1 Flashcards
(500 cards)
1
Q
What is the physiologic source of human chorionic gonadotropin (hCG)?
A
Produced by placental syncytiotrophoblasts, first appears in maternal blood 10 d after fertilization, peaking at 9–10 wks, then falling to a plateau at 20–22 wks. Glycoprotein with 2 subunits. Alpha–subunit is similar to LH, FSH, TSH. Beta is specific.
2
Q
What are the purposes of beta–hCG?
A
Maintains corpus luteum production of progesterone until placenta can synthesize progesterone and take over maintenance of pregnancy. Regulates steroid biosynthesis in placenta and fetal adrenal.
3
Q
What is the signifiance of beta–hCG levels in pregnancy?
A
Inadequate beta–hCG levels indicate ectopic, threatened abortion, missed abortion.
4
Q
What is the structure of human placental lactogen?
A
Structure is similar to anterior pituitary growth hormone and prolactin. The level of HPL parallels placental growth, rising throughout pregnancy.
5
Q
What is the role of human placental lactogen?
A
Antagonizes cellular action of insulin, decreasing insulin utilization, thereby contributing to the predisposition of pregnancy to glucose intolerance and diabetes. Low levels indicate a risk of threatened abortion, intrauterine growth restriction (IUGR).
6
Q
What is progesterone?
A
Steroid hormone produced after ovulation by the luteal cells of the corpus luteum. Induces endometrial secretory changes favorable for blastocyst implantation.
7
Q
What is the source of progesterone?
A
Initially produced exclusively by the corpus luteum up to menstrual weeks 6–7. Between 7 and 9 weeks, both the corpus luteum and the placenta produce progesterone. After 9 wks, corpus luteum involutes, and progesterone is exclusively made by placenta.
8
Q
What is the significance of an elevated progesterone level during pregnancy?
A
Twin pregnancy, hydatidiform mole, choriocarcinoma, embryonal carcinoma
9
Q
What are the purposes of progesterone?
A
In early pregnancy, progesterone induces endometrial secretory changes favorable for blastocyst implantation. In later pregnancy, progesterone induces immune tolerance for the pregnancy and prevents myometrial contractions.
10
Q
What are estrogens?
A
Steroid hormones, which occur in three forms, estradiol, estriol, and estrone.
11
Q
What is estradiol?
A
Predominant moiety during nonpregnant reproductive years is estradiol. It is converted from androgens in follicular theca cells; androgens diffuse into follicular granulosa cells where aromatase completes the transformation into estradiol.
12
Q
What is estriol?
A
Main estrogen during pregnancy. Dehydroepiandrosterone–sulfate (DHEAS) from the fetal adrenal gland is the precursor for 90% of estriol converted by sulfatase enzyme in the placenta.
13
Q
What is estrone?
A
Main form of estrogen during menopause. Postmenopausal adrenal androstenedione is converted in peripheral adipose tissue to estrone.
14
Q
What are the skin changes during pregnancy?
A
Striae gravidarum are stretch marks” on abdomen. Spider angiomata and palmer erythema from increased skin vascularity. Linea nigra is pigmentation of from pubis to umbilicus. Chloasma is blotchy pigmentation of nose and face.”
15
Q
What is the Chadwick sign?
A
Bluish or purplish discoloration of the vagina and cervix as a result of increased vascularity.
16
Q
What are the blood pressure changes during pregnancy?
A
Systolic and diastolic decline early in 1st trimester, nadir by 24–28 weeks, then pressures gradually rise toward term but never return completely to prepregnancy baseline. Diastolic falls more than systolic. Elevated BP is never normal in pregnancy.
17
Q
What are the plasma volume changes during pregnancy?
A
Plasma volume increases up to 50% with a significant increase by the first trimester. Maximum increase is by 30 weeks. Plasma volume increases with multiple fetuses.
18
Q
What are the systemic vascular resistance changes during pregnancy?
A
SVR equals blood pressure (BP) divided by cardiac output (CO). Because BP decreases and CO increases, SVR declines by 30%, reaching its nadir by 20 weeks, enhancing uteroplacental perfusion.
19
Q
What are the cardiac output changes during pregnancy?
A
CO increases up to 50%. HR increases by 20 beats/min by 3rd trimester. SV increases by 30% by end of 1st trimester. CO is lowest supine because of inferior vena cava compression. CO is highest in left lateral position.
20
Q
What is the effect of pregnancy on heart murmurs?
A
A systolic ejection murmur along the left sternal border is normal in pregnancy because of increased CO through the aortic and pulmonary valves. Diastolic murmurs are never normal in pregnancy and must be investigated.
21
Q
What are the red blood cells mass changes during pregnancy?
A
RBC mass increases by 30%; O2–capacity increases. Because plasma volume increases by 50%, the calculated hemoglobin and hematocrit values decrease by 15%. Nadir of Hb is at 28–30 weeks’ gestation. Decreases in Hb and Hct are dilutional effects.
22
Q
What are the white blood cell changes during pregnancy?
A
WBC count increases progressively during pregnancy with a mean value of up to 16,000/mm3 in the third trimester. ESR increases in pregnancy because of the increased gamma globulins. Platelet count is unchanged in pregnancy.
23
Q
What is the effect of pregnancy on coagulation factors?
A
Factors VII, VIII, LX, and X increase progressively in pregnancy, resulting in a hypercoagulable state.
24
Q
How does pregnancy affect the stomach?
A
Gastric motility decreases and emptying time increases from progesterone effect. Increase in stomach residual volume and upward displacement of intraabdominal contents by gravid uterus predisposes to aspiration pneumonia with anesthesia.
25
What is the effect of pregnancy on the large bowel?
Colonic motility decreases and transit time increases from the progesterone effect on smooth muscle. These changes predispose to increased colonic fluid absorption, resulting in constipation.
26
How does pregnancy affect tidal volume?
Tidal volume (Vt) is volume of air that moves in and out of the lungs at rest. Vt increases with pregnancy to 40%. Tidal volume is the only lung volume that does not decrease with pregnancy.
27
How does pregnancy affect minute ventilation?
Te increases up to 40%, with the major increase by 20 weeks. Te is the product of respiratory rate (RR) and Vt. RR remains unchanged with Vt increasing steadily throughout the pregnancy into the third trimester.
28
How does pregnancy affect residual volume?
RV is the volume of air trapped in the lungs after deepest expiration. RV decreases up to 20% by the third trimester because of the upward displacement of intraabdominal contents against diaphragm by the gravid uterus.
29
How does pregnancy affect blood gases?
The rise in Vt produces a respiratory alkalosis with a decrease in Pco2 from 40 to 35 mm Hg, and an increase in pH from 7.40 to 7.45. An increased renal loss of bicarbonate compensates for the alkalosis, resulting in alkalotic urine.
30
How does pregnancy affect the kidneys?
The kidneys increase in size during pregnancy because of increased renal blood flow. Ureteral diameter increases because of the progesterone effect on smooth muscle. GFR, renal plasma flow, creatinine clearance increase 50% at end 1st trimester.
31
What is the effect of pregnancy on blood urea nitrogen, creatinine, and uric acid?
25% decrease in serum blood urea nitrogen, creatinine, and uric acid.
32
How does pregnancy affect urine glucose?
Glucosuria. Urine glucose normally increases. Glucose is freely filtered and actively reabsorbed. Urine protein remains unchanged.
33
What hormones stimulate breast development in females?
From infancy to puberty, there is no difference between female and male breasts. With beginning of female puberty, release of estrogen, and then progesterone, causes the breasts to change into mature form over 3 to 4 years, and complete by 16.
34
What is the anatomy of the female breast?
Fibrous and fatty tissue and 15–20 lobes in each breast. 80% of breast is fat during reproductive years. Lobes are further divided into lobules containing alveoli of secretory cells with ducts that conduct to a reservoir under the nipple.
35
What are the breast structure changes of pregnancy?
During pregnancy, the alveoli enlarge; and during lactation, the cells secrete milk proteins and lipids. With the release of oxytocin, the muscular cells surrounding the alveoli contract to express the milk during lactation.
36
What are Cooper?s ligaments?
Cooper's ligaments keep the breasts in the characteristic shape and position and support breast tissue. In the elderly or during pregnancy, these ligaments become loose or stretched.
37
What is the effect of estrogen on the breasts?
Estrogen, released from the ovarian follicle, promotes the growth ducts.
38
What is the effect of progesterone on the breasts?
Progesterone, released from the corpus luteum, stimulates the development of milk– producing alveolar cells.
39
What is the effect of prolactin on the breasts?
Prolactin, released from the anterior pituitary gland, stimulates milk production.
40
What is the purpose of oxytocin?
Released from the posterior pituitary in response to suckling, causes milk ejection from the lactating breast.
41
What are the breasts changes during pregnancy?
Breasts become fully developed under influence of estrogen, progesterone, and prolactin during pregnancy. Prolactin causes production of milk. Oxytocin release from suckling reflex causes ducts to eject milk from the nipple.
42
What is the first secretion of the mammary gland after delivery?
Colostrum, which contains more protein and less fat than milk. Contains IgA that impart passive immunity to infant. Milk production occurs 1 to 3 days after delivery. Expulsion of placenta initiates milk production; causes drop in E and P.
43
What is the effect of suckling on milk production?
Physical stimulation of suckling causes the release of oxytocin and stimulates prolactin secretion, causing increased milk production.
44
What is the most significant event of postconceptional week 1?
Implantation of the blastocyst on the endometrium. Week 1 begins with fertilization of the egg and ends with implantation of the blastocyst onto the endometrial surface. Fertilization usually occurs in the distal part of the oviduct.
45
For what period of time is the egg fertilizable?
The egg is capable of being fertilized for 12–24 hours. The sperm is capable of fertilizing for 24–48 hours.
46
What events occur in postconception of week 2?
Development of bilaminar germ disk with epiblast and hypoblast layers. Layers give rise to 3 germ layers. Invasion of maternal sinusoids by syncytiotrophoblast occurs. beta–hCG is produced in syncytiotrophoblast and enters maternal blood.
47
What event occurs during postconception week 3?
Migration of cells through the primitive streak between the epiblast and hypoblast to form the trilaminar germ disk with ectoderm, mesoderm, and endoderm layers. These layers will give rise to the major organs and organ systems.
48
What event occurs during postconception weeks 4–8?
Major organs are formed. Period of major teratogenic risk. Ectoderm forms central and peripheral nervous systems; organs of seeing, hearing; integument. Mesoderm: muscles, cartilage, CVS, urogenital. Endoderm forms lining GI, respiratory tracts.
49
What happens to the paramesonephric (Mullerian) duct in males?
Present in all early embryos and is primordium of female system. In males, Y chromosome induces gonadal secretion of Mullerian inhibitory factor, which causes Mullerian duct to involute.
50
What happens to the paramesonephric (Mullerian) duct in females?
In females, without Mullerian inhibitory factor, the Mullerian duct develops into the fallopian tubes, uterus, cervix, and proximal vagina.
51
What hormonal stimulation is needed for differentiation of the external female genitalia?
No hormonal stimulation is needed for differentiation of the external genitalia into labia majora, labia minora, clitoris, and distal vagina.
52
What is the mesonephric (Wolffian) duct?
Present in early embryos and is primordium of male system. T causes development of vas deferens, seminal vesicles, epididymis, efferent ducts. In females, Wolffian duct regresses.
53
What will happen to the Wolffian duct if a genetic male has absence of testosterone receptors?
If a genetic male has absence of androgen receptors, the Wolffian duct will regress and there will be absence of vas deferens, seminial vesicles, epidymis, and efferent ducts.
54
What hormonal stimulation is causes differentiation of the male external genitalia?
Dihydrotestosterone stimulation is needed for differentiation of the external genitalia into a penis and scrotum. If a genetic male has an absence of androgen receptors, external genitalia will differentiate into a female phenotype.
55
What are the infectious teratogens?
Bacteria (eg, chlamydia and gonorrhea cause neonatal eye and ear infections), viral (eg, rubella, cytomegalovirus, herpes virus), spirochetes (eg, syphilis), or protozoa (eg, toxoplasmosis).
56
What weeks of gestation are associated with greatest risk of teratogenicity from ionizing radiation?
No increase is seen in fetal anomalies or pregnancy losses with exposure of
57
What are the adverse pregnancy effects of cocaine?
Tobacco is associated with intrauterine growth restriction (IUGR) and preterm delivery, but no specific syndrome.
