renal V. R ovarian V. Drains to IVC o
Male and Female derivatives of embryonic urogenital structures Structure Male Female Labioscrotal swelling Scrotum Labia majora Urogenital folds Penile urethra Labia minora/nymphae Genital tubercle Penis Clitoris Phallus Penis bulb Vesibular bulbs Urogenital sinus Prostate gland Urehral / Skene’s glands Prostatic utricle Vagina Bulbourethral glands Vestibular glands Cooper’s glans Bartholin’s glands Mesonephric duct Epididymis Epiophoron Ductus deferens Gartner’s duct Gonad Testis Ovary Gubernaculums Gubernaculums testis Round lig. of uterus
Important Facts Escutcheon in mons pubis [triangular in female, diamond in male]. Labia minora & breast are the only areas of the body rich in sebaceous glands w/o hair follicles. Lowest part of embryonic urogenital sinus – vestibule. MC large cystic structure of vulva – Bartholin’s duct cyst. Vagina: o Normal pH: 3.8 – 7.2 rd o Lower 3 : close w/ endopelvic fascia & ligament rd o Middle 3 : supported by levator ani M.& cardinal ligament [lower part] rd o Upper 3 : supported by cardinal ligament [upper] & parametria o Blood supply: Vaginal A. Either directly from uterine A. or as a branch of internal iliac A. Pudendal V. Principal venous drainage
CONGENITAL ABNORMALITIES OF FEMALE REPRODUCTIVE TRACT Key terms: Androgen resistance syndrome – 46 X,Y individual w testis, absent uterus, normal female phenotype and scanty body hair. Arcuate uterus – minimum septate uterus Bicornuate uterus – partial lack of fusion of 2 uterine corpura w/ single cervix present. Didelphic uterus – compete duplication of uterus and cervix w/o fusion of 2 cavities. Rokitansky-Kuster-Hauser syndrome – 46 X,X female w/ mullerian failure showing absence of all or most of the vagina, c ervix, uterus, and FT. Unicolic/unicornuate uterus – represents a complete arrest of 1 mullerian duct. MC cause of labial fusion is c ongenital adrenal hyperplasia.
HISTORY, P.E, AND PREVENTIVE HEALH CARE Keyterms: Ectropion – presence of endocervical [glandular] epithelium on potrio vaginalis of cervix; may result from scarring of external os or congenital. Total procidencia – prolapse of uterus and cervix thru i ntroitus Stages of uterine prolapse; Stage 1 Minimum descent of cervix into vaginal canal Stage 2 Descent of cervix to introitus Stage 3 Prolapse of cervix or uterus thru introitus
Nerve supply: vaginal plexus, pudendal nerve; pain fibers [S1-4] o Lymphatics: Upper 3rd External iliac nodes Middle 3rd Common & internal iliac nodes Lower 3rd Common iliac, superficial inguinal & perirectal nodes o
Surgical procedures for vagina: colpectomy, colposcopy & colphorrhapy Cervix: o Blood supply: descending branch of uterine A., cervical A. & azygos A. o Lymphatics: obturator, common iliac, internal/external iliac nodes o Nerve supply: S2-4 Majority of arterial supply to cervix is at 3 or 9 o’ clock position. Removal of narrow lower par of uterus is c alled trachelectomy. Uterus: Nulliparous External os is round
Trichomonas: use 1% NaCl while KOH is used in c andidiasis
RAPE, INCEST AND DOMESTIC VIOLENCE Key terms MC acquired infection in STD is chamydia. [Tx: ceftriaxone and doxycycline] Survival time of sperm: Source Motile sperm Sperm Aid phosphatase Vagina Up to 8 hrs Up to 7-9 days Variable Pharynx 6 hrs Unknown 100 IU Rectum Undetermined 20-24 hrs 100 IU
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Cervix
Up to 5 days
Up to 17 days
Variable
Classic Sx of intraductal papilloma is spontaneous bloody discharge from 1 nipple. Intraductal papilloma and fibrocystic changes are the 2 MC etiology of spontaneous nonmilky discharge. Usual etiology of fat necrosis is tr auma. Most accurate conventional method of determining nonpalpable breast CA is mammography, often mediolateral oblique position. Indirect signs of breast CA: 1. single dilated duct w/ intraductal CA 2. asymptomatic architectural distortion in dense breast 3. developing density isolated clusters of tiny calcific ation are the MC and important diagnostic sign of early CA. Diagnostic test for breast CA is MRI. The |presence and number of axilla node metastasis is the single best predictor of survival. Most frequently prescribed hormonal agent for breast CA is tamoxifen/raloxifen.
DIAGNOSTIC PROCEDURES Keyterms Hysterosalpingography – xray whereby uterine cavity and lumina of FT are visualized by injecting contrast material thru cervical canal. Hysteroscopy – direct visualization of endometrial cavity using an endoscope. Laparoscopy – examination and inspection of uterine cavity and pelvic organs by endoscope. Sonohysterography – imaging of uterine cavity by instilling saline.
Important facts Sonography is the method of choice for locating a missing I UD. Endovaginal UTZ is the mainstay in evaluation of pregnant woman w/ 1 st trimester vaginal bleeding. CT scan is very accurate in dx cystic teratoma, and is an exc ellent techique to confirm dx of ovarian vein thrombosis. Endometrial sampling is the standard diagnostic test to confirm endometritis. CT is the most accurate in dx of appendicitis. Most frequent problem in performing endometrial sampling is cervical stenosis or spasm. Major complication following endometrial biopsy is uterine perforation. Laparoscopy is adopted as method of choice for female sterilization. Cervical punch biopsy is diagnostic for pxs w/ abnormal papsmear.
PEDIATRIC GYNECOLOGY Keyterms Adhesive vulvitis – a self-limiting consequence of chronic vulvitis in w/c denuded epithelium of labia minora agglutinates and fuses the 2 labia together. McCune-Albright Syndrome/Polycystic Fibrous dyplasia – triad: café-au lait spots, fibrous dysplasia, and cysts of skull and l ung bones. Incomplete or pseudoprecosious puberty – premature female sexual maturation and uterine bleeding w/o associated ovulation. Precocious puberty – the appearance of secondary sexual maturation at an age > 2.5 standard deviations below the mean for the population to w/c the child belongs.
Important facts Vulvovaginitis – MC gynecological disease of children and premenarcheal females. [+] identification of T. vaginalis, N. gonorrhea, and Chlamydia often indicates sexual abuse. Why is a child susceptible to vulvar infections: 1. they lack labial fat pads and pubic hair 2. her vulvar and vaginal epithelium lack protective effects of estrogen thus are sensitive to irritation or infection 3. labia minora are thin and vulvar skin i s red 4. vaginal epithelium is of neutral pH providing an excellent medium for bacterial growth. 5. her vagina lacks glycogen, lactobacilli, and antibodies to help resists infection. The major factor in childhood vulvovaginitis is poor perineal hygiene. Classic Sx of E. vermicularis infection is nocturnal vulvar and perineal itching. The classic perineal “figure of 8 or hourglass rash” indicates l ichen sclerosus. MC cause of bleeding in childhood is foreign bodies, w/c is MC among 3-9 y.o and are due to small wads of toilet tissue. Classic Sx: foul, bloody vaginal discharge. Usual cause of accidental genital trauma is fall [mostly straddle injury]. Calcification in an ovarian mass indcates a dx of ovarian teratoma. MC malignancy in preadolescent females is germ cell tumor. MC malignant neoplasm is dysgerminoma. MC tumor in children is benign teratoma. MC DDX of abdominopelvic mass in children that is not an ovarian mass is a benign cyst of mesentery or omentum. MC cause of pseudoprecocious puberty is an estrogen-secretig ovarian tumor, of w/c the MC type is granulose cell tumors. DOC for GnRH-dependent precocious puberty is GnRH agonists. Spontaneous discharge from nipple is a Sx of intraductal papilloma. MC of all benign breast conditions is fibrocystic changes. Its classic Sx is cyclic bilateral breast pain; signs include ↑ engorgement and density of breast, excessive nodularity, rapid change and fluctuation in size of cystic tenderness and spontaneous nipple discharge. 3 clinical stage of fibrocystic changes: 1st stage / Mazoplasia Breast pain in upper outer quadrant, intense stromal proliferation 2nd stage / Adenosis Seen in early 20s, w/ marked proliferation and hyperplasia of duct, ductules, and alveolar cells 3rd stage / cystic Seen in their 40s, w/ no severe breast pain but there is sudden phase pain and tenderness w/ a lump, straw-colored fluid DOC for fibrocystic changes: Danazol MC breast tumor in adolescents is fibroadenomas. It does not produce breast pain and tenderness. MC breast sarcoma is Cystosarcoma phylloides. MC breast malignancy is infiltrating ductal CA.
DIFFERENTIAL DIAGNOSIS OF MAJOR GYNECOLOGIC PROBLEMS Keyterms Hematocolpos – distenion of an obstructed vagina [caused by imperforate hymen or transverse vaginal septum] w/ blood products. Hematometria – uterus distended w/ blood secondary to partial or complete obstruction of any part of lower genital tract.
Important facts Implantation bleeding occurs at time of 1 st missed menstrual period and last a very s hort time, may be present 1-2 days w/ flow to menstrual period, it can be seen as brownishtinged cervical mucus. Common cause of DUB in puberty is anovuation. MC benign condition causing postmenopausal bleeding. MC example of recurrent pelvic pain among women. Pelvic congestion syndrome is characterized by pain and heaviness in pelvis that occurs after arising and becomes worst as day progresses, uterus appears dusky-blue & mottled, often w/ varicosities of veins of broad li gament. MC benign neoplasms of adnexa are s erous cystadenoma and benign cystic t eratoma [dermoid cyst]. MC benign ovarian neoplasm among different age groups: Age 19 Benign cystic teratoma Age 20-44 Serous cystadenoma Ages 20 to beyond 75 cystadenocarcinoma
Abdominal masses in young childhood are more likely to be Wilm’s tumor or neuroblastomas. Solid or mixed solid and cystic adnexal masses in children include dysgerminoma and teratoma. Majority of adnexal masses in adolescents are functional cysts of ovary [benign cystic teratoma]. It is also the MC neoplastic masses in reproductive years. Benign fibromas of the ovary may be associated w/ ascites and pleural effusion call ed Meig’s syndrome. Struma ovarii refers to a teratoma w/ thyroid elements present. Tumor makers: CA-125 Epithelial tumors Serum HCG and AFP Germ-cell tumors
BENIGN GYNECOLOGIC LESIONS Keyterms Degeneration of myoma – myoma outgrowths its blood supply and begin to necrose centrally. Endometrial poyp – localized outgrowth of endometrial gland and stroma projecting beyond surface of endometrium including is vascular stalk. Gartner’s duct cyst - cyst primarily of mesonephric origin found laterally in vagina. Hidradenoma – rare, small benign vulvar tumor of apocrine sweat glands. Hydatid cyst of Morgagni – pedunculated, paratubal cysts found near fimbria of oviduct. Hyperreactio luteinalis – multiple theca lutein cysts causing bil ateral ovarian enlargement during pregnancy. Leiomyomatosis peritonealis disseminate – benign disease w/ multiple small nodules over pelvic surface and abdominal peritoneum mimicking disseminated CA or sarcoma. Luteoma of pregnancy – rare, specific, benign hyperplastic reaction of ovarian t heca lutein cells during pregnancy. Nabothian cysts – cervical retention cysts li ned by endocervical –type columnar cells. Syringoma – benign tumor of eccrine sweat glands.
