RED ARROWS (Robia) & UNDERLINED (Ozark) Flashcards

1
Q

Meiosis II of ovum is completed at

A

fertilization (discontinuous)

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2
Q

Spermatogenesis results in how many germ cells

A

4

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3
Q

Oogenesis restults in how many germ cells

A

1

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4
Q

Normal sperm production requires

A

reduced temp

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5
Q

What receptor (and where) is upregulated in pregnancy promote cause GERD?

A

B-receptors on LES

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6
Q

What steroid hormone peaks during labor, and promotes partuition?

A

cortisol

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7
Q

What is progesterone’s role during pregnancy?

A

maintains uterine quiescence and sustains fetus

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8
Q

What is estrogen’s role during pregnancy?

A

Promotes partuition, increases sensitivity to OXY

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9
Q

Ovary development depends on presence of

A

2x and no y

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10
Q

loss of one x results in

A

ovarian dysgenesis but no lose of female ducts or genitalia (turners)

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11
Q

How is it possible to have XX male and XY female?

A

presence or absence of XY, respectively

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12
Q

What promotes relaxin? What does it do?

A

hCG promotes relaxin. It relaxes the pelvic bones (looser)…

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13
Q

XY without SRY looks like

A

turners

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14
Q

When male hormones are absent, default is

A

female genital tract, external genitals

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15
Q

What blocks 5-alpha reductase?

A

Propecia (finesteride)

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16
Q

XO is

A

turners

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17
Q

Seminifereous tubule dysgenesis disease

A

XXY klinefelters

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18
Q

What causes male pseudohermaphroditism

A

Androgen resistance

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19
Q

Main cause of congenital adrenal hyperplasia

A

21 hydroxylase deficiency

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20
Q

21 hydroxylase deficiency main cause of

A

CAH

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21
Q

Lack cortisol/aldosterone. Main cause

A

CAH - 21 hydroxylase deficiency

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22
Q

slide 21…

A

COME BACK TO THIS

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23
Q

clitoromegaly….retention of urogenital sinus and fusion of labia…these features are exhibited in

A

female pseudohermaphroditism … virilization by androgens….

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24
Q

T to E2

A

aromatase

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25
Q

T to DHT

A

5-alpha hydroxylase (blocked by propecia, finesteride)

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26
Q

Male pattern baldness caused by

A

DHT

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27
Q

What is the function of the intercellular bridges between secondary spermatocytes?

A

Synchronizes development, sharing resources…large enough to pass organelles by MT’s

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28
Q

What’s an acrosome?

A

A cap of membrane containing digestive enzymes

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29
Q

Continuous exposure (not pulsatile) of GnRH

A

inhibitory FSH and LH release

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30
Q

What keeps T high near developing sperm?

A

ABP from sertoli cells (which are stimulated by T and FSH)

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31
Q

Paracrine inhibin from sertoli does what to leydig?

A

PROMOTES it (opposite)

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32
Q

Paracrine activin from sertoli does what to leydig?

A

INHIBITS it (opposite)

33
Q

Ovulatory phase

A

short 1-3 days, time of final oocyte maturation and release into reproductive tract. LH/FSH surge

34
Q

as the follicular phase progresses, what happens to E2?

A

E2 synthesis from ovary increases past certain threshold, and SWITCHES from negative to positive feedback at ant. pituitary: LH SURGE.

35
Q

What hormone is secreted at IMPLANTATION

A

hCG

36
Q

Theca cells are analogous to sertoli cells. What enzyme is lacking in theca cells?

A

aromatase

37
Q

Granulosa cells are analogous to leydig cells. What enzyme is not lacking?

A

aromatase. Androstenedione from theca cells can be made into E2

38
Q

Describe ovulatory mucus secretions

A

Crystalized mucus looks like “Fern”

Most “stretch”

39
Q

Female infertility quadruples between ages

A

20 and 40

40
Q

Describe the acrosomal reaction

A

spermatozoan has receptors for glycoprotein of zona pellucida, called “ZP3”. binding causes increased IP3, leading to INCREASED CALCIUM, and membrane fusion, forcing enzyme rich contents out

41
Q

Mechanism of polyspermy?

A

Sperm penetration promotes release of enzymes that harden glycoproteins of zona pellucida. Oocyte’s internal vesicles release hydrolytic enzymes that digest ZP2, altering the membrane to modified ZP3, which is HARDENED so polyspermy can’t occur

42
Q

Ca2+ increase that caused cortical reaction also triggers

A

second meiotic division of oocyte

43
Q

how many sperm actually arrive at the distal end of fallopian tube

A

50 or less

44
Q

What is the failure rate of implantation

A

70%

45
Q

What happens to the zona pellucida during adhesion of the zygote to uterine wall?