58
What are the teratogenic effects of alcohol?
Fetal alcohol syndrome: midfacial hypoplasia, microcephaly, mental retardation, and IUGR.
59
What are the adverse pregnancy effects of cocaine?
Placental abruption, preterm delivery, intraventricular hemorrhage, and IUGR. Marijuana is associated with preterm delivery but not with any syndrome.
60
What is a FDA pregnancy category A drug?
Controlled studies show no risk. Adequate studies show no risk to the fetus in any pregnancy trimester. Category A includes acetaminophen, thyroxine, folic acid, and magnesium sulfate.
61
What is a FDA pregnancy category B drug?
No evidence of risk in humans. Controlled studies show no risk to humans despite adverse findings in animals. Category B includes penicillin, cephalosporins, methyldopa, insulin, Pepcid, Reglan, Tagamet, Vistaril, Paxil, Prozac, Benadryl, and Dramamine.
62
What is a FDA category C drug?
Risk cannot be ruled out. Controlled studies are lacking in humans and animals. Category C includes codeine, Decadron, methadone, Bactrim, Cipro, AZT, beta–blockers, Prilosec, heparin, Protamine, Thorazine, Robitussin, and Sudafed.
63
What is a FDA category D drug?
Positive evidence of risk. Studies demonstrate fetal risk, but potential benefits of the drug may outweigh the risk. Category D includes aspirin, Valium, tetracycline, Dilantin, Depakote, and lithium.
64
What is a FDA category X drug?
Contraindicated in pregnancy. Studies demonstrate fetal risk, which outweighs any possible benefit. Category X includes Accutane (isotretinoin), Danocrine, Pravachol, coumadin, and Cafergot.
65
What is the teratogenic effect of alcohol?
Fetal alcohol syndrome: IUGR, midfacial hypoplasia, developmental delay, short palpebral fissures, long philtrum, joint anomalies, cardiac defects.
66
What is the teratogenic effect of diethylstilbestrol?
DES syndrome: T–shaped uterus, vaginal adenosis (predisposition to vaginal clear cell carcinoma), cervical hood, incompetent cervix, preterm delivery.
67
What is the teratogenic effect of dilantin?
Fetal hydantoin syndrome: IUGR, craniofacial dysmorphism (epicanthal folds, depressed nasal bridge, oral clefts), mental retardation, microcephaly, nail hypoplasia, heart defects.
68
What is the teratogenic effect of isotretinoin (Accutane)?
Congenital deafness, microtia, CNS defects, congenital heart defects.
69
What is the teratogenic effect of lithium?
Ebstein's anomaly (right heart defect).
70
What is the teratogenic effect of streptomycin?
Cranial nerve VIII damage, hearing loss.
71
What is the teratogenic effect of tetracycline?
Deciduous teeth discoloration after the fourth month.
72
What is the teratogenic effect of thalidomide?
Phocomelia, limb reduction defects, ear/nasal anomalies, cardiac defects, pyloric or duodenal stenosis.
73
What is the teratogenic effect of trimethadione?
Facial dysmorphism (short upturned nose, slanted eyebrows), cardiac defects, IUGR, mental retardation.
74
What is the teratogenic effect of valproic acid (Depakote)?
Neural tube defects (spina bifida), cleft lip, renal defects.
75
What is the teratogenic effect of warfarin (Coumadin)?
Chondrodysplasia (stippled epiphysis), microcephaly, mental retardation, optic atrophy.
76
What is gravidity?
The total number of pregnancies, irrespective of pregnancy duration. A nulligravida is a woman who is not currently pregnant and has never been pregnant. A primigravida is a woman who is pregnant currently for first time.
77
What is a multigravida?
Woman who is pregnant for more than first time. Parity is total number of pregnancies achieving >20 weeks' gestation.
78
What is a nullipara?
A nullipara is a woman who has never carried a pregnancy achieving 20 weeks' gestation. A primipara is a woman who has carried one pregnancy to 20 weeks' gestation.
79
What is multipara?
A woman who has carried more than one pregnancy to 20 weeks' gestation.
80
What is puerpera?
Woman who has just given birth.
81
What is an abortion?
Pregnancy loss prior to 20 menstrual weeks.
82
What is an antepartum death?
Fetal death between 20 menstrual weeks and the onset of labor.
83
What is an intrapartum death?
Fetal death from onset of labor to birth.
84
What is a fetal death?
Fetal death between 20 menstrual weeks and birth.
85
What is a perinatal death?
Fetal/neonatal death from 20 menstrual weeks to 28 days after birth.
86
What is a neonatal death?
Newborn death between birth and the first 28 days of life.
87
What is birth rate?
Number of live births per 1,000 total population.
88
What is the fetal mortality rate?
Number of fetal deaths per 1,000 total births.
89
What is the neonatal mortality rate?
Number of neonatal deaths per 1,000 live births.
90
What is a perinatal mortality rate?
Number of fetal plus neonatal deaths per 1,000 total births.
91
What is infant mortality rate?
Number of infant deaths per 1,000 live births.
92
What is the maternal mortality rate?
Number of maternal deaths per 100,000 live births.
93
What is an advanced maternal age?
Women
94
What is aneuploidy?
Cells do not contain 2 complete sets of 23 chromosomes. Most common aneuploidy is trisomy, presence of an extra chromosome. Most trisomies result in spontaneous abortions.
95
What is the most common trisomy at term?
The most common trisomy at term is trisomy 21. The most common trisomy in first–trimester losses is trisomy 16.
96
What is polyploidy?
Cells contain complete sets of extra chromosomes. Most common polyploidy is triploidy, with 69 chromosomes, followed by tetraploidy, with 92 chromosomes. Incomplete mole is a triploidy caused by fertilization of 1 egg by 2 sperm.
97
What are structural chromosomal alterations?
Conditions in which chromosomal material is deleted, gained, or rearranged. Alterations can involve single or multiple chromosomes. An example of a chromosomal deletion is cri du chat syndrome, which is a deletion of short arm of chromosome 5.
98
What is mosaicism?
Two or more cytogenetically distinct cell lines in the same individual. Mosaicism can involve the placenta, the fetus, or both. Gonadal mosaicism can result in premature ovarian failure and predispose to gonadal malignancies.
99
What is a reciprocal translocation?
Involves any 2 or more nonhomologous chromosomes when there is a breakage and reunion of portions of chromosomes to yield new products.
100
What is the chromosomal composition of carriers of balanced reciprocal translocations?
Carriers of balanced reciprocal translocations have 46 chromosomes, with both derivative chromosomes present.
101
What is a Robertsonian translocation?
Involves acrocentric chromosomes, and centric fusion after loss of satellite region of short arms of original chromosome. Karyotype will have 45 chromosomes; however, full complement of genetic material is present; no clinical effects.
102
What percentage of miscarried abortuses have abnormal chromosomes?
At least 50% of 1st trimester abortuses have abnormal chromosomes. 2 most common aneuploidies in miscarriages are trisomy 16 and monosomy X. Fifty percent of these abnormalities are autosomal trisomies, with trisomy 16 most common.
103
What is Turner syndrome?
Also known as gonadal dysgenesis. Seen in 1 in 10,000 births. In most cases it is the result of loss of the paternal X chromosome. 98% of these conceptions abort spontaneously. Ultrasound shows nuchal skin–fold thickening, cystic hygroma.
104
What are the clinical manifestations of Turner syndrome?
Absence of secondary sexual, short stature, streak gonads, primary amenorrhea, infertility, broad chest, web neck. Urinary tract anomalies, aortic coarctation are common. Intelligence is usually normal.
105
What is Klinefelter syndrome?
Klinefelter syndrome is seen in 1 in 2,000 births. Diagnosis is made at puberty. Tall stature, testicular atrophy, azoospermia, gynecomastia, and truncal obesity. Learning disorders and low IQ.
106
What is incidence of Down syndrome?
Trisomy 21. One in 800 births; 50% of cytogenetic diseases at term. Increases with maternal age.
107
What are the clinical signs of trisomy 21?
Mental retardation, short stature, hypotonia, brachycephaly, short neck. Oblique orbital fissures, flat nasal bridge, small ears, nystagmus, protruding tongue. Endocardial cushion defects, duodenal atresia.
108
What is Edward syndrome?
Trisomy 18 causes profound mental retardation, rocker–bottom feet and clenched fists. Survival to 1 year of age by only 40%. Seen more frequently with advancing maternal age.
109
What is Patau syndrome?
Trisomy 13 is profound mental retardation, cyclopia, proboscis, holoprosencephaly, and severe cleft lip with palate. Survival to 1 year of age by only 40%. Seen more frequent with advancing maternal age.
110
What is the triad of Down syndrome?
Short stature, mental retardation, endocardial cushion cardiac defects.
111
What percentage of live born infants have a congenital Mendelian genetic disorder?
1% of liveborn infants have a Mendelian disorder. 15% of all birth defects are Mendelian disorders. 70% of Mendelian disorders are autosomal dominant. Remainder are autosomal recessive, X–linked, or multifactorial.
112
What are the genetics of autosomal dominant disorders?
Transmission equally to males, females; serial generations are affected. Each affected individual has affected parent. Affected individuals will transmit disease to 50% of offspring. Unaffected individuals bear unaffected children. No carrier states.
113
What are the most common clinical manifestations of autosomal dominant disorders?
Most common findings are anatomic abnormalities. Age of onset is delayed, with variability in expression.
114
What are the most common autosomal dominant disorders?
Polydactyly, Marfan syndrome, Huntington chorea, myotonic dystrophy, achondroplasia, polycystic kidneys, neurofibromatosis, osteogenesis imperfecta.
115
What are the genetics of autosomal recessive disorder?
Transmission equally to males and females; often skips generations. Enzyme deficiencies most common. Age of onset is earlier. If both parents are heterozygous, 25% of offspring affected, 50% are carriers, 25% are normal. Carrier states common.
116
What is the heritance pattern if one parent is homozygous and one parent is heterozygous for autosomal recessive disorders?
If one parent homozygous and one heterozygous, 50% of offspring affected, and 50% will be carriers. If both parents homozygous, 100% of children affected.
117
What are the most common autosomal recessive disorders?
Deafness, cystic fibrosis, Thalassemia, albinism, sickle cell anemia, Tay–Sachs disease, phenylketonuria, congenital adrenal hyperplasia, Wilson disease
118
What are the genetics of X–linked recessive disorders?
Conditions are dominant in men, but dominant or recessive in women.
119
What is the transmission pattern for X–linked recessive disorders?
No male–to–male transmission (because father gives only his Y to his son). Transmission is 100% male–to–female. Transmission from heterozygous females to male offspring in an autosomally dominant pattern.
120
What is the the pattern of expression for X–linked recessive disorders?
Disease is expressed in all males who carry gene, and disease is expressed only in male relatives with the gene.
121
What are the most common X–linked recessive disorders?
Hemophilia A, color blindness, diabetes insipidus, G–6–PD deficiency, hydrocephalus, Duchenne muscular dystrophy, complete androgen insensitivity.
122
What is the triad of autosomal dominant disorders?
Transmitted by both sexes. All generations affected. No carrier states.
123
What is the triad of autosomal recessive disorders?
Transmitted by both sexes. Often skips generations. Male and female carriers.
124
What is the triad of X–Linked recessive disorders?
No male–male transmission. Expressed only in males. Female carriers.
125
What are the genetics of X–linked dominant disorders?
The disease is manifested in female heterozygotes as well as carrier males (hemizygotes); hypophosphatemic rickets. The disease is manifested in female heterozygotes, but is lethal in males, causing abortion; incontinentia pigmenti.
126
What is the prevalence of multifactorial birth defects?
Majority of birth defects (70%) are multifactorial; caused by interaction of multiple genes with environmental factors. Increased frequency of disorder in families. Recurrence rate is 2–3%. The more severe the malformation, the higher the recurrence.
127
What are the most common multifactorial birth defects?
Neural tube defects, congenital heart disease, cleft lip and palate, and pyloric stenosis.
128
What are neural tube defects?
Incidence is 2 per 1,000 births. Failure of neural tube closure. Anencephaly and spina bifida occur with equal frequency. Preconception folic acid supplementation decreases incidence NTD.
129
What is the incidence of congenital heart disease?
1% of births. Majority multifactorial. Distinguish isolated defects should be distinguished from those that are part of a syndrome with a higher recurrence risk. Preconception folate reduces the risk of CHD and neural tube defects.
