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Physiology II > Reproductive > Flashcards

Reproductive Flashcards

1
Q

HPG Axis

A

Hypothalamus: GnRH (Gonadotropin Releasing hormone

Anterior Pituitary: Gonadotropins - LH and FSH

Gonads: Testes - testosterone, inhibin; Estrogen - Estrogens, progestin, inhibin

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2
Q

HPG regulates

A

Gametogenesis

Hormone Secretion

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3
Q

Gonadotropin Releasing Hormone

A

Produced in the preoptic or rostrum nucleus of the hypothalamus. Stored in vesicles of the terminal axons in the median eminence.

GnRH can also be produced by neurons that originate in epithelium of the olfactory pit.

Released circhorally in to the hypothalmo-hypophyseal portal blood. The half life is less than 1 minute.

Binds to GPCR on gonadotropes and activates PLC

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4
Q

Kalimann syndrome

A

Genetic disorder in which the patient has hypogonadism and anosmia (cannot smell)

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5
Q

GnRH regulation

A

Synthesis and secretion of GnRH and are under feedback control from gonadal hormones.

Also controlled by:
Stress
Pheromones
Light/dark cycles
Kisspeptins
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6
Q

LH and FSH

A

Bind to GPCRs in the gonads to activate cAMP
LH can activate phospholipase C
General actions are meant to promote Gametogensis (FSH dominant) and gonadal hormone secretion (estrogens, progestin, testosterone) is LH dominant.

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7
Q

Control of FSH and LH

A

Secretion is by GnRH which generally has negative feedback to GnRH at the level of hypothalamus

Negative feedback is directed toward the tonic center for GnRH in the arcuate nuclei of the hypothalamus.
LH and FSH have a short feedback loop of inhibition. Estradiol and testosterone can also inhibit LH and to a less extent FSH

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8
Q

GnRH, FSH, LH in gestation

A

Male fetus: tesosterone is converted to estradiol in the brain to defiminize the GnRH surge center

Female fetus:Alpha fetal protein prevents estradiol from corssing the blood brain barrier. Allows for the development of GnRH surge center

GnRH secretion begins 4th week of gestation and levels remain low until puberty
FSH and LH secretion begins in weeks 10-12 and remains low until puberty (Peak midway through gestation and drop to low levels before birth)

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9
Q

GnRH surge center

A

Dominant in females andplays an important role in GnRH secretion during ovulation

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10
Q

GnRH, FSH, and LH in Childhood

A

Levels of FSH and LH rise gradually in childhood with FSH levels higher than LH
GnRH frequency and amplitude are low in a child and increase in the months prior to puberty

In prepubescent girls, GnRH is highly sensitive to negative regulation by estradiol
As estradiol accumulates, GnRH becomes desensitized to the inhibitory effects of estradiol
In prepubescent boys, low GnRH, LH, and FSH develop leydig and sertoli cells, but testosterone remains low because there must be a critical threshold of leydig cells to make pubertal levels of testosterone.

Pre-pubertal GnRH inhibition is highly sensitive to testosterone, as in girls.

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11
Q

FIrst kiss and kisspeptin

A

Hypothalamic neurons for kisspeptin are essential in establishing circhoral secretion of GnRH from the tonic center.
Helps establish negative feedback in adults.
Also establishes the surge center in women
Humans deficient in Kiss1r have pubertal delays

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12
Q

Senescence

A

Gradual loss of gonadal (target cell) responsiveness to gondaotropin stimulation around 40-60 years of age in both sexes

Gradual in Male and Sudden in female

Gonadotropin secretion rates increase further due to lack of negative feedback. FSH levels are higher than LH levels because a hormone called inhibin that favors FSH inhibition is lower

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13
Q

Senescence and the sexes

A

More gradual in men and may be capable into the 90s. Spermatogonia are active but FSH receptors are fewer.

