AUB Flashcards

1
Q

AUB causes divided into 9 categories which are …?

A

PALM-COEIN: polyp, adenomyosis, leiomyoma, malignancy and hyperplasia, coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, and not yet classified.

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2
Q

CAUSES OF PRIMARY AMENORRHEA if Breasts Absent and Uterus Present

A

A. Gonadal failure: 1.45,X (Turner syndrome), 2. 46,X, abnormal X (e.g., short- or long-arm deletion)
3. Mosaicism (e.g., X/XX, X/XX,XXX) 4. 46,XX or 46,XY pure gonadal dysgenesis
5. 17α-hydroxylase deficiency with 46,XX
B. Hypothalamic failure secondary to inadequate GnRH release: 1. Insufficient GnRH secretion because of neurotransmitter defect 2. Inadequate GnRH synthesis (Kallmann syndrome) 3. Congenital anatomic defect in central nervous system 4. CNS neoplasm (craniopharyngioma)
C. Pituitary failure: 1. Isolated gonadotrophin insufficiency (thalassemia major, retinitis pigmentosa) 2. Pituitary neoplasia (chromophobe adenoma) 3. Mumps, encephalitis 4. Newborn kernicterus 5. Prepubertal hypothyroidism.

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3
Q

the most common cause of primary amenorrhea, occurring in almost 50% of those with this symptom.

A

Gonadal failure which is most frequently caused by a chromosomal disorder or deletion of all (as occurs in Turner syndrome) or part of an X chromosome, but it is sometimes caused by another genetic defect and, rarely, 17α-hydroxylase deficiency.
An occasional individual with mosaicism, an abnormal X chromosome, pure gonadal dysgenesis (46,XX), or even Turner syndrome (45,X) may have a few follicles that develop under endogenous gonadotropin stimulation early in puberty and may synthesize enough estrogen to induce breast development and a few episodes of uterine bleeding, resulting early in premature ovarian failure, usually before age 25. Rarely, ovulation and pregnancy can occur.

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4
Q

Turner syndrome features

A

primary amenorrhea and absent breast development, short stature (<60 inches in height), webbing of the neck, a short fourth metacarpal, and cubitus valgus. Cardiac abnormality, renal abnormalities, and hypothyroidism are also more prevalent.

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5
Q

Causes of primary amenorrhea if Breast development; uterus absent:

A

A. Androgen resistance (testicular feminization) B. Congenital absence of uterus (uterovaginal agenesis)

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6
Q

Causes of primary amenorrhea if Absent breast development; uterus absent

A

A. 17,20-desmolase deficiency B. Agonadism C. 17α-hydroxylase deficiency with 46,XY karyotype

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7
Q

Causes of primary amenorrhea if Breast development; uterus present

A

A. Hypothalamic cause B. Pituitary cause C. Ovarian cause D. Uterine cause

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8
Q

The — genes are important for uterine development, and mutations (e.g., in —-) have been found in genetic syndromes with uterine abnormalities (e.g., hand-foot-genital and Guttmacher syndromes) and also in cases of bicornuate uterus.

A

The Hox genes are important for uterine development, and mutations (e.g., in Hox-A13) have been found in genetic syndromes with uterine abnormalities (e.g., hand-foot-genital and Guttmacher syndromes) and also in cases of bicornuate uterus.

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9
Q

the second most frequent cause of primary amenorrhea. It occurs in 1 in 4000 to 5000 female births and accounts for approximately 15% of individuals with primary amenorrhea.

A

Congenital Absence of the Uterus (Uterine Agenesis, Uterovaginal Agenesis, Mayer-Rokitansky-Küster-Hauser Syndrome)

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10
Q

MANAGEMENT of primary amenorrhea if hypergonadotropic hypogonadism

A

After a history is obtained and a physical examination performed, including measurement of height, span, and weight, those with primary amenorrhea can be grouped into one of the four general categories.
Women with hypergonadotropic hypogonadism (FSH >30 mIU/mL), not those with hypogonadotropic hypogonadism, should have a peripheral white blood cell karyotype obtained to determine whether a Y chromosome is present. If a Y chromosome is present, the streak gonads should be excised, because the incidence of subsequent malignancy, mainly gonadoblastomas, is relatively high.
All women with an elevated FSH level and an XX karyotype should have electrolyte and serum progesterone levels measured to rule out 17α-hydroxylase deficiency; a clue is if the patient is hypertensive. In addition to hypernatremia and hypokalemia, individuals with 17α-hydroxylase deficiency have an elevated serum progesterone level (>3 ng/mL), a low 17α-hydroxyprogesterone level (<0.2 ng/mL), and an elevated serum deoxycorticosterone level (>17 ng/100 mL) and usually have hypertension.

