Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo Repro Exam II > Puberty, Disorders of Development, & Menstrual Disorders > Flashcards

Puberty, Disorders of Development, & Menstrual Disorders Flashcards

1
Q

A major characteristic of follicular growth and estradiol secretion is explained by the 2 cell theory of ovarian follicular development. What is the 2 cell theory?

A

LH stimulates the theca cells to produce androgens

FSH stimulates the granulosa cells to convert those androgens to estrogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hormone changes during the luteal phase

A

LH and FSH are significantly suppresed through negative feedback effect of elevated circulating estradiol and progesterone

If conception does not occur, progesterone and estradiol level decline near the end of the luteal phase as a result of corpus luteal regression

FSH will then rise which initiates new follicular growth for the next cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

______ appears to enhance the hypothalamic release of GnRH and induce the midcycle LH surge

A

Estradiol

[during early follicular development, estradiol levels are low; approx 1 wk before ovulation, estradiol levels begin to increase; during the luteal phase, estradiol rises to a maximum 5-7 days after ovulation and returns to baseline before menstruation]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe changes in secretion of progestins during the ovarian cycle

A

During follicular development, the ovary secretes only a small amount of progesterone

Prior to ovulation, the unruptured luteinizing graafian follicle begins to produce increasing amounts of progesterone

Secretion of progesterone by the corpus luteum reaches a maximum 5-7 days after ovulation and returns to baseline before menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

At about 8-10 weeks of fetal development, oocytes become surrounded by precursor granulosa cells. This oocyte-granulosa cell complex is called a ____

A

Primordial follicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In the ADULT ovary, a graafian follicle forms. The innermost 3-4 layers of multiplying granulosa cells become cuboidal and adherent to the ovum; this is known as the _____

A

Cumulus oophorus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

After ovulation, the granulosa cells of the ruptured follicle undergo luteinization. The luteinized granulosa cells, theca cells, capillaries, and CT form the corpus luteum. The corpus luteum produces copious amounts of _____ and some estradiol

A

Progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What histologic portion of the endometrium contains spiral arteries and undergoes cyclic changes during the menstrual cycle and is sloughed off at menstruation?

A

Functionalis

[the basalis layer contains basal arteries, remains relatively unchanged during each cycle, and produces stem cells for renewal of functionalis layer]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

During which phase of the uterine cycle is endometrial lining at its maximal thickness?

A

Secretory phse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is an intact coagulation pathway important in regulating menstruation?

A

Menstruation disrupts blood vessels, but with normal hemostasis, the injured vessels are rapidly repaired

Restoration of these blood vessels requires successful interaction of platelets and clotting factors

[certain medications and clotting disorders are associated heavy bleeding]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The median age of menarche is _____. Menarche usually occurs within 2-3 years after ______ at tanner stage IV, rarely before tanner stage III.

A

12.43; thelarche

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define primary amenorrhea

A

No menstruation by 13 y/o without secondary sexual development OR by the age of 15 with secondary sexual characteristics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Length of normal menstrual cycle in adults

A

21-35 days

[in first few years after menarche may be 21-45 days]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Normal vs. excessive menstrual flow

A

Normal mean blood loss per menstrual period is 30 cc — most report changing a pad 3-6x/day

Excess is >80cc — often associated with anemia [changing a pad q1-2 hrs is considered excessive especially if bleeding is lasting >7 days]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Onset of puberty is determined primarily by what 3 factors?

A

Genetic factors (including race)

Geographic location

Nutritional status (obese children have earlier puberty, malnourished later, mean weight of 106 lbs required to start menarche)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The female infant acquires the lifetime peak number of oocytes of 6-7 million by midgestation (16-20 wks). The HPO axis is _____ between the ages of 4-10 y/o.

A

Suppressed

[low levels of gonadotropins and sex steroids during prepubertal period are due to both negative feedback by low levels of estradiol as well as intrinsic CNS inhibition of GnRH secretion]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Between ages of 8-11 there is an increase in which 3 hormones responsible for axillary and pubic hair development?