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14
Q

GnRH, FSH, and LH in Puberty

A

Transition from reproductive to non-reproductive state
Defining moment of puberty is circhoral secretion of GnRH (frequency produces greater FSH and LH)
LH levels are higher than FSH levels in puberty

Stimulates the development of the GnRH tonic centers

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15
Q

Male Reproductive system

A

Regulation, synthesis and secretion of hormones
Spermatogenesis
Parasympathetic sex - controls erection
Sympathetic sex - controls emission and ejaculation

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16
Q

Male hormones and leydig cells

A

Hypothalamus makes GnRH, gonadotropes of anterior pituitary FSH, LH
Leydig cells are 20% of testes in an adult (few in childhood but many in women and children
Leydig cells express the LH receptor and produce testosterone, dihydrotestosterone, androstenedione

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17
Q

Testosterone in men and reproduction

A

testosterone and FSH are required for spermatogenesis (FSH takes importance)
Testosterone directly inhibits LH from the gonadotropes
Testosterone from leydig cells may also stimulate inhibin
Secondary sex characteristics

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18
Q

Sertoli Cells and male hormones

A

Sertoli cells express the FSH receptor and promote spermatogenesis
Produce inhibin in response to FSH stimulation

Inhibin directly inhibits FSH from gonadotropes

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19
Q

Negative feedback of sertoli cells

A

Classic feedback between Sertoli cells and anterior pituitary
FSH stimulates release of Inhibin and Inhibin suppresses FSH release

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20
Q

Inhibin cycle

A 
Decreased spermatogenesis
Decreased Inhibin
Increased secretion of FSH 
Increased spermatogenesis
Increased Inhibin 
Diminish FSH secretion 
REPEAT
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21
Q

Control of spermatogenesis

A

Not well understood
Sertoli cells contain the highest conectration of receptors for:
Androgen, Estrogen, Insulin, GH and Insulin Like Growth Factor 1, Thyroid hormones

FSH most directly controls spermatogenesis. (essential for the process during puberty)
Fetal gonadotropins transform primordial germ cells into spermatogonia in the seminiferous tubules. Spermatogonia contain FSH receptors and are activated by FSH at puberty

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22
Q

Process of spermatogenesis

A

LH stimulates leydig cells to produce testosterone

Testosterone is essential for growth metabolism and division of germ cells. Testosterone stimulates sertoli cell division. The number of sperm is directly related to the number of sertoli cells

Proliferation, differentiation and apoptosis are all affected by the actions of estradiol receptors in testes cells

FSH stimulates sertoli cells at puberty and aids in spermatogenesis
GH controls the metabolic function of testes aiding in division of spermatogonia
Sertoli cells produce androgen binding protein via FSH
ABP concentrates androgens to support spermatogenesis

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23
Q

Estradiol in males

A

Produced by leydig and sertoli and is involved in negative feedback to GnRH and LH

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24
Q

Androgen synthesis

A

95% of male androgens are synthesized by leydig cells

5% come from zona reticularis of the adrenal cortex

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25
Q

Androgen receptors

A

Bind to aromatized androgens to promote growth an development of gonads and secondary sex characteristics
Leydig cells will aromatize androgens (making testosterone, estrogens, DHT)

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26
Q

Three most active androgens in men

A

testosterone
Dihydrotestosterone: higher affinity for androgen receptor. Synthesized from testosterone in some target tissues.
Androstenedione: precursor of testosterone; 1/10 the activity

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27
Q

Transport of androgens

A

97-98% of androgens circulate in the plasma bound to sex hormone binding globulin (SHBG) or albumin. can be in blood for 30min - several hours

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28
Q

Active testosterone

A

2-3% of plasma testosterone is biologically active
Used within minutes in the target tissue
Used directly as testosterone
May be converted to dihydrotestosterone by 5-alpha reductase.

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29
Q

Excretion of testosterone

A

Converted to other metabolites. Converted in liver to DHEA and excreted through liver via bile or kidney via urine.

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30
Q

Testosterone secretion

A

Diurnal pattern
Lower plasma levels at night (8pm)
Higher plasma levels in the morning (8am)

Age patterns:
Fetal - High level related to the formation of masculine genitals; stim by hCG, SRY, etc.
Childhood - low levels with low levels of gonadotropins
Puberty - Rapid increase with the increase in GnRH and gonadotropins
Adult - Remains high and constant

Senescence - modest decline after 60
Results from Leydig cells losing responsiveness to LH
May cause loss of libido , but spermatogenesis will occur (sperm count is lower with less testosterone due to less sertoli cells)
Diurnal pattern still present

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31
Q

Mechanism of testosterone

A

Binds to cytoplasmic receptors WITHIN the cells
Enters nucleus for gene expression
Stimultes the production of protein snearly everywhere in the body
The proteins are then responsible for all occurring changes namely the expression of secondary sex characteristics.