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11
Q

MANAGEMENT of primary amenorrhea if hypogonadotropic hypogonadism

A

the underlying disorder is in the CNShypothalamic-pituitary region, and the serum PRL level should be determined. Even if the PRL level is not elevated, all women with hypogonadotropic hypogonadism should have a head CT scan or MRI to rule out a lesion. Ovulation can be induced in women with this disorder because their ovaries are normal. Initially, they should receive estrogen-progestogen treatment to induce breast development and cause epiphyseal closure. When fertility is desired, human menopausal gonadotropins or pulsatile GnRH should be administered. Clomiphene citrate will be ineffective because of low endogenous E2 levels.

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12
Q

The differential diagnosis of androgen resistance from uterine agenesis can easily be made by

A

the presence in the latter condition of normal body hair, ovulatory and premenstrual-type symptoms, biphasic basal temperature, and a normal female testosterone level. Because women with uterine agenesis have normal female endocrine function, they do not require hormone therapy. A renal scan should be performed because of the high incidence of renal abnormalities. They may need surgical reconstruction of an absent vagina (McIndoe procedure), but progressive mechanical dilation with plastic dilators. Individuals with androgen resistance have an XY karyotype and male levels of testosterone. After full breast development is attained and epiphyseal closure occurs, the gonads should be removed because of their malignant potential.

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13
Q

The estrogen came from peripheral adipose tissue conversion is called

A

Estrone

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14
Q

Ovarian hyperthtcosis,

A

considered a more severe form of PCOS, is a rare condition characterized by nests of lutcinizcd thcca cells distributed throughout the ovarian stroma. Affected women exhibit severe hyperandrogenism and greater degree of insulin resistance

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15
Q

(HAIRAN)

A

Hypmmdrogmic-insulin mistant-acanthosis nigricans (HAIRAN) syndrome also is uncommon and consists of marked hyperan-drogenism, severe insulin resistance, and acanthosis nigricans.

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16
Q

Oligomcnorrhca definition

A

(fewer than nine menstrual periods in l year)

17
Q

amenorrhea

A

(absence of menscs for 3 or more consecutive months)

18
Q

The prevalence of metabolic syndrome approximates ___ percent in women with PCOS compared with 4 percent in age-adjusted controls

A

The prevalence of metabolic syndrome approximates 45 percent in women with PCOS compared with 4 percent in age-adjusted controls

19
Q

In women with PCOS, the risk of cndomctrial cancer is increased –· to — fold

A

In women with PCOS, the risk of cndomctrial cancer is increased three· to fourfold

20
Q

the American College of Obstetricians and Gynecologists (2016) recommends endometrial assessment (sampling) in

A
  • any woman older than 45 years with abnormal uterine bleeding.
  • younger than 45 years with a history of unopposed estrogen exposure such as seen in obesity or PCOS,
  • those with failed medical management, and women with persistent bleeding are ideally sampled.
21
Q

PCOS Complications in Pregnancy

A

Women with PCOS who become pregnant experience a higher rate (30 to 50 percent) of early miscarriage compared with a baseline rate of approximately 15 percent in the general population.
higher risks of gestational diabetes, pregnancy-induced hypertension, and preterm birth have been noted. raise the risk of multifetal gesta-tions, which are associated with elevated rates of maternal and neonatal complications due to increase use of ovulation induction medications or IVF to conceive.

