Endocrine - Female Reproductive

Front 1

What hormones are pulsatile and therefore must be measured at specific times?

Back 1

Melatonin
ACTH
Corisol

Front 2

What nucleus secretes GnRH into the pituitary portal circulation?

Back 2

Arcuate nucleus

Front 3

What hormone is required for normal pituitary function?

Back 3

Pulsatile GnRH

-pulse frequency is slowed by progesterones and androgens, slow frequency favors FSH release

-pulse amplitude is reduced by estrogens

Front 4

What ovarian follicle cells have FSH receptors?

Back 4

Granulosa cells

Front 5

What ovarian follicle cells have LH receptors?

Back 5

Theca cells

Front 6

What are the structural similarites and differences of FSH and LH?

Back 6

Both hormones share alpha-subunits.

Functional specificity is conferred by beta-subunits

Front 7

What is the effect of low-level estrogen on gonadotropin release from the pituitary?

Back 7

Favors gonadotropin release, predominantly FSH

Front 8

What is the effect of rising/high estrogen levels on gonadotropin release from the pituitary?

Back 8

Inhibits gonadotropin release, facilitates storage

Front 9

What is the effect of high estrogen with rising progesterone levels on gonadotropin release from the pituitary?

Back 9

facilitates mid-cycle gonadotropin surge

Front 10

What is the effect of high-level progesterone on gonadotropin release from the pituitary?

Back 10

inhibits LH release during luteal phase

Front 11

What is the role of LH during the follicular phase?

Back 11

activates Theca cells to produce androgens

Front 12

What is the role of FSH during the follicular phase?

Back 12

acts on Granulosa cells to:
-induce LH receptors
-induce FSH receptors
-mitosis
-activation of aromatase enzyme system

Front 13

Rising estrogen levels during the follicular phase have two effects.

Back 13

1. Negative feedback
2. Proliferation of the endometrium

Front 14

What are the levels of estrogen and progesterone in the early Luteal phase? What effect does this have?

Back 14

Estrogen and progesterone are both at high levels.

The high levels provide endometrial changes in preparation for implantation.

Front 15

Reproductive Endocrine Disorders (4)

Back 15

1. Menstrual disorders
2. Hyperandrogenic disorders
3. Hyperprolactinemic disorders
4. Infertility

Front 16

Classification of Amenorrhea.

What is the differentiation based upon?

Back 16

FSH level

Front 17

Hypergonadotropic Primary Amenorrhea

causes (3)

Back 17

1. Prepubertal surgical ablation, infection, chemotherapy
2. Gonadal dysgenesis (Turner syndrome)
3. Androgen Insensitivity Syndrome

Front 18

Turner Syndrome

Back 18

(45,X) genotype or mosaic variants

Elevated FSH and LH

Gonadal dysgenesis due to accelerated postnatal follicular atresia. Multiple somatic abnormalities, infantile female genitalia.

Nonfunctional ovaries, absent secondary sexual characteristics.

Front 19

Androgen Insensitvity Syndrome

Back 19

(46,XY) with androgen receptor defect

Female external genitalia (failed masculinization) without female internal genitalia

Gonadectomy after puberty to elimnate risk of tumor

Hypergonadotropic Primary Amenorrhea

Front 20

Eugonadotropic and Hypogonadotropic primary amenorrhea

-distinguish between endocrine vs. anatomical disorder

Back 20

Differentiate by presence of secondary sexual characteristics

-presence indicates anatomical cause (hormones are working)

-absence indicates hypothalamic-pituitary cause

Front 21

Steroid Challenge Tests

-progestin challenge

Back 21

Administer sufficient dose to cause secretory endometrial change, then withdraw.

Bleeding implies estrogen primed endometrium and confirms patent outflow tract

Front 22

Steroid Challenge Tests

-estrogen-progestin challenge

Back 22

Administer sequential estrogen then progestin to cause endometrial proliferation then secretory change, then withdraw

Bleeding confims patent outflow tract

Front 23

Eugonadotropic/Hypogonadotropic primary amenorrhea without normal sexual characteristics

-functional and organic causes

Back 23

Ovaries are presumed functional since FSH is not elevated

Functional causes: stress, extreme weight changes, excessive exercise, familial delay, systemic illnes

Organic causes: craniopharyngioma, pituitary tumor, CNS infection, CNS inflammation, congenital (Kallman) - neurons dont migrate

Front 24

Hypergonadotropic Secondary Amenorrhea

-main cause

Back 24

Acquired ovarian failure
-autoimmune, chemo, infection, incomplete gonadal dysgenesis
-repetitive FSH > 45 with low Estrogen

Front 25

Eugonadotropic/ Hypogonadotropic secondary amenorrhea

-causes (2)

Back 25

1. Acquired mullerian disorder (may present with progressive hypomenorrhea and dysmenorrhea before amenorrhea)
2. Dysfunction/failure of hypothalamic - pituitary center

Differentiate via progestin/ estrogen-progestin challenge

Front 26

Eugonaodotropic/Hypogonadotropic secondary amenorrhea

-Endocrine disorder
-causes (4)

Back 26

Problems with GnRH secretion, action or response by pituitary gonadotropes.