Generally testosterone is a proliferation and differentiation hormone (especially in muscles) and has a long term effect on gene expression

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32
Q

Converting testosterone

A

In many tissues testosterone is enzymatically converted to active metabolites

Testosterone via aromatase makes estradiol (in adipose, testes, liver, brain tissue)

Testosterone via 5-alpha reductase makes dihydrotestosterone (in testes, prostate, adrenals, external genital tissue, and hair follicles and sebum)

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33
Q

Effect of taking end production androgens

A

It effectively works as a form of birth control. As GnRH is highly sensitive to the inhibitory effects of estradiol and testosterone

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34
Q

During puberty receptors

A

become desensitized due to increased concentration of testosterone and estradiol.

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35
Q

Regular circhoral expression of GnRH is established

A

At the end of puberty
Sustains a regular secretion of gonadotropins
sustains regular gonad production of sex hormone

Establishes adulthood

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36
Q

Stimulation of Kisspeptin neurons

A

can be stimulated by either testosterone or estradiol

Kiss peptin stimulation will stimulate the development of GnRH

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37
Q

Lack of kisspeptin/receptor

A

Kallman’s sydrome

Delayed onset of puberty

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38
Q

With increased testosterone in relation to FSH receptor

A

Greater Testosterone leads to more sertoli cells. Increases the metabolic capacity of sertoli. Greater density of FSH receptor and greater gametogenesis.

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39
Q

Testosterone in-utero

A

Production of testosterone begins during the 7th week. Stimulated by hCG secretion of placenta.
Supresses formation of female genital organs by expressing Wolffian ducts.
Promotes formation of male sex organs and formation of duct system.

Effect on hypothalamus to make it more “male”

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40
Q

Testosterone in puberty

A

Further growth and secretion of sex organs
Increased muscle size
Enlarges larynx and thickens vocal cords
Bone growth and closing of epiphyseal plate
Decreases growth of hair on head

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41
Q

Reproductive function of testosterone

A

Promotes secretion of male genital tract
Required for normal sex drive
Testosterone is essential for sperm maturation and semen production

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42
Q

Release of hormones in females

A

GnRH is released from the hypothalamus with the same circorhal rhythm as males
LH and FSH from the anterior pituitary that is stimulated by GnRH, will in turn stimulate estrogen and progestin in the ovary.

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43
Q

HPG activity pre-puberty

A

HPG axis is very low or inactive until puberty when pulsatile secretion of GnRH establishes gonadotropin and ovarian hormone levels sufficient to stimulate menarche

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44
Q

Progestrin/estrogen and follicular phase and luteal phase

A

Estradiol levels are low at the beginning of follicular phase and increases towards the end. Follicular phase remains high during luteal phase.
Progesterone levels rise towards the end of follicular phase. Dips and maintains high levels during follicular phase

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45
Q

During the female reproductive phase progesterone and estrogen regulate changes in

A 
Ovary
Endometrium
Secretion of GnRH 
Secretion of LH 
Secretion of FSH
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46
Q

GnRH feedback loops in females

A

GnRH from the surge center is responsive to negative feedback via estradiol (surge center release is usually low and constant with feedback)

GnRH from the surge center is stimulated by estradiol and progesterone to create a spike in LH and FSH. (late follicular phase)

LH (dominant) and FHS spike is required for ovulation

After ovulation the GnRH surge center is inhibited and LH FSH and estradiol levels decrease

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47
Q

Becoming a woman begins as a fetus

A

Fetal ovary responds to hCG, GH, and fetal gonadotropins to form oogonia and initiate the formation of primary oocytes
Granulosa cells surround the primary oocyte to form primordial follicle
All ovum are generated in the 2nd trimester, but oogenesis is suspended at prophase 1 of meiosis until puberty

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48
Q

Eggs in the ovary with age

A

Gestation: 7 million
Birth: 2 million
Puberty: 400,000
Only 400 ova released at ovulation during reproductive ages.

