1 What is the normal duration of the menstrual cycle? What are the two ovarian phases, and which occurs first?

Normal cycle time is approximately 28 days, and the ovarian phases consist of the follicular and luteal phases, with the follicular phase occurring first. The first day of the menstrual cycle (and follicular phase) is defined as the day on which menstruation begins (Fig. 9-1).

Figure 9-1 Menstrual cycle. FSH, follicle-stimulating hormone; LH, luteinizing hormone.

(From Brown TA: Rapid Review Physiology. Philadelphia, Mosby, 2007.)

2 Which phase of the ovarian cycle is generally responsible for the cycle being longer or shorter?

The luteal phase is fixed at 14 days in a majority of women, so the differences in the length of the follicular phase account for cycle length differences. For boards, you should simply assume that the luteal phase accounts for 14 days of the menstrual cycle.

3 During the follicular phase, what hormonal changes occur in the pituitary and the ovary?:

Because the corpus luteum has involuted prior to the beginning of the follicular phase, and because this structure is the principal source of estrogen during the preceding luteal phase, plasma estrogen levels at the beginning of the follicular phase are low. This reduces estrogen’s negative feedback effect on pituitary production of follicle-stimulating hormone (FSH), so FSH secretion begins to rise. Note that the corpus luteum is also the major source of progesterone during the luteal phase, so progesterone levels are low during the follicular phase.

During the follicular phase, the rising FSH stimulates the development of several ovarian follicles, eventually causing the emergence of a dominant follicle, which becomes a site of estrogen synthesis. The growing follicle secretes increasing amounts of estrogen, which has the effect of inhibiting pituitary FSH production, thereby gradually reducing serum FSH levels in the later part of the follicular phase. However, the dominant follicle becomes increasingly sensitive to circulating FSH, so plasma estrogen levels still continue to rise throughout the follicular phase.

Note: Inhibin is also secreted by the ovaries and selectively inhibits FSH secretion with no effect on luteinizing hormone (LH) secretion.

4 What occurs in the uterus during the follicular phase?

The estrogen secreted by the ovaries stimulates proliferation of the endometrial lining of the uterus throughout the follicular phase.

5 What happens to cause ovulation at the end of the follicular phase?

When plasma estrogen reaches a critical level, it switches from causing negative feedback on the pituitary to causing positive feedback by sensitizing gonadotropes to gonadotropin-releasing hormone (GnRH). This stimulates the pituitary to release a surge of LH and FSH. The surge of these hormones causes rupture of the follicle and release of the ovum. This is an elegant design feature, because high estrogen levels indicate to the pituitary that the ovarian follicle is sufficiently “mature” to be released.

6 What happens in the ovary and endometrium during the luteal phase?

After ovulation, the cells that lined the follicle (granulosa cells and theca interna cells) form the corpus luteum (“yellow body”) under the influence of LH. The corpus luteum synthesizes both estrogen and a large amount of progesterone. The progesterone stimulates the endometrium to become more secretory and glandular in preparation for implantation. It also stimulates the spiral arteries to develop. These arteries empty into the intervillous space so that chorionic villi from the cytotrophoblast can extract oxygen if fertilization occurs. If fertilization does not occur, the corpus luteum degenerates, the levels of estrogen and progesterone fall, and the endometrium sloughs off as the menstrual flow.

You are expected to be able to differentiate between the histologic appearances of the endometrial lining during the follicular and luteal phases (Fig. 9-2). Notice the glandular hypertrophy, irregular shape of glands, and well-developed spiral arteries in the luteal (secretory) phase. In contrast, the glands in the follicular phase are smaller and straighter, and there is less vascularity in the stroma.

Figure 9-2 Low-magnification view of the uterine endometrium during the proliferative (estrogenic) phase of the reproductive cycle. Growing endometrial glands have straight profiles.

(From Telser A, Young J, Baldwin K: Elsevier’s Integrated Histology. Philadelphia, Mosby, 2008.)

7 In women with amenorrhea (absence of menses), why does bleeding after the cessation of a brief course of progesterone indicate that the cause of amenorrhea is due to the lack of ovulation?

In order to answer this question, one has to have a thorough comprehension of the normal physiology of the menstrual cycle; hence, this is a good board-style question.