130
What is the incidence of cleft lip and palate?
The incidence is 1 per 1,000 births. The risk of cleft lip in a second child of unaffected parents is 4%. If two children are affected, the risk of the third child being affected is 10%.
131
What is the heritance pattern for pyloric stenosis?
More common in males. The risk of the condition in the offspring of an affected parent is much greater if the affected parent is female.
132
What is the epidemiology of induced abortions?
Nearly half of all pregnancies among American women are unintended, and four in 10 of these are terminated by abortion. A quarter of all pregnancies end in abortion.
133
What are the risks associated with induced abortion?
Early first–trimester abortions pose virtually no long–term risk of infertility, ectopic pregnancy, spontaneous abortion. 0.3% of abortion patients experience a complication that requires hospitalization.
134
What is vacuum curettage–dilation and curettage?
D&C is most common abortion procedure (90%), and is performed before 13 weeks'. Prophylactic antibiotics, conscious sedation, paracervical block. The cervical canal is dilated with cervical dilators or hygroscopic/osmotic dilators.
135
What are the complications of vacuum curettage?
Complications are rare but include endometritis, treated with outpatient antibiotics; and retained products of conception, treated by repeat curettage. Maternal mortality rate is 1 per 100,000 women.
136
What is a medical abortion?
Induction of abortion using oral mifepristone (Mifeprex; a progesterone antagonist) and buccal misoprostol (Cytotec; prostaglandin E1). Limited to first 63 days of amenorrhea. 85% abort within 3 days.
137
What are the complications of mifepristone/misoptostol induction of abortion?
2% abort incompletely and require vacuum curettage. Clostridium sordellii sepsis is a rare complication.
138
What is dilation and evacuation?
Most common 2nd trimester abortion procedure. Laminaria dilators placed 24 hours. Early 2nd trimester abortions can be performed by vacuum aspiration alone. If the fetus is more than 14 weeks, the fetus is morcellated with ultrasound guidance.
139
What is an intact D&E?
Involves more advanced pregnancies. 2 days of Laminaria for wide cervical dilation, allowing assisted breech delivery under ultrasound. Decompression of calvaria with the fetus delivered intact. Also called a partial birth" abortion."
140
What are the complications of induced abortions?
Immediate complications may include uterine perforation, retained tissue, hemorrhage, infection, and, rarely, disseminated intravascular coagulation.
141
What labor induction methods are used for intact induced abortion?
Hypertonic, intra–amniotic saline or urea, prostaglandins (intraamniotic PGF2a), vaginal PGE2 (dinoprostone), IM 15–methyl PGF2a (Hemabate), PGE1 (misoprostol). Delivery of a live fetus may require feticidal, intracardiac KCl or digoxin.
142
What is spontaneous abortion?
Bleeding that occurs before 12 weeks' gestation. The most common cause of early pregnancy loss is fetal abnormalities.
143
What is the etiology of most cases of spontaneous abortion?
Cytogenetic abnormalities cause the majority of early pregnancy losses because of gross chromosomal abnormalities of the fetus. Other losses may be caused by Mendelian autosomal or X–linked dominant or recessive diseases.
144
What antibody is associated with repeat spontaneous abortions?
Anticardiolipin antibody is an uncommon cause of early pregnancy loss. Some women with SLE produce antibodies against vascular system and fetoplacental tissues. This is known as antiphospholipid syndrome.
145
What is the treatment of spontaneous abortion?
Speculum exam for vaginal or cervical lesions. RhoGAM for all Rh–negative gravidas who undergo dilatation and curettage. Molar and ectopic pregnancy should be ruled out by ultrasound in all patients with early pregnancy bleeding.
146
What are the signs of missed abortion?
Ultrasound finding of a nonviable pregnancy without vaginal bleeding, uterine cramping, or cervical dilation.
147
What is the management of missed abortion?
Scheduled suction D&C, conservative management awaiting a spontaneous completed abortion, or induce contractions with misoprostol (Cytotec).
148
What are the signs of threatened abortion?
Ultrasound finding of a viable pregnancy with vaginal bleeding but absence of cervical dilation. Half of threatened abortions will continue to term successfully. Management is observation.
149
What is the presentation of inevitable abortion?
Vaginal bleeding and uterine cramping leading to cervical dilation, but no product of conception has been passed.
150
What is the management of inevitable abortion?
Emergency suction D&C to prevent further blood loss and anemia.
151
What is an incomplete abortion?
Vaginal bleeding and uterine cramping leading to cervical dilation, with some, but not all, product of conception have been passed. Management is emergency suction D&C to prevent further blood loss and anemia.
152
What is the presentation of completed abortion?
Vaginal bleeding and uterine cramping after all product of conception has been passed. Confirmed by a sonogram showing no intrauterine contents or debris.
153
What is the management of completed abortion?
Conservative. If an intrauterine pregnancy has been previously confirmed. Otherwise, serial beta–human chorionic gonadotropin levels should be obtained weekly until negative to verify that an ectopic pregnancy has not been missed.
154
What is intrauterine fetal demise?
In utero death of a fetus after 20 weeks' gestation before birth. Antenatal demise occurs before labor. Intrapartum demise occurs after the onset of labor.
155
What is the most serious complication of intrauterine fetal demise?
Disseminated intravascular coagulation may occur with prolonged fetal demise (>2 weeks), resulting from release of tissue thromboplastin from deteriorating fetal organs.
156
What are the causes of intrauterine fetal demise?
Most commonly idiopathic. Other causes include antiphospholipid syndrome, overt maternal diabetes, maternal trauma, severe maternal isoimmunization, fetal aneuploidy, and fetal infection.
157
What is the presentation of intrauterine fetal demise?
Before 20 weeks' gestation, the most common finding is uterine fundus less than dates. After 20 weeks' gestation, the most common symptom is maternal report of absence of fetal movements.
158
How is intrauterine fetal demise diagnosed?
Ultrasound demonstrates lack of fetal cardiac activity.
159
What is the management of intrauterine fetal demise if DIC is present?
Coagulopathy should be assessed with platelet count, d–dimer, fibrinogen, prothrombin time, partial thromboplastin time. If DIC is identified, immediate delivery is necessary with selective blood product transfusion if indicated.
160
What is the management of intrauterine fetal demise if DIC is not present?
A dilatation and evacuation may be appropriate in pregnancies of 20 weeks or if a fetal autopsy is indicated.
161
What tests may identify the cause of intrauterine fetal demise?
Cervical and placental cultures for suspected infection, autopsy for suspected lethal anatomic syndrome, karyotype for aneuploidy, total body x–ray for suspected osteochondrodysplasia, maternal blood for Kleihauer–Betke.
162
What is ectopic pregnancy?
Pregnancy in which implantation has occurred outside of the uterine cavity. The most common location is in the oviduct.
163
What is the differential diagnosis of abnormal vaginal bleeding with a positive pregnancy test?
Threatened abortion, incomplete abortion, ectopic pregnancy, and hydatidiform mole. The possibility of pregnancy or a complication of pregnancy should always be considered.
164
What are the risk factors for ectopic pregnancy?
Scarring from PID, IUD, tubal ligation, tubal surgery, or congenital (diethylstilbestrol exposure). 1% of pregnancies are ectopic pregnancies, and if the patient has had one ectopic pregnancy, the incidence becomes 15%.
165
What is the triad of ectopic pregnancy?
Secondary amenorrhea. Unilateral abdominal/pelvic pain. Vaginal bleeding.
166
What are the symptoms of ectopic pregnancy?
The classic triad with an unruptured ectopic pregnancy is amenorrhea, vaginal bleeding, and unilateral pelvic–abdominal pain. Ruptured ectopic pregnancy causes symptoms of intraperitoneal bleeding and irritation.
167
What are the signs of ectopic pregnancy?
Unilateral adnexal and cervical motion tenderness. Uterine enlargement and fever are absent. Ruptured ectopic pregnancy, causes signs of peritoneal irritation (guarding/rigidity), hypovolemia. Hypotension, tachycardia indicate significant blood loss.
168
What are the laboratory abnormalities in ectopic pregnancy?
Beta–hCG test will be positive. Sonography may reveal an adnexal mass; but no intrauterine pregnancy will be seen even though the beta–HCG is positive.
169
How is ectopic pregnancy diagnosed?
Failure to see a normal intrauterine gestational sac when the serum beta–hCG titer is >1,500 mIU is presumptive diagnosis of an ectopic pregnancy.
170
What are the signs of ruptured ectopic pregnancy?
The diagnosis of ruptured ectopic pregnancy is presumed with a history of amenorrhea, vaginal bleeding, and abdominal pain in the presence of a hemodynamically unstable patient. Laparoscopic intervention to stop the bleeding is necessary.
171
What is the management of intrauterine pregnancy with bleeding?
If the sonogram reveals an IUP, the diagnosis is threatened abortion, the patient should be placed on bed rest. If the diagnosis is hydatidiform mole, the patient should be treated with a suction curettage and followed up on a weekly basis with beta–hCG.
172
What is the management of a possible ectopic pregnancy?
If sonogram does not reveal IUP, but beta–hCG is 1,500 mIU.
173
What is the management of unruptured ectopic pregnancy?
Medical management with methotrexate is preferred.
174
What is the criteria for use of methotrexate for ectopic pregnancy?
Folate antagonist attacks proliferating tissues including trophoblastic villi. Criteria: pregnancy mass
175
What is the follow–up management after methotrexate for ectopic pregnancy?
Follow–up serial beta–hCG levels to ensure pregnancy resolution. Rh–negative women should receive RhoGAM.
176
What is the treatment of ectopic pregnancy if methotrexate is contraindicated?
Salpingostomy. Isthmic tubal pregnancies are managed with segmental resection. Salpingectomy is for ruptured ectopic pregnancy or if no desire for further fertility.
177
What is the follow–up management after a salpingostomy for ectopic pregnancy?
After a salpingostomy, beta–hCG titers should be obtained weekly. Rh–negative women receive Rho GAM.
178
What is chorionic villus sampling?
Performed under ultrasound without anesthesia. Catheter is placed transcervically or transabdominally into placenta. Chorionic villi (placental precursors) are aspirated between 10–12 wks, and sent for karyotyping. Loss in 0.7%.
179
What is amniocentesis?
Performed after 15 wks under ultrasound without anesthesia. Needle is placed into amniotic fluid under ultrasound guidance, aspirating fluid containing desquamated fetal amniocytes. Pregnancy loss rate 0.5%.
180
What tests are done on fetal amniocytes after amniocentesis?
Fetal karyotyping is performed on amniocytes. Neural tube defect screening is performed on amniotic fluid with biochemical analysis (AF–AFP and acetylcholinesterase).
181
What is percutaneous umbilical blood sampling?
PUBS is a transabdominal procedure under ultrasound; aspirates fetal blood from umbilical vein after 20 wks'. Blood gases, karyotype, IgG and IgM antibodies; intrauterine transfusion with fetal anemia. Loss rate 2%.
182
What is fetoscopy?
Transabdominal with a fiberoptic scope in operating room after 20 weeks under anesthesia. Intrauterine surgery or fetal skin biopsy for ichthyosis. Laser of placental vessels in twin–twin transfusion syndrome. Pregnancy loss rate 2–5%.
183
What is cervical cerclage?
Transvaginal therapeutic procedure performed between 14 and 24 weeks' gestation, placing a suture that encircles the cervix to prevent cervical dilation. Performed under either regional or general anesthesia in cervical insufficiency.
184
What are the presumptive signs of pregnancy?
Presumptive signs of pregnancy include amenorrhea, breast tenderness, nausea and vomiting, increased skin pigmentation, and skin striae.
185
What are probable signs of pregnancy?
Enlargement of the uterus, maternal sensation of uterine contractions or fetal movement, Hegar sign (softening of the junction between the corpus and cervix), and positive beta–hCG.
186
What are the positive signs of pregnancy?
Hearing fetal heart tones, sonographic visualization of a fetus, perception of fetal movements by an external examiner, and x–ray showing a fetal skeleton.
187
What is normal pregnancy duration postconception?
266 days or 38 weeks. However, most women can't identify conception date accurately.
188
What is the normal duration of pregnancy from the last menstrual period?
280 days or 40 weeks from the LMP. Assumes a 28–day menstrual cycle in which ovulation occurs on day 14 after the beginning of the LMP. Only 10% of women have a 28–day cycle.