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49
Q

Process to progress to an antrum

A

12-20 preantral eggs enter the 65 day process to become antrum. Only one antrum will be selected to ovulate
Non-selected antrum will undergo apoptosis

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50
Q

LH spike

A

Midcycle and stimulates ovulation
Stimulates a change in the cells of the ovary to produce more lutenizing cells
This defines the luteal phase

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51
Q

Menstrual cycle phases

A

Follicular phase first

Luteal phase second

52
Q

What hormone builds with follicular phase

A

Estradiol (peaks at the end)
Switches from negative feedback in early follicular phase to positive feedback late phase due to increased concentrations
Increased sex hormone production

53
Q

Follicular phase begins with…

A

Menses
Uterine wall sloughs off
Sex hormones are very low
Gonadotropin levels are high

54
Q

Follicular phase endometrial lining will rebuild with…

A

Increased estradiol levels

Lining will reach a peak as one enters the luteal phase

55
Q

Uterine Milk

A

Produced with high levels of pregesterone during the luteal phase
Aids with implantation

56
Q

Negative feedback to positive feedback switch is accomplished by

A

Reaching peak levels of estradiol at the end of follicular stage.

57
Q

Granulosa cells

A

Surround the primary oocyte (ovum) to form primordial follicle
Protect ovum

58
Q

Primordial follicle cells are maintained throughout live by…

A

Oocyte maturation inhibitor produced by granulosa cells. Does so by preventing FSH receptor expression

59
Q

As oocyte maturation inhibitor declines…

A

Granulosa cells are able to express FSH receptor.
The more FSH receptor the better response to FSH and primordial follicle will progress to preantral follicle

Declines with high and cyclic levels of FSH (in senescence FSH levels are high but not cyclic)

60
Q

Each cycle six primordial follicles express enough _____ to become _____

A

FSH receptor
preantrum follicle

Process takes 300 days

61
Q

Preantral (primary follicle) cell

A

Has a thicker layer of granulosa cells than primordial

Progresses to antrum cells

62
Q

Antrum (secondary follicle) is characterized by ___

A

Presence of thecal cells

63
Q

Thecal cells

A

Once proliferation of granulosa cells by FSH receptor reaches a critical point thecal cells appear

Express the LH receptor

64
Q

The antrum

A

can produce sex hormones thanks to the thecal cells that differentiate at this stage. Thecal cells express LH receptor

65
Q

Thecal cell hormone production

A

Cholesterol and intracellular acetate to Pregnenolone
Pregnenolone to progesterone
Progesterone to 17a-hydroxyprogesterone

17a-hydro… to Androstenedione
Androstenedione to testosterone
Testosterone to Estradiol

Thecal cells are similar to Leydig cells in males for the ability to produce hormones

LH receptor of thecal cells of antrum is respo0nsible for the uptake of cholesterol and its metabolism to hormones

66
Q

Antrum (secondary follicle) forms __ days before ovulation

A

65

67
Q

During follicular phase thecal cells of antrum dominantly make ___

A

Estradiol

May also make low levels of progesterone and testosterone

68
Q

Inner granulosa cells of the antrum…

A

express FSH receptor and convert theca derived androsterone and tesosterone to estradiol

FSH receptor signaling increases aromatase to produce estradiol

69
Q

Estradiol production of females every month comes from

A

30-60 immature follicles with thecal cells

70
Q

Selection of dominant pre-ovulatory follicles….

A

10 days before ovulation and 2 days after the start of the cycle

FSH levels are high at this time and the selected follicle has the highest level of granulosa cell proliferation. The dominant follicle is the one that is best able to concentrate the most FSH in the antral fluid of teh antrum and foster estradiol production and proliferation

71
Q

Thecal cells of the dominant preovulatory follicle

A

Can also produce estradiol

72
Q

Dominant (graffian) follicle regulates GnRH, FSH, and LH

A

Estradiol from granulosa cells of developing follicles inhibits LH, FSH, and tonic GnRH (day 5-14)
Leads to the positive threshold
day 10-12 estradiol spike will stimulate the GnRH surge center and LH production in the gonadotropes

73
Q

Inhibin in females is made by the…

A

dominant follicle around day 10 and will decrease FSH

74
Q

Hypothesis about GnRH and LH surge

A

Estradiol increases from granulosa cells prior to ovulation, but 1-2 days before ovulation LH and FSH levels surge

