Brainscape's Knowledge GenomeTM

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


See full index

Pathophysiology - Endocrine and Reproductive > Female Reproductive System Endocrine Pathophysiology > Flashcards

Female Reproductive System Endocrine Pathophysiology Flashcards

1
Q

What is the relative hormonal requirement for ovulation, menstrual cycle proliferation, mucus production, and development of vagina, urethra, and breasts / how is this relevant?

A

Vagina/urethra/breasts < glandular mucus production < menstrual cycle proliferative phase < ovulation

  • > smallest amount is needed to initiate puberty and development of secondary sexual characteristics
  • > events of puberty happen in a predictable fashion based on circulating estrogen levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What characterizes the onset of puberty in terms of LH?

A

Nocturnal rise in LH levels due to pulsatile GnRH release at night -> leads to increased testosterone
-> occurs during REM sleep

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

Why do we think puberty is happening earlier nowadays?

A

Related to nutrition

-> being a greater mass allows puberty to ensue faster (you’ve met your nutritional requirements)

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

Place the following in the correct order, and define them:

Growth spurt, adrenarche, pubarche, thelarche, menarche

A 
Thelarche - breast bud / breast growth
Pubarche - pubic hair growth
Adrenarche - axillary hair growth (think adrenal glands make hair)
Growth spurt - follow hair growth
Menarche - first menstrual bleed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the average timespan between thelarche and menarche and who tends to get it earlier? During what Tanner stage does menarche usually occur?

A

Around 2.5 years, tends to occur earlier in African Americans, with mild obesity

Tanner Stage 3 - Menarche

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

What is the definition of precocious vs delayed puberty in females?

A

Precocious - Tanner Stage 2 at <8 years

Delay - Tanner Stage 1 at age 13, or no menses by age 16.

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

What is the definition of true precocity and what are the main causes in women?

A

GnRH dependent or central precocioius puberty (driven by hypothalamus)

  1. Idiopathic is primary cause
  2. CNS problem can also be the cause - unwanted activation of hypothalamus pulse generator.
    - > this reason is more common in girls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the most common causes of precocious pseudopuberty in boys and girls? What is this also called?

A

GnRH-independent puberty (peripheral puberty)

Boys - Testicular tumor (either theca cell or choriocarcinoma secreting hCG)

Girls - Ovarian tumor (i.e. granulosa cell making estrogen)

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

What usually causes hypergonadotropic hypogonadism?

A

Usually a chromosomal abnormal causing gonadal dysgenesis
-> i.e. Turner syndrome

Gonadotrope levels are high, but gonads are not responding

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

What are some reversile causes of hypogonadotropic hypogonadism?

A

Physiologic delay in puberty
Weight loss
Hypothyrodism
Prolactinoma

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

What are some causes of irreversible hypogonadotropic hypogonadism?

A

GnRH deficiency - i.e. Kallmann
Hypopituitarism
Craniopharyngioma / other pituitary tumors
Congenital CNS defects

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

What is the normal range of the menstrual cycle and the average duration of menses? How much blood is lost?

A

Normal - 21 to 35 days, mean 28 days

Average menses - 3-8 days -> about 30 mL is lost (1 oz)

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

What is the rate of GnRH pulses during follicular and luteal phase?

A

Follicular phase - quickly to stimulate follicule - every 60 minutes

Luteal phase - slowly to maintain endometrium - 90 minutes

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

What does an activin do? What produces them?

A

It is produced by the same cells as inhibins (Ovarian stromal cells), except they do the opposite of inhibins -> they STIMULATE gonadotropes to release FSH

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

What marker do primary follicles express, and what stage of Meiosis are they found in? When do they move on?

A

They express anti-Mullerian hormone -> can be used to track the development of the primary follicles

They are stuck in Prophase I of Meiosis I, they will move on when the corona radiata (inner layer of granulosa cells) stops delivering cAMP thru the zona pellucida (distinct mucopolysaccharide band) during the Graafian follicle stage -> secondary oocyte will arrest at Metaphase II until fertilization.

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

What are the ovarian and endometrial cycles and relative timing?

A

Ovarian: Starts with follicular phase, then ovulation occurs, then you have the luteal phase (corpus luteum)

Endometrial: Starts with proliferative phase (under influence of estrogens), then enters secretory phase (during luteal phase of ovarian cycle)

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

Defining as day 1 as the first day after menses, when is a dominant follicle selected and how is it selected? What happens to the other follicles?

