Reproductive Flashcards

1
Q

What is the most likely diagnosis?

A

Abruptio placentae. The presence of painful vaginal bleeding in the second or third trimester suggests abruption, and the presence of contractions is an additional clinical hint. The laboratory values, particularly the mild thrombocytopenia (normal platelet count in pregnancy is > 100,000/mm3) and decreased plasma fibrinogen (normal fibrinogen is > 400 mg/dL in pregnancy), also suggest placental abruption with developing consumptive coagulopathy.

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2
Q

What is the differential diagnosis of painful vaginal bleeding in the third trimester?

A

Abruption often presents as painful vaginal bleeding, whereas placenta previa (a complication of pregnancy in which placental tissue either partially or fully covers the cervical os) presents as painless vaginal bleeding. Other causes of third-trimester painful bleeding include labor, genital laceration, and uterine rupture (typically seen during labor in women who attempt vaginal delivery after cesarean section).

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3
Q

What is the pathophysiology of Abruptio placentae?

A

Abruptio placentae is the premature separation of a normal placenta from the uterus occurring after 20 weeks’ gestation and before delivery. The rupture of maternal blood vessels at the anchoring villi of the placenta causes a separation from the endometrium in which blood can accumulate. The hemorrhage can be external or concealed (Figure 13-1). This in turn disrupts the fetal blood supply and in severe cases can lead to fetal death.

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4
Q

What risk factors are associated with Abruptio placentae?

A

Risk factors that can increase disruption or weakening of the maternal blood vessels include trauma, maternal hypertension, cigarette smoking, cocaine use, thrombophilia, increased parity, direct abdominal trauma, amniocentesis, and multifetal gestation.

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5
Q

What complication are patients with Abruptio placentae at greatly increased risk for developing?

A

Disseminated intravascular coagulation (DIC) occurs in approximately 10%–20% of cases of serious abruption with fetal death. In these cases, it is thought that the death of the fetus releases procoagulants into the mother’s circulation, triggering DIC. This initiates intravascular activation of coagulation and results in consumption of platelets and clotting factors. Fibrin may deposit in the microcirculation, causing ischemic organ damage and hemolytic anemia and then fibrinolysis of the fibrin deposition. Ultimately, this can cause a bleeding diathesis along with clinical manifestations of thrombosis.

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6
Q

What is the most likely diagnosis?

A

Androgen insensitivity syndrome (also known as testicular feminization syndrome) should be suspected in a woman with primary amenorrhea, little or no axillary/pubic hair, and an inguinal mass. The disease affects approximately 1:100,000 chromosomal males.

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7
Q

What is the clinical presentation of Androgen insensitivity syndrome?

A

There are two main presentations of this disorder:
1. In newborns it presents as an inguinal mass.
2. In adolescents it presents as primary amenorrhea.
The inguinal mass seen in newborns is caused by aberrant descent of the testes, which usually remain in the abdomen.

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8
Q

What is the pathophysiology of Androgen insensitivity syndrome?

A

This disorder results from dysfunction of the androgen receptors in a genetically male patient. The testes are present and secrete testosterone and müllerian inhibiting factor (MIF). However, the person cannot respond to this testosterone because the peripheral receptors are nonfunctional. Instead, the testosterone is converted into estradiol in peripheral tissues (especially adipose tissue), which initiates breast development. The vagina is often present but may be short and blind-ending. The MIF secretion inhibits normal development of the ovaries and uterus. Figure 13-2 illustrates genetic regulation of gonadal development.

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9
Q

What would confirmatory testing show in Androgen insensitivity syndrome?

A
  • On karyotype, these patients are 46,XY.
  • Pelvic ultrasound can show testes and the absence of a uterus and ovaries.
  • Polymerase chain reaction assay can show mutations of the androgen receptor.
  • Testosterone and dihydrotestosterone (DHT) levels should also be measured. Both should be normal
    or high. Low testosterone may indicate testicular dysgenesis or Leydig cell aplasia/hypoplasia. If testosterone levels are normal but DHT levels are low, 5α-reductase deficiency is suspected because testosterone is converted to DHT by 5α-reductase.
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10
Q

What is the appropriate treatment for Androgen insensitivity syndrome?