Important facts Urethral curuncle, small fleshy outgrowth at distal end of urethra common in postmenopausal women usually located at ectropion of posterior urethral wall. Common S/Sx includes dysuria, frequency, urgency and pain or tenderness. It is not a precursor for urethral CA.
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Urethral prolapse is MC in children. It appears as annular rosette of friable edematous prolapsed mucosa. Tx; hot sitz bath and antibiotics, topical estrogen and excision of redundant mucosa. MC large vulvar cyst is Bartholin’s duct cyst [often located at posterolateral aspect] MC small vulvar cyst is Epidermal inclusion cyst [often located at anterior half of labia majora]. It is not related to trauma unlike inclusion cy st of vagina. Urethral CA: o MC in elderly women, usually squamous cell ori gin, found in distal urethra. S/Sx: bleeding, frequency, dysuria, urethral mass and tenderness, induration of urethra. Most vulvar epidermal cysts do not have sebaceous cells. MC benign neoplasm in females is nevus/mole of vulva or vulvar nevi. A flat junctional nevus and dysplastic nevus have greatest potential for malignant transformation. MC benign solid tumors of vulva are fibroma [often located at labia majora]. 2nd MC benign vulvar mesenchymal tumors are lipoma [often at labia majora]. Hidradenoma are treated by excisional biopsy. Fox-Fordyce disease are multiple retention cyst of apocrine gland w/ skin i nflammation. Von Recklinghausen’s Disease are generalized neurofibromatous nodules from neural sheath associated w/ café-au-lait spots. Vulvar hematomas are treated conservatively and by surgery [> 10 cm, expanding]. Burning vulvar syndrome – persistent vulvodynia w/o any cause. Psoriasis is dx by [+] silver scales and bleeding or scraping of plaques. Seborrheic dermatitis is characterized by presence of oily scales. Lichen planus is characterized by presence of shiny, vi olaceous papules. Urethral diverticulum are MC seen from posterior urethra, middle 3 rd], characterized by dysuria, dyspareunia and dribbling of urine. Classic sign is presence of purulent material on expression of sub-urethral area. MC cystic structure in vagina is inclusion cyst usually found in posterior and lateral walls of 1/3 of the vagina. Types of dysontogenic cyst of vagina: Mesonephros Gartner’s duct cyst Mullerian cyst Perimesonephrium Urogenital sinus Vestibular cyst Most frequent etiology of trauma to lower genital tract of adult females is coitus, usually a transverse tear of posterior fornix. Tx: suturing. MC benign tumor of cervix is endocervical/cervical polyps. Cervical myomas commonly arise from isthmus of uterus. Cervical lacerations arise from 3 and 9 o’ clock position. Tx: suturing Cervical stenosis often occurs in internal os. Endometrial polyp often arises in fundus of uterus.3 components include endometrial gland and stroma, and central vascular channels. Most frequent pelvic tumors are leiomyoma [often found in corps of uterus]. Submucosal myoma are most troublesome clinically. MC form of leiomyomas and is the mildest – hyaline degeneration. Most acute form of l eiomyomas, often painful – red or carneous degeneration. “Spaghetti tumor” is characteristic of intravenous leiomyomatosis. MC ovarian cysts are follicular cysts [often located at ovarian cortex]. Halban’s triad of corpus luteum cyst: delayed me nses w/ menorrhagia, unilateral pelvic pain, & small, tender adnexal mass. MC ovarian neoplasms are benign cystic teratom/dermoid cyst/mature teratoma [often found among prepubertal female and teenagers]. Tx: cystectomy MC complication of dermoid cysts is torsion. Triad of endometrioma: pelvic pain, dyspareunia and infertility. MC benign solid neoplasm of ovary is fibroma. Triad of Meig’s sy ndrome: ovarian fibroma, ascites, hydrothorax. “coffee-bean” appearing nucleus is found i n Brenner’s tumor/Transitional cell tumors. Leiomyomas of oviduct are usually seen in interstitial portion of tubes. MC benign tumor of oviduct i s Angiomyoma / Adenomatoid tumor.
Doesn’t respond to hormonal stimulation Non-cyclical
Responds to estrogen Cyclical
Common sites of endometriosis: ovary [MC], c ul-de-sac, fallopian tubes, uterosacral ligaments, bowel. Less common sites: cervix, vagina, bladder. Rare sites: nasopharynx, lungs A 37 y/o female complains of hemoptysis w/ each period: endometriosis of nasopharynx or lung Maximum time on estrogen suppression should be 6 mos. due to adverse effects 3 cardinal histologic features in endometriosis: ectopic endometrial glands and str oma, hemosiderin-laden macrophages. Classic pelvic finding is fixed, retroverted uterus w/ scarring and tenderness posterior to uterus. Nodularity of uterosacral ligaments & cul-de-sac of Douglas Tx for endometriosis: o Medical – if < 1-2 c m, primary goal: induction of amenorrhea, drugs used include: danazol 800 mg/d x 6-9 mos.; GnRH agonists; OCPs; and medroxyprogeserone [for pxs who has completed childbirth]. o Conservative surgery: laparoscopy or TAHBSO [definitive surgery] GIT endometriosis [sigmoid olon and anterior wall of rectum] is the MC site of extrapelvic endometriosis. Most serious consequence of urinary tract endometriosis [often at trigone] is ureteral obstruction. Adenomyosis / endometriosis interna is often found at posterior wall of uterus. Standard criterion: endometrial gland and stroma > 1 LPF [2.5mm] from basalis layer of endometrium. Classic Sx of adenomyosis: primary & secondary dysmenorrheal and dyspareunia. Mgt of adenomyosis: o Medical: GnRH agonists, cyclic hormone prostaglandin synthetase inhibitors o Surgery: definitive tx is hysterectomy.
ANATOMIC DEFECTS OF ABDOMINAL WALL AND PELVIC FLOOR Keyterms Cystocele – protrusion of bladder into vagina, significant relaxation of fascial supports of bladder. Common in women w/ android or anthropoid pelvis. Descensus of cervix & uterus [prolapse, procidencia] – protrusion of cervix and uterus into barrel of vagina. st o 1 degree: prolapse into upper vagina nd degree: prolapse near uterus 2 o rd o 3 [complete]: total prolpase thru introitus th o 4 degree: body of uterus is out of introitus o Tx: Nonoperative Pessaries, estrogen Operative Vaginal hysterectomy w anterior & posterior repair + perineorrhaphy to reinforce introitus
Dovetail sign – loss of anterior perianal folds i ndicates a defect in external anal sphincter or chronic degree laceration. Enterocele – herniation of pouch of Douglas [cul-de-sac] btw uterosacral li gament into rectovaginal septum, usually contains small bowel. Pessary – a prosthesis inserted into vagina to support pelvic structure. Urethrocele – protrusion of urethra into vagina, significant loss of fascial supports of urethra. Common in women w/ gynecoid pelvis. MC traumatic cause of rectovaginal fistula is obstetric [due to prolonged 2 nd stage of labor]. It usually occur in lower 3 rd of vagina.
ENDOMETRIOSIS AND ADENOMYOSIS Keyterms Adenomyosis – growth of endometrial glands and stroma into uterine musculature to a depth of at least 2.5 mm from basalis layer of endometrium. Chocolate cysts – a cystic area of endometriosis in ovary. Dyschezia – difficult/painful evacuation of feces from rectum. Endometriosis – presence and growth of glands and stroma identical t o lining of uterus in aberrant location. Retrograde menstruation – menstrual flow, endometrial cells, and debris, blood flow via FT into peritoneal cavity. MC etiology.
UROGYNECOLOGY Keyterms Genuine stress incontinence – loss of urine when intravesical pressure exceeds maximum urethral pressure in absence of detrusor acivity. Interstitial cystitis – complex inflammatory condition of bladder usually associated w/ altered epithelial permeability, mast cell activation and upregulation of secondary afferent nerve. Overflow incontinence – loss of urine when intravesical pressure exceeds the maximum urethral pressure secondary to elevtion of intravesical pressure associated w/ bladder distention but in absence of detrusor activity. Reflex incontinence – loss of urine caused by abnormal reflex activity in spinal cord in absence of sensation that is usually associated w/ desire to micturate. True incontinence – loss of urine w/o abnormal bladder function due to fistulas or other damage to urinary tract Urge incontinence – loss of urine associated w/ strong desire to void directly into motor urge incontinence [uninhibited detrusor contractions] and sensory urge incontinence.