If the administration and withdrawal of progesterone cause menses, this indicates that the endometrium has been sufficiently primed by estrogen and requires only a course of progesterone to have menses. However, the only source of endogenous progesterone is the corpus luteum, which forms only after ovulation. If there is no ovulation, there is no progesterone secretion, and there will not be menses.

The most common causes of anovulation are obesity, polycystic ovary syndrome, eating disorders (can result in decreased GnRH levels), premature ovarian failure, hyperprolactinemia (prolactin inhibits GnRH release), thyroid disorders (increased thyrotropin-releasing hormone [TRH] levels can stimulate prolactin release), adrenal insufficiency, and Asherman’s syndrome.

8 How does fertilization prevent degeneration of the corpus luteum?

If the ovum is fertilized, the developing embryo will synthesize human chorionic gonadotropin (hCG), which acts similarly to LH and maintains the corpus luteum.

9 How does the corpus luteum function in the maintenance of pregnancy?

During the first 6 weeks of pregnancy the corpus luteum is the primary producer of estrogen and progesterone, hormones required for the continuation of pregnancy. After the sixth week of pregnancy, the placenta begins to take over as the principal site of steroidogenesis. After delivery and removal of the placenta, both estrogen and progesterone levels fall markedly.

10 Describe the hormones associated with normal testicular descent

Normal testicular descent involves a transabdominal phase, which is mediated by müllerian-inhibiting factor (MIF) (a product of Sertoli cells), and a scrotal phase, which is mediated by androgens and β-hCG. Cryptorchidism refers to incomplete descent of the testes into the scrotal sac. The most common location of undescended testes is in the inguinal canal. Generally, the condition is unilateral and resolves spontaneously by 3 months. If uncorrected, cryptorchidism can result in infertility secondary to arrested germ cell maturation (sperm prefer the cooler temperature of the scrotal sac), increased risk of seminoma, and testicular infarction secondary to torsion of the undescended testes.

11 What is the function of the SRY gene?

The SRY gene is located on the Y chromosome and is responsible for testicular development (mediated by testis-determining factor). Testes contain Leydig and Sertoli cells. Leydig cells secrete testosterone, which stimulates the development of the mesonephric ducts. The mesonephric ducts develop into all of the male internal genitalia except for the prostate (epididymis, seminal vesicles, ejaculatory duct, and ductus deferens). Testosterone can also be converted into dihydrotestosterone (DHT), which stimulates the development of the male external genitalia and prostate. Sertoli cells produce MIF, which permits the degeneration of the paramesonephric duct. If degeneration does not occur, the paramesonephric duct develops by default into the female internal genitalia (uterus, fallopian tubes, and upper third of the vagina).

12 What is hermaphroditism?

A true hermaphrodite is a person who has both male and female internal genitalia (ovotestes). This condition is very rare. Pseudohermaphroditism is more common; the term describes any person in whom there is discordance between the sex of the internal and external genitalia. Because female pseudohermaphrodites lack a Y chromosome, they do not have an SRY gene and thus do not develop testes. Lack of MIF production results in development of female internal genitalia from the paramesonephric duct. Exposure to excessive androgen concentrations during the early gestational period (either by exogenous intake during pregnancy or through congenital adrenal hyperplasia) stimulates production of virilized external genitalia. Male pseudohermaphrodites, on the other hand, do contain a Y chromosome and thus develop testes. Because their testes produce MIF, they do not develop female internal genitalia. However, their external genitalia are feminized. This is most often due to androgen insensitivity syndrome, in which there is a defect in the androgen receptor. As a result, genotypic males are unable to develop male external genitalia but have high concentrations of testosterone and estrogen because there is no negative feedback from the pituitary due to lack of receptor stimulation.

13 What is 5α-reductase deficiency?

The enzyme 5α-reductase is responsible for converting testosterone into DHT. Because DHT stimulates the production of male external genitalia and the prostate, lack of DHT at birth leads to ambiguous external genitalia in these males. Internal genitalia are unaffected, because testicular development is governed exclusively by the presence of the Y chromosome. At puberty, increased concentrations of testosterone are adequate to stimulate development of the male external genitalia (Table 9-1). Patients with this autosomal recessive condition are thus said to develop a “penis at 12.”

Table 9-1 Conditions Affecting Development of the Genitalia

1 What important information should you find out before prescribing hormonal contraceptives?

It would be important to ask about tobacco use, breastfeeding, risk for sexually transmitted diseases (STDs), past medical history, and current medications because these factors may influence decisions about which type of contraceptive to prescribe.

