SDR Flashcards

1
Q

When does differentiation begin?

A

6-8wks

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2
Q

What does the presence of testis-determining factor cause and where is it located? (+SRY)

A
  • Gonads develop into a testis

- Located on the Y chromosome

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3
Q

What does the absence of testis-determining factor cause? (-SRY)

A

-Gonad differentiates into an ovary

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4
Q

What are the different but related ducts that form beside the undifferentiated gonads?

A

Wolfian Ducts

Mullerian ducts

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5
Q

Explain what happens in the presence of SRY (+SRY)

A
  • The Y chromosome carries the SRY gene
  • Gonads differentiate into testes
  • The presence of testosterone causes the wolfian ducts to develop into the internal male structures
  • The presence of anti-mullerian hormone causes degeneration and atrophy of mullerian ducts
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6
Q

What are the internal male structures that develop?

A

Epididymis
Vas deferens
Seminal vesicles
Ejaculatory ducts

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7
Q

Explain what happens in the absence of SRY (-SRY)

A
  • Gonads differentiate into ovaries
  • The absence of testosterone causes degeneration and atrophy of the wolfian duct
  • The absence of the anti-mullerian hormone allows for mullerian ducts to develop into the internal female structures
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8
Q

What are the internal female structures that develop?

A

Uterus
Fallopian tubes
Upper part of the vagina

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9
Q

Describe the process of puberty:

A

-Pulsatile release of GnRH followed by an increase in LH and FSH ->Results in episodic peaks of estradiol and testosterone-> Initiates secondary sexual maturation in girls and boys

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10
Q

Delayed puberty:

A
  • No secondary sex characteristics; in females by 13 and males by 14
  • Etiology: undernutrition, athletics, HPG defects, stress, environmental exposures
  • 95% of the time: normal hormone levels, HPG axis intact, maturation just slow.
  • Often familial
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11
Q

Precocious puberty:

A
  • Sexual maturation before ages 6-7 in females and 9 in boys
  • Central: GnRH-dependent-short stature d/t premature closing of the epiphysis
  • Peripheral: GnRH independent- gonadal tumors, testotoxicosis, exposure to exogenous sex steroids
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12
Q

What are the male sex hormones (4) and what do they do?

A
  1. GnRH- released from hypothalmus, stimulates the anterior pituitary to secrete FSH and LH
  2. FSH- stimulates spermatogenesis (Sertoli cells)
  3. LH- stimulates the secretion of testosterone (Leydig cells)
  4. Testosterone- stimulates spermatogenesis, stimulates the development of male secondary sex characteristics
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13
Q

Describe hormonal regulation of the hypothalmus-pituitary-testes axis (?)

A

The hypothalamus releases GhRH which stimulates the anterior to release FSH and LH. LH stimulates the Leydig cells to secrete testosterone which stimulates spermatogenesis and secondary sex characteristics. FSH (and testosterone) stimulate the Sertoli cell which leads to spermatogenesis.

  • *Testosterone provides negative feedback to hypothalamus= if too high will not produces more GnRH.
  • *Inhibin works to inhibit FSH release from the ant. pit
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14
Q

Outline the Uterine Cycle (aka Menstrual Cycle)

A
  1. Menstrual phase: bleeding. Day 1 to day 3-5; function layer of the endometrial lining and blood leave the uterus through the vagina
  2. Proliferative phase (follicular)- Begins at end of menstruation; repair and growth of inner endometrial lining
  3. Secretory phase (luteal)- Due to secretion of progesterone by the corpus luteum= causes endometrial lining to thicken (forming nutritious environment awaiting the arrival of a fertilized ovum)
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15
Q

What hormone is the follicular phase dominated by?

A

Estrogen

Hypothalamus secretes GnRH->gonadotropin release by ant pit gland-> FSH and small amounts of LH stimulate growth and maturation of the ovarian follicle-> maturing ovarian follicle secretes large amounts of estrogen-> estrogen aids in maturation of follicle and builds lining -> ends with sharp rise of LH which causes ovulation.

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16
Q

What hormone is the luteal phase dominated by?