Important facts Classic Sx of endometriosis is cycl ic pelvic pain. Its most popular theory is retrograde menstruation. Other Sx: infertility and abnormal bleeding Differences: Adenomyosis Endometriosis Usually in older women Young women
Important facts Innervation of bladder & urethra: Continence Bladder Symph [NEp] = relaxation w/c prevents micturition Sphincter Contraction = prevents micturition
Micturition Parasymph [Ach] = contraction causing micturition Relaxation
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Giemsa/wright stain: [+] Donovan bodies – clusters of dark-staining baceria w/ bipolar safety pin appearance [pathognomonic] o Mgt: TMP-SMZ, Doxycycline, Erythromycin, Ciprofloxacin Lymphogranuloma venereum o Etiology: C. trachomatis o S/Sx: tender, enlarged, matted nodes [bubos] nd o Classic clinical sign of 2 stage:: double-genitocrural fold or groove sign rd o Classic sign of 3 stage: multiple draining sinuses or fistula [rupture bubos] o Dx: CFAb titer – mos frequently used serum mehod o Mgt: doxycycline, RCN, eryhromycin Chancroid o Soft chancre – painful and tender o Hard chancre – asymptomatic o Etiology: haemophilus ducreyi o Dx: culture of purulent material - “school of fish” o Mgt: erythromycin, ciprofloxacin, azithromycin Syphilis o Etiology: treponema pallidum o Stages: Primary syphilis Hard chancre, painless ulcer Secondary syphilis Red macules & papules over palms & soles of feet Latent stage No evidence of diseas Tertiary syphilis Gumma [like cold abscesses o
Resting bladder pressure is btw 20 & 30 cm H2O . Highest pressure zone in urethra is about midpoint in functional urethra, roughly 0.5 cm proximal to urogenital diaphragm. For continence to be present, UCP > bladder pressure Cystoscopy and cystometry are best used for Dx of detrusor hyperactivity MC cause of lower urinary tract infection is E. coli. Common etiologic agents in urethritis include Neisseria and Chlamydia. MC form of UTI is cystitis. Common etiologic agents in urethral diverticulum include gonococcus and E. coli. Most urethral diverticula emanate from ventral wall of urethra. MC urinary incontinence is genuine stress incontinence. 2nd MC cause of urinary i ncontinence is urge incontinence. MC groin hernias in males is i nguinal hernia, in females is femoral hernia. Anterior colporrhaphy is indicated for urethrocele and cystocele. Posterior colporrhaphy is indicated for rectocele. Classic Sx in rectocele is “heavy or falling out feeling in vagina w/ constipation or imcomplete emptying of rectal vault. Enterocele is the only type of hernia that can occur after abdominal or vaginal hysterectomy. It is usually due to weakened pouch of Douglas. Important supports in its prevention are the uterosacral and cardinal ligaments. Mixed incontinence is motor urge incontinence as a result of detrusor overactivity and stress incontinence.
INFECTIONS OF LOWER GENITAL TRACT Keyterms Clue cells – epithelial cells w/ c lusters of bacterial adherent to external surface, have granular/stippled appearance and are associated w/ bacterial vaginosis Donovan bodies – pathognomonic clusters of dark-staining bacteria found in cytoplasm of large mononuclear cells in pxs w/ granuloma inguinale. Groove sign – depression btw groups of inflammed nodes producing a double genitocrural fold in pxs w/ lymphogranuloma venereum. Gumma – infectious granuloma characteristic of late or tertiary syphilis Koilocytosis – histologic appearance of cells w/ perinuclear halo consistent w/ HPV infection Whiff test – smell of vaginal discharge after addition of 10% KOH w/c is [+] for either bacterial vaginosis or trichomonas infections.
Important facts Specific sign of acute bacterial cystitis i s suprapubic tenderness. Vulvovaginitis [external dysuria], cystitis [internal dysuria] MC pathogens causing acute urethritis: C. trachomatis & N. gonorrheae MC etiology is ascendinng infection from introitus and distal urethra. Most frequently involved pathogens in uncomplicated lower UTI are E. coli, Staph saprophyticus. Gold standard: > 10 5 uropathogens/ml Mgt of acute bacterial cystitis: o Acute uncomplicated type: TMP-SMZ x 3 days o Complicated type: quinolones BID [DOC] o Chronic/pregnant/DM – TMP- SMZ x 7-14 days o Recurrent cystitis – TMP-SMZ, nitrofurantoin Bartholin’s duct cyst is located in labia majora while bartholin’s glands are found in base of labia minora. Tx of bartholin’s duct cyst is marsupialization [if symptomatic] Most contagious of all sexually transmitted disease is pediculosis pubis, w/c is caused by phthirus pubis [crab louse]. Scabies is aka “great dermatologic imitator”, caused by Sarcoptes scabiei [itch mite ], Sx: intense pruritus at night, Tx: permethrin 5% Characteristic lesion in molluscum contagiosum [by pox virus] is [+] umbilicated papules, or water wart, Dx: intracytoplasmic molluscum bodies. MC viral sexually transmitted disease is condyloma acuminatum [by HPV]. o HPV 16, and 18 – high risk, associated w/ aneuploid, premalignant & malignant lesions. o HPV 6, 11 – associated w/ benign, euploid lesions o MC subtype of condyloma acuminatus is cauliflower-shaped. o Progress of the infection is by autoinoculation. o Classic finding is [+] cells w/ perinuclear bodies [Refer to p. 56 of OB-GYN handy notes f or clinical features of genital ulcers] Genital ulcers/genital herpes o HSV 2 – cause ulceration below waist o HSV 1 – infects epithelium above waist o Latent phase: viruses reside at dorsal root ganglia of S2-4 o Cell culture – gold standard o Western blot assay – most specific serologic test o Mgt: Acyclovir, famcyclovir, valacyclovir Granuloma inguinale [donovanosis] o Etiology: calymmatobacterium granulomatis o Characteristic lesion of ulcer: beefy-red painless ulcer w/ fresh granulation tissue
Dx: FTA-ABS & MHA-TP Mgt: PCN G – DOC for syphilis, can cause Jarisch-Herxheimer reaction Vaginitis o pH > 5.0 o 4 diagnostic criteria: 1. homogenous-grayish white discharge 2. vaginal ph > 4.5 3. [+] whiff test 4. clue cells > 20% of epithelial cells o 3 MC vaginal infections: Bacterial vaginosis Candidiasis / Moniliasis Trichomoniasis Gardnerella vaginalis C. albicans / glabrata Trichomonas vaginalis Musty/fishy odor, pruritus Pruritus, edema, Copious, frothy w/ bubbles, is rare erythema, odorless malodorous discharge Gary or white thin sticky White “cottage cheese” Green-yellow “bubbly” [+} clue cells Yeast + pseuudohyphae Flagellated protozoa [+] whiff test ‘fishy amine’ [-] whiff test May be [-/+], hanging drop tech. Metro or clindamycin Synthetic Imidazoles Metronidazole pH > 4.5 pH < 4.5 pH < 4.5 o o
Most prevalent cause of vaginitis is bacterial vaginosis/Non-specific vaginitis. MC nonviral, non-chlamydial STD of females is Trichomoniasis. Classic sign of trichomoniasis: “colpitis macularis” – strawberry-like appearance of upper vagina and cervix, [+] patchy erythema Toxic shock syndrome: o S. pyogenes – common in postpartum o S. aureus – common in children o Mgt: PCN, clindamycin, gentamycin, vancomycin, aminoglycosides Most specific test for AIDS is PCR. Cervicitis – etiology: Endocervicitis N. gonorrhea and C trachomatis Ectocervicitis T. vaginalis Mucopurulent cervicitis [urethritis in males] o Etiology: Chlamydia trachomatis, gonorrhea o Dx: modified-thayer martin [gonorrhea], McCoy cell monolayers [C. trachomatis] o Tx: azithromycin, doxycycline, erythromycin, ofloxacin
INFECTIONS OF LOWER GENITAL TRACT Keyterms Fitz-Hugh-Curtis syndrome – syndrome of perihepatic inflammation, origin from transperitoneal or vascular dissemination of either N. gonorrhea or C. trachomatis. PID – infection of upper genital tract, often use as acute s alpingitis Tubo-ovarian complex – collection of pus w/in an anatomic space created by adherence of organs involving the oviducts, ovaries
Important facts Endometritis o Etiology: C. trachomatis, N. gonorrhea, S, agalactiae o Tx: tetracycline - DOC PID o 3 major sequelae: ectopic pregnancy, chronic pain, infertility o MC cause: salpingitis [oviducts], caused by C. trachomatis o Highest risk: menstruating teenager w/ multiple sex partners w/o contraception
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Cervicitis is not included in PID Mode of infection: ascending infection from bacterial flora of vagina o Triad: fever, elevated ESR, adnexal tenderness and mass o MC complain is lower abdominal pain [hallmark] o Laparoscopy is the gold standard for Dx of PID o [Refer to p. 58 of OB-GYN handy notes for CDC guidelines in DX of Acute PID] o Mgt: ofloxacin, metronidazole, clindamycin, ceftriaxone, cefoxitin, doxycycline Actinomyces infection o Etiology: actinomyces israelli o Dx: [+] tubo-ovarian abscess – sulfur granules in gm [+] filaments Pelvic tuberculosis o Etiology: M. tb, M. bovis o Primary and predominant site of pelvic Tb are the oviducts. o Other sites: endometrium, ovaries o Gross appearance: “tobacco-appearance” in FT o Classic histologic features: giant cells, granulomas, caseous necrosis o Mgt: INH, pyrazinamide, rifampicin, streptomycin o o
PRINCIPLES OF RADIATION TX & CHEMOTHERAPY IN GYNECOLOGIC CANCER Keyterms Brachytherapy – a radiotherapy in w/c source is applied to tumor thru needles implanted into tumor [interstitial], or placed in vagina or c ervical canal [internal]. Fractionation - direct radiotherapy tx into numerous small doses to reduce damage o normal tissue Teletherapy – a form of radiotherapy w/ placement of radioactive source of a distance from px [external treatment]
Important facts Radiation primarily acts on cells in M phase, making rapidly proliferating cells the most radiosensitive. Most chemotherapeutic drugs are severely myelosuppressive except bleomycin and vincristine. Adverse effects of some chemotherapeutic drugs: Vincristine & cisplatin Severe peripheral neurotoxicity Bleomycin Severe pulmonary toxicity Doxurubicin Severe cardiomyopathy Cisplatin Nephrotoxic and myelosuppressive Taxol Severe neuropenia and neurotoxicity
INTRA-EPITHELIAL NEOPLASIA OF CERVIX Keyterms CA in situ – gives rise to or is usually present in vicinity of invasive CA, full thickness of epithelium is replaced by neoplastic cells CIN – premaalignant change in cervical epithelium that can progress to cervical CA Conization – excisional technique to remove a cone-shaped central core of c ervix for Dx and Tx of intraepithelial neoplasia Cryotherapy – freezing of cervix to abate abnormal epithelium Dysplasia Mild Involves 1/3 of epithelium [CIN 1] Moderate Involves 2/3 of epithelium [CIN 2] Severe Involves full thickness of epithelium [CIN 3]
Endocervical curettage – obtain cervical tissue for histologic section Koilocytosis – associated w/ HPV infection, including perinuclear cavitation and nuclear atypicality Leukoplakia – described an area that appears white to naked eye even before application of 3% acetic acid. Mosaic pattern – rosette appearance of capillary vessels in tr ansformation zone Punctation – stippled appearance of capillary vessels in transformation zone
Important facts Risk of progression for CIN I to a higher grade is 16%. Precise of cause of CIN is unknown but associated w/ sexual activity and HPV infection Cigarette smoking increases risk for IN, while vitamin A and E decreases risk for CIN. PAP smear is done by taking samples from endo/ectocervix, and lateral vaginal wall. [Refer to p. 65 for Modified Bethesda Classification of PAP smear in OB-GYN handy notes] Abnormal colposcopic findings: 1. Punctation or red stippling aceowhite epithelium 2. leukoplakia 3. 4. mosaic pattern of sharp-bordered lesions w/ vessels HIV infected pxs have highest risk when CD4 counts < 200. HPV infections spontaneously regress w/in 2 years. Goal of tx in CIN: eradication of all abnormal tissue. Benign vs. Malignant lesions Characteristic Benign Malignant Occurrence Unilateral Bilateral
Consistency Cystic Solid Surface Smooth Irregular Mobility Mobile Fixed Weight loss, ascites, color flow Absent Present Cervical dysplasia almost always forms at transformation zone. Papsmear only gives cytology while colposcopy and biopsy are needed for histology; w/c is needed for diagnosis, s taging and treatment. A papsmear [+] for CIN shows chromatin clumping, and decreased cytoplasm resulting in higher nucleus/cytoplasm ratio. 90% of women w. abnormal cytologic findings can be adequately evaluated w/ colposcopy. Indications for cone bopsy/LEEP: o Inadequate view of transformation zone on colposcopy o [=] ECC o + grade 2 discrepancy between colposcopic biopsy and papsmear o Tx of HGSIL and adenocarcinoma n situ Indications for cryotherapy: o Tx of LGSIL or HGSIL only if it is a l esion completely visualized on colposcopic exam Indications for laser therapy: o Excision or ablasion of CIN o Ablation during laparoscopic surgery [ex. Endometriosis]
MALIGNANT DISEASE OF THE CERVIX Keyterms Barrel-shaped cervix – contains large CA generally of endocervical origin that has replaced much of the cervix causing its di ameter to widen [>4cm]. Modified radical hysterectomy – removes uterus and cervix and some paracervical tissue but does no dissect ureters distal to uterine arteries. Persistent tumor – identification of invasive disease at si te of primary tx at < 6 mos. after therapy. Radical hysterectomy – removes uterus, upper 3 rd of vagina, cervix and paracervicalparametrial tissue. Pelvic ureters are dissected to the uterovesical junction. It is usually combined w/ pelvic LN dissection. Recurrent tumor – identification of invasive disease 6 mos. or more after therapy.
Important facts Most squamous cell CA of cervix is large cell, nonkeratinizing type. Carcinoma of the cervix o HPV 18 – common in adenocarcinoma o HPV 16 – common in SCCA [more c ommon] [Refer to p. 66 of OB-GYN handy notes f or classification of Cervical CA] [Refer to p. 67 of OB-GYN handy notes f or clinical stages of Cervix uteri] Tumor marker for adenocarcinoma is CA-125. Definitive dx of microinvasive CA is established by cervical conization. Microinvasive cervical CA effectively tx by total hysterectomy. Most cervical CA are treated by irradiation [teleherapy and brachytherapy]. Cervical CA is the 3rd MC malignancy of lower genital tract. Cervical CA is the 3rd MC gynecologic malignancy [breast CA -1 st, ovarian CA – 2nd] Symptoms of cervical CA become evident when cervical lesions are of moderate size, looks like “cauliflower”. Cancers that metastasize to cervix: RIBE [rectal, intra-abdominal, bladder, endometrial] Uremia and pyelonephritis are common causes of death in cervical CA.
MALIGNANT DISEASES OF FALLOPIAN TUBE Keyterms Hydrops tubae profluens – sx complex of abnormal vaginal discharge preceded by pain and a mass that may disappear after the discharge is noted. Tubal CA staging: Stage 1 Confined to tubes Stage 2 Spread to ovaries or pelvic tissue Stage 3 Intraperitoneal spread or involvement of retroperitoneal nodes Stage 4 Metastasis to liver parenchyma, outside peritoneum, or malignant cells in pleural fluid
Important facts 80-90% of FT malignancy are metastatic from other sites usually from ovaries , uterus, or GIT. Pathognomonic for tubal pregnancy: abnormal vaginal discharge/bleeding, lower abdominal pain, and adnexal tenderness in postmenopausal women. [triad] Peritoneum is the most frequent site of metastatic spread in tubal CA. Chemotherapy w/ cisplatin prolongs survival in tubal CA.
GESTATIONAL TROPHOBLASTIC DISEASE Keyterms Choriocarcinoma – highly malignant trophoblastic neoplasia, both c ytotrophic and syncytiotrophic growth in malignant fusion. Complete mole – molar pregnancy w/ swelling of all placental villi, absent fetal tissue
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High-risk GTD – px w/ pretreatment serum HCG > 40, 000 mIU/ml or > 4 mos. duration of disease or previous chemotherapy failure, brain or liver metastasis Hydatidiform mole – placental abnormality involving swollen placental villi and trophoblastic hyperplasia w/ loss of fetal blood vessels, may spread to extrauterine sites. Low-risk GTD – pxs w/ metastatic disease outside uterus excluding brain, liver, serum HCG < 40, 000 mIU/ml, duration < 4 mos. w/ no prior chemotherapy. Partial mole – molar pregnancy w/ some normal and swollen villi, fetal cord, and amniotic membrane elements. Placental site trophoblastic tumor – rare GTT arising from uterus and s ecretes HPL and HCG, often resistant to chemotherapy. Stages of GTT: Stage 1 Confined to corpus uteri Stage 2 Metastasis to pelvis and vagina Stage 3 Metastasis to lungs Stage 4 Distant metastasis [liver, brain, etc.] Theca-lutein cells – ovarian enlargements occurring w/ H mole and consists of theca lutein cells, regresses after tx of mole. DNA of complete mole is always paternal while DNA of partial mole i s both maternal and paternal. All early [< 20 weeks] preeclampsia is molar pregnancy GTN secrete HCG, lactogen and thyrotropin. “Sheets of trophoblast” w/ extensive hemorrhage and necrosis is diagnostic of choriocarcinoma. [it also has no villi]
NEOPLASTIC DISEASE OF OVARIES Keyterms AFP – secretory product of endodermal sinus tumors in serum and serves as specific tumor marker. Brenner tumors – resembling urothelium and so called “Walthard nest of ovary”, mixed w/ ovarian stroma. Clear cell tumor/mesonephroma – an ovarian neoplasm consists of clear cell s w/ glycogen or “hobnail cells” resemble clear cell tumors from endocervix, endometrium and vagina. Dermoid – benign, cystic germ cell tumor [cystic teratoma] w/ elements of all 3 germ layers, MC ovarian neoplasm in < 30 y.o Dysgerminoma – MC ovarian malignant germ cell tumors, w/ primitive germ cells. Endodermal sinus tumor – malignant germ cell tumor, recapitulates extraembryonic tissue and resembles yolk sac of rodent placenta. Endometriod tumor – ovarian epithelial tumor whose cells resemble uterine endometrial adenocarcinoma. Epithelial stromal tumors – MC type of ovarian neoplasms, from surface [coelomic epithelium and ovarian stroma]. Fibroma – MC benign ovarian solid tumors, compost of stromal cells and fibroblasts, and are associated w/ ascites and hydrothorax in Meig’s syndrome. Germ cell tumors – 2nd MC type of ovarian tumors, containing cells that r ecapitulate embryonic tissue [ecto, meso, endoderm] Gonadoblastoma – arises from abnormal dysgenetic gonads and consists of s ex cords stromal elements and germ cells. Granulosa-theca cell tumor – sex cord stromal tumors that secretes estrogens and consists of granulosa cells [sex cord] and ovarian stromal cells [theca cells, fibroblasts], demonstrates “Call-Exner bodies” [eosinophilic bodies in granulose cells]. Krukenberg tumor – metastasis to ovary, bilateral, w/ signet ri ng cells from GIT, most frequently from stomach and large i ntestine. Pseudomyxoma peritonei – intraperitoneal spread of mucin-secreting cells from ovarian mucinous cystadenoma or cystadenocarcinoma or from appendix leading to recurrent abdominal masses and bowel obstruction. Small cell CA – highly virulent, often accompanied by hypercalcemia. Stages of ovarian CA: Stage 1 Confined to 1 or both ovaries Stage 2 Extension to pelvic structures Stage 3 Extension to outside pelvis or retroperitoneal/inguinal nodes Stage 4 Extends outside peritoneal cavity or liver parenchyma
Important facts Trophoblastic tissues normally regresses w/in 2-3 wks after deliv ery Finding of trophoblastic cells in uterus > 3 wks after delivery signifies a [+] choriocarcinoma TOC for placental site trophoblastic tumor/trophoblastic pseudotumor is hysterectomy. H mole o A prior H mole is a major risk factor for development of gestational choriocarcinoma. o MC presenting Sx is abnormal bleeding. o Dxtic aid: snowstorm pattern on UTZ o Most effective method of emptying uterus in molar pregnancy is by suction curettage. Gestational trophoblastic neoplasia o Most frequent site of metastatic GTT are the lungs, less frequent are li ver, brain, ovary and vagina. o Non-metastatic GTT: methotrexate, actinomycin D, citravorum o High-risk GTT: methrotrexate, actinomycin D, chlorambucil or cyclophosphamide o Pxs treated for GTT should not become pregnant for 6-12 mos. after tx to allow accurate assessment of B-HCG levels. Risk of developing a molar pregnancy after a primary molar pregnancy is 20-40x greater than initial risk.
Struma ovarii – specialized ovarian stroma consists of thyroid tissue component.
Important facts Ovarian Ca is the 2nd MC malignancy of the lower part of f emale genital tract. [endometrial > ovarian > cervix]. It has the highest mortality because of its late detection. Pxs w/ ovarian CA are at increased risk for breast and endometrial CA. Most frequent ovarian neoplasms are epithelial s tromal tumors. [Refer to p. 70 of OB-GYN handy notes f or classification of ovarian neoplasms] [Refer to p. 72 of OB- GYN handy notes for Sassone’s criteria in Dx of Ovarian Malignancy + FIGO classification] Serous tumors are the most frequent ovarian epithelial tumors. It also has the worst prognosis. MC malignancy among teens and early 20s are germ cell tumors. Tumor markers: P53 tumor suppressor gene, CA-125 Ovarian epithelial CA c-myc oncogene Serous CA k-ras oncogene Borderline ovarian CA Serum LDH Dysgerminoma AFP Endodermal sinus tumors hCG Choriocarcinoma
NEOPLASTIC DISEASE OF THE VULVA Keyterms Keye’s punch – used to biopsy the vulva Lichen sclerosus – vulvar abnormality usually characterized by thinning of epithelium w/ loss of subcutaneous adnexal structure, hyalinization of superficial dermis and lymphocytic infiltrates below zone of dermal homogenization. Microinvasive vulvar CA – superficially invasive CA of vulva not associated w/ LN metastasis. Lesion < 2 cm in diameter, invasion of 1 mm into stroma. Paget’s disease of vulva – itchy, usually erythematous lesion containing large cells same to paget’s disease of breast. Stages of vulvar CA: Stage 1 < 2cm, confined to vulva and perineum Stage 2 > 2cm, confined to vulva and perineum Stage 3 Extends to anus or lower urethra, unilateral LN metastasis Stage 4 Spreads to bladder, rectum, pelvic bone, or upper urethra or nonvulvar site, bilateral LN metastasis
Important facts Vulvar CA o Mostly are squamous cell CA [usually in postmenopausal women] o Major Sx: pruritus o MC vulvar atypia is lichen sclerosus. o HPV types 6 and 11 are most frequently associated w/ benign vulvar warts. o Most lesions are located at posterior perineal area. Melanoma is the MC non-squamous cell malignancy of vulva. o Pigmented lesions of vulva are usually junctional nevi. o Mostly occur at labia minora or clitoris. o 2 MC varieties: s uperficial spreading melanoma and nodular melanoma. Intraepithelial vulvar neoplasia spontaneously regress, VIN 3 has 3-4 % risk of progression to invasive CA. A basal cell CA of vulva is treated by wide local excision. MC site of vulvar dysplasia: labia majora AdenoCA of vagina is associated w/ DES, and often presents in the young.
Benign conditions w/ elevated CA-125: 1. endometriosis 4. pregnancy 2. hemorrhagic ovarian cysts 5. leiomyoma 3. liver disease 6. PID MC germ cell tumors are benign cystic teratoma / dermoids MC malignant germ cell umor is dysgerminoma. Immature teratoma – multiple agent chemotherapy o VAC regimen: vincristine, actinomycin D and cycophosphamide o VBP regimen: vinblastine, bleomycin, cisplatin Embryonal CA is dx by both HCG and AFO [+] Polyembryomas is dx by both HCG and HPL [+] Most frequently found elements in mixed germ cell tumors are dysgerminomas and teratomas. Metastatic ovarian cell tumors frequently origi nate from endometrium and fallopian tube. Most ovarian neoplasms are dx at stage 3 or 4. Majority of ovarian epithelial tumor cell types recapitulate mullerian-type epithelium [serous-endosalpinx, mucinous-endocervix, endometrioid-endometrium].
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Malignant germ cell tumors are usually unilateral except dysgerminomas and teratomas. Risk of ovarian CA is decreased by O CPs use, BTL, and hysterectomy. 2nd MC gynecologic malignancy and is the 5 TH MC cancer in women: ovarian CA It is also the deadliest of all gynecologic malignancy MC type of ovarian CA: serous type of epithelial ovarian CA A postmenopausal woman w/ widening girth notices that she can no longer button her pants: ovarian CA Ovarian CA metastasis to umbilicus is “Sister Mary Joseph’s nodules” Ovarian and endometrial CA is staged surgically and not clinically unlike cervical CA w/c is staged clinically. MC type of ovarian GCT: dysgerminioma [tumor marker – LDH] Most aggressive GCT: endodermal sinus tumor [characterized by schiller-duval bodies] Embryonal and choriocarcinoma tumor marker: beta-HCG GCTs are very chemosensitive. Least common gynecologic malignancy: fallopian cell CA [usually adenoCA] Pathognomonic finding in fallopian tube CA: hydrops tubae perfluens In any postmenopausal bleeding or discharge that cannot be explained by endometrial biopsy, fallopian cell CA should be considered.
NEOPLASTIC DISEASE OF VAGINA Keyterms Clear cell adenocarcinoma – a vaginal or cervical malignancy occur primarily after 14 y/o, often associated w/ prenatal exposure to DES. Pelvic exenteration – extensive pelvic operation to treat central pelvic recurrence of cervical CA after radiation, a total exenteration involving removal of bladder, uterus, cervix and rectum. An anterior exenteration spares the rectum while posterior exenteration spares the bladder. Pseudosarcoma botryoides – benign tumor occurring in vagina of i nfants and pregnant females. Sarcoma botryoides / embryonal rhabdomyosarcoma – rare, often fatal vaginal malignancy occurring in infants and children. Staging of vaginal tumors: Stage 0 CIS Stage 1 CA limited to vaginal wall Stage 2 CA involving subvaginal tissuebut not extend thru pelvic wall Stage 3 CA extending to pelvic wall Stage 4 CA extending beyond true pelvis or involving mucosa of bladder or rectum
Abnormal vaginal bleeding is the MC complaint in endometrial hyperplasia. Most important prognostic factor in uterine tumors is the level of estrogen and progesterone. Leiomyosarcomas are the MC type of uterine tumors. TOC for mullerian adenosarcoma is TAHBSO. Most pxs who develop endometrial CA are btw 50-65 y.o [peri/posmenopausal years]. It is the MC malignancy of the genital tract. [Refer to p. 69 of OB-GYN handy notes f or FIGO classification of Endometrial CA] [Refer to p. 68 of OB-GYN handy notes f or classication of Endometrial hyperplasia] Chronic unopposed estrogen stimulation leads to endometrial hyperplasia and adenocarcinoma. Other predisposing factors include obesity, nulliparity, late menopause and DM. Cytologic atypia w/ endometrial hyperplasia is the most important factor in determining premalignant potential. Key determinant to risk of nodal spread is the depth of myometrial invasion w/c is often related to tumor grade. Histologic variants of enometril CA w/ poor prognosis include serous CA and cl ear cell CA. Most frequent sites of distant metastasis of adenoCA of endometrium are the l ungs, retroperitoneal nodes and abdomen. CA-125 > 35 U/ml usually suggest extrauterine disease Recurrences of uterine myomas are most frequent in pelvis, abdomen and lungs. Metastatic endolymphatic stromal myosis is tx by progestin [200 mg/d].
NEOPLASTIC DISEASE OF THE ENDOMETRIUM Important facts MC gynecologic CA: endometrial CA Gold standard for diagnosing endometrial hyperplasia and CA: biopsy MC subtype of endometrial CA: endometriod [ciliaed adenoarcinoma] Subtype w/ very poor prognosis: papillary serous CA Grade is the most important prognostic indicator in endometriod CA. Side effects of chemotherapeutic dugs: doxyrubicin [cardiotoxicity], ci splatin [nephrotoxicity], ifosphamide [hemorrhagic cystiis], etopiside [blood dyscrasia], bleomycin [pulmonary fibrosis]
REPRODUCTIVE ENDOCRINOLOGY Keyterms Activin – same structure to inhibin, stimulates pituitary FSH release and ovarian estradiol formation. Arcuate nucleus – lies on medial part of hypothalamus above median eminence, major source of GnRH secretion. Beta-endorphin – potent opioid peptide in hypothalamus and pituitary, it inhibits LH secretion. FSH – stimulates granulosa cell synthesis in females Inhibin – produced by ovarian granulose cells w/c i nhibits FSH secretion. LH – stimulates ovarian steroid synthesis in females. SHBG – serum globulin w/ high affinity to dihydroestosterone, testosterone, estradiol and androgens.
VAIN 1 / LGSIL – least severe type, mild dysplasia, l ocated in lower 3 rd epithelium VAIN 2 – intermediate severity, moderate dysplasia, a lower 2/3 of epithelium VAIN 3 – most severe type, severe dysplasia and CIS, full thickness of epithelium
Important facts VAIN 2 an 3 are combined into high-grade squamous epithelial lesion Radiation tx is the most frequent mode of treatment for SCCA of vagina. MC sx is vaginal bleeding or discharge. Most cases of VAIN occur in upper 1/3 of vaginal epithelium. VAIN can be treated by excision, laser or 5-F U. MC primary vaginal malignancy is squamous cell CA. Most CA occurring in vagina is metastatic. Vaginal CA constitutes < 2% of gynecologic malignancy. Clear cell adenoCA of vagina is associated w/ prenatal DES exposure.
NEOPLASTIC DISEASE OF THE UTERUS Keyterms Endolymphatic stromal myosis – low grade, < 10 mitoses/10 hpf endometrial stromal sarcoma Endometrial CA grading: Grade 1 Well-differentiated Adenocanthoma Grade 2 Intermediate Grade 3 Poorly differentiated Adenosquamous CA
Important facts Control of reproduction: Locus Messenger prod. Higher brain NEp, dopa, endorphins areas Hypothalamus GnRH
Anterior pituitary Ovary
Endometrial CA staging: Stage 1 Confined to uterine corpus Stage 2 Involves corpus and cervix Stage 3 Spreading outside uterus but confined in pelvis Stage 4 Spreading outside pelvis or into mucosa of bladder/rectum Complex hyperplasia – glands are irregular in s hape and often close together, low malignant potential Simple hyperplasia – consisting of proliferating glands, some dilated and w/ abundant stroma.
Important facts Postmenopausal bleeding and abnormal perimenopausal bleeding are the primary Sx of endometrial CA.
FSH, LH Estrogen, androgens & progesterone
Stimulant prod. Estrogen
Inhibitory prod. Estrogen
NEp, progesterone, estrogen GnRH, estrogen, androgen,progesterone FSH, LH
Endorphins, dopa, estrogen, androgen, Estrogen, androgen, inhibin GnRH, FSH, LH
Cell bodies that produce GnRH are located in anterior hypothalamus and medial basal/tuberal hypothalamus. Tanycytes are specialized ependymal cells from lumen of 3 rd ventricle into outermost zone of median eminence. PGE2 is luteotrophic while PGF2α is luteolytic. Normal number of oocytes; At birth 2M At 7 mos. AOG 6M Neonatal period 2M Menarche 400, 000 If ovulated < 500 Events in follicular stimulation: Recruitment Days 1-4 Selection Days 5-7 Dominance Days 8-12 Follicle monitoring Done at days 8, 10, and 12 [UTZ]
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Summary of ovarian cycle: Follicular phase Estradiol Luteal phase ↑ progesterone & estradiol Premenstrual ↓ progesterone & phase estrogen
Growth & maturation of graafian follicle Growth & maturation of corpus l uteum Regression of corpus luteum, a “cohort of follicles” start o develop
Pelvic congestion syndrome – valvular engorgement of uterus and vessels of broad ligament & lateral pelvic walls, w/c may lead to chronic pelvic pain. PMS – group of Sx, both physical & behavioral, that occur in 2 nd half of menstrual cycle & often interfere w/ work & personal relationships, ffd by period entirely free of Sx.
Important facts ↑ PGF2α levels were found in secretory endometrium than proliferative. TOC for primary dysmenorrhea is prostaglandin synthetase inhibitors [NSAIDS] OCP – DOC for pxs who desire contraception. Factors affecting prevalence & severity of dysmenorrhea: Hx of vaginal delivery Decreased OCP use Decreased Smoking Decreased Duration & amount of menstrual flow Increased Early menarche Increased Family hx among mothers and sisters Increased
Summary of menstrual cycle: Proliferative phase or Estrogen causes proliferation of stromal & epithelial cells, estrogen phase endometrium thickens [2-3 mm] w/ vessel proliferation, LH surge occurs 2 days before ovulation Secretory phase or Progesterone is secreted from corpus luteum, marked swelling & progesterone phase for mation of tortous glands and vessels, ↑ lipid & glycogen deposits, endometrium thickens about 4-6 mm Menstruation ↓ in progesterone & estrogen secretions causing vasospasm of blood vessels & initiates uterine contracion leading to desquamation
Cytologic hormonal maturation index: st rd o 1 number [parabasal cells], middle [intermediate], 3 number [superficial cells] o Ex: 0/10/90 = adequate marked estrogen effect; 200/75/5 = poor estrogen effect; 100/0/0 = no estrogen [ex. postmenopausal], 0/100/0 = maximum progesterone effect [ex. pregnancy] Most feminizing Sx are abnormal menstruation or menorrhagia. Most musculinizing Sx is hirsutism. Morphologic changes after ovulation: Day 25 Pseudodecidual reaction occurs Day 23 Active glandular secretion and stromal edema Day 18 Basal vacuolation occurs
MC causes of secondary dysmenorrhea: endometriosis>adenomyosis, IUD Common historical findings in PMS pxs include a [+] hx of maternal PMS, low levels of exercise, younger age, and higher parity. Bromocriptine is effective in relieving breast tenderness in PMS.
ABNORMAL UTERINE BLEEDING Keyterms Amenorrhea – no menses for at least 6 mos. DUB – excessive uterine bleeding w/ no demonstrable organic cause [gental/extragenital], MC due to abnormality of endocrine origin particularly anovulation. Intermenstrual bleeding – bleeding of variable amounts btw regular menses. Menometrorrhagia – prolonged uterine bleeding occurring at irregular intervals. Menorrhagia or hypermenorrhea – prolonged [> 7 days] or excessive [> 80 ml] uerine bleeding occurring at regular intervals. Metrorrhagia – uterine bleeding occurring at irregular but frequent intervals, amount being variable. Oligomenorrhea – infrequent uterine bleeding at intervals between 35 days to 6 mos. Polymenorrhea – uterine bleeding occurring at regular intervals of < 21 days, or 16-23 d.
Important events in menstrual cycle: Day 5 Glandular & stromal mitosis Day 16 Basal vacuolation Day 22 Active glandular secretion & stromal edema Day 26 Pseudodecidualization In humans, GnRH is secreted in pulsatile manner w/ T1/2 of 2-4 mins. It is more r apid in follicular phase [1 pulse/hr], luteal phase [1 pulse/2-3 hrs] NEp stimulates GnRH release while serotonin inhibits it. Principal metabolite of serotonin is 5-HIAA. Neuropeptide-Y stimulate pulsatile GnRH release and in pituitary it potentiates gonadotropin response to GnRH. Somatostatin inhibits releaseof GH, prolatin and TSH. Leuprolide acetate is a GnRH agonists while Nal-Glu i s a potent GnRH antagonist. Main action of LH is to stimulate androgen synthesis by theca cells and progesterone synthesis by corpus luteum Prostanoids produced by endometrium; PGE2, PGF2α, PGI2, and TXA2 Ovary secretes 3 primary steroids: estradiol [folli cle], progesterone [corpus luteum] and androstenedione [stroma]. Ovary lacks the ffg enzymes: 21-hydroxylase, 11-β hydroxylase and 18-hydroxylase. Estrone sulfate is the largest component of the pool of circulating estrogens. Pregnanediol-3-glucuronide is the major urinary metabolite of progesterone. Estradiol inhibits FSH while progesterone inhibits LH. Mean average of menarche = 13 y.o, for menopause = 51 y.o Duration of menses = 38 yrs Mean duration of menstrual cycle length = 28 + 7 days o Short cycles = < 21 days [polymenorrhea] o Longer cycles = > 35 days [oligmenorrhea] Mean duration of menstrual flow = 4 + 2 days Subnuclear vacuolization is the 1st histological indication of the effect of progesterone but is not evidence that ovulation has occurred. T1/2 of LH IS 30 mins while FSH is 3.9 hrs Progestin challenge tests: give progestin for 5 days then stop. This simulates progesterone withdrawal. If ovaries are secreting estrogen, sloughing will occur and menses results. No menses indicates no ovaries, no estrogen, or blood flow obstruction. Prolactin inhibits GnRH pulsations and therefore inhibits ovulation.
PRIMARY AND SECONDARY DYSMENORRHEA Keyterms Dysmenorrhea – painful cramping sensation i n lower abdomen accompanied by sweating, tachycardia, HA, NAV, diarrhea, tremulousness w/c occur j ust before or during menses. o Primary dysmenorrhea – begin at or shorlty after menarche [ovulatory cycle], not associated w/ pelvic pathologic conditions. [< 20 yo] o Secondary dysmenorrhea – arises after menarche [anovulatory cycle] and is associated w/ other pelvic conditions. [>20 y.o] Mitteschmerz – midcycle pelvic pain us ually related to ovulation, unknown mechanism.
Important facts Mean duration of menses is 4 days. Methods to quantify blood loss include: o Radioisotope labeling of RBCs o Photometric measurement to quantify hematin collected onto sanitary napkins – MC o Alkaline hematin method – most precise Mean amount of MBL in normal women is about 35 ml. MC cause of DUB i n postmenarcheal and premenopausal yrs is anovulation secondary to alterations in neuroendocrinologic function. 2 mechanisms of hemostasis during menses: o Hemostatic plug formation – most important mechanism in functional endometrium o Vasoconstriction – most important mechanism in basalis layer Progestins are the TOC for women w/ anovulatory DUB. It produces normal bleeding episode after estrogen is withdrawn. D and C is the TOC for women w/ DUB who suffer hypovolemia/hypotension and for older women who are at risk for endometrial neoplasia. Hysterectomy is indicated for women w/ persistent ovulatory DUB, or w/ leiomyomas and uterine prolapse. [alternatives: D and C, ablation] Postcoital bleeds suggests trauma, infections or cervical cancer. Always do an endometrial biopsy when encountering postmenopausal bleeding because of he strong possibility of endometrial cancer. Other bleeding tips: o Postcoital bleed in pregnant woman: consider placenta previa o Postcoital bleeding in non-pregnant woman: consider cervical cancer o Postmenopausal bleeding: c onsider endometrial cancer o Premenopausal bleeding: c onsider PCOD
Summary of tx for DUB: Observation For mild bleeding OCP For pxs who are sexually active Progesterone If not sexually active, premenopausal women Clomiphene If w/ infertility problems, induction of ovulation Average loss of iron in each menses is 13 mg. Organic cause of abnormality in uterine bleeding vs. DUB Organic cause DUB Any age Extremes of age Ovulatory Anovulatory [MC cause] Regular, cyclic dysmenorrhea Irregular, non-cyclic, no pain Not responsive to treatment Responsive to hormonal tx Secretory endomerium Proliferating or hyperplastic
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Biphasic BBT
Summary for DUB: Menorrhagia Metrorrhagia Menometrorrhagia Hypermenorrhea Hypomenorrhea Oligomenorrhea Polymenorrhea
Monophasic BBT
Regular Irregular Irregular Regular Regular Irregular Regular
Prolonged + prolonged + prolonged Normal Normal or ↓ Variable [>35d] Regular [ 30 mIUml]. Hypothalamic dysfunction – secondary amenorrhea caused by abnormal pattern of GnRH pulsatility & circulatory estradiol levels > 40 pg/ml. Hypothalamic failure – secondary amenorrhea due to abnormal pattern of GnRH pulsatility & estradiol levels < 40 pg/ml. Intrauterine adhesions / synechiae/ Ashermann’s syndrome – fibrous tissue partially/completely obliterates uterine cavity. Pituitary destruction – damage or necrosis of pituitary gland caused by anoxia, thrombosis or hemorrhage. It is known as Sheehan’s syndrome when related to pregn ancy and Simmond’s disease when unrelated to pregnancy. Polycystic ovarian syndrome – characterized by excessive androgen production, inappropriate gonadotropin secretion & chronic anovulation, begins perimenarcheally manifesting w/ hyperandrogenism [hirsutism, oligo/amenorrhea] Premature ovarian failure – cessation of menses due to depletion of ovarian follicles or failure of primordial follicles to respond to gonadotropins. Sheehan’s syndrome – postpartum pituitary necrosis Sigmond’s syndrome – pituitary hemorrhage not related to pregnancy
Presumptions: breast present means that estrogen is produced uterus present means Y chromosome is absent
HYPERPROLACTINEMIA, GALACTORRHEA, AND PITUITARY ADENOMAS Keyterms Bromocriptine – dopa-receptor agonists use to treat hyperprolactnemia. Carbegoline – dopa-receptor agonist that directly inhibits secretion of prolactin from pituitary and is an effective tx for hyperprolactinemia. Empty-sella syndrome – an intrasellar extension of subarachnoid space resulting in compression of pituitary gland and an enlarged sella turcica associated w/ galactorrhea and hyperprolactinemia. Galactorrhea – non-puerperal secretion from breast of watery or milky fluid that contains either pus or blood. Hyperprolactinemia – levels of circulating prolac tin above normal [> 20-25 ng/ml] that can cause galactorrhea or amenorrhea or both. PIF – neurotransmitter [dopa] that inhibits prolactin synthesis and release. Prolactinoma – MC pituitary tumor arising from c hromophobic cells that secrete prolactin.
Important facts Main function of Prolactin is to stimulate growth of mammary tissue as well as produce & secrete milk into alveoli. Major physiologic inhibitor of prolactin release is dopamine. Most frequent cause of slightly elevated prolactin levels is stress. Diagnostic test of choice for prolactinoma is MRI. Main Sx in hyperprolactemia are galactorrhea and amenorrhea.
HYPERANDROGENISM Keyterms Acanthosis nigricans – dark, raised hyperpigmentation of skin found on nape and axilla. Crytic hyperandrogenism – elevated levels of circulating androgens w/o clinical manifestation of hirsutism or acne, accompanied by anovuation. Hilus cell tumor – small testosterone-secreting ovarian tumor developing after menopause. Hyperandrogenic chronic anovulation – consists of endocrine findings in polycystic ovarian syndrome w/o morphologic and sonographic findings of polycystic ovaries. Idiopathic hirsutism [constitutional/familial hirsutism] – MC d/o associated w/ androgen excess, due to increased peripheral androgen metabolism, normal circulating levels of testosterone and DHEAS. PCOS – characterized by excessive ovarian androgen production, abnormal gonadotropin secretion, chronic anovulation, w/ morphologic changes in ovary consisting of multiple small subcapsular follicles, increased stromal tissues & ovarian enargement. Sertoli or leydig cell tumors – testosterone secreting ovarian tumors usually unilateral. Spironolactone – aldosterone antagonist acting as anti-androgen by binding to peripheral androgen receptor w/o inducing androgenic activity. It also inhibits steroidogenesis by interfering w/ ovarian enzymatic activity in pilosebaceous unit. Stromal hyperthecosis – characterized by nests of luteinized theca cells w/in stroma of bilaterally enlarged ovaries, associated w/ virilization.