Progesterone (also secreted by granulosa cells) before LH surge may be essential for the switch to positive feedback of LH by estradiol

High Estrogen may be directed at the GnRh surge center impacting amplitude and frequency

GnRH receptor # increases (by estradiol?) in the pituitary and could impact the switch

75
Q

Tertiary follicle

A

Similar to the secondary follicle

Has antral fluid. Accumulates between the oocyte and granulosa layer and has FSH receptor tht can concentrate FSH

76
Q

Dominant (graffian follicle)

A

Has a differentiation event so that granulosa cells make LH receptor and thecal cells make FSH receptor
All cell layers are now able to produce estradiol
Will also produce Inhibin to suppress FSH

77
Q

Ovulation occurs…

A

14 days after teh first day of menses

2 days before ovulation LH secretion drastically increazses

78
Q

Sweling of the dominant follicle is caused by

A

increased LH and FSH levels

Outer wall of follicle swells which creates a protrusion of the ovary
Fluid oozes and then the ovum ruptures
release of ovum and granulosa cells that are now called corona radiata

79
Q

Peak LH

A

converts granulosa cells and thecal cells to progesterone producing leutin cells and beginning the luteal phase

requires appropriate levels of estradiol

80
Q

Signs and symptoms of ovulation

A

Mittleschmertz: pain during the middle of the cycle
cervical mucous thins
Body temp rises after ovulation,,, estradiol cools the body and progesterone raises body temp
Regular monthly period
LH spike (urine ovulation predictor kits)
PMS
Serum progesterone increases (d14-21)

81
Q

Leutin cells

A

Produce low levels of inhibin that prevent FSH

If FSH is present in the luteal phase another cycle will start! (prevents fertilization)

82
Q

Luteal phase

A

Low levels FSH and LH
Pregesterone, estradiol, inhibin all inhibit gonadotropin

Small amounts of LH are required to maintain function of the corpus luteum. Keeps the leutin cells alive and producing hormones fo r12 days

83
Q

Progesteroen in luteal phase

A

produced by leutin cells
Pro-Gestation
12 days post ovulation functionality for implantation

84
Q

If not pregnant

A

Corpus luteum dies and becomes corpus albicans, scar tissue
No more sex hormone production
Pituitary will tehn secrete LH and FSH to drive the new cycle
Menstruation

85
Q

If pregnant then

A

Placenta hCG will feed the corpus luteum for the entire first trimester

86
Q

Uterine cycle

A

Fluctuation of the endometrium that coincides with the ovarian cycle
Influenced by estradiol and progesterone

87
Q

Complete lack of estrogen and progesterone

A

Seen with Corpus albicans

Leads to the destruction of the uterine lining and vasospasm

88
Q

Fibrinolysis

A

Produced during menses to prevent blood clotting

89
Q

Clots during menstruation

A

Indicates a uterine pathology

90
Q

Uterine cycle endometrium

A

High estrogen before ovulation stimulates proliferation of the endometrium (also generates mucous layer to direct sperm)

High progesterone after ovulation stimulates secretory development and activity. Secretes uterine milk to nourish a fertilized ovum before implantation. Estradiol is still present and still leads to proliferation

91
Q

Female puberty is activated by…

A

Established circorrohal expression of GnRH form HP axis.
This results in the stimulation of primordial follicles to antrum. This is a long process that in total takes a full year.
Requires ovarian production of estradiol to an amount significant enough to cause a positive switch

Menarche occurs 2 years after the activation of HPG axis

92
Q

Estrogen in menopause

A

Ovarian burnout
Insufficient follicles to be stimulated by LH and FSH

Possible to run out of estrogen because there are no granulosa cells to make aromatase

93
Q

Inhibin in menopause

A

Runout of dominant follicle and luteal cells which wil result in a sharp increase in gonadotropin with FSH levels higher than LH

94
Q

Hormones during follicular phase

A

Progesterone, androstenedione, and testosterone are synthesized first but are all converted to estradiol by aromatase

95
Q

Hormones during luteal phase

A

There is less aromatase which leads to excessive amounts of progesterone

96
Q

3 types of estrogens

A

Keep in mind that during pregnancy the placenta can ALSO produce estrogen

Estradiol

Estrone - low potency, from peripheral conversion of adrenal/ovarian testosterone