189
What is Naegele's Rule?
Assuming 28–day cycles, the due date can be estimated as the LMP minus 3 months plus 7 days.
190
What is the duration of the first trimester?
Assuming a 40 menstrual week pregnancy, the first trimester is assumed to extend from conception through to 13 weeks.
191
What are the common complaints associated with the first trimester?
Nausea, vomiting, fatigue, breast tenderness, frequent urination are normal. Spotting and bleeding in 20% of pregnancies, 50% of which will continue successfully. Average weight gain is 5–8 pounds.
192
What are the normal symptoms during the second trimester?
2nd trimester extends from 13 to 26 wks. Normal symptoms are sense of well–being, round ligament pain, Braxton–Hicks contractions (painless, low–intensity, long–duration contractions). Avg weight gain is 1 lb/wk after 20 wks.
193
When does quickening occur during pregnancy?
Quickening (maternal awareness of fetal movement) is detected at 18–20 weeks by primigravidas and 16–20 weeks by multigravidas.
194
What complications can occur in the second trimester?
Complications include incompetent cervix (painless cervical dilation leading to delivery of a nonviable fetus); premature membrane rupture, and premature labor.
195
What are the normal symptoms during the third trimester?
3rd trimester extends from 26 to 40 wks. Decreased libido, lower back/leg pain, frequency, Braxton–Hicks. Lightening is descent of head, resulting in pelvic pressure. Bloody show is passage of bloody mucus from cervical dilation before labor.
196
What is the average weight gain during the third trimester?
Average weight gain is 1 pound per week after 20 weeks.
197
What are the complications of the third trimester?
Complications include premature membrane rupture, premature labor, preeclampsia, urinary tract infection, anemia, and gestational diabetes.
198
What are the breast changes in pregnancy?
Breast enlargement. Each breast increases in size by 400 grams. Management is a support bra.
199
What percentage of women develop carpal tunnel syndrome during pregnancy?
50% of pregnant women will experience numbness, tingling, burning, or pain in at least two of the three digits supplied by the median nerve. Management is a wrist splint (resolves after delivery).
200
What are the complexion changes of pregnancy?
Some women develop brownish or yellowish patches called chloasma on their faces. Linea nigra may develop on lower abdominal midline. Hyperpigmentation of nipples and genitalia may also occur.
201
What is the fluid change of pregnancy?
Increased circulating steroid levels and decreased serum albumin results in edema in half of pregnant women. Edema is not a criterion for preeclampsia. Management is elevating legs and using support hose.
202
What are the hair and nail changes of pregnancy?
Hair shedding decreases in pregnancy. Telogen effluvium is the excessive shedding of hair occurring 1–5 months after pregnancy. Telogen effluvium occurs in 40–50% of women. Nails become more brittle.
203
What is the cause of headache during pregnancy?
Muscle contraction and migraine headaches are more common in pregnancy because of increased estrogen. Management is ice packs, acetaminophen.
204
What is the treatment of leg cramps during pregnancy?
Lower extremity muscle cramps are frequent in pregnancy. Management is hydration, stretching exercises, and calcium supplementation.
205
What is the treatment of morning sickness during pregnancy?
Nausea and vomiting are common in early pregnancy and are mediated by elevated hCG. Management is eating small meals with crackers and carbohydrates.
206
What is the treatment of stress incontinence during pregnancy?
Pressure on the bladder with an enlarging uterus frequently causes involuntary loss of urine. Management is Kegel exercises.
207
What is the treatment of varicose veins during pregnancy?
Lower–extremity varicosities are caused by increased blood volume, the relaxing effect of progesterone on smooth muscle, and an increased lower–extremity venous pressure. Discourage prolonged standing and sitting.
208
What are the causes of vaginal bleeding during pregnancy?
Early (spontaneous abortion). Later (abruption, previa).
209
What are the causes of vaginal fluid leakage during pregnancy?
Membrane rupture (ROM). Urinary incontinence.
210
What is a serious cause of epigastric pain during pregnancy?
Severe preeclampsia.
211
What are the causes of uterine cramping during pregnancy?
Preterm labor, preterm contractions.
212
What is a possible cause of decreased fetal movement during pregnancy?
Fetal compromise.
213
What are the causes of persistent vomiting during pregnancy?
Hyperemesis (early), hepatitis, pyelonephritis.
214
What are the serious causes of headache and visual changes during pregnancy?
Severe preeclampsia
215
What are the causes of pain with urination during pregnancy?
Cystitis, pyelonephritis.
216
What are the causes of chills and fever during pregnancy?
Pyelonephritis, chorioamnionitis.
217
What are the safe immunizations during pregnancy?
Antigens from killed or inactivated organisms: killed influenza (all pregnant women in flu season); hepatitis B (pre– and postexposure); hepatitis A (pre– and postexposure); pneumococcus (high–risk women); meningococcus (in outbreaks).
218
Which vaccinations are unsafe during pregnancy?
Unsafe immunizations include antigens from live attenuated organisms: measles, mumps, polio, rubella, yellow fever, varicella.
219
What is the normal pregnancy hemoglobin?
Reference range is 10–12 g/dL. The nonpregnant female hemoglobin reference range is 12–14 g/dL. Values in pregnancy reflect dilutional effect of greater plasma volume increase than red blood cell mass.
220
What is the most reliable predictor of anemia during pregnancy?
MCV is the most reliable predictor of true anemia. A low hemoglobin and low MCV (100) suggests folate deficiency.
221
What are the causes of a low platelet count during pregnancy?
A low platelet count (
222
What are the causes of a low leukocyte count during pregnancy?
White blood cell count in pregnancy is normally up to 16,000/mm3. Leukopenia suggests immune suppression or leukemia.
223
What is the significance of a positive rubella IgG antibody test in pregnancy?
The presence of rubella antibodies rules out a primary infection during pregnancy. Antibodies derived from a natural, wild infection lead to lifelong immunity. Antibodies from live–attenuated virus are less durable.
224
What is the management of a negative rubella IgG during pregnancy?
Absence of antibodies is risk for a primary rubella infection in pregnancy, which can be teratogenic, particularly in 1st trimester. Rubella immunization is contraindicated in pregnancy because it is live. Immunize after delivery.
225
What is the significance of a positive hepatitis B Virus (HBV) surface antibody test?
HBV surface antibodies are expected from a successful vaccination.
226
What is the significance of a positive hepatitis surface antigen?
HBV surface antigen represents either a previous or current infection and high risk for vertical transmission of HBV from the mother to the fetus or neonate. S antigen is the only hepatitis test obtained on prenatal laboratory panel.
227
What is the significance of a positive hepatitis B E antigen?
The presence of HBV E antigen signifies a highly infectious state.
228
What is the significance of a positive direct Coombs test?
The patient's blood type and Rh is determined with the direct Coombs test. If the patient is Rh negative, she is at risk for anti–D isoimmunization.
229
What is the significance of a positive indirect Coombs test or atypical antibody test?
The presence of atypical RBC antibodies is determined with the indirect Coombs test. Isoimmunization is identified if atypical antibodies are present. Follow–up testing is necessary to identify whether the fetus is at risk.
230
What is the prenatal screening for syphilis?
Nonspecific screening tests (VDRL or rapid plasma reagin [RPR]) are performed on all pregnant women. Positive screening tests must be followed with treponema–specific tests (MHATP or FTA).
231
What urine screening is included in prenatal labs?
Assessment of proteinuria, ketones, glucose, leukocytes, and bacteria is important to screen for underlying renal disease, diabetes, and infection.
232
What is the significance of asymptomatic bacteriuria?
Eight percent of pregnant women have ASB. 30% of ASB progresses to pyelonephritis if untreated, which is associated with septic shock, pulmonary edema, and adult respiratory distress syndrome.
233
What is the significance of a positive PPD or Tine test?
Screening skin test that determines previous exposure to TB. A positive test is induration, not erythema. If the screening test is negative, no further follow–up is necessary. TB screening should be done only on high–risk populations.
234
What is the management of a positive PPD test during pregnancy?
Chest x–ray to rule out active disease. If chest x–ray negative, start isoniazid and vitamin B6 are given for 9 months. If chest x–ray positive, induced sputum is cultured and triple medications begun. AntiTb drugs are safe in pregnancy.
235
At what time after infection is the HIV ELISA test positive?
This screening test assesses presence of detectable HIV antibodies. A 3–month lag exists between HIV infection and a positive ELISA test. All babies born to HIV–positive women will be HIV antibody positive from passive maternal antibodies.
236
What is the management of a positive HIV Western blot test during pregnancy?
Triple antiviral therapy is recommended for HIV–positive women starting at 14 weeks and continuing through delivery. With cesarean delivery and triple antiviral therapy, the transmission rate is 1%.
237
What are the second trimester laboratory tests?
Maternal serum alpha–fetoprotein, ultrasound, triple screen.
238
At what time does alpha–fetoprotein peak in the maternal serum?
AFP is the major serum glycoprotein of the embryo. Peaks at 12 weeks in fetus, then rises until 30 weeks in maternal serum.
239
What is the significance of an elevated maternal serum alpha–fetoprotein?
Fetal neural tube defects and ventral wall defects result in increased spillage of AFP. Other causes include twin pregnancy, placental bleeding, fetal renal disease, and sacrococcygeal teratoma.
240
When is MS–AFP testing performed?
MS–AFP is always performed as part of multiple marker screenings. Maternal serum testing is performed at 15–20 weeks.
241
What is the management of an elevated MS–AFP?
A positive high value is >2.5 multiples of the media. The next step in management is to obtain an obstetric ultrasound to confirm gestational dating. The most common cause of an elevated MS–AFP is dating error.
242
What is the management of an elevated MS–AFP if the dates are incorrect?
If true gestational age is more advanced than the assumed gestational age, it would explain the positive high value. In cases of dating error, repeat MS–AFP if pregnancy is still within 15–20 wk window. A normal MS–AFP will be reassuring.
243
What is the management of an elevated MS–AFP if the dates are correct?
If dates are correct and no explanation on sonogram, perform amniocentesis for AF–AFP and acetylcholinesterase activity. Elevated levels of amniotic fluid acetylcholinesterase activity are specific to open neural tube defects.
244
What is the meaning of an unexplained elevated MS–AFP but normal AF–AFP?
The pregnancy is statistically at risk for intrauterine growth restriction (IUGR), stillbirth, and preeclampsia.
245
What is the management of a low MS–AFP?
Positive low value is
246
What is the management of a low MS–AFP with correct dates?
If the dates are correct and no explanation is seen on sonogram, perform amniocentesis for karyotype.
247
What is the triple marker screen?
The sensitivity for trisomy 21 can be increased to 70% by performing maternal serum screen for MS–AFP, hCG, and estriol. The window for testing is 15–20 weeks. Accurate dating is important because reference values are gestational age specific.
248
What are the triple marker screen abnormalities in trisomy 21?
With Down syndrome, levels for MS–AFP and estriol are decreased, but hCG is increased. Perform an amniocentesis for karyotype.
249
What are the triple marker screen abnormalities in trisomy 18?
With Edward syndrome, levels for all three markers (MS–AFP, estriol, and hCG) are decreased. Perform an amniocentesis for karyotype.
250
What is the quadruple marker screen?
Adding a fourth marker (inhibin A) to the triple marker screen can increase the Down syndrome detection rate to 80%.
251
What are the third trimester laboratory tests?
Oral glucose tolerance test, complete blood count, atypical antibody screen.
252
What is the 1–h 50–g oral glucose tolerance test (OGTT)?
Screening test administered between 24 and 28 wks. Nonfasting. 50–g glucose load is given, and glucose is measured 1 h later. Normal is 140 mg/dL.
253
What test should be obtained if the 1–hoiur 50–g oral glucose tolerance test is >140 mg/dL?
If the 1–hour test is abnormal, the next step is a 3–h 100–g OGTT.
254
What percentage of women with an abnormal 1–hour glucose tolerance test have diabets?
15% of women with an abnormal 1–hour test will have gestational diabetes.
255
What is the 100–g oral glucose tolerance test?
Definitive test for glucose intolerance. After overnight fast, an FBS >125 mg/dL indicates overt diabetes, and no further testing is performed. If the FBS is
256
What are the normal values for a 100–g oral glucose tolerance test?
FBS
257
What is the criteria for anemia during pregnancy?