A

DHEA, DHEA-S, and androstenedione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe onset of puberty around age 11

A

Around age 11, there is a gradual loss of sensitivity to the negative feedback of sex steroids + intrinsic loss of CNS inhibition of hypothalamic GnRH release

Sleep-associated increases in GnRH occur and gradually shift into adult type secretory patterns

The increase in GnRH promotes ovarian follicular maturation and sex steroid production, which leads to the deveopment of secondary sex characteristics

By mid to late puberty, the positive-feedback mechanism of estradiol on LH release from the anterior pituitary gland is complete and ovulatory cycles are established

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Stages of normal pubertal development

A
  1. Thelarche (first physical sign of puberty, requires estrogen)
  2. Pubarche/adrenarche (requires androgens)
  3. Peak height velocity (occurs about 1 yr before onset of menses)
  4. Menarche (requires pulsatile GnRH from hypothalamus, FSH and LH, estrogen and progesterone, and normal outflow tract)
  5. Mature sexual hair and breasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tanner staging of breast development

A

Stage 1: preadolescent; elevation of papilla only

Stage 2: breast bud stage; elevation of breast and papillla as a small mound with enlargement of the areolar region

Stage 3: Further enlargement of breast and areola without separation of their contours

Stage 4: projection of areola and papilla to form a secondary mound above the level of the breast

Stage 5: mature stage; projection of papilla only, resulting from recession of the areola to the general contour of the breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Tanner staging of pubic hair

A

Stage 1: Preadolescent; absence of pubic hair

Stage 2: Sparse hair along the labia; hair downy with slight pigment

Stage 3: Hair spreads sparsely over junction of pubes; hair is darker and coarser

Stage 4: adult-type hair; there is no spread to the medial surface of the thighs

Stage 5: adult-type hair with spread to the medial thighs assuming an inverted triangle pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define precocious puberty

A

Development of any sign of secondary sex characteristics prior to an age 2.5 standard deviations earlier than the expected age of pubertal onset (in North America — 8 y/o for girls, 9 y/o for boys)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

75% of cases of precocious puberty are idiopathic. Why is it important to do a thorough evaluation?

A

To eliminate a serious disease and to arrest potential osseous maturation that can affect normal growth patterns (can lead to premature fusion of the long bones epiphysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is heterosexual precocious puberty and what are 3 potential causes?

A

Development of secondary sexual characteristics opposite those of anticipated phenotypic sex

Causes include virilizing neoplasms, congenital adrenal hyperplasia, and exposure to endogenous androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define isosexual precocious puberty and its primary cause

A

Premature sexual maturation that is appropriate for the phenotype of the affected individual

Cause is typically constitutional and organic brain disease (tumors, trauma, infectious process)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

One potential cause of heterosexual precocity is a virilizing neoplasm. These are very rare in childhood and typically originate in the ovaries (Sertoli-Leydig cell) or adrenals. How are these diagnosed and treated?

A

Diagnosed by PE and radiology

Treated with surgical removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

One potential cause of heterosexual precocity is congenital adrenal hyperplasia, most commonly resulting from a defect of the adrenal enxyme 21-hydroxylase leading to excess androgen production. What is the difference between classical vs. non classical congenital adrenal hyperplasia?

A

Classical — most severe forms can cause birth of female w/ ambiguous genitalia; if untreated, progressive virilization and short adult status will result

Nonclassical — late-onset, can cause premature pubarche and an adult disorder resembling PCOS

28
Q

True isosexual precocity arises from premature activation of the normal process of pubertal development involving the HPO axis. What is pseudoisosexual precocity?

A

Increased estrogen levels and sexual characteristic maturation WITHOUT activation of the HPO axis (i.e., estrogen producing tumors)

29
Q

75% of true isosexual precocious puberty is constitutional or idiopathic. How is it diagnosed and treated?

A

Diagnose with administration of exogenous GnRH and see a resultant rise in LH levels consistent with older girls who are undergoing normal puberty

Tx with GnRH agonist — this will suppress pituitary release of FSH/LH, resulting in decline of gonadotrophins to prepubertal levels and arrest of gonadal sex steroid secretion

[note: 10% of cases are caused by CNS disorder and are dx by MRI of the head]

30
Q

Cause of pseudoisosexual precocity involving somatic mutation during embryogenesis which causes them to function independent of their normal stimulating hormones; associated with multiple cystic bone defects, cafe au lait spots, and adrenal hypercortisolism

A

McCune-Albright syndrome

31
Q

Cause of pseudoisosexual precocity associated with a sex cord tumor that secretes estrogen; associated with GI polyposis and mucocutaneous pigmentation

A

Peutz-Jeghers syndrome

32
Q

When is puberty considered delayed?