Estriol - made in the bile of the liver to be excreted to the urine

97
Q

Progestins

A

Progesterone

17-a-hydroxyprogesterone with the same effects of progesterone

98
Q

Progesterone secretion timing

A

non-pregnant: secreted in significant amounts only during the last 12 days of monthly cycle by corpus luteum

Pregnancy: Progesterone is also secreted by the placenta, especially during teh 4th month

99
Q

Transport of female sex hormone

A

Use liver-derived Sex Hormone Binding Protein

Loose binding and hormones is released to tissue after 30 minutes

100
Q

Metabolism of Female Sex Hormones

A

Liver is the primary site for degradation of ovarian steroids and secreted in bile or urine

Liver will make estriol (E3) from Estradiol (E1) or esterone (E2)
In liver disease estrogen activity increases
Progesterone is also converted to nearly inactive metabolites.

101
Q

Endocrien actions in females

A

Estradiol: generallly proliferation and differentiation and growth of genital tract

Progesterone: a secretion hormone, prepare uterus for pregnancy and breast for lactation

102
Q

Estrogen actions

A

Ovary: synergize with FSh to promote growth of granulosa cells
Uterus: thickens endometrial layer
Vagina: Stratified epithelium - resistant to trauma and infection. Makes vagina more acidic (degrades sperm outside of ovulation)
Fallopian tube: Growth of glandular and ciliated epithelial cells, promotes ciliary action

External genitalia: growth and maintenance
Breasts: Proliferate and differentiate breasts. Growth of ducts and deposition of adipose

Cervical mucous: peak estradiol. produces a less acidic musous to guide sperm in

Na and water RETENTION (peak estradiol can be associated with hypertension)

Increased thickness of skin.

Relax pelvic ligaments in pregnancy
Affects rate of early cell production in fetus
Stimulates prostoglandins

103
Q

General estrogen actions

A

General anabolic activity. Increase cell metabolism and BMR. Slight increase of body protein and deposition of subcutaneous fat

Effects skeletal growth: inhibit osteoclast and stimulate osteoblast. Aids in closure of epiphyseal plate,
With menopause and lack of estrogen osteoclasts are favored

104
Q

Estrogen excess

A

Severe cramps during menses because estrogen stimulates prostaglandins (stimulate smooth muscle contractions)
Unusually severe nausea or edema during pregnancy or menses
Enlarged uterus, uterine fibroids
Fibrocystic breast changes
Menorrhagia (heavy menses

105
Q

Estrogen deficiency

A 
Scant menses
Small uterus
Small breasts
Midcycle spotting
Infertility due to lack of ovulation
106
Q

Progesterone actions

A

Progestation
Conteract proliferative phase of estradiol and promote and secretory phase
Inhibit prostoglandin = lower levels of uterine contraction and a better chance for implantation
Promotes secretion of fallopian tube lining for nutrition of ovum
Develpment of preasts and alveoli

Increases basal body temperature

CNS effects: increased apetite, decrease in wakefullness, increased sensitivity to CO2

107
Q

Progesterone Excess

A 
Edema (due to secretion)
Bloating
Headache (Hypertension)
Depression (associated with lack of sleep)
Weight gain  
Tiredness
Hypertension, varicose veins
108
Q

Progesterone deficiency

A

Similar to symptoms of : no ovulation, endometriosis, adenomyosis, endometrial hyperplasia
Due to loack of estrogen inhibition

Prolonged menses
Heavy menses (menorrhagia)
Severe cramps
Luteal spotting (cannot lengthen luteal phase)
109
Q

Hormonal contraceptives

A

Progesterone and estradiol work on anterior pituitary to inhibit LH and FSH preventing ovulation
Progestins thicken the cervical mucous and creates a barrier to sperm. During follicular phase causes a thin endometrium to prevent implantation

110
Q

Contraceptives have 4 types

A

Progesterone only = Best for nursing mothers as estrogen can prevent milk production
Monophasic = 21 days of equal dose progestin/estrogen
Biphasic = Day 1-14 have less progestin than monophasic
Triphasic = every 5, 7. 9 days the concentration of progestin increases compared to estrogen

Biphasic and triphasic were created to allow enometrial lining to increase with lower progestin.