A

Selected around day 5-7

Depends on follicle’s intrinsic capacity to synthesis estrogen (highest estrogen to androgen ratio due to most utilization of FSH by granulosa cells)
-> this is based on the number of FSH receptors expressed.

All other follicles become atretic

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

How does estrogen act synergistically with FSH in follicle development?

A

Estrogen induces LH receptors and induces FSH receptors in granulosa and theca -> helps stimulate and nuture production of testosterone via theca cells to give to granulosa cells.

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

What triggers the LH surge and what affect does this have on the follicle during and after ovulation?

A

Estradiol reaches a threshold concentration, which leads to LH surge

LH surge causes rupture of follicular wall with ovum release

Granulosa cells become “luteinized” from exposure to so much LH -> become filled with lipid via upregulation of LDL receptor. Also upregulate 3b hydroxysteroid DH to make more progesterone-> primarily progesterone (aromatase is turned off, no estrogen made)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does progesterone do during the luteal phase?

A
  1. Suppresses maturation of other follicles in ipsilateral ovary
  2. Thermogenic activity - accounts for the 0.5 degree increase in basal body temp during ovulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What triggers menses?

A

Overtime, the corpus luteum loses sensitivity to gonadotropins -> stops secretion of estrogen and progresterone.

Can only be saved by hCG

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

What are the two main layers of the endometrium?

A
  1. Basal layer - adjacent to myometrium, remains intact throughout the menstrual cycle. These are basically the stem cells of the uterus.
  2. Functional layer - Layer which proliferates from basal layer under influence of estrogen, and will die when spiral arteries become ischemic (mainly due to prostaglandin-mediated constriction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is characteristic of the secretory / luteal phase in the endometrium (stroma, glands, and arteries)? What is the overall process / change which is occurring in the endometrium?

A

Mostly under influence of progesterone: Mitotic activity is severely restricted, endometrial glands produce and secrete glycogen-rich vacuoles.

Stroma becomes edematous, enlarged, and corkscrew-shaped.

Spiral arterioles develop and extend nearly to the surface

-> this is the “decidualization” which occurs in preparation for the bb

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

What are the sources of androgens in women?

A
  1. Adrenal cortex - primary source of androgens, mostly DHEA and androstenedione
  2. Ovary - a small amount is made, mostly androstenedione

Androstenedione is converted peripherally to testosterone to some degree

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

What are the clinical features of hyperandrogenism in women?

A
  1. Hirsutism
  2. Acne
  3. Male pattern baldness - central loss of hair with recession of temporal area
  4. Android obesity (apple shaped rather than pear-shaped) - increased waist to hip ration (>0.85)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the two places women never make hair unless it’s pathologic?

A
  1. The chest (excluding the breast)

2. The small of the back

27
Q

How will the ovaries appear in polycystic ovarian syndrome (PCOS)?

A

Enlarged, bilateral cystic ovaries from unruptured follicular cysts -> cysts are not rupturing due to hormonal imbalance

These are secondary follicles which weren’t selected for and don’t regress.

28
Q

What is the clinical definition of PCOS?

A

2/3 of the following:

  1. Irregular uterine bleeding
  2. Hyperandrogenism - either seen clinically or measured
  3. Polycystic ovaries
29
Q

What condition is easily confused with PCOS and what causes that condition?

A

Non-classic Congenital Adrenal Hyperplasia
-> Increased androgens due to loss of 21-hydroxylase enzyme.

Main distinguishing factor: Non-classic CAH has very high levels of 17-OH-Progesterone (upstream from the block)

30
Q

What is going wrong hormonally in PCOS which accounts for the symptoms?

A

Hyperinsulinemia / insulin resistance alter the hypothalamic hormonal balance and cause:

  1. Increased LH:FSH ratio, which stimulates increased androgen production from theca interna cells –> hirsutism.
  2. High circulating androgen levels are converted to estrone via adipose tissue (these women are obese with insulin resistance) -> feedback by estrone decreases FSH levels secreted by anterior pituitary.
  3. Since FSH is low, androgens are not rapidly turned into estrogen via granulosa cells -> slowed rate of follicular maturation. This leads to small follicular cysts and anovulation -> infertility.
31
Q

What is the classic presentation of someone with PCOS then?

A

An obese young woman (adipose tissue required to make estrogen) with infertility, oligomenorrhea, hirsutism/hyperandrogenism, and often insulin resistance (obese)

32
Q

What two conditions are you at increased risk of developing in the future due to PCOS?