A

Secondary sexual characteristics have not appeared by age 13

Thelarche has not occurred by 14

No menarche by 15-16

No menarche 5 years after onset of thelarche

33
Q

Causes of delayed puberty

A

Hypergonadotropic hypogonadism (Turner syndrome)

Hypogonadotropic Hypogonadism (Constitutional delay, Kallman syndrome, anorexia/extreme exercise, pituitary tumors/disorders, hyperprolactinemia, drug use)

Anatomic causes (mullerian agenesis, imperforate hymen, transverse vaginal septum)

34
Q

Define secondary amenorrhea

A

Patient with prior menses has absent menses for 6+ months

35
Q

Primary amenorrhea with absence of secondary sexual characteristics as well as diagnostic findings of FSH and LH <5 IU/L indicates hypogonadotropic hypogonadism. what is the most common cause of this type of delayed puberty?

A

Constitutional (physiologic) delay

36
Q

Cause of hypogonadotropic hypogonadism characterized by absence of migration of GnRH neurons into the hypothalamus as well as anosmia

A

Kallman syndrome

37
Q

Describe workup for pt who presents with primary amenorrhea in whom secondary sex characteristics are ABSENT

A

Measure FSH and LH levels

If FSH and LH < 5 IU/L, it is hypogonadotropic hypogonadism which can be due to many causes including hypothalamic or pituitary lesions, anorexia, hyperprolactinemia, Kallman syndrome, or most commonly constitutional (physiologic) delay

If FSH > 20 IU/L and LH >40 IU/L, it is hypergonadotropic hypogonadism. Next step is a karyotype analysis. If karyotype is 46, XX it is premature ovarian failure. If karyotype is 45,XO, it is Turners syndrome

38
Q

Most common form of female gonadal dysgenesis, characterized by absent secondary sexual characteristics, webbed neck, shield chest, short stature, streak ovaries, and coarctation of aorta

A

Turner’s syndrome

39
Q

Describe workup for pt who presents with primary amenorrhea in whom secondary sex characteristics are PRESENT

A

First perform uterine ultrasound.

If uterus is absent or abnormal, do a karyotype analysis. 46,XY = androgen insensitivity syndrome. 46,XX = mullarian agenesis.

If uterus is present or normal, check for outflow obstruction. If there is no outflow obstruction, evaluate for secondary amenorrhea. If there is an outflow obstruction, evaluate for imperforate hymen vs. transverse vaginal septum

40
Q

Condition in which there are male levels of testosterone in a female, as well as testes in the abdominal wall secreting normal amounts of antimullerian hormone — thus there is no uterus formation but external genitalia appear female w/ absent or sparse pubic hair, as well as breast development with smaller than normal areola/nipples

A

Androgen insensitivity syndrome (46,XY)

41
Q

Tx for androgen insensitivity syndrome

A

Gonadectomy after puberty to avoid neoplasm (gonadoblastomas and dysgerminomas)

Can create neovagina by surgical and nonsurgical methods; consider HRT

42
Q

Most common cause of primary amenorrhea in women with normal breast development

A

Mullerian agenesis (Meyer-Rokitansky-Kuster-Hauser) [46,XX]

[failure of mullerian ducts to fuse distally, so uterus is absent but may have unilateral or bilateral rudimentary uterine tissue, tubes, and ovaries; normal female testosterone levels; renal anomalies are common so check IVP]

43
Q

Outflow obstruction suspected in adolescents who present complaining of monthly dysmenorrhea without vaginal bleeding, vaginal bulge, and midline cystic mass

A

Imperforate hymen

[confirm with US, showing normal uterus and hematocolpos]

Tx with hymenectomy

44
Q

Condition that presents similar to imperforate hymen but will not have vaginal bulge; usually dx by MRI and corrected with surgery

A

Transverse vaginal septum

45
Q

The first step in the workup of a pt who presents with secondary amenorrhea and a negative pregnancy test is to check a TSH and prolactin level. What is the next step if both of these are normal?