A

Initially, removal of the testes is performed because of the high risk of cancer development without such a procedure. Thereafter, treatments are mainly hormone replacement therapy and psychological support. Estrogen, but not progesterone, is given because no uterus is present. Estrogen is given to replace the loss of sex hormone production with the removal of the testes. Psychological therapy is given because of the potential for gender confusion. Surgical reconstruction may be needed to create a “functional” vagina, although if found earlier the use of dilators may obviate surgical intervention.

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11
Q

What is the most likely diagnosis? What organism causes this condition?

A

Bacterial vaginosis (BV). The presence of clue cells, which are squamous epithelial cells with smudged borders (Figure 13-3), is strong evidence that the infection is bacterial in origin. An elevated pH (> 4.5) and a positive whiff test (amine release with potassium hydroxide results in a fishy smell) may aid in the diagnosis.
BV is not generally considered a sexually transmitted infection (STI), and it can also occur in women who have not had intercourse. It is caused by an imbalance of naturally occurring bacterial flora within the vagina, with a decrease in favorable bacteria (lactobacilli) and an overgrowth of existing commensal bacteria (eg, Gardnerella vaginalis).

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12
Q

What other conditions should be considered in the differential diagnosis of Bacterial vaginosis?

A

As this woman is in a monogamous relationship she is not at high risk for STIs such as Trichomonas, Neisseria gonorrhoeae, or Chlamydia. Most women with chlamydia and gonorrhea are asymptomatic, although they can have cervical motion tenderness on pelvic exam. Trichomonas often causes a frothy discharge. Candida is another common cause of vaginitis, which is not sexually transmitted. Women with candida often present with vaginal itching and increased white, curdlike discharge.

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13
Q

What is the appropriate treatment for Bacterial vaginosis (BV)?

A

Metronidazole (oral or vaginal gel) is used to treat bacterial vaginosis (BV). Chlamydia is treated with azithromycin. Gonorrhea is treated with ceftriaxone. Candida is treated with fluconazole.

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14
Q

What is the most likely diagnosis?

A

Benign prostatic hyperplasia (BPH). BPH increases with age and is found in approximately one half of men 51–60 years of age.

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15
Q

What are the typical signs and symptoms of Benign prostatic hyperplasia (BPH)?

A
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16
Q

What is the pathophysiology of Benign prostatic hyperplasia (BPH)?

A

The prostate gland has a central region surrounding the urethra and a peripheral region. In BPH the central region hypertrophies in response to stimulation from the growth hormone dihydrotestosterone (DHT). In prostate cancer, it is often the peripheral region that grows.

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17
Q

What are the potential complications of Benign prostatic hyperplasia (BPH)?

A

Complications of BPH include the following:
- UTI secondary to urine stasis
- Bladder stone formation secondary to urine stasis.
- Daytime sleepiness and exhaustion due to repeated nighttime awakenings from nocturia.
- Acute urinary retention, which presents with symptoms such as abdominal pain and a suprapubic
mass (the filled bladder). This can be spontaneous or secondary to triggers such as anticholinergics, antihistamines, or α-receptor agonists (eg, cold medications), all of which decrease bladder contractility.

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18
Q

What is the appropriate treatment for Benign prostatic hyperplasia (BPH)?

A

Medical options include cholinergics (eg, bethanechol), α-blockers (eg, prazosin), and 5α-reductase inhibitors (eg, finasteride). Cholinergics help increase bladder contractility, whereas α-blockers relax the bladder neck so that urine flows more easily. The 5α-reductase inhibitors prevent the formation of DHT so that prostate growth is retarded. Side effects of finasteride include sexual dysfunction and postural hypotension. Surgery is also an option.

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19
Q

What is the most likely diagnosis?

A

Approximately 90% of breast lumps discovered in women between 20 and 50 years of age are benign. Fibroadenomas are the most common breast tumors seen in young women. They are benign, often arise quickly, and reabsorb within several weeks to months. Fibroadenomas do not carry an increased risk of breast cancer. Approximately 20% of fibroadenomas are bilateral or multiple. The risk associated with having a first-degree relative with breast cancer is higher the younger the relative is at diagnosis.

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20
Q

What are Cooper ligaments?

A

The superficial and deep pectoral fascia surrounding the breast are connected by fibrous bands known as Cooper suspensory ligaments.