A
  1. Type 2 diabetes - insulin resistance
  2. Endometrial cancer - due to unopposed circulating estrone and estrogen from anovulatory cycles -> corpus luteum is never made.
33
Q

What “type” of insulin resistance do patients with PCOS have?

A

“Selective” insulin resistance

  • > Ovary / liver are sensitive to insulin and will increase androgen synthesis in ovary, and suppress SHBG production by liver (increases free testosterone levels)
  • > muscle / adipose are reesistant to insulin, causing obesity
34
Q

What is the treatment algorithm for PCOS?

A
  1. Weight reduction
  2. OCPs -> prevent endometrial hyperplasia due to unopposed estrogen (provide hormones exogenously)
  3. Clomiphene - infertility treatment which blocks estrogen receptor negative feedback in hypothalamus
  4. Metformin - to combat insulin resistance
  5. Spironolactone / ketoconazole -> block androgen receptor as well as production
  6. Statins - for treatment of metabolic syndrome.
35
Q

What is the definition of infertility? When should a consultation be offered?

A

Failure to conceive after 12 months of regular coital activity in the absence of contraception

Should be offered after 1 year, or if older than 35, evaluate at 6 months (little time)

36
Q

What is primary vs secondary infertility?

A

Primary - no previous pregnancies have occurred

Secondary - prior pregnancy has occurred, but not necessarily a live birth

37
Q

How has the rate of infertility been changing since 1950 and why?

A

It has increased, since marriages are happening later, and contraception is improved.

  • > As you get older, it becomes harder and harder to conceive
  • > by age 40, you are about half as fertile as you were at 20.
38
Q

What are the common causes of anovulation in females?

A

PCOS, obesity, HPO axis abnormalities, premature ovarian failure, hypothyroidism, adrenal dysfunction (high or low)

39
Q

What are tubal / uterine factors which can cause infertility?

A

Uterine abnormalities -> fibroids / polyps
Pelvic inflammatory diseases
Endometriosis

40
Q

What are some environmental toxins which can cause infertility?

A

Smoking (accelerated menopause), marijuana (inhibits GnRH pulsatility), alcohol, caffeine, anesthetic gases

41
Q

What is the clinical definition of menopause? What is the underlying mechanism? What usually precedes it?

A

No menses for 12 months

  • > Apoptotic depletion of ovarian follicles (highest levels in the fetus, and number of follicles rapidly decreases until menopause)
  • > Usually preceded by 4-5 years of abnormal menstrual cycles
42
Q

What is premature ovarian failure? What type of disorder is it?

A

Menopause before age 40

This is primary ovarian insufficiency -> hypergonadotrophic hypogonadism

43
Q

What is the approximate age of onset of normal menopause, and what marker is specific for it?

A

Approximately 51 years (can be earlier in smokers)

Increased FSH levels are specific (loss of negative feedback on FSH due to decreased estrogen levels)

44
Q

What is the source of estrogen in menopause, and what are the general symptoms to remember?

A

Peripheral conversion of androgen to estrogen. (LH stimulates the theca cells). These increased androgens can lead to hirsutism.

Remember HAVOCS:
Hot Flashes
Atrophy of ->
Vagina
Osteoporosis (first three from decreased estrogen)
Coronary Artery Disease
Sleep Disturbances (from hot flashes and night sweats)

45
Q

What are vasomotor symptoms and what helps them? Are they common?

A

Vasomotor symptoms = hot flashes.

Extremely common, but only 25% of women actually seek treatment.

Estrogen therapy reduces them.

46
Q

What is one consequence of vaginal atrophy during menopause which is very distressing?

A

“Genital Syndrome of Menopause”

Dyspareunia (annotate page 600) -> “difficulty + lying with” -> painful sexual intercourse because it’s bone dry
-> loss of libido

47
Q

What is the treatment for genital syndrome of menopause?

A

Local estrogen -> safe and effective at any age

48
Q

How do you diagnose osteoporosis in a postmenopausal women? How can this be measured easily? How do you treat?

A

If they’ve lost more than 1” from their driver’s license reported height, they most likely have vertebral osteoporosis

  • > Crown to pubis / pubis to floor ratio is about 1 for easier measurement
  • > Treat with hormone replacement therapy (estrogen), the earlier the better
49
Q

What is the definition of primary amenorrhea? How do you differentiate between hypogonadotropic hypogonadism / gonadal dysgenesis?

A

Never having had menstruation on their own accord (without OCPs)

Hypogonadotropic hypogonadism - FSH will be low / inappropriate normal

Gonadal dygenesis - FSH will be high

50
Q

What is the most common cause of primary amenorrhea? Why does it occur in this condition?