A

it dissolves

46
Q

During adhesion stage of implantation, the blastocyst secretes _____ which increases integrins in endometrial cells

A

IL1

47
Q

What does osteopontin do?

A

The embryo and the endometrium both have increased integrins. Osteopontins bridge the two integrin-rich interfaces during adhesion.

48
Q

What do stream cells do, during adhesion?

A

stromal cells form decidua and SECRETE NUTRIENTS. Later this becomes a barrier and endocrine organ.

49
Q

What is the role of the synctiotrophoblast?

A

Responsible for most endocrine functions “acts like pituitary”

50
Q

What is the role of the cytotrophoblast?

A

Secrete CRH, TRH, and somatostatin “acts like hypothalamus”

51
Q

Thick layer of well vascularized endometrium

A

ideal for implantation of embryo. Occurs during luteal phase. Maintained by progesterone from corpus luteum. If fertilization occurs, hCG from placenta maintains corpus luteum to maintain the endometrium

52
Q

hCG from placenta

A

increases by LOG SCALE (a lot) and negatively regulates pituitary release of LH/FSH so another follicle doesn’t develop

53
Q

What inhibits RPL

A

progesterone and estrogen during pregnancy, and dopamine

54
Q

What happens to the size of fetal adrenal gland, as it starts cranking out DHEA-S for estrogen synthesis?

A

grows to 20x original size

55
Q

Marker for fetal wellbeing? How is it made?

A

Estradiol.

Cholesterol from mom, is made into pregnenalone (via desmolase) in the placenta. The pregnenalone goes to the fetal adrenal gland, where it is converted to DHEA-S. DHEAS-S goes to fetal liver, where it becomes 16-OH DHEA-S. 16-OH DHEA-S then goes to the placenta, where it is made into Estriol.

Although estriol is the major estrogen during pregnancy, it has weak estrogenic activity.

56
Q

What prevents premature lactogenesis?

A

High E2/Progesterone from the fetus

57
Q

What happens to LES during pregnancy

A

decreased tone. more heartburn

58
Q

Ferguson reflex

A

More distention of cervix, more OXY release, which promotes prostaglandin release, which promotes contractions.

59
Q

Cortisol promotes

A

surfactant production in baby

60
Q

What stimulates maternal behavior during pregnancy, and after birth? OXY or prolactin?

A

prolactin

61
Q

Whale milk has what % fat?

A

40-65%

62
Q

What are the two effects of prolactin?

A

Mammogenic (breast development)

Galactogenic (milk production)

63
Q

Removing dopamine release inhibition on

A

prolactin secreting lactotrophs in anterior pituitary, promoting milk production

64
Q

What does suckling do to GnRH

A

Inhibits arcuate and POA….decrease GnRH….

65
Q
FSH stimulates which cells? Pick 2
A. Granulosa
B. Sertoli
C. Theca
E. Leydig
A

Granulosa and sertoli

66
Q

LH stimulates which cells? Pick 2

A. Granulosa
B. Sertoli
C. Theca
E. Leydig

A

C and E

67
Q

Menarche. When usually occurs?

A

(First menses): usually between 11-14 yo in USA

68
Q

What’s abnormal for menarche?

A

Menarche that’s more than 2.5 years after thelarche

69
Q

What tanner stage do you get COURSE pubic hair (both men and women)

A

3

70
Q

In the 2nd male tanner stage, testicular volume size increases by how much?

A

> 3mL

71
Q

Describe precocious puberty in women

A

younger than 6 years old

72
Q

Describe precocious puberty in men

A

younger than 9 years old

73
Q

Primary amenorrhea

A

no menses by 16, or 2.6 years after thelarche

74
Q

Secondary amenorrhea

A

absence of 3 consecutive cycles following the establishment of regular cyclic menstrual periods of 6 months of amenorrhea.

75
Q

HYPERgonadotrophic hypogonadism

A

Low E2, high LH/FSH

Eg. Turner’s

76
Q

HYPOgonadotrophic hypogonadism

A

Low E2, low LH/FSH
Eg. Kallmans
Eg. hypopituitary, infarct, stress

77
Q

Abnormal gap in tanner stages

A

> 2 tanner stage difference

78
Q

First sign of pubertal development in females

A

breast buds

79
Q

Normal cycles depend on what kind of feedback

A

positive