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21
Q

What is the structure of breast tissue?

A

Breast tissue is found between the second and sixth ribs and is made of parenchyma and stroma (Figure 13-4). The parenchyma has 15–25 lobes, each of which has 20–40 lobules composed of alveoli. Lactiferous ducts offer drainage to the corresponding lobe. The ducts are dilated immediately before the nipple, forming the lactiferous sinuses.

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22
Q

What are the muscles of the breast tissue, and how are they innervated? (4)

A
  1. The serratus anterior is innervated by the long thoracic nerve.
  2. The latissimus dorsi is innervated by the thoracodorsal nerve.
  3. The pectoralis minor is innervated by the medial pectoral nerve.
  4. The pectoralis major is innervated by the pectoral nerve.
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23
Q

What is the appropriate treatment for Fibroadenomas of the breast?

A

Because of their benign nature, no treatment is necessary. The patient should be followed up in 1–2 months to assess for reabsorption. If there remains concern for breast cancer, a needle or excision biopsy is indicated.

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24
Q

What is the most likely diagnosis?

A

Ectopic pregnancy. Ectopic pregnancy occurs at a rate of 17:1000 pregnancies. The majority (98%) of cases occur in the fallopian tubes, most often (90%) in the ampulla.

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25
Q

What signs and symptoms are commonly associated with Ectopic pregnancy?

A
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26
Q

What are 7 risk factors associated with this condition?

A
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27
Q

What are the typical laboratory findings in Ectopic pregnancy?

A

The β-hCG level in an ectopic pregnancy is typically < 6500 IU/L, which is markedly lower than in a uterine pregnancy. The serum progesterone level (typically < 15 ng/mL) is also much lower than in a uterine pregnancy. In a normal intrauterine pregnancy, the β-hCG level increases by 50% every 48 hours. If this trend does not occur on serial laboratory results, then an ectopic pregnancy is suspected.

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28
Q

What are the appropriate treatments for ectopic pregnancy?

A

Treatment may be medical or surgical depending on the clinical situation. The usual medical treatment is methotrexate, which may be given if the ectopic pregnancy is < 3 cm, the β-hCG level is < 12,000 IU/L, no fetal heart rate is present, and the mother’s liver and renal tests are normal. β-hCG levels must be checked serially after administration of methotrexate to ensure the proper decline in β-hCG, indicating ectopic demise. Surgery is indicated if the criteria for medical intervention are not met. Surgery may remove part or all of the fallopian tube. Segmental resection might be necessary for an ischemic ectopic pregnancy. Salpingectomy is usually reserved for a ruptured ectopic pregnancy.

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29
Q

What is the most likely diagnosis?

A

Endometriosis

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30
Q

What signs and symptoms are commonly associated with this condition?

A
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31
Q

What is the pathophysiology of endometriosis?

A

In endometriosis, endometrial tissue is found outside the endometrial cavity, usually in the ovary and pelvic peritoneum. It is thought that this endometrial tissue is either transported via the lymphatic system, causing peritoneal tissue to undergo metastatic change to become functional endometrial tissue, or that it is transported through the fallopian tubes in retrograde menstruation. Endometrial tissue causes adhesions, fibrosis, and severe inflammation.

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32
Q

What risk factors are associated with Endometriosis?

A

Endometriosis occurs in 10%–15% of women overall but is more common (30%–40%) in women with infertility. The risk of endometriosis is seven-fold higher in women who have a first-degree relative with the condition. Endometriosis has also been linked to autoimmune disorders such as lupus. It is less commonly identified in African-American women.

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33
Q

What are the appropriate treatments for Endometriosis?

A

Medical treatment includes alleviating symptoms (with nonsteroidal anti-inflammatory drugs) and suppressing menstrual cycles to allow the lesions to involute. This is done with continuous oral contraceptive pills, medroxyprogesterone (inducing “pseudopregnancy”), androgen derivatives, or gonadotropin- releasing hormone agonists (inducing “pseudomenopause”). Surgical treatment may be necessary in refractory cases.

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34
Q

What is the most likely diagnosis?

A

Erectile dysfunction (ED) affects up to 50% of men 40–70 years of age.

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35
Q

What physiologic factors are necessary to maintain an erection?