CBC performed between 24 and 28 weeks' in all women. The increasing diversion of iron to the fetus in the second and third trimester causes iron deficiency. A hemoglobin
258
What is the significance of a positive atypical antibody screen at 28 weeks gestation in a Rh–negative woman?
Before giving prophylactic RhoGAM to an Rh–negative woman, an indirect Coombs test is performed at 28 weeks to ensure she has not become isoimmunized. Two–tenths of a percent of Rh–negative women will become isoimmunized.
259
What is late pregnancy bleeding?
Vaginal bleeding occurring after 20 weeks' gestation. Prevalence is
260
What are the causes of late pregnancy bleeding?
Cervical erosion, polyps, and, rarely, carcinoma. Vaginal varicosities and lacerations. Abruptio placenta, placenta previa, and vasa previa.
261
What is the initial clinical assessment of late pregnancy bleeding?
Assess fetal heart tones, fetal monitor status, nature and duration of the bleeding. Pain or contractions. Determine the location of placental implantation by ultrasound.
262
What is the laboratory evaluation of late pregnancy bleeding?
CBC, DIC workup (platelets, PT, PTT, fibrinogen, D–dimer), type and cross–match, sonogram for placental location. Do not perform a digital or speculum examination until ultrasound rules out previa.
263
What is the initial management of late pregnancy bleeding?
Large–bore IV; if maternal vital signs unstable, administer isotonic fluids without dextrose wide open and place a urinary catheter to monitor urine. If fetal jeopardy is present or gestational age is ±36 weeks, immediate delivery.
264
What is the abruptio placenta?
Separation of a placenta from uterine wall before delivery. Partial or complete. Most commonly bleeding is overt and external. Less commonly, bleeding remains concealed. Retroplacental hematoma remains in uterus, resulting in increased fundal height.
265
What is the triad of abruptio placenta?
Late trimester painful bleeding. Normal placental implantation. Disseminated intravascular coagulopathy.
266
How is placental abruption diagnosed?
Painful, late–trimester vaginal bleeding with a normal fundal or lateral uterine wall placental implantation not over the lower uterine segment.
267
What is the most common cause of late–third trimester bleeding?
Abruptio placenta is most common cause of late–trimester bleeding, occurring in 1% of pregnancies. It is the most common cause of painful, late–trimester bleeding. Ultrasound may show retroplacental hematoma.
268
What is mild placental abruption?
Vaginal bleeding is minimal and there are no fetal monitor abnormalities. There is localized uterine pain and tenderness with incomplete relaxation between contractions.
269
What is moderate abruption?
Symptoms of uterine pain and moderate vaginal bleeding, gradual in onset. From 25 to 50% of placental surface is separated. Fetal monitoring may show tachycardia, decreased variability, or mild late decelerations.
270
What is severe abruption?
Symptoms are abrupt with a continuous knifelike uterine pain. Greater than 50% of placental separation. Severe late decelerations, bradycardia, or fetal death. Severe disseminated intravascular coagulation may occur.
271
What are the risk factors for placental abruption?
Previous abruption, hypertension, and maternal trauma. Maternal cocaine abuse and premature membrane rupture.
272
What is the management of placental abruption?
Emergency cesarean delivery is performed if maternal or fetal jeopardy. Vaginal delivery is performed if bleeding is heavy but controlled and pregnancy is >36 weeks. Perform amniotomy and induce labor.
273
What is the management of placental abruption remote from term?
Conservative in–hospital observation if mother/fetus stable and
274
What are the complications of abruptio placenta?
Hemorrhagic shock with acute tubular necrosis from profound hypotension; DIC from release of tissue thromboplastin from the disrupted placenta.
275
What is the triad of placenta previa?
Late trimester bleeding. Lower segment placental implantation. Absence of pain.
276
What is placenta previa?
Placenta is implanted in lower uterus. Placenta previa is found in only 0.5% of pregnancies. Placenta previa causes painless vaginal bleeding as the lower uterine segment stretches in late pregnancy.
277
How is placenta previa diagnosed?
Painless late–trimester vaginal bleeding with an ultrasound showing placental implantation over the lower uterine segment.
278
What is the presentation of placenta previa?
Painless late–pregnancy bleeding, which may be preceded by trauma, coitus, or pelvic examination. The uterus is nontender.
279
What are the risk factors for placenta previa?
Previous placenta previa and multiple gestation. Multiparity and advanced maternal age.
280
What is the management of placenta previa if theere is maternal or fetal jeopardy?
Cesarean if maternal or fetal jeopardy despite stabilization with crystalloid and PRBCs.
281
What is the management of placenta previa if the mother and fetus are stable and remote from term?
Conservative in–hospital observation for preterm gestations if mother and fetus are stable. Confirm abnormal placental implantation with sonogram and replace blood loss with crystalloid, PRBCs.
282
What is the mode of delivery for placenta previa?
Vaginal delivery may be attempted if placental edge is >2 cm from internal cervical os. Scheduled cesarean delivery is performed if the mother has been stable after fetal lung maturity has been confirmed by amniocentesis, usually at 36 wks.
283
What are the complications of severe hypotension from placenta previa?
If placenta previa occurs over a uterine scar, villi may invade into deeper layers of decidua basalis and myometrium, resulting in intractable bleeding, requiring cesarean hysterectomy. Profound hypotension may cause Sheehan syndrome or ATN.
284
What is placenta accreta?
The placental villi invade the deeper layers of the endometrial deciduus basalis but do not penetrate the myometrium. Placenta accreta is the most common form of placenta accreta, accounting for 75% of cases.
285
What is placenta increta?
Occurs when the villi invade the myometrium but do not reach the uterine serosal surface or the bladder. Placenta increta accounts for 15% of all cases.
286
What is placenta percreta?
The placental villi invade to the uterine serosa or into the bladder. Placenta percreta is the least common form of placenta increta, accounting for 5% of cases.
287
What is vasa previa?
Vasa previa is present when fetal vessels traverse fetal membranes over internal cervical os. If fetal vessels rupture the bleeding will be from the fetoplacental circulation, and fetal exsanguination will rapidly occur, leading to fetal death.
288
How is vasa previa diagnosed?
Rarely confirmed before delivery, but vasa previa may be suspected when antenatal sonogram with color–flow Doppler reveals a vessel crossing the membranes over the internal cervical os.
289
What is the presentation of vasa previa?
The classic triad is rupture of membranes and painless vaginal bleeding, followed by fetal bradycardia. Management is immediate cesarean delivery.
290
What is uterine rupture?
Complete separation of the wall of the pregnant uterus with or without expulsion of the fetus. The rupture may be incomplete (not including the peritoneum) or complete (including the visceral peritoneum).
291
What is the presentation of uterine rapture?
Vaginal bleeding, loss of fetal heart rate, abdominal pain, loss of station of fetal head. Rupture may occur before labor on during labor.
292
What are the risk factors for uterine rupture?
The most common risk factors are previous classic uterine incision, myomectomy, and excessive oxytocin stimulation. Other risk factors are grand multiparity and marked uterine distention.
293
Which type of cesarian section incision is most likely to rupture?
A vertical fundal uterine scar is 20 times more likely to rupture than a low segment incision. Maternal and perinatal mortality is also much higher with the vertical incision rupture.
294
What is the management of uterine rupture?
Immediate cesarian delivery of the fetus. Uterine repair is indicated in a stable young woman to conserve fertility. Hysterectomy is performed in the unstable patient or one who does not desire further childbearing.
295
What is group B beta–hemolytic streptococcus?
GBS is a bacterium commonly found in normal GI tract flora. Thirty percent of women have asymptomatic vaginal colonization with GBS. Most neonates delivered to colonized mothers will be culture positive.
296
What is the significance of group B beta–hemolytic streptococcus?
1 in 500 neonates develop serious infections. Early onset infection is most common, within a few hours to days; characterized by fulminant pneumonia, sepsis. 50% mortality. Late–onset infection occurs after first week with meningitis.
297
What is the triad of group B beta–hemolytic streptococcus neonatal sepsis?
Newborn sepsis. Within hours of birth. Bilateral diffuse pneumonia.
298
What is the prevention of group B beta–hemolytic streptococcus infection?
Intrapartum antibiotic prophylaxis of neonatal GBS sepsis is given with IV penicillin G. If the patient is penicillin allergic, use clindamycin or erythromycin.
299
What is the management of women with a positive GBS urine culture?
All women with a positive GBS urine culture or a previous baby with GBS sepsis will receive intrapartum prophylaxis. Prophylaxis of other women is based on either of the following two protocols.
300
What is the management of women with a positive third trimester vaginal GBS culture?
Third–trimester vaginal cultures are obtained at 36–37 weeks gestational age, and intrapartum prophylaxis is administered only to those with positive GBS cultures.
301
What is the management of a pregnant woman with intrapartum risk factors for GBS infection?
Screening by intrapartum risk factors. No vaginal cultures are obtained. Intrapartum prophylaxis is given on basis of risk factors being present: preterm gestation, membranes ruptured >18 h, or maternal fever.
302
What is the triad of congenital toxoplasma?
Chorioretinitis. Intracranial calcifications. Symmetrical IUGR.
303
What are the CT findings in CNS toxoplasmosis?
Toxoplasma causes intracranial calcifications CMV causes periventricular calcifications.
304
What is toxoplasmosis?
Caused by ingestion of cat feces or raw goat milk or undercooked, meat. 40% of women are toxo IgG positive. 1st–trimester infection risk 15%, but infections are serious or lethal. 3rd trimester infection risk is 65%, but asymptomatic.
305
What are the manifestations of fetal toxoplasmosis?
Symmetric IUGR, nonimmune fetal hydrops, microcephaly, and intracranial calcifications. Chorioretinitis, seizures, hepatosplenomegaly, and thrombocytopenia.
306
What is the prevention of intrapartum toxoplasmosis?
Avoid infected cat feces, raw goat milk, and undercooked meat.
307
What is the treatment of toxoplasmosis?
Pyrimethamine and sulfadiazine are used to treat a known infection. Spiramycin is used to prevent vertical transmission from the mother to the fetus.
308
When is the risk of fetal or neonatal varicella infection highest?
Greatest risk is if maternal rash appears between 5 days antepartum and 2 days postpartum.
309
What are the maternal complications of varicella infection?
10% of mothers with varicella will develop varicella pneumonia. Communicabable 1–2 days before vesicles appear until all vesicles are crusted. Pruritic vesicles begin on head and neck, progressing to the trunk. Infection can trigger labor.
310
What is the prevention of varicella in pregnancy?
Administer VZIG (varicella zoster immune globulin) to a susceptible gravida within 72 h of exposure. Live–attenuated varicella virus (Varivax III) can be administered to nonpregnant or postpartum, varicella IgG–antibody–negative women.
311
What is the treatment of varicella pneumonia?
IV acyclovir for varicella pneumonia, encephalitis, or the immunocompromised.
312
What is the triad of congenital rubella?
Congenital deafness. Congenital cataracts. Congenital heart disease.
313
What is the fetal infection rate for rubella?
Transplacental infection rate is >90% in the first 10 weeks of pregnancy, but 5% in the third trimester.
314
What are the manifestations of congenital rubella syndrome?
Symmetric IUGR, microcephaly, or ventriculoseptal defect. Congenital deafness (most common sequelae), cataracts, mental retardation, hepatosplenomegaly, thrombocytopenia, and blueberry muffin" rash."
315
What is the prevention of congenital rubella syndrome?
All pregnant women undergo rubella IgG screening. Rubella–susceptible women should avoid contact with rubella cases, then receive vaccine after delivery (live attenuated virus); pregnancy should be avoided for 1 mth after immunization.
316
What are the manifestations of congenital cytomegalovirus infection?
Nonimmune hydrops, symmetric IUGR, microcephaly, periventricular cerebral calcifications. 2% of newborns have in utero exposure. CMV is most common congenital viral syndrome; most common cause deafness.
317
What are the signs of newborn cytomegalovirus infection?
Only 10% of infected infants have clinical disease, which includes petechiae, meningoencephalitis, periventricular calcifications, hepatosplenomegaly, thrombocytopenia, and jaundice.
318
What are the manifestations of maternal CMV infection?
Mild, low–morbidity, mononucleosis–like syndrome with hepatitis.
319
What is the treatment of maternal CMV infection?
Antiviral therapy with ganciclovir.
320
What is the most common route of HSV fetal infection?