2 What are you concerned about in this woman’s history in regard to hormonal contraception?

Estrogen-containing hormonal contraceptives alone increase the risk for various thrombotic and thromboembolic phenomena, including stroke, myocardial infarction, deep venous thrombosis, and pulmonary embolism (PE). In women who smoke, such contraceptives increase this risk substantially (as does this woman’s hypertension) and should therefore be used with caution. If this woman were over 35 as well as a smoker, estrogen-containing contraceptives would be contraindicated.

3 What are the absolute contraindications to using estrogen-containing contraceptives?

Smoker older than 35, history of thromboembolic phenomena (PE, stroke), coronary artery disease, hepatic tumors (estrogens can make hepatic tumors grow and rupture), and personal history of estrogen-dependent cancers such as endometrial carcinoma or breast carcinoma, unexplained vaginal bleeding, and impaired liver function.

4 What do oral contraceptives typically consist of and what is their mechanism of action?

The two general types of oral contraceptive are the combination pills (estrogen and progesterone) and the progesterone-only pills. In the combination pills, the constant level of estrogen supplied continuously suppresses pituitary gonadotropin secretion, thereby removing the stimulus for ovulation. The progesterone in the combination pills serves two functions: first, it thickens the cervical mucus secretions, essentially making the vaginal/uterine environment less “receptive” to sperm, and second, it opposes the proliferative effects of estrogen, causing thinning of the uterine lining (which is important in reducing the risk of endometrial cancer from unopposed estrogen). The progesterone-only pills are only about 50% effective at inhibiting ovulation, but as mentioned, they also work by thickening the cervical mucus and altering the motility and secretions of the fallopian tubes, as well as thinning the endometrium.

Important in this woman’s history is that she wishes to breastfeed her baby. Combination hormonal contraceptives post partum can interfere with milk production, so prescribing a progesterone-only contraceptive would be recommended.

Other methods of hormonal contraception:

Other types of contraception include the intrauterine device (IUD) with or without hormones; barrier methods (condoms, diaphragm, cervical cap); or tubal ligation/vasectomy.

5 How can menstrual cycles be made regular by hormonal contraceptives?

In order for menstruation to occur, there must first be estrogenic stimulation of endometrial proliferation; then progesterone must induce maturation and stimulate secretion by the endometrial glands. Menses begin following the decline in progesterone and estrogen levels near the end of the menstrual cycle. In many women, these hormonal events do not occur in such a well-orchestrated manner. Consequently, the estrogen and progesterone stimulation of the uterus can be provided artificially, which can mimic the natural menstrual period. Typically, to achieve this type of control, estrogens are given with progesterones for 21 days, and then placebo pills are given for 7 days to allow for menstruation.

6 Your patient asks if taking hormonal contraceptives will increase her risk for endometrial cancer. How does taking oral contraceptives affect the risk of endometrial, ovarian, and breast cancer? What is supposed to explain this effect?

Hormonal contraceptives (combined) actually decrease the risk of ovarian as well as endometrial cancer. The proposed explanation for decreasing risk of ovarian cancer is that by inhibiting ovulation, oral contraceptives reduce the inflammatory response and cell proliferation that usually occurs on the ovarian surface after each follicle ruptures through the ovarian surface, which is what predisposes ovarian surface epithelium to malignancy. The proposed explanation for decreasing the risk of endometrial cancer is the effect progesterone has on thinning the uterine lining and preventing unopposed growth by estrogen.

The risk of breast cancer is controversial: Studies show either no effect or a slight increase in risk.

7 How do ovarian cysts form and how do oral contraceptives reduce their occurrence?

The most common ovarian cysts are “functional cysts” that form when the normal follicular maturation and the corpus luteum formation process becomes somewhat aberrant. These are the follicular cysts and corpus lutein cysts, respectively. Follicular cysts develop after failure of a mature ovarian follicle to rupture and be ovulated. Corpus lutein cysts are formed during the luteal phase and occur when the corpus luteum becomes abnormally large or hemorrhagic (corpus hemorrhagicum). Clearly, the inhibition of follicular maturation and ovulation by oral contraceptives should reduce the chance that these cysts will develop.

8 Why may the drugs phenytoin, phenobarbital, and rifampin make oral contraceptives less effective at preventing pregnancy?