A

Developing and maintaining an erection depends on neurologic, vascular, and hormonal factors (Figure 13-5). Neurologic control of erectile function is via the dorsal nerve of the penis, a branch of the pudendal nerve which provides autonomic innervation to the pelvis. Vascularly, significant arterial flow into the penis (specifically into the corpora cavernosa and corpora spongiosum) must be maintained and venous outflow prevented. Adequate blood flow is achieved through cyclic guanosine monophosphate (cGMP)-mediated relaxation of the smooth muscle of the corporae, which requires nitric oxide. Hormonally, adequate production of testosterone is required.

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36
Q

What risk factors are associated with Erectile dysfunction (ED)?

A

The main risk factors for developing ED are primarily vascular (hypertension, cardiovascular disease, and diabetes mellitus).
Other risk factors include obesity, sedentary lifestyle, nerve injury, pelvic trauma/radiation, spinal cord injury, prostate surgery, and psychiatric disorders (eg, depression, performance anxiety, fear of sudden death).

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37
Q

What drugs most commonly cause Erectile dysfunction (ED)?

A
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38
Q

What is the appropriate treatment for Erectile dysfunction (ED)?

A

The main treatment for ED is phosphodiesterase inhibitors, such as sildenafil and vardenafil. These work by preventing the degradation of cGMP, thereby allowing dilatation of the corpora and adequate blood flow into the penis. Other treatments include vacuum pumps, penile prosthesis, and direct injection of α-blockers (eg, phentolamine) into the penis. Depression should be treated as appropriate. SSRIs and behavioral therapy are helpful in the treatment of performance anxiety.

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39
Q

What is the most likely diagnosis?

A

Pelvic inflammatory disease (PID) is the most likely diagnosis. This condition occurs as a complication of ascending gonococcal or chlamydial infection. Ascending infection by these agents can also cause tubo- ovarian abscess or Fitz-Hugh–Curtis syndrome (perihepatitis resulting in right upper quadrant pain).

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40
Q

What 6 signs and symptoms are commonly associated with this condition?

A
  1. Fever.
  2. Pelvic pain.
  3. Cervical motion tenderness.
  4. Adnexal tenderness.
  5. WBC elevation.
  6. ESR >15.
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41
Q

What is the pathophysiology of Pelvic inflammatory disease (PID)?

A

Chlamydia is the most common cause of PID. Neisseria gonorrhoeae also causes PID.

42
Q

What risk factors are associated with Pelvic inflammatory disease (PID)?

A
  1. Cigarette smoking.
  2. High frequency of intercourse.
  3. Multiple partners.
  4. New sexual partner within 1 month of symptom onset.
  5. Recent history of douching.
  6. Use of an intrauterine device.
  7. Young age at first intercourse.
43
Q

What are the likely Gram stain and culture findings in a patient with Pelvic inflammatory disease (PID) ?

A

PCR is the gold standard to detect Chlamydia or N gonorrhoeae. The sample can be done with a first-catch urine or a cervical swab. Urine PCR is as specific, but less sensitive than a cervical swab.

44
Q

What are the appropriate treatments for Pelvic inflammatory disease (PID)?

A

Uncomplicated PID is treated as an outpatient with ceftriaxone and doxycycline. If the patient is pregnant, has a tubo-ovarian abscess, or is nauseous and cannot tolerate oral medications, she must be hospitalized for administration of intravenous antibiotics. Surgery is indicated in cases of tubo-ovarian abscess.

45
Q

What is the most likely diagnosis?

A

Gestational diabetes mellitus (DM) is defined as glucose intolerance first documented in pregnancy.

46
Q

What is the pathophysiology of Gestational diabetes mellitus (DM)?

A

Gestational DM occurs in approximately 4% of all pregnancies. Normal pregnancy is a diabetogenic (pro- diabetic) state characterized by insulin resistance and decreased peripheral uptake of glucose. This is mediated by the production of counterregulatory (anti-insulin) hormones by the placenta, including human placental lactogen, cortisol, and placental growth hormone.

47
Q

How is Gestational DM diagnosed?

A

Gestational DM is most often asymptomatic and is usually detected at 24–28 weeks’ gestation by a routine OGTT.
In gestational DM, any two of the following levels are diagnostic: 1-hour postprandial glucose > 190 mg/dL, 2-hour postprandial glucose > 165 mg/dL, and/or 3-hour postprandial glucose > 145 mg/dL. Other signs include glycosuria, hyperglycemia, and fetus large for gestational age.