The most common route of fetal infection is contact with maternal genital lesions during a recurrent HSV episode. Transplacental transmission from mother to fetus can occur with viremia during the primary infection but is rare.
321
How is HSV infection diagnosed?
The definitive diagnosis is a positive HSV culture from fluid obtained from a ruptured vesicle or debrided ulcer.
322
What are the manifestations of fetal HSV infection?
The transplacental infection rate is 50% with maternal primary infections. Manifestations may include spontaneous abortions, symmetric IUGR, microcephaly, and cerebral calcifications.
323
What is the neonatal attack rate after exposure to herpes simplex virus?
With passage through an HSV–infected birth canal, neonatal attack rate is 50% with primary infection, but
324
What are the neonatal findings of HSV infection?
Skin, eye, mucous membrane disease or disseminated infection or CNS infection. Neonatal mortality 50%. Survivors have meningoencephalitis, mental retardation, pneumonia, hepatosplenomegaly, jaundice, and petechiae.
325
What is the prevention of neonatal herpes simplex virus infection?
Cesarean section should be performed in the presence of genital HSV lesions at the time of labor. If membranes have been ruptured >8–12 h, the virus may already have infected the fetus and cesarean delivery would be of no value.
326
What is the treatment of herpes simplex virus infection in pregnancy?
Women with active, recurrent genital herpes should be offered suppressive acyclovir at 36 months.
327
What is the major route of fetal HIV infection?
Major route of vertical transmission is contact with infected genital secretions with vaginal delivery.
328
What is the rate of transmission of maternal HIV infection with zidovudine treatment?
Without maternal zidovudine, vertical transmission rate is 30%, but with ZDV, the infection rate is lowered to 10% with vaginal delivery. With elective cesarean before membrane rupture, infection rate
329
What are the neonatal findings of HIV infection?
At birth neonates of HIV–positive women will have a positive HIV tests from transplacental passive IgG passage. HIV–infected breast milk can transmit disease to newborn. Progression from HIV to AIDS in infants is more rapid.
330
What is the antiviral prophylaxis against HIV infection in pregnancy?
HIV–infected pregnant women should be offered triple–drug therapy, including zidovudine, starting at 14 weeks and continuing throughout pregnancy, intrapartum, and after delivery.
331
What is the mode of delivery for HIV–infected pregnant women?
Cesarean at 38 wks, unless mother has very low (
332
What precautions should be taken in HIV–infected women who are to deliver vaginally?
HIV–infected women may deliver vaginally if
333
What is the transmission rate for syphilis in pregnancy?
Transplacental infection is common with vertical transmission rates of 60% in primary and secondary syphilis. The rate of fetal infection with latent or tertiary syphilis is lower.
334
What are the manifestations of early congenital syphilis?
Nonimmune hydrops, macerated skin, anemia, thrombocytopenia, and hepatosplenomegaly. Fetal death rates are high, with perinatal mortality rates approaching 50%. The placenta is typically large and edematous.
335
What is the treatment of syphilis in pregnancy?
Benzathine penicillin 2.4 million units IM x 1. Other antibiotics do not cross placenta. Penicillin–allergic gravidas should be given a full penicillin dose using an oral desensitization regimen.
336
What is the mode of infection for hepatitis B virus?
Hepatitis B is spread by body secretions. Sharing needles, sexual intercourse, perinatal transmission. Vertical transmission accounts for 40% of all chronic HBV infections. Most HBV infections are asymptomatic.
337
What is the major route of hepatitis B fetal infection?
The main route of fetal or neonatal infection is from infected genital secretions wirh vaginal delivery. There is no perinatal transmission risk if the mother is positive for HBV surface antibodies but negative for HBV surface antigen.
338
What is the rate of neonatal infection with hepatitis B?
Neonatal HBV develops 10% of mothers positive for HBsAg, but in 80% of those positive for both HBsAg and HBeAg. Of those neonates who get infected, 80% will develop chronic hepatitis, compared with 10% of infected adults.
339
What is the most common type of maternal hepatitis B infection?
Majority are asymptomatic. Hepatitis B surface Ag is screening test used for existing infection and is obtained on all pregnant women. A positive HBsAg test is followed with a hepatitis panel and liver enzymes, assessing for active or chronic hepatitis.
340
What are the maternal signs of cute hepatitis B?
Acute and chronic HBV infections can result in right upper quadrant pain and lethargy. Elevated bilirubin and high liver enzymes. The majority of patients with acute hepatitis will recover normal liver function.
341
What is the mode of delivery for pregnant women with hepatitis B?
Vaginal delivery is indicated. Cesarean section is indicated only for obstetric indications.
342
What is the prevention of hepatitis B vertical transmission?
Avoid scalp electrodes. Neonates receive passive immunization with hepatitis B immunoglobulin and hepatitis B vaccine. Breast feeding is allowed after neonate has received vaccine and HBIG.
343
What are the indications for maternal immunization for hepatitis B?
HBsAg–negative mothers at high risk for hepatitis B should receive HBIg passive immunization. Active immunization is safe in pregnancy because the agent is a killed virus.
344
What is the treatment of hepatitis B in pregnancy?
There is no specific therapy for acute hepatitis. Chronic HBV can be treated with either interferon or lamivudine.
345
27–year–old primigravida at 18 weeks' with pelvic pressure without uterine contractions. Fetal membranes bulging into vagina, and fetal feet can be felt through the membranes. Prior cervical conization. What is the diagnosis?
Cervical insufficiency
346
What is cervical insufficiency"?"
Inability of the uterine cervix to retain a pregnancy to viability in the absence of contractions or labor.
347
What are the causes of cervical insufficiency?
Forceful cervical dilation associated with second trimester abortion procedures, cervical laceration from rapid delivery, injury from deep cervical conization, or congenital weakness from diethylstilbestrol exposure.
348
What is the criteria for diagnosis of cervical insufficiency?
Elective cervical cerclage is beneficial with a history of two or more unexplained second–trimester pregnancy losses. Serial transvaginal ultrasound evaluations of the cervix after 16–20 weeks may be helpful.
349
What is the management of cervical insufficiency?
Elective cerclage at 13–16 weeks' is appropriate after sonographic demonstration for fetal normality. Cerclage may be considered with sonographic evidence of cervical insufficiency after ruling out labor and chorioamnionitis.
350
What is the triad of cervical insufficiency?
Pregnant 18–22 weeks. Painless cervical dilation. Delivery of previable baby.
351
What are the methods of cervical cerclage?
McDonald cerclage places a removable suture in cervix. Cerclage removal at 36–37 weeks, after fetal lung maturity but before labor. Shirodkar cerclage utilizes submucosal suture, which is left in place, requiring cesarean.
352
What are the risk factors for multiple gestation?
Dizygotic multiple gestations are most common. Risk factors: race, geography, family history, ovulation induction. Risk is 10% with clomiphene, 30% with human menopausal gonadotropin. Monozygotic multiple gestation has no risk factors.
353
What are the complications for twin pregnancies?
Anemias (iron and folate), preeclampsia, preterm labor (50%), malpresentation (50%), cesarean delivery (50%), and postpartum hemorrhage.
354
What are the clinical findings in twin gestations?
Hyperemesis gravidarum is more common from high levels of beta–hCG. Uterus is larger than dates. Maternal serum alpha–fetoprotein is higher than with one fetus.
355
What is the antepartum management of twin gestations?
Give mother iron and folate supplementation to prevent anemia, monitor NP to detect preeclampsia, and perform serial ultrasounds, looking for twin–twin transfusion (amniotic fluid discordance).
356
What is the intrapartum management of twin gestation?
Vaginal delivery if both twins are cephalic presentation (50%); cesarean delivery if first twin in noncephalic presentation. Observe for postpartum hemorrhage from uterine atony.
357
What is isoimmunization?
A pregnant woman has developed antibodies to foreign red blood cells, most commonly against those of her current or previous fetus(es), but also caused by transfusion of mismatched blood.
358
What are the causes of isoimmunization?
The most common RBC antigens are of Rh system (C, c, D, E, e), with most common being D. Antibodies to RBC antigens are detected by indirect Coombs test (atypical antibody test). Concentration of antibodies is reported in dilutional titers.
359
What is hemolytic disease of the newborn?
HDN is ranges from hyperbilirubinemia to erythroblastosis fetalis. Caused by maternal antibodies crossing into fetal circulation and targeting antigen–positive fetal RBCs, resulting in hemolysis, anemia, fetal hydrops, death.
360
What are the risk factors for isoimmunization?
Isoimmunization most commonly occurs when fetal RBCs enter mother's circulation transplacentally at delivery. Other risk factors are amniocentesis, ectopic pregnancy, D&C, abruptio, previa.
361
What are the requirements for isoimmunization?
Mother must be antigen negative. Fetus must be antigen positive, which means the father of the pregnancy must also be antigen positive.
362
What are the obstetric complications of isoimmunization?
Fetal RBCs must cross over into maternal circulation to stimulate her lymphocytes to produce Ab to fetal RBC Ag. Significant titer of maternal Ab is requried to cross into fetal circulation, causing fetal hemolysis.
363
What is the management of isoimmunization?
1. Determine whether there is any fetal risk. 2. Assess degree of fetal anemia if the fetus is antigen positive. 3. Intervene if severe anemia
364
What criteria indicate that the fetus is at risk for isoimmunization?
Fetal risk is present only if atypical antibodies antibodies are associated with HDN, antibodies in mother have titer >1:8, and father is antigen positive. Fetal blood type may be determined by amnio or PUBS. If fetus is Ag neg, there is no fetal risk.
365
What criteria indicate that the fetus is not at risk for isoimmunization?
No fetal risk if maternal atypical antibody test is negative, maternal antibodies are present but are not associated with HDN, Ab titer is
366
How is the degree of fetal anemia assessed if the at–risk fetus is RBC antigen positive or if fetal blood typing is impossible?
Serial amniocentesis or PUBS: amniotic fluid bilirubin indicates fetal hemolysis. Ultrasound Doppler: as fetal anemia worsens, the peak flow of middle cerebral artery velocity rises.
367
What is the intervention for severe fetal anemia?
Intrauterine intravascular transfusion is performed if gestational age is 34 weeks.
368
What is RhoGAM?
Pooled anti–D IgG antibodies that are given IM to a pregnant woman when there is significant risk of fetal RBCs passing into her circulation. Passive IgG attaches to foreign RBC Ag, causing lysis before maternal lymphocytes become stimulated.
369
When is RhoGAM given?
Rho GAM is given to Rh(D)–negative mothers at 28 w, and after chorionic villus sampling, amniocentesis, or D&C. Also given within 72 h of delivery of an Rh(D)–pos infant.
370
What is Kleihauer–Betke test?
Quantitates volume of fetal RBCs in maternal circulation by differential staining fetal and maternal RBCs. Determines if more than 1 vial of RhoGAM needs to be given when large fetal–maternal bleeding may have occured (abruptio).
371
A 25–year–old woman, G2 P1, at 28 weeks' gestation with regular uterine contractions every 7–10 min. She is a smoker with chronic hypertension. What is the diagnosis?
Preterm labor
372
What is preterm labor?
Preterm delivery is the most common cause of perinatal morbidity and mortality. 12% of pregnancies deliver prematurely. Many patients will have preterm contractions but not be in preterm labor.
373
What is the criteria for preterm labor?
3 criteria: Pregnancy >20 weeks, but 2 cm.
374
What are the risk factors for preterm labor?
Multiple pregnancy, uterine anomalies, PROM, previous preterm. Pyelonephritis, chorioamnionitis, smoking, physical labor, polyhydramnios, abdominal–pelvic surgery, periodontal disease, bacterial vaginosis, trichomoniasis, cervix
375
What are the symptoms of preterm labor?
Lower abdominal pain or pressure, lower back pain, increased vaginal discharge, or bloody show. The symptoms may be present for several hours to days but are not recognized as contractions by the patient.
376
What is the triad of preterm labor?
Pregnancy 20–36 weeks. >3 contractions in 30 min. Dilated cm or changing.
377
What is the triad of preterm contractions?
Pregnancy 20–36 weeks. Contractions in 30 min. Dilated
378
What is the triad of magnesium toxicity?
Preterm labor tocolysis. Respiratory depression. Muscle weakness.
379
What are the contraindications to tocolysis?
Severe abruptio placenta, ruptured membranes, chorioamnionitis. Fetal lethal anomaly, fetal demise repetitive late decelerations. Eclampsia, severe preeclampsia, advanced cervical dilation.