These drugs all induce hepatic cytochrome P-450 enzymes, which can accelerate the rate of hepatic catabolism of estrogen and progesterone compounds.

1 What is the differential diagnosis for secondary amenorrhea?

The differential diagnosis for secondary amenorrhea includes pregnancy (which is most common), tumor of ovary or adrenals, anatomic abnormalities (such as Asherman’s syndrome, in which intrauterine adhesions may occur following uterine surgery), ovarian failure or polycystic ovary syndrome (PCOS), hypothyroidism, hyperprolactinemia, and central nervous system (CNS) or hypothalamic disorder.

2 What laboratory tests should you order?

Even though the woman is emphatic that she cannot be pregnant, a serum β-hCG should always be done first to rule out pregnancy. If the β-HCG test is negative, one then can then proceed with further testing: thyroid-stimulating hormone (TSH), prolactin level, a progesterone-only challenge test, estrogen and progesterone challenge, FSH level, and LH level.

If withdrawal bleeding is present with the progesterone-only challenge test, then the amenorrhea is secondary to anovulation (see question 7 under Basic Concepts section for further discussion). If withdrawal bleeding is absent with progesterone alone, but present with estrogen and progesterone, then suspect inadequate endogenous estrogen and evaluation of FSH and LH levels might help distinguish between a hypothalamic/pituitary process and ovarian failure. If withdrawal bleeding is completely absent, an anatomic disorder such as Asherman’s syndrome might be present. Asherman’s syndrome refers to the removal of the stratum basalis owing to repeated curettage. Because the stratum basalis serves as the stem cell layer of the endometrium, destruction of this layer prevents regeneration of the functional endometrial tissue. Instead, endometrial fibrosis persists.

3 Does an elevated β-human chorionic gonadotropin level always indicate a developing embryo/fetus?

It does not necessarily mean she is pregnant, because gestational trophoblastic tumors (hydatiform moles/invasive moles/choriocarcinoma) as well as several germ cell tumors of the ovary also elaborate β-hCG. Note, however, that these are all rare entities. You should confirm the presence of a developing embryo within the uterus by ultrasound.

4 What is β-human chorionic gonadotropin and what is its normal function, aside from serving as a marker for pregnancy?

The hormone β-hCG is similar in structure and activity to LH. It is secreted early in pregnancy by the placenta (specifically, the syncytiotrophoblast cells) and functions to maintain the corpus luteum, which is the principal site of ovarian steroidogenesis during the luteal phase. Production begins approximately 1 week after conception and doubles in quantity every 2 days. The hormone is detectable in the blood by 8 days after conception and in the urine approximately 14 days after conception (around the time a woman would expect her next period). Plasma levels of β-hCG peak in the first trimester (by 10 weeks of gestation). Then, as the placenta begins to take over as the main site of maternal estrogen and progesterone secretion, β-hCG levels taper off (Fig. 9-3).

Figure 9-3 Human chorionic gonadotropin stimulates production of estrogen and progesterone by the corpus luteum. As the levels of this hormone drop, the placenta takes over as the major site of synthesis of ovarian steroids.

(From Guyton AC, Hall J: Textbook of Medical Physiology, 11th ed. Philadelphia, WB Saunders, 2007.)

5 Relative to a normal pregnancy, how would the β-human chorionic gonadotropin level differ for an ectopic pregnancy?

In ectopic pregnancy there is poor placentation (there are fewer syncytiotrophoblast cells to produce β-hCG), and therefore, the serum β-hCG is significantly lower than would be expected for normal pregnancy of the same gestational age. As a general rule of thumb, if β-hCG levels do not double appropriately and reach expected levels, you should suspect an abnormality with the pregnancy.

6 Assuming the positive β-human chorionic gonadotropin test confirms a pregnancy in this woman, what was the approximate date of conception?

Because ovulation occurs approximately 2 weeks after the onset of menses, and her last menses began 9 weeks ago, the approximate date of conception was 7 weeks ago.

7 What is the difference between the gestational age and the time since conception (developmental age)?

The gestational age is the period that has elapsed since the first day of her last menstrual period. It is not the time since conception, a mistake students commonly make. Because conception typically occurs 2 weeks later, the time since conception is 2 weeks shorter than the gestational age. Gestational age is most commonly used: She is 9 weeks by gestation.

