Reproductive System Flashcards

1
Q

How long does it take to produce mature sperm?

A

21 days (complete turnover every 60d)

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2
Q

3 differences between spermatogenesis and oogenesis

A
  • timing of mitosis: f- prior to birth/ m-after puberty
  • f: 1 oocyte–> 1 mature ovum, 3 polar bodies // m: primary spermatocyte–> 4 spermatozoa
  • f: 2nd meiotic division after fertilization
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3
Q

What is produced by seminal vesicles? prostate? role of each component???

A
  • s.v.- fructose, citric acid, nutrients, (nourish), prostaglandins (motility), fibrinogen (clot)
  • prostate- calcium, citrate, clotting enzyme, alkaline fluid (neutralization)
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4
Q

Sperm count considered infertile

A
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5
Q

Role of acrosome, cortical granules

A
  • acrosome- enzymes in sperm head help penetrate wall of ovum
  • cortical granules- in egg, inactivate receptors once sperm enters to prevent polyspermy
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6
Q

Mullerian vs Wolffian ducts

At what point in utero is sex determined?

A
8 weeks (2nd month)
testosterone expressed or not
- Mullerian ducts turn into female, wolffian ducts turn into male, we start with both
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7
Q

DHT is? Roles?

A

DHT= potent derivative of testosterone

  • fetal development of male reproductive system
  • pubertal growth of scrotum, prostate, hair, sebaceous glands
  • prostatic secretion
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8
Q
Function of:
testes
epididymis/ductus deferens
seminal vesicles
prostate gland
bulbourethral glands
A
  • testes- produce sperm, testosterone
  • epi/dd- sperm storage/maturation
  • sv- bulk of semen-fructose, prostaglandins, clotting
  • prostate- alkaline, clotting
  • bulbourethral- mucus
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9
Q

Males- targets of GnRH, LH, FSH

A

GnRH- hypothalamus to ant pituitary, release LH/FSH

  • LH–> leydig cells –> testosterone
  • FSH–> sertoli cells –> spermatogenesis and inhibin for negative feedback on hypothalamus
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10
Q

ADT and prostate cancer

A

Androgen Deprivation Therapy- testosterone nourishes cancer cells, ADT–> lose bone density, muscle mass

  • Prostate cancer- late 60s/early 70s, predisposed if obese, sedentary, poor dietary habits
  • Higher incidence in caucasians, higher mortality in african americans
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11
Q

Andropause

A

late in life, gradual
testosterone down –> decreased libido, strength, bone density, body mass
protein synthesis, CV function

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12
Q

Arteriosclerosis effects on male reproductive

A

can cause erectile dysfunction, blocks small vessels around penis

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13
Q

Ovarian cycle (days)

A
  • Follicular phase- 15 d on avg (9-23)
  • Ovulatory phase- 1-3 d, ends w ovulation
  • Luteal phase- 13 d
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14
Q

Endometrial cycle

A

AKA thickness of endometrium

  • proliferative phase (11 d, thickens, ovaries produce estrogen)
  • secretory phases (12 d, thickened, CL makes progesterone)
  • Menstrual phase (5 d, low E+P)
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15
Q

Atresia

A

6-12 follicles start to mature each month due to FSH, atresia = breakdown of all but 1

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16
Q

Role of corpus luteum

A
  • depends on LH (lutenizing homone)
  • Follicle after ovulation, provides estrogen & progesterone to implant blastocyst, maintain zygote until placenta grown
  • degenerates in 14 d (inhibin) if no fertilization
17
Q

Functions of estradiol (estrogens)

A
  • pubertal growth
  • fat deposition
  • increase vascularization of skin
  • inhibits osteoclasts
18
Q

Functions of progesterone

A
  • secretory changes in uterus

- breast development

19
Q

Perimenopause v menopause

A
  • perimenopause- changes in menstrual cycle, body temp up, sleep disturbances, anxiety, depression
  • menopause- early 50s, hot flashes, night sweats, insomnia, low libido, headaches, mood swings, vaginal dryness, bone loss
20
Q

Why use/not use hormone therapy?

A

Negative side effects- cancer, heart disease

- prescribed for maximum of 5 yrs if severe symptoms of menopause

21
Q

hCG (human chorionic gonadotropin)

A
  • produced 8-9 d after fertilization
  • maintains corpus luteum, stimulates P + E production by CL
  • stimulates testosterone production in male fetus
  • hCG receptors in endometrium can inhibit contractions produced by oxytocin
22
Q

Function of estrogens during pregnancy

A
  • estradiol produced by CL for 1st 5-6 wk stimulated by hCG, then placenta
  • increases uterine blood flow, stimulates growth of myometrium
  • growth (w progesterone) of ductal breast tissue
  • (w relaxin) softens pelvic ligaments
23
Q

Parturition - 4 phases

A

Parturition = labor

0: conception to start of labor
1: …to delivery of fetus
2: …to delivery of placenta
3: postpartum, involution of uterus

24
Q

Positive feedback theory of parturition

A

Cervical stretch by baby’s head excites fundic (uterine) contraction, et cetera

25
Q

Prolactin

A

Promotes milk secretion (along with E, P)

- suckling reflex –> hypothalamus –> PRH –> ant pituitary –> prolactin –> milk

26
Q

Colostrum

A

first milk

27
Q

4 ways to diagnose fetal well being

A
  • ultrasound- transvaginal before 10 w, then abdominal
  • amniocentesis- 14-16 wk, 20 mL fluid, DNA tests
  • chorionic villus sampling- piece of placenta if high risk
  • fetal blood sampling- from 17 wks, if high risk
28
Q

BRCA1 and BRCA2

A
  • tumor suppressor genes, repair DNA damage or get rid of unrepaired DNA
  • risk of breast and ovarian cancer much higher if mutated
  • BRCA1 worse (65% risk breast cancer, 40% ovarian cancer w gene)
29
Q

Breast cancer- ER, PR, HER2 receptor subtypes

A
  • positive= cancer uses estrogen, progesterone, or human epidermal growth factor to grow
  • HR+/HER2- most common form (73% cases), best prognosis
  • HR-/HER2- triple negative, most lethal, 13% cases, higher incidence if black
30
Q

Determining stages of breast cancer

A
  • Tumor size
  • Nodes- number + or -
  • Metastasis- automatically becomes stage 4
31
Q

Recommended age of 1st mammogram

A

50, can request earlier

32
Q

Herceptin

A
  • drug targeting HER2 (cancer cells have too many HER2 receptors)
  • 12 mo regimen, cardiotoxicity side effects interfere w compliance (monitor ejection fraction every 3 mo)
33
Q

Endocrine therapies for breast cancer

A
Antiestrogen drugs (Tamoxifen)
Aromatase inhibitors - blocks conversion of androgens to estrogen.