48
Q

What risk factors are associated with Gestational diabetes mellitus (DM)?

A

Risk factors include age < 25 years, family or past history of gestational DM, fetus large for gestational age, glycosuria at first prenatal visit, obesity, polycystic ovarian syndrome, previous stillbirths or abortions, maternal birthweight > 4.1 kg (9 lb), and Hispanic or African American race.

49
Q

What are 4 common fetal complications associated with Gestational DM?

A

Common fetal complications include:
1. Congenital defects.
2. Macrosomia.
3. Perinatal mortality (2%–5%).
4. Shoulder dystocia.

50
Q

What are the appropriate treatments for Gestational diabetes mellitus (DM)?

A

Affected women should adhere to a diabetic diet. Fasting blood glucose and 2-hour postprandial glucose levels should be routinely monitored. If levels remain high for 2 weeks, insulin therapy, rather than oral hypoglycemics, should be instituted. Fetal growth should also be monitored.

51
Q

What is the most likely diagnosis?

A

Klinefelter syndrome.

52
Q

What is the pathogenesis of Klinefelter syndrome?

A
53
Q

What tests and/or imaging tools could be used to confirm the diagnosis of Klinefelter syndrome?

A
  • Elevated follicle-stimulating hormone (FSH) levels are a key finding in Klinefelter. Because the seminiferous tubules are unformed, there is a lack of Sertoli cells; therefore, no inhibin (made by Sertoli cells) is produced. Without inhibin, there is a loss of negative feedback on FSH, causing elevated levels (Figure 13-6). LH levels are also elevated as a result.
  • Testosterone levels are low, whereas estradiol levels are high.
  • The definitive diagnosis requires karyotype.
54
Q

What is the appropriate treatment for Klinefelter syndrome?

A

Androgen replacement therapy should begin around puberty. Androgen replacement has been shown to help with virilization, psychosocial development, hair growth, muscle mass, libido, testicular size, and precocious osteoporosis. Also, the patient needs to be educated and counseled about the fact that he is infertile.

55
Q

What can be done to increase the fertility of patients with Klinefelter syndrome?

A

Most men with Klinefelter produce small amounts of sperm, but it is typically not found in the ejaculate. Since some sperm are produced, they can be extracted from the testicles for use in vitro fertilization.

56
Q

What is the most likely diagnosis?

A

The heavy vaginal bleeding and palpable masses suggest leiomyomas, or uterine fibroids.

57
Q

What is the epidemiology of Uterine fibroids?

A

Uterine fibroids can be found in 25% of all reproductive-aged women. The incidence of leiomyoma is greatly increased in African-American women (two to three times increased risk compared to white women). Leiomyoma is the most common benign neoplasm in females.

58
Q

Which cells of the uterus are most commonly affected in Uterine fibroids?

A

Smooth muscle cells of the myometrium are most commonly affected, although fibroids can also occur in subendometrial or subperitoneal areas (Figure 13-7). Fibroids within the uterus can be submucosal, subserosal, or intramural. Submucosal fibroids are most often associated with abnormal bleeding, whereas subserosal fibroids are most often the cause of pressure due to mass effect.

59
Q

How does the size of Uterine fibroids change with age?

A

The estrogen sensitivity of leiomyomas usually results in increased size during the first trimester of pregnancy and shrinkage after menopause.

60
Q

Are patients with leiomyosarcomas at increased risk for uterine malignancy?

A

Most leiomyosarcomas arise de novo and malignant transformation of leiomyomas into leiomyosarcoma is rare. Approximately 9% of uterine malignancies are leiomyosarcomas.

61
Q

What uterine abnormality is associated with an increased risk of endometrial cancer?

A

Endometrial hyperplasia, which is characterized by abnormal glandular proliferation, is considered to be a premalignant lesion. This is caused by increased estrogen stimulation and, like uterine fibroids, often presents with abnormal vaginal bleeding. Therefore, its presence must be distinguished from abnormal vaginal bleeding secondary to uterine fibroids. This can be accomplished by histological examination of the endometrium obtained by endometrial biopsy.

62
Q

What is the usual treatment for Uterine fibroids (leiomyomas)?