A

Progesterone

Follows ovulation
Follicular cells of the ruptured follicle on the surface of the ovary form the corpus luteum
LH stimulates the corpus luteum to secrete progesterone and small amounts of estrogen-> progesterone and estrogen exert a negative feedback effect on the ant pit gland-> inhibiting FSH and LH
Progesterone supports the endometrial lining of the uterus during the second half of the cycle
When corpus luteum dies, secretion of progesterone and estrogen decline -> FSH and LH are once again secreted and cycle repeats

17
Q

What is the corpus luteum?

A

During the luteal phase, the site of the ruptured/old follicle becomes the corpus luteum which secretes estrogen and progesterone. These hormones stimulate continued thickening of the endometrium. Cells of the corpus luteum become enlarged and fatty. If pregnancy does not occur the corpus luteum begins to degenerate and estrogen and progesterone levels fall.

18
Q

If fertilization dose occur what supports the corpus luteum?

A

hCG

19
Q

Describe the positive feedback loop of menstruation.

A

(mid cycle)
Hypothalamus release GnRH-> ant pit release LH stimulating the Theca cells to produce androgens to stimulate Granulosa cells which are also stimulated by FSH -> estrogen production-> loops back to hypothalmus to continue to release GnRH= spike in FSH and LH causing ovulation

20
Q

Describe the negative feedback loop happening in menstruation.

A

Hypothalamus releases GnRH->ant pit releases LH to stimulate theca cell to produce androgen which stimulates the Granulosa cell which is also stimulated by FSH-> estrogen and progesterone production. When estrogen and progesterone increases, hypothalamus slows production of GnRH.

Inhibin also plays part in decreasing LH and FSH from ant pit.

21
Q

Primary Amenorrhea

A

Failure of menarche and the absence of menstruation by age 14; without development of secondary sex characteristics by age 16

22
Q

Secondary Amenorrhea

A

Absence of menstruation for a time equivalent to 3+cycles or 6 months in women who have previously menstrated

23
Q

What is the primary hormone problem with PCOS?

A

FSH low and LH elevated

Disruption in H-P-G axis:
	FSH low
	LH high
	Androgen high
	Estrogen high
24
Q

What is the leading cause of infertility?

A

Polycystic Ovarian Syndrome

25
Q

T/F: Hyperinsulinemia causes an increase in severity of symptoms of PCOS

A

True

26
Q

T/F: Polycystic ovaries are a requirement for diagnosis of PCOS

A

False

27
Q

What are some common culprits of pelvic pain?

A
  • Pelvic inflammatory disease
  • Ovarian cysts
  • Leiomyomas (uterine fibroids)
  • Endometriosis
  • Endometrial polyps
28
Q

Causes of endometriosis (4 theories).

A
  1. Regurgitation through fallopian tubes; during retrograde menstruation some of the endometrial cells relfux up the fallopian tube and reimplant ectoptically
  2. Lymphatic dissemination; transport of endometrial cells throughout the lymphatics
  3. Extrapelvic dissemination through pelvic veins
  4. Metaplastic differentiation of epithelial cells= turn into endometrial cells
29
Q

What is endometriosis?

A

Endometriosis is the presence of endometrial tissue outside the lining of the uterine cavity

30
Q

Classic symptoms of endometriosis:

A

Classic symptoms:
Dysmenorrhea
Abnormal uterine bleeding
Infertility
Pain
Begins 5 to 7 days before menses, peaks, and lasts for 2 to 3 days
Severity does not reflect extent of disease

31
Q

Cervical cancer is related to:

A

HPV

32
Q

Vaginal cancer:

A
R/t prenatal exposure to diethylstilbestrol
May also be caused by:
Spread of cervical cancer
Human papillomavirus infection
Chronic local irritation
33
Q

Endometrial cancer:

A

Good prognosis, bleeding is an early symptom in post menopausal women, removal of uterus can be curative

34
Q

Ovarian cancerous tumors:

A

Bad Prognosis
Associated with family history of ovarian and breast cancer
Causes vague GI symptoms
Up to 75% of cases have metastasized by the time they are discovered
No good screening tests available
Ovariectomy

Dx
Ultrasound
CA-125: tumor marker
Laparotomy and biopsy

**Ovarian cancer- BRCA 1 gene