8 At what time during development is the embryo/fetus most susceptible to teratogens?

The fetus is most susceptible during the third to eighth weeks (days 15-56, the “embryonic period”), when organogenesis occurs. Common teratogens include alcohol, cocaine, nicotine, excessive vitamin A, lithium, warfarin, angiotensin-converting enzyme (ACE) inhibitors, alkylating agents, certain antibiotics, and valproic acid, to name a few.

9 What is fetal alcohol syndrome?

Fetal alcohol syndrome is the leading cause of congenital malformations in the United States and results from excessive alcohol intake during pregnancy. It is associated with a wide range of congenital defects including mental retardation, microcephaly, seizures, and motor disorders, all of which result from a disruption of neuroblast migration. Other defects include limb dislocation, heart abnormalities, and facial abnormalities (flat nasal bridge, upturned nose, “railroad track” ears, epicanthal folds, smooth philtrum, and small palpebral fissures) (Fig. 9-4).

Figure 9-4 Infant with fetal alcohol syndrome. Note short palpebral fissures, mild ptosis, appearance of the nostrils, smooth philtral area, and narrow vermilion of the upper lip.

(From Gilbert-Barness E: Potter’s Pathology of the Fetus, Infant and Child, 2nd ed. Philadelphia, Mosby, 2007.)

10 The risk of which fetal developmental abnormalities can be reduced by taking supplemental folic acid early during pregnancy?

The risk of developmental abnormalities of the CNS and the spinal cord, which may cause neural tube defects such as spina bifida and anencephaly, may be reduced. Ideally, prenatal supplements are taken prior to pregnancy, because significant neural development may already have occurred by the time a woman realizes she is pregnant.

11 Is the woman in Case 9-2 at high or low risk for having a baby with Down syndrome (trisomy 21)?

The incidence of Down syndrome increases significantly with maternal age (as ova age, they acquire mutations), and because this woman is only 26, her risk is quite low. The risk increases with age from approximately 1 in 1500 for babies of 16-year-old mothers to approximately 1 in 25 babies for 45-year-old mothers.

Note: Maternal serum α-fetoprotein (AFP) levels are often checked around the 16th week of pregnancy. High levels may indicate a neural tube defect such as spina bifida whereas low levels may indicate Down syndrome. Other laboratory findings associated with Down syndrome include decreased estriol and elevated β-hCG and inhibin A.

12 Why should ergot alkaloids (e.g., ergonovine), triptans (e.g., sumatriptan), and synthetic prostaglandins (e.g., misoprostol) all be stringently avoided during pregnancy?

These agents all cause powerful uterine contractions that can result in abortion. The effects of ergot alkaloids and triptans are principally mediated through serotonin receptors. Misoprostol is a synthetic prostaglandin that causes contractions in an analogous fashion to endogenous prostaglandins.

1 What is the differential diagnosis for first-trimester bleeding (<12-14 weeks)?

The differential diagnosis for first-trimester bleeding includes spontaneous abortion, ectopic pregnancy, molar pregnancy, and postcoital bleeding, as well as other non–pregnancy-related causes such as vaginal laceration or trauma.

Case 9-3 continued:

She has not been seen in clinic, but she knows she is pregnant by a positive urine pregnancy test. She has had severe nausea and vomiting but thinks that is normal “morning sickness.” You are concerned about a spontaneous abortion and ectopic pregnancy. A pelvic ultrasound (Fig. 9-5) reveals a “snowstorm” pattern and no discernible fetus. Serum β-hCG levels are elevated far and above what would be expected during pregnancy.

Figure 9-5 Pelvic ultrasound from patient in Case 9-3.

(From Gabbe SG, Niebyl JR, Simpson JL: Obstetrics—Normal and Problem Pregnancies, 4th ed. Philadelphia, Churchill Livingstone, 2002.)

2 What is the diagnosis?

Molar pregnancy (hydatidiform mole) is likely. Molar pregnancy is one subtype of gestational trophoblastic disease (GTD).

3 How can β-human chorionic gonadotropin levels differentiate between a normal pregnancy and a molar pregnancy (complete or incomplete mole)?

Because these moles are made exclusively of trophoblastic (placental) tissue, the site of β-hCG synthesis, serum β-hCG levels are substantially elevated in comparison to a normal pregnancy of similar “gestational age.” Other features that suggest a molar pregnancy include severe vaginal bleeding early in the pregnancy and vaginal passage of molar vesicles.