A

Expectant management is often considered in mild cases. Hormonal therapies (oral contraceptive pills) are commonly prescribed for symptomatic treatment. For definitive treatment, surgery, including myomectomy or hysterectomy, can be performed. Other possibilities include uterine artery embolization and MRI-guided focused ultrasound surgery.

63
Q

What is the most likely diagnosis?

A

The start of menopause. Menopause is defined as 12 months without a period (amenorrhea) in a woman older than 45 years of age without another cause for amenorrhea. The average age of menopause onset is 51 years. In women younger than 40 years of age, a full workup should be performed to evaluate the cause of what would be called premature ovarian failure.

64
Q

What is the differential diagnosis for irregular vaginal bleeding, and how should it be evaluated?

A
65
Q

What are the signs, symptoms, and laboratory values associated with menopause?

A

Signs and symptoms of menopause include a change in menstrual cycle length, skipped periods, hot flashes, sleep disturbance, vaginal dryness (resulting in itching and dyspareunia), and an increase in urinary tract infections (due to increased vaginal pH). Laboratory values in menopause include elevated follicle-stimulating hormone and, in early menopause, elevated estradiol levels.

66
Q

What complications are associated with menopause?

A

One complication is morbidity from the symptoms of menopause, such as vasomotor flushing. Menopause also increases a woman’s risk of developing osteoporosis. It is estimated that women can lose up to 20% of their bone density in the years surrounding menopause. This occurs because estrogen, which normally inhibits bone resorption, is decreased. Women undergoing menopause are also at risk for depression.

67
Q

What are the appropriate treatments for menopause and its complications?

A

Short-term estrogen therapy (2–3 years and not more than 5 years) is recommended for moderate to severe vasomotor flushing. Long-term therapy is not recommended. The benefits of reducing hot flash symptoms must be weighed carefully with the increase in cardiovascular adverse events. Topical estrogen can be applied to treat vaginal dryness. For women with osteoporosis or at high risk for the disease, bisphosphonates, which prevent bone resorption, are the preferred first-line agent. The selective estrogen receptor modulator raloxifene is another alternative. These therapies should be used in addition to calcium/vitamin D, exercise, and smoking cessation. Selective serotonin reuptake inhibitors can be given for depressive symptoms.

68
Q

What is the most likely diagnosis?

A

Hydatidiform mole or molar pregnancy. In North American and European countries, rates tend to be 1:1000–1500 pregnancies, whereas in Asian and Latin American countries the rates are higher, reaching 1:12–500 pregnancies.

69
Q

What risk factors are associated with this condition?

A
70
Q

What risk factors are associated with Hydatidiform mole (molar pregnancy)?

A

The main risk factor is extremes of reproductive age (younger than 20 or older than 35 years). A history of molar pregnancy is also predictive.

71
Q

How does Hydatidiform mole or molar pregnancy develop?

A

A complete mole develops when an enucleate egg is fertilized by a haploid sperm that then replicates. This results in 46 chromosomes (all paternal) but no fetal parts. A partial mole results from a haploid ovum and two sperm. The karyotype is typically triploid (69 chromosomes) and fetal parts may be present. There are some cases of recurrent moles that are due to a loss of maternal imprinting.

72
Q

What are the typical signs, symptoms, and clinical presentation of this condition?

A
73
Q

What 4 complications are associated with Hydatidiform mole or molar pregnancy?

A
  1. Increased risk for preeclampsia.
  2. Ovarian theca-lutein cysts (which are benign and resolve when the mole is removed).
  3. Respiratory distress (secondary to trophoblastic embolization).
  4. Choriocarcinoma (other causes of choriocarcinoma are spontaneous or induced abortion, ectopic
    pregnancy, and normal pregnancy).
74
Q

What is the appropriate treatment for Hydatidiform mole or molar pregnancy?

A

This condition is highly sensitive to chemotherapy (usually methotrexate or actinomycin D) and has a low rate of recurrence. The most common site of metastasis is the lungs, and the metastases also resolve with chemotherapy. Patients who develop choriocarcinoma are asked not to get pregnant for a year so that they can be monitored for recurrence through serial β-hCG levels.

75
Q

What is the most likely diagnosis?