A

Turner syndrome (XO) -> gonadal dysgenesis

Occurs because the single cuboidal layer of granulosa cells does not properly form around the egg units -> no protection for the eggs. Thus, the follicles rapidly degrade in utero and become replaced by connective tissue (streak gonads).

51
Q

How does nutrition affect the onset of menarche?

A

Malnutrition (anorexia / bulimia) -> delay menarche, due to lower fat to lean body weight ratio

Moderate obesity -> earlier menarche, due to increased estrogen conversion from adipose tissue

52
Q

What is the question you have to ask yourself when evaluating primary amenorrhea?

A

Is there normal development of female secondary sexual characteristics.

If NO -> hypogonadism, hyper or hypogonadotropic (as explained before)

If YES -> Mullerian anomalies, outflow obstruction, androgen insensitivity, or weight/exercise issue

53
Q

What is Mayer-Rokitansky-Kuster-Hauser syndrome also called, and how will the patient present?

A

Mullerian agenesis

Presents as primary amenorrhea in females with fully developed secondary sexual characteristics (ovaries are functional, not derived from Mullerian duct)

54
Q

Why do patients with Mullerian agenesis have primary amenorrhea? How will their gonads look?

A

Mullerian ducts give rise to fallopian tubes, uterus, and upper vagina.

  • > uterus and upper vagina + fallopian tubes will be absent
  • > lower 1/3 of vagina formed via urogenital sinus, will be present as blind vagina.
55
Q

What does the paramesonephric duct become in the male?

A

Two blind-ended sacs

  • > prostatic utricle
  • > appendix of the testis
56
Q

What medical condition causes hematocolpos? What is the clinical presentation

A

Hematocolpos = condition where vagina fills with blood “blood + vagina”

Imperforate hymen -> requires surgical correction

Cyclical abdominal pain during periods, with urinary retention, nausea, and diarrhea

57
Q

What genitalia will those with androgen insensitivity have?

A

They have normal female external genitalia, but blind vagina / absent uterus / upper vagina (Wolffian / mesonephric duct formed in utero)
-> testes will be present with normal circulating levels of testosterone for a male, the only difference is end-organ response

58
Q

What is the management for patients with androgen insensitivity syndrome? Will they have hair?

A

Gonadectomy after puberty with estrogen therapy
-> testes will be present as inguinal masses, need to be removed to prevent tumorigenesis (like cryptorchidism)

If they have complete androgen insensitivity (there is a spectrum, these patients are viewed as intersex) -> no axillary or pubic hair (requires some testosterone response)

59
Q

What is the first step in the algorithm for secondary amenorrhea (amenorrhea which has started after menarche)? What does a positive test mean?

A

Progesterone / progestin challenge test

  • > Withdrawal bleeding 2-7 days after giving progesterone (and levels have dropped) indicates that there is a presence of estrogen, but ovulation and thus formation of corpus luteum has not been occurring
  • > endometrium stuck in proliferative phase, never reaches secretory phase to turn over

Basically, withdrawal bleed = ANOVULATION, where estrogen is present

60
Q

What do you do if there is no withdrawal bleed after the progestin challenge? What are the possible results?

A

Estrogen + Progesterone challenge

If bleeding -> reason for amenorrhea is low estrogen. Check FSH levels to see if gonadal failure or CNS failure.

If no bleeding -> uterus / anatomical outflow tract problem

61
Q

What is Asherman syndrome and what typically causes it?

A

Secondary amenorrhea due to loss of basalis (regenerative layer) of endometrium, with scarring

Normally caused by overaggressive dilation and curettage (obestetrical procedure)

Refer to pathoma

62
Q

How is the diagnosis of functional hypothalamic amenorrhea made, and is it common?

A

Low estrogen levels, with no withdrawal bleed from progestin challenge

It is one of the most common causes of amenorrhea

63
Q

What are some common causes of functional hypothalamic amenorrhea?

A
  1. Low weight (eating disorders like anorexia / bulimia) -> we said these are causes of anovulation as well
  2. Endocrine conditions (hypothyroid, hyperprolactinemia, diabetes)

Stress and exercise also contribute
-> results in ultimately low GnRH

64
Q

What is the female athletic triad?

A
  1. Disordered eating -> social pressures
  2. Menstrual dysfunction -> due to low GnRH from excessive stress / exercise
  3. Osteoporosis -> due to low estrogen

Pathophysiology - Endocrine and Reproductive (27 decks)

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