380
Hat are the indications for tocolytic agents?
Parenteral agents may prolong pregnancy but for no more than 72 h to provide time for maternal IM betamethasone to enhance fetal pulmonary surfactant. Oral tocolytic agents are no more effective than placebo.
381
What is the tocolytic mechanism of magnesium sulfate?
Magnesium sulfate is a competitive inhibitor of calcium. Clinical monitoring is based on decreasing but maintaining detectable deep tendon reflexes.
382
What are the side effects of magnesium sulfate?
Muscle weakness, respiratory depression, and pulmonary edema. Magnesium overdose is treated with IV calcium gluconate. Contraindications include renal insufficiency and myasthenia gravis.
383
What is the mechanism of terbutaline inhibition of labor?
Terbutaline is beta–Adrenergic agonists. Tocolytic effect depends on stimulating the beta2–adrenergic receptor which inhibits myometrial activity.
384
What are the side effects of terbutaline?
Hypertension, tachycardia from beta1 receptor cardiovascular activity. Other side effects are hyperglycemia, hypokalemia, and pulmonary edema.
385
What are the contraindications to terbutaline?
Cardiac disease, diabetes mellitus, uncontrolled hyperthyroidism.
386
What are the side effects of calcium–channel blockers for tocolysis?
Tachycardia, hypotension, and myocardial depression. Contraindications to nifedipine include hypotension.
387
What is the tocolytic mechanism of prostaglandin synthetase inhibitors?
Decrease smooth muscle contractility by decreasing prostaglandin production (e.g., indomethacin).
388
What are the side effects of indomethacin in pregnancy?
Oligohydramnios, in utero ductus arteriosus closure, and neonatal necrotizing enterocolitis. Contraindications include gestational age >32 weeks.
389
What is the management of preterm labor?
Isotonic fluids. MgSO4 tocolysis 5 g, then 2 g/h. Cervical and urine cultures before giving IV penicillin G for group B beta Strep prophylaxis. Maternal IM betamethasone to stimulate fetal type II pneumocyte surfactant production if
390
What is the prevention of preterm labor?
Weekly intramuscular of 17a–OH progesterone caproate starting at 20 weeks' gestation has been shown to decrease preterm deliveries in women with a history of previous idiopathic preterm deliveries.
391
What is premature rupture of membrane?
Rupture of the fetal membranes before the onset of labor, whether at term or pre– term.
392
What are the risk factors for premature rupture of membrane?
Ascending infection from the lower genital tract is the most common risk factor for PROM. Other risk factors are local membrane defects and cigarette smoking.
393
What is the presentation of premature rupture of membrane?
Sudden gush of copious vaginal fluid. On external examination, clear fluid is flowing out of the vagina. Oligohydramnios is seen on ultrasound examination.
394
How is premature rupture of membrane diagnosed?
Sterile speculum exam: pooling positive: clear, watery amniotic fluid is seen in the posterior vaginal fornix. Nitrazine positive: fluid turns pH–sensitive paper blue. Fern positive when allowed to dry on slide
395
What is the triad of ruptured membranes?
Posterior fornix pooling. Fluid is nitrazine (+). Glass slide drying: fern (+).
396
What are the signs of Chorioamnionitis?
Diagnosed clinically with all the following criteria: maternal fever and uterine tenderness in the presence of confirmed PROM in the absence of a URI or UTI.
397
What is the management of premature rupture of membranes if uterine contractions occur?
If uterine contractions occur, tocolysis is contraindicated. If chorioamnionitis is present, obtain cervical cultures, start broad–spectrum IV antibiotics, and initiate prompt delivery.
398
What is the management of premature rupture of membranes before viability in the absence of infection or contractions?
Before viability (
399
What is the management of premature rupture of membranes with preterm viability in the absence of infection or contractions?
With preterm viability (24–33 wks), hospitalize at bed rest, betamethasone to enhance fetal lung maturity if 34 weeks), induce labor with oxytocin/ prostaglandin. Or cesarean.
400
What are the hazards associated with PROM?
Neonatal infection and sepsis, deformations, umbilical cord compression, pulmonary hypoplasia. Maternal chorioamnionitis, sepsis, deep venous thrombosis.
401
What are the complications of preterm delivery?
Neonatal respiratory distress syndrome (most common), patent ductus arteriosus, intraventricular hemorrhage, necrotizing enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, cerebral palsy.
402
What is postterm pregnancy?
Pregnancy that continues for 40 weeks or >280 days postconception. Or a pregnancy that continues 42 weeks or for 294 days after the first day of the last menstrual period.
403
What is the triad of chorioamnionitis?
Ruptured membranes. Maternal fever. No UTI or URI.
404
What are the causes of postterm pregnancy?
The most common cause of true postdates are idiopathic. More common in young primigravidas and rarely with placental sulfatase deficiency. Pregnancies with anencephalic fetuses are the longest pregnancies.
405
What is the significance of postterm pregnancy?
Perinatal mortality is increased 3x because of decreased placental function. Cesarean rate is increased. Shoulder dystocia is more common. Dysmaturity syndrome: decreased placental function causes subcutaneous loss.
406
What is the management of postterm pregnancy?
Assess accuracy of gestational age being >42 weeks. Assess the likelihood of successful induction by evaluating cervical dilation, effacement, position, consistency, station. Favorable cervix is dilated, effaced, soft, and anterior to mid position.
407
What is the management of post term pregnancy with dates sure, favorable cervix?
There is no benefit to the fetus or mother in continuing the pregnancy. Induce labor with IV oxytocin and artificial rupture of membranes.
408
What is the management of post term pregnancy with dates sure, unfavorable cervix?
Cervical ripening initiated with vaginal or cervical prostaglandin E2 followed by IV oxytocin. Or management could be conservative with twice weekly NSTs and AFIs awaiting spontaneous labor.
409
What is the management of meconium amniotic fluid?
To prevent meconium aspiration syndrome: Amnioinfusion may be helpful. Suctioning of fetal nose and pharynx is not routinely performed. Laryngoscopic visualization of vocal cords is only indicated if the neonate is depressed.
410
20–year–old primigravida at 32 weeks' gestation. Blood pressure (BP) is 155/95, which is persistent on repeat BP check spot urine dipstick is negative. What is the diagnosis?
Gestational hypertension
411
What is gestational hypertension?
BP >140/90 after 20 weeks without proteinuria. The BP returns to normal postpartum. No symptoms of preeclampsia (no headache, epigastric pain, visual disturbances). Laboratory tests are normal for pregnancy.
412
What is the management of gestational hypertension?
Conservative outpatient management is appropriate. Appropriate laboratory testing should be performed to rule out preeclampsia, e.g., urine protein, hemoconcentration assessment.
413
What is the triad of gestational hypertension?
Pregnancy >20 wk. Nonsustained hypertension. No proteinuria.
414
20–year–old primigravida at 32 weeks', gained 10 pounds in 2 weeks. BP is 156/95. 2+ pedal edema, and her fingers appear swollen. Urine dipstick 2+ protein. What is the diagnosis?
Preeclampsia.
415
What is preeclampsia?
Sustained BP elevation in pregnancy after 20 weeks' gestation in the absence of preexisting hypertension.
416
What is the diagnostic criteria for mild preeclampsia?
The diagnostic dyad includes the following: Sustained BP elevation of >140/90. Proteinuria on dipstick of 1–2+ or >300 mg on a 24–h urine collection.
417
What are the risk factors for preeclampsia?
Preeclampsia is found 8 times more frequently in primiparas. Other risk factors are multiple gestation, hydatidiform mole, diabetes mellitus, age extremes, chronic hypertension, and chronic renal disease.
418
What is the pathophysiology of preeclampsia?
Vasospasm caused vasoactive angiotensin; increases in vasoconstrictor, thromboxane, and decreases in vasodilator, prostacyclin. Intravascular constriction, decreased perfusion of placenta, kidneys, liver, brain, heart.
419
What are the symptoms of mild preeclampsia?
Excess weight gain and fluid retention. Presence of new onset of persistent headache, epigastric pain, or visual disturbances would move the diagnosis from mild to severe preeclampsia.
420
What are the laboratory abnormalities of mild preeclampsia?
Hemoconcentration is shown by elevation of Hb, hematocrit, blood urea nitrogen, serum creatinine, and serum uric acid. Proteinuria. DIC or liver enzyme elevation would change the diagnosis from mild to severe preeclampsia.
421
What is the management of mild preeclampsia?
The only definitive cure is delivery and removal of all fetal–placental tissue. Delivery may be deferred in mild preeclampsia to minimize neonatal complications of prematurity.
422
Before 36 weeks' gestation, mild preeclampsia is managed in the hospital, watching for possible progression to severe preeclampsia. No antihypertensive agents or MgSO4 are used.
Delivery. At >36 weeks' gestation, delivery is indicated with dilute IV oxytocin induction of labor and continuous infusion of N MgSO4 to prevent eclamptic seizures.
423
What is the triad of mild preeclampsia?
Pregnancy >20 wk. Sustained HTN (>140/90 mm Hg). Proteinuria WOO mg/24 h.
424
20–year–old primigravida at 32 weeks', headache, epigastric pain, light flashes. 10 lb weight gain in 2 weeks. BP is 170/115. 2+ pedal edema, finger swelling. Urine dipstick 4+ protein. What is the diagnosis?
Severe preeclampsia
425
What are the diagnostic findings in severe preeclampsia?
Mild preeclampsia plus one of following: BP >160/110. Proteinuria 3–4+. Evidence of maternal jeopardy: headache, epigastric pain, visual changes, platelets
426
What are the risk factors for severe preeclampsia?
These are the same as mild preeclampsia with the addition of diseases with small vessel disease such as systemic lupus and longstanding overt diabetes.
427
What are the symptoms of severe preeclampsia?
New onset of persistent headache, epigastric pain, or visual disturbances is characteristic of severe preeclampsia.
428
What are the laboratory abnormalities of severe preeclampsia?
Severe hemoconcentration. Proteinuria. DIC and hepatocellular injury.
429
What is the management of severe preeclampsia with maternal or fetal jeopardy?
Prompt delivery; MgSO4 to prevent convulsions; 5–g loading dose, then continue infusion of 2 g/h. Lower BP to diastolic 90–100 mm Hg with IV hydralazine or labetalol. Vaginal delivery with oxytocin if mother and fetus stable.
430
What are the indications for conservative management of severe preeclampsia?
Conservative inpatient management may rarely be attempted in absence of maternal and fetal jeopardy with gestational age 26–34 weeks if BP can be lowerd to
431
What is the triad of severe preeclampsia?
Pregnancy >20 wk. Sustained hypertension (>160/110 mm Hg). Proteinuria (>5 grams/24 h)
432
20–year–old primigravida with a tonic–clonic seizure at 32 weeks'. Headache. Gained 10 lbs in 2 weeks. Unresponsive. BP is 180/115, and urine dipstick shows 4+ protein. What is the diagnosis?
Eclampsia
433
What is eclampsia?
Unexplained tonic–clonic seizures in a hypertensive, proteinuric pregnant woman in the last half of pregnancy.
434
What are the risk factors for eclampsia?
These are the same as mild and severe preeclampsia. A primary seizure disorder does not predispose to eclampsia.
435
What is the etiology of eclampsia?
Severe diffuse cerebral vasospasm resulting in cerebral perfusion deficits and cerebral edema.
436
What is the management of eclampsia?
Protect airway. MgSO4, 5 g to stop seizures, then 2 g/h. Prompt delivery after stabilization. Vaginal delivery with oxytocin if stable. Lower diastolic to 90–100 mm Hg with IV hydralazine or labetalol.
437
What is the triad of chronic hypertension?
Pregnancy 140/90 mm Hg). +/– proteinuria.
438
36–year–old multigravida at 12 weeks' with BP 160/95. Chronic hypertension for last 5 years. Spot urine dipstick protein is 2+. Creatinine is 1.2 mg/dl. What is the diagnosis?
Chronic hypertension in pregnancy
439
What are the risk factors for chronic hypertension?
Most chronic hypertension is idiopathic without specific antecedents. Risk factors are obesity, advanced maternal age, positive family history, renal disease, diabetes, systemic lupus erythematosus.
440
How is chronic hypertension in pregnancy diagnosed?
BP 140/90 with onset before the pregnancy or before 20 weeks' gestation.