4 What is the difference between an invasive mole and choriocarcinoma and from what does each generally arise?

An invasive mole invades the myometrium but does not normally metastasize. A majority of them arise from benign molar pregnancies. Choriocarcinoma, on the other hand, is often metastatic and spreads hematogenously. Half of these develop from benign molar pregnancies, one fourth after normal term pregnancy, and one fourth after miscarriage, abortion, or ectopic pregnancy. A key histologic distinction between invasive moles and choriocarcinomas is that choriocarcinomas are less differentiated and lack a villous pattern.

5 Cover the columns on the right side of Table 9-2 and try to identify the characteristics of the different gestational trophoblastic diseases

See Table 9-2 and Figure 9-6.

Table 9-2 Gestational Trophoblastic Diseases

Figure 9-6 Patterns of fertilization to account for chromosomal origin of complete (46,XX) and triploid partial moles (XXY). In a complete mole, one or two sperm fertilize an egg that has lost its chromosomes. Partial moles are due to fertilization of an egg by one diploid or two haploid sperm, depicted in this example as one 23,X and one 23,Y.

(From Kumar V, Abbas AK, Fausto N: Robbins and Cotran Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2005.)

1 What is the differential diagnosis?

The differential diagnosis for palpitations and heat intolerance includes hyperthyroidism, normal pregnancy, anxiety, cardiac arrhythmia, and pheochromocytoma.

2 What would you like to do for further workup?

A thyroid panel to rule out hyperthyroidism would be helpful.

3 What is the diagnosis?

These results suggest gestational hyperthyroidism. In pregnancy, the total T₄ is usually elevated because estrogen increases the synthesis of thyroxine-binding globulin by the liver. Notice, however, that this woman had elevated free T₄, levels as well and it is this elevated free T₄ (or free T₃) that causes hyperthyroidism.

4 How does the pregnant state predispose to hyperthyroidism?

This effect is due to the presence of hCG in the maternal circulation. hCG is a glycoprotein synthesized and secreted by the placenta in large amounts. Owing to its similarity in structure to TSH (TSH, FSH, LH, and β-hCG all share the same α-subunit), it often hyperstimulates the thyroid gland during pregnancy, resulting in gestational hyperthyroidism. This condition often spontaneously resolves following delivery of the fetus and placenta.

5 How are maternal levels of follicle-stimulating hormone and luteinizing hormone likely to be affected in this woman, given that she is pregnant?

They should be low and virtually undetectable because of the significant negative feedback that the high levels of estrogen and progesterone seen with pregnancy produce on the pituitary.

6 Why is the decline in estrogen and progesterone after delivery beneficial for the beginning of lactation?

Both estrogen and progesterone inhibit lactation, and their withdrawal allows the elevated prolactin present at the time of delivery to facilitate milk letdown and lactation. Recall that the placenta is the major site of progesterone and estrogen secretion, so its expulsion after delivery will reduce the levels of these hormones.

7 How does breastfeeding act as a natural contraceptive?

Nipple suckling by the baby stimulates the release of prolactin by the anterior pituitary gland. Because one of the functions of prolactin is to inhibit the hypothalamic secretion of GnRH, this results in reduced FSH and LH secretion by the pituitary. Reduced levels of these gonadotropins inhibit ovulation in the nursing mother and acts as a natural birth control pill. However, breastfeeding must be practiced continuously in order to be efficacious as a contraceptive method.

1 What is the diagnosis?

Preeclampsia is defined by new-onset hypertension (>140/90 mm Hg) and proteinuria (>300 mg/day) occurring after 20 weeks’ gestation. Although the definitive cause of preeclampsia is still unknown, the underlying cause is thought to be generalized arterial vasospasm.

Note: The severity of preeclampsia is generally determined by the degree of proteinuria and blood pressure elevation.

2 How should this patient be managed?

This woman is classified as having mild preeclampsia. Because she is not yet at term (37 weeks), bed rest and expectant management would be appropriate, as one would not want to induce premature labor. She could also be given steroids such as betamethasone to enhance fetal lung maturity in the event that premature delivery is necessary.

Case 9-5 continued:

The next week she develops right upper quadrant (RUQ) pain, her proteinuria worsens, and her blood pressure increases to 170/115 mm Hg.

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