22
Q

Diagnosis of late-onset CAH

A

With late-onset CAH, the most commonly affected enzyme is 21·hydroxylase, and deficiency leads to accumula-tion of its substrate, 17-hydroxyprogcstcronc. Scrum values arc drawn in the morning from a fasting patient. Threshold values of 17·hydroxyprogestcronc that measure >200 ng/dL should prompt an ACTH stimulation test. With this test, syn· thetic ACTH, 250 µg, is injected intravenously, and a scrum 17-hydroxyprogestcronc levd is measured 1 hour later.

23
Q

Diagnostic tests of cushing syndrome

A

24-hour urine collection for uri-nary free cortisol excretion can be obtained. Alternatively, a dexamethasone suppression test administers 1 mg of dexa-methasone orally at 11 PM, and a plasma cortisol level is mea-sured at 8 AM the following morning. In women with a normal functioning feedback loop, administration of the corticosteroid dexamethasone lowers ACTH secretion and thus diminishes adrenal cortisol production. Normal testing values arc < 5 µg/ dL. However, if a woman has an exogenous or an ectopic endogenous source of cortisol, then cortisol levels during suppression testing will remain elevated

24
Q

Important points regarding PCOM Polycystic ovarian morphology in US

A
  • More recently, follicle number per ovazy (FNPO) threshold values have bet:n raised due to improved sonographic imaging resolution. Namely, an FNPO threshold of> 20 follicles and/or ovarian volume > 10 mL in either ovazy has been adopted by ESHRE and ASRM.
  • PCOM often reflects normal adolescent ovarian physiology. Thus, sonography fur PCOS evaluation is not recommended within 8 years of menarche,
25
Q

In patients with PCOS who are not candidates fur combination hormonal contraception,

A

progesterone withdrawal is recommended every 1 to 3 months. Examples of regimens used include: medroxyprogesterone acetate (MPA), 5 to 10 mg orally daily day for 12 days, or micronized progesterone, 200 mg orally each evening for 12 days.
Patients arc counseled that intermittent progcstins will not reduce symptoms of acne or hirsutism, nor do they provide contraception. For those requiring birth conuol, a continuous progestin only contraceptive pill, depot medroxyprogesterone acetate, or a progestin releasing implant or intrauterine device may be used and will act to thin the cndomctrium.

26
Q

hirsutism treatment

A
  • COCs first-line option for who are candidates for it. However, medical therapies will not eliminate hair already present, treatments may require 6 -12 months before clinical improvement is apparent.
  • Hair Removal Both depilation and epilation are suitable techniques.
  • Eflornithine Hydrochloride This antimetabolite topical cream is applied twice daily to affected areas and is an irreversible inhibitor of ornithine decarboxylase. FDA-approved for treatment of female facial hirsutism. It may require 4-8 wks of use before changes are noticed. S.E. Local burning and erythema.
  • Spironolactone not FDA-approved for this indication, It is a competitive inhibitor of androgen binding to the androgen receptor. This drug also directly inhibits 5n-reductase. The typical dosage is 50 to 100 mg orally twice daily. if used as monotherapy, intermenstrual bleeding frequently deveops, spironolactone is also a potassium-sparing diuretic. As such, it is not prescribed for chronic use in combination with agents that can also raise blood potassium levels.
  • Flutamide is another antiandrogen marketed for the treat-ment of prostate cancer. It is uncommonly used for hirsutism due to its potential hepatotoxicity. As an antiandrogen, teratogenicity is a concern.
  • Finasteride is a 5n-reductase inhibitor, blocks conversion of testosterone to DHT. 5-mg daily doses for women found finasteride to be modestly effective for hirsutism treatment S.E. decreased libido risk of male fetal teratogenicity is present, and effective contraception must be used concurrently.
27
Q

Most common causes of postmenopausal bleeding are:

A

• vaginal atrophy (59 %)
• endometrial hyperplasia (10 %)
• endometrial polyp (9 %)
• uterine cancer (5-10 %)
• bleeding related to the use of HRT
Rare causes of postmenopausal bleeding include:
• uterine fibroids
• adenomyosis (often during HRT usage)
• cervical polyp
• cervical cancer
• vaginal cancer
• tubal- and ovarian cancer

28
Q

postcoital bleeding ddx

A

Cervical cancer, cervical polyp, ectropion, urogenital atrophy or cervicitis secondary to chlamydial infection.