A

Ovarian cancer is the second most common gynecologic malignancy. It is also the fifth most likely cause of cancer death in women.

76
Q

What are the typical signs and symptoms of Ovarian cancer?

A

Nonspecific symptoms are characteristic in ovarian cancer and include abdominal and pelvic pain, bloating, vaginal bleeding, and changes in bowel habits.
Physical signs are usually present only in advanced disease and include palpable ovarian or pelvic masses, ascites, pleural effusions, and bowel obstruction.

77
Q

What are the different forms of ovarian cancer?

A

Most ovarian cancers (90%) are epithelial in origin. There are two types of epithelial ovarian cancer: serous and mucinous. The serous type is slightly more common and is often bilateral. The mucinous type can progress to pseudomyxoma peritonei. Pseudomyxoma peritonei is a condition in which the mucinous adenocarcinoma cells seed the peritoneum. These cells continue to produce mucous and fill the abdominal cavity, eventually obstructing the bowel.
Other types of ovarian cancers include sex cord stromal tumors, germ cell tumors, and metastatic cancer to the ovaries.

78
Q

What 6 risk factors are associated with ovarian cancer?

A
  1. Early menarche or late menopause.
  2. Nulligravidity.
  3. Infertility.
  4. Endometriosis.
  5. Family history of ovarian or breast cancer.
  6. BRCA mutation or Lynch syndrome.
    Conversely, protective factors include multiple pregnancies and oral contraceptive pill use. It is theorized that protection against ovarian cancer results from a decreased number of ovulatory cycles.
79
Q

What tests and/or imaging tools can be used to confirm the diagnosis of ovarian cancer?

A

Initial tests include transvaginal ultrasound, CT, and screening for the tumor marker CA-125. CT and ultrasound often miss cancers, however, and CA-125 is better able to detect recurrences than to establish an initial diagnosis. If suspicion remains high even with negative initial testing, exploratory surgery is usually recommended; findings are used to stage the disease.

80
Q

What is the appropriate treatment for ovarian cancer?

A

Treatment is usually debulking surgery followed by chemotherapy, although choice of therapy depends on the clinical presentation of the cancer.

81
Q

What is the most likely diagnosis?

A

Paget disease of the breast, an eczematous skin lesion in the area of the nipple, is associated with underlying invasive or in situ breast carcinoma (Figure 13-8). In approximately 50% of cases, Paget disease is associated with a palpable breast mass. Paget disease is often mistaken for a benign skin lesion such as eczema.

82
Q

What is the pathophysiology of Paget disease of the breast?

A

The skin lesion likely develops from underlying mammary adenocarcinoma cells that migrate through the ducts to the epidermis. However, an alternative theory suggests that epidermal keratinocytes transform into malignant cells independent of the underlying carcinoma.

83
Q

What are the most likely findings on histology in Paget disease of the breast?

A

Histology often shows large cells with a halo of clear cytoplasm surrounding a prominent nucleolus. Additionally, the cytoplasm stains positive for mucin.

84
Q

What are the most common sites of metastasis for breast carcinoma?

A
  1. Bone is the most common site for metastatic disease.
  2. Other common organ sites include liver and lung.
  3. Less common sites include bone marrow, brain, ovaries, spinal cord, and eye.
85
Q

What is the lymphatic drainage of the breast?

A

Approximately 75% of lymphatic drainage of the breast is to the axillary lymph nodes, which include the pectoral (majority of drainage), apical, subscapular, lateral, and central node groups. The nipple drains to the pectoral group. The remaining lymph drains to the infraclavicular, supraclavicular, and parasternal (also known as the internal thoracic) nodes. To assess for lymph node metastasis in breast cancer, a sentinel lymph node biopsy is performed. To do this, a dye is injected into the tumor, and the first lymph node that the tumor drains into is dyed first. This lymph node is then biopsied to assess for lymphatic invasion.

86
Q

Molecular analysis of a biopsy reveals that the cells express c-erbB-2 in high levels. What is the significance of this, and how does it affect treatment?

A

The human epithelial growth factor receptor (HER)-2/neu (also known as c-erbB-2) protein is a transmembrane growth factor receptor kinase. Overexpression of this molecule (present in 18%–20% of breast cancers) has been associated with a poorer prognosis. The drug trastuzumab is a humanized recombinant monoclonal antibody directed against this protein. The binding of trastuzumab to the extracellular portion of the molecule stimulates a cytotoxic immune response, leading to death of the cancer cells.