111
Q

Placenta derived hormones

A

hCG (Human Chorionic Gonadotropin)
Estrogens
Progesterone
hCS (Human Chorionic Somatomammotropin)

112
Q

hCG

A

Resembles LH from pituitary
Informs corpus luteum that pregnancy has occurred and prevents involution

Diabetogenic effect to direct glucose to embryo

Continues synthesis of progesterone and estrogen to:
Maintain uterine lining by inhibiting menstruation
Promote endometria growth and storage of nutrients
Suppress new follicular development

Encourages development of alveoli in maternal breasts
Encourages development of leydig cells in male fetus

weight loss but DANGEROUS

113
Q

hCG secretion

A

Secreted by syncytiotrophoblast cells into maternal fluids 2-3 days post-implantation
Measured in maternal blood and urine 8-9 days after ovulation
Used as basis for pregnancy test

Secretion rises to max
within 10-12 weeks of pregnancy
Decreases back to low level by 16-20 weeks and stays low thereafter

114
Q

hCS Pattern of secretion

A

begin in the 5th week of pregnancy
The more cells of the placenta the more hCS
Produced in proportion to the weight of the placenta
greatest concentration of all placenta-derived hormones

115
Q

hCS actions

A

partial development of the breasts
weak growth on protein tissues
Decreased insulin sensitivity and decreased glucose uptake and oxidation in the mother making more glucose available for the fetus
Promotes release of free fatty acids from fat stores for use by fetus

116
Q

Progesterone synthesis in pregnancy

A

secreted by corpus luteum for first trimester
after it is synthesized and secreted by syncytiotrophoblast of placenta
Increases 10X
From circulating maternal cholesterol
Placenta converts cholesterol to progesterone

117
Q

Progesterone action during pregnancy

A

Development of decidual cells in uterus important for nourishment of early embryo
Decreases contraction of myometrium
Aids in cell cleavage in developing embryo
Prepares breasts for lactation

118
Q

Estrogen synthesis in pregnancy

A

Produced to the sync. cells of the placenta
Synthesis requires DHEA (a weak androgen produced in materanland fetal adrenals, mostly from the fetus)
DHEA is transported to the fetal liver and then the placenta where it creates estradiol

119
Q

More Hormone actions in pregnancy

A

Anterior pituitary of mother enlarges 50% inpregnancy to accomodate CRH, TRH, and prolactin
Placenta makes CRH to enhance maternal glucocorticoid action
Enhances maternal cortisol action (diabetogenic and mobilize aa for fetus)
2X increase in aldosterone that may cause hypertension
Thyroid enlrages and incresed T4 production vic hCG

PTH increases causing increased Ca reabsorption from mom to use with fetus. Increased with lactation
Relaxin secreted by ovaries softens cervix and relaxes ligaments
Oxytocin synthesized by hypothalamus, secreted by posterior pituitary to increase uterine contraction via neurogenic stretch reflex

120
Q

Changes in mom with pregnancy

A 
Weight gain
Increase BMR (sensation of overheating)

Ca, phosphate, iron and vitamin deficiency may lead to anemia and other diseases
Cardiac output is increased
Increased BV due to aldosterone, estrogen, and excess RBC
20% greater respiratory rate (increased biodemands and progesterone increases respiratory rate)
Increased filtration rate (loss of water and electrolytes)

121
Q

Preeclampsia

A

Hypertension associated with protein in the urine
Excess salt and water retention
Impaired blood flow
Filtration rate and renal blood flow drop, despite normal tendencies to increase in pregnancy

122
Q

Possible causes of preeclampsia

A

Placental and adrenal hormones (aldosterone)
Autoimmune
Insufficient blood to placenta

123
Q

Placenta action

A

Transfer food for the baby
Diffusion of oxygen from maternal blood to fetal blood via passive diffusion (different hemoglobin that has different binding for BPG and offloading of oxygen)
Removal of CO2 from fetal tissue
During 2nd and 3rd trimester the placenta will produce steroids and hCG

124
Q

Oxytocin in third trimester

A

Receptor expression increases and allows positive feedback between oxytocin and uterine contraction
initiated by dilation of teh cervix and fetal pituitary

125
Q

Lactation

A

Extrogen will inhibit the production of milk

Prolactin aids lactation

Physiology II (4 decks)

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