Important facts 1st sign of puberty is appearance of breast budding followed by appearance of pubic hair. Earliest sign of puberty is breast budding & menarche. Mean interval btw breast budding and menarche is 2-3 yrs. Arbitrary age of primary amenorrhea is 16 ½ yrs. Ratio of fat to both total body weight & lean body weight is the most relevant factor tha determines time of onset f puberty and menstruation. The most frequent antecedent factor of intrauterine adhesions is endometrial curettage associated w/ pregnancy. It is confirmed by hysterography or hysteroscopy. MC cause of secondary amenorrhea in adolescent women is anorexia nervosa, w/c is due to hypothalamic dysfunction. MC cause of primary amenorrhea is gonadal failure. 2nd MC cause of primary amenorrhea is uterovaginal agenesis. Dx of gonadal failure or hyeprgonadotrophic hypogonadism can be established by FSH levels > 30 mIU/ml. MC non-prolactin secreting pituitary tumors are chromophobe adenomas. MC mullerian anomaly is imperforate hymen. Tx: cruciate incision MC form of hypogonadism in females is Turner’s syndrome. MC cause of delayed puberty is constitutional delay. Some etiologies of amenorrhea: o Kallman’s syndrome: congenital lack of GnRH o Sheehan’s syndrome: pituitary infarction resulting from hypotension during delivery, usually resulting from hemorrhage. o Premature ovarian failure: menopause before age 35 o Savage’s syndrome: ovarian resistance to FSH/LH o Turner’s syndrome [XO karyotype]: ovarian dys genesis
Important facts Major androgen produced by ovaries is testosterone, for adrenal gland is DHEAS. Ovaries secrete about 0.1 mg of testosterone/day from thce-stromal cells MC cause of androgen excess in females is idiopathic hirsutism. “Halo sign” in UTZ is characteristic of PCOS. Its S/Sx include amenorrhea, hirsutism and obesity. MC cause of sexual ambiguity in newborn is congenital adrenal hyperplasia. Spironolactone is the TOC for PCOS and idiopathic hirsutism. Summary of tx for hirsutism: If w/ ↑ testosterone, excess ovarian androgen production OCPs If w/ ↑ DHEAS, excess androgen secretion Dexamethasone If neither is increased Spironolactone
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3 markers of androgen production: Ovary Testosterone Adrenal gland DHEAS Peripheral 3α–diol-G
o
Hair-Van syndrome triad: acanthosis nigricans, hyperandrogenism, insulin resistance.
INFERTILITY Keyterms Artificial insemination – sperm placed in female reproductive tract other than by sex. It is also known as donor or therapeutic donor insemination. Asthenospermia – loss or r eduction of motility of spermatozoa. Azoospermia – absence of sperm in semen. [i.e Klinefelter, varicocele] Clomiphene citrate – given to induce ovulation in anovulatory females w/ circulating estradiol levels of > 40 pg/ml. Gamete intrafallopian transfer [GIFT] – placement of human ova and sperm into distal end of oviduct. In vitro fertilization [IVF] – fertilization of human ova by sperm in the lab. Infertility – inability of couples of reproductive age to establish a pregnancy by having sexual intercourse w/in a certain period of time [usually 1 yr] Oligospermia - < 20 M sperm/ml of semen Ovarian hyperstimulation syndrome – ovarian enlargement to a diameter of > 6 cm due to stimulation of multiple follicles. Primary infertility – occurs in woman who has never been pregnant Salpingitis isthmica nodosa – diverticula of endosalpinx in muscularis of isthmic part of oviduct. Secondary infertility – it occur after 1 or more pregnancy Spinbarkeit – property of elasticity or disensibiity of cervical mucus. Teratozoosermia – greater than normal incidence of abnormal forms of sperm in semen analysis.
Important facts Measurement of LH by urinary LH immunoassays is the best way to detect optimal time to have intercourse or insemination. Clomiphene citrate is the TOC for females w oligomenorrhea as well as amenorrhea who have sufficient ovarian estradiol production. S/E: ovarian cyst formation Intracytoplasmic sperm injection is now the TOC for all causes of male infertility as well as for those w/ no known cause of infertility. If GnRH is used for ovulation induction, it needs to be administered in a pulsatile manner at intervals of 1-2 hours. [Refer to p. 76-77 of OB-GYN handy notes for causes of Infertility]
MC cause of primary amenorrhea: gonadal dysgenesis MC cause of fetal morbidity and mortality: preterm labor o MC reason for neonatal sepsis: chorioamnionitis [GBS, E. coli] o MC congenital adrenal hyperplasia: 21-hydroxyase deficiency High LH: FSH ratio in the context of androgen excess indicates that ovary is the source. A baby w ambiguous genitalia, dangerously hypotensive, and w/ elevated 17hydroxyproesterone: 21-hydroxylase deficiency 11-β hydroxylase deficiency: low cortisol, high mi neral corticoids [hypertensive], and high androgens + elevated 11-deoxycortisol. 21-hydroxylase deficiency: low cortisol and mineral corticoids [hypotensive], high androgens + 17-hydroxyprogesterone is elevated. 24 y/o obese woman w/ facial hair comes in w/ complaints of amenorrhea. LH: FSH ratio is elevated: PCOS [tx w/ OCPs] A baby w/ ambiguous genitalia is born to a mother who complains of increased facial hair growth over the last few months: luteoma of pregnancy o
Pelvic pain Chronic pelvic pain is defines as > 6 mos. of pain. MC cause of chronic pelvic pain: PID Pelvic pain associated w/ ovulation: mittelschmerz Final conclusive step in diagnosing pelvic pain: l aparoscopy MC cause of acute pelvic pain ruptured cysts
Pelvic masses Histories suggestive of diagnosis: Context in w/c pelvic mass is found Painless abnormal uterine bleeding Amenorrhea Dysmenorrhea Reproductive age
Postmenopausal Hx of PID Hx of surgery/endometriosis
Likely diagnosis Leiomyoma Pregnancy, ovarian cysts Endometriosis Preganancy, ovarian cysts, leiomyoma, TOA, ovarian neoplasm Neoplasm S/sx of systemic illness [TOA, adhesion] Adhesions
MENOPAUSE Keyterms Atrophic vaginitis – inflammation of vaginal epithelium due to atrophy secondary to decreased circulating estrogen. Climacteric – physiologic product in female life during w/c there is regression of ovarian function. Apparent clinically over 3-5 yrs around menopause. HRT – administration of estrogen and progestin. Hot flush – pathognomonic sign of menopause caused by decreased in circulating estrogen levels. Menopause – complete or permanent cessation of menses indicated by finl menstrual period, often during the climacteric. Interval of 6-12 mos. is needed, usual age: 45-55 y.o Premature ovarian failure / premature menopause – cessation of menses due to depletion of ovarian follicles before age 35-40. Raloxifene – estrogen agonist effect on bone by suppressing bone resorption & an estrogen antagonist effect on endometrium and breast tissue. Selective estrogen receptor stimulator [SERM] – agents that bind to estrogen receptor and have estrogen agonist effect on other tissue. Tibolone – synthetic steroid w/ estrogenic, progestogenic and androgenic activity, reduces hot flushes, increases bone density and does not stimulate endometrial proliferation when given orally.
MC causes of undiagnosed pelvic masses: leiomyomas Diagnostic tests for various causes of pelvic masses: Ovarian cysts PE + UTZ for confirmation Leiomyomas PE + UTZ, hysteroscopy for confirmation Ovarian neoplasm UTZ, CT scan, CA-125, family hx, age suspicion Endometrial neoplasm ECC and D and C Tubo-ovarian abscess Hx of PID, tender mass, KUB xray [ileus]
Important facts Initial fall in inhibin levels is the 1st index of declining ovarian function. Most effective tx for hot flushes is estrogen, alternative is progestogen. Spine and hip are the MC location of osteoporotic fractures. Contraindications to estrogen treatment: presence of breast or endometrial CA, active thrombophlebitis and undiagnosed AUB. Median age of onset of menopause is 47.5 yrs, and is median length is 4 yrs.
MC functional ovarian cysts: follicular cyst MC indication for hysterectomy leiomyoma Extremely rarely do leiomyomas progress to malignancy [leiomyosarcoma] MC type of leiomyomas: subserous type Leiomyomas/fibroids are hormonally responsive smooth muscle tumors. Changes in uterine fibroids over time: hyaline degeneration, calcification, red degeneration [painful interstitial hemorrhage w/ pregnancy, and cystic degeneration] Uterine locations of leiomyomas: Submucous Just below endometrium, tend o bleed Menorrhagia Intramural w/in the uterine wall Menorrhagia Subserous Just below he serosa/peritoneum Torsion Pregnancy w/ fibroids does carry increased risk for preterm labor and feral malpresentation.