441
What are the risk factors for chronic hypertension with superimposed preeclampsia?
Occurs in 25% of patients with chronic hypertension. Risk factors include renal insufficiency, HTN for previous 4 years, and HTN in a previous pregnancy. Abruptio placenta incidence is markedly increased.
442
What are the criteria for chronic hypertension with superimposed preeclampsia?
Established chronic HTN with: rising BP ; worsening proteinuria; maternal jeopardy (headache, epigastric pain, visual changes, platelet count
443
What are the laboratory abnormalities of chronic hypertension with superimposed preeclampsia?
Those with renal disease may have proteinuria, lowered creatinine clearance, and elevated BUN, creatinine, and uric acid.
444
What is the treatment of severe HTN in pregnancy?
The drug of choice is methyl–dopa because of fetal safety. Labetalol and atenolol are acceptable alternatives. However, beta–blocking agents are associated with intrauterine growth restriction.
445
What is the triad of chronic HTN with superimposed preeclampsia?
Chronic hypertension. Worsening BP. Worsening proteinuria.
446
What antihypertensive medications are contraindicated in pregnancy?
Angiotensin–converting enzyme inhibitors are contraindicated in pregnancy because of fetal hypocalvaria, renal failure, oligohydramnios, and death. Diuretics are contraindicated because of adverse fetal effects.
447
What is the management of hypertension during pregnancy?
Reduction of BP to normal levels may jeopardize uteroplacental blood flow. Maintain diastolic 90–100 mm Hg. Sonograms and NSTs after 30 weeks' to monitor for IUGR. BP and urine protein assessments. Induce labor at term if cervix is favorable.
448
What is the management of hypertension during labor?
IV MgSO4 during labor to prevent convulsions. Keep diastolic BP between 90 and 100 mm Hg with IV hydralazine and/or labetalol. Attempt vaginal delivery with IV oxytocin infusion if mother and fetus are stable.
449
36–year–old multigravida is at 32 weeks'. BP 160/105. Increased total bilirubin, lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase, platelets 80,000. What is the diagnosis?
HELLP syndrome.
450
What is HELLP syndrome?
Occurs in 5–10% of preeclamptic patients and is characterized by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). HELLP syndrome occurs twice as often in multigravidas as primigravidas.
451
What is the management of HELLP syndrome?
Prompt delivery at any gestational age is appropriate. Maternal corticosteroids may enhance postpartum normalization of liver enzymes and platelet count.
452
What are the complications of HELLP syndrome?
DIC, abruptio placenta, fetal demise, ascites, and hepatic rupture.
453
What are the causes of hyperthyroidism in pregnancy?
Underlying etiology may be Graves disease, toxic nodular goiter, hydatidiform mole, toxic diffuse goiter. Hyperthyroidism is associated with increased spontaneous abortions, prematurity, intrauterine growth restriction, perinatal morbidity and mortality.
454
What is the treatment of thyroid storm in pregnancy?
Pyrexia, tachycardia, and severe dehydration. Management is propylthiouracil, beta–blocking agents, steroids, and iodine.
455
What is the pathophysiology of Graves disease in pregnancy?
Mediated by autoimmune production of thyrotropin–receptor antibodies (TSHR–Ab) which stimulates thyroid hormone production. TSHR–Ab can cross placenta, causing fetal hyperthyroidism. Elevated free T4 and TSHR–Ab, and low TSH.
456
What is the management of Graves disease?
PTU and methimazole block thyroid synthesis; can be used in pregnancy. Subtotal thyroidectomy is indicated when medical therapy fails. Radioactive iodine (I131) is contraindicated because can cross placenta.
457
What is the effect of hypothyroidism on pregnancy?
If uncontrolled it is associated with spontaneous abortion. If controlled with thyroid replacement, normal fertility and pregnancy outcomes are noted.
458
What are the risk factors for gestational diabetes?
Obesity, age >30 yrs, family history are the most common risk factors. Other risk factors are fetal macrosomia, unexplained stillbirth or neonatal death, polyhydramnios, previous traumatic delivery. Prevalence of glucose intolerance 2–3%.
459
What is gestational diabetes mellitus?
The most common type with onset during pregnancy, usually diagnosed in the last half. Diabetogenic effect of human placental lactogen, placental insulinase, cortisol, and progesterone. 35% of GDM will develop diabetes within 5–10 yrs.
460
What is white class A1 diabetes?
Gestational diabetes with normal fasting blood sugar not requiring insulin.
461
What is White class A2 diabetes?
Gestational diabetes with elevated fasting blood sugar requiring insulin
462
What is White class B diabetes?
Overt diabetes mellitus onset after age 20 years and duration
463
What is White class C diabetes?
Overt DM onset age 10–19 years or duration 10–19 years.
464
What is the screening for diabetes in pregnancy?
All pregnant women are screened between 24 and 28 weeks' gestation. Patients with risk factors (obesity) are screened on the first prenatal visit then repeated at 24–28 weeks if initially negative.
465
What is the screening test for diabetes in pregnancy?
1–h 50–g OGTT with normal value 140 mg/dL, then proceed to a definitive 3–h 100–g OGTT. If screening value is >200 mg/dL, and a subsequent FBS is >125mg/dl, GDM is diagnosed.
466
What is the 3–h oral glucose tolerance test?
Performed on all patients with an abnormal 1–h screening test. Performed after an overnight fast. 100g glucose is given, then 4 glucose values are obtained. Normal values are FBS
467
What is impaired glucose tolerance?
Diagnosed if only one value on the 3–h oral glucose tolerance test is abnormal.
468
What is gestational diabetes mellitus?
GDM is diagnosed if at least two values are abnormal. If the fasting blood sugar is >125, overt diabetes is diagnosed, and the 100–g glucose load should not be given.
469
What are the indications for insulin therapy in diabetes in pregnancy?
SQ insulin with type 1, type 2 DM, and with GDM if home glucose values are consistently above target. Initial dose is based on pregnancy trimester. Glyburide is being used for patients with GDM who cannot be controlled by diet.
470
What are the home blood glucose monitoring goals for diabetes in pregnancy?
Patient checks her blood glucose values at least four times a day with target values of FBS 60–90 mg/dL and 1 h after a meal of
471
What abnormalities are associated with diabetes in pregnancy?
The most common fetal anomalies with overt DM are neutral tube defects and congenital heart disease. An uncommon anomaly, but one highly specific for overt DM, is caudal regression syndrome.
472
What are the assessments for anomalies in diabetes during pregnancy?
Obtain a triple–marker screen at 16–18 weeks to assess for neutral tube defects and a targeted ultrasound at 18–20 weeks for structural anomalies. Fetal echocardiogram at 22–24 weeks to assess for congenital heart disease.
473
What is the antepartum fetal surveillance for diabetes in pregnancy?
Weekly NSTs and AFI at 32 weeks if taking insulin, macrosomia, previous stillbirth, HTN. NSTs and AFIs at 26 weeks if small vessel disease or poor control. BPPs can be performed at time of monthly sonograms for macrosomia or IUGR.
474
What is the intrapartum timing of delivery for diabetes in pregnancy?
Target delivery gestational age is 40 wks, but earlier delivery may be necessary if fetal jeopardy. An amniotic L/S ratio of 2.5 in the presence of phosphatidyl glycerol assures lung maturity.
475
What is the intrapartum glycemic control in pregnant diabetics?
Maintain maternal blood glucose levels between 80 and 100 mg/dL using a 5% dextrose in water infusion and an insulin drip.
476
What is the criteria for anemia in pregnancy?
A hemoglobin concentration of
477
How is iron deficiency anemia diagnosed in pregnancy?
Iron deficiency anemia is the most common anemia in women because of menstrual and pregnancy needs. RBCs are microcytic and hypochromic. Hb 15.
478
What are the symptoms of iron deficiency anemia?
None to general malaise, palpitations, and ankle edema. Treatment is FeSO4 325 mg po tid. Prevention is with elemental iron 30 mg per day.
479
What is the screening test for sickle cell anemia?
Peripheral blood tests used to detect the presence of hemoglobin S. Screening tests do not differentiate between disease and trait.
480
What is the triad of iron deficiency anemia in pregnancy?
Hemoglobin 15%.
481
What is the triad of folate deficiency anemia?
Hemoglobin 100 mcL. RDW >15%.
482
What is the definitive diagnostic test for sickle cell anemia?
Hemoglobin electrophoresis will differentiate between SA trait (40% hemoglobin S).
483
What are the effects of sickle cell anemia on pregnancy?
With SS, the pregnancy may be complicated by increased spontaneous abortions, IUGR, fetal deaths, and preterm delivery.
484
30–year–old primigravida woman at 20 weeks' twin gestation of Norwegian descent and complains of intense skin–itching. No rash is noted. Urine appears dark–colored. What is the diagnosis?
Cholestasis of pregnancy.
485
What is intrahepatic cholestasis of pregnancy?
Stimulated by estrogen in second half of pregnancy. Risk is increased with multiple pregnancy. Bile acids are incompletely cleared by liver and accumulate in plasma. 0.5% in North America, Europe. High recurrence.
486
What are the signs of intrahepatic cholestasis of pregnancy?
Intractable pruritus of palms and soles of the feet, worse at night. Mild elevation of bilirubin, serum bile acids are increased 10– to 100–fold. Preterm births and stillbirths are increased.
487
What is the management of intrahepatic cholestasis of pregnancy?
Oral antihistamines, cholestyramine. Ursodeoxycholic acid is the treatment of choice. Antenatal fetal testing should be initiated at 34 weeks.
488
30 year–old primigravida at 34 weeks' with nausea, vomiting, anorexia. BP is 150/95 mm Hg. PTT 65 seconds. Creatinine 2.6. Uric acid 13, LDH 1100, ALT 220, AST 370, total bilirubin 8.8. Ammonia elevated. Urine protein 3+. What is the diagnosis?
Acute fatty liver
489
What is acute fatty liver?
Rare life–threatening complication of pregnancy in 3rd trimester. Caused by a disordered metabolism of fatty acids by mitochondria in fetus; deficiency in long–chain 3–hydroxyacyl–coenzyme A dehydrogenase.
490
What is the presentation of acute fatty liver?
Flu–like symptoms, nausea, vomiting, anorexia, epigastric pain, jaundice, fever. HTN, proteinuria, edema. ARF, pancreatitis, hepatic encephalopathy, coma. Elevated LFTs, hyperbilirubinemia, DIC. Hypoglycemia, increased ammonia.
491
What is the management of acute fatty liver?
Intensive care unit stabilization with acute IV hydration and monitoring. Prompt delivery.
492
What is asymptomatic bacteriuria of pregnancy?
The most common UTI in pregnancy. No symptoms or signs are present. If not treated, 30% of cases will develop acute pyelonephritis. Positive urine culture >100K colony–forming units of a single organism.
493
What are the complications of acute pyelonephritis in pregnancy?
Preterm labor and delivery sepsis, anemia, and pulmonary failure.
494
What is the triad of asymptomatic bacteriuria?
No urgency, frequency, or burning. No fever. Urine culture (+).
495
What is the triad of acute cystitis?
Urgency, frequency, and burning. No fever. Positive urine culture.
496
What is the triad of acute pyelonephritis?
Urgency, frequency, and burning. Fever and costovertebral angle tenderness. Positive urine culture.
497
What are the thrombophilias?
Disorders that promote clotting because of excess clotting factors or deficiency of anticlotting proteins. Prevalence 20%; most asymptomatic. DVT may occur during surgery, pregnancy. Thrombophilias cause miscarriages, stillbirths, abruption, preeclampsia.
498
What are the inherited thrombophilias?
Inherited thrombophilias are the most common thrombophilias. Two most common thrombophilias are factor V Leiden and prothrombin mutations. Hyperhomocysteinemia affects 10%. Antithrombin III deficiency (uncommon, severe), protein C, protein S deficiencies.
499
What is antiphospholipid syndrome?
Acquired autoimmune thrombophilia, in which antiphospholipid antibodies cause blood clots. One–third of SLE have antiphospholipid antibodies that may increase miscarriage. APS causes 15% of repeated miscarriages.
500
What is the treatment of thrombophilias during pregnancy?
SQ heparin does not cross placenta and is safe. Low–dose aspirin may be given with heparin. Low molecular–weight heparin is safer than unfractionated heparin. Warfarin is used postpartum for 6–8 wks; safe during breastfeeding; contraindicated antepartum.