Degree of abnormality reflected by basal FSH
1. Stress, systemic illness
2. Weight changes
3. Exercise
4. Pituitary tumor, infection, infiltration

Front 27

Menstrual Disorders

-differentiation between causes (2)

Back 27

Differentiate organic causes of abnormal uterine bleeding from endocrine causes

Front 28

Dysfunctional Uterine Bleeding
-cause

Back 28

ALWAYS implies an endocrine cause

Endometrium is responding normally to abnormal endocrine signals

-Estrogen/Progesterone withdrawl
-Estrogen/Progesterone breakthrough

Front 29

Hyperandrogenic Disorders
-sources of androgens (3)

Back 29

1. Ovary
2. Adrenal
3. Peripheral interconversion

Front 30

Hyperandrogenic Disorders
-clinically significant androgens (3)

Back 30

1. Testosterone - most potent
2. DHEAS - most specific (adrenal secretion)
3. 17-dihydroxyprogesterone

Front 31

Hyperandrogenic Disorders
-clinical manifestations(3)

Back 31

1. Hirsutism, skin changes
2. Menstrual abnormalitites
3. Insulin resistance

Front 32

Hirsutism

Back 32

Irreversible conversion of vellus to terminal hair in a male distribution pattern
Increase androgen action at the hair follicle
Progression of hyperandrogenic signs and symptoms
-menstrual irregularity, skin changes
-hirsutism
-defeminization and masculinization

Front 33

Adrenal Hyperandrogenism
-causes (4)

Back 33

1. DHEAS and other androgens elevated
2. Adrenocortical carcinoma
3. Cushing's Syndrome or Disease
4. Congenital Adrenal Hyperplasias
-late onset exceedingly common (21-hydoxylase deficiency most common)

Front 34

Congenital Adrenal Hyperplasia
-pathogenesis
-symptoms
-treatment

Back 34

Deficient glucocorticoid production upregulates ACTH, w/overproduction of androgenic intermediates
Androgen elevation leads to hirsutism, acne, menstrual irregularity
Salt wasting or retention w/HTN
Diagnose with ACTH stimulation test
Treat with exogenous glucocorticoid

Front 35

Ovarian Hyperandrogenism - Neoplasms
-cell-types
-presentation of syptoms
-diagnosis

Back 35

Granulosa cell, Hilar cell and Sertoli-Leydig cell (rare)
Testosterone elevations are significant and rapidly progessive, leading to significant signs and symptoms in a short time
Diagnose with ultrasound/MRI, failure to supress using GnRH analogs

Front 36

Polycystic Ovary Disease
-pathogenesis

Back 36

Overstimulation of theca with insuffcient aromatase activity to convert A --> E
Abnormal FSH/LH secretion maintained by hyperandrogenic state
Chronic anovulation, hyperandrogenism, variable estrogens
Insulin-resistence associated with dyslipidemias, atherogenesis and DM

Front 37

Polycystic Ovary Disease
-Rotterdam Criteria

Back 37

At least two of the following:
-Menstural irregularity -- oligo/amonorrhea
-Hyperandrogenism and/or hyperandrogenemia
-Sonographic evidence of follicular atresia (cysts) and/or stromal hyperplasia

Front 38

Polycystic Ovary Disease
-clinical presentation (5)

Back 38

1. Menstrual irregularity, possible endometrial hyperplasia, early endometrial adenocarcinoma
2. Central obesity
3. Enlarged, polycystic ovaries
4. Hyperandrogenic manifestations - hirsutism, acanthosis nigracans
5. Insulin resistance - metabolic syndrome

Front 39

Polycystic Ovary Disease
-treatment (4)

Back 39

1. Lifestyle modification
2. Exogenously cycle enometrium (birth control)
3. Insulin sensitizing agents
4. Ovulation induction

Front 40

Prolactin
-what tonically inhibits it?

Back 40

Dopamine

Front 41

Galactorrhea
-definition
-causes

Back 41

Bilateral inappropriately timed lactation
Unilateral discharge or any other discharge requires investigation for breat pathology
Hyperprolactinemia
Frequently associated with ovulatory dysfunction and resulting menstrual disorders

Front 42

Hyperprolactinemia
-causes (6)

Back 42

1. Nipple stimulation
2. Chest wall trauma
3. Chronic herpes zoster
4. Drugs that alter dopaminergic tone
5. Primary hyperthyroidism -TSH stimulates PRL release
6. Pituitary adenoma

Front 43

Hyperprolactinemia
-evalutation
-treatment

Back 43

Confirm hyperprolactinemia
Exclude primary hyperthyroidism or other causes
Sellar imaging for adenoma
Treat with dopamine agonists or surgery (rare)

Front 44

Infertility
-definition

Back 44

One year of regular, unprotected intercourse without conception (10-12% incidence in couples trying to conceive)

Fertility declines in women with advancing age (not true with men until much later in life)

Front 45

Infertility
-Male factors (40% of couples) (4)

Back 45

1. Hypothalamic-pituitary
2. Testicular - environment/viral/varicocele
3. Obstructive - vasectomy/infection
4. Ejaculatory - retrograde ejaculation in diabetes, autonomic dysfunction

Front 46

Infertility
-Female factors (3)

Back 46

1. Ovulatory dysfunction or failure
2. Female reproductive tract abnormalities
-Cervical
-Uterine: polyps, fibroids
-Fallopian tube: blockage, adhesions
-Peritoneal: endometriosis, adhesions
3. Immunologic