A

Progesterone challenge test

If there is withdrawal bleeding, it is normogonadotropic hypogonadism (causes include PCOS, nonclassic CAH, Cushings, Sertoli-leydig tumor, exogenous androgens)

If there is no withdrawal bleeding, proceed with estrogen/progesterone challenge test. If there is withdrawal bleeding, check FSH/LH, if elevated it is hypergonadotropic hypogonadism; if FSH/LH low then do MRI to check for pituitary adenoma. If there is no withdrawal bleeding, it is likely an outflow obstruction

46
Q

First step in workup of pt with secondary amenorrhea

A

Pregnancy test

47
Q

Leading cause of female anovulatory infertility, associated with insulin resistance and increased circulating testosterone

A

PCOS

48
Q

Tx for PCOS

A

Weight loss

OCPs — suppresses FSH and LH, estrogen stimulates SHBG

Clomiphene citrate — can induce ovulation

Ovarian diathermy/laser tx

Spironolactone and/or electrolysis

Insulin-sensitizing agents - metformin

49
Q

The first step in the workup of a pt who presents with secondary amenorrhea and a negative pregnancy test is to check a TSH and prolactin level. What is the next step if the prolactin is normal but the TSH is abnormal?

A

Treat thyroid disease

[note: mild hypothyroidism is more often associated with hypermenorrhea or oligomenorrhea; tx should restore menses w/i a few months]

50
Q

The first step in the workup of a pt who presents with secondary amenorrhea and a negative pregnancy test is to check a TSH and prolactin level. What is the next step if TSH is normal but prolactin is abnormal?

A

If prolactin is <100, consider other causes

If prolactin is >100, perform MRI to evaluate for prolactinoma. If MRI is negative, consider other causes — ectopic prolactin production (bronchogenic carcinoma, ovarian dermoid cyst, RCC, gonadoblastoma), breastfeeding and stimulation, excessive exercise, severe head trauma, hypothyroid, liver or renal failure, meds (OCPs, antipsychotics, antidepressants, antihypertensives, H2 blockers, opiates, cocaine)

51
Q

PE considerations in pts presenting with hyperandrogenism

A

Degree of hirsutism, acne, and alopecia should be documented

Acanthosis nigricans — sign of insulin resistance

Bimanual exam assessing for ovarian enlargement

52
Q

What labs should you do on someone who presents with apparent hyperandrogenism?

A

17-hydroxyprogesterone level to exclude 21 hydroxylase deficiency CAH

24 hr free urinary cortisol or overnight dexamethasone suppression test — will rule out cushing syndrome

Prolactin and TSH to exclude hyperprolactinemia +/- thyroid dysfunction

Glucose, lipid levels

Testosterone and DHEA-S — high testosterone suspect ovarian androgen producing tumor; DHEA-S suspect adrenal androgen producing tumor

53
Q

Abnormally frequent menses at intervals <21 days

A

Polymenorrhea

54
Q

Excess and/or prolonged bleeding (>80mL and >7days) occurring at normal intervals

A

Menorrhagia

55
Q

Irregular episodes of uterine bleeding

A

Metrorrhagia

56
Q

Heavy and irregular uterine bleeding

A

Menometrorrhagia

57
Q

Define intermenstrual bleeding

A

Scant bleeding at ovulation for 1-2 days

58
Q

Menstrual cycles occurring >35 days but less than 6 months

A

Oligomenorrhea

59
Q

PALM-COEIN classification system for abnormal bleeding in reproductive age women

A 
PALM: Structural Causes
Polyp
Adenomyosis
Leiomyoma (or other myoma)
Malignancy and Hyperplasia
COEIN: Nonstructural Causes
Coagulopathy
Ovulatory Dysfunction
Endometrial
Iatrogenic (IUD, hormones)
Not yet classified
60
Q

Medical history considerations in pt that presents with abnormal uterine bleeding

A 
Age of menarche and menopause
Menstrual bleeding patterns
Severity of bleeding
Pain
Medical conditions
Surgical hx
Medications
Signs/symptoms of bleeding d/o
61
Q

PE considerations in pt that presents with DUB

A

General exam

Pelvic exam — external, speculum with pap if needed, bimanual

62
Q

Lab and other diagnostic tests to consider in pts that present with DUB

A 
Pregnancy test
CBC
Targeted screening for bleeding d/o (VonW, PT, PTT)
TSH
Chlamydia

Consider transvaginal US, saline infusion sonohysterography, MRI, hysteroscopy, endometrial biopsy

63
Q

Treatment for AUB in which there is massive bleeding

A

Hospitalization and transfusions if hemodynamically unstable

25 mg IV conjugated estrogens, then hormonal tx (combo therapy, Mirena)

64
Q

Treatment for AUB in which there is moderate bleeding

A

Combination OCPs

Mirena

65
Q

Treatments to consider for AUB in which bleeding is unresponsive to conservative therapy

A

D and C, polypectomy, myomectomy, endometrial ablation, hysterectomy

Endo Repro Exam II (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions