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► Med Misc 06 > OB/GYN III > Flashcards

OB/GYN III Flashcards

1
Q

How is a molar pregnancy categorized

A

abnormal proliferation of the placental trophoblastic cells Abnormal cells distend the uterus and secrete hCG, mimicking a normal pregnancy. There are 2 types complete (classic) and partial (incomplete)

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2
Q

What defines a complete mole

A

Empty ovum fertilized by sperm.

46XX by one sperm occurs 90% of the time
46XX or 46 XY by two sperm occurs 10%

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3
Q

What is the most common clinical presentation of a molar pregnancy

A

Abnormal uterine bleeding (most common)
Uterine size greater than expected for GA
lack of fetal heart tones
hCG greater than 100,000 and uterine cavity filled with small vessicles

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4
Q

What defines an incomplete mole

A

a normal ovum is fertilized by two sperm. The resulting karyotype is 69 XXX, XXY, or XYY

A fetus may or may not be present, but will not viable if present

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5
Q

What are the most common clinical presentation of an incomplete molar pregnancy

A

Abnormal heavy bleeding
hCG is not as elevated as it is with a complete mole

Many spontaneous abortions are the result of a partial mole

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6
Q

How long should a patient wait for reattempting pregnancy following a molar pregnancy

A

at least 1 year

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7
Q

Gestational Trophoblastic Tumors may become metastatic to what locations

A

Lung (80%)
Vagina (30%)
Liver (10%)
Brain (10%)

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8
Q

How is a GTT diagnosed

A

After evacuation of a molar pregnancy

  1. increase in hCG
  2. the value of hCG reaches a plateau for 3 weeks
  3. metastatic disease is identified
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9
Q

What is used to treat non metastatic GTT

A

Single agent chemotherapy

  1. Methotrexate
  2. Actinomycin D
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10
Q

What drug is given with methotrexate to preserve normal cells

A

leucovorin

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11
Q

What is the mechanism of methotrexate

A

Anitmetabolite inhibits purine synthesis by blocking the dihydrofolate reductase enzyme required to process folic acid. Results in arrested synthesis of DNA, RNA and proteins

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12
Q

What is the mechanism of actinomycin D

A

Antibiotic that intercalates DNA strands

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13
Q

How should you monitor a patient with GTT

A

hCG titers should be taken weekly until normal fro 3 months, then monthly for 6 months
Contraception is preferred for 1 year

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14
Q

What carries a good prognosis with metastatic GTT

A

Rules of 4

  • duration less than 4 months
  • less than 40,000 hCG pretreatment
  • No foreign metastasis to brain or liver
  • no previous chemotherapy
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15
Q

What is the treatment for poor prognosis metastatic GTT

A

EMA-CO

Etoposide
Methotrexate
Actinomycin D
Cyclophosphamide
Oncovin (vincristine)
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16
Q

How long should treatment last for poor prognosis metastatic GTT

A

Three additional chemo sessions after a negative hCG titer

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17
Q

What are the phases of the menstrual cycle

A

Follicular

Secretory

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18
Q

What is polymenorrhea

A

menstrual cycles that last less than 21 days in duration

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19
Q

What is oligomenorrhea

A

menstrual cycles that last more than 35 days in duration

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20
Q

When are menstrual cycles most irregular

A

2 years following menarche
3 years preceding menopause

During both times anovulation is common

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21
Q

What is the follicular or proliferative phase

A

lasts from the first day of menses until ovulation, during which time follicles within the oveary grow in response to FSH and in the uterus enometrial glands proliferate under the influence of estrogen, primarily estradiol produced by the follicle

Characterized by:
Variable length (average of 14 days)
development of ovarian follicles in response to FSH
Secretion of estrogen from the ovary
Proliferation of the endometrium in response to estrogen
Low basal body temperature

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22
Q

What causes ovulation to occur

A

response to the LH surge

Characterized by:
release of the oocytes from the follicle in response to FSH induction of collagenases
Resumption of meiosis, with oocytes progressing from prophase I to metaphase II
Formation of the corpus luteum with in the follicle

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23
Q

What is the luteal or secretory phase

A

Begins with ovulation and last until menses

The corpus luteum, stimulated by LH, produces progesterone, which causes secretory changes in the endometrium necessary fro preparing the endometrium for implantation.

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24
Q

What characterizes the luteal phase

A

Fairly constant duration of 12-16 days
elevated basal temperature in response progesterone production
sustaining of the corpus lute in the ovary

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25
Q

Where is GnRH produced and what is the frequency of release

A

Produced by hypothalamic neurons from the arcuate nucleus and transported to the portal plexus to the anterior pituitary.

Released in a pulsatile manner:
Follicular phase has one pulse every 60-90 minutes
Luteal phase has one pulse ever 2-3 hours

Amplitude and frequency is modulated by feedback of estrogen and progesterone

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26
Q

What is the role of FSH

A

production of estrogen and growth of the follicle. FSH receptors exist primarily on the ovarian granulosa cell membrane

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27
Q

What is the role of LH

A

responsible for the initiation of the luteal phase (ovulation) and maintenance of the luteal phase of the menstrual cycle

LH receptors exist primarily on ovarian theca cells at all stages of the cycle and on granulosa cells after the follicle matures under the influence of FSH and estradiol

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28
Q

What is the 2 cell hypothesis of estrogen production

A
  1. LH acts on the theca cells to stimulate the conversion of cholesterol to androgens
  2. Androgens are transported from the theca cells to the granulosa cells
  3. Under the influence of FSH, androgens are aromatized to form estrogens by the enzyme aromatase in the granulosa cells
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29
Q

What are the key steps in the process of oogenesis

A
  1. primordial follicle
  2. Primary follicle
  3. Preantral follicle
  4. Antral follicle
  5. Preovulatory follicle
  6. Ovulation
  7. Early corpus luteum
  8. Mature corpus luteum
  9. Corpus Albicans
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30
Q

What is a primordial follicle

A

contains an oocyte surrounded by a single layer of granulosa cells. Each oocyte is arrested in Prophase I

A woman is born with a finite number of follicles that peaks at 20 weeks gestation. The decline is independent of the menstrual cycle and ovulation

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31
Q

What are the estrogen effects on the preantral follicle

A
  1. stimulates preantral follicle growth
  2. with FSH, increases FSH receptor content of the follicle
  3. in the presence of FSH, stimulate mitosis of granulosa cells
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32
Q

What are the effects of the follicular increase of estradiol

A

Negative feedback on FSH

positive feed back on LH

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33
Q

Where is inhibin secreted from

A

granulosa cells in response to FSH

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34
Q

What are the two types of inhibin

A

Inhibin A: under the influence of LH suppresses FSH during the luteal phase of the cycle.

Inhibin B: directly suppresses pituitary FSH secretion in the follicular phase of the cycle

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35
Q

What is activin

A

Augments secretion of FSH and increases pituitary response to GnRH by enhancing GnRH receptor formation on the pituitary

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36
Q

When do estrogens peak

A

24-36 hours before ovulation

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37
Q

What is the effect of LH on the follicle

A

initiates luetinization and progesterone production

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38
Q

What effect does a preovulatory rise in progesterone have

A

causes a midcycle FSH surge by enhancing pituitary response to GnRH and facilitating the positive feedback action of estrogen

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39
Q

When does ovulation occur

A

10-12 hours after peak of LH

24-36 hours after peak of Estradiol

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40
Q

When can an oocyte become fertilized

A

only after it has reached metaphase II

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41
Q

What does the LH surge stimulate

A

Resumption of meiosis in the oocyte
Luteinization of the granulosa cell
Synthesis of progesterone and prostaglandin

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42
Q

When are peak levels of progesterone obtained

A

7-8 days after ovulation

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43
Q

What happens in the absence of pregnancy to the corpus luteum

A

will undergo apoptosis and cease to produce progesterone by 12-14 days after ovulation

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44
Q

What effect does the decrease in estrogen and progesterone have on the endometrium

A

leads to coiling and constriction of the spiral arteries in the endometrium

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45
Q

What causes menstrual cramps

A

the result of uterine contraction which are stimulated by prostaglandins. Therefore the cramps can be controlled with prostaglandin synthetase inhibitors (NSAIDs)

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46
Q

What is amenorrhea

A

absence of menses for 6 months or longer

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47
Q

What is primary amenorrhea

A

Absence of menses by 14 years of age ingirls without appropriate development of secondary sexual characteristics or by 16 years of age regardless of secondary sex characteristics

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48
Q

What are the categories of amenorrhea

A

Hypergonadotropic: elevated gonadotropins (typically FSH more than 20 IU/L; LH more than 40 IU/L)

Hypogonadotropic: low levels of gonadotropins (FSH and LH less than 5 IU)

Eugonadotropic: normal gonadotropin levels (FISH and LH of 5-20 IU/L)

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49
Q

What are the etiologies of hypergonadotropic amenorrhea

A
  1. turner syndrome
  2. Premature ovarian failure
  3. Gonadal dysgenesis
  4. Gonadal agenesis
  5. Resistant ovary syndrome
  6. Galactosemia
  7. Enzyme deficiency
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50
Q

What are the phenotypic characteristics of turner syndrome

A

Short stature
webbed neck
shield chest
increased carrying angle at the elbow

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51
Q

What are the etiologies of hypogonadotropic amenorrhea

A
  1. anorexia
  2. Female athlete triad
  3. Kallman syndrome
  4. Postpill amenorrhea
  5. Medication or drugs
  6. Pituitary disease
  7. Stress
  8. Delayed puberty
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52
Q

What is the female athlete triad

A

Syndrome of disordered eating, amenorrhea, and osteopenia or osteoporosis

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53
Q

What percent of body fat is generally needed to initiate menarche and maintain regularity

A

17% to initiate

22% to maintain

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54
Q

What is kallman syndrome

A

Deficient secretion of GnRH associated with anosmia or hyposmia.

Involves the failure of olfactory axonal and GnRH neuronal migration from the olfactory placode in the nose

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55
Q

How does stress lead to amenorrhea

A

stress leads to an increased output of corticotropin releasing hormone, which subsequently results indecreased GnRH pulsatile secretion and thus decreased secretion of FSH and LH

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56
Q

What are the etiologies of Eugonadotropic amenorrhea

A
  1. Disorders of Androgen excess (PCOS)
  2. Disorders of the outflow tract or uterus
    a. Mullerian agenesis
    b. Mullerian anomalies
    c. androgen insensitivity syndrome (AIS)
    d. Asherman Syndrome
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57
Q

What is the triad assocated with PCOS

A
  1. Menstrual irregularity signifying oligo or anovulations
  2. Appearance of multiple small ovarian cysts on ultrasound “string of pearls”
  3. Clinical or laboratory evidence of hyperandrogenism

loss of 5-10% body weight may help patients reestablish ovulatory cycles.

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58
Q

When and how may an imperforate hymen present

A

generally not until 6-12 months after menarche. The vagina maybe distended with more than 1 Liter of old blood

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59
Q

What is the problem with Androgen insensitivity syndrome

A

The defect is in the androgen receptor and can not respond to the androgen. The individual is phenotypically female and is usually raised female

Testosterone levels will be in the male range, but they will not have any pubic or axillary hair. Normal breast development because the testosterone is converted to estrogen

Gonadectomy is required to prevent gonadoblastoma

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60
Q

What should be suspected if a female patient presents with bilateral inguinal hernia

A

AIS

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61
Q

What is asherman syndrome

A

Intrauterine scarring usually a result of viorous curettage during a hypoestrogenic state or in the presence of an intrauterine infection.

Adhesions can develop

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62
Q

What is the goal of hormone replacement for the treatment in patients with hypergonadotropic amenorrhea

A

prevent bone loss, vasomotor symptoms, urogenital atrophy, and cardiovascular disease due to lack of estrogen

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63
Q

When is it safe to consider an estrogen only treatment

A

in women without a uterus

Progesterone is needed as it is protective of the uterus

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64
Q

What is the mechanism behind using OCP for the treatment of PCOS

A

Progestin component suppresses endogenously elevate LH levels, thereby decreasing androgen overproduction

Estrogen component of the pill increases the sex hormone binding globulin levels thereby decreasing the amounts of free estrogens and androgens

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65
Q

What is the rotterdam criteria

A

It is the criteria established in 2003 that is used to diagnose PCOS. It requires 2 of the following 3:

a. Menstrual irregularities
b. Hyperandrogenism
c. Polycystic ovaries

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66
Q

What are the results of irregular ovulations

A

lack of adequate progesterone and experience chronic estrogen exposure to the endometrium. Increases risk for endometrial hyperplasia and endometrial cancer

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67
Q

What is the Ferriman-Gallwey score

A

It is a score used for diagnosing hirsutism.