Sexually transmitted diseases Gold standard for diagnosis of PID: laparoscopy Chandelier sign: when you touch the cervix, there is so much pain that she jumps to the chandelier. Common causative agents in PID: N. gonorrhea, C. trachomatis, E. coli, Bacteroides Gold standard for diagnosis of gonorrhea: culture on Thayer-Martin agar There is 50-90% chance of transmission after 1 exposure to gonorrhea. Fitz-Hugh-Curtis perihepatitis presents as RUQ pain, fever, nausea and vomiting. It can be caused by chlmydia or gonorrhea. Use erythromycin rather than doxyycline for pregnant women or children w/ chlamydia. CS delivery is indicated for active herpes infection. A very specific test in dx of AIDS western blot Whiff test: combining vaginal secretions w 10% KOH: amines rel eased will give fishy odor, indicating a [+] tests
Important Gynecologic concepts Some most common: o MC cause of hirsutism: PCOD o MC reason for hospitalization in women of reproductive age: endometriosis o MC post-operative complication: pulmonary atelectasis
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MISCELLANEOUS [OBSTETRICS & GYNECOLOGY] Most common MC cause of gynecologic malignancy MC CA in women MC liver CA associated w/ OCP use MC CA invading female GUT MC type of endometrial adenoCA MC form of ductal CA in-situ of breast MC CA of breast – primary, malignant Least common CA of the breast MC CA of breast – primary, benign MC congenital anomaly of breast MC malignant neoplasm of breast w/ calcifications MC breast disorder/breast mass MC breast CA presenting w/ architectural distortion w/o a discrete density MC mammographic presentation of an invasive CA MC cause of bloody nipple discharge in F > 50 y.o MC cause of green, straw-colored nipple discharge MC cause of breast mass after a trauma MC breast mass in postmenopausal women MC CA of connective tissue/soft issue – benign MC site of origin of metastatic tumor to ovary MC site of vaginal epithelial tumor MC CA of ovary during pregnancy MC CA of ovary – benign, primary MC CA of ovary – malignant, primary MC CA of ovary – benign MC germ cell tumor of ovary MC germ cell tumor of anterior mediastinum Most important criteria for dx btw borderline ovarian tumor & frank CA MC uterine site for implantation MC finding in uterine rupture MC CA of uterus – primary MC CA of uterus MC CA of vulvar & cervix MC CA of testicles & the most malignant MC CA of testicles [overall] MC CA in uncircumcised men Most radiosensitive testicular tumor MC germinal tumor in males MC fusion defect of the urethra in men MC metastatic site of prostate CA MC cause of acute urinary retention in men MC cause of venereal disease in men MC cause of UTI in males MC CA of breast in males MC cause of PID MC cause of UTI in young women MC cause of STD [overall] MC cause of STD in adolescents MC cause of venereal disease in women MC cause of ectopic tubal pregnancy MC cause of vaginitis & vulvar infections / pruritus MC cause of vulvovaginitis MC viral cause of vulvo-vaginal infections MC bacterial cause of vulvo-vaginal infections MC cause of hemosalpinx MC cause of suppurative salpingitis MC cause of ambiguous genitalia MC chromosomal anomaly in early spontaneous abortion MC chromosomal anomaly in 1 st trimester abortion MC chromosomal anomaly in cysti c hygroma in 2 nd or 3rd trimester MC chromosomal anomaly associated w/ choroids plexus cyst MC chromosomal disorder MC ectopic tubal implantation site Most definitive treatment for CIN Most sensitive pregnancy test Most specific test of Amniotic fluid to exclude i ntraamniotic infection MC cause of stillbirth
Endometrial CA Leiomyoma Hepatocellular adenoma Endometrial adenoCA Endometrial CA Comedo DCIS Invasive ductal CA Papillary CA Fibroadenoma Supernumerary nipples [vs. accessory nipples] Ductal CA in situ Fibrocystic changes Lobular CA Speculated density Ductal papilloma Fibrocystic disease Fat necrosis Breast carcinoma Lipoma Stomach [Krukenberg tumor] Upper part of posterior wall Dysgerminoma Serous cystadenoma Serous cystadenocarcinoma Mature teratoma [epithelial tumors] Mature cystic teratoma Seminoma Stromal invasion Upper posterior wall Fetal distress Leiomyoma adenoCA SCCA chorioCA Seminoma SCCA Seminoma Seminoma Hypospadias Pelvis BPH Non-gonococcal urethritis Prostatic hypertrophy Infiltrating ductal CA N. gonorrhea > C. trachomatis E. coli, S. saprophyticus Chlamydia Condyloma acuminatum Gonorrhea PID Candidiasis [C. albicans] Candidiasis & moniliasis HPV [condyloma acuminatum] G. vaginalis Ectopic pregnancy [MC complaint = pain] Gonococcus Androgenital syndrome 45 X Autosomal trisomy Monosomy X Trisomy 18 Down’s syndrome or trisomy 21 Ampulla Hysterectomy b-HCG Gram stain Syphilis
Main lesion in syphilis MC neonatal infection or white plaques in children MC site of metastatic trophoblastic disease MC CA of placenta – benign MC placental lesion MC Sx in placenta previa In abruption placenta MC pregnancy complication in women w/ unicornuate uterus MC serious medical complication of pregnancy MC serious liver disease in pregnancy MC cause of Cushing syndrome in pregnancy MC benign mesenteric masses MC cause of SAH during pregnancy Most likely cause of spider angioma in pregnancy Most important characteristic of baseline FHR Most sensitive method to dx CMV infection MC method of family planning MC complication of multiple gestation MC complication of SLE during pregnancy MC neurologic abnormality in neonatal period MC neurologic disorder of neonatal period MC congenital anomaly of he nervous system MC cause of neonatal sepsis MC cause of primary amenorrhea MC cause of fetal morbidity & mortality MC cause of acute & chronic pelvic pain MC type of fistula formation after prolonged obstructive labor MC cause of undiagnosed pelvic masses MC functional ovarian cyst MC reason for hospitalization in women of reproductive age MC indication for hysterectomy MC used test to detect APAS antibodies Most specific clotting test to identify lupus MC source of cerebral artery embolism during pregnancy MC pregnancy complication of benign ovarian cyst MC fetal presentation to enter the pelvis MC cause of oligohydramnios MC cause of innocent heart murmur in childhood MC type of conjoined twin MC intrapartum presentation of twins Most critical period w/ regards to developmental malformations Most likely the cause of fetal-maternal hemorrhage MC inherited bleeding disorder Most significant fetal consequence of GDM MC birth defect in women w/ overt DM Most appropriate method of contraception for DM MC maternal complication of hydramnios MC recognizable COD in fetus MC cause of severe DIC in pregnancy MC cause of PP he requiring hysterectomy MC cause of primary LTCS MC postpartum complication of precipitous labor MC breech presentation MC finding in molar pregnancy MC finding in uterine rupture Most significant factor in postpartum metritis Most ideal anesthetic for replacing inverted uterus Most ideal anesthetic for non-OB surgery at preg. MC extrauterine disease requiring surgical treatment during pregnancy MC cause of episiotomy breakdown MC cause of dystocia MC cause of uterine rupture MC cause of fetal tachycardia Most reliable sign of fetal compromise MC deceleration pattern during labor Most reliably detected part of fetal ECG Earliest morphologic evidence of ovulation found i n endometrium MC site of endometriosis MC site of breast CA
Endarteritis Thrush [candidal stomatitis] Lungs Cavernous hemangioma [vs. chorioangioma] Placental infarcts Painless vaginal bleeding Painful vaginal bleeding Abortion Pyelonephritis Hepatitis Benign adrenal tumor Chylous or mesenteric cyst Ruptured cerebral aneurysm Estrogen Beat-to-beat variability CMV IgM titer Tubal sterilization Preterm delivery HPN Asphyxial brain injury Hypotonia Myelomeningocoele Chorioamnionitis Gonadal dysgenesis Preterm labor Rupture ovarian cyst & PID Vesico-vaginal fistula Leiomyomas Follicular cyst Endometriosis Leiomyomas ELISA Platelet neutralization Heart Torsion LOT Renal anomalies Still’s murmur Thoracophagus Cephalic-cephalic Embryonic period Chorioangioma Von willebrand disease Macrosomia CHD Sterilization Abruption placenta Abruption placenta Abruption placenta Placenta accrete Dystocia Hemorrhage Frank breech Increase uterine size Fetal distress Route of delivery Halothane General anesthesia Appendicitis Infection Pelvic contraction & uterine dysfunction Separation of previous CS scar Maternal fever Reduced baseline variability Variable deceleration R wave peak Basal vacuolation Ovaries Upper outer quadrant
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RAPID REVIEW Treatment for breastfeeding mastitis MC cause of non-obstetric postpartum death Postmaturity syndrome characteristics Cardinal movements of labor
A pregnant w/ Hct = 10, is this normal? Test used to detect NTDs Test at 10 th wk AOG to screen for chromosomal abnormalities Antihypertensive in px w/ severe preeclampsia Abnormal HR pattern in CST Seizure prophylaxis in severe preeclampsia Cure for ecclmpsia & preeclampsia Cause of erythroblastosis fetalis Cause of hydrops fetalis Preeclampsia in 1st trimester is Primary causes of 3 rd trimester bleeding Chromosomal pattern of complete mole Molar pregnancy containing fetal tissue Antibiotics w/ teratogenic effects Shortest AP diameter of pelvis Meds given to accelerate fetal lung maturity MC cause of postpartum hemorrhage Tx of postpartum hemorrhage Typical antibiotics for GBS prophylaxis Px fails to lactate after CS w/marked blood loss Cause of amenorrhea w/ normal prolactin, no response to estrogen, progesterone challenge & hx of D and C Therapy for PCOS Medication used to induce ovulation Dxtic step required in postmenopausal women w/ vaginal bleeding Indications for medical treatment of ectopic pregnancy Medical options for endometriosis Uterine bleeding at 8 wks AOG, no products expelled, cervical os is closed Uterine bleeding at 18 wks AOG, no products expelled, membrane ruptured, cervical os open Laparoscopic findings in endometriosis Natural history of melanoma Px w/ increased vaginal discharge & petechial patches in upper vagina & cervix Tx for bacterial vaginosis Contraception that protects against PID Unopposed estrogen is contraindicated in Px w/ recent PID & RUQ pain Annual screening for women w/ strong family hx of ovarian CA Lab values suggestive of menopause MC cause of female infertility 2 consecutive findings of ASCUS, next step?
Continue BF & give PO antibiotics Thromboembolic disease Oligohydramnios & passage of meconium in utero, “scrawny” neonate w/ dry, peeling skin Engagement, descent, flexion, internal rotation, extension, external rotation, expulsion No. a Hct < 11 should raise IDA suspect AFP or amniocentesis Chorionic villous sampling Hydralazine & labetalol Late decelerations [fetal hypoxia] IV magnesium sulfate Delivery Maternal antibodies against infant’s Rh-[+] RBC result in fetal RBC hemolysis ↓ protein production by fetal liver l eading to ↓ oncotic pressure, edema & cardiac failure H mole Abruption placenta & placenta previa 46, XX Partial mole TCN, fluoroquinolones, aminoglycosides, sulfonamides Obstetric conjugate [btw sacral & pubis] Betamethasone or dexamethasone x 48 hrs Uterine atony Uterine massage or oxytocin IV PCN or ampicillin Sheehan’s syndrome [postpartum necrosis] Ashermann’s syndrome
Weight loss & OCPs Clomiphene citrate Endometrial biopsy Stable, unruptured ectopic pregnancy of < 3.5 cm at 6 wks gestation OCPs, danazol, GnRH agonists Threatened abortion Inevitable abortion
“chocolate cysts & powder burns” Regresses after menopause Trichomonas vaginitis Oral or topical metronidazole OCP & barrier contraception Endometrial or estrogen receptor [+] CA Fitz-Hugh-Curtis syndrome CA-125 & transvaginal UTZ Elevated serum FSH Endometriosis Colposcopy & endocervical curettage
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