87
Q

What is the most likely diagnosis?

A

Preeclampsia and eclampsia are the two most common causes of pregnancy-induced hypertension (PIH). Preeclampsia can occur at 20+ weeks of gestation. Preeclampsia is characterized by proteinuria and blood pressure > 140/90 mm Hg. Eclampsia is preeclampsia associated with seizures and/or coma.

88
Q

What signs and symptoms are commonly associated with Preeclampsia & eclampsia?

A
89
Q

What is HELLP syndrome?

A

HELLP is a subcategory of preeclampsia that results in a high rate of stillbirth (10%–15%) and neonatal death (~ 25%). HELLP stands for Hemolysis, Elevated Liver enzymes, and Low Platelets.

90
Q

What are the appropriate treatments for Preeclampsia?

A

If the baby is term, the fetal lungs are mature, or the case is severe, delivery is the best treatment. Mild preeclampsia is treated with bed rest, close monitoring, and blood pressure control with antihypertensive agents. In severe cases the mother should be hospitalized, and magnesium sulfate should be given for seizure prophylaxis (continued for 24 hours postpartum), in addition to antihypertensive agents. If severe, immediate delivery may be indicated to save the life of the mother.

91
Q

What is the most likely diagnosis?

A

Testicular torsion. Testicular torsion is usually seen in adolescent males aged 16–18 years, although it can also occur in infancy. Approximately 50% of instances occur during sleep, but it can also occur at rest or with physical activity. Some patients have repeated episodes that spontaneously resolve (presumably because the testis is undergoing repeated torsion and detorsion).

92
Q

What signs and symptoms are typically associated with Testicular torsion?

A

Symptoms of testicular torsion include the following:
1. Sudden, acute onset of pain in the scrotum, often on one side.
2. Swelling/reddening of the scrotum.
3. Abdominal pain.
4. Nausea/vomiting.
Signs of testicular torsion include the affected side’s being higher than the other and horizontal in orientation as well as absent cremasteric reflex.

93
Q

What 7 conditions should be included in the differential diagnosis?

A
94
Q

What complications are associated with testicular torsion?

A

Testicular torsion results in the twisting of the spermatic cord, which contains the testicular artery, pampiniform plexus, and vas deferens. The main danger is the twisting of the testicular artery, which cuts off the blood supply to the testicle. If this is not reversed rapidly, it will result in testicular atrophy and necrosis. This is a true surgical emergency.

95
Q

What is the appropriate treatment for testicular torsion?

A

Manually untwisting the testis will produce immediate and dramatic pain relief if successful. The success of this method can be confirmed by evidence of return of blood flow to the testis on Doppler ultrasound. Even if successful, surgery should be performed to suture the testis in place to prevent repeated torsion. If manual detorsion does not work, emergent surgery must be performed. Treatment must be initiated within 6 hours of presentation to assure viability of the testicle. If it is not treated within 24 hours, there is little chance of the testicle’s viability.

96
Q

What is the most likely diagnosis?

A

Turner syndrome, characterized by gonadal dysgenesis secondary to the presence of a single X chromosome (XO) (Figure 13-9). This syndrome is the most common cause of primary amenorrhea. This genetic disorder affects 3% of all conceptions, but only 1:1000 45X embryos survives to term.

97
Q

What other conditions can cause primary amenorrhea?

A
98
Q

What diagnostic test is indicated based on the patient’s clinical features?

A

Karyotype analysis should be performed.

99
Q

What diagnostic test is indicated based on the patient’s clinical features?

A

Karyotype analysis should be performed.

100
Q

Other than primary amenorrhea, What 7 other conditions are associated with Turner syndrome?

A
  1. Coarctation of the aorta.
  2. Bicuspid aortic valve.
  3. Hypothyroidism.
  4. Sensorineural hearing loss.
  5. Renal abnormalities.
  6. Gastrointestinal telangiectasias.
  7. Osteoporosis.
101
Q

What are the appropriate treatments for Primary amenorrhea in Turners Syndrome?

A

Recombinant human growth hormone and hormone replacement therapy can initiate puberty and complete growth. Treatment of other associated conditions is also advised.