Greater than 8 is an abnormal score

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68
Q

If a patient experience an rapid onset of hirsutism, what is the most likely etiology

A

Drug induced or Androgen secreting tumor

Suspect a tumor with levels of testosterone greater than 200 ng/dL

PCOS will likely have a more gradual onset of hirsutism

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69
Q

What defines polycystic ovaries by ultrasound criteria

A

12 or more antral follicles between 2 and 9 mm in size and peripheral in location in at least one ovary

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70
Q

What is the pathophysiology of LH in PCOS

A

increased LH pulse frequency and amplitude stimulated by GnRH
LH stimulates production of androgens from the theca cells in the ovary leading to hyperandrogenism

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71
Q

What is the pathophysiology of Insulin resistance in PCOS

A

With PCOS insulin resistance is present regardless of obesity
Insulin has been shown to increase production of androgens in women with PCOS
a. IGF-I receptor binding
b. Decreases production of sex hormone binding globulin produced by the liver. Increases free metabolically active testosterone

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72
Q

What are the health consequences of PCOS

A 
Diabetes
Obesity
Metabolic syndrome
Cardiovascular disease
Endometrial Hyperplasia
Infertility
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73
Q

What is the cause of cushings syndrome

A

Excess cortisol from ACTH

Diagnosed by 24 hour urine collection of free cortisol with the level greater than 100 on two determinations

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74
Q

What is ancanthosis nigricans

A

Raised, velvety, hyper pigmentation of skin, typically seen on the axilla, neck and intertriginous areas
Marker of insulin resistance
Will go away as insulin resistance improves

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75
Q

How can an insulin and glucose be used to determine insulin sensitivity

A

Glucose/Insulin Ratio

Ratio less than 4.5 in obese adult women
Ratio less than 7 in adolescents

suggested to diagnose insulin resistance

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76
Q

What is the underlying condition in PCOS and how can it be medically treated

A

Insulin resistance

Metformin
Thiazolidinediones

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77
Q

What is lanugo hair

A

soft, short hair covering the fetus that is shed in late gestation and during the neonatal period

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78
Q

What is vellus hair

A

soft, fine, unpigmented hair that covers apparently hairless areas of the body

79
Q

What is terminal hair

A

longer, coarse, pigmented hair that may grow in response to sex hormones or may be sex hormone independent

80
Q

What is hypertrichosis

A

excessive growth of androgen independent hair in nonsexual areas such as forearms and legs

81
Q

What is hirsutism

A

the presence of terminal hair in androgen dependent sites where hair does not normally grow in women.

82
Q

What is virilization

A

hirsutism associated with other signs of hyperandrogenism, such as increased muscle mass, clitormegaly, temporal balding, voice deepening and increased libido

83
Q

What is the normal level of testosterone in women

A

less than 70 ng/dL

84
Q

What are the percentages of free testosterone in women, women with hirsutism and men

A

women: 1%
hirsutism: 2%
men: 2-3%

85
Q

Is it possible to have hirsutism with normal testosterone levels

A

YEP…

The active testosterone is unbound. With a decreased level of SHBG there is an increased level of free or unbound testosterone

86
Q

What effect does cirrhosis have on SHBG

A

Increases the plasma levels therefore decreasing free testosterone

87
Q

What factors may lead to the development of hirsutism

A
  1. Increased concentration of serum androgens, especially free testosterone
  2. Decreased levels of SHBG, resulting in increased bioavailable androgen
  3. Increased activity of 5a-reductase
88
Q

What is NCAH

A

Nonclassic Adrenal Hyperplasia

This is a less severe form of congenital adrenal hyperplasia that is diagnosed in the newborn and is associated with amigos genitalia and salt wasting

89
Q

What drug exposure may cause hirsutism without virilization

A 
Pheyntoin
diazoxide
minoxidil
danazol
corticosteroids
cyclosporin
90
Q

What is the goal of treatment of hirsutism

A

The major goal is arresting the virilization process, not removing the hair. Once terminal hair has been established, withdrawal of androgens does not affect the established hair pattern

91
Q

What is the benefit of using Combination hormonal contraceptive for the treatment of hirsutism

A

Both estrogen and progestin in the hormonal contraceptives cause a decrease in goadotropin secretion with a consequent decrease in ovarian androgen production

a. Estrogen also stimulate an increase in SHBG, causing increased binding of testosterone and decreased free testosterone levels
b. Progestin also may displace active androgens at the hair follicle and may inhibit 5a-reductase activity

92
Q

What are some androgen receptor blockers that may be used for hirsutism

A

Spironolactone (5a-reductase inhibitor properties)
Flutamide (nonsteroidal antiandrogen)
Cyproterone acetate

93
Q

What are some structural causes of abnormal bleeding

A

fibroids
endometrial polyps
adenomyosis
endometrial or uterine cancer

94
Q

What is dysfunctional uterine bleeding (DUB)

A

abnormal bleeding that can be excessive or prolonged, or unpredictable, reflects a disturbance in normal ovulatory function. It is a manifestation of abnormal hormonal stimulation of the endometrium

95
Q

What is metrorrhagia

A

bleeding at irregular intervals

96
Q

What is menometrorrhagia

A

excessive bleeding at irregular intervals

97
Q

What is menorrhagia

A

excessive or prolonged bleeding at regular intervals. Generally not associated with DUB because of the regular cycles

98
Q

What causes the irregularity associated with DUB

A

unopposed estrogen stimulation that allows the endometrium to slough off in isolated locations at various times

99
Q

What is the etiology of DUB

A
  1. PCOS
  2. Immaturity of the hypothalamic pituitary ovarian axis
    3 Dysfunction of the hypothalamic pituitary ovarian axis
  3. Abnormalities of the normal feedback signals
100
Q

What is estrogen withdrawal bleeding

A

Bleeding that may occur at MIDCYCLE when estrogen levels decline briefly just before ovulation

101
Q

What are some organic causes of abnormal uterine bleeding

A
  1. polyps
  2. uterine fibroids
  3. endometritis
  4. endometrial hyperplasia
  5. pregnancy
  6. blood dyscrasia
102
Q

What increased risk does DUB carry

A

Increases risk of endometrial hyperplasia and cancer

103
Q

30% of adolescents who present with severe blood loss will generally have what pathology

A

associated coagulapathy such as Von Willebrand Disease in which platelets are dysfunctional

104
Q

What type of sonography is more sensitive in detecting endometrial polyps

A

Transvaginal

105
Q

What are the orally administer progestins administered to control bleeding

A
  1. Medroxyprogesterone acetate 10mg daily for 10-12 days
  2. Norethindrone acetate 5 mg daily for 10-12 days
  3. Oral Micronized progesterone 200 mg daily for 10-12 days
106
Q

How soon should a response be noted when utilizing OCP for control of bleeding

A

with in 24 hours of therapy initiation. If no response has occured by this time, another treatment for the DUB should be initiated

107
Q

Can estrogen be used to stop DUB bleeding

A

Yes.

Rapidly stops bleeding with in 12-24 hours of treatment

It is effective when bleeding has been prolonged or is secondary to progesterone breakthrough bleeding

108
Q

What is the mechanism of high dose estrogen to control bleeding

A

initiation of clotting at the capillary level

109
Q

What role do NSAIDs have with DUB

A

limiting menstrual blood loss in women who ovulate, and they reduce excess blood loss by as much as 50%

110
Q

What is the success rate of endometrial ablation

A

50% of women will achieve amenorrhea

90% will see a significant reduction

111
Q

What are some common names for uterine leiomyomas

A

myomas
fibroids
ibromyomas

112
Q

What are leiomyomas

A

porliferative well circumscribed, pseudoencapsulated, benign tumors composed of smooth muscle and fibrous connective tissue. Primarily located in the uterus but may be found in areas outside the uterus

113
Q

What is the most common uterine mass

A

leiomyomas

present in 20-40% of women over the age of 35

114
Q

How are leiomyomas classified

A

according to location

  1. Intramural leiomyomas: most common variety. Occurs within the myometrium of the uterus as isolated, ecapsulated nodules of varying size
  2. Submucous leiomyomas: located beneath the endometrium and can grow into the uterine cavity
  3. Subserosal leiomyomas: located just beneath the serosal surface and how out toward the peritoneal cavity and causing distortion of the peritoneal surface
115
Q

How are leiomyosarcomas diagnosed

A

based on a mitotic count of 10 mitotic figures per 10 high power fields

116
Q

What are the associated symptoms of leiomyomas

A
  1. Abnormal Uterine Bleeding
  2. Pain
  3. Pressure (GU and GI problems)
  4. Reproductive disorders
  5. Pregnancy related disorders
117
Q

What should be done initially for treatment of leiomyomas

A

Expectant management.

Bimanual exam every 3-6 months to determine uterine size and rate of tumor growth

NSAIDs on a regular schedule to limit blood loss

118
Q

What are the indications for surgery for leiomyomas

A

When symptoms fail to respond to conservative management.

Excessive bleeding
Protrusion
Rapid growth
Repetitive pregnancy loss
Infertility
Enlarged Uterine size
119
Q

What are the types of surgical procedures available for leiomyomas

A
  1. Myomectomy
    a. Abdominal myomectomy
    b. Hysteroscopic resection
    c. Laparoscopic myomectomy
    d. MRI guided focused Ultrasound
    e. Laproscopic myolysis or cryomyolysis
  2. Hysterectomy
  3. Uterine Artery Embolization (UAE)
120
Q

What is endometriosis

A

the presence of functioning endometrial glands and stroma outside their usual location within the uterine cavity

121
Q

Where does endometriosis occur

A

It is primarily a pelvic disease with implants in or adhesions of the ovaries, fallopian tubes, uterosacral ligaments, rectosigmoid, bladder, and appendix

Less common it can be located outside the pelvis suggesting a metastatic disease

122
Q

What are the causes of endometriosis

A
  1. Retrograde menstrual flow
  2. Hematogenous or lymphatic spread
  3. Metaplasia of the coelomic epithelium
  4. Genetic and immunologic influences
123
Q

What causes the pain associated with endometriosis

A
  1. Irritation or direct ivasion of pelvic floor nerves by infiltrating implants
  2. Effects of active bleeding from implants
  3. may result from growth factors, cytokines, prostaglandins, and histamines in endometriotic tissue and peritoneal fluid of women with endometriosis
124
Q

How is fertility effected with endometriosis

A

Moderate to sever endometriosis is thought to cause infertility by causing adhesions and scarring of the ovaries and fallopian tubes

125
Q

What are the signs and symptoms of endometriosis

A
  1. dysmenorrhea
  2. pain with ovulation
  3. chronic pelvic pain
  4. dyspareunia
  5. infertility
  6. GI and GU disturbances
    a. 1/3 will urinary tract involvement
    b. up to 1/3 will have bowel involvement
126
Q

What is dyschezia

A

pain with defication

127
Q

How is endometriosis diagnosed

A

the only way to diagnose the condition is by visualization at surgery or by biopsy of implants

128
Q

What is a marker for endometriosis

A

CA-125

Not specific

129
Q

What pathologies will elevate CA-125

A

Endometriosis
Ovarian Ca
PID
IBD

130
Q

What will a typical pelvic exam demonstrate on a patient with endometriosis

A
  1. Nodularity and tenderness of the uterosacral ligaments
  2. Endometriomas
  3. Uterus is often in a fixed retroverted position
  4. Usually normal pelvic examination for minimal endometriosis
131
Q

What are endometriomas

A

ovarian cysts filled with old blood from endometriosis, forming “chocolate cysts”. Palpated as adnexal masses often fixed to the lateral pelvic walls or to the posterior cull-de-sac

132
Q

What is the appearance of endometriosis

A

brown or black pigmentation known as powder burn lesions

Lesions that are clear vesicular, white opacified, glandular excrescences, polypoid or red hemorrhagic vesicles are consider to be “atypical” lesions. May be more metabollically active

White scarring of pelvic peritoneum suggests old burned-out endometriosis

133
Q

What is the basis of medical therapy for the treatment of endometriosis

A

hormonal suppression of menses

134
Q

What are the medical options available for the treatment of endometriosis

A
  1. OCP
  2. GnRH agonist
  3. Danazol
  4. Aromatase inhibitors
135
Q

What is the mechanism of OCP

A

creates a pseduopregnancy state associated with amenorrhea

136
Q

What is the mechanism for GnRH agonist

A

Chemical alteration of the amino acids at positions 6 and 10 produce synthetic derivatives of GnRH that resist cleavage by endopeptidases but retain a high affinity for the pituitary GnRH receptor.

The effect is down regulation and desensitization of the pituitary with resulting lack of ovarian estrogen production

137
Q

What are the side effects associated with GnRH agonist

A
  1. menopausal symptoms

2. Bone loss with prolonged use

138
Q

What is the mechanism of danazol

A

adrogenic testosterone derivative that suppresses FSH and LH as well as ovarian estrogen and progesterone production

139
Q

What are the adverse effects of danazol

A

Hirsutism
acne
weight gain
decreased breast size

140
Q

What is the mechanism for aromatase inhibitors

A

Aromatase enzyme converts androgen precursors suchas androstenedione and testosterone to estrone and estradiol.

Inhibitors such as letrozole and anastrazole will inhibit the production of estrogen within the endometriotic lesion. They will increase FSH and LH by blocking estrogens negative feedback on the pituitary.

Currently only indicated for Breast cancer and this treatment option is considered investigational

141
Q

What is the treatment choice for adhesions associated with endmetriosis

A

Surgery

142
Q

What is the physiology of splanchnic pain

A

occurs when an irritable stimulus is appreciated in a specific organ secondary to tension, peritoneal irritation or inflammation, hypoxia or necrosis of viscera, or production of prostanoids

143
Q

What is the physiology of referred pain

A

Occurs when autonomic impulses arise from a diseased visceral organ, eliciting an irritable response within the spinal cord. pain is sensed in the dermatomes corresponding to cells receiving those impulses

144
Q

When is laparoscopy indicated for pelvic pain

A

cases that are unresponsive to medical therapy or when an organic cause of the pain is suspected

145
Q

What should be included as differential for ACUTE pelvic pain

A 
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion
PID
GI disorders
Urologic causes
146
Q

what is mittleschmerz

A

pain the lower abdomen noticed at or near the time of ovulation. May be associated with a ruptured ovarian cyst

147
Q

What should be included as differential for CHRONIC pelvic pain

A 
Dysmenorrhia
Pelvic Adhesions
Endometriosis
Adenomyosis
Mullerian anomalies
148
Q

What is the success rate of laporascopic separation of adhesions

A

75% report improvement in pain that is sustained at least 6-12 months

149
Q

What is adenomyosis

A

a condition characterized by the presence of ectopic foci of endometrium within the myometrium, may also cause chronic pelvic pain and dysmenorrhea

150
Q

What are the locations of ectopic pregnancies

A
  1. Tubal (99%) and most common sight is the ampulla
  2. Ovarian
  3. Abdominal
  4. Cervical
  5. Heterotropic
151
Q

What is a heterotropic ectopic pregnancy

A

both intrauterine and ectopic pregnancy occurring simultaneously

152
Q

What is the prevalence of ectopic pregnancy

A

2%

153
Q

What are the signs and symptoms of an ectopic pregnancy

A

Vaginal bleeding
Abdominal pain
Other symptoms related to hypotension
Pregnancy status

154
Q

How does smoking effect ectopic pregnancy

A

smoking causes tubal ciliary dysfunction

155
Q

What approach is needed to diagnose an ectopic pregnancy

A
  1. Transvaginal ultrasound to rule out an intrauterine pregnancy
  2. hCG
  3. D&C
  4. Serial hCG if below discriminatory zone
  5. Laparoscopy
  6. Serum progesterone levels: Levels less than 5 ng/mL are considered nonviable
156
Q

What is the discriminatory zone

A

the quantitative hCG level above which all viable intrauterine pregnancies are visible by ultra sound. Generally this is 2000 IU/mL

157
Q

What are the surgical approaches available for treatment of an ectopic pregnancy

A
  1. Salpingectomy
  2. Linear Salpingotomy
  3. Operative laparoscopy
  4. Laparotomy
  5. Cornual resection
158
Q

What are the medical approaches available for treatment of an ectopic pregnancy

A

Methotrexate

folic acid antagonist that interferes with DNA synthesis

159
Q

how is infertility defined

A

no conception after 1 year of unprotected intercourse.

160
Q

what is fecundability

A

monthly probability of pregnancy. Which is rough 20% among fertile couples. The cumulative probability of pregnancy after 1 year reaches 85%

161
Q

How can hypothyroidism induce oligo/anovulation.

A

increased thyrotropin-releasing hormone (TRH) secretion stimulates prolactin secretion

High levels of prolactin cause thalamic dysfunction and lack of progesterone, leading to miscarriage

162
Q

What is the treatment for ovulatory dysfunction

A
  1. Correcting the underlying problem

2. clomiphene citrate: Most commonly prescribed fertility drug and is indicated for the treatment of anovulation

163
Q

What is the mechanism of clomiphen citrate

A

estrogen antagonist and works best in women with functioning hypothalamic pituitary ovarian axis

It triggers endogenous release of FSH, which then stimulates follicular development

164
Q

How is a decreased ovarian reserve diagnosed

A
  1. Elevated menstrual cycle day 3 FSH is a marker for decreased number and quality of oocyte.
165
Q

What is the definition of ovarian failure

A

FSH greater than 40 mIU/mL associated with amenorrhea.

If these findings are before the age of 40, it is considered premature ovarian failure

166
Q

What is the treatment for decreased ovarian reserve

A
  1. Donor oocytes

2. Adoption

167
Q

What are the common causes of tubal disease

A

Pelvic inflammatory disease
tubal ligation
endometriosis

168
Q

How is tubal disease diagnosed

A
  1. HSG: hysterosalpingography - fluoroscopic view of the uterine cavity
  2. Laproscopy
169
Q

What is the treatment for tubal disease

A
  1. IVF
  2. Surgery
    a. Tubal reanastomosis
    b. Lysis of peritubal adhesions
170
Q

What are the WHO standards for a semen fertility sample

A
  1. Volume: 1.5 - 5.0mL
  2. Concentration greater than 20 million sperm/mL
  3. Total sperm greater than 40 million per ejaculate
  4. Percent motility greater than 50%
  5. Progression greater than 2
  6. Morphology more than 30% normal
  7. WBC less than 1 million/mL
171
Q

what is azoospermia

A

absence of sperm in the ejaculate

172
Q

What karyotype is associate with azoospermia

A

kleinfelter syndrome

173
Q

what is CBAVD

A

congenital bilateral agenesis of the vas deferens

2/3 with CBAVD will have Cystic Fibrosis.

174
Q

When is a woman’s most fertile days

A

up to 4 days prior to ovulation and the day of ovulation

175
Q

What are the assisted reproductive technology options

A
  1. IVF (in vitro fertilization)
  2. ICSI (intracytoplasmic sperm injection)
  3. PGD (preimplantation genetic diagnosis)
  4. GIFT (famete intrafallopian transfer)
  5. ZIFT (zygote intrafallopian transfer)
176
Q

What is RPL

A

Recurrent pregnancy loss

177
Q

What defines recurrent pregnancy loss

A

two to three or more CONSECUTIVE spontaneous abortions of clinically recognized pregnancies prior to 15 weeks gestation

178
Q

What is the incidence of RPL

A

5%

179
Q

What are the etiology of miscarriages in the general reproductive population

A 
Advanced age
Chromosome anomaly
Congenital anomaly
Structural anomalies of the uterus
Hormonal conditions
180
Q

What is the etiology of RPL

A 
50% is idiopathic
Genetic/parental chromosomal abnormality
Antiphospholipid syndrome
Anatomic cause
Endocrinologic factors
181
Q

What is a robertsonian translocation

A

occurs when genetic information is exchanged between two acrocentric chromosomes.

182
Q

What are acrocentric chromosomes

A

13, 14, 15, 21, 22

unique because their centromeres are near the end of the chromosome and their short arms encode redundant genes

183
Q

How is APS (Antiphospholipid Syndrome) diagnosed

A

1 of the 2 clinical criteria

a. Thrombosis
b. Pregnancy morbidity

1 of the 2 laboratory criteria

a. Anticardiolipin antibodies, IgM or IgG in medium or high titers
b. Lupus anticoagulant antibodies

184
Q

What do the muellarian ducts develop into

A

fallopian tubes and fuse to form the uterus, cervix and upper third of the vagina

185
Q

What are the common muellarian anomalies associated with RPL

A

Uterine septum
Unicornuate uterus
Bicornuate uterus
Uterin didelphys

186
Q

What is a uterine septum

A

results when fusion of the paired mullerian duct has occurred normally but the medial septum between the ducts has not been completely resorbed. Most common uterine abnormality diagnosed with RPL

187
Q

What is a unicornuate uterus

A

occurs when one of the paired mullerian ducts fails to develop. A uterus with a limited cavity results

188
Q

What is a bicornuate uterus

A

arises due to the incomplete fusion of the mulllerian ducts resulting in two separate uterine cavities joined at a common cervix

189
Q

What is a uterine didelphys

A

the result of complete failure of the mullerian ducts to fuse, but normal differentiation of each duct system. The final out come is two separate uteri and cervices, with each uterine horn a smaller than normal uterus

190
Q

How are uterine abnormalities diagnosed

A
  1. HSG hysterosalpinogography
  2. Ultrasound
  3. Saline sonohysterography
  4. MRI
  5. Hysteroscopy
191
Q

At what point will DM become a significant risk for inducing RPL

A

A1C above 8%. Well controlled diabetes has little effect on RPL

192
Q

What is the treatment for APS

A

heparin injections and low dose aspirin throughout pregnancy

The benefit is in its prevention of placental microthrombi and possible treatment of inflammation

193
Q

What is a metroplasty

A

a surgical procedure to unify the cavities and reconstruct the uterus and can be performed when pregnacy outcomes have been particularly poor despite excellent and aggressive prenatal care in previous pregnancies

Can be done for bicornuate uterus and uterine didelphys

194
Q

What is the treatment option for a unicornuate uterus

A

cerclage

► Med Misc 